TY  - JOUR
T1  - Erythropoietin Action in Stress Response, Tissue Maintenance and Metabolism
AN  - 1842512051; PQ0002450017
AB  - Erythropoietin (EPO) regulation of red blood cell production and its induction at reduced oxygen tension provides for the important erythropoietic response to ischemic stress. The cloning and production of recombinant human EPO has led to its clinical use in patients with anemia for two and half decades and has facilitated studies of EPO action. Reports of animal and cell models of ischemic stress in vitro and injury suggest potential EPO benefit beyond red blood cell production including vascular endothelial response to increase nitric oxide production, which facilitates oxygen delivery to brain, heart and other non-hematopoietic tissues. This review discusses these and other reports of EPO action beyond red blood cell production, including EPO response affecting metabolism and obesity in animal models. Observations of EPO activity in cell and animal model systems, including mice with tissue specific deletion of EPO receptor (EpoR), suggest the potential for EPO response in metabolism and disease.
JF  - International Journal of Molecular Sciences
AU  - Zhang, Yuanyuan
AU  - Wang, Li
AU  - Dey, Soumyadeep
AU  - Alnaeeli, Mawadda
AU  - Suresh, Sukanya
AU  - Rogers, Heather
AU  - Teng, Ruifeng
AU  - Noguchi, Constance Tom
AD  - Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA, connien@helix.nih.gov
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 10296
EP  - 10333
PB  - Molecular Diversity Preservation International, Matthaeusstr 11 Basel 4057 Switzerland
VL  - 15
IS  - 6
SN  - 1422-0067, 1422-0067
KW  - Toxicology Abstracts
KW  - erythropoietin
KW  - erythropoietin receptor
KW  - signal transduction
KW  - stress response
KW  - wound healing
KW  - endothelial
KW  - brain
KW  - cardiovascular
KW  - inflammation
KW  - metabolism
KW  - obesity
KW  - Heart
KW  - Obesity
KW  - Brain injury
KW  - Oxygen tension
KW  - Erythrocytes
KW  - Cloning
KW  - Brain
KW  - Animal models
KW  - Anemia
KW  - Stress
KW  - Cell culture
KW  - Ischemia
KW  - Erythropoietin
KW  - Reviews
KW  - Nitric oxide
KW  - Metabolism
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842512051?accountid=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=International+Journal+of+Molecular+Sciences&rft.atitle=Erythropoietin+Action+in+Stress+Response%2C+Tissue+Maintenance+and+Metabolism&rft.au=Zhang%2C+Yuanyuan%3BWang%2C+Li%3BDey%2C+Soumyadeep%3BAlnaeeli%2C+Mawadda%3BSuresh%2C+Sukanya%3BRogers%2C+Heather%3BTeng%2C+Ruifeng%3BNoguchi%2C+Constance+Tom&rft.aulast=Zhang&rft.aufirst=Yuanyuan&rft.date=2014-01-01&rft.volume=15&rft.issue=6&rft.spage=10296&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Molecular+Sciences&rft.issn=14220067&rft_id=info:doi/10.3390%2Fijms150610296
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Heart; Obesity; Brain injury; Oxygen tension; Erythrocytes; Anemia; Animal models; Brain; Cloning; Stress; Cell culture; Ischemia; Erythropoietin; Reviews; Nitric oxide; Metabolism
DO  - http://dx.doi.org/10.3390/ijms150610296
ER  - 



TY  - JOUR
T1  - Failure to Consider the Menstrual Cycle Phase May Cause Misinterpretation of Clinical and Research Findings of Cardiometabolic Biomarkers in Premenopausal Women
AN  - 1780522218; PQ0002856577
AB  - Biomarker assessment plays a critical role in the study and prevention of disease. However, variation in biomarkers attributable to the menstrual cycle in premenopausal women may impair understanding the role of certain biomarkers in disease development and progression. Thus, in light of the recently increasing evidence of menstrual cycle variability in multiple cardiometabolic biomarkers, a reexamination of approaches for appropriately studying and diagnosing cardiovascular disease in premenopausal women is warranted. We reviewed studies (from 1934 through 2012) evaluating changes in cardiometabolic biomarkers across phases of the menstrual cycle, including markers of oxidative stress, lipids, insulin sensitivity, and systemic inflammation. Each was observed to vary significantly during the menstrual cycle. For example, nearly twice as many women had elevated cholesterol levels warranting therapy ( greater than or equal to 200 mg/dL) during the follicular phase compared with the luteal phase (14.3% vs. 7.9%), with only 3% having consistently high levels during all phases of the cycle. Similarly, nearly twice as many women were classified as being at an elevated risk of cardiovascular disease (high sensitivity C-reactive protein >3 mg/L) during menses compared with other phases (12.3% vs. 7.4%). Menstrual cycle-associated variability in cardiometabolic biomarkers is an important source of variability that should be accounted for in both research and clinical settings.
JF  - Epidemiologic Reviews
AU  - Schisterman, Enrique F
AU  - Mumford, Sunni L
AU  - Sjaarda, Lindsey A
AD  - Correspondence to Dr. Enrique F. Schisterman, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Boulevard, Suite 7B03N, Bethesda, MD 20892.
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 71
EP  - 82
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 36
IS  - 1
SN  - 0193-936X, 0193-936X
KW  - Health & Safety Science Abstracts
KW  - biomarkers, cardiometabolic
KW  - inflammation
KW  - menstrual cycle
KW  - variability
KW  - Bioindicators
KW  - Risk assessment
KW  - Sensitivity
KW  - Lipids
KW  - Cholesterol
KW  - Insulin
KW  - Prevention
KW  - Oxidative stress
KW  - Reviews
KW  - Proteins
KW  - Cardiovascular diseases
KW  - Females
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780522218?accountid=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=Epidemiologic+Reviews&rft.atitle=Failure+to+Consider+the+Menstrual+Cycle+Phase+May+Cause+Misinterpretation+of+Clinical+and+Research+Findings+of+Cardiometabolic+Biomarkers+in+Premenopausal+Women&rft.au=Schisterman%2C+Enrique+F%3BMumford%2C+Sunni+L%3BSjaarda%2C+Lindsey+A&rft.aulast=Schisterman&rft.aufirst=Enrique&rft.date=2014-01-01&rft.volume=36&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Epidemiologic+Reviews&rft.issn=0193936X&rft_id=info:doi/10.1093%2Fepirev%2Fmxt007
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-04-01
N1  - Last updated - 2016-04-29
N1  - SubjectsTermNotLitGenreText - Risk assessment; Bioindicators; Sensitivity; Prevention; Oxidative stress; Lipids; Reviews; Proteins; Cholesterol; Females; Cardiovascular diseases; Insulin
DO  - http://dx.doi.org/10.1093/epirev/mxt007
ER  - 



TY  - JOUR
T1  - Spline interpolation for modelling of accumulated effects of ozone
AN  - 1762143372; 20670911
AB  - An alternative approach for computing exposure indices, such as AOT40 of the ground-level ozone, is considered in this paper. The aim of the study is to compare it with the traditional way of calculating the exposure indices in order to discover possible weaknesses or strengths of both approaches. The problem under consideration is of great importance when modelling results, obtained after running large-scale air pollution models, have to be compared with experimental data. Usually the data are received in a form of mesh-function. At the same time, accumulated effects have to be considered as integrals of smooth (at least continuous) functions. Cubic spline interpolation over data of ozone concentrations is considered as a tool for computing accumulated effects. Practical computations include estimations for measurements of several stations over Europe for two different years. The results obtained with the proposed procedure are compared with those achieved from the calculations according to the classical definition.
JF  - International Journal of Environment and Pollution
AU  - Chervenkov, Hristo
AU  - Dimov, Ivan
AU  - Zlatev, Zahari
AD  - Department of Meteorology, National Institute of Meteorology and Hydrology (NIMH), Bulgarian Academy of Sciences (BAS), Tsarigradsko Shose Blvd. 66, 1784 Sofia, Bulgaria
PY  - 2014
SP  - 17
EP  - 31
PB  - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom
VL  - 54
IS  - 1
SN  - 0957-4352, 0957-4352
KW  - Materials Business File (MB); Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE); ANTE: Abstracts in New Technologies and Engineering (AN)
KW  - ENERGY AND ENVIRONMENT
KW  - Environment and Sustainable Development
KW  - Air pollution
KW  - Computation
KW  - Mathematical models
KW  - Exposure
KW  - Splines
KW  - Ozone
KW  - Models
KW  - Interpolation
KW  - Yes:(AN)
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1762143372?accountid=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=International+Journal+of+Environment+and+Pollution&rft.atitle=Spline+interpolation+for+modelling+of+accumulated+effects+of+ozone&rft.au=Chervenkov%2C+Hristo%3BDimov%2C+Ivan%3BZlatev%2C+Zahari&rft.aulast=Chervenkov&rft.aufirst=Hristo&rft.date=2014-01-01&rft.volume=54&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Environment+and+Pollution&rft.issn=09574352&rft_id=info:doi/10.1504%2FIJEP.2014.064048
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Last updated - 2016-02-03
DO  - http://dx.doi.org/10.1504/IJEP.2014.064048
ER  - 



TY  - JOUR
T1  - Role of myeloid derived suppressor cells in tuberculosis infection and disease
AN  - 1753484724; 19993378
JF  - BMC Infectious Diseases
AU  - Kumar, Nathella Pavan
AU  - Sridhar, Rathinam
AU  - Banurekha, Vaithilingam V
AU  - Jawahar, Mohideen S
AU  - Nutman, Thomas B
AU  - Babu, Subash
AD  - National Institutes of Health international Center for Excellence in Research, Chennai, India
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 1
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - Suppl 3
SN  - 1471-2334, 1471-2334
KW  - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts
KW  - Infectious diseases
KW  - Human immunodeficiency virus
KW  - Mycobacterium
KW  - Tuberculosis
KW  - Suppressor cells
KW  - Infection
KW  - V 22360:AIDS and HIV
KW  - J 02500:Book & Conference Notices
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753484724?accountid=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=conference&rft.jtitle=BMC+Infectious+Diseases&rft.atitle=Role+of+myeloid+derived+suppressor+cells+in+tuberculosis+infection+and+disease&rft.au=Kumar%2C+Nathella+Pavan%3BSridhar%2C+Rathinam%3BBanurekha%2C+Vaithilingam+V%3BJawahar%2C+Mohideen+S%3BNutman%2C+Thomas+B%3BBabu%2C+Subash&rft.aulast=Kumar&rft.aufirst=Nathella&rft.date=2014-01-01&rft.volume=14&rft.issue=Suppl+3&rft.spage=O18&rft.isbn=&rft.btitle=&rft.title=BMC+Infectious+Diseases&rft.issn=14712334&rft_id=info:doi/10.1186%2F1471-2334-14-S3-O18
L2  - http://www.biomedcentral.com/1471-2334/14/S3/O18
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-01-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Infectious diseases; Suppressor cells; Tuberculosis; Infection; Mycobacterium; Human immunodeficiency virus
DO  - http://dx.doi.org/10.1186/1471-2334-14-S3-O18
ER  - 



TY  - JOUR
T1  - Precancer Risk Perceptions Predict Postcancer Subjective Well-Being
AN  - 1732826515; PQ0002227756
AB  - Objective: The present study used longitudinal data to explore whether subjective well-being in cancer survivors was related to predisease judgments of their likelihood of getting cancer. Method: Subjective well-being was assessed in terms of affective well-being (frequency of positive and negative affective states) and satisfaction with one's life overall. The sample consisted of 158 participants in the National Survey of Midlife Development in the U.S. (MIDUS) who developed cancer during the 8-10 years between the first and second waves of the survey (average time since diagnosis = 3.37 years; SD= 2.48), and 3,243 control participants who reported no history of cancer at either wave. Results: Controlling for demographic variables and well-being at Wave 1, the effect of cancer on well-being depended on whether, prior to being diagnosed, people judged themselves to be at low or high risk of cancer. For those perceiving a high risk, a cancer diagnosis had a modest but significant negative impact on affect and life satisfaction, whereas no negative impact emerged for those perceiving a low risk. Similar effects were not observed for heart attack risk perceptions, or for measures of trait optimism or depression, suggesting that the effect was domain-specific. Conclusions: Low precancer risk perceptions were associated with long-term benefits for subjective well-being in people who developed cancer.
JF  - Health Psychology
AU  - Persoskie, Alexander
AU  - Ferrer, Rebecca A
AU  - Nelson, Wendy L
AU  - Klein, William M P
AD  - National Cancer Institute, Bethesda, Maryland, persoskieai@mail.nih.gov
PY  - 2014
SP  - 1023
EP  - 1032
PB  - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States
VL  - 33
IS  - 9
SN  - 0278-6133, 0278-6133
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - risk perception
KW  - cancer
KW  - subjective well-being
KW  - resilience
KW  - optimism
KW  - Risk assessment
KW  - Demography
KW  - Health risks
KW  - Historical account
KW  - Depression
KW  - Perception
KW  - Cancer
KW  - Quality of life
KW  - H 11000:Diseases/Injuries/Trauma
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732826515?accountid=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=Precancer+Risk+Perceptions+Predict+Postcancer+Subjective+Well-Being&rft.au=Persoskie%2C+Alexander%3BFerrer%2C+Rebecca+A%3BNelson%2C+Wendy+L%3BKlein%2C+William+M+P&rft.aulast=Persoskie&rft.aufirst=Alexander&rft.date=2014-01-01&rft.volume=33&rft.issue=9&rft.spage=1023&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fhea0000074
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-11-01
N1  - Last updated - 2015-12-23
N1  - SubjectsTermNotLitGenreText - Demography; Risk assessment; Historical account; Health risks; Depression; Perception; Cancer; Quality of life
DO  - http://dx.doi.org/10.1037/hea0000074
ER  - 



TY  - JOUR
T1  - Epstein-Barr Virus Antibodies and the Risk of Associated Malignancies: Review of the Literature
AN  - 1701483205; PQ0001756125
AB  - Epstein-Barr virus (EBV), a ubiquitous herpes virus that infects 90% of humans by adulthood, is linked to the development of various cancers, including nasopharyngeal carcinoma, gastric cancer, Burkitt lymphoma, non-Hodgkin lymphoma (NHL), and Hodgkin lymphoma. We reviewed the literature published since 1980 regarding an association between antibodies against EBV proteins and the risk of EBV-associated malignancies. Immunoglobulin A antibody levels that are elevated before diagnosis have consistently been associated with the risk of nasopharyngeal carcinoma, and patients with Hodgkin lymphoma have significantly higher immunoglobulin G antibody levels than disease-free controls. However, the link between the immune response to EBV and other EBV-associated malignancies was less clear. Although evidence of an association between the risk of Burkitt lymphoma and immunoglobulin G antibodies was consistent for available studies, the sample sizes were limited. Evidence for a link between antibodies against EBV and risk of either gastric cancer or NHL was inconsistent. Future investigations should account for tumor EBV status because only 7%-10% of gastric tumors and select NHL subtypes are related to EBV infection. Comparing differences in the associations between the humoral immune response to EBV and disease risk across cancers may help elucidate how this ubiquitous virus contributes to distinct tumors globally.
JF  - American Journal of Epidemiology
AU  - Coghill, Anna E
AU  - Hildesheim, Allan
AD  - Correspondence to Dr. Anna E. Coghill, National Cancer Institute, 9609 Medical Center Drive, Rockville, MD 20892, anna.coghill@nih.gov
PY  - 2014
SP  - 687
EP  - 695
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 180
IS  - 7
SN  - 0002-9262, 0002-9262
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Risk Abstracts
KW  - Burkitt lymphoma
KW  - EBV antibodies
KW  - EBV immune response
KW  - EBV serology
KW  - gastric carcinoma
KW  - Hodgkin lymphoma
KW  - nasopharyngeal carcinoma
KW  - non-Hodgkin lymphoma
KW  - Hodgkin's disease
KW  - Herpesvirus
KW  - Infection
KW  - Herpes simplex
KW  - Non-Hodgkin's lymphoma
KW  - Burkitt's lymphoma
KW  - Epstein-Barr virus
KW  - Malignancy
KW  - Immune response (humoral)
KW  - Gastric cancer
KW  - Lymphoma
KW  - Tumors
KW  - Cancer
KW  - Health risks
KW  - Immunoglobulin A
KW  - Nasopharyngeal carcinoma
KW  - Literature reviews
KW  - Reviews
KW  - Immunoglobulin G
KW  - Proteins
KW  - Immune response
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - V 22350:Immunology
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701483205?accountid=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=Epstein-Barr+Virus+Antibodies+and+the+Risk+of+Associated+Malignancies%3A+Review+of+the+Literature&rft.au=Coghill%2C+Anna+E%3BHildesheim%2C+Allan&rft.aulast=Coghill&rft.aufirst=Anna&rft.date=2014-01-01&rft.volume=180&rft.issue=7&rft.spage=687&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu176
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-08-01
N1  - Last updated - 2015-12-23
N1  - SubjectsTermNotLitGenreText - Hodgkin's disease; Tumors; Infection; Herpes simplex; Burkitt's lymphoma; Malignancy; Immunoglobulin A; Nasopharyngeal carcinoma; Literature reviews; Immunoglobulin G; Immune response; Gastric cancer; Immune response (humoral); Non-Hodgkin's lymphoma; Health risks; Reviews; Proteins; Lymphoma; Cancer; Epstein-Barr virus; Herpesvirus
DO  - http://dx.doi.org/10.1093/aje/kwu176
ER  - 



TY  - JOUR
T1  - Reduced Cerebrospinal Fluid Levels of Brain-Derived Neurotrophic Factor Is Associated With Cognitive Impairment in Late-Life Major Depression
AN  - 1683502982
AB  - Objectives. Late-life depression (LLD) is associated with reduced neurotrophic support and abnormalities in neurodegenerative cascades. The aim of the present study is to determine the concentrations of brain-derived neurotrophic factor (BDNF), amyloid-[beta] 42, total Tau, and phosphorylated Tau in the cerebrospinal fluid (CSF) of patients with LLD and cognitive impairment compared to healthy older adults. Method. We included 25 antidepressant-free patients with LLD (10 with mild cognitive impairment [LLD + MCI] and 15 with no cognitive decline [LLD + NCD]) and 25 healthy older adults as a comparison group. Depressive symptoms were assessed by the 21-item Hamilton Depression Rating Scale (HDRS-21) and cognitive performance by a comprehensive cognitive battery. Results. Patients with LLD + MCI showed significantly lower CSF BDNF levels compared to LLD + NCD and healthy controls (p = .003). There were no significant differences in Alzheimerʼs disease-related CSF biomarkers between groups. CSF BDNF concentrations were positively correlated with Cambridge Cognitive Test (CAMCOG) scores (r = .36, p = .02). Discussion. The present study adds to the growing body of evidence that abnormalities in the BDNF system are involved in the pathophysiology of LLD. The reduction of the availability of BDNF in the central nervous system may indicate increased vulnerability to the development of several age-related neuropsychiatric disorders as well as to adverse cognitive outcomes.
JF  - The Journals of Gerontology.  Series B, Psychological Sciences and Social Sciences
AU  - Diniz, Breno S
AU  - Teixeira, Antonio L
AU  - Machado-Vieira, Rodrigo
AU  - Talib, Leda L
AU  - Radanovic, Marcia
AU  - Gattaz, Wagner F
AU  - Forlenza, Orestes V
AD  - Department of Mental Health, Faculty of Medicine, Federal University of Minas Gerais School, Av. Alfredo Balena, 190, Belo Horizonte, Minas Gerais 30130-100, Brazil; Department and Institute of Psychiatry, Faculty of Medicine, University of Sao Paulo, Brazil; National Institute of Science and Technology - Molecular Medicine (INCT-MM), Federal University of Minas Gerais, Belo Horizonte, Brazil ; Department of Internal Medicine, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil ; Department and Institute of Psychiatry, Faculty of Medicine, University of Sao Paulo, Brazil; National Institute of Mental Health (NIMH), National Institutes of Health, Bethesda, Maryland ; Department and Institute of Psychiatry, Faculty of Medicine, University of Sao Paulo, Brazil ; Department of Mental Health, Faculty of Medicine, Federal University of Minas Gerais School, Av. Alfredo Balena, 190, Belo Horizonte, Minas Gerais 30130-100, Brazil; Department and Institute of Psychiatry, Faculty of Medicine, University of Sao Paulo, Brazil; National Institute of Science and Technology - Molecular Medicine (INCT-MM), Federal University of Minas Gerais, Belo Horizonte, Brazil
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 845
EP  - 851
CY  - Washington
PB  - Oxford University Press, UK
VL  - 69
IS  - 6
SN  - 1079-5014
KW  - Gerontology And Geriatrics
KW  - Alzheimerʼs disease
KW  - Amyloid-[beta]42
KW  - BDNF
KW  - Cerebrospinal fluid
KW  - Cognition
KW  - Late-life depression
KW  - Abnormality
KW  - Nervous system
KW  - Pathophysiological aspects
KW  - Vulnerability
KW  - Elderly
KW  - Brain
KW  - Cognitive Development
KW  - Depression (Psychology)
KW  - Patients
KW  - Symptoms
KW  - Age differences
KW  - Antidepressant drugs
KW  - Biological markers
KW  - Central nervous system
KW  - Cognitive impairment
KW  - Cognitive performance
KW  - Depression
KW  - Elderly people
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683502982?accountid=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+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.atitle=Reduced+Cerebrospinal+Fluid+Levels+of+Brain-Derived+Neurotrophic+Factor+Is+Associated+With+Cognitive+Impairment+in+Late-Life+Major+Depression&rft.au=Diniz%2C+Breno+S%3BTeixeira%2C+Antonio+L%3BMachado-Vieira%2C+Rodrigo%3BTalib%2C+Leda+L%3BRadanovic%2C+Marcia%3BGattaz%2C+Wagner+F%3BForlenza%2C+Orestes+V&rft.aulast=Diniz&rft.aufirst=Breno&rft.date=2014-01-01&rft.volume=69&rft.issue=6&rft.spage=845&rft.isbn=&rft.btitle=&rft.title=The+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.issn=10795014&rft_id=info:doi/10.1093%2Fgeronb%2Fgbu096
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2015-04-15
N1  - Last updated - 2016-05-16
DO  - http://dx.doi.org/10.1093/geronb/gbu096
ER  - 



TY  - JOUR
T1  - No Impact of Lentiviral Transduction on Hematopoietic Stem/Progenitor Cell Telomere Length or Gene Expression in the Rhesus Macaque Model
AN  - 1680440786; PQ0001472073
AB  - The occurrence of clonal perturbations and leukemia in patients transplanted with gamma-retroviral (RV) vector-transduced autologous hematopoietic stem and progenitor cells (HSPCs) has stimulated extensive investigation, demonstrating that proviral insertions may perturb adjacent proto-oncogene expression. Although enhancer-deleted lentiviruses are less likely to result in insertional oncogenesis, there is evidence that they may perturb transcript splicing, and one patient with a benign clonal expansion of lentivirally transduced HPSC has been reported. The rhesus macaque model provides an opportunity for informative long-term analysis to ask whether transduction impacts on long-term HSPC properties. We used two techniques to examine whether lentivirally transduced HSPCs from eight rhesus macaques transplanted 1-13.5 years previously are perturbed at a population level, comparing telomere length as a measure of replicative history and gene expression profile of vector positive versus vector negative cells. There were no differences in telomere lengths between sorted GFP super(+) and GFP super(-) blood cells, suggesting that lentiviral (LV) transduction did not globally disrupt replicative patterns. Bone marrow GFP super(+) and GFP super(-) CD34 super(+) cells showed no differences in gene expression using unsupervised and principal component analysis. These studies did not uncover any global long-term perturbation of proliferation, differentiation, or other important functional parameters of transduced HSPCs in the rhesus macaque model.
JF  - Molecular Therapy
AU  - Sellers, Stephanie E
AU  - Dumitriu, Bogdan
AU  - Morgan, Mary J
AU  - Hughes, William M
AU  - Wu, Colin O
AU  - Raghavarchari, Nalini
AU  - Yang, Yanqin
AU  - Uchida, Naoya
AU  - Tisdale, John F
AU  - An, Dong S
AD  - Hematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 52
EP  - 58
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 22
IS  - 1
SN  - 1525-0016, 1525-0016
KW  - Virology & AIDS Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Autografts
KW  - Tumorigenesis
KW  - Bone marrow
KW  - Transcription
KW  - CD34 antigen
KW  - Expression vectors
KW  - Gene expression
KW  - Differentiation
KW  - Telomeres
KW  - Leukemia
KW  - Splicing
KW  - Stem cells
KW  - Lentivirus
KW  - Principal components analysis
KW  - Hemopoiesis
KW  - Macaca mulatta
KW  - Population levels
KW  - Blood cells
KW  - Proto-oncogenes
KW  - Benign
KW  - G 07730:Development & Cell Cycle
KW  - W 30920:Tissue Engineering
KW  - V 22370:Oncology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680440786?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=No+Impact+of+Lentiviral+Transduction+on+Hematopoietic+Stem%2FProgenitor+Cell+Telomere+Length+or+Gene+Expression+in+the+Rhesus+Macaque+Model&rft.au=Sellers%2C+Stephanie+E%3BDumitriu%2C+Bogdan%3BMorgan%2C+Mary+J%3BHughes%2C+William+M%3BWu%2C+Colin+O%3BRaghavarchari%2C+Nalini%3BYang%2C+Yanqin%3BUchida%2C+Naoya%3BTisdale%2C+John+F%3BAn%2C+Dong+S&rft.aulast=Sellers&rft.aufirst=Stephanie&rft.date=2014-01-01&rft.volume=22&rft.issue=1&rft.spage=52&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2013.168
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-05-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Autografts; Tumorigenesis; Bone marrow; Transcription; CD34 antigen; Gene expression; Expression vectors; Leukemia; Telomeres; Differentiation; Stem cells; Splicing; Principal components analysis; Hemopoiesis; Population levels; Blood cells; Proto-oncogenes; Benign; Lentivirus; Macaca mulatta
DO  - http://dx.doi.org/10.1038/mt.2013.168
ER  - 



TY  - JOUR
T1  - National Library of Medicine Disaster Information Management Research Center: Achieving the vision, 2010-2013
AN  - 1680140076; 201503986
AB  - From 2010 to 2013, the National Library of Medicine (NLM) Disaster Information Management Research Center (DIMRC) continued to build its programs and services on the foundation laid in its starting years, 20082010. Prior to 2008, NLM had a long history of providing health information, training, and tools in response to disasters. Aware of this legacy, the NLM long range plan (Charting a Course for the 21st Century: NLM's Long Range Plan 20062016) called for creation of a center to show a strong commitment to disaster remediation and to provide a platform for demonstrating how libraries and librarians can be part of the solution to this national problem. NLM is continuing efforts to ensure that medical libraries have plans for the continuity of their operations, librarians are trained to understand their roles in preparedness and response, online disaster health information resources are available for many audiences and in multiple formats, and research is conducted on tools to enhance the exchange of critical information during and following disasters. This paper describes the 2010-2013 goals and activities of DIMRC and its future plans. Adapted from the source document.
JF  - Information Services & Use
AU  - Love, Cynthia B
AU  - Arnesen, Stacey J
AU  - Phillips, Steven J
AU  - Windom, Robert E
AD  - Disaster Information Management Research Center, Specialized Information Services Division, National Library of Medicine, National Institutes of Health, U.S. Department of Health and Human Services, Bethesda, MD, USA
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 149
EP  - 170
PB  - IOS Press, Amsterdam, The Netherlands
VL  - 34
IS  - 1-2
SN  - 0167-5265, 0167-5265
KW  - National Library of Medicine
KW  - Disaster Information Management Research Center
KW  - history
KW  - preparedness
KW  - response
KW  - recovery
KW  - medicine
KW  - disasters
KW  - public health emergencies
KW  - emergency management
KW  - libraries
KW  - librarians
KW  - informationists
KW  - Bethesda Hospitals' Emergency Preparedness Partnership
KW  - hazards
KW  - databases
KW  - Internet
KW  - Web
KW  - research and development
KW  - WISER
KW  - REMM
KW  - CHEMM
KW  - Disaster Lit
KW  - Resource Guide for Disaster Medicine and Public Health
KW  - Resource Guide for Public Health Preparedness
KW  - National Network of Libraries of Medicine
KW  - NN/LM
KW  - Research centers
KW  - National libraries
KW  - Disasters
KW  - Medical libraries
KW  - article
KW  - 3.19: SCIENCE, TECHNOLOGY, MEDICINE LIBRARIES
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680140076?accountid=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=Information+Services+%26+Use&rft.atitle=National+Library+of+Medicine+Disaster+Information+Management+Research+Center%3A+Achieving+the+vision%2C+2010-2013&rft.au=Love%2C+Cynthia+B%3BArnesen%2C+Stacey+J%3BPhillips%2C+Steven+J%3BWindom%2C+Robert+E&rft.aulast=Love&rft.aufirst=Cynthia&rft.date=2014-01-01&rft.volume=34&rft.issue=1-2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Information+Services+%26+Use&rft.issn=01675265&rft_id=info:doi/
LA  - English
DB  - Library & Information Science Abstracts (LISA)
N1  - Date revised - 2015-06-01
N1  - Last updated - 2016-09-27
N1  - CODEN - ISUSDX
N1  - SubjectsTermNotLitGenreText - Research centers; National libraries; Disasters; Medical libraries
ER  - 



TY  - JOUR
T1  - Using the Internet to Seek Information About Genetic and Rare Diseases: A Case Study Comparing Data From 2006 and 2011
AN  - 1665171201
AB  - The Genetic and Rare Disease Information Center (GARD) is a major provider of Web-based information on genetic and rare diseases. Little is known about the type of Web-based information individuals seek about genetic and rare diseases or their reasons for seeking. The objective of this paper is to describe the types of Web-based information sought about genetic and rare diseases and the reasons for seeking it from GARD by examining inquiries from 2006 and 2011. Findings from this study indicate that lay people contacting a genetic and rare disease information center most often seek information about disease prognosis, finding a specialist, and obtaining a diagnosis for symptoms. Unique characteristics of individuals searching the Internet for genetic and rare diseases information, includes a growing interest in participating in clinical research studies and a desire to supplement or better understand information discussed during a visit with a health care provider. These efforts represent advancements in patient self-advocacy.
JF  - Journal of Medical Internet Research
AU  - Morgan, Tamandra
AU  - Schmidt, Johanna
AU  - Haakonsen, Christy
AU  - Lewis, Janine
AU  - Della Rocca, Maria
AU  - Morrison, Stephanie
AU  - Biesecker, Barbara
AU  - Kaphingst, Kimberly A
AD  - ICE International, 530 Gaither Road, Rockville, MD, United States ; Childrenʼs National Medical Center, Washington, DC, United States ; The Harvey Institute for Human Genetics, Baltimore, MD, United States ; ICF International, Rockville, MD, United States ; National Human Genome Research Institute, Bethesda, MD, United States ; Washington University School of Medicine, St Louis, MO, United States ; ICE International, 530 Gaither Road, Rockville, MD, United States
Y1  - 2014
PY  - 2014
DA  - 2014
CY  - Toronto
PB  - Gunther Eysenbach MD MPH, Associate Professor
VL  - 16
IS  - 2
SN  - 1438-8871
KW  - Medical Sciences--Computer Applications
KW  - rare disease
KW  - genetic disease
KW  - patient education
KW  - information seeking
KW  - Internet use
KW  - Lay people
KW  - Desire
KW  - Genetic factors
KW  - Diagnosis
KW  - Health care
KW  - Clinical research
KW  - Advocacy
KW  - Prognosis
KW  - Computer based
KW  - Internet
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665171201?accountid=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+Medical+Internet+Research&rft.atitle=Using+the+Internet+to+Seek+Information+About+Genetic+and+Rare+Diseases%3A+A+Case+Study+Comparing+Data+From+2006+and+2011&rft.au=Morgan%2C+Tamandra%3BSchmidt%2C+Johanna%3BHaakonsen%2C+Christy%3BLewis%2C+Janine%3BDella+Rocca%2C+Maria%3BMorrison%2C+Stephanie%3BBiesecker%2C+Barbara%3BKaphingst%2C+Kimberly+A&rft.aulast=Morgan&rft.aufirst=Tamandra&rft.date=2014-01-01&rft.volume=16&rft.issue=2&rft.spage=%5Bnp%5D&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Internet+Research&rft.issn=14388871&rft_id=info:doi/10.2196%2Fresprot.2916
LA  - eng
DB  - Applied Social Sciences Index & Abstracts (ASSIA); Library & Information Science Abstracts (LISA)
N1  - Date revised - 2015-01-09
N1  - Last updated - 2015-05-01
N1  - SubjectsTermNotLitGenreText - Advocacy; Clinical research; Computer based; Desire; Diagnosis; Genetic factors; Health care; Internet; Lay people; Prognosis
DO  - http://dx.doi.org/10.2196/resprot.2916
ER  - 



TY  - JOUR
T1  - Collaborative Biomedicine in the Age of Big Data: The Case of Cancer
AN  - 1665167127
AB  - Biomedicine is undergoing a revolution driven by high throughput and connective computing that is transforming medical research and practice. Using oncology as an example, the speed and capacity of genomic sequencing technologies is advancing the utility of individual genetic profiles for anticipating risk and targeting therapeutics. The goal is to enable an era of "P4" medicine that will become increasingly more predictive, personalized, preemptive, and participative over time. This vision hinges on leveraging potentially innovative and disruptive technologies in medicine to accelerate discovery and to reorient clinical practice for patient-centered care. Based on a panel discussion at the Medicine 2.0 conference in Boston with representatives from the National Cancer Institute, Moffitt Cancer Center, and Stanford University School of Medicine, this paper explores how emerging sociotechnical frameworks, informatics platforms, and health-related policy can be used to encourage data liquidity and innovation. This builds on the Institute of Medicine€™s vision for a "rapid learning health care system" to enable an open source, population-based approach to cancer prevention and control.
JF  - Journal of Medical Internet Research
AU  - Shaikh, Abdul R
AU  - Butte, Atul J
AU  - Schully, Sheri D
AU  - Dalton, William S
AU  - Khoury, Muin J
AU  - Hesse, Bradford W
AD  - PricewaterhouseCoopers LLP 1800 Tysons Boulevard, McLean, VA, 22102, United States ; Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, United States ; Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, United States ; DeBartolo Family Personalized Medicine Institute at the Moffitt Cancer Center, Moffitt Cancer Center, Tampa, FL, United States ; PricewaterhouseCoopers LLP 1800 Tysons Boulevard, McLean, VA, 22102, United States
Y1  - 2014
PY  - 2014
DA  - 2014
CY  - Toronto
PB  - Gunther Eysenbach MD MPH, Associate Professor
VL  - 16
IS  - 4
SN  - 1438-8871
KW  - Medical Sciences--Computer Applications
KW  - biomedical research
KW  - crowdsourcing
KW  - health information technology
KW  - innovation
KW  - precision medicine
KW  - Learning
KW  - Health care
KW  - Medical research
KW  - Innovation
KW  - Clinical practice
KW  - Biomedicine
KW  - Oncology
KW  - Discovery
KW  - Individualized
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665167127?accountid=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+Medical+Internet+Research&rft.atitle=Collaborative+Biomedicine+in+the+Age+of+Big+Data%3A+The+Case+of+Cancer&rft.au=Shaikh%2C+Abdul+R%3BButte%2C+Atul+J%3BSchully%2C+Sheri+D%3BDalton%2C+William+S%3BKhoury%2C+Muin+J%3BHesse%2C+Bradford+W&rft.aulast=Shaikh&rft.aufirst=Abdul&rft.date=2014-01-01&rft.volume=16&rft.issue=4&rft.spage=%5Bnp%5D&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Internet+Research&rft.issn=14388871&rft_id=info:doi/10.2196%2Fjmir.2496
LA  - eng
DB  - Applied Social Sciences Index & Abstracts (ASSIA); Library & Information Science Abstracts (LISA)
N1  - Name - National Cancer Institute; Stanford University School of Medicine
N1  - Date revised - 2015-01-09
N1  - Last updated - 2015-05-01
N1  - SubjectsTermNotLitGenreText - Biomedicine; Cancer; Clinical practice; Discovery; Health care; Individualized; Innovation; Learning; Medical research; Oncology
DO  - http://dx.doi.org/10.2196/jmir.2496
ER  - 



TY  - JOUR
T1  - Older Adult Experience of Online Diagnosis: Results From a Scenario-Based Think-Aloud Protocol
AN  - 1665159936
AB  - Searching for online information to interpret symptoms is an increasingly prevalent activity among patients, even among older adults. As older adults typically have complex health care needs, their risk of misinterpreting symptoms via online self-diagnosis may be greater. The intent of the study was to describe the processes that a sample of older adults may use to diagnose symptoms online as well as the processes that predict accurate diagnosis. Older adult participants tended to rely on matching strategies to interpret symptoms, but many still utilized existing medical knowledge and previous illness experiences as a guide for diagnosis. Many participants also had difficulty navigating the Internet tools, which suggests an increased need for navigation aids in Web design. Furthermore, participants who were inaccurate in their diagnosis had more difficulty with the Internet tools and confusion with the task than those who were accurate. Future work in this area may want to utilize additional study design such as eye-tracking to further understand the coordination between Web navigation, online symptom information processing, and diagnostic strategies.
JF  - Journal of Medical Internet Research
AU  - Luger, Tana M
AU  - Houston, Thomas K
AU  - Suls, Jerry
AD  - eHealth Quality Enhancement Research Initiative, Center for Healthcare Organization and Implementation Research, Edith Nourse Rogers Memorial Veteranʼs Hospital, Building 70 (152), 200 Springs Road, Bedford, MA, 01730, United States ; eHealth Quality Enhancement Research Initiative, Center for Healthcare Organization and Implementation Research, Edith Nourse Rogers Memorial Veteranʼs Hospital, Bedford, MA, United States; Health Informatics and Implementation Science, Quantitative Health Sciences, University of Massachusetts Medical School, Worcester, MA, United States ; Behavioral Research Program, National Cancer Institute, Bethesda, MD, United States ; eHealth Quality Enhancement Research Initiative, Center for Healthcare Organization and Implementation Research, Edith Nourse Rogers Memorial Veteranʼs Hospital, Building 70 (152), 200 Springs Road, Bedford, MA, 01730, United States
Y1  - 2014
PY  - 2014
DA  - 2014
CY  - Toronto
PB  - Gunther Eysenbach MD MPH, Associate Professor
VL  - 16
IS  - 1
SN  - 1438-8871
KW  - Medical Sciences--Computer Applications
KW  - information seeking behavior
KW  - Internet
KW  - age factors
KW  - Symptoms
KW  - Elderly people
KW  - Diagnostic testing
KW  - Coordination
KW  - Diagnosis
KW  - Health care
KW  - Information processing
KW  - Confusion
KW  - Navigation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665159936?accountid=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+Medical+Internet+Research&rft.atitle=Older+Adult+Experience+of+Online+Diagnosis%3A+Results+From+a+Scenario-Based+Think-Aloud+Protocol&rft.au=Luger%2C+Tana+M%3BHouston%2C+Thomas+K%3BSuls%2C+Jerry&rft.aulast=Luger&rft.aufirst=Tana&rft.date=2014-01-01&rft.volume=16&rft.issue=1&rft.spage=%5Bnp%5D&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Internet+Research&rft.issn=14388871&rft_id=info:doi/10.2196%2Fjmir.2924
LA  - eng
DB  - Applied Social Sciences Index & Abstracts (ASSIA); Library & Information Science Abstracts (LISA)
N1  - Date revised - 2015-01-09
N1  - Last updated - 2015-05-01
N1  - SubjectsTermNotLitGenreText - Confusion; Coordination; Diagnosis; Diagnostic testing; Elderly people; Health care; Information processing; Internet; Navigation; Symptoms
DO  - http://dx.doi.org/10.2196/jmir.2924
ER  - 



TY  - JOUR
T1  - The pathophysiology of extracellular hemoglobin associated with enhanced oxidative reactions.
AN  - 1652446584; 25642190
AB  - Hemoglobin (Hb) continuously undergoes autoxidation producing superoxide which dismutates into hydrogen peroxide (H2O2) and is a potential source for subsequent oxidative reactions. Autoxidation is most pronounced under hypoxic conditions in the microcirculation and for unstable dimers formed at reduced Hb concentrations. In the red blood cell (RBC), oxidative reactions are inhibited by an extensive antioxidant system. For extracellular Hb, whether from hemolysis of RBCs and/or the infusion of Hb-based blood substitutes, the oxidative reactions are not completely neutralized by the available antioxidant system. Un-neutralized H2O2 oxidizes ferrous and ferric Hbs to Fe(IV)-ferrylHb and OxyferrylHb, respectively. FerrylHb further reacts with H2O2 producing heme degradation products and free iron. OxyferrylHb, in addition to Fe(IV) contains a free radical that can undergo additional oxidative reactions. Fe(III)Hb produced during Hb autoxidation also readily releases heme, an additional source for oxidative stress. These oxidation products are a potential source for oxidative reactions in the plasma, but to a greater extent when the lower molecular weight Hb dimers are taken up into cells and tissues. Heme and oxyferryl have been shown to have a proinflammatory effect further increasing their potential for oxidative stress. These oxidative reactions contribute to a number of pathological situations including atherosclerosis, kidney malfunction, sickle cell disease, and malaria. The toxic effects of extracellular Hb are of particular concern with hemolytic anemia where there is an increase in hemolysis. Hemolysis is further exacerbated in various diseases and their treatments. Blood transfusions are required whenever there is an appreciable decrease in RBCs due to hemolysis or blood loss. It is, therefore, essential that the transfused blood, whether stored RBCs or the blood obtained by an Autologous Blood Recovery System from the patient, do not further increase extracellular Hb.
JF  - Frontiers in physiology
AU  - Rifkind, Joseph M
AU  - Mohanty, Joy G
AU  - Nagababu, Enika
AD  - Molecular Dynamics Section, Laboratory of Molecular Gerontology, National Institute on Aging Baltimore, MD, USA ; Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions Baltimore, MD, USA. ; Molecular Dynamics Section, Laboratory of Molecular Gerontology, National Institute on Aging Baltimore, MD, USA. ; Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions Baltimore, MD, USA.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 500
VL  - 5
KW  - oxidative reactions
KW  - proinflammatory reactions
KW  - heme
KW  - hydrogen peroxide
KW  - Fe(IV)hemoglobins
KW  - hemoglobin autoxidation
KW  - extracellular hemoglobin
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652446584?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Frontiers+in+physiology&rft.atitle=The+pathophysiology+of+extracellular+hemoglobin+associated+with+enhanced+oxidative+reactions.&rft.au=Rifkind%2C+Joseph+M%3BMohanty%2C+Joy+G%3BNagababu%2C+Enika&rft.aulast=Rifkind&rft.aufirst=Joseph&rft.date=2014-01-01&rft.volume=5&rft.issue=&rft.spage=500&rft.isbn=&rft.btitle=&rft.title=Frontiers+in+physiology&rft.issn=&rft_id=info:doi/10.3389%2Ffphys.2014.00500
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-02-02
N1  - Date created - 2015-02-02
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.3389/fphys.2014.00500
ER  - 



TY  - JOUR
T1  - Effect of elevated oxygen concentration on bacteria, yeasts, and cells propagated for production of biological compounds
AN  - 1647026390; 21316107
AB  - The response of bacteria, yeast, and mammalian and insects cells to oxidative stress is a topic that has been studied for many years. However, in most the reported studies, the oxidative stress was caused by challenging the organisms with H sub(2)O sub(2) and redox-cycling drugs, but not by subjecting the cells to high concentrations of molecular oxygen. In this review we summarize available information about the effect of elevated oxygen concentrations on the physiology of microorganisms and cells at various culture conditions. In general, increased oxygen concentrations promote higher leakage of reactive oxygen species (superoxide and H sub(2)O sub(2)) from the respiratory chain affecting metalloenzymes and DNA that in turn cause impaired growth and elevated mutagenesis. To prevent the potential damage, the microorganisms and cells respond by activating antioxidant defenses and repair systems. This review described the factors that affect growth properties and metabolism at elevated oxygen concentrations that cells may be exposed to, in bioreactor sparged with oxygen enriched air which could affect the yield and quality of the recombinant proteins produced by high cell density schemes.
JF  - Microbial Cell Factories
AU  - Baez, Antonino
AU  - Shiloach, Joseph
AD  - Biotechnology Core Laboratory, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda 20892, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 181
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1475-2859, 1475-2859
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts
KW  - Hyperoxia
KW  - Oxidative stress
KW  - ROS
KW  - Protein oxidation
KW  - SOD activity
KW  - Hyperoxygenation
KW  - Leakage
KW  - Antioxidants
KW  - Cell density
KW  - Cell culture
KW  - Mutagenesis
KW  - Reactive oxygen species
KW  - Hydrogen peroxide
KW  - Insect cells
KW  - Bioreactors
KW  - Reviews
KW  - Superoxide
KW  - Microorganisms
KW  - DNA
KW  - Electron transport
KW  - Drugs
KW  - Metabolism
KW  - J 02410:Animal Diseases
KW  - W 30950:Waste Treatment & Pollution Clean-up
KW  - A 01450:Environmental Pollution & Waste Treatment
KW  - K 03310:Genetics & Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647026390?accountid=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=Microbial+Cell+Factories&rft.atitle=Effect+of+elevated+oxygen+concentration+on+bacteria%2C+yeasts%2C+and+cells+propagated+for+production+of+biological+compounds&rft.au=Baez%2C+Antonino%3BShiloach%2C+Joseph&rft.aulast=Baez&rft.aufirst=Antonino&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Microbial+Cell+Factories&rft.issn=14752859&rft_id=info:doi/10.1186%2Fs12934-014-0181-5
L2  - http://www.microbialcellfactories.com/content/13/1/181
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Number of references - 68
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Antioxidants; Leakage; Cell density; Cell culture; Mutagenesis; Reactive oxygen species; Hydrogen peroxide; Oxidative stress; Superoxide; Reviews; Bioreactors; Insect cells; DNA; Microorganisms; Electron transport; Drugs; Metabolism
DO  - http://dx.doi.org/10.1186/s12934-014-0181-5
ER  - 



TY  - JOUR
T1  - In vitro Screening of Compounds against Laboratory and Field Isolates of Human Hookworm Reveals Quantitative Differences in Anthelmintic Susceptibility
AN  - 1647024265; 21172693
AB  - A panel of 80 compounds was screened for anthelmintic activity against a laboratory strain of Ancylostoma ceylanicum and field isolates of hookworm obtained from school children in the Kintampo North District of the Brong Ahafo Region of Ghana. Although the laboratory strain of A. ceylanicum was more susceptible to the compounds tested than the field isolates of hookworm, a twofold increase in compound concentration resulted in comparable egg hatch percent inhibition for select compounds. These data provide evidence that the efficacy of anthelmintic compounds may be species-dependent and that field and laboratory strains of hookworm differ in their sensitivities to the anthelmintics tested. These data also suggest that both compound concentration and hookworm species must be considered when screening to identify novel anthelmintic compounds.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Treger, Rebecca S
AU  - Otchere, Joseph
AU  - Keil, Martin F
AU  - Quagraine, Josephine E
AU  - Rai, Ganesha
AU  - Mott, Bryan T
AU  - Humphries, Debbie L
AU  - Wilson, Michael
AU  - Cappello, Michael
AU  - Vermeire, Jon J
AD  - Department of Pediatrics and Program in International Child Health, Yale University School of Medicine, New Haven, Connecticut; Noguchi Memorial Institute for Medical Research, University of Ghana, Legon, Ghana; Chemical Genomics Center, National Institutes of Health, Bethesda, Maryland; Yale School of Public Health, Yale University, New Haven, Connecticut, jon.vermeire@yale.edu
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 71
EP  - 74
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 90
IS  - 1
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  - Screening
KW  - Ghana
KW  - Data processing
KW  - Children
KW  - Hygiene
KW  - Education establishments
KW  - K 03400:Human Diseases
KW  - Q5 08504:Effects on organisms
KW  - J 02400:Human Diseases
KW  - Q1 08102:Institutes and organizations
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647024265?accountid=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=In+vitro+Screening+of+Compounds+against+Laboratory+and+Field+Isolates+of+Human+Hookworm+Reveals+Quantitative+Differences+in+Anthelmintic+Susceptibility&rft.au=Treger%2C+Rebecca+S%3BOtchere%2C+Joseph%3BKeil%2C+Martin+F%3BQuagraine%2C+Josephine+E%3BRai%2C+Ganesha%3BMott%2C+Bryan+T%3BHumphries%2C+Debbie+L%3BWilson%2C+Michael%3BCappello%2C+Michael%3BVermeire%2C+Jon+J&rft.aulast=Treger&rft.aufirst=Rebecca&rft.date=2014-01-01&rft.volume=90&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0547
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-10-26
N1  - SubjectsTermNotLitGenreText - Screening; Hygiene; Education establishments; Data processing; Children; Ghana
DO  - http://dx.doi.org/10.4269/ajtmh.12-0547
ER  - 



TY  - JOUR
T1  - Association Between Stool Enteropathogen Quantity and Disease in Tanzanian Children Using TaqMan Array Cards: A Nested Case-Control Study
AN  - 1647024235; 21172703
AB  - Etiologic studies of diarrhea are limited by uneven diagnostic methods and frequent asymptomatic detection of enteropathogens. Polymerase chain reaction-based stool pathogen quantification may help distinguish clinically significant infections. We performed a nested case-control study of diarrhea in infants from a community-based birth cohort in Tanzania. We tested 71 diarrheal samples and pre-diarrheal matched controls with a laboratory-developed TaqMan Array Card for 19 enteropathogens. With qualitative detection, no pathogens were significantly associated with diarrhea. When pathogen quantity was considered, rotavirus (odds ratio [OR] = 2.70 per log sub(10) increase, P < 0.001), astrovirus (OR = 1.49, P = 0.01), and Shigella/enteroinvasive Escherichia coli (OR = 1.47, P = 0.04) were associated with diarrhea. Enterotoxigenic E. coli (0.15 SD decline in length-for-age z score after 3 months per log sub(10) increase, P < 0.001) and Campylobacter jejuni/C. coli (0.11 SD decline, P = 0.003) in pre-diarrheal stools were associated with poor linear growth. Quantitative analysis can help refine the association between enteropathogens and disease in endemic settings.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Platts-Mills, James A
AU  - Gratz, Jean
AU  - Mduma, Esto
AU  - Svensen, Erling
AU  - Amour, Caroline
AU  - Liu, Jie
AU  - Maro, Athanasia
AU  - Saidi, Queen
AU  - Swai, Ndealilia
AU  - Kumburu, Happiness
AU  - McCormick, Benjamin J J
AU  - Kibiki, Gibson
AU  - Houpt, Eric R
AD  - Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia, Charlottesville, Virginia; Haydom Lutheran Hospital, Haydom, Tanzania; Kilimanjaro Clinical Research Institute, Moshi, Tanzania; Fogarty International Center, National Institutes of Health, Bethesda, Maryland, erh6k@virginia.edu
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 133
EP  - 138
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 90
IS  - 1
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Health & Safety Science Abstracts
KW  - Rotavirus
KW  - Tanzania
KW  - Diarrhea
KW  - Community involvement
KW  - Quantitative analysis
KW  - Shigella
KW  - Pathogens
KW  - Infection
KW  - Children
KW  - Astrovirus
KW  - Campylobacter jejuni
KW  - Escherichia coli
KW  - Feces
KW  - Infants
KW  - K 03300:Methods
KW  - J 02400:Human Diseases
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647024235?accountid=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=Association+Between+Stool+Enteropathogen+Quantity+and+Disease+in+Tanzanian+Children+Using+TaqMan+Array+Cards%3A+A+Nested+Case-Control+Study&rft.au=Platts-Mills%2C+James+A%3BGratz%2C+Jean%3BMduma%2C+Esto%3BSvensen%2C+Erling%3BAmour%2C+Caroline%3BLiu%2C+Jie%3BMaro%2C+Athanasia%3BSaidi%2C+Queen%3BSwai%2C+Ndealilia%3BKumburu%2C+Happiness%3BMcCormick%2C+Benjamin+J+J%3BKibiki%2C+Gibson%3BHoupt%2C+Eric+R&rft.aulast=Platts-Mills&rft.aufirst=James&rft.date=2014-01-01&rft.volume=90&rft.issue=1&rft.spage=133&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0439
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Diarrhea; Pathogens; Children; Infection; Feces; Infants; Community involvement; Quantitative analysis; Rotavirus; Astrovirus; Campylobacter jejuni; Escherichia coli; Shigella; Tanzania
DO  - http://dx.doi.org/10.4269/ajtmh.13-0439
ER  - 



TY  - JOUR
T1  - Schistosomiasis Elimination Strategies and Potential Role of a Vaccine in Achieving Global Health Goals
AN  - 1647024189; 21172713
AB  - In March 2013, the National Institute of Allergy and Infectious Diseases and the Bill and Melinda Gates Foundation co-sponsored a meeting entitled "Schistosomiasis Elimination Strategy and Potential Role of a Vaccine in Achieving Global Health Goals" to discuss the potential role of schistosomiasis vaccines and other tools in the context of schistosomiasis control and elimination strategies. It was concluded that although schistosomiasis elimination in some focal areas may be achievable through current mass drug administration programs, global control and elimination will face several significant scientific and operational challenges, and will require an integrated approach with other, additional interventions. These challenges include vector (snail) control; environmental modification; water, sanitation, and hygiene; and other future innovative tools such as vaccines. Defining a clear product development plan that reflects a vaccine strategy as complementary to the existing control programs to combat different forms of schistosomiasis will be important to develop a vaccine effectively.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Mo, Annie X
AU  - Agosti, Jan M
AU  - Walson, Judd L
AU  - Hall, B Fenton
AU  - Gordon, Lance
AD  - Neglected Infectious Diseases, Global Health, Infectious Diseases, Bill and Melinda Gates Foundation, Seattle, Washington; Departments of Global Health, Medicine, Pediatrics, Epidemiology, University of Washington, Seattle, Washington; Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institute of Health, 6610 Rockledge Drive, Bethesda, MD 20892, annie.mo@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 54
EP  - 60
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 90
IS  - 1
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Health & Safety Science Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW  - Disease control
KW  - Intervention
KW  - Hosts
KW  - Allergies
KW  - Environmental factors
KW  - Product development
KW  - Public health
KW  - Allergic reactions
KW  - Hypersensitivity
KW  - Sanitation
KW  - Infectious diseases
KW  - Schistosoma
KW  - Drugs
KW  - Innovations
KW  - Control programs
KW  - Schistosomiasis
KW  - Vaccines
KW  - Hygiene
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - K 03450:Ecology
KW  - H 4000:Food and Drugs
KW  - J 02450:Ecology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647024189?accountid=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=Schistosomiasis+Elimination+Strategies+and+Potential+Role+of+a+Vaccine+in+Achieving+Global+Health+Goals&rft.au=Mo%2C+Annie+X%3BAgosti%2C+Jan+M%3BWalson%2C+Judd+L%3BHall%2C+B+Fenton%3BGordon%2C+Lance&rft.aulast=Mo&rft.aufirst=Annie&rft.date=2014-01-01&rft.volume=90&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0467
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Allergic reactions; Infectious diseases; Disease control; Schistosomiasis; Hosts; Vaccines; Hygiene; Product development; Environmental factors; Hypersensitivity; Sanitation; Control programs; Drugs; Intervention; Allergies; Innovations; Public health; Schistosoma
DO  - http://dx.doi.org/10.4269/ajtmh.13-0467
ER  - 



TY  - JOUR
T1  - Needs for Monitoring Mosquito Transmission of Malaria in a Pre-Elimination World
AN  - 1647022968; 21172685
AB  - As global efforts to eliminate malaria intensify, accurate information on vector populations and transmission dynamics is critical for directing control efforts, developing new control tools, and predicting the effects of these interventions under various conditions. Currently available sampling tools for mosquito population monitoring suffer from well-recognized limitations. As reported in this workshop summary, a recent gathering of medical entomologists, modelers, and malaria experts reviewed these issues and agreed that efforts are needed to improve methods to monitor key transmission parameters. Identified needs include standardized methods for sampling of both mosquito adults and larvae, improved tools for mosquito species identification and age-grading, and a better means for determining the entomological inoculation rate.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - James, Stephanie
AU  - Takken, Willem
AU  - Collins, Frank H
AU  - Gottlieb, Michael
AD  - Laboratory of Entomology, Wageningen University and Research Center, Wageningen, The Netherlands; University of Notre Dame, Notre Dame, Indiana; Science Division, Foundation for the National Institutes of Health, 9650 Rockville Pike, Bethesda, MD 20814, sjames@fnih.org
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 6
EP  - 10
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 90
IS  - 1
SN  - 0002-9637, 0002-9637
KW  - Entomology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts B: Bacteriology
KW  - Environmental monitoring
KW  - Human diseases
KW  - Conferences
KW  - Vectors
KW  - Culicidae
KW  - Pest control
KW  - Malaria
KW  - Hosts
KW  - Disease transmission
KW  - Public health
KW  - Entomologists
KW  - Reviews
KW  - Inoculation
KW  - Sampling
KW  - Hygiene
KW  - Aquatic insects
KW  - J 02410:Animal Diseases
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Z 05350:Medical, Veterinary, and Agricultural Entomology
KW  - Q5 08502:Methods and instruments
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022968?accountid=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=Needs+for+Monitoring+Mosquito+Transmission+of+Malaria+in+a+Pre-Elimination+World&rft.au=James%2C+Stephanie%3BTakken%2C+Willem%3BCollins%2C+Frank+H%3BGottlieb%2C+Michael&rft.aulast=James&rft.aufirst=Stephanie&rft.date=2014-01-01&rft.volume=90&rft.issue=1&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0175
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Entomologists; Environmental monitoring; Human diseases; Malaria; Pest control; Hosts; Hygiene; Aquatic insects; Public health; Conferences; Reviews; Inoculation; Vectors; Sampling; Disease transmission; Culicidae
DO  - http://dx.doi.org/10.4269/ajtmh.13-0175
ER  - 



TY  - JOUR
T1  - Training Programs Within Global Networks: Lessons Learned in the Fogarty International Clinical Research Scholars and Fellows Program
AN  - 1647022843; 21172711
AB  - The Fogarty International Clinical Research Scholars and Fellows Support Center at Vanderbilt describes administrative lessons learned from the management of 436 scholars (American students or host country junior trainees) and 122 post-doctoral fellows (Americans or host country nationals). Trainees spent 10-11 months working on mentored research projects at 61 well-vetted sites in 27 low- or middle-income host countries (LMICs) with strong US partners. Economies of scale, strong centralized information exchange, and effective standardized operations linking US institutions with LMIC field sites were achieved in a program that minimized administrative overhead. Advantages and drawbacks of this approach are presented and discussed. Training of a new generation of global research leaders is greatly facilitated by an overseas mentored research experience that is administratively streamlined to optimize the use of resources for training, research, and capacity building.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Carothers, Catherine L
AU  - Heimburger, Douglas C
AU  - Schlachter, Sarah
AU  - Gardner, Pierce
AU  - Primack, Aron
AU  - Warner, Tokesha L
AU  - Vermund, Sten H
AD  - Institute for Global Health and Fogarty International Clinical Research Scholars and Fellows Support Center at Vanderbilt University, Nashville, Tennessee; Stony Brook University School of Medicine, Stony Brook, New York; Fogarty International Center, National Institutes of Health, Bethesda, Maryland; Vanderbilt University Institute for Global Health, 2525 West End Avenue, Suite 750, Nashville, TN 37203, catherine.lem@vanderbilt.edu
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 173
EP  - 179
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 90
IS  - 1
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology
KW  - K 03420:Plant Diseases
KW  - J 02450:Ecology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022843?accountid=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=Training+Programs+Within+Global+Networks%3A+Lessons+Learned+in+the+Fogarty+International+Clinical+Research+Scholars+and+Fellows+Program&rft.au=Carothers%2C+Catherine+L%3BHeimburger%2C+Douglas+C%3BSchlachter%2C+Sarah%3BGardner%2C+Pierce%3BPrimack%2C+Aron%3BWarner%2C+Tokesha+L%3BVermund%2C+Sten+H&rft.aulast=Carothers&rft.aufirst=Catherine&rft.date=2014-01-01&rft.volume=90&rft.issue=1&rft.spage=173&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0512
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
DO  - http://dx.doi.org/10.4269/ajtmh.12-0512
ER  - 



TY  - JOUR
T1  - Computer Aided-Diagnosis of Prostate Cancer on Multiparametric MRI: A Technical Review of Current Research
AN  - 1647014688; 21220704
AB  - Prostate cancer (PCa) is the most commonly diagnosed cancer among men in the United States. In this paper, we survey computer aided-diagnosis (CADx) systems that use multiparametric magnetic resonance imaging (MP-MRI) for detection and diagnosis of prostate cancer. We review and list mainstream techniques that are commonly utilized in image segmentation, registration, feature extraction, and classification. The performances of 15 state-of-the-art prostate CADx systems are compared through the area under their receiver operating characteristic curves (AUC). Challenges and potential directions to further the research of prostate CADx are discussed in this paper. Further improvements should be investigated to make prostate CADx systems useful in clinical practice.
JF  - BioMed Research International
AU  - Wang, Shijun
AU  - Burtt, Karen
AU  - Turkbey, Baris
AU  - Choyke, Peter
AU  - Summers, Ronald M
AD  - Imaging Biomarkers and Computer-Aided Diagnosis Laboratory, Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Building 10, Room 1C224, Bethesda, MD 20892-1182, USA, rms@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Prostate cancer
KW  - Classification
KW  - Reviews
KW  - Computers
KW  - Magnetic resonance imaging
KW  - Segmentation
KW  - Image processing
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647014688?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Computer+Aided-Diagnosis+of+Prostate+Cancer+on+Multiparametric+MRI%3A+A+Technical+Review+of+Current+Research&rft.au=Wang%2C+Shijun%3BBurtt%2C+Karen%3BTurkbey%2C+Baris%3BChoyke%2C+Peter%3BSummers%2C+Ronald+M&rft.aulast=Wang&rft.aufirst=Shijun&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F789561
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Prostate cancer; Classification; Computers; Reviews; Magnetic resonance imaging; Segmentation; Image processing
DO  - http://dx.doi.org/10.1155/2014/789561
ER  - 



TY  - JOUR
T1  - The Role of MRI in Prostate Cancer Active Surveillance
AN  - 1647011343; 21220700
AB  - Prostate cancer is the most common cancer diagnosis in American men, excluding skin cancer. The clinical behavior of prostate cancer varies from low-grade, slow growing tumors to high-grade aggressive tumors that may ultimately progress to metastases and cause death. Given the high incidence of men diagnosed with prostate cancer, conservative treatment strategies such as active surveillance are critical in the management of prostate cancer to reduce therapeutic complications of radiation therapy or radical prostatectomy. In this review, we will review the role of multiparametric MRI in the selection and follow-up of patients on active surveillance.
JF  - BioMed Research International
AU  - Johnson, Linda M
AU  - Choyke, Peter L
AU  - Figg, William D
AU  - Turkbey, Baris
AD  - Molecular Pharmacology Section, Medical Oncology Branch, National Cancer Institute, Bethesda, MD 20852, USA, figgw@helix.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Metastases
KW  - Prostate cancer
KW  - Radiation
KW  - Reviews
KW  - Magnetic resonance imaging
KW  - Skin cancer
KW  - Tumors
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647011343?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+Role+of+MRI+in+Prostate+Cancer+Active+Surveillance&rft.au=Johnson%2C+Linda+M%3BChoyke%2C+Peter+L%3BFigg%2C+William+D%3BTurkbey%2C+Baris&rft.aulast=Johnson&rft.aufirst=Linda&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F203906
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Metastases; Prostate cancer; Radiation; Reviews; Magnetic resonance imaging; Skin cancer; Tumors
DO  - http://dx.doi.org/10.1155/2014/203906
ER  - 



TY  - JOUR
T1  - Pharmacogenomics of cetuximab in metastatic colorectal carcinoma
AN  - 1642616788; 21155334
AB  - Cetuximab is a chimeric monoclonal antibody that has revolutionized the treatment of metastatic colorectal cancer. Knowledge of the mechanisms that underlie its effectiveness, as well as the primary and secondary resistance mechanisms, have led to important developments in the understanding of cetuximab biology. In light of knowledge gained from recent trials, the efficacy of cetuximab has been clearly demonstrated to depend upon RAS mutational status, moreover cetuximab should only be used in a subset of patients who may benefit. In this article, we critically review clinical and pharmacogenetic issues of cetuximab, focusing on the cost-effectiveness involved with the use of the drug.
JF  - Pharmacogenomics
AU  - Silvestris, Nicola
AU  - Vincenzi, Bruno
AU  - Brunetti, Anna Elisabetta
AU  - Loupakis, Fotious
AU  - Dell'Aquila, Emanuela
AU  - Russo, Antonio
AU  - Scartozzi, Mario
AU  - Giampieri, Riccardo
AU  - Cascinu, Stefano
AU  - Lorusso, Vito
AU  - Tonini, Giuseppe
AU  - Falcone, Alfredo
AU  - Santini, Daniele
AD  - super(1)Medical Oncology Unit, National Cancer Institute "Giovanni Paolo II", Bari, Italy
PY  - 2014
SP  - 1701
EP  - 1715
PB  - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL  - 15
IS  - 13
SN  - 1462-2416, 1462-2416
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - cetxuximab
KW  - colorectal carcinoma
KW  - cost-effectiveness
KW  - EGFR
KW  - pharmacogenomics
KW  - predictive
KW  - RAS
KW  - resistance
KW  - Metastases
KW  - Monoclonal antibodies
KW  - Colorectal cancer
KW  - Colorectal carcinoma
KW  - Clinical trials
KW  - Drugs
KW  - Pharmacogenetics
KW  - G 07880:Human Genetics
KW  - W 30940:Products
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642616788?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenomics&rft.atitle=Pharmacogenomics+of+cetuximab+in+metastatic+colorectal+carcinoma&rft.au=Silvestris%2C+Nicola%3BVincenzi%2C+Bruno%3BBrunetti%2C+Anna+Elisabetta%3BLoupakis%2C+Fotious%3BDell%27Aquila%2C+Emanuela%3BRusso%2C+Antonio%3BScartozzi%2C+Mario%3BGiampieri%2C+Riccardo%3BCascinu%2C+Stefano%3BLorusso%2C+Vito%3BTonini%2C+Giuseppe%3BFalcone%2C+Alfredo%3BSantini%2C+Daniele&rft.aulast=Silvestris&rft.aufirst=Nicola&rft.date=2014-01-01&rft.volume=15&rft.issue=13&rft.spage=1701&rft.isbn=&rft.btitle=&rft.title=Pharmacogenomics&rft.issn=14622416&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Number of references - 93
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Metastases; pharmacogenomics; Monoclonal antibodies; Colorectal cancer; Colorectal carcinoma; Drugs; Clinical trials; Pharmacogenetics
ER  - 



TY  - JOUR
T1  - Hyperspectral Visible-Near Infrared Determination of Arsenic Concentration in Soil
AN  - 1635028501; 21085013
AB  - The development of rapid techniques, such as hyperspectral spectrophotometry, for investigating arsenic (As) soil contamination could be of great value with respect to conventional methods. This study was conducted to detect As concentrations in artificially polluted soils (from 25 to 1045 mg kg super(-1)) through hyperspectral visible-near infrared spectrophotometry and to compare two multivariate statistical regression analyses: partial least squares and support vector machines. The correlation coefficient r is greater in the partial least squares in both model (0.93%) and test (0.87%) with respect to support vector machines (0.88% for the model and 0.82% for the test). The most important model variables extracted from the variable importance in projection scores resulted the absorption peaks at 580, 660, 715, and 780 nm. Bands in the visible spectra are not directly associated to As, but the metalloid can interact with the main spectrally active components of soil permitting to multivariate statistical models to screen As concentrations.
JF  - Communications in Soil Science and Plant Analysis
AU  - Stazi, Silvia Rita
AU  - Antonucci, Francesca
AU  - Pallottino, Federico
AU  - Costa, Corrado
AU  - Marabottini, Rosita
AU  - Petruccioli, Maurizio
AU  - Menesatti, Paolo
AD  - Dipartimento per l'Innovazione nei Sistemi Biologici, Agroalimentari e Forestali (DIBAF), Universita degli Studi della Tuscia, Viterbo, Italy
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 2911
EP  - 2920
PB  - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL  - 45
IS  - 22
SN  - 0010-3624, 0010-3624
KW  - Pollution Abstracts; Aqualine Abstracts; Water Resources Abstracts
KW  - Regression Analysis
KW  - Correlation Coefficient
KW  - Model Testing
KW  - Soil
KW  - Absorption
KW  - Spectrophotometry
KW  - Arsenic
KW  - Mathematical models
KW  - Soil Contamination
KW  - Soil contamination
KW  - Projections
KW  - Model Studies
KW  - SW 5010:Network design
KW  - P 5000:LAND POLLUTION
KW  - AQ 00008:Effects of Pollution
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635028501?accountid=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=Communications+in+Soil+Science+and+Plant+Analysis&rft.atitle=Hyperspectral+Visible-Near+Infrared+Determination+of+Arsenic+Concentration+in+Soil&rft.au=Stazi%2C+Silvia+Rita%3BAntonucci%2C+Francesca%3BPallottino%2C+Federico%3BCosta%2C+Corrado%3BMarabottini%2C+Rosita%3BPetruccioli%2C+Maurizio%3BMenesatti%2C+Paolo&rft.aulast=Stazi&rft.aufirst=Silvia&rft.date=2014-01-01&rft.volume=45&rft.issue=22&rft.spage=2911&rft.isbn=&rft.btitle=&rft.title=Communications+in+Soil+Science+and+Plant+Analysis&rft.issn=00103624&rft_id=info:doi/10.1080%2F00103624.2014.954716
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-12-01
N1  - Last updated - 2015-01-21
N1  - SubjectsTermNotLitGenreText - Soil; Arsenic; Mathematical models; Absorption; Spectrophotometry; Soil contamination; Regression Analysis; Correlation Coefficient; Soil Contamination; Model Testing; Projections; Model Studies
DO  - http://dx.doi.org/10.1080/00103624.2014.954716
ER  - 



TY  - JOUR
T1  - Inhibition of Hep G2 Hepatic Cancer Cell Growth and CCl sub(4) Induced Liver Cytotoxicity in Swiss Albino Mice by Mahua Extract
AN  - 1635027433; 21023302
AB  - Mahua flower extract may provide protective effects against hepatotoxicity. The effect of Mahua flower extract (ME) was investigated on Hep G2 cell line and carbon tetrachloride (CCl sub(4))-induced liver damages in Swiss albino mice. To investigate its cytotoxic effect in liver cancer, Hep G2 cells were treated with different doses of ME, and cell proliferation as well as colony formation assays demonstrated dose-dependent cytotoxicity of ME towards Hep G2 cells in tissue culture. Further gene expression studies showed significant down-regulation of AKT1/2/3, p-AKT, and COX-2 proteins including up-regulation of active caspase-3 in ME treated Hep G2 cells. In in vivo experiments, the mice were pretreated with ME for 15 days. On the 16th day CC1 sub(4) was injected intraperitoneally and after 24 h all mice were sacrificed. The antioxidant enzyme activities were measured in liver homogenates. CCl sub(4)-induced hepatotoxicity was evidenced by significant increase in lipid peroxidation and decrease in activities of antioxidant enzymes such as GST, GSH, SOD, CAT, and GPx. Histological studies showed CCl sub(4)-induced centrilobular necrosis and formation of fatty vacuoles in cirrhotic mice liver. Treatment with ME at a dose of 2 mg and 4 mg/kg exhibited the potential to prevent significant liver toxicity. The expression of active caspase-3 protein was down-regulated in ME treated groups compared to CCl sub(4) exposed animals. This study demonstrated ME mediated antioxidant activity and hepatoprotective effects; therefore it could be used in the future for treating hepatic disorders including liver cancer, especially in combination with chemotherapeutics.
JF  - Journal of Environmental Pathology, Toxicology and Oncology
AU  - Ray, Sudipta
AU  - Murmu, Nabendu
AU  - Adhikari, Jyotirmay
AU  - Bhattacharyya, Sayantan
AU  - Adhikari, Sumanto
AU  - Banerjee, Samir
AD  - Department of Signal Transduction & Biogenic Amines, Chittaranjan National Cancer Institute, Kolkata, India, nabendu.murmu@cnci.org.in
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 295
EP  - 314
PB  - Begell House Inc., 79 Madison Avenue, Suite 1201 New York NY 10016-7892 United States
VL  - 33
IS  - 4
SN  - 0731-8898, 0731-8898
KW  - Toxicology Abstracts
KW  - Madhuca indica
KW  - hepatotoxicity
KW  - oxidative stress
KW  - COX-2
KW  - Cyclooxygenase-2
KW  - Flowers
KW  - Liver diseases
KW  - Antioxidants
KW  - Liver cancer
KW  - Enzymes
KW  - Toxicity
KW  - Tissue culture
KW  - Lipid peroxidation
KW  - Gene expression
KW  - Cytotoxicity
KW  - Necrosis
KW  - Colonies
KW  - Superoxide dismutase
KW  - Vacuoles
KW  - Caspase-3
KW  - AKT1 protein
KW  - Cell proliferation
KW  - X 24300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635027433?accountid=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+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.atitle=Inhibition+of+Hep+G2+Hepatic+Cancer+Cell+Growth+and+CCl+sub%284%29+Induced+Liver+Cytotoxicity+in+Swiss+Albino+Mice+by+Mahua+Extract&rft.au=Ray%2C+Sudipta%3BMurmu%2C+Nabendu%3BAdhikari%2C+Jyotirmay%3BBhattacharyya%2C+Sayantan%3BAdhikari%2C+Sumanto%3BBanerjee%2C+Samir&rft.aulast=Ray&rft.aufirst=Sudipta&rft.date=2014-01-01&rft.volume=33&rft.issue=4&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Journal+of+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.issn=07318898&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-12-01
N1  - Number of references - 38
N1  - Last updated - 2015-04-16
N1  - SubjectsTermNotLitGenreText - Cyclooxygenase-2; Flowers; Antioxidants; Liver diseases; Liver cancer; Enzymes; Tissue culture; Toxicity; Lipid peroxidation; hepatotoxicity; Gene expression; Colonies; Necrosis; Cytotoxicity; Superoxide dismutase; Vacuoles; Caspase-3; AKT1 protein; Cell proliferation
ER  - 



TY  - JOUR
T1  - Impact of accelerometer data processing decisions on the sample size, wear time and physical activity level of a large cohort study
AN  - 1635023623; 21092286
AB  - Background: Accelerometers objectively assess physical activity (PA) and are currently used in several large-scale epidemiological studies, but there is no consensus for processing the data. This study compared the impact of wear-time assessment methods and using either vertical (V)-axis or vector magnitude (VM) cut-points on accelerometer output. Methods: Participants (7,650 women, mean age 71.4 y) were mailed an accelerometer (ActiGraph GT3X+), instructed to wear it for 7 days, record dates and times the monitor was worn on a log, and return the monitor and log via mail. Data were processed using three wear-time methods (logs, Troiano or Choi algorithms) and V-axis or VM cut-points. Results: Using algorithms alone resulted in "mail-days" incorrectly identified as "wear-days" (27-79% of subjects had >7-days of valid data). Using only dates from the log and the Choi algorithm yielded: 1) larger samples with valid data than using log dates and times, 2) similar wear-times as using log dates and times, 3) more wear-time (V, 48.1 min more; VM, 29.5 min more) than only log dates and Troiano algorithm. Wear-time algorithm impacted sedentary time (~30-60 min lower for Troiano vs. Choi) but not moderate-to-vigorous (MV) PA time. Using V-axis cut-points yielded ~60 min more sedentary time and ~10 min less MVPA time than using VM cut-points. Conclusions: Combining log-dates and the Choi algorithm was optimal, minimizing missing data and researcher burden. Estimates of time in physical activity and sedentary behavior are not directly comparable between V-axis and VM cut-points. These findings will inform consensus development for accelerometer data processing in ongoing epidemiologic studies.
JF  - BMC Public Health
AU  - Keadle, Sarah Kozey
AU  - Shiroma, Eric J
AU  - Freedson, Patty S
AU  - Lee, I-Min
AD  - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1210
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2458, 1471-2458
KW  - Health & Safety Science Abstracts
KW  - Physical activity
KW  - Measurement
KW  - Exposure assessment
KW  - Behavioral epidemiology
KW  - Sedentary behavior
KW  - Age
KW  - Data processing
KW  - Accelerometers
KW  - Wear
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635023623?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Public+Health&rft.atitle=Impact+of+accelerometer+data+processing+decisions+on+the+sample+size%2C+wear+time+and+physical+activity+level+of+a+large+cohort+study&rft.au=Keadle%2C+Sarah+Kozey%3BShiroma%2C+Eric+J%3BFreedson%2C+Patty+S%3BLee%2C+I-Min&rft.aulast=Keadle&rft.aufirst=Sarah&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=1210&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-14-1210
L2  - http://www.biomedcentral.com/1471-2458/14/1210
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-12-01
N1  - Number of references - 38
N1  - Last updated - 2015-02-12
N1  - SubjectsTermNotLitGenreText - Age; Data processing; Physical activity; Accelerometers; Wear
DO  - http://dx.doi.org/10.1186/1471-2458-14-1210
ER  - 



TY  - JOUR
T1  - Malaria Immunity in Man and Mosquito: Insights into Unsolved Mysteries of a Deadly Infectious Disease
AN  - 1635016036; 21103000
AB  - Malaria is a mosquito-borne disease caused by parasites of the obligate intracellular Apicomplexa phylum the most deadly of which, Plasmodium falciparum, prevails in Africa. Malaria imposes a huge health burden on the world's most vulnerable populations, claiming the lives of nearly one million children and pregnant women each year. Although there is keen interest in eradicating malaria, we do not yet have the necessary tools to meet this challenge, including an effective malaria vaccine and adequate vector control strategies. Here we review what is known about the mechanisms at play in immune resistance to malaria in both the human and mosquito hosts at each step in the parasite's complex life cycle with a view toward developing the tools that will contribute to the prevention of disease and death and, ultimately, to the goal of malaria eradication. In so doing, we hope to inspire immunologists to participate in defeating this devastating disease.
JF  - Annual Review of Immunology
AU  - Crompton, Peter D
AU  - Moebius, Jacqueline
AU  - Portugal, Silvia
AU  - Waisberg, Michael
AU  - Hart, Geoffrey
AU  - Garver, Lindsey S
AU  - Miller, Louis H
AU  - Barillas, Carolina
AU  - Pierce, Susan K
AD  - Laboratory of Immunogenetics, spierce@niaid.nih.gov
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 157
EP  - 187
PB  - Annual Reviews, Inc., 4139 El Camino Way Palo Alto CA 94303-0139 United States
VL  - 32
SN  - 0732-0582, 0732-0582
KW  - Entomology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW  - malaria
KW  - mosquito immunity
KW  - human immunity
KW  - human adaptive immunity
KW  - Parasites
KW  - Human diseases
KW  - Life cycle
KW  - Malaria
KW  - Hosts
KW  - Public health
KW  - Disease transmission
KW  - Infectious diseases
KW  - Aquatic insects
KW  - Play
KW  - Vectors
KW  - Culicidae
KW  - Pest control
KW  - Plasmodium falciparum
KW  - Immunity
KW  - Children
KW  - Pregnancy
KW  - Reviews
KW  - Africa
KW  - Apicomplexa
KW  - Vaccines
KW  - Z 05340:Ecology and Behavior
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635016036?accountid=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=Annual+Review+of+Immunology&rft.atitle=Malaria+Immunity+in+Man+and+Mosquito%3A+Insights+into+Unsolved+Mysteries+of+a+Deadly+Infectious+Disease&rft.au=Crompton%2C+Peter+D%3BMoebius%2C+Jacqueline%3BPortugal%2C+Silvia%3BWaisberg%2C+Michael%3BHart%2C+Geoffrey%3BGarver%2C+Lindsey+S%3BMiller%2C+Louis+H%3BBarillas%2C+Carolina%3BPierce%2C+Susan+K&rft.aulast=Crompton&rft.aufirst=Peter&rft.date=2014-01-01&rft.volume=32&rft.issue=&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Annual+Review+of+Immunology&rft.issn=07320582&rft_id=info:doi/10.1146%2Fannurev-immunol-032713-120220
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-12-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Life cycle; Pest control; Malaria; Hosts; Aquatic insects; Disease transmission; Public health; Play; Infectious diseases; Reviews; Vectors; Immunity; Vaccines; Children; Pregnancy; Culicidae; Apicomplexa; Plasmodium falciparum; Africa
DO  - http://dx.doi.org/10.1146/annurev-immunol-032713-120220
ER  - 



TY  - JOUR
T1  - The association between the upper digestive tract microbiota by HOMIM and oral health in a population-based study in Linxian, China
AN  - 1627969123; 20927837
AB  - Background: Bacteria affect oral health, but few studies have systematically examined the role of bacterial communities in oral diseases. We examined this relationship in a large population-based Chinese cancer screening cohort. Methods: Human Oral Microbe Identification Microarrays were used to test for the presence of 272 human oral bacterial species (97 genera) in upper digestive tract (UDT) samples collected from 659 participants. Oral health was assessed using US NHANES (National Health and Nutrition Examination Survey) protocols. We assessed both dental health (total teeth missing; tooth decay; and the decayed, missing, and filled teeth (DMFT) score) and periodontal health (bleeding on probing (BoP) extent score, loss of attachment extent score, and a periodontitis summary estimate). Results: Microbial richness, estimated by number of genera per sample, was positively correlated with BoP score (P = 0.015), but negatively correlated with tooth decay and DMFT score (P = 0.008 and 0.022 respectively). Regarding beta -diversity, as estimated by the UniFrac distance matrix for pairwise differences among samples, at least one of the first three principal components of the UniFrac distance matrix was correlated with the number of missing teeth, tooth decay, DMFT, BoP, or periodontitis. Of the examined genera, Parvimonas was positively associated with BoP and periodontitis. Veillonellacease [G-1] was associated with a high DMFT score, and Filifactor and Peptostreptococcus were associated with a low DMFT score. Conclusions: Our results suggest distinct relationships between UDT microbiota and dental and periodontal health. Poor dental health was associated with a less microbial diversity, whereas poor periodontal health was associated with more diversity and the presence of potentially pathogenic species.
JF  - BMC Public Health
AU  - Yu, Guoqin
AU  - Dye, Bruce A
AU  - Gail, Mitchell H
AU  - Shi, Jianxin
AU  - Klepac-Ceraj, Vanja
AU  - Paster, Bruce J
AU  - Wang, Guo-Qing
AU  - Wei, Wen-Qiang
AU  - Fan, Jin-Hu
AU  - Qiao, You-Lin
AU  - Dawsey, Sanford M
AU  - Freedman, Neal D
AU  - Abnet, Christian C
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1110
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2458, 1471-2458
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Health & Safety Science Abstracts
KW  - Microbiota
KW  - Oral health
KW  - Dental caries
KW  - Periodontitis
KW  - Bleeding on probe
KW  - Attachment loss
KW  - Teeth
KW  - Peptostreptococcus
KW  - Population studies
KW  - Nutrition
KW  - Cancer
KW  - Public health
KW  - Digestive tract
KW  - Oral diseases
KW  - Species diversity
KW  - Bleeding
KW  - China, People's Rep.
KW  - Decay
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - A 01450:Environmental Pollution & Waste Treatment
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627969123?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Public+Health&rft.atitle=The+association+between+the+upper+digestive+tract+microbiota+by+HOMIM+and+oral+health+in+a+population-based+study+in+Linxian%2C+China&rft.au=Yu%2C+Guoqin%3BDye%2C+Bruce+A%3BGail%2C+Mitchell+H%3BShi%2C+Jianxin%3BKlepac-Ceraj%2C+Vanja%3BPaster%2C+Bruce+J%3BWang%2C+Guo-Qing%3BWei%2C+Wen-Qiang%3BFan%2C+Jin-Hu%3BQiao%2C+You-Lin%3BDawsey%2C+Sanford+M%3BFreedman%2C+Neal+D%3BAbnet%2C+Christian+C&rft.aulast=Yu&rft.aufirst=Guoqin&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=1110&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-14-1110
L2  - http://www.biomedcentral.com/1471-2458/14/1110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Number of references - 41
N1  - Last updated - 2015-07-23
N1  - SubjectsTermNotLitGenreText - Teeth; Digestive tract; Oral diseases; Periodontitis; Bleeding; Population studies; Nutrition; Cancer; Public health; Species diversity; Decay; Peptostreptococcus; China, People's Rep.
DO  - http://dx.doi.org/10.1186/1471-2458-14-1110
ER  - 



TY  - JOUR
T1  - PTEN expression and function in adult cancer stem cells and prospects for therapeutic targeting
AN  - 1622614941; 20857592
AB  - Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a non-redundant lipid phosphatase that restrains and fine tunes the phosphatidylinositol-3-kinase (PI3K) signaling pathway. PTEN prevents tumorigenesis through multiple mechanisms and regulates a plethora of cellular processes, including survival, proliferation, energy metabolism and cellular architecture. Most recently, studies have shown that PTEN is also critical for stem cell maintenance and that PTEN loss can lead to the emergence and proliferation of cancer stem cell (CSC) clones. In this review, we will focus on the role of PTEN expression and function and downstream pathway activation in cancer stem cell biology and regulation of the tumorigenic potential; the emerging role of PTEN in mediating the crosstalk between the PI3K and MAPK pathways will also be discussed, together with prospects for the therapeutic targeting of tumors lacking PTEN expression.
JF  - Advances in Biological Regulation
AU  - Ciuffreda, Ludovica
AU  - Falcone, Italia
AU  - Incani, Ursula Cesta
AU  - Del Curatolo, Anais
AU  - Conciatori, Fabiana
AU  - Matteoni, Silvia
AU  - Vari, Sabrina
AU  - Vaccaro, Vanja
AU  - Cognetti, Francesco
AU  - Milella, Michele
AD  - Division of Medical Oncology A, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy, ludovicaciuffreda@hotmail.com
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 66
EP  - 80
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 56
SN  - 2212-4926, 2212-4926
KW  - Biotechnology and Bioengineering Abstracts
KW  - PTEN
KW  - Cancer stem cells
KW  - PI3K
KW  - MAPK
KW  - Crosstalk
KW  - Feedback loops
KW  - Combination therapy
KW  - Cell survival
KW  - Stem cells
KW  - 1-Phosphatidylinositol 3-kinase
KW  - MAP kinase
KW  - Chromosomes
KW  - Energy metabolism
KW  - Lipids
KW  - Tumorigenesis
KW  - PTEN protein
KW  - Cancer
KW  - Signal transduction
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622614941?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=PTEN+expression+and+function+in+adult+cancer+stem+cells+and+prospects+for+therapeutic+targeting&rft.au=Ciuffreda%2C+Ludovica%3BFalcone%2C+Italia%3BIncani%2C+Ursula+Cesta%3BDel+Curatolo%2C+Anais%3BConciatori%2C+Fabiana%3BMatteoni%2C+Silvia%3BVari%2C+Sabrina%3BVaccaro%2C+Vanja%3BCognetti%2C+Francesco%3BMilella%2C+Michele&rft.aulast=Ciuffreda&rft.aufirst=Ludovica&rft.date=2014-01-01&rft.volume=56&rft.issue=&rft.spage=66&rft.isbn=&rft.btitle=&rft.title=Advances+in+Biological+Regulation&rft.issn=22124926&rft_id=info:doi/10.1016%2Fj.jbior.2014.07.002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Cell survival; Chromosomes; MAP kinase; 1-Phosphatidylinositol 3-kinase; Stem cells; Energy metabolism; Lipids; Tumorigenesis; PTEN protein; Cancer; Signal transduction
DO  - http://dx.doi.org/10.1016/j.jbior.2014.07.002
ER  - 



TY  - JOUR
T1  - A decision exercise to engage cancer patients and families in Deliberation about Medicare Coverage for advanced Cancer Care
AN  - 1622614907; 20450901
AB  - Background: Concerns about unsustainable costs in the US Medicare program loom as the number of retirees increase and experiences serious and costly illnesses like cancer. Engagement of stakeholders, particularly cancer patients and their families, in prioritizing insured services offers a valuable strategy for informing Medicare coverage policy. We designed and evaluated a decision exercise that allowed cancer patients and family members to choose Medicare benefits for advanced cancer patients. Methods: The decision tool, Choosing Health plans All Together (CHAT) was modified to select services for advanced cancer patients. Patients with a cancer history (N = 246) and their family members (N = 194) from North Carolina participated in 70 CHAT sessions. Variables including participants' socio-demographic characteristics, health status, assessments of the exercise and results of group benefit selections were collected. Routine descriptive statistics summarized participant characteristics and Fisher's exact test compared group differences. Qualitative analysis of group discussions were used to ascertain reasons for or against selecting benefits. Results: Patients and family members (N = 440) participated in 70 CHAT exercises. Many groups opted for such services as palliative care, nursing facilities, and services not currently covered by the Medicare program. In choosing among four levels of cancer treatment coverage, no groups chose basic coverage, 27 groups (39%) selected intermediate coverage, 39 groups (56%) selected high coverage, and 4 groups (6%) chose the most comprehensive cancer coverage. Reasons for or against benefit selection included fairness, necessity, need for prioritizing, personal experience, attention to family needs, holistic health outlook, preference for comfort, freedom of choice, and beliefs about the proper role of government. Participants found the exercise very easy (59%) or fairly easy (39%) to understand and very informative (66%) or fairly informative (31%). The majority agreed that the CHAT exercise led to fair decisions about priorities for coverage by which they could abide. Conclusions: It is possible to involve cancer patients and families in explicit discussions of their priorities for affordable advanced cancer care through the use of decision tools designed for this purpose. A key question is whether such a conversation is possible on a broader, national level.
JF  - BMC Health Services Research
AU  - Danis, Marion
AU  - Abernethy, Amy P
AU  - Zafar, S Yousuf
AU  - Samsa, Gregory P
AU  - Wolf, Steven P
AU  - Howie, Lynn
AU  - Taylor, Donald H, Jr
AD  - Department of Bioethics, National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 315
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1472-6963, 1472-6963
KW  - Physical Education Index
KW  - Medicare
KW  - Hospice benefit
KW  - Health priorities
KW  - Insurance benefits
KW  - Public participation
KW  - Experience
KW  - Programs
KW  - Health (services)
KW  - Family
KW  - Patients
KW  - Exercise
KW  - Illness
KW  - Cancer
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622614907?accountid=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=BMC+Health+Services+Research&rft.atitle=A+decision+exercise+to+engage+cancer+patients+and+families+in+Deliberation+about+Medicare+Coverage+for+advanced+Cancer+Care&rft.au=Danis%2C+Marion%3BAbernethy%2C+Amy+P%3BZafar%2C+S+Yousuf%3BSamsa%2C+Gregory+P%3BWolf%2C+Steven+P%3BHowie%2C+Lynn%3BTaylor%2C+Donald+H%2C+Jr&rft.aulast=Danis&rft.aufirst=Marion&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=315&rft.isbn=&rft.btitle=&rft.title=BMC+Health+Services+Research&rft.issn=14726963&rft_id=info:doi/10.1186%2F1472-6963-14-315
L2  - http://www.biomedcentral.com/1472-6963/14/315
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2014-11-01
N1  - Number of references - 12
N1  - Last updated - 2014-11-12
N1  - SubjectsTermNotLitGenreText - Experience; Programs; Health (services); Medicare; Family; Patients; Exercise; Illness; Cancer
DO  - http://dx.doi.org/10.1186/1472-6963-14-315
ER  - 



TY  - JOUR
T1  - Curcumin Augments the Efficacy of Antitumor Drugs Used in Leukemia by Modulation of Heat Shock Proteins Via HDAC6
AN  - 1622606536; 20889198
AB  - Heat shock proteins (HSPs) and histone deacetylase 6 (HDAC6) are induced under oxidative stress, which promotes oncogenesis. HSPs are regulated by heat shock factori (HSF1). HDAC6, a class lib deacetylase, plays an essential role in tumorigenesis and cell stress response. HSPs, HSF1, and HDAC6 are up-regulated in cancer. In the present study, we explored the effect of curcumin, a phytochemical, on HSPs (27, 70, and 90), HSF1, and HDAC6 in two different leukemia cell lines (K-562 and HL-60). The association between HDAC6, HSPs, and intrinsic oxidative stress was also investigated. Overexpressions of HSPs (27, 70, and 90), HSF1, and HDAC6 in leukemia cells were down-regulated by curcumin, and the effects on HSPs 27 and 70 were less than that on HSP 90. This resulted in cell cycle arrest at the G2/M stage, leading to apoptosis. Different cell cycle regulatory proteins (p53, p21, cyclin B1, COK1, and Cdc25C) and some apoptosis-related proteins (Bc1-2, Bax, Bid, Bad, Apaf1, AIF, and Cyt c) were altered by curcumin. Increased ROS levels in leukemia cells were quenched by curcumin. A probable association between high ROS level and the overexpression of tumor markers was established in this study. Thus, curcumin enhanced the efficacy of anti-tumor drugs imatinib-mesylate and cytarabine through the inhibition of the tumor markers.
JF  - Journal of Environmental Pathology, Toxicology and Oncology
AU  - Sarkar, Ruma
AU  - Mukherjee, Apurba
AU  - Mukherjee, Sutapa
AU  - Biswas, Raj
AU  - Biswas, Jaydip
AU  - Roy, Madhumita
AD  - Department of Environmental Carcinogenesis & Toxicology, Chittaranjan National Cancer Institute, Calcutta, India, mitacnci@yahoo.co.in
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 247
EP  - 263
PB  - Begell House Inc., 79 Madison Avenue, Suite 1201 New York NY 10016-7892 United States
VL  - 33
IS  - 3
SN  - 0731-8898, 0731-8898
KW  - Toxicology Abstracts
KW  - HSPs
KW  - HSF1
KW  - HDAC6
KW  - curcumin
KW  - ROS
KW  - leukemia
KW  - Histone deacetylase
KW  - Heat shock proteins
KW  - cytarabine
KW  - Tumor markers
KW  - Curcumin
KW  - Apoptosis
KW  - Tumorigenesis
KW  - Cell cycle
KW  - Cancer
KW  - p53 protein
KW  - Tumor cell lines
KW  - regulatory proteins
KW  - Oxidative stress
KW  - Cyclin B1
KW  - Hsp27 protein
KW  - Apoptosis-inducing factor
KW  - Drugs
KW  - Antitumor activity
KW  - HSF1 protein
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622606536?accountid=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+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.atitle=Curcumin+Augments+the+Efficacy+of+Antitumor+Drugs+Used+in+Leukemia+by+Modulation+of+Heat+Shock+Proteins+Via+HDAC6&rft.au=Sarkar%2C+Ruma%3BMukherjee%2C+Apurba%3BMukherjee%2C+Sutapa%3BBiswas%2C+Raj%3BBiswas%2C+Jaydip%3BRoy%2C+Madhumita&rft.aulast=Sarkar&rft.aufirst=Ruma&rft.date=2014-01-01&rft.volume=33&rft.issue=3&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Journal+of+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.issn=07318898&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Number of references - 85
N1  - Last updated - 2015-04-16
N1  - SubjectsTermNotLitGenreText - Histone deacetylase; Heat shock proteins; Apoptosis; Curcumin; Tumor markers; cytarabine; Cell cycle; Tumorigenesis; Cancer; p53 protein; Tumor cell lines; regulatory proteins; Cyclin B1; Oxidative stress; Hsp27 protein; Apoptosis-inducing factor; Drugs; HSF1 protein; Antitumor activity
ER  - 



TY  - JOUR
T1  - Physicians' knowledge, beliefs, and use of race and human genetic variation: new measures and insights
AN  - 1622605948; 20846348
AB  - Background: Understanding physician perspectives on the intersection of race and genomics in clinical decision making is critical as personalized medicine and genomics become more integrated in health care services. There is a paucity of literature in the United States of America (USA) and globally regarding how health care providers understand and use information about race, ethnicity and genetic variation in their clinical decision making. This paper describes the development of three scales related to addressing this gap in the literature: the Bonham and Sellers Genetic Variation Knowledge Assessment Index--GKAI, Health Professionals Beliefs about Race-HPBR, and Racial Attributes in Clinical Evaluation-RACE scales. Methods: A cross-sectional, web survey of a national random sample of general internists in the USA (N = 787) was conducted. Confirmatory factor analysis was used to assess the construct validity of the scales. Scale items were developed through focus groups, cognitive interviews, expert advisory panels, and exploratory factor analysis of pilot data. Results: GKAI was measured as a count of correct answers (Mean = 3.28 SD = 1.17). HPBR yielded two domains: beliefs about race as a biological phenomenon (HPBR-BD, alpha = .69, 4 items) and beliefs about the clinical value of race and genetic variation for understanding risk for disease (HPBR-CD alpha = .61, 3 items). RACE yielded one factor (alpha = .86, 7 items). Conclusions: GKAI is a timely knowledge scale that can be used to assess health professional knowledge of race and human genetic variation. HPBR is a promising new tool for assessing health professionals' beliefs about the role of race and its relationship with human genetic variation in clinical practice. RACE offers a valid and reliable tool for assessing explicit use of racial attributes in clinical decision making.
JF  - BMC Health Services Research
AU  - Bonham, Vence L
AU  - Sellers, Sherrill L
AU  - Woolford, Sam
AD  - Social and Behavioral Research Branch, National Human Genome Research Institute, National Institutes of Health, 31 Center Drive, Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 456
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1472-6963, 1472-6963
KW  - Risk Abstracts
KW  - Scale development
KW  - Medical decision making
KW  - Personalized medicine
KW  - RACE (Racial Attributes in Clinical Evaluation)
KW  - GKAI (Genetic Variation Knowledge Assessment Index)
KW  - Explicit use of race
KW  - Risk assessment
KW  - Decision making
KW  - USA
KW  - Health care
KW  - Risk factors
KW  - Genetic diversity
KW  - Ethnic groups
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622605948?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Health+Services+Research&rft.atitle=Physicians%27+knowledge%2C+beliefs%2C+and+use+of+race+and+human+genetic+variation%3A+new+measures+and+insights&rft.au=Bonham%2C+Vence+L%3BSellers%2C+Sherrill+L%3BWoolford%2C+Sam&rft.aulast=Bonham&rft.aufirst=Vence&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=456&rft.isbn=&rft.btitle=&rft.title=BMC+Health+Services+Research&rft.issn=14726963&rft_id=info:doi/10.1186%2F1472-6963-14-456
L2  - http://www.biomedcentral.com/1472-6963/14/456
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Number of references - 45
N1  - Last updated - 2014-11-26
N1  - SubjectsTermNotLitGenreText - Risk assessment; Decision making; Health care; Risk factors; Genetic diversity; Ethnic groups; USA
DO  - http://dx.doi.org/10.1186/1472-6963-14-456
ER  - 



TY  - JOUR
T1  - Cytogenetic as an Important Tool for Diagnosis and Prognosis for Patients with Hypocellular Primary Myelodysplastic Syndrome
AN  - 1618161870; 20821731
AB  - We analyzed cytogenetically 105 patients with hypocellular primary MDS and their clinical implications. The main chromosomal abnormalities found were del(5q)/-5, del(6q)/+6, del(7q)/-7, del(11q), and del(17p). Pediatric patients had a higher frequency of abnormal karyotypes compared with adult patients ( P < 0,05). From our patients, 18% showed evolution of the disease. The chromosomal abnormalities presented in the diagnosis of patients who evolved to AML included numerical (-7, +8) and structural del(6q), del(7q), i(7q), t(7; 9), i(9q), and del(11q) abnormalities and complex karyotypes. Although the frequency of evolution from hypocellular MDS to AML is low, our results suggest that some chromosomal alterations may play a critical role during this process. We applied the IPSS in our patients because this score system has been proved to be useful for predicting evolution of disease. When we considered the patients according to group 1 (intermediate-1) and group 2 (intermediate-2 and high risk), we showed that group 2 had a high association with respect to the frequency of abnormal karyotypes ( P < 0,0001), evolution of disease ( P < 0,0001), and mortality ( P < 0,001). In fact, the cytogenetic analysis for patients with hypocellular primary MDS is an important tool for diagnosis, prognosis, in clinical decision-making and in follow-up.
JF  - BioMed Research International
AU  - Correa de Souza, Daiane
AU  - de Souza Fernandez, Cecilia
AU  - Camargo, Adriana
AU  - Apa, Alexandre Gustavo
AU  - Sobral da Costa, Elaine
AU  - Bouzas, Luis Fernando
AU  - Abdelhay, Eliana
AU  - de Souza Fernandez, Teresa
AD  - Bone Marrow Transplantation Center, National Cancer Institute (INCA), 20230-130 Rio de Janeiro, RJ, Brazil, teresafernandez@inca.gov.br
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Myelodysplastic syndrome
KW  - Mortality
KW  - Decision making
KW  - Pediatrics
KW  - Risk factors
KW  - Prognosis
KW  - Karyotypes
KW  - Evolution
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618161870?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytogenetic+as+an+Important+Tool+for+Diagnosis+and+Prognosis+for+Patients+with+Hypocellular+Primary+Myelodysplastic+Syndrome&rft.au=Correa+de+Souza%2C+Daiane%3Bde+Souza+Fernandez%2C+Cecilia%3BCamargo%2C+Adriana%3BApa%2C+Alexandre+Gustavo%3BSobral+da+Costa%2C+Elaine%3BBouzas%2C+Luis+Fernando%3BAbdelhay%2C+Eliana%3Bde+Souza+Fernandez%2C+Teresa&rft.aulast=Correa+de+Souza&rft.aufirst=Daiane&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F542395
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-11-12
N1  - SubjectsTermNotLitGenreText - Decision making; Mortality; Myelodysplastic syndrome; Pediatrics; Risk factors; Prognosis; Karyotypes; Evolution
DO  - http://dx.doi.org/10.1155/2014/542395
ER  - 



TY  - JOUR
T1  - Multiparametric MRI in Biopsy Guidance for Prostate Cancer: Fusion-Guided
AN  - 1618159947; 20821926
AB  - Prostate cancer (PCa) is the most common solid-organ malignancy among American men and the second most deadly. Current guidelines recommend a 12-core systematic biopsy following the finding of an elevated serum prostate-specific antigen (PSA). However, this strategy fails to detect an unacceptably high percentage of clinically significant cancers, leading researchers to develop new, innovative methods to improve the effectiveness of prostate biopsies. Multiparametric-MRI (MP-MRI) has emerged as a promising instrument in identifying suspicious regions within the prostate that require special attention on subsequent biopsy. Fusion platforms, which incorporate the MP-MRI into the biopsy itself and provide active targets within real-time imaging, have shown encouraging results in improving the detection rate of significant cancer. Broader applications of this technology, including MRI-guided focal therapy for prostate cancer, are in early phase trials.
JF  - BioMed Research International
AU  - Rothwax, Jason T
AU  - George, Arvin K
AU  - Wood, Bradford J
AU  - Pinto, Peter A
AD  - Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1210, USA, pintop@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Malignancy
KW  - Prostate cancer
KW  - Magnetic resonance imaging
KW  - Biopsy
KW  - prostate-specific antigen
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618159947?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Multiparametric+MRI+in+Biopsy+Guidance+for+Prostate+Cancer%3A+Fusion-Guided&rft.au=Rothwax%2C+Jason+T%3BGeorge%2C+Arvin+K%3BWood%2C+Bradford+J%3BPinto%2C+Peter+A&rft.aulast=Rothwax&rft.aufirst=Jason&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F439171
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Malignancy; Prostate cancer; Magnetic resonance imaging; Biopsy; prostate-specific antigen
DO  - http://dx.doi.org/10.1155/2014/439171
ER  - 



TY  - JOUR
T1  - Physical and Dosimetric Optimization of Laser Equipment in Dermatology: A Preliminary Study
AN  - 1618159064; 20823307
AB  - The aim of this preliminary study is to investigate the correlation between clinical set-up at present used in the treatment of specific skin conditions and laser beam absorbed power in the tissue. This study focused on the CO sub(2) and Nd-Yag laser equipment used in the daily clinical practice in the Department of Dermatology of San Gallicano Institute in Rome. Different types of tissue-equivalent material with various water and haemoglobin concentrations were tested to evaluate laser beam attenuation power. In particular, thinly sliced pork loin, of uniform consistency and without fat, was selected for its high content of haemoglobin to mimic human tissues. An optical power meter was used to measure the power or energy of a laser beam. During measurements, the tissue equivalent phantoms were positioned on the detector head and the laser beam was orthogonally oriented. The results of two experimental set-ups are reported here. The dependence of residual power (W) as a function of ex vivo tissue thickness (mm) for different laser output powers was studied. Data were fitted by a parametric logistic equation. These preliminary data allow for more accurately determining the energy fraction released from lasers to the tissues in order to improve clinical outcomes.
JF  - BioMed Research International
AU  - Soriani, A
AU  - D'Alessio, D
AU  - Cattelan, V
AU  - Cameli, N
AU  - Mariano, M
AU  - Ungania, S
AU  - Guerrisi, M
AU  - Strigari, L
AD  - Medical Physics Laboratory, Regina Elena National Cancer Institute, 00144 Rome, Italy, soriani@ifo.it
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Hemoglobin
KW  - Data processing
KW  - Skin
KW  - Mathematical models
KW  - Head
KW  - Energy
KW  - Dermatology
KW  - Pork
KW  - Lasers
KW  - Carbon dioxide
KW  - Physical training
KW  - W 30935:Food Biotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618159064?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Physical+and+Dosimetric+Optimization+of+Laser+Equipment+in+Dermatology%3A+A+Preliminary+Study&rft.au=Soriani%2C+A%3BD%27Alessio%2C+D%3BCattelan%2C+V%3BCameli%2C+N%3BMariano%2C+M%3BUngania%2C+S%3BGuerrisi%2C+M%3BStrigari%2C+L&rft.aulast=Soriani&rft.aufirst=A&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F151969
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Hemoglobin; Mathematical models; Skin; Data processing; Head; Energy; Pork; Dermatology; Lasers; Carbon dioxide; Physical training
DO  - http://dx.doi.org/10.1155/2014/151969
ER  - 



TY  - JOUR
T1  - High Guanidinium Permeability Reveals Dehydration-Dependent Ion Selectivity in the Plasmodial Surface Anion Channel
AN  - 1618154622; 20823708
AB  - Malaria parasites grow within vertebrate erythrocytes and increase host cell permeability to access nutrients from plasma. This increase is mediated by the plasmodial surface anion channel (PSAC), an unusual ion channel linked to the conserved clag gene family. Although PSAC recognizes and transports a broad range of uncharged and charged solutes, it must efficiently exclude the small Na super(+) ion to maintain infected cell osmotic stability. Here, we examine possible mechanisms for this remarkable solute selectivity. We identify guanidinium as an organic cation with high permeability into human erythrocytes infected with Plasmodium falciparum , but negligible uptake by uninfected cells. Transport characteristics and pharmacology indicate that this uptake is specifically mediated by PSAC. The rank order of organic and inorganic cation permeabilities suggests cation dehydration as the rate-limiting step in transport through the channel. The high guanidinium permeability of infected cells also allows rapid and stringent synchronization of parasite cultures, as required for molecular and cellular studies of this pathogen. These studies provide important insights into how nutrients and ions are transported via PSAC, an established target for antimalarial drug development.
JF  - BioMed Research International
AU  - Bokhari, Abdullah AB
AU  - Mita-Mendoza, Neida K
AU  - Fuller, Alexandra
AU  - Pillai, Ajay D
AU  - Desai, Sanjay A
AD  - The Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA, sdesai@niaid.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Biotechnology and Bioengineering Abstracts
KW  - Parasites
KW  - Human diseases
KW  - Anions
KW  - Pharmacology
KW  - Synchronization
KW  - Erythrocytes
KW  - Nutrients
KW  - Cell culture
KW  - Cell permeability
KW  - Malaria
KW  - Gene families
KW  - Public health
KW  - Permeability
KW  - Solutes
KW  - Ion channels
KW  - Anion channels
KW  - Osmotic stability
KW  - Drug development
KW  - Plasmodium falciparum
KW  - Pathogens
KW  - Cations
KW  - Uptake
KW  - Dehydration
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618154622?accountid=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=BioMed+Research+International&rft.atitle=High+Guanidinium+Permeability+Reveals+Dehydration-Dependent+Ion+Selectivity+in+the+Plasmodial+Surface+Anion+Channel&rft.au=Bokhari%2C+Abdullah+AB%3BMita-Mendoza%2C+Neida+K%3BFuller%2C+Alexandra%3BPillai%2C+Ajay+D%3BDesai%2C+Sanjay+A&rft.aulast=Bokhari&rft.aufirst=Abdullah&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F741024
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Number of references - 1
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Solutes; Parasites; Permeability; Human diseases; Anions; Erythrocytes; Uptake; Malaria; Public health; Pharmacology; Synchronization; Osmotic stability; Cell permeability; Cell culture; Nutrients; Drug development; Pathogens; Gene families; Cations; Ion channels; Anion channels; Dehydration; Plasmodium falciparum
DO  - http://dx.doi.org/10.1155/2014/741024
ER  - 



TY  - JOUR
T1  - A nested real-time PCR assay for the quantification of Plasmodium falciparum DNA extracted from dried blood spots
AN  - 1618153825; 20846349
AB  - Background: As public health efforts seek to eradicate malaria, there has been an emphasis on eliminating low-density parasite reservoirs in asymptomatic carriers. As such, diagnosing submicroscopic Plasmodium infections using PCR-based techniques has become important not only in clinical trials of malaria vaccines and therapeutics, but also in active malaria surveillance campaigns. However, PCR-based quantitative assays that rely on nucleic acid extracted from dried blood spots (DBS) have demonstrated lower sensitivity than assays that use cryopreserved whole blood as source material. Methods: The density of Plasmodium falciparum asexual parasites was quantified using genomic DNA extracted from dried blood spots (DBS) and the sensitivity of two approaches was compared: quantitative real-time PCR (qPCR) targeting the P. falciparum 18S ribosomal RNA gene, either with an initial conventional PCR amplification prior to qPCR (nested qPCR), or without an initial amplification (qPCR only). Parasite densities determined by nested qPCR, qPCR only, and light microscopy were compared. Results: Nested qPCR results in 10-fold higher sensitivity (0.5 parasites/[mu]l) when compared to qPCR only (five parasites/ul). Among microscopy-positive samples, parasite densities calculated by nested qPCR correlated strongly with microscopy for both asymptomatic (Pearson's r = 0.58, P < 0.001) and symptomatic (Pearson's r = 0.70, P < 0.0001) P. falciparum infections. Conclusion: Nested qPCR improves the sensitivity for the detection of P. falciparum blood-stage infection from clinical DBS samples. This approach may be useful for active malaria surveillance in areas where submicroscopic asymptomatic infections are prevalent.
JF  - Malaria Journal
AU  - Tran, Tuan M
AU  - Aghili, Amirali
AU  - Li, Shanping
AU  - Ongoiba, Aissata
AU  - Kayentao, Kassoum
AU  - Doumbo, Safiatou
AU  - Traore, Boubacar
AU  - Crompton, Peter D
AD  - Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Twinbrook 2, Room 125, 12441 Parklawn Drive, Rockville, Maryland 20852, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 393
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1475-2875, 1475-2875
KW  - Biochemistry Abstracts 2: Nucleic Acids; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Plasmodium falciparum
KW  - Nucleic acid testing
KW  - Quantitative PCR
KW  - Nested PCR
KW  - Dried blood spot
KW  - Passive surveillance
KW  - rRNA 18S
KW  - Biological surveys
KW  - Parasites
KW  - Human diseases
KW  - Nucleotide sequence
KW  - Asymptomatic infection
KW  - Malaria
KW  - Clinical trials
KW  - Cryopreservation
KW  - Public health
KW  - Blood
KW  - nucleic acids
KW  - DNA
KW  - Polymerase chain reaction
KW  - genomics
KW  - Vaccines
KW  - Nucleic acids
KW  - K 03300:Methods
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - N 14810:Methods
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618153825?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Malaria+Journal&rft.atitle=A+nested+real-time+PCR+assay+for+the+quantification+of+Plasmodium+falciparum+DNA+extracted+from+dried+blood+spots&rft.au=Tran%2C+Tuan+M%3BAghili%2C+Amirali%3BLi%2C+Shanping%3BOngoiba%2C+Aissata%3BKayentao%2C+Kassoum%3BDoumbo%2C+Safiatou%3BTraore%2C+Boubacar%3BCrompton%2C+Peter+D&rft.aulast=Tran&rft.aufirst=Tuan&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-13-393
L2  - http://www.malariajournal.com/content/13/1/393
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Number of references - 19
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Biological surveys; Parasites; Human diseases; Nucleotide sequence; DNA; Polymerase chain reaction; Malaria; Nucleic acids; Public health; rRNA 18S; Blood; nucleic acids; Asymptomatic infection; Vaccines; genomics; Cryopreservation; Clinical trials; Plasmodium falciparum
DO  - http://dx.doi.org/10.1186/1475-2875-13-393
ER  - 



TY  - JOUR
T1  - Levels of Soluble E-Cadherin in Breast, Gastric, and Colorectal Cancers
AN  - 1618153742; 20823323
AB  - Soluble E-cadherin is a 80 kDa protein fragment coming from the proteolytic cleavage of the extracellular domain of the full length epithelial cadherin, a molecule involved in cell adhesion/polarity and tissue morphogenesis. In comparison with normal epithelia, cancer cells show a decreased cadherin-mediated intercellular adhesion, and sE-cad levels normally increase in body fluids (blood and urine). This review focuses on soluble E-cadherin in sera of patients affected by three solid cancers (breast, gastric, and colorectal cancers) and how its levels correlate or not with some cancer parameters (e.g., dimension, progression, and localisation). We will describe the main proteomics approaches adopted to measure sE-cad both in vivo and in vitro and the most important findings about its behaviour in cancer dynamics.
JF  - BioMed Research International
AU  - Repetto, Ombretta
AU  - De Paoli, Paolo
AU  - De Re, Valli
AU  - Canzonieri, Vincenzo
AU  - Cannizzaro, Renato
AD  - Facility of Bio-Proteomics, Centro di Riferimento Oncologico (CRO), Aviano National Cancer Institute, Via F. Gallini 2, 33081 Aviano, Italy, vdere@cro.it
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Proteolysis
KW  - Morphogenesis
KW  - Colorectal cancer
KW  - E-Cadherin
KW  - Cell adhesion
KW  - Blood
KW  - Urine
KW  - Reviews
KW  - Cadherin
KW  - Breast cancer
KW  - Polarity
KW  - proteomics
KW  - Gastric cancer
KW  - Cell adhesion molecules
KW  - Body fluids
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618153742?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Levels+of+Soluble+E-Cadherin+in+Breast%2C+Gastric%2C+and+Colorectal+Cancers&rft.au=Repetto%2C+Ombretta%3BDe+Paoli%2C+Paolo%3BDe+Re%2C+Valli%3BCanzonieri%2C+Vincenzo%3BCannizzaro%2C+Renato&rft.aulast=Repetto&rft.aufirst=Ombretta&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F408047
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Number of references - 1
N1  - Last updated - 2015-10-15
N1  - SubjectsTermNotLitGenreText - Proteolysis; Morphogenesis; Colorectal cancer; E-Cadherin; Cell adhesion; Blood; Urine; Cadherin; Reviews; Breast cancer; Polarity; proteomics; Gastric cancer; Body fluids; Cell adhesion molecules
DO  - http://dx.doi.org/10.1155/2014/408047
ER  - 



TY  - JOUR
T1  - Multiparametric MRI in the PSA Screening Era
AN  - 1618153700; 20823667
AB  - Prostate cancer remains significant public health concern amid growing controversies regarding prostate specific antigen (PSA) based screening. The utility of PSA has been brought into question, and alternative measures are investigated to remedy the overdetection of indolent disease and safeguard patients from the potential harms resulting from an elevated PSA. Multiparametric MRI of the prostate has shown promise in identifying patients at risk for clinically significant disease but its role within the current diagnostic and treatment paradigm remains in question. The current review focuses on recent applications of MRI in this pathway.
JF  - BioMed Research International
AU  - George, Arvin K
AU  - Pinto, Peter A
AU  - Rais-Bahrami, Soroush
AD  - National Cancer Institute, Urologic Oncology Branch, National Institutes of Health, 10 Center Drive, 2950-W, Building 10, CRC Room 2W-5940, Bethesda, MD 20892-1210, USA, arvin.george@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Prostate cancer
KW  - Magnetic resonance imaging
KW  - Public health
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618153700?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Multiparametric+MRI+in+the+PSA+Screening+Era&rft.au=Correa+de+Souza%2C+Daiane%3Bde+Souza+Fernandez%2C+Cecilia%3BCamargo%2C+Adriana%3BApa%2C+Alexandre+Gustavo%3BSobral+da+Costa%2C+Elaine%3BBouzas%2C+Luis+Fernando%3BAbdelhay%2C+Eliana%3Bde+Souza+Fernandez%2C+Teresa&rft.aulast=Correa+de+Souza&rft.aufirst=Daiane&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F542395
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Prostate cancer; Magnetic resonance imaging; Public health
DO  - http://dx.doi.org/10.1155/2014/465816
ER  - 



TY  - JOUR
T1  - The Role of Chemoattractant Receptors in Shaping the Tumor Microenvironment
AN  - 1611635719; 20792713
AB  - Chemoattractant receptors are a family of seven transmembrane G protein coupled receptors (GPCRs) initially found to mediate the chemotaxis and activation of immune cells. During the past decades, the functions of these GPCRs have been discovered to not only regulate leukocyte trafficking and promote immune responses, but also play important roles in homeostasis, development, angiogenesis, and tumor progression. Accumulating evidence indicates that chemoattractant GPCRs and their ligands promote the progression of malignant tumors based on their capacity to orchestrate the infiltration of the tumor microenvironment by immune cells, endothelial cells, fibroblasts, and mesenchymal cells. This facilitates the interaction of tumor cells with host cells, tumor cells with tumor cells, and host cells with host cells to provide a basis for the expansion of established tumors and development of distant metastasis. In addition, many malignant tumors of the nonhematopoietic origin express multiple chemoattractant GPCRs that increase the invasiveness and metastasis of tumor cells. Therefore, GPCRs and their ligands constitute targets for the development of novel antitumor therapeutics.
JF  - BioMed Research International
AU  - Zhou, Jiamin
AU  - Xiang, Yi
AU  - Yoshimura, Teizo
AU  - Chen, Keqiang
AU  - Gong, Wanghua
AU  - Huang, Jian
AU  - Zhou, Ye
AU  - Yao, Xiaohong
AU  - Bian, Xiuwu
AU  - Wang, Ji Ming
AD  - Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA, wangji@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Invasiveness
KW  - Angiogenesis
KW  - Homeostasis
KW  - Tumors
KW  - Tumor cells
KW  - Chemotaxis
KW  - Fibroblasts
KW  - Leukocyte migration
KW  - Endothelial cells
KW  - Metastases
KW  - G protein-coupled receptors
KW  - Chemotactic factors
KW  - Microenvironments
KW  - Immune response
KW  - Mesenchyme
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611635719?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+Role+of+Chemoattractant+Receptors+in+Shaping+the+Tumor+Microenvironment&rft.au=Zhou%2C+Jiamin%3BXiang%2C+Yi%3BYoshimura%2C+Teizo%3BChen%2C+Keqiang%3BGong%2C+Wanghua%3BHuang%2C+Jian%3BZhou%2C+Ye%3BYao%2C+Xiaohong%3BBian%2C+Xiuwu%3BWang%2C+Ji+Ming&rft.aulast=Zhou&rft.aufirst=Jiamin&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F751392
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Number of references - 3
N1  - Last updated - 2015-10-15
N1  - SubjectsTermNotLitGenreText - Invasiveness; Angiogenesis; Tumors; Homeostasis; Chemotaxis; Tumor cells; Fibroblasts; Metastases; Endothelial cells; Leukocyte migration; G protein-coupled receptors; Chemotactic factors; Microenvironments; Immune response; Mesenchyme
DO  - http://dx.doi.org/10.1155/2014/751392
ER  - 



TY  - JOUR
T1  - Diffusion Tensor Histogram Analysis of Pediatric Diffuse Intrinsic Pontine Glioma
AN  - 1611634288; 20792214
AB  - Purpose . To evaluate tumor structure in children with diffuse intrinsic pontine glioma (DIPG) using histogram analyses of mean diffusivity (MD), determine potential treatment and corticosteroid-related effects on MD, and monitor changes in MD distributions over time. Materials and Methods . DTI was performed on a 1.5T GE scanner. Regions of interest included the entire FLAIR-defined tumor. MD data were used to calculate histograms. Patterns in MD distributions were evaluated and fitted using a two-normal mixture model. Treatment-related effects were evaluated using the super(R2) statistic for linear mixed models and Cox proportional hazards models. Results . 12 patients with DIPG underwent one or more DTI exams. MD histogram distributions varied among patients. Over time, histogram peaks became shorter and broader ( P=0.0443 ). Two-normal mixture fitting revealed large lower curve proportions that were not associated with treatment response or outcome. Corticosteroid use affected MD histograms and was strongly associated with larger, sharper peaks ( super(R2) =0.51 , P=0.0028 ). Conclusions . MD histograms of pediatric DIPG show significant interpatient and intratumoral differences and quantifiable changes in tumor structure over time. Corticosteroids greatly affected MD and must be considered a confounding factor when interpreting MD results in the context of treatment response.
JF  - BioMed Research International
AU  - Steffen-Smith, Emilie A
AU  - Sarlls, Joelle E
AU  - Pierpaoli, Carlo
AU  - Shih, Joanna H
AU  - Bent, Robyn S
AU  - Walker, Lindsay
AU  - Warren, Katherine E
AD  - Pediatric Oncology Branch, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Building 10, Room 1-5750, 9000 Rockville Pike, Bethesda, MD 20892, USA, warrenk@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Brain tumors
KW  - Corticoids
KW  - Pediatrics
KW  - Statistical analysis
KW  - Tumors
KW  - Glioma
KW  - Children
KW  - Models
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611634288?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diffusion+Tensor+Histogram+Analysis+of+Pediatric+Diffuse+Intrinsic+Pontine+Glioma&rft.au=Steffen-Smith%2C+Emilie+A%3BSarlls%2C+Joelle+E%3BPierpaoli%2C+Carlo%3BShih%2C+Joanna+H%3BBent%2C+Robyn+S%3BWalker%2C+Lindsay%3BWarren%2C+Katherine+E&rft.aulast=Steffen-Smith&rft.aufirst=Emilie&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F647356
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Last updated - 2015-10-15
N1  - SubjectsTermNotLitGenreText - Brain tumors; Corticoids; Pediatrics; Statistical analysis; Glioma; Tumors; Children; Models
DO  - http://dx.doi.org/10.1155/2014/647356
ER  - 



TY  - JOUR
T1  - Diagnostic Features and Subtyping of Thymoma Lymph Node Metastases
AN  - 1611633827; 20792639
AB  - Aim. The purpose of the present study was to characterize the morphological features of thymoma metastases in lymph nodes and to evaluate the possibility of their subtyping according to the 2004 WHO classification of thymus tumors. Materials and Methods. We reviewed 210 thymoma cases in our series of thymic epithelial tumors (TET), including their recurrences and lymphogenous metastases. Three cases of lymph node metastases, one case occurring synchronously with the primary tumor and one synchronously with the first relapse (both in intrathoracic location) and one case of metastasis observed in a laterocervical lymph node subsequently to two thymoma relapses were found. Results. The metastatic nodes were variably but extensively involved in all cases. The histological features were similar in both primary tumors and metastases. Thymoma metastases were subtyped according to the WHO classification as B3 (one case) and B2 (two cases), and distinctive features in comparison to metastatic epithelial neoplasias from other sites were observed. Conclusion. Thymoma lymph node metastases, although rare, can be subtyped according to the WHO classification on the basis of their morphological and immunohistochemical features. Clinically, the presence of nodal metastases may herald subsequent relapses and further metastases even in extrathoracic sites.
JF  - BioMed Research International
AU  - Sioletic, Stefano
AU  - Lauriola, Libero
AU  - Gallo, Enzo
AU  - Martucci, Robert
AU  - Evoli, Amelia
AU  - Palmieri, Giovannella
AU  - Melis, Enrico
AU  - Pizzi, Giuseppe
AU  - Rinaldi, Massimo
AU  - Lalle, Maurizio
AU  - Pescarmona, Edoardo
AU  - Granone, Pierluigi
AU  - Facciolo, Francesco
AU  - Marino, Mirella
AD  - Department of Pathology, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy, mirellamarino@inwind.it
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Metastases
KW  - Classification
KW  - Reviews
KW  - Thymus
KW  - Tumors
KW  - thymoma
KW  - Lymph nodes
KW  - Neoplasia
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611633827?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diagnostic+Features+and+Subtyping+of+Thymoma+Lymph+Node+Metastases&rft.au=Sioletic%2C+Stefano%3BLauriola%2C+Libero%3BGallo%2C+Enzo%3BMartucci%2C+Robert%3BEvoli%2C+Amelia%3BPalmieri%2C+Giovannella%3BMelis%2C+Enrico%3BPizzi%2C+Giuseppe%3BRinaldi%2C+Massimo%3BLalle%2C+Maurizio%3BPescarmona%2C+Edoardo%3BGranone%2C+Pierluigi%3BFacciolo%2C+Francesco%3BMarino%2C+Mirella&rft.aulast=Sioletic&rft.aufirst=Stefano&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F546149
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Number of references - 3
N1  - Last updated - 2014-10-30
N1  - SubjectsTermNotLitGenreText - Metastases; Classification; Reviews; Thymus; Tumors; thymoma; Neoplasia; Lymph nodes
DO  - http://dx.doi.org/10.1155/2014/546149
ER  - 



TY  - JOUR
T1  - Challenges in malaria modeling
AN  - 1566857979; 20749856
JF  - Malaria Journal
AU  - McKenzie, F Ellis
AD  - Fogarty International Center, National Institutes of Health, Bethesda, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - Suppl 1
SN  - 1475-2875, 1475-2875
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Human diseases
KW  - Malaria
KW  - Modelling
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566857979?accountid=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=conference&rft.jtitle=Malaria+Journal&rft.atitle=Challenges+in+malaria+modeling&rft.au=McKenzie%2C+F+Ellis&rft.aulast=McKenzie&rft.aufirst=F&rft.date=2014-01-01&rft.volume=13&rft.issue=Suppl+1&rft.spage=O14&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-13-S1-O14
L2  - http://www.malariajournal.com/content/13/S1/O14
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Human diseases; Malaria; Modelling
DO  - http://dx.doi.org/10.1186/1475-2875-13-S1-O14
ER  - 



TY  - JOUR
T1  - Activity and Safety of Bevacizumab Plus Fotemustine for Recurrent Malignant Gliomas
AN  - 1566839282; 20727308
AB  - Background . No established chemotherapeutic regimen exists for the treatment of recurrent malignant gliomas (rMGs). Herein, we report the activity and safety results of the bevacizumab (B) plus fotemustine (FTM) combination for the treatment of rMGs. Patients and Methods . An induction phase consisted of B 10 mg/kg days 1, 15 plus FTM 65 mg/m super(2) days 1, 8, and 15. Nonprogressive patients entered the maintenance phase with B 10 mg/kg plus FTM 75 mg/m super(2) every 3 weeks. The primary endpoint was response rate; secondary endpoints included safety, progression free survival (PFS), and overall survival (OS). Results . Twenty-six patients affected by recurrent MGs (50% glioblastoma) were enrolled. Eight partial responses (31%) were observed. Median PFS and OS were 4 (95% C.I.: 2.8-5.1) and 6 months (95% C.I.: 4.2-7.8), respectively. Responses were significantly associated with both improved PFS and OS ( P=0.002 and P=0.001 , resp.). Treatment adverse events were mostly mild to moderate in intensity. Bevacizumab-related adverse events included grade 3 venous thromboembolic event (8%), grade 2 epistaxis (4%), hypertension (8%), and gastrointestinal perforation (4%). Conclusions . Bevacizumab plus FTM showed activity and good tolerability in pretreated MGs. Further investigations are needed in order to verify the benefits deriving from the addition of B to a cytotoxic in this clinical setting of patients.
JF  - BioMed Research International
AU  - Vaccaro, V
AU  - Fabi, A
AU  - Vidiri, A
AU  - Giannarelli, D
AU  - Metro, G
AU  - Telera, S
AU  - Vari, S
AU  - Piludu, F
AU  - Carosi, MA
AU  - Villani, V
AU  - Cognetti, F
AU  - Pompili, A
AU  - Marucci, L
AU  - Carapella, C M
AU  - Pace, A
AD  - Department of Medical Oncology, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy, alessandra.fabi@virgilio.it
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Brain tumors
KW  - Glioblastoma
KW  - Cytotoxicity
KW  - Survival
KW  - Bevacizumab
KW  - Glioma
KW  - Thromboembolism
KW  - Hypertension
KW  - N3 11027:Neurology & neuropathology
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566839282?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Impact+of+Immunogenetic+IL28B+Polymorphism+on+Natural+Outcome+of+HCV+Infection&rft.au=De+Re%2C+Valli%3BGragnani%2C+Laura%3BFognani%2C+Elisa%3BPiluso%2C+Alessia%3BIzzo%2C+Francesco%3BMangia%2C+Alessandra%3BCrovatto%2C+Marina%3BGava%2C+Graziella%3BCasarin%2C+Pietro%3BSansonno%2C+Domenico%3BRacanelli%2C+Vito%3BDe+Vita%2C+Salvatore%3BPioltelli%2C+Pietro%3BCaggiari%2C+Laura%3BDe+Zorzi%2C+Mariangela%3BBerretta%2C+Massimiliano%3BGini%2C+Andrea%3BZucchetto%2C+Antonella%3BBuonaguro%2C+Franco+Maria%3BDe+Paoli%2C+Paolo%3BZignego%2C+Anna+Linda&rft.aulast=De+Re&rft.aufirst=Valli&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F710642
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Number of references - 1
N1  - Last updated - 2015-10-15
N1  - SubjectsTermNotLitGenreText - Brain tumors; Glioblastoma; Cytotoxicity; Survival; Glioma; Bevacizumab; Thromboembolism; Hypertension
DO  - http://dx.doi.org/10.1155/2014/351252
ER  - 



TY  - JOUR
T1  - Phenotypic divergence among the members of the African malaria mosquitoes and strategies of persistence throughout the dry season
AN  - 1566834953; 20749870
JF  - Malaria Journal
AU  - Lehmann, Tovi
AU  - Dao, Adama
AU  - Yaro, Alpha S
AU  - Huestis, Diana L
AU  - Diallo, Moussa
AU  - Timbine, Seydou
AU  - Kassogue, Yaya
AU  - Adamou, Alpha
AU  - Traore, Adama I
AU  - Samake, Djibril
AD  - Laboratory of Malaria and Vector Research, NIAID, NIH, Rockville, MD, 20852, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - Suppl 1
SN  - 1475-2875, 1475-2875
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Human diseases
KW  - Africa
KW  - Culicidae
KW  - Malaria
KW  - Divergence
KW  - Dry season
KW  - Aquatic insects
KW  - Phenotypes
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566834953?accountid=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=conference&rft.jtitle=Malaria+Journal&rft.atitle=Phenotypic+divergence+among+the+members+of+the+African+malaria+mosquitoes+and+strategies+of+persistence+throughout+the+dry+season&rft.au=Lehmann%2C+Tovi%3BDao%2C+Adama%3BYaro%2C+Alpha+S%3BHuestis%2C+Diana+L%3BDiallo%2C+Moussa%3BTimbine%2C+Seydou%3BKassogue%2C+Yaya%3BAdamou%2C+Alpha%3BTraore%2C+Adama+I%3BSamake%2C+Djibril&rft.aulast=Lehmann&rft.aufirst=Tovi&rft.date=2014-01-01&rft.volume=13&rft.issue=Suppl+1&rft.spage=O2&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-13-S1-O2
L2  - http://www.malariajournal.com/content/13/S1/O2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Human diseases; Malaria; Divergence; Dry season; Phenotypes; Aquatic insects; Culicidae; Africa
DO  - http://dx.doi.org/10.1186/1475-2875-13-S1-O2
ER  - 



TY  - JOUR
T1  - Efficient drug delivery of Paclitaxel glycoside: a novel solubility gradient encapsulation into liposomes coupled with immunoliposomes preparation.
AN  - 1566822738; 25264848
AB  - Although the encapsulation of paclitaxel into liposomes has been extensively studied, its significant hydrophobic and uncharged character has generated substantial difficulties concerning its efficient encapsulation into the inner water core of liposomes. We found that a more hydrophilic paclitaxel molecule, 7-glucosyloxyacetylpaclitaxel, retained tubulin polymerization stabilization activity. The hydrophilic nature of 7-glucosyloxyacetylpaclitaxel allowed its efficient encapsulation into the inner water core of liposomes, which was successfully accomplished using a remote loading method with a solubility gradient between 40% ethylene glycol and Cremophor EL/ethanol in PBS. Trastuzumab was then conjugated onto the surface of liposomes as immunoliposomes to selectively target human epidermal growth factor receptor-2 (HER2)-overexpressing cancer cells. In vitro cytotoxicity assays revealed that the immunoliposomes enhanced the toxicity of 7-glucosyloxyacetylpaclitaxel in HER2-overexpressing cancer cells and showed more rapid suppression of cell growth. The immunoliposomes strongly inhibited the tumor growth of HT-29 cells xenografted in nude mice. Notably, mice survived when treated with the immunoliposomes formulation, even when administered at a lethal dose of 7-glucosyloxyacetylpaclitaxel in vivo. This data successfully demonstrates immunoliposomes as a promising candidate for the efficient delivery of paclitaxel glycoside.
JF  - PloS one
AU  - Shigehiro, Tsukasa
AU  - Kasai, Tomonari
AU  - Murakami, Masaharu
AU  - Sekhar, Sreeja C
AU  - Tominaga, Yuki
AU  - Okada, Masashi
AU  - Kudoh, Takayuki
AU  - Mizutani, Akifumi
AU  - Murakami, Hiroshi
AU  - Salomon, David S
AU  - Mikuni, Katsuhiko
AU  - Mandai, Tadakatsu
AU  - Hamada, Hiroki
AU  - Seno, Masaharu
AD  - Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama, Japan. ; Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, United States of America. ; Ensuiko Sugar Refining Co., Ltd., Tokyo, Japan. ; Faculty of Life Science, Kurashiki University of Science and the Arts, Kurashiki, Japan. ; Faculty of Science, Okayama University of Science, Okayama, Japan.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 9
KW  - Drug Carriers
KW  - 0
KW  - Glycosides
KW  - Liposomes
KW  - Paclitaxel
KW  - P88XT4IS4D
KW  - Index Medicus
KW  - Animals
KW  - Solubility
KW  - Humans
KW  - Mice
KW  - HT29 Cells
KW  - Mice, Inbred BALB C
KW  - Female
KW  - Paclitaxel -- chemistry
KW  - Paclitaxel -- administration & dosage
KW  - Glycosides -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566822738?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Efficient+drug+delivery+of+Paclitaxel+glycoside%3A+a+novel+solubility+gradient+encapsulation+into+liposomes+coupled+with+immunoliposomes+preparation.&rft.au=Shigehiro%2C+Tsukasa%3BKasai%2C+Tomonari%3BMurakami%2C+Masaharu%3BSekhar%2C+Sreeja+C%3BTominaga%2C+Yuki%3BOkada%2C+Masashi%3BKudoh%2C+Takayuki%3BMizutani%2C+Akifumi%3BMurakami%2C+Hiroshi%3BSalomon%2C+David+S%3BMikuni%2C+Katsuhiko%3BMandai%2C+Tadakatsu%3BHamada%2C+Hiroki%3BSeno%2C+Masaharu&rft.aulast=Shigehiro&rft.aufirst=Tsukasa&rft.date=2014-01-01&rft.volume=9&rft.issue=9&rft.spage=e107976&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0107976
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-06-15
N1  - Date created - 2014-09-30
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Control Release. 2000 Jan 3;63(1-2):19-30 [10640577]
Mol Med Rep. 2013 Mar;7(3):947-52 [23291923]
Eur J Cancer. 2001 Sep;37(13):1590-8 [11527683]
Int J Pharm. 2002 Mar 20;235(1-2):179-92 [11879753]
Clin Cancer Res. 2002 Apr;8(4):1172-81 [11948130]
AAPS PharmSci. 2003 Nov 21;5(4):E32 [15198520]
Cancer Treat Rev. 1993 Oct;19(4):351-86 [8106152]
Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):2031-5 [9050899]
Int J Cancer. 1997 Mar 28;71(1):103-7 [9096672]
Cancer Lett. 1997 Oct 14;118(2):153-60 [9459205]
Mol Cancer Ther. 2005 Mar;4(3):435-42 [15767552]
Clin Cancer Res. 2006 Feb 15;12(4):1317-24 [16489089]
Biomaterials. 2006 Oct;27(28):4975-83 [16757022]
Cancer Res. 2006 Jul 1;66(13):6732-40 [16818648]
Crit Rev Oncol Hematol. 2007 Mar;61(3):222-9 [17092739]
Int J Pharm. 2007 Jun 29;338(1-2):317-26 [17368984]
Cell Prolif. 2007 Aug;40(4):580-94 [17635524]
J Control Release. 2007 Jul 31;120(3):169-77 [17586082]
Pharm Res. 2007 Dec;24(12):2402-11 [17828616]
J Pharm Sci. 2010 May;99(5):2309-19 [19904827]
J Control Release. 2010 Jun 15;144(3):332-40 [20202473]
J Control Release. 2010 Sep 15;146(3):264-75 [20385184]
Biomaterials. 2011 May;32(13):3459-70 [21296406]
Adv Drug Deliv Rev. 2011 Mar 18;63(3):161-9 [20869415]
Int J Pharm. 2011 Jun 30;412(1-2):132-41 [21507344]
J Cell Mol Med. 2011 Nov;15(11):2525-38 [21323863]
J Control Release. 2012 Jun 10;160(2):117-34 [22484195]
J Control Release. 2012 Nov 10;163(3):322-34 [22989535]
Adv Drug Deliv Rev. 2013 Jan;65(1):36-48 [23036225]
J Control Release. 2001 Jul 6;74(1-3):95-113 [11489487]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0107976
ER  - 



TY  - JOUR
T1  - Atomic layer deposition coating of carbon nanotubes with aluminum oxide alters pro-fibrogenic cytokine expression by human mononuclear phagocytes in vitro and reduces lung fibrosis in mice in vivo.
AN  - 1562427363; 25216247
AB  - Multi-walled carbon nanotubes (MWCNTs) pose a possible human health risk for lung disease as a result of inhalation exposure. Mice exposed to MWCNTs develop pulmonary fibrosis. Lung macrophages engulf MWCNTs and produce pro-fibrogenic cytokines including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and osteopontin (OPN). Atomic layer deposition (ALD) is a novel process used to enhance functional properties of MWCNTs, yet the consequence of ALD-modified MWCNTs on macrophage biology and fibrosis is unknown.
          The purpose of this study was to determine whether ALD coating with aluminum oxide (Al2O3) would alter the fibrogenic response to MWCNTs and whether cytokine expression in human macrophage/monocytes exposed to MWCNTs in vitro would predict the severity of lung fibrosis in mice. Uncoated (U)-MWCNTs or ALD-coated (A)-MWCNTs were incubated with THP-1 macrophages or human peripheral blood mononuclear cells (PBMC) and cell supernatants assayed for cytokines by ELISA. C57BL6 mice were exposed to a single dose of A- or U-MWCNTs by oropharyngeal aspiration (4 mg/kg) followed by evaluation of histopathology, lung inflammatory cell counts, and cytokine levels at day 1 and 28 post-exposure. ALD coating of MWCNTs with Al2O3 enhanced IL-1β secretion by THP-1 and PBMC in vitro, yet reduced protein levels of IL-6, TNF-α, and OPN production by THP-1 cells. Moreover, Al2O3 nanoparticles, but not carbon black NPs, increased IL-1β but decreased OPN and IL-6 in THP-1 and PBMC. Mice exposed to U-MWCNT had increased levels of all four cytokines assayed and developed pulmonary fibrosis by 28 days, whereas ALD-coating significantly reduced fibrosis and cytokine levels at the mRNA or protein level.
          These findings indicate that ALD thin film coating of MWCNTs with Al2O3 reduces fibrosis in mice and that in vitro phagocyte expression of IL-6, TNF-α, and OPN, but not IL-1β, predict MWCNT-induced fibrosis in the lungs of mice in vivo.
JF  - PloS one
AU  - Taylor, Alexia J
AU  - McClure, Christina D
AU  - Shipkowski, Kelly A
AU  - Thompson, Elizabeth A
AU  - Hussain, Salik
AU  - Garantziotis, Stavros
AU  - Parsons, Gregory N
AU  - Bonner, James C
AD  - Environmental and Molecular Toxicology Program, Department of Biological Sciences, North Carolina State University, Raleigh, North Carolina, United States of America. ; Department of Chemical & Biomolecular Engineering, North Carolina State University, Raleigh, North Carolina, United States of America. ; Clinical Research Unit, 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  - 9
KW  - Cytokines
KW  - 0
KW  - Interleukin-1beta
KW  - Interleukin-6
KW  - Nanotubes, Carbon
KW  - Soot
KW  - Tumor Necrosis Factor-alpha
KW  - Osteopontin
KW  - 106441-73-0
KW  - Aluminum Oxide
KW  - LMI26O6933
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Osteopontin -- metabolism
KW  - Interleukin-6 -- metabolism
KW  - Lung -- metabolism
KW  - Lung -- pathology
KW  - Cell Death -- drug effects
KW  - Macrophages -- drug effects
KW  - Soot -- pharmacology
KW  - Pulmonary Fibrosis
KW  - Interleukin-1beta -- biosynthesis
KW  - Mice, Inbred C57BL
KW  - Lung -- drug effects
KW  - Macrophages -- ultrastructure
KW  - Osteopontin -- secretion
KW  - Tumor Necrosis Factor-alpha -- metabolism
KW  - Cell Line
KW  - Surface Properties
KW  - Inflammation -- pathology
KW  - Macrophages -- metabolism
KW  - Nanotubes, Carbon -- chemistry
KW  - Phagocytes -- metabolism
KW  - Nanotubes, Carbon -- ultrastructure
KW  - Leukocytes, Mononuclear -- metabolism
KW  - Aluminum Oxide -- pharmacology
KW  - Nanotechnology -- methods
KW  - Cytokines -- metabolism
KW  - Phagocytes -- drug effects
KW  - Leukocytes, Mononuclear -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562427363?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Atomic+layer+deposition+coating+of+carbon+nanotubes+with+aluminum+oxide+alters+pro-fibrogenic+cytokine+expression+by+human+mononuclear+phagocytes+in+vitro+and+reduces+lung+fibrosis+in+mice+in+vivo.&rft.au=Taylor%2C+Alexia+J%3BMcClure%2C+Christina+D%3BShipkowski%2C+Kelly+A%3BThompson%2C+Elizabeth+A%3BHussain%2C+Salik%3BGarantziotis%2C+Stavros%3BParsons%2C+Gregory+N%3BBonner%2C+James+C&rft.aulast=Taylor&rft.aufirst=Alexia&rft.date=2014-01-01&rft.volume=9&rft.issue=9&rft.spage=e106870&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0106870
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-05-28
N1  - Date created - 2014-09-13
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Hum Pathol. 2002 Aug;33(8):819-25 [12203215]
Nanotoxicology. 2014 Feb;8(1):17-27 [23094697]
Exp Lung Res. 2004 Oct-Nov;30(7):585-98 [15371094]
Am J Respir Cell Mol Biol. 2005 Apr;32(4):342-9 [15653932]
Toxicol Appl Pharmacol. 2005 Sep 15;207(3):221-31 [16129115]
PLoS Med. 2005 Sep;2(9):e251 [16128620]
N Engl J Med. 2005 Oct 13;353(15):1564-73 [16221779]
Science. 2006 Feb 3;311(5761):622-7 [16456071]
Toxicol Pathol. 2007 Jan;35(1):148-53 [17325983]
Acc Chem Res. 2008 Jan;41(1):60-8 [17867649]
Am J Respir Cell Mol Biol. 2009 Mar;40(3):349-58 [18787175]
Biomed Mater. 2009 Apr;4(2):025001 [19208941]
Hypertension. 2009 May;53(5):751-3 [19307468]
Toxicology. 2009 May 17;259(3):113-21 [19428951]
Nat Nanotechnol. 2009 Nov;4(11):747-51 [19893520]
Toxicol Sci. 2009 Dec;112(2):468-81 [19584127]
Toxicol Sci. 2010 Jan;113(1):226-42 [19822600]
Part Fibre Toxicol. 2010;7:5 [20307263]
Am J Respir Cell Mol Biol. 2010 Aug;43(2):142-51 [19738159]
ACS Nano. 2010 Jul 27;4(7):3661-70 [20593840]
Nat Nanotechnol. 2011 Feb;6(2):121-5 [21278749]
Am J Pathol. 2011 May;178(5):1975-85 [21514415]
Part Fibre Toxicol. 2011;8:21 [21781304]
ACS Nano. 2011 Sep 27;5(9):6861-70 [21800904]
Am J Respir Cell Mol Biol. 2011 Oct;45(4):858-66 [21398620]
Nat Nanotechnol. 2011 Oct;6(10):645-50 [21926980]
Langmuir. 2011 Dec 6;27(23):14497-507 [22070742]
ACS Nano. 2011 Dec 27;5(12):9772-87 [22047207]
Adv Mater. 2012 Feb 21;24(8):1017-32 [22278762]
Int J Nanomedicine. 2012;7:1387-97 [22457596]
Part Fibre Toxicol. 2012;9:8 [22472194]
Nat Med. 2012 Jul;18(7):1028-40 [22772564]
ACS Nano. 2012 Jul 24;6(7):5820-9 [22717232]
Small. 2012 Sep 24;8(18):2904-12 [22777948]
Part Fibre Toxicol. 2012;9:22 [22713230]
Inhal Toxicol. 2012 Dec;24(14):995-1008 [23216160]
J Pathol. 2013 Jan;229(2):157-67 [23023641]
Toxicol Lett. 2013 Feb 27;217(2):91-101 [23266719]
Environ Health Perspect. 2013 Jun;121(6):683-90 [23649538]
Am J Pathol. 2013 Sep;183(3):758-73 [23886891]
Cytokine Growth Factor Rev. 2003 Dec;14(6):479-88 [14563350]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0106870
ER  - 



TY  - JOUR
T1  - Differential sensitivity of prefrontal cortex and hippocampus to alcohol-induced toxicity.
AN  - 1560587166; 25188266
AB  - The prefrontal cortex (PFC) is a brain region responsible for executive functions including working memory, impulse control and decision making. The loss of these functions may ultimately lead to addiction. Using histological analysis combined with stereological technique, we demonstrated that the PFC is more vulnerable to chronic alcohol-induced oxidative stress and neuronal cell death than the hippocampus. This increased vulnerability is evidenced by elevated oxidative stress-induced DNA damage and enhanced expression of apoptotic markers in PFC neurons. We also found that one-carbon metabolism (OCM) impairment plays a significant role in alcohol toxicity to the PFC seen from the difference in the effects of acute and chronic alcohol exposure on DNA repair and from exaggeration of the damaging effects upon additional OCM impairment in mice deficient in a key OCM enzyme, methylenetetrahydrofolate reductase (MTHFR). Given that damage to the PFC leads to loss of executive function and addiction, our study may shed light on the mechanism of alcohol addiction.
JF  - PloS one
AU  - Fowler, Anna-Kate
AU  - Thompson, Jeremy
AU  - Chen, Lixia
AU  - Dagda, Marisela
AU  - Dertien, Janet
AU  - Dossou, Katina Sylvestre S
AU  - Moaddel, Ruin
AU  - Bergeson, Susan E
AU  - Kruman, Inna I
AD  - Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America. ; Laboratory of Clinical Investigation, NIA, National Institutes of Health, Baltimore, Maryland, United States of America.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 9
KW  - Biomarkers
KW  - 0
KW  - Microtubule-Associated Proteins
KW  - Mtap2 protein, mouse
KW  - Homocysteine
KW  - 0LVT1QZ0BA
KW  - Ethanol
KW  - 3K9958V90M
KW  - Methylenetetrahydrofolate Reductase (NADPH2)
KW  - EC 1.5.1.20
KW  - Index Medicus
KW  - Acute Disease
KW  - Animals
KW  - Microtubule-Associated Proteins -- metabolism
KW  - Neurons -- metabolism
KW  - Apoptosis
KW  - DNA Damage
KW  - Gene Expression
KW  - Organ Specificity
KW  - Mice
KW  - Methylenetetrahydrofolate Reductase (NADPH2) -- deficiency
KW  - Neurons -- pathology
KW  - Mice, Knockout
KW  - Homocysteine -- metabolism
KW  - Microtubule-Associated Proteins -- genetics
KW  - Oxidative Stress
KW  - Mice, Inbred C57BL
KW  - Biomarkers -- metabolism
KW  - Chronic Disease
KW  - Male
KW  - Stereotaxic Techniques
KW  - Methylenetetrahydrofolate Reductase (NADPH2) -- genetics
KW  - DNA Repair -- genetics
KW  - Prefrontal Cortex -- metabolism
KW  - Alcoholism -- pathology
KW  - Prefrontal Cortex -- pathology
KW  - Hippocampus -- metabolism
KW  - Ethanol -- toxicity
KW  - Alcoholism -- metabolism
KW  - Hippocampus -- pathology
KW  - Alcoholism -- genetics
KW  - Prefrontal Cortex -- drug effects
KW  - Hippocampus -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560587166?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+sensitivity+of+prefrontal+cortex+and+hippocampus+to+alcohol-induced+toxicity.&rft.au=Fowler%2C+Anna-Kate%3BThompson%2C+Jeremy%3BChen%2C+Lixia%3BDagda%2C+Marisela%3BDertien%2C+Janet%3BDossou%2C+Katina+Sylvestre+S%3BMoaddel%2C+Ruin%3BBergeson%2C+Susan+E%3BKruman%2C+Inna+I&rft.aulast=Fowler&rft.aufirst=Anna-Kate&rft.date=2014-01-01&rft.volume=9&rft.issue=9&rft.spage=e106945&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0106945
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-12-04
N1  - Date created - 2014-09-05
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Nature. 1993 Apr 22;362(6422):709-15 [8469282]
Brain. 2004 May;127(Pt 5):1108-26 [14985269]
Mutat Res. 1995 Dec;345(3-4):191-6 [8552140]
Circulation. 1999 Jun 1;99(21):2757-64 [10351969]
Exp Biol Med (Maywood). 2004 Nov;229(10):988-95 [15522834]
Mutat Res. 2005 Sep 4;577(1-2):203-16 [15922368]
Brain Res Dev Brain Res. 2005 Dec 7;160(2):130-45 [16226814]
Neuropsychopharmacology. 2006 Jun;31(6):1301-9 [16251993]
Nat Neurosci. 2006 Sep;9(9):1161-8 [16921368]
Neuropsychopharmacology. 2007 Jun;32(6):1251-60 [17119541]
Toxicol Pathol. 2007 Jun;35(4):495-516 [17562483]
Am J Psychiatry. 2007 Aug;164(8):1149-59 [17671276]
Biol Psychiatry. 2007 Sep 15;62(6):627-34 [17336938]
Neurochem Res. 2008 Jun;33(6):1117-28 [18259862]
Brain Res Rev. 2008 Jun;58(1):192-208 [18440072]
Ann N Y Acad Sci. 2008 Oct;1141:105-30 [18991954]
Alcohol Alcohol. 2009 Mar-Apr;44(2):136-40 [19147798]
Physiol Rev. 2009 Apr;89(2):649-705 [19342616]
Nat Rev Neurosci. 2009 Jun;10(6):410-22 [19455173]
Behav Brain Res. 2009 Sep 14;202(2):225-31 [19463705]
Pharmacol Biochem Behav. 2009 Sep;93(3):237-47 [19410598]
J Nutr. 2009 Dec;139(12):2402-5 [19812215]
Neuropsychopharmacology. 2010 Jan;35(1):217-38 [19710631]
DNA Repair (Amst). 2010 Aug 5;9(8):898-906 [20634149]
Neurosci Biobehav Rev. 2010 Nov;35(2):232-47 [20493211]
Methods Mol Biol. 2011;682:3-13 [21057916]
Mutat Res. 2010 Nov 28;703(1):59-65 [20601098]
Behav Brain Res. 2011 Jun 1;219(2):234-9 [21255611]
Brain. 2011 Jul;134(Pt 7):2013-24 [21690575]
J Neurosci Res. 2011 Sep;89(9):1461-70 [21656845]
Hum Brain Mapp. 2012 Feb;33(2):319-33 [21391268]
Antioxid Redox Signal. 2012 May 15;16(10):1033-45 [22098189]
J Neural Transm (Vienna). 2012 Aug;119(8):891-910 [22212484]
Exp Biol Med (Maywood). 2012 Jul;237(7):740-7 [22829701]
Alcohol Clin Exp Res. 2012 Dec;36(12):2017-27 [22577873]
World J Biol Psychiatry. 2013 Dec;14(8):549-64 [24236956]
J Neurochem. 2014 Jun;129(5):770-80 [24521073]
Neuropharmacology. 2014 Sep;84:101-10 [23978384]
Mol Cell Biochem. 2014 Aug;393(1-2):43-57 [24671494]
Eur J Neurosci. 2013 Oct;38(7):3018-26 [23815783]
J Biol Chem. 2012 Dec 21;287(52):43533-42 [23118224]
Nutrition. 2000 Apr;16(4):296-302 [10758367]
J Neural Transm Suppl. 2000;(60):187-96 [11205139]
Hum Mol Genet. 2001 Mar 1;10(5):433-43 [11181567]
Neuropsychologia. 2001;39(4):376-89 [11164876]
Biol Psychiatry. 2002 Jan 15;51(2):134-42 [11822992]
Neuropsychologia. 2002;40(10):1675-89 [11992656]
Neuropsychologia. 2002;40(10):1690-705 [11992657]
Science. 2002 Jul 26;297(5581):552-7 [12142524]
Nat Rev Cancer. 2003 Sep;3(9):701-8 [12951589]
Curr Med Chem. 2003 Dec;10(24):2693-703 [14529459]
Alcohol Clin Exp Res. 2004 Apr;28(4):650-61 [15100618]
Cognition. 1994 Apr-Jun;50(1-3):7-15 [8039375]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0106945
ER  - 



TY  - JOUR
T1  - Purified cell wall from the probiotic bacterium Lactobacillus gasseri activates systemic inflammation and, at higher doses, produces lethality in a rat model
AN  - 1560111054; 20504057
AB  - Introduction: One proposed benefit of probiotic therapy is that probiotic bacterial cell-wall binding to intestinal cell pathogen-recognition receptors activates protective innate immunity. However, in critically ill patients, intestinal epithelium disruption by shock or other insults may compromise this compartmentalized response and cause systemic bacteria and cell-wall translocation. The effects of intravascular introduction of probiotic bacterial cell wall are unclear. Methods: We investigated 24-hour infusions of purified cell wall from Lactobacillus gasseri ATC33323 (L. gasseri), a probiotic bacterium, in Sprague-Dawley rats (n = 49). Results: Increasing cell-wall doses (0 (control), 10, 20, 40, 80, or 160 mg/kg over 24 hours) produced dose-ordered decreases in survival measured after 168 hours (11 survivors/11 total (100%), seven of seven (100%), seven of seven (100%), six of eight (75%), five of eight (63%), and one of nine (11%), respectively, P < 0.0001). The L. gasseri cell wall was equally or more lethal than Staphylococcus aureus cell wall, which was previously studied (100% to 88% survival with the same increasing doses). During challenge, compared with controls, L. gasseri cell wall produced increases in blood IL-1[beta], IL-10, tumor necrosis factor-[alpha], migratory inhibitory protein-1[alpha], monocyte chemotactic protein-1, and nitric oxide, and decreases in neutrophils, lymphocytes, and platelets that were greater with higher versus lower doses (P less than or equal to 0.05). Medium-dose cell wall (40 and 80 mg/kg combined) progressively decreased blood pressure and increased heart rate, and all doses increased lactate, hepatic transaminases, and creatinine phosphokinase (P less than or equal to 0.05). Conclusion: Although L. gasseri, like other probiotic bacteria, is considered safe, its cell wall can stimulate the maladaptive inflammatory response associated with pathogenic bacteria. Such effects deserve study, especially regarding critically ill patients.
JF  - Critical Care
AU  - Xu, Xinhui
AU  - Hicks, Caitlin
AU  - Li, Yan
AU  - Su, Junwu
AU  - Shiloach, Joseph
AU  - Kaufman, Jeanne B
AU  - Fitz, Yvonne
AU  - Eichacker, Peter Q
AU  - Cui, Xizhong
AD  - Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 1
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 18
IS  - 4
SN  - 1364-8535, 1364-8535
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology
KW  - Cell survival
KW  - Heart rate
KW  - Animal models
KW  - Lymphocytes
KW  - transaminase
KW  - Interleukin 10
KW  - Blood pressure
KW  - Epithelium
KW  - Cell migration
KW  - Staphylococcus aureus
KW  - Translocation
KW  - Monocyte chemoattractant protein 1
KW  - probiotics
KW  - Leukocytes (neutrophilic)
KW  - Immunity
KW  - Inflammation
KW  - Lethality
KW  - Creatinine
KW  - Shock
KW  - Lactic acid
KW  - Intestine
KW  - Platelets
KW  - Liver
KW  - Lactobacillus gasseri
KW  - Nitric oxide
KW  - Cell walls
KW  - J 02410:Animal Diseases
KW  - A 01330:Food Microbiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560111054?accountid=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=Critical+Care&rft.atitle=Purified+cell+wall+from+the+probiotic+bacterium+Lactobacillus+gasseri+activates+systemic+inflammation+and%2C+at+higher+doses%2C+produces+lethality+in+a+rat+model&rft.au=Xu%2C+Xinhui%3BHicks%2C+Caitlin%3BLi%2C+Yan%3BSu%2C+Junwu%3BShiloach%2C+Joseph%3BKaufman%2C+Jeanne+B%3BFitz%2C+Yvonne%3BEichacker%2C+Peter+Q%3BCui%2C+Xizhong&rft.aulast=Xu&rft.aufirst=Xinhui&rft.date=2014-01-01&rft.volume=18&rft.issue=4&rft.spage=R140&rft.isbn=&rft.btitle=&rft.title=Critical+Care&rft.issn=13648535&rft_id=info:doi/10.1186%2Fcc13966
L2  - http://ccforum.com/content/18/4/R140
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Number of references - 40
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Cell survival; Monocyte chemoattractant protein 1; Heart rate; Leukocytes (neutrophilic); probiotics; Animal models; Lymphocytes; Immunity; Blood pressure; Interleukin 10; transaminase; Inflammation; Creatinine; Lethality; Shock; Liver; Platelets; Intestine; Lactic acid; Nitric oxide; Epithelium; Cell migration; Translocation; Cell walls; Lactobacillus gasseri; Staphylococcus aureus
DO  - http://dx.doi.org/10.1186/cc13966
ER  - 



TY  - JOUR
T1  - Growing burden and impact of road crashes in India: need for a safe systems approach
AN  - 1560103298; 20619333
AB  - As per estimates, nearly 175,000 (136,900 as per official reports) persons died due to road crashes in India in 2011 along with hospitalisations and disabilities among survivors. More than 70-80% of these deaths and injuries occurred among young people, men and among pedestrians, two wheeler riders and pillions, and cyclists. The economic loss due to road crashes is an estimated $550 billion (INR 55,000 crores) or 3% of GDP (at 2004 prices) every year. Road safety in India requires a scientific approach for making road users safer in all traffic environments considering the limitations of human behaviour. There is need for strong road safety policies and programmes, a lead agency to coordinate activities, capacity strengthening, human resources, dedicated funding, strong advocacy, implementing scientific interventions, along with monitoring and evaluation. The 4'E's of Engineering, Enforcement, Education and Emergency Care need to be addressed through an intersectoral approach. In India, road deaths and other injuries are publicly glaring, while road safety is professionally lacking and politically missing and needs to be corrected for making road environments safer through multipronged approaches.
JF  - International Journal of Vehicle Safety
AU  - Gururaj, G
AD  - Department of Epidemiology, WHO Collaborating Centre for Injury Prevention & Safety Promotion, Centre for Public Health, National Institute of Mental Health & Neuro Sciences, Bangalore 560029, Karnataka, India
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 282
EP  - 295
PB  - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom
VL  - 7
IS  - 3-4
SN  - 1479-3105, 1479-3105
KW  - Health & Safety Science Abstracts
KW  - SCIENCE, ENGINEERING AND TECHNOLOGY
KW  - RISK, SAFETY AND EMERGENCY MANAGEMENT
KW  - Automotive and Vehicle Technology and Systems
KW  - Design and Product Development
KW  - Risk, Reliability and Safety
KW  - Mortality
KW  - Injuries
KW  - Pedestrians
KW  - Safety
KW  - Intervention
KW  - India
KW  - Education
KW  - Safety engineering
KW  - Disabilities
KW  - Economics
KW  - Traffic safety
KW  - Emergency medical services
KW  - H 2000:Transportation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560103298?accountid=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=International+Journal+of+Vehicle+Safety&rft.atitle=Growing+burden+and+impact+of+road+crashes+in+India%3A+need+for+a+safe+systems+approach&rft.au=Gururaj%2C+G&rft.aulast=Gururaj&rft.aufirst=G&rft.date=2014-01-01&rft.volume=7&rft.issue=3-4&rft.spage=282&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Vehicle+Safety&rft.issn=14793105&rft_id=info:doi/10.1504%2FIJVS.2014.063261
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Mortality; Education; Safety engineering; Injuries; Disabilities; Pedestrians; Safety; Economics; Intervention; Traffic safety; Emergency medical services; India
DO  - http://dx.doi.org/10.1504/IJVS.2014.063261
ER  - 



TY  - JOUR
T1  - First complex, then simple
AN  - 1554953326; 20459072
JF  - BioData Mining
AU  - Malley, James D
AU  - Moore, Jason H
AD  - Center for Information Technology, The National Institutes of Health, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 13
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 7
IS  - 1
SN  - 1756-0381, 1756-0381
KW  - Biotechnology and Bioengineering Abstracts
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554953326?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioData+Mining&rft.atitle=First+complex%2C+then+simple&rft.au=Padron%2C+Alejandro%3BMolina-Cruz%2C+Alvaro%3BQuinones%2C+Mariam%3BRibeiro%2C+Jose+MC%3BRamphul%2C+Urvashi%3BRodrigues%2C+Janneth%3BShen%2C+Kui%3BHaile%2C+Ashley%3BRamirez%2C+Jose+Luis%3BBarillas-Mury%2C+Carolina&rft.aulast=Padron&rft.aufirst=Alejandro&rft.date=2014-01-01&rft.volume=15&rft.issue=1&rft.spage=636&rft.isbn=&rft.btitle=&rft.title=BMC+Genomics&rft.issn=14712164&rft_id=info:doi/10.1186%2F1471-2164-15-636
L2  - http://www.biodatamining.org/content/7/1/13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 3
N1  - Last updated - 2014-08-21
DO  - http://dx.doi.org/10.1186/1756-0381-7-13
ER  - 



TY  - JOUR
T1  - In depth annotation of the Anopheles gambiae mosquito midgut transcriptome
AN  - 1554948702; 20503957
AB  - Background: Genome sequencing of Anopheles gambiae was completed more than ten years ago and has accelerated research on malaria transmission. However, annotation needs to be refined and verified experimentally, as most predicted transcripts have been identified by comparative analysis with genomes from other species. The mosquito midgut-the first organ to interact with Plasmodium parasites-mounts effective antiplasmodial responses that limit parasite survival and disease transmission. High-throughput Illumina sequencing of the midgut transcriptome was used to identify new genes and transcripts, contributing to the refinement of An. gambiae genome annotation. Results: We sequenced similar to 223 million reads from An. gambiae midgut cDNA libraries generated from susceptible (G3) and refractory (L35) mosquito strains. Mosquitoes were infected with either Plasmodium berghei or Plasmodium falciparum, and midguts were collected after the first or second Plasmodium infection. In total, 22,889 unique midgut transcript models were generated from both An. gambiae strain sequences combined, and 76% are potentially novel. Of these novel transcripts, 49.5% aligned with annotated genes and appear to be isoforms or pre-mRNAs of reference transcripts, while 50.5% mapped to regions between annotated genes and represent novel intergenic transcripts (NITs). Predicted models were validated for midgut expression using qRT-PCR and microarray analysis, and novel isoforms were confirmed by sequencing predicted intron-exon boundaries. Coding potential analysis revealed that 43% of total midgut transcripts appear to be long non-coding RNA (lncRNA), and functional annotation of NITs showed that 68% had no homology to current databases from other species. Reads were also analyzed using de novo assembly and predicted transcripts compared with genome mapping-based models. Finally, variant analysis of G3 and L35 midgut transcripts detected 160,742 variants with respect to the An. gambiae PEST genome, and 74% were new variants. Intergenic transcripts had a higher frequency of variation compared with non-intergenic transcripts. Conclusion: This in-depth Illumina sequencing and assembly of the An. gambiae midgut transcriptome doubled the number of known transcripts and tripled the number of variants known in this mosquito species. It also revealed existence of a large number of lncRNA and opens new possibilities for investigating the biological function of many newly discovered transcripts.
JF  - BMC Genomics
AU  - Padron, Alejandro
AU  - Molina-Cruz, Alvaro
AU  - Quinones, Mariam
AU  - Ribeiro, Jose MC
AU  - Ramphul, Urvashi
AU  - Rodrigues, Janneth
AU  - Shen, Kui
AU  - Haile, Ashley
AU  - Ramirez, Jose Luis
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///0,
PY  - 2014
DA  - 0, 2014
SP  - 636
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 15
IS  - 1
SN  - 1471-2164, 1471-2164
KW  - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Entomology Abstracts
KW  - Genomes
KW  - Parasites
KW  - Geographical distribution
KW  - non-coding RNA
KW  - Survival
KW  - Malaria
KW  - Infection
KW  - DNA microarrays
KW  - Disease transmission
KW  - Models
KW  - Public health
KW  - Gene expression
KW  - Midgut
KW  - Antiprotozoal agents
KW  - Aquatic insects
KW  - Pest control
KW  - Plasmodium falciparum
KW  - Endoparasites
KW  - Anopheles gambiae
KW  - Plasmodium berghei
KW  - Databases
KW  - Bibliographic information
KW  - Homology
KW  - Boundaries
KW  - G 07810:Insects
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Z 05320:Physiology, Anatomy, and Biochemistry
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554948702?accountid=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=BMC+Genomics&rft.atitle=In+depth+annotation+of+the+Anopheles+gambiae+mosquito+midgut+transcriptome&rft.au=Padron%2C+Alejandro%3BMolina-Cruz%2C+Alvaro%3BQuinones%2C+Mariam%3BRibeiro%2C+Jose+MC%3BRamphul%2C+Urvashi%3BRodrigues%2C+Janneth%3BShen%2C+Kui%3BHaile%2C+Ashley%3BRamirez%2C+Jose+Luis%3BBarillas-Mury%2C+Carolina&rft.aulast=Padron&rft.aufirst=Alejandro&rft.date=2014-01-01&rft.volume=15&rft.issue=1&rft.spage=636&rft.isbn=&rft.btitle=&rft.title=BMC+Genomics&rft.issn=14712164&rft_id=info:doi/10.1186%2F1471-2164-15-636
L2  - http://www.biomedcentral.com/1471-2164/15/636
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 42
N1  - Last updated - 2016-10-26
N1  - SubjectsTermNotLitGenreText - Genomes; Parasites; Bibliographic information; Geographical distribution; Pest control; Endoparasites; Aquatic insects; Public health; non-coding RNA; Survival; Malaria; Infection; DNA microarrays; Models; Disease transmission; Gene expression; Databases; Homology; Boundaries; Antiprotozoal agents; Midgut; Plasmodium falciparum; Anopheles gambiae; Plasmodium berghei
DO  - http://dx.doi.org/10.1186/1471-2164-15-636
ER  - 



TY  - JOUR
T1  - Individual education, area income, and mortality and recurrence of myocardial infarction in a Medicare cohort: the National Longitudinal Mortality Study
AN  - 1554947721; 20450868
AB  - Background: The Medicare program provides universal access to hospital care for the elderly; however, mortality disparities may still persist in this population. The association of individual education and area income with survival and recurrence post Myocardial Infarction (MI) was assessed in a national sample. Methods: Individual level education from the National Longitudinal Mortality Study was linked to Medicare and National Death Index records over the period of 1991-2001 to test the association of individual education and zip code tabulation area median income with survival and recurrence post-MI. Survival was partitioned into 3 periods: in-hospital, discharge to 1 year, and 1 year to 5 years and recurrence was partitioned into two periods: 28 day to 1 year, and 1 year to 5 years. Results: First MIs were found in 8,043 women and 7,929 men. In women and men 66-79 years of age, less than a high school education compared with a college degree or more was associated with 1-5 year mortality in both women (HRR 1.61, 95% confidence interval 1.03-2.50) and men (HRR 1.37, 1.06-1.76). Education was also associated with 1-5 year recurrence in men (HRR 1.68, 1.18-2.41, < High School compared with college degree or more), but not women. Across the spectrum of survival and recurrence periods median zip code level income was inconsistently associated with outcomes. Associations were limited to discharge-1 year survival (RR lowest versus highest quintile 1.31, 95% confidence interval 1.03-1.67) and 28 day-1 year recurrence (RR lowest versus highest quintile 1.72, 95% confidence interval 1.14-2.57) in older men. Conclusions: Despite the Medicare entitlement program, disparities related to individual socioeconomic status remain. Additional research is needed to elucidate the barriers and mechanisms to eliminating health disparities among the elderly.
JF  - BMC Public Health
AU  - Coady, Sean A
AU  - Johnson, Norman J
AU  - Hakes, Jahn K
AU  - Sorlie, Paul D
AD  - Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, 2 Rockledge Ctr, 6701 Rockledge Dr., Rm10200 MSC 7936, Bethesda 20817 MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 705
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2458, 1471-2458
KW  - Health & Safety Science Abstracts
KW  - Myocardial infarction
KW  - Epidemiology
KW  - Mortality
KW  - Socio-economic
KW  - Elderly
KW  - Education
KW  - Age
KW  - Survival
KW  - Socioeconomics
KW  - Income
KW  - Hospitals
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554947721?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Public+Health&rft.atitle=Individual+education%2C+area+income%2C+and+mortality+and+recurrence+of+myocardial+infarction+in+a+Medicare+cohort%3A+the+National+Longitudinal+Mortality+Study&rft.au=Coady%2C+Sean+A%3BJohnson%2C+Norman+J%3BHakes%2C+Jahn+K%3BSorlie%2C+Paul+D&rft.aulast=Coady&rft.aufirst=Sean&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=705&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-14-705
L2  - http://www.biomedcentral.com/1471-2458/14/705
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 31
N1  - Last updated - 2014-09-18
N1  - SubjectsTermNotLitGenreText - Mortality; Age; Education; Elderly; Socioeconomics; Survival; Myocardial infarction; Hospitals; Income
DO  - http://dx.doi.org/10.1186/1471-2458-14-705
ER  - 



TY  - JOUR
T1  - Innovation is often unnerving: the door into summer
AN  - 1554947231; 20450727
JF  - BioData Mining
AU  - Malley, James D
AU  - Moore, Jason H
AD  - Center for Information Technology, The National Institutes of Health, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 12
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 7
IS  - 1
SN  - 1756-0381, 1756-0381
KW  - Biotechnology and Bioengineering Abstracts
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554947231?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioData+Mining&rft.atitle=Innovation+is+often+unnerving%3A+the+door+into+summer&rft.au=Malley%2C+James+D%3BMoore%2C+Jason+H&rft.aulast=Malley&rft.aufirst=James&rft.date=2014-01-01&rft.volume=7&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=BioData+Mining&rft.issn=17560381&rft_id=info:doi/10.1186%2F1756-0381-7-12
L2  - http://www.biodatamining.org/content/7/1/12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 1
N1  - Last updated - 2014-08-21
DO  - http://dx.doi.org/10.1186/1756-0381-7-12
ER  - 



TY  - JOUR
T1  - Biological activities of 'noninfectious' influenza A virus particles
AN  - 1554945316; 20455967
AB  - ABSTRACT: Only a small fraction of influenza A virus (IAV) particles within a viral population register as infectious by traditional infectivity assays. Despite constituting the most abundant product of influenza infection, the role that the 'noninfectious' particle fraction plays in the biology of the virus has largely been ignored. This review shines a light on this oft-ignored population by highlighting studies, both old and new, that describe the unique biological activities of these particles, and discussing what this population can tell us about the biology of IAV evolution and disease.
JF  - Future Virology
AU  - Brooke, Christopher B
AD  - Laboratory of Viral Diseases, National Institute of Allergy & Infectious Diseases, Bethesda, MD, USA; , brookecb@niaid.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 41
EP  - 51
PB  - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL  - 9
IS  - 1
SN  - 1746-0794, 1746-0794
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - aggregation
KW  - DI particles
KW  - genome packaging
KW  - influenza
KW  - noninfectious
KW  - semi-infectious
KW  - virion heterogeneity
KW  - virus
KW  - Influenza
KW  - Infectivity
KW  - Influenza A virus
KW  - Reviews
KW  - Population studies
KW  - Particulates
KW  - Infection
KW  - Evolution
KW  - Light effects
KW  - H 0500:General
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554945316?accountid=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=Future+Virology&rft.atitle=Biological+activities+of+%27noninfectious%27+influenza+A+virus+particles&rft.au=Brooke%2C+Christopher+B&rft.aulast=Brooke&rft.aufirst=Christopher&rft.date=2014-01-01&rft.volume=9&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Future+Virology&rft.issn=17460794&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 103
N1  - Last updated - 2015-02-12
N1  - SubjectsTermNotLitGenreText - Infectivity; Population studies; Infection; Evolution; Light effects; Influenza; Reviews; Particulates; Influenza A virus
ER  - 



TY  - JOUR
T1  - The independent and combined effects of exercise training and reducing sedentary behavior on cardiometabolic risk factors
AN  - 1554942751; 20461774
AB  - This pilot study examined if the combination of exercise training and reducing sedentary time (ST) results in greater changes to health markers than either intervention alone. Fifty-seven overweight/obese participants (19 males/39 females) (mean plus or minus SD; age, 43.6 plus or minus 9.9 years; body mass index (BMI), 35.1 plus or minus 4.6 kg.m super(-2)) completed the 12-week study and were randomly assigned to (i) EX: exercise 5 days.week super(-1) for 40 min.session super(-1) at moderate intensity; (ii) rST: reduce ST and increase nonexercise physical activity; (iii) EX-rST: combination of EX and rST; and (iv) CON: maintain behavior. Fasting lipids, blood pressure (BP), peak oxygen uptake, BMI, and 2-h oral glucose tolerance tests were completed pre- and post-intervention. EX and EX-rST increased peak oxygen uptake by 10% and decreased systolic BP (both p >) suscite plus de modifications chez les marqueurs de la sante que l'une ou l'autre des interventions isolees. Cinquante-sept sujets obeses ou presentant du surpoids (19 hommes, 39 femmes) (moyenne plus or minus e.-t. : age, 43,6 plus or minus 9,9 ans, indice de masse corporelle (IMC), 35,1 plus or minus 4,6 kg.m super(-2)) participent a une etude durant 12 semaines et sont repartis aleatoirement dans l'un des quatre groupes suivants: (i) >, exercice physique d'intensite moderee a raison de 40 min par seance, 5 jours par semaine; (ii) >, diminution du ST et augmentation de l'activite physique sans exercices; (iii) >, combinaison d'EX et de rST; et (iv) >, maintien du comportement. Avant et apres les interventions, on evalue les lipides sanguins a jeun, la pression sanguine (BP), de la consommation d'oxygene de pointe, l'IMC et l'epreuve d'hyperglycemie provoquee par voie orale d'une duree de 2 h. Dans les groupes EX et EX-rST, on observe une augmentation de la consommation d'oxygene de pointe de 10 % et une diminution de la BP (p > de 17,8 % (de 2,8 a 32,8 %) et une diminution de 19,4 % (de -31,4 a -7,3 %) de la surface de l'insuline sous la courbe. Les autres groupes ne presentent pas d'amelioration sur le plan de l'action de l'insuline. Dans le groupe rST, le ST diminue de 7 % (50 min.jour super(-1)), mais seule la BP, variable associee a la sante, s'ameliore. Les groupes EX et EX-rST presentent une amelioration de la consommation d'oxygene de pointe et de l'IMC, encore une autre demonstration en faveur des effets benefiques de l'exercice physique d'intensite moderee. L'analyse intragroupe fournit des observations preliminaires selon lesquelles la pratique d'exercice physique et la diminution du ST suscitent des ameliorations au niveau des biomarqueurs metaboliques qu'on n'observe pas lors de la seule pratique d'exercice physique, et ce, nonobstant le fait que les differences entre les groupes n'atteignent pas le niveau de signification statistique. Il faut realiser d'autres etudes sur des echantillons plus grands pour analyser les resultats en matiere de sante issus d'une plus grande diminution du ST et sur une plus longue periode. [Traduit par la Redaction]
JF  - Applied Physiology, Nutrition, and Metabolism
AU  - Kozey Keadle, Sarah
AU  - Lyden, Kate
AU  - Staudenmayer, John
AU  - Hickey, Amanda
AU  - Viskochil, Richard
AU  - Braun, Barry
AU  - Freedson, Patty S
AD  - Department of Kinesiology, University of Massachusetts Amherst, Amherst, MA 01003, USA., Sarah.keadle@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 770
EP  - 780
PB  - NRC Research Press
VL  - 39
IS  - 7
SN  - 1715-5312, 1715-5312
KW  - Physical Education Index
KW  - sitting
KW  - training
KW  - cardiometabolic risk factors
KW  - insulin resistance
KW  - assis
KW  - entrainement
KW  - facteurs de risque cardiometabolique
KW  - insulinoresistance
KW  - Obesity
KW  - Behavior
KW  - Exercise (intensity)
KW  - Body mass
KW  - Lipids
KW  - Analysis
KW  - Hormones
KW  - Exercise (programs)
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554942751?accountid=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=Applied+Physiology%2C+Nutrition%2C+and+Metabolism&rft.atitle=The+independent+and+combined+effects+of+exercise+training+and+reducing+sedentary+behavior+on+cardiometabolic+risk+factors&rft.au=Kozey+Keadle%2C+Sarah%3BLyden%2C+Kate%3BStaudenmayer%2C+John%3BHickey%2C+Amanda%3BViskochil%2C+Richard%3BBraun%2C+Barry%3BFreedson%2C+Patty+S&rft.aulast=Kozey+Keadle&rft.aufirst=Sarah&rft.date=2014-01-01&rft.volume=39&rft.issue=7&rft.spage=770&rft.isbn=&rft.btitle=&rft.title=Applied+Physiology%2C+Nutrition%2C+and+Metabolism&rft.issn=17155312&rft_id=info:doi/10.1139%2Fapnm-2013-0379
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2014-08-01
N1  - Number of references - 48
N1  - Last updated - 2014-09-18
N1  - SubjectsTermNotLitGenreText - Obesity; Behavior; Exercise (intensity); Analysis; Lipids; Body mass; Exercise (programs); Hormones
DO  - http://dx.doi.org/10.1139/apnm-2013-0379
ER  - 



TY  - JOUR
T1  - Cardiovascular complications following chronic treatment with cocaine and testosterone in adolescent rats.
AN  - 1553710182; 25121974
AB  - Concomitant use of anabolic androgenic steroids and cocaine has increased in the last years. However, the effects of chronic exposure to these substances during adolescence on cardiovascular function are unknown. Here, we investigated the effects of treatment for 10 consecutive days with testosterone and cocaine alone or in combination on basal cardiovascular parameters, baroreflex activity, hemodynamic responses to vasoactive agents, and cardiac morphology in adolescent rats. Administration of testosterone alone increased arterial pressure, reduced heart rate (HR), and exacerbated the tachycardiac baroreflex response. Cocaine-treated animals showed resting bradycardia without changes in arterial pressure and baroreflex activity. Combined treatment with testosterone and cocaine did not affect baseline arterial pressure and HR, but reduced baroreflex-mediated tachycardia. None of the treatments affected arterial pressure response to either vasoconstrictor or vasodilator agents. Also, heart to body ratio and left and right ventricular wall thickness were not modified by drug treatments. However, histological analysis of left ventricular sections of animals subjected to treatment with testosterone and cocaine alone and combined showed a greater spacing between cardiac muscle fibers, dilated blood vessels, and fibrosis. These data show important cardiovascular changes following treatment with testosterone in adolescent rats. However, the results suggest that exposure to cocaine alone or combined with testosterone during adolescence minimally affect cardiovascular function.
JF  - PloS one
AU  - Engi, Sheila A
AU  - Cruz, Fábio C
AU  - Leão, Rodrigo M
AU  - Spolidorio, Luís C
AU  - Planeta, Cleopatra S
AU  - Crestani, Carlos C
AD  - Laboratory of Pharmacology, Department of Natural Active Principles and Toxicology, School of Pharmaceutical Sciences, Univ. Estadual Paulista-UNESP, Araraquara, SP, Brazil; Joint UFSCar-UNESP Graduate Program in Physiological Sciences, São Carlos, SP, Brazil. ; Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, US National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland, United States of America. ; Department of Physiology and Pathology, School of Dentistry of Araraquara, Univ. Estadual Paulista-UNESP, Araraquara, SP, Brazil.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 8
KW  - Testosterone
KW  - 3XMK78S47O
KW  - Cocaine
KW  - I5Y540LHVR
KW  - Index Medicus
KW  - Rats
KW  - Animals
KW  - Heart Rate -- drug effects
KW  - Rats, Wistar
KW  - Blood Pressure -- drug effects
KW  - Male
KW  - Testosterone -- administration & dosage
KW  - Testosterone -- toxicity
KW  - Cocaine -- toxicity
KW  - Cardiovascular System -- drug effects
KW  - Cocaine -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553710182?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cardiovascular+complications+following+chronic+treatment+with+cocaine+and+testosterone+in+adolescent+rats.&rft.au=Engi%2C+Sheila+A%3BCruz%2C+F%C3%A1bio+C%3BLe%C3%A3o%2C+Rodrigo+M%3BSpolidorio%2C+Lu%C3%ADs+C%3BPlaneta%2C+Cleopatra+S%3BCrestani%2C+Carlos+C&rft.aulast=Engi&rft.aufirst=Sheila&rft.date=2014-01-01&rft.volume=9&rft.issue=8&rft.spage=e105172&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0105172
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2016-03-31
N1  - Date created - 2014-08-15
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Regul Toxicol Pharmacol. 2010 Jun;57(1):117-23 [20153798]
Fundam Appl Toxicol. 1994 Jan;22(1):113-21 [8125204]
Clin Cardiol. 2010 May;33(5):264-9 [20513064]
Neurosci Res. 2010 Aug;67(4):317-26 [20472007]
Am J Cardiol. 2010 Sep 15;106(6):893-901 [20816133]
Mini Rev Med Chem. 2011 May;11(5):409-24 [21443510]
Eur J Pharmacol. 2011 Nov 30;670(2-3):527-33 [21963526]
Heart. 2011 Dec;97(24):2056-62 [21690608]
J Cardiovasc Pharmacol. 2012 Mar;59(3):231-40 [22030898]
J Psychopharmacol. 2012 Oct;26(10):1366-74 [22767371]
J Neurosci. 2013 Mar 13;33(11):4913-22 [23486962]
Neuroscience. 2013 Dec 3;253:29-39 [23994153]
J Clin Periodontol. 2014 Mar;41(3):295-302 [24433307]
Physiol Behav. 2014 Mar 14;126:15-24 [24382485]
Pediatrics. 1995 Jul;96(1 Pt 1):23-8 [7596717]
Drug Alcohol Depend. 1995 Nov;40(1):9-15 [8746919]
Drug Alcohol Depend. 1997 Jan 10;44(1):11-29 [9031816]
J Stud Alcohol. 1997 Sep;58(5):464-73 [9273910]
J Hum Hypertens. 1997 Aug;11 Suppl 1:S19-27 [9321736]
Health Educ Behav. 1997 Dec;24(6):746-58 [9408788]
Prog Cardiovasc Dis. 1998 Jul-Aug;41(1):1-15 [9717856]
Am J Hypertens. 1998 Nov;11(11 Pt 1):1279-83 [9832169]
Curr Pharm Des. 2004;10(29):3579-89 [15579055]
Eur J Pharmacol. 1999 Oct 21;383(1):57-68 [10556682]
Neurosci Biobehav Rev. 2000 Jun;24(4):417-63 [10817843]
Eur J Pharmacol. 2000 Jun 16;398(2):263-72 [10854839]
Eur J Neurosci. 2002 Feb;15(3):539-44 [11876781]
Acta Cient Venez. 2002;53(3):225-31 [12658872]
Neurosci Biobehav Rev. 2003 Jan-Mar;27(1-2):163-78 [12732232]
Thromb Res. 2003 Feb 15;109(4):195-201 [12757774]
Am J Psychiatry. 2003 Jun;160(6):1041-52 [12777258]
Psychopharmacology (Berl). 2004 Apr;172(4):384-92 [14668974]
Neurosci Lett. 2004 Nov 11;370(2-3):201-5 [15488323]
Am J Epidemiol. 1980 Dec;112(6):736-49 [7457467]
J Auton Nerv Syst. 1987 Dec;21(2-3):203-13 [3450695]
Lancet. 1990 Apr 7;335(8693):827-38 [1969567]
Circulation. 1992 Feb;85(2):407-19 [1346509]
N Engl J Med. 1993 Apr 1;328(13):922-6 [8446139]
J Steroid Biochem Mol Biol. 2005 Jan;93(1):43-8 [15748831]
Pharmacology. 2005 Dec;75(1):5-12 [15897678]
Cardiovasc Toxicol. 2005 Fall;5(4):377-90 [16382175]
Prog Cardiovasc Dis. 2006 May-Jun;48(6):407-15 [16714160]
Brain Res. 2006 May 23;1090(1):58-68 [16674926]
Neuropsychopharmacology. 2006 Sep;31(9):2055-64 [16482089]
Eur J Pharmacol. 2006 Nov 21;550(1-3):95-106 [17011546]
Dev Psychobiol. 2008 Mar;50(2):127-33 [18286579]
Horm Behav. 2008 Feb;53(2):378-85 [18201704]
Psychopharmacology (Berl). 2009 Jan;201(4):589-99 [18797848]
Semin Diagn Pathol. 2009 Feb;26(1):10-7 [19292024]
Exp Toxicol Pathol. 2009 Jul;61(4):317-23 [19027274]
Psychopharmacology (Berl). 2009 Sep;206(1):1-21 [19547960]
Physiol Res. 2009;58(5):605-12 [19093712]
Brain Cogn. 2010 Feb;72(1):73-85 [19616355]
Pflugers Arch. 2010 May;459(6):995-1004 [20127126]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0105172
ER  - 



TY  - JOUR
T1  - Spatial-temporal excess mortality patterns of the 1918-1919 influenza pandemic in Spain
AN  - 1551615117; 20290754
AB  - Background: The impact of socio-demographic factors and baseline health on the mortality burden of seasonal and pandemic influenza remains debated. Here we analyzed the spatial-temporal mortality patterns of the 1918 influenza pandemic in Spain, one of the countries of Europe that experienced the highest mortality burden. Methods: We analyzed monthly death rates from respiratory diseases and all-causes across 49 provinces of Spain, including the Canary and Balearic Islands, during the period January-1915 to June-1919. We estimated the influenza-related excess death rates and risk of death relative to baseline mortality by pandemic wave and province. We then explored the association between pandemic excess mortality rates and health and socio-demographic factors, which included population size and age structure, population density, infant mortality rates, baseline death rates, and urbanization. Results: Our analysis revealed high geographic heterogeneity in pandemic mortality impact. We identified 3 pandemic waves of varying timing and intensity covering the period from Jan-1918 to Jun-1919, with the highest pandemic-related excess mortality rates occurring during the months of October-November 1918 across all Spanish provinces. Cumulative excess mortality rates followed a south-north gradient after controlling for demographic factors, with the North experiencing highest excess mortality rates. A model that included latitude, population density, and the proportion of children living in provinces explained about 40% of the geographic variability in cumulative excess death rates during 1918-19, but different factors explained mortality variation in each wave. Conclusions: A substantial fraction of the variability in excess mortality rates across Spanish provinces remained unexplained, which suggests that other unidentified factors such as comorbidities, climate and background immunity may have affected the 1918-19 pandemic mortality rates. Further archeo-epidemiological research should concentrate on identifying settings with combined availability of local historical mortality records and information on the prevalence of underlying risk factors, or patient-level clinical data, to further clarify the drivers of 1918 pandemic influenza mortality.
JF  - BMC Infectious Diseases
AU  - Chowell, Gerardo
AU  - Erkoreka, Anton
AU  - Viboud, Cecile
AU  - Echeverri-Davila, Beatriz
AD  - Division of International Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 371
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2334, 1471-2334
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Risk Abstracts
KW  - 1918-1919 influenza pandemic
KW  - Spain
KW  - Spanish influenza
KW  - Spring-summer wave
KW  - Excess death rates
KW  - Relative risk of death
KW  - Transmissibility
KW  - Provinces
KW  - Geography
KW  - Spatial heterogeneity
KW  - Urbanization
KW  - Population density
KW  - Respiratory diseases
KW  - Models
KW  - Demography
KW  - Influenza
KW  - pandemics
KW  - Sulfur dioxide
KW  - Islands
KW  - Infectious diseases
KW  - Risk factors
KW  - Latitude
KW  - Waves
KW  - Mortality
KW  - Age composition
KW  - Data processing
KW  - Climate
KW  - Spain, Balearic Is.
KW  - Immunity
KW  - Children
KW  - Mortality patterns
KW  - Infant mortality
KW  - Population number
KW  - Infants
KW  - H 1000:Occupational Safety and Health
KW  - R2 23060:Medical and environmental health
KW  - V 22400:Human Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551615117?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Infectious+Diseases&rft.atitle=Spatial-temporal+excess+mortality+patterns+of+the+1918-1919+influenza+pandemic+in+Spain&rft.au=Chowell%2C+Gerardo%3BErkoreka%2C+Anton%3BViboud%2C+Cecile%3BEcheverri-Davila%2C+Beatriz&rft.aulast=Chowell&rft.aufirst=Gerardo&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=BMC+Infectious+Diseases&rft.issn=14712334&rft_id=info:doi/10.1186%2F1471-2334-14-371
L2  - http://www.biomedcentral.com/1471-2334/14/371
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 49
N1  - Last updated - 2014-10-02
N1  - SubjectsTermNotLitGenreText - Mortality; Age composition; Data processing; Urbanization; Climate; Population density; Immunity; Children; Models; Influenza; Demography; pandemics; Islands; Risk factors; Waves; Infants; Respiratory diseases; Mortality patterns; Infant mortality; Sulfur dioxide; Infectious diseases; Latitude; Population number; Spain, Balearic Is.
DO  - http://dx.doi.org/10.1186/1471-2334-14-371
ER  - 



TY  - JOUR
T1  - Impairment of translation in neurons as a putative causative factor for autism
AN  - 1551614961; 20291137
AB  - Background: A dramatic increase in the prevalence of autism and Autistic Spectrum Disorders (ASD) has been observed over the last two decades in USA, Europe and Asia. Given the accumulating data on the possible role of translation in the etiology of ASD, we analyzed potential effects of rare synonymous substitutions associated with ASD on mRNA stability, splicing enhancers and silencers, and codon usage. Presentation of the hypothesis: We hypothesize that subtle impairment of translation, resulting in dosage imbalance of neuron-specific proteins, contributes to the etiology of ASD synergistically with environmental neurotoxins. Testing the hypothesis: A statistically significant shift from optimal to suboptimal codons caused by rare synonymous substitutions associated with ASD was detected whereas no effect on other analyzed characteristics of transcripts was identified. This result suggests that the impact of rare codons on the translation of genes involved in neuron development, even if slight in magnitude, could contribute to the pathogenesis of ASD in the presence of an aggressive chemical background. This hypothesis could be tested by further analysis of ASD-associated mutations, direct biochemical characterization of their effects, and assessment of in vivo effects on animal models. Implications of the hypothesis: It seems likely that the synergistic action of environmental hazards with genetic variations that in themselves have limited or no deleterious effects but are potentiated by the environmental factors is a general principle that underlies the alarming increase in the ASD prevalence. Reviewers: This article was reviewed by Andrey Rzhetsky, Neil R. Smalheiser, and Shamil R. Sunyaev.
JF  - Biology Direct
AU  - Poliakov, Eugenia
AU  - Koonin, Eugene V
AU  - Rogozin, Igor B
AD  - Laboratory of Retinal Cell & Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 16
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 9
IS  - 1
SN  - 1745-6150, 1745-6150
KW  - Ecology Abstracts
KW  - Synonymous mutations
KW  - Single nucleotide polymorphism
KW  - Codon usage
KW  - Splicing enhancer
KW  - Splicing silencer
KW  - mRNA secondary structure
KW  - Transcription factor binding
KW  - Neurotoxin
KW  - Translation
KW  - mRNA stability
KW  - Etiology
KW  - Data processing
KW  - Statistical analysis
KW  - Animal models
KW  - Environmental factors
KW  - Enhancers
KW  - Splicing
KW  - Reviews
KW  - Neurons
KW  - Codons
KW  - Neurotoxins
KW  - Autism
KW  - Mutation
KW  - D 04040:Ecosystem and Ecology Studies
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551614961?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+Direct&rft.atitle=Impairment+of+translation+in+neurons+as+a+putative+causative+factor+for+autism&rft.au=Poliakov%2C+Eugenia%3BKoonin%2C+Eugene+V%3BRogozin%2C+Igor+B&rft.aulast=Poliakov&rft.aufirst=Eugenia&rft.date=2014-01-01&rft.volume=9&rft.issue=1&rft.spage=16&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-9-16
L2  - http://www.biologydirect.com/content/9/1/16
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 124
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Translation; Etiology; mRNA stability; Data processing; Animal models; Statistical analysis; Environmental factors; Enhancers; Splicing; Neurons; Reviews; Codons; Neurotoxins; Mutation; Autism
DO  - http://dx.doi.org/10.1186/1745-6150-9-16
ER  - 



TY  - JOUR
T1  - In vitro stability of free and glucuronidated cannabinoids in urine following controlled smoked cannabis
AN  - 1551048135; 19974689
AB  - Analyte stability is an important factor in urine test interpretation, yet cannabinoid stability data are limited. A comprehensive study of [Delta] super(9)-tetrahydrocannabinol (THC), 11 -hydroxy-THC (11-OH-THC), 11-nor-9-carboxy-THC (THCCOOH), cannabidiol, cannabinol, THC-glucuronide, and THCCOOH-glucuronide stabilities in authentic urine was completed. Urine samples after ad libitum cannabis smoking were pooled to prepare low and high pools for each study participant; baseline concentrations were measured within 24 h at room temperature (RT), 4 [degrees]C and -20 [degrees]C. Stability at RT, 4 [degrees]C and -20 [degrees]C was evaluated by Friedman tests for up to 1 year. THCCOOH, THC-glucuronide, and THCCOOH-glucuronide were quantified in baseline pools. RT THCCOOH baseline concentrations were significantly higher than -20 [degrees]C, but not 4 [degrees]C baseline concentrations. After 1 week at RT, THCCOOH increased, THCCOOH-glucuronide decreased, but THC-glucuronide was unchanged. In RT low pool, total THCCOOH (THCCOOH+THCCOOH-glucuronide) was significantly lower after 1 week. At 4 [degrees]C, THCCOOH was stable 2 weeks, THCCOOH-glucuronide 1 month and THC-glucuronide for at least 6 months. THCCOOH was stable frozen for 1 year, but 6 months high pool results were significantly higher than baseline; THC-glucuronide and THCCOOH-glucuronide were stable for 6 months. Total THCCOOH was stable 6 months at 4 [degrees]C, and frozen 6 months (low) and 1 year (high). THC, cannabidiol and cannabinol were never detected in urine; although not detected initially, 11-OH-THC was detected in 2 low and 3 high pools after 1 week at RT. Substantial THCCOOH-glucuronide deconjugation was observed at RT and 4 [degrees]C. Analysis should be conducted within 3 months if non-hydrolyzed THCCOOH or THCCOOH-glucuronide quantification is required.
JF  - Analytical and Bioanalytical Chemistry
AU  - Desrosiers, Nathalie A
AU  - Lee, Dayong
AU  - Scheidweiler, Karl B
AU  - Concheiro-Guisan, Marta
AU  - Gorelick, David A
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; Program in Toxicology, University of Maryland Baltimore, 655 W. Baltimore Street, Baltimore, MD 21201, USA, mhuestis@intra.nida.nih.gov
PY  - 2014
SP  - 785
EP  - 792
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 406
IS  - 3
SN  - 1618-2642, 1618-2642
KW  - Aqualine Abstracts; Water Resources Abstracts
KW  - Cannabinoids
KW  - Urine
KW  - Stability
KW  - Glucuronide
KW  - Testing Procedures
KW  - Temperature
KW  - Pools
KW  - AQ 00001:Water Resources and Supplies
KW  - SW 5010:Network design
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551048135?accountid=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=In+vitro+stability+of+free+and+glucuronidated+cannabinoids+in+urine+following+controlled+smoked+cannabis&rft.au=Desrosiers%2C+Nathalie+A%3BLee%2C+Dayong%3BScheidweiler%2C+Karl+B%3BConcheiro-Guisan%2C+Marta%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Desrosiers&rft.aufirst=Nathalie&rft.date=2014-01-01&rft.volume=406&rft.issue=3&rft.spage=785&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-013-7524-7
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-12-01
N1  - Number of references - 29
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Testing Procedures; Urine; Temperature; Pools
DO  - http://dx.doi.org/10.1007/s00216-013-7524-7
ER  - 



TY  - JOUR
T1  - Drinking and Parenting Practices as Predictors of Impaired Driving Behaviors Among U.S. Adolescents
AN  - 1550986651; 201426120
AB  - Objective: The purpose of this study was to identify the extent to which 10th-grade substance use and parenting practices predicted 11th-grade teenage driving while alcohol-/other drug-impaired (DWI) and riding with alcohol-other drug-impaired drivers (RWI). Method: The data were from Waves 1 and 2 of the NEXT Generation study, with longitudinal assessment of a nationally representative sample of 10th graders starting in 2009-2010. Multivariate logistic regression analysis was used to examine the prospective associations between proposed predictors (heavy episodic drinking, illicit drug use, parental monitoring knowledge and control) in Wave 1 and DWI/RWI. Results: Heavy episodic drinking at Wave I predicted Wave 2 DWI (odds ratio [OR] = 3.73, p < .001) and RWI (OR = 3.92, p < .001) after controlling for parenting practices and selected covariates. Father's monitoring knowledge predicted lower DWI prevalence at Wave 2 when controlling for covariates and teenage substance use (OR = 0.66, p < .001). In contrast, mother's monitoring knowledge predicted lower RWI prevalence at Wave 2 when controlling for covariates only (OR = 0.67, p < .05). but the effect was reduced to nonsignificance when controlling for teen substance use. Conclusions: Heavy episodic drinking predicted DWI and RWI. In addition, parental monitoring knowledge, particularly by fathers, was protective against DWI, independent of the effect of substance use. This suggests that the enhancement of parenting practices could potentially discourage adolescent DWI. The findings suggest that the parenting practices of fathers and mothers may have differential effects on adolescent impaired-driving behaviors. Adapted from the source document.
JF  - Journal of Studies on Alcohol and Drugs
AU  - LI, KAIGANG
AU  - Simons-Morton, Bruce G
AU  - Brooks-Russell, Ashley
AU  - Ehsani, Johnathon
AU  - Hingson, Ralph
AD  - Health Behavior Branch, National Institute of Child Health & Human Development, Bethesda, Maryland; Health Behavior Branch, Division of Intramural Population Health Research, National Institute of Child Health & Human Development, 6100 Executive Blvd. 7B13B, Bethesda, MD 20892-7510 kaigang.li@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 5
EP  - 15
PB  - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway
VL  - 75
IS  - 1
SN  - 1937-1888, 1937-1888
KW  - Binge drinking
KW  - Parenting
KW  - Parents
KW  - Adolescents
KW  - Substance abuse
KW  - Prevalence
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550986651?accountid=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=Drinking+and+Parenting+Practices+as+Predictors+of+Impaired+Driving+Behaviors+Among+U.S.+Adolescents&rft.au=LI%2C+KAIGANG%3BSimons-Morton%2C+Bruce+G%3BBrooks-Russell%2C+Ashley%3BEhsani%2C+Johnathon%3BHingson%2C+Ralph&rft.aulast=LI&rft.aufirst=KAIGANG&rft.date=2014-01-01&rft.volume=75&rft.issue=1&rft.spage=5&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 - Substance abuse; Parenting; Adolescents; Parents; Binge drinking; Prevalence
ER  - 



TY  - JOUR
T1  - New Research Findings Since the 2007 Surgeon General's Call to Action to Prevent and Reduce Underage Drinking: A Review
AN  - 1550984118; 201425706
AB  - Objective: In 2007, the U.S. Department of Health and Human Services issued The Surgeon General's Call To Action To Prevent And Reduce Underage Drinking, a publication documenting a problem linked to nearly 5,000 injury deaths annually and poor academic performance, potential cognitive deficits, risky sexual behavior, physical and sexual assaults, and other substance use. This report reviews subsequent underage drinking and related traffic fatality trends and research on determinants, consequences, and prevention interventions. Method: New research reports, meta-analyses, and systematic literature reviews were examined. Results: Since the Call to Action, reductions in underage frequency of drinking, heavy drinking occasions, and alcohol-related traffic deaths that began in the 1980s when the drinking age nationally became 21 have continued. Knowledge regarding determinants and consequences, particularly the effects of early-onset drinking, parental alcohol provision, and cognitive effects, has expanded. Additional studies support associations between the legal drinking age of 21, zero tolerance laws, higher alcohol prices, and reduced drinking and related problems. New research suggests that use/lose laws, social host liability, internal possession laws, graduated licensing, and night driving restrictions reduce traffic deaths involving underage drinking drivers. Additional studies support the positive effects of individually oriented interventions, especially screening and brief motivational interventions, web and face-to-face social norms interventions, college web-based interventions, parental interventions, and multicomponent community interventions. Conclusions: Despite reductions in underage alcohol consumption and related traffic deaths, underage drinking remains an enduring problem. Continued research is warranted in minimally studied areas, such as prospective studies of alcohol and brain development, policy studies of use/lose laws, internal possession laws, social host liability, and parent-family interventions. (J. Stud. Alcohol Drugs, 75, 158-169, 2014). Adapted from the source document.
JF  - Journal of Studies on Alcohol and Drugs
AU  - Hingson, Ralph
AU  - White, Aaron
AD  - Division of Epidemiology and Prevention Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland rhingson@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 158
EP  - 169
PB  - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway
VL  - 75
IS  - 1
SN  - 1937-1888, 1937-1888
KW  - Alcohol consumption
KW  - Underage
KW  - Death
KW  - Surgeons
KW  - Interventions
KW  - Traffic
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550984118?accountid=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=New+Research+Findings+Since+the+2007+Surgeon+General%27s+Call+to+Action+to+Prevent+and+Reduce+Underage+Drinking%3A+A+Review&rft.au=Hingson%2C+Ralph%3BWhite%2C+Aaron&rft.aulast=Hingson&rft.aufirst=Ralph&rft.date=2014-01-01&rft.volume=75&rft.issue=1&rft.spage=158&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; Underage; Interventions; Death; Traffic; Surgeons
ER  - 



TY  - JOUR
T1  - Design, synthesis and pharmacological evaluation of novel vanadium-containing complexes as antidiabetic agents.
AN  - 1548639681; 25057899
AB  - Based on the data about structure and antidiabetic activity of twenty seven vanadium and zinc coordination complexes collected from literature we developed QSAR models using the GUSAR program. These QSAR models were applied to 10 novel vanadium coordination complexes designed in silico in order to predict their hypoglycemic action. The five most promising substances with predicted potent hypoglycemic action were selected for chemical synthesis and pharmacological evaluation. The selected coordination vanadium complexes were synthesized and tested in vitro and in vivo for their hypoglycemic activities and acute rat toxicity. Estimation of acute rat toxicity of these five vanadium complexes was performed using a freely available web-resource (http://way2drug.com/GUSAR/acutoxpredict.html). It has shown that the selected compounds belong to the class of moderate toxic pharmaceutical agents, according to the scale of Hodge and Sterner. Comparison with the predicted data has demonstrated a reasonable correspondence between the experimental and predicted values of hypoglycemic activity and toxicity. Bis{tert-butyl[amino(imino)methyl]carbamato}oxovanadium (IV) and sodium(2,2'-Bipyridyl)oxo-diperoxovanadate(V) octahydrate were identified as the most potent hypoglycemic agents among the synthesized compounds.
JF  - PloS one
AU  - Fedorova, Elena V
AU  - Buryakina, Anna V
AU  - Zakharov, Alexey V
AU  - Filimonov, Dmitry A
AU  - Lagunin, Alexey A
AU  - Poroikov, Vladimir V
AD  - Saint-Petersburg State Chemical Pharmaceutical Academy, Ministry of Healthcare and Social Development of Russian Federation, Saint-Petersburg, Russian Federation. ; National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America; Orekhovich Institute of Biomedical Chemistry of Russian Academy of Medical Sciences, Moscow, Russian Federation. ; Orekhovich Institute of Biomedical Chemistry of Russian Academy of Medical Sciences, Moscow, Russian Federation.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 7
KW  - (2,2'-bipyridyl)oxodiperoxovanadate(V)
KW  - 0
KW  - Coordination Complexes
KW  - Hypoglycemic Agents
KW  - bis(tert-butyl(amino(imino)methyl)carbamato)oxovanadium(IV)
KW  - Vanadium
KW  - 00J9J9XKDE
KW  - Epinephrine
KW  - YKH834O4BH
KW  - Index Medicus
KW  - Molecular Structure
KW  - Animals
KW  - Primary Cell Culture
KW  - Mice
KW  - Drug Design
KW  - Adipocytes -- drug effects
KW  - Adipocytes -- cytology
KW  - Rats
KW  - Quantitative Structure-Activity Relationship
KW  - Rats, Wistar
KW  - Adipocytes -- metabolism
KW  - Inhibitory Concentration 50
KW  - Male
KW  - Hypoglycemic Agents -- chemical synthesis
KW  - Hyperglycemia -- drug therapy
KW  - Coordination Complexes -- chemical synthesis
KW  - Hyperglycemia -- metabolism
KW  - Hyperglycemia -- chemically induced
KW  - Coordination Complexes -- pharmacology
KW  - Hypoglycemic Agents -- pharmacology
KW  - Coordination Complexes -- chemistry
KW  - Vanadium -- chemistry
KW  - Hyperglycemia -- pathology
KW  - Hypoglycemic Agents -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548639681?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Public+Health&rft.atitle=Individual+education%2C+area+income%2C+and+mortality+and+recurrence+of+myocardial+infarction+in+a+Medicare+cohort%3A+the+National+Longitudinal+Mortality+Study&rft.au=Coady%2C+Sean+A%3BJohnson%2C+Norman+J%3BHakes%2C+Jahn+K%3BSorlie%2C+Paul+D&rft.aulast=Coady&rft.aufirst=Sean&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=705&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-14-705
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-04-21
N1  - Date created - 2014-07-25
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Inorg Biochem. 2000 May 30;80(1-2):123-31 [10885472]
Dalton Trans. 2013 Sep 7;42(33):11900-11 [23787783]
SAR QSAR Environ Res. 2003 Oct-Dec;14(5-6):339-47 [14758978]
Acta Med Scand. 1967 Sep;182(3):353-61 [6058364]
Biol Pharm Bull. 1995 May;18(5):719-25 [7492989]
J Biol Chem. 1964 Feb;239:375-80 [14169133]
J Inorg Biochem. 2006 Sep;100(9):1535-46 [16824605]
SAR QSAR Environ Res. 2007 May-Jun;18(3-4):285-98 [17514571]
J Biol Inorg Chem. 2009 Aug;14(6):841-51 [19290551]
SAR QSAR Environ Res. 2009 Oct;20(7-8):679-709 [20024804]
J Inorg Biochem. 2010 Sep;104(9):987-92 [20627316]
Biometals. 2009 Dec;22(6):895-905 [19404749]
Eur J Med Chem. 2011 Sep;46(9):4374-82 [21802177]
Acta Biochim Pol. 2012;59(2):195-200 [22693688]
Future Med Chem. 2012 Oct;4(15):1933-44 [23088274]
Chem Res Toxicol. 2012 Nov 19;25(11):2378-85 [23078046]
J Inorg Biochem. 2003 Aug 1;96(2-3):321-30 [12888267]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0100386
ER  - 



TY  - JOUR
T1  - Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
AN  - 1548630598; 25058030
AB  - Despite an overall decrease in incidence of and mortality from cancer, about 40% of Americans will be diagnosed with the disease in their lifetime, and around 20% will die of it. Current approaches to test carcinogenic chemicals adopt the 2-year rodent bioassay, which is costly and time-consuming. As a result, fewer than 2% of the chemicals on the market have actually been tested. However, evidence accumulated to date suggests that gene expression profiles from model organisms exposed to chemical compounds reflect underlying mechanisms of action, and that these toxicogenomic models could be used in the prediction of chemical carcinogenicity.
          In this study, we used a rat-based microarray dataset from the NTP DrugMatrix Database to test the ability of toxicogenomics to model carcinogenicity. We analyzed 1,221 gene-expression profiles obtained from rats treated with 127 well-characterized compounds, including genotoxic and non-genotoxic carcinogens. We built a classifier that predicts a chemical's carcinogenic potential with an AUC of 0.78, and validated it on an independent dataset from the Japanese Toxicogenomics Project consisting of 2,065 profiles from 72 compounds. Finally, we identified differentially expressed genes associated with chemical carcinogenesis, and developed novel data-driven approaches for the molecular characterization of the response to chemical stressors. Here, we validate a toxicogenomic approach to predict carcinogenicity and provide strong evidence that, with a larger set of compounds, we should be able to improve the sensitivity and specificity of the predictions. We found that the prediction of carcinogenicity is tissue-dependent and that the results also confirm and expand upon previous studies implicating DNA damage, the peroxisome proliferator-activated receptor, the aryl hydrocarbon receptor, and regenerative pathology in the response to carcinogen exposure.
JF  - PloS one
AU  - Gusenleitner, Daniel
AU  - Auerbach, Scott S
AU  - Melia, Tisha
AU  - Gómez, Harold F
AU  - Sherr, David H
AU  - Monti, Stefano
AD  - Bioinformatics Program, Boston University, Boston, Massachusetts, United States of America; Department of Computational Biomedicine, Boston University Medical Campus, Boston, Massachusetts, United States of America. ; Biomolecular Screening Branch, Division of the National Toxicology Program at the National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, North Carolina, United States of America. ; Bioinformatics Program, Boston University, Boston, Massachusetts, United States of America. ; Department of Environmental Health, Boston University School of Public Health, Boston, Massachusetts, United States of America.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 7
KW  - Carcinogens
KW  - 0
KW  - Drugs, Investigational
KW  - Peroxisome Proliferator-Activated Receptors
KW  - Receptors, Aryl Hydrocarbon
KW  - Index Medicus
KW  - Sensitivity and Specificity
KW  - Gene Expression -- drug effects
KW  - Animals
KW  - Area Under Curve
KW  - DNA Damage
KW  - Organ Specificity
KW  - Peroxisome Proliferator-Activated Receptors -- metabolism
KW  - Peroxisome Proliferator-Activated Receptors -- genetics
KW  - Rats
KW  - Gene Expression Profiling
KW  - Quantitative Structure-Activity Relationship
KW  - Carcinogenicity Tests -- methods
KW  - Databases, Factual
KW  - Toxicogenetics
KW  - Receptors, Aryl Hydrocarbon -- metabolism
KW  - Receptors, Aryl Hydrocarbon -- genetics
KW  - Drugs, Investigational -- toxicity
KW  - Male
KW  - DNA Repair
KW  - Models, Genetic
KW  - Carcinogens -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548630598?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genomic+models+of+short-term+exposure+accurately+predict+long-term+chemical+carcinogenicity+and+identify+putative+mechanisms+of+action.&rft.au=Gusenleitner%2C+Daniel%3BAuerbach%2C+Scott+S%3BMelia%2C+Tisha%3BG%C3%B3mez%2C+Harold+F%3BSherr%2C+David+H%3BMonti%2C+Stefano&rft.aulast=Gusenleitner&rft.aufirst=Daniel&rft.date=2014-01-01&rft.volume=9&rft.issue=7&rft.spage=e102579&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0102579
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-04-21
N1  - Date created - 2014-07-25
N1  - Date revised - 2017-01-14
N1  - Genetic sequence - GSE57822; GEO
N1  - SuppNotes - Cited By:
Cancer Res. 2011 Nov 1;71(21):6590-600 [21900402]
Toxicol Sci. 2011 Nov;124(1):54-74 [21813463]
Lancet Oncol. 2012 Jun;13(6):564-5 [22575586]
Nucleic Acids Res. 2013 Jan;41(Database issue):D1104-14 [23093600]
Int J Mol Sci. 2013;14(4):7742-56 [23574936]
N Engl J Med. 2000 Jul 13;343(2):78-85 [10891514]
Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421]
Nat Genet. 2003 Jul;34(3):267-73 [12808457]
Toxicol Pathol. 2004 Jul-Aug;32(4):393-401 [15307212]
Genome Biol. 2004;5(10):R80 [15461798]
N Engl J Med. 1988 Mar 24;318(12):727-32 [3347221]
Dig Dis Sci. 1991 Jul;36(7):962-72 [1649041]
JAMA. 1996 Jan 3;275(1):55-60 [8531288]
Toxicol Sci. 2004 Dec;82(2):363-6 [15456919]
Toxicol Sci. 2005 Jun;85(2):747-808 [15800034]
J Biotechnol. 2005 Sep 29;119(3):219-44 [16005536]
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517]
Toxicol Sci. 2006 Jan;89(1):51-6 [16221960]
Life Sci. 2006 May 8;78(24):2787-96 [16360708]
Crit Rev Toxicol. 2006 Nov-Dec;36(10):781-92 [17118728]
Mol Carcinog. 2006 Dec;45(12):914-33 [16921489]
Toxicol Sci. 2007 Sep;99(1):90-100 [17557906]
Biomed Pharmacother. 2007 Dec;61(10):614-22 [17669614]
Mutat Res. 2008 Jan 1;637(1-2):23-39 [17689568]
Toxicol Sci. 2008 May;103(1):28-34 [18281259]
Med Ref Serv Q. 2008 Fall;27(3):303-11 [19042710]
Environ Health Perspect. 2008 Nov;116(11):1439-42 [19057693]
Nat Protoc. 2009;4(1):44-57 [19131956]
Nature. 2009 Nov 5;462(7269):108-12 [19847166]
Biostatistics. 2010 Apr;11(2):242-53 [20097884]
Mol Nutr Food Res. 2010 Feb;54(2):218-27 [20041446]
Exp Toxicol Pathol. 2010 Sep;62(5):497-502 [19616417]
Nat Biotechnol. 2010 Aug;28(8):827-38 [20676074]
Mutat Res. 2010 Dec;705(3):184-200 [20399889]
Bioinformatics. 2011 Jun 15;27(12):1739-40 [21546393]
Database (Oxford). 2011;2011:bar049 [22083790]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0102579
ER  - 



TY  - JOUR
T1  - Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis
AN  - 1547869833; 20291079
AB  - Background: Cognitive impairment, including dementia, is a major health concern with the increasing aging population. Preventive measures to delay cognitive decline are of utmost importance. Alzheimer's disease (AD) is the most frequent cause of dementia, increasing in prevalence from 40% above 85 years of age. Methods: We systematically reviewed selected modifiable factors such as education, smoking, alcohol, physical activity, caffeine, antioxidants, homocysteine (Hcy), n-3 fatty acids that were studied in relation to various cognitive health outcomes, including incident AD. We searched MEDLINE for published literature (January 1990 through October 2012), including cross-sectional and cohort studies (sample sizes > 300). Analyses compared study finding consistency across factors, study designs and study-level characteristics. Selecting studies of incident AD, our meta-analysis estimated pooled risk ratios (RR), population attributable risk percent (PAR%) and assessed publication bias. Results: In total, 247 studies were retrieved for systematic review. Consistency analysis for each risk factor suggested positive findings ranging from ~38.9% for caffeine to ~89% for physical activity. Education also had a significantly higher propensity for "a positive finding" compared to caffeine, smoking and antioxidant-related studies. Meta-analysis of 31 studies with incident AD yielded pooled RR for low education (RR = 1.99; 95% CI: 1.30-3.04), high Hcy (RR = 1.93; 95% CI: 1.50-2.49), and current/ever smoking status (RR = 1.37; 95% CI: 1.23-1.52) while indicating protective effects of higher physical activity and n-3 fatty acids. Estimated PAR% were particularly high for physical activity (PAR% = 31.9; 95% CI: 22.7-41.2) and smoking (PAR%=31.09%; 95% CI: 17.9-44.3). Overall, no significant publication bias was found. Conclusions: Higher Hcy levels, lower educational attainment, and decreased physical activity were particularly strong predictors of incident AD. Further studies are needed to support other potential modifiable protective factors, such as caffeine.
JF  - BMC Public Health
AU  - Beydoun, May A
AU  - Beydoun, Hind A
AU  - Gamaldo, Alyssa A
AU  - Teel, Alison
AU  - Zonderman, Alan B
AU  - Wang, Youfa
AD  - Laboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, 251 Bayview Blvd., Suite 100, Room #: 04B118, Baltimore, MD 21224, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 643
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2458, 1471-2458
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Risk assessment
KW  - Alcohol
KW  - Age
KW  - Physical activity
KW  - Alzheimer's disease
KW  - Aging
KW  - Smoking
KW  - Education
KW  - Cognitive ability
KW  - Risk factors
KW  - Reviews
KW  - Dementia disorders
KW  - Fatty acids
KW  - Caffeine
KW  - H 12000:Epidemiology and Public Health
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547869833?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Public+Health&rft.atitle=Epidemiologic+studies+of+modifiable+factors+associated+with+cognition+and+dementia%3A+systematic+review+and+meta-analysis&rft.au=Beydoun%2C+May+A%3BBeydoun%2C+Hind+A%3BGamaldo%2C+Alyssa+A%3BTeel%2C+Alison%3BZonderman%2C+Alan+B%3BWang%2C+Youfa&rft.aulast=Beydoun&rft.aufirst=May&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=643&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-14-643
L2  - http://www.biomedcentral.com/1471-2458/14/643
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-07-01
N1  - Number of references - 307
N1  - Last updated - 2014-08-21
N1  - SubjectsTermNotLitGenreText - Risk assessment; Alcohol; Age; Physical activity; Aging; Alzheimer's disease; Smoking; Education; Cognitive ability; Reviews; Risk factors; Dementia disorders; Fatty acids; Caffeine
DO  - http://dx.doi.org/10.1186/1471-2458-14-643
ER  - 



TY  - JOUR
T1  - Effect of ingested human antibodies induced by RTS, S/AS01 malaria vaccination in children on Plasmodium falciparum oocyst formation and sporogony in mosquitoes
AN  - 1547853558; 20297218
AB  - Background: The circumsporozoite protein (CS protein) on the malaria parasites in mosquitoes plays an important role in sporogony in mosquitoes. The RTS,S/AS01 malaria vaccine candidate, which has shown significant efficacy against clinical malaria in a large Phase 3 trial, targets the Plasmodium falciparum CS protein, but the ability of serum from vaccinated individuals to inhibit sporogony in mosquitoes has not been evaluated. Methods: Previously a double-blind, randomized trial of RTS,S/AS01 vaccine, as compared with rabies vaccine, in five- to 17-month old children in Tanzania was conducted. In this study, polyclonal human antibodies were purified from the pools of sera taken one month after the third vaccination. IgGs were purified from four pools of sera from 25 RTS,S/AS01 vaccinated children each, and two pools of sera from 25 children vaccinated with rabies vaccine each. The ability of antibodies to inhibit P. falciparum oocyst formation and/or sporogony in the mosquito host was evaluated by a standard membrane-feeding assay. The test antibodies were fed on day 0 (at the same time as the gametocyte feed), or on days 3 or 6 (serial-feed experiments). The oocyst and sporozoite counts were performed on days 8 and 16, respectively. In addition, two human anti-CS monoclonal antibodies (mAb) and a control mAb were also evaluated. Results: Polyclonal anti-CS IgG preparations from RTS,S-vaccinated children tested at concentrations of 149-210 ELISA units (EU)/ml did not show significant inhibition in oocyst and sporozoite formation when the antibodies were fed with gametocytes at the same time, or later (serial-feed experiments). Similarly, anti-CS mAbs tested at 6,421 or 7,122 EU/ml did not show reduction in oocyst and sporozoite formation. Conclusions: This study does not support the concept that anti-CS antibodies induced by the RTS,S/AS01 vaccines in humans noticeably reduce malaria transmission by blocking P. falciparum sporozoite development or salivary gland invasion in mosquitoes when taken up during feeding.
JF  - Malaria Journal
AU  - Miura, Kazutoyo
AU  - Jongert, Erik
AU  - Deng, Bingbing
AU  - Zhou, Luwen
AU  - Lusingu, John P
AU  - Drakeley, Chris J
AU  - Fay, Michael P
AU  - Long, Carole A
AU  - Vekemans, Johan
AD  - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12735 Twinbrook Parkway, Rockville, MD 20852, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 263
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1475-2875, 1475-2875
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - RTS,S/AS01
KW  - Oocyst formation
KW  - Sporogony
KW  - Standard membrane feeding assay
KW  - Parasites
KW  - Human diseases
KW  - Tanzania
KW  - Disease control
KW  - Malaria
KW  - Salivary gland
KW  - Clinical trials
KW  - Disease transmission
KW  - Public health
KW  - circumsporozoite protein
KW  - Rabies
KW  - Aquatic insects
KW  - Feeding
KW  - Enzyme-linked immunosorbent assay
KW  - Gametocytes
KW  - Oocysts
KW  - Monoclonal antibodies
KW  - Sporozoites
KW  - Culicidae
KW  - Pest control
KW  - Plasmodium falciparum
KW  - Children
KW  - Vaccination
KW  - Antibodies
KW  - Immunoglobulin G
KW  - Vaccines
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547853558?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Malaria+Journal&rft.atitle=Effect+of+ingested+human+antibodies+induced+by+RTS%2C+S%2FAS01+malaria+vaccination+in+children+on+Plasmodium+falciparum+oocyst+formation+and+sporogony+in+mosquitoes&rft.au=Miura%2C+Kazutoyo%3BJongert%2C+Erik%3BDeng%2C+Bingbing%3BZhou%2C+Luwen%3BLusingu%2C+John+P%3BDrakeley%2C+Chris+J%3BFay%2C+Michael+P%3BLong%2C+Carole+A%3BVekemans%2C+Johan&rft.aulast=Miura&rft.aufirst=Kazutoyo&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-13-263
L2  - http://www.malariajournal.com/content/13/1/263
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-07-01
N1  - Number of references - 31
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Antibodies; Human diseases; Disease control; Pest control; Malaria; Vaccines; Aquatic insects; Public health; Feeding; Enzyme-linked immunosorbent assay; Oocysts; Sporogony; Gametocytes; Monoclonal antibodies; Sporozoites; Salivary gland; Children; Vaccination; Clinical trials; Disease transmission; circumsporozoite protein; Rabies; Immunoglobulin G; Culicidae; Plasmodium falciparum; Tanzania
DO  - http://dx.doi.org/10.1186/1475-2875-13-263
ER  - 



TY  - JOUR
T1  - Neuroinflammation and neurodegeneration in adult rat brain from binge ethanol exposure: abrogation by docosahexaenoic acid.
AN  - 1546219489; 25029343
AB  - Evidence that brain edema and aquaporin-4 (AQP4) water channels have roles in experimental binge ethanol-induced neurodegeneration has stimulated interest in swelling/edema-linked neuroinflammatory pathways leading to oxidative stress. We report here that neurotoxic binge ethanol exposure produces comparable significant effects in vivo and in vitro on adult rat brain levels of AQP4 as well as neuroinflammation-linked enzymes: key phospholipase A2 (PLA2) family members and poly (ADP-ribose) polymerase-1 (PARP-1). In adult male rats, repetitive ethanol intoxication (3 gavages/d for 4 d, ∼ 9 g/kg/d, achieving blood ethanol levels ∼ 375 mg/dl; "Majchrowicz" model) significantly increased AQP4, Ca+2-dependent PLA2 GIVA (cPLA2), phospho-cPLA2 GIVA (p-cPLA2), secretory PLA2 GIIA (sPLA2) and PARP-1 in regions incurring extensive neurodegeneration in this model--hippocampus, entorhinal cortex, and olfactory bulb--but not in two regions typically lacking neurodamage, frontal cortex and cerebellum. Also, ethanol reduced hippocampal Ca+2-independent PLA2 GVIA (iPLA2) levels and increased brain "oxidative stress footprints" (4-hydroxynonenal-adducted proteins). For in vitro studies, organotypic cultures of rat hippocampal-entorhinocortical slices of adult age (∼ 60 d) were ethanol-binged (100 mM or ∼ 450 mg/dl) for 4 d, which augments AQP4 and causes neurodegeneration (Collins et al. 2013). Reproducing the in vivo results, cPLA2, p-cPLA2, sPLA2 and PARP-1 were significantly elevated while iPLA2 was decreased. Furthermore, supplementation with docosahexaenoic acid (DHA; 22:6n-3), known to quell AQP4 and neurodegeneration in ethanol-treated slices, blocked PARP-1 and PLA2 changes while counteracting endogenous DHA reduction and increases in oxidative stress footprints (3-nitrotyrosinated proteins). Notably, the PARP-1 inhibitor PJ-34 suppressed binge ethanol-dependent neurodegeneration, indicating PARP upstream involvement. The results with corresponding models support involvement of AQP4- and PLA2-associated neuroinflammatory pro-oxidative pathways in the neurodamage, with potential regulation by PARP-1 as well. Furthermore, DHA emerges as an effective inhibitor of these binge ethanol-dependent neuroinflammatory pathways as well as associated neurodegeneration in adult-age brain.
JF  - PloS one
AU  - Tajuddin, Nuzhath
AU  - Moon, Kwan-Hoon
AU  - Marshall, S Alex
AU  - Nixon, Kimberly
AU  - Neafsey, Edward J
AU  - Kim, Hee-Yong
AU  - Collins, Michael A
AD  - Department of Molecular Pharmacology & Therapeutics, Loyola University Chicago, Stritch School of Medicine, Maywood, Illinois, United States of America. ; Department of Pharmaceutical Sciences, University of Kentucky, Lexington, Kentucky, United States of America. ; Laboratory of Molecular Signaling, NIAAA, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 7
KW  - Aquaporin 4
KW  - 0
KW  - Docosahexaenoic Acids
KW  - 25167-62-8
KW  - Ethanol
KW  - 3K9958V90M
KW  - Parp1 protein, rat
KW  - EC 2.4.2.30
KW  - Poly (ADP-Ribose) Polymerase-1
KW  - Poly(ADP-ribose) Polymerases
KW  - Phospholipases A2
KW  - EC 3.1.1.4
KW  - Index Medicus
KW  - Rats
KW  - Phospholipases A2 -- metabolism
KW  - Animals
KW  - Rats, Sprague-Dawley
KW  - Dose-Response Relationship, Drug
KW  - Inflammation -- chemically induced
KW  - Inflammation -- drug therapy
KW  - Inflammation -- metabolism
KW  - Poly(ADP-ribose) Polymerases -- metabolism
KW  - Male
KW  - Aquaporin 4 -- metabolism
KW  - Ethanol -- adverse effects
KW  - Entorhinal Cortex -- metabolism
KW  - Docosahexaenoic Acids -- pharmacology
KW  - Hippocampus -- metabolism
KW  - Entorhinal Cortex -- drug effects
KW  - Docosahexaenoic Acids -- therapeutic use
KW  - Hippocampus -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1546219489?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neuroinflammation+and+neurodegeneration+in+adult+rat+brain+from+binge+ethanol+exposure%3A+abrogation+by+docosahexaenoic+acid.&rft.au=Tajuddin%2C+Nuzhath%3BMoon%2C+Kwan-Hoon%3BMarshall%2C+S+Alex%3BNixon%2C+Kimberly%3BNeafsey%2C+Edward+J%3BKim%2C+Hee-Yong%3BCollins%2C+Michael+A&rft.aulast=Tajuddin&rft.aufirst=Nuzhath&rft.date=2014-01-01&rft.volume=9&rft.issue=7&rft.spage=e101223&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0101223
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-03-09
N1  - Date created - 2014-07-17
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Neurosci. 2003 Mar 15;23(6):2348-56 [12657694]
Kidney Int. 2004 Feb;65(2):551-63 [14717925]
J Neurochem. 2004 Jun;89(6):1368-77 [15189339]
J Neurochem. 2004 Aug;90(3):637-45 [15255941]
Psychopharmacologia. 1975 Sep 17;43(3):245-54 [1237914]
Alcohol. 1985 Jan-Feb;2(1):133-8 [2861830]
J Stud Alcohol. 1991 Sep;52(5):448-53 [1943100]
Alcohol. 1993 Nov-Dec;10(6):559-61 [8123218]
Biophys J. 1995 May;68(5):1888-94 [7612831]
Alcohol Clin Exp Res. 1996 Apr;20(2):284-92 [8730219]
Alcohol Clin Exp Res. 1996 Nov;20(8):1406-11 [8947317]
FASEB J. 1998 Feb;12(2):221-30 [9472987]
J Neurophysiol. 1998 Mar;79(3):1441-9 [9497423]
Alcohol Clin Exp Res. 1998 Feb;22(1):217-24 [9514310]
J Stud Alcohol. 1999 May;60(3):400-6 [10371269]
Brain Res. 2005 Feb 9;1034(1-2):11-24 [15713255]
Lipids. 2004 Nov;39(11):1125-32 [15726828]
J Pharmacol Exp Ther. 2005 Aug;314(2):780-8 [15878999]
Curr Drug Targets CNS Neurol Disord. 2005 Aug;4(4):435-52 [16101559]
Lipids. 2005 Jul;40(7):719-28 [16196423]
Life Sci. 2005 Nov 19;78(1):74-81 [16214179]
Metab Brain Dis. 2005 Dec;20(4):285-94 [16382339]
J Neurosci Res. 2006 Feb 15;83(3):432-40 [16397898]
Neuroscience. 2006 Jun 30;140(2):547-53 [16563639]
Acta Physiol (Oxf). 2006 May-Jun;187(1-2):75-85 [16734744]
Prog Lipid Res. 2006 Nov;45(6):487-510 [16814865]
J Neurochem. 2006 Oct;99(1):107-18 [16987239]
Biochem Biophys Res Commun. 2006 Nov 17;350(2):399-404 [17010308]
Hepatology. 2006 Nov;44(5):1218-30 [17058263]
Alcohol Clin Exp Res. 2006 Nov;30(11):1938-49 [17067360]
Front Biosci. 2007;12:2616-30 [17127267]
J Neurochem. 2007 May;101(3):577-99 [17257165]
J Neurosci Res. 2007 May 15;85(7):1568-78 [17387686]
Hum Mol Genet. 2008 Feb 1;17(3):440-57 [17984171]
Glia. 2008 Apr 15;56(6):587-96 [18286643]
J Lipid Res. 2008 May;49(5):939-44 [18252846]
Neurosci Res. 2008 May;61(1):18-26 [18406487]
Chem Phys Lipids. 2008 May;153(1):34-46 [18359292]
Alcohol Clin Exp Res. 2008 Jun;32(6):929-36 [18445110]
J Biol Chem. 2008 May 30;283(22):15280-6 [18375385]
J Lipid Res. 2008 Jul;49(7):1477-87 [18398221]
Neurochem Res. 2009 Feb;34(2):260-7 [18592376]
Front Biosci (Landmark Ed). 2009;14:1116-28 [19273119]
J Cereb Blood Flow Metab. 2009 Apr;29(4):820-9 [19190653]
Lancet. 2009 Jun 27;373(9682):2223-33 [19560604]
J Neuroinflammation. 2009;6:21 [19678934]
J Neurotrauma. 2009 Feb 11;26(2):261-73 [19236167]
Biol Psychiatry. 2010 May 1;67(9):823-30 [20132926]
Prostaglandins Leukot Essent Fatty Acids. 2010 Apr-Jun;82(4-6):165-72 [20207120]
J Neurosurg. 2010 May;112(5):1095-104 [19731985]
Neuromolecular Med. 2010 Jun;12(2):133-48 [19855947]
Neuroscience. 2010 Jul 28;168(4):1036-46 [19682555]
Curr Med Chem. 2010;17(25):2746-63 [20586719]
Addict Biol. 2011 Jan;16(1):43-54 [20331561]
Am J Physiol Endocrinol Metab. 2010 Dec;299(6):E879-86 [20858748]
J Alzheimers Dis. 2010;22(3):939-48 [20858964]
Curr Opin Clin Nutr Metab Care. 2011 Mar;14(2):158-67 [21178607]
J Neurotrauma. 2011 Mar;28(3):371-81 [21204635]
FASEB J. 2011 May;25(5):1556-66 [21257712]
Annu Rev Nutr. 2011 Aug 21;31:321-51 [21756134]
J Neuroinflammation. 2011;8:101 [21846384]
Prostaglandins Other Lipid Mediat. 2011 Nov;96(1-4):114-20 [21810478]
Am J Pathol. 2012 Jan;180(1):17-23 [22051773]
Front Biosci (Elite Ed). 2012;4:1358-67 [22201960]
PLoS One. 2012;7(6):e39257 [22720084]
Neuroscience. 2012 Oct 11;222:147-58 [22842515]
Mol Neurobiol. 2012 Aug;46(1):85-95 [22476944]
Behav Brain Res. 2013 Jan 1;236(1):270-82 [22985845]
Neurotox Res. 2013 Jan;23(1):105-10 [23184649]
PLoS One. 2013;8(1):e51923 [23300957]
Prostaglandins Leukot Essent Fatty Acids. 2013 Jan;88(1):105-14 [22727983]
Prostaglandins Leukot Essent Fatty Acids. 2013 Jan;88(1):97-103 [22770766]
Prostaglandins Leukot Essent Fatty Acids. 2013 Jan;88(1):127-9 [23022417]
Alcohol. 2013 Feb;47(1):39-45 [23102656]
J Neuroinflammation. 2012;9:279 [23270503]
Alcohol Clin Exp Res. 2013 Mar;37(3):425-34 [23347220]
Neurochem Res. 2013 Apr;38(4):753-60 [23371482]
Neurochem Int. 2013 Apr;62(5):664-73 [23357477]
Neurochem Int. 2013 Apr;62(5):626-36 [23439385]
Neurobiol Dis. 2013 Jun;54:239-51 [23313316]
J Nutr Biochem. 2013 May;24(5):760-9 [22841392]
J Neurochem. 2013 Jun;125(6):869-84 [23570577]
Neurosci Lett. 2013 Sep 13;551:7-11 [23872044]
Nat Neurosci. 2013 Oct;16(10):1392-400 [23974709]
PLoS One. 2013;8(10):e75333 [24098376]
J Neurochem. 2013 Nov;127(3):378-93 [23919613]
Addict Biol. 2014 Jan;19(1):27-36 [22500955]
Semin Cell Dev Biol. 2014 Nov;35:24-32 [24582829]
Alcohol. 2000 Jul;21(3):201-6 [11091022]
Alcohol Clin Exp Res. 2000 Nov;24(11):1712-23 [11104119]
Brain Res. 2001 May 11;900(2):219-26 [11334801]
Alcohol Clin Exp Res. 2001 May;25(5):717-25 [11371721]
Exp Biol Med (Maywood). 2001 Nov;226(10):927-33 [11682699]
Lipids. 2001 Sep;36(9):945-59 [11724467]
Alcohol Clin Exp Res. 2002 Apr;26(4):547-57 [11981132]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0101223
ER  - 



TY  - JOUR
T1  - NCI-60 whole exome sequencing and pharmacological CellMiner analyses.
AN  - 1546218733; 25032700
AB  - Exome sequencing provides unprecedented insights into cancer biology and pharmacological response. Here we assess these two parameters for the NCI-60, which is among the richest genomic and pharmacological publicly available cancer cell line databases. Homozygous genetic variants that putatively affect protein function were identified in 1,199 genes (approximately 6% of all genes). Variants that are either enriched or depleted compared to non-cancerous genomes, and thus may be influential in cancer progression and differential drug response were identified for 2,546 genes. Potential gene knockouts are made available. Assessment of cell line response to 19,940 compounds, including 110 FDA-approved drugs, reveals ≈80-fold range in resistance versus sensitivity response across cell lines. 103,422 gene variants were significantly correlated with at least one compound (at p<0.0002). These include genes of known pharmacological importance such as IGF1R, BRAF, RAD52, MTOR, STAT2 and TSC2 as well as a large number of candidate genes such as NOM1, TLL2, and XDH. We introduce two new web-based CellMiner applications that enable exploration of variant-to-compound relationships for a broad range of researchers, especially those without bioinformatics support. The first tool, "Genetic variant versus drug visualization", provides a visualization of significant correlations between drug activity-gene variant combinations. Examples are given for the known vemurafenib-BRAF, and novel ifosfamide-RAD52 pairings. The second, "Genetic variant summation" allows an assessment of cumulative genetic variations for up to 150 combined genes together; and is designed to identify the variant burden for molecular pathways or functional grouping of genes. An example of its use is provided for the EGFR-ERBB2 pathway gene variant data and the identification of correlated EGFR, ERBB2, MTOR, BRAF, MEK and ERK inhibitors. The new tools are implemented as an updated web-based CellMiner version, for which the present publication serves as a compendium.
JF  - PloS one
AU  - Reinhold, William C
AU  - Varma, Sudhir
AU  - Sousa, Fabricio
AU  - Sunshine, Margot
AU  - Abaan, Ogan D
AU  - Davis, Sean R
AU  - Reinhold, Spencer W
AU  - Kohn, Kurt W
AU  - Morris, Joel
AU  - Meltzer, Paul S
AU  - Doroshow, James H
AU  - Pommier, Yves
AD  - Developmental Therapeutic Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Developmental Therapeutic Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; HiThru Analytics LLC, Laurel, Maryland, United States of America. ; Developmental Therapeutic Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; Centro de Estudos em Células Tronco, Terapia Celular e Genética Toxicológica, Programa de Pós-Graduação em Farmácia, Universidade Federal de Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil. ; Developmental Therapeutic Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; SRA International, Fairfax, Virginia, United States of America. ; Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Developmental Therapeutic Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Developmental Therapeutic Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; Developmental Therapeutic Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 7
KW  - Antineoplastic Agents
KW  - 0
KW  - Index Medicus
KW  - Base Sequence
KW  - Genomics -- methods
KW  - Humans
KW  - Databases, Factual
KW  - Genetic Variation -- genetics
KW  - Cell Line, Tumor
KW  - Sequence Analysis, DNA
KW  - Antineoplastic Agents -- pharmacology
KW  - Neoplasms -- drug therapy
KW  - Genome -- genetics
KW  - Data Mining -- methods
KW  - Computational Biology -- methods
KW  - Exome -- genetics
KW  - Neoplasms -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1546218733?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=NCI-60+whole+exome+sequencing+and+pharmacological+CellMiner+analyses.&rft.au=Reinhold%2C+William+C%3BVarma%2C+Sudhir%3BSousa%2C+Fabricio%3BSunshine%2C+Margot%3BAbaan%2C+Ogan+D%3BDavis%2C+Sean+R%3BReinhold%2C+Spencer+W%3BKohn%2C+Kurt+W%3BMorris%2C+Joel%3BMeltzer%2C+Paul+S%3BDoroshow%2C+James+H%3BPommier%2C+Yves&rft.aulast=Reinhold&rft.aufirst=William&rft.date=2014-01-01&rft.volume=9&rft.issue=7&rft.spage=e101670&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0101670
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-12-18
N1  - Date created - 2014-07-18
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Pharmacogenomics. 2013 Jul;14(9):1065-84 [23837481]
Cell Rep. 2013 Aug 15;4(3):609-20 [23933261]
Genome Res. 2002 Apr;12(4):656-64 [11932250]
Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11445-50 [14504390]
Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14229-34 [14623978]
Cancer Res. 2010 Mar 15;70(6):2191-203 [20215517]
Stem Cells. 2010 Apr;28(4):649-60 [20178109]
Mol Cancer Ther. 2010 May;9(5):1451-60 [20442306]
Mol Endocrinol. 2010 Jun;24(6):1287-96 [20375240]
Mol Cancer Ther. 2010 Dec;9(12):3105-14 [21159603]
Biomark Med. 2011 Jun;5(3):293-305 [21657839]
BMC Mol Biol. 2011;12:23 [21586152]
BMC Cancer. 2011;11:206:1-13 [21619594]
PLoS One. 2012;7(2):e31628 [22347499]
Nature. 2012 Mar 29;483(7391):544-5 [22460893]
Nature. 2012 Mar 29;483(7391):570-5 [22460902]
Nature. 2012 Mar 29;483(7391):603-7 [22460905]
Science. 2012 May 25;336(6084):1040-4 [22628656]
Future Oncol. 2012 May;8(5):509-23 [22646766]
Nature. 2012 Jun 21;486(7403):405-9 [22722202]
Acta Histochem. 2012 Nov;114(7):641-6 [22172707]
Cancer Discov. 2012 Jul;2(7):591-7 [22705984]
Am J Hum Genet. 2012 Jul 13;91(1):97-108 [22703879]
Cancer Res. 2012 Jul 15;72(14):3499-511 [22802077]
Neurology. 2012 Jul 31;79(5):396-7 [22744653]
Neurology. 2012 Jul 31;79(5):406-11 [22744673]
Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14592-7 [22912405]
J Clin Endocrinol Metab. 2012 Sep;97(9):E1774-81 [22740705]
Proc Natl Acad Sci U S A. 2012 Sep 11;109(37):15030-5 [22927417]
Hum Mutat. 2012 Nov;33(11):1610-5 [22730194]
Science. 2013 Mar 29;339(6127):1546-58 [23539594]
Cancer Res. 2003 Dec 15;63(24):8634-47 [14695175]
Cancer Cell. 2004 Aug;6(2):129-37 [15324696]
DNA Repair (Amst). 2004 Nov 2;3(11):1389-407 [15380096]
J Natl Cancer Inst. 1989 Jul 19;81(14):1088-92 [2738938]
Cancer Res. 2013 Jul 15;73(14):4372-82 [23856246]
Mol Cancer Ther. 2009 Apr;8(4):713-24 [19372543]
DNA Repair (Amst). 2014 Jan;13:1-9 [24355542]
Clin Pharmacol Ther. 2014 Mar;95(3):269-80 [24136381]
PLoS One. 2014;9(3):e92047 [24670534]
J Natl Cancer Inst. 1990 Jul 4;82(13):1113-8 [2359137]
Mol Pharmacol. 1994 Oct;46(4):627-38 [7969041]
Cancer Res. 1995 Jan 15;55(2):303-6 [7812962]
Mol Cancer Ther. 2006 Apr;5(4):853-67 [16648555]
Nat Rev Cancer. 2006 Oct;6(10):813-23 [16990858]
Mol Cancer Ther. 2006 Nov;5(11):2606-12 [17088437]
Cancer Res. 2006 Dec 1;66(23):11100-5 [17145850]
Oncogene. 2007 Jan 4;26(1):77-90 [16799634]
Mol Cancer Ther. 2007 May;6(5):1483-91 [17483436]
Cancer Res. 2008 Jan 15;68(2):415-24 [18199535]
Jpn J Cancer Res. 1999 Oct;90(10):1139-45 [10595743]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0101670
ER  - 



TY  - JOUR
T1  - A global assembly of adult female mosquito mark-release-recapture data to inform the control of mosquito-borne pathogens
AN  - 1544018961; 20178832
AB  - Background: Pathogen transmission by mosquitos is known to be highly sensitive to mosquito bionomic parameters. Mosquito mark-release-recapture (MMRR) experiments are a standard method for estimating such parameters including dispersal, population size and density, survival, blood feeding frequency and blood meal host preferences. Methods: We assembled a comprehensive database describing adult female MMRR experiments. Bibliographic searches were used to build a digital library of MMRR studies and selected data describing the reported outcomes were extracted. Results: The resulting database contained 774 unique adult female MMRR experiments involving 58 vector mosquito species from the three main genera of importance to human health: Aedes, Anopheles and Culex. Crude examination of these data revealed patterns associated with geography as well as mosquito genus, consistent with bionomics varying by species-specific life history and ecological context. Recapture success varied considerably and was significantly different amongst genera, with 8, 4 and 1% of adult females recaptured for Aedes, Anopheles and Culex species, respectively. A large proportion of experiments (59%) investigated dispersal and survival and many allowed disaggregation of the release and recapture data. Geographic coverage was limited to just 143 localities around the world. Conclusions: This MMRR database is a substantial contribution to the compilation of global data that can be used to better inform basic research and public health interventions, to identify and fill knowledge gaps and to enrich theory and evidence-based ecological and epidemiological studies of mosquito vectors, pathogen transmission and disease prevention. The database revealed limited geographic coverage and a relative scarcity of information for vector species of substantial public health relevance. It represents, however, a wealth of entomological information not previously compiled and of particular interest for mosquito-borne pathogen transmission models.
JF  - Parasites & Vectors
AU  - Guerra, Carlos A
AU  - Reiner, Robert C, Jr
AU  - Perkins, T Alex
AU  - Lindsay, Steve W
AU  - Midega, Janet T
AU  - Brady, Oliver J
AU  - Barker, Christopher M
AU  - Reisen, William K
AU  - Harrington, Laura C
AU  - Takken, Willem
AU  - Kitron, Uriel
AU  - Lloyd, Alun L
AU  - Hay, Simon I
AU  - Scott, Thomas W
AU  - Smith, David L
AD  - Fogarty International Center, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 276
PB  - BioMed Central Ltd., Floor 6 London WC1X 8HL United Kingdom
VL  - 7
IS  - 1
SN  - 1756-3305, 1756-3305
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Entomology Abstracts
KW  - Mosquito
KW  - Vector
KW  - Mark-release-recapture
KW  - Database
KW  - Pathogen transmission models
KW  - Bionomics
KW  - Parasites
KW  - Anopheles
KW  - Population density
KW  - Survival
KW  - Blood meals
KW  - Hosts
KW  - Models
KW  - Public health
KW  - Disease transmission
KW  - Geography
KW  - Aquatic insects
KW  - Feeding
KW  - Aedes
KW  - Data processing
KW  - Vectors
KW  - Pest control
KW  - Pathogens
KW  - Host preferences
KW  - Disaggregation
KW  - Culex
KW  - Databases
KW  - Blood
KW  - Life history
KW  - Dispersal
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Z 05350:Medical, Veterinary, and Agricultural Entomology
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544018961?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parasites+%26+Vectors&rft.atitle=A+global+assembly+of+adult+female+mosquito+mark-release-recapture+data+to+inform+the+control+of+mosquito-borne+pathogens&rft.au=Guerra%2C+Carlos+A%3BReiner%2C+Robert+C%2C+Jr%3BPerkins%2C+T+Alex%3BLindsay%2C+Steve+W%3BMidega%2C+Janet+T%3BBrady%2C+Oliver+J%3BBarker%2C+Christopher+M%3BReisen%2C+William+K%3BHarrington%2C+Laura+C%3BTakken%2C+Willem%3BKitron%2C+Uriel%3BLloyd%2C+Alun+L%3BHay%2C+Simon+I%3BScott%2C+Thomas+W%3BSmith%2C+David+L&rft.aulast=Guerra&rft.aufirst=Carlos&rft.date=2014-01-01&rft.volume=7&rft.issue=1&rft.spage=276&rft.isbn=&rft.btitle=&rft.title=Parasites+%26+Vectors&rft.issn=17563305&rft_id=info:doi/10.1186%2F1756-3305-7-276
L2  - http://www.parasitesandvectors.com/content/7/1/276
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-07-01
N1  - Number of references - 54
N1  - Last updated - 2015-06-26
N1  - SubjectsTermNotLitGenreText - Parasites; Population density; Pest control; Hosts; Pathogens; Geography; Aquatic insects; Disease transmission; Public health; Feeding; Bionomics; Data processing; Vectors; Survival; Blood meals; Host preferences; Models; Disaggregation; Blood; Databases; Life history; Dispersal; Culex; Aedes; Anopheles
DO  - http://dx.doi.org/10.1186/1756-3305-7-276
ER  - 



TY  - JOUR
T1  - Inflammasome activation in airway epithelial cells after multi-walled carbon nanotube exposure mediates a profibrotic response in lung fibroblasts
AN  - 1544018790; 20178914
AB  - Background: In vivo studies have demonstrated the ability of multi-walled carbon nanotubes (MWCNT) to induce airway remodeling, a key feature of chronic respiratory diseases like asthma and chronic obstructive pulmonary disease. However, the mechanism leading to remodeling is poorly understood. Particularly, there is limited insight about the role of airway epithelial injury in these changes. Objectives: We investigated the mechanism of MWCNT-induced primary human bronchial epithelial (HBE) cell injury and its contribution in inducing a profibrotic response. Methods: Primary HBE cells were exposed to thoroughly characterized MWCNTs (1.5-24 mu g/mL equivalent to 0.37-6.0 mu g/cm super(2)) and MRC-5 human lung fibroblasts were exposed to 1:4 diluted conditioned medium from these cells. Flow cytometry, ELISA, immunostainings/immunoblots and PCR analyses were employed to study cellular mechanisms. Results: MWCNT induced NLRP3 inflammasome dependent pyroptosis in HBE cells in a time- and dose-dependent manner. Cell death and cytokine production were significantly reduced by antioxidants, siRNA to NLRP3, a caspase-1 inhibitor (z-WEHD-FMK) or a cathepsin B inhibitor (CA-074Me). Conditioned medium from MWCNT-treated HBE cells induced significant increase in mRNA expression of pro-fibrotic markers (TIMP-1, Tenascin-C, Procollagen 1, and Osteopontin) in human lung fibroblasts, without a concomitant change in expression of TGF-beta. Induction of pro-fibrotic markers was significantly reduced when IL-1[beta], IL-18 and IL-8 neutralizing antibodies were added to the conditioned medium or when conditioned medium from NLRP3 siRNA transfected HBE cells was used. Conclusions: Taken together these results demonstrate induction of a NLRP3 inflammasome dependent but TGF-beta independent pro-fibrotic response after MWCNT exposure.
JF  - Particle and Fibre Toxicology
AU  - Hussain, Salik
AU  - Sangtian, Stacey
AU  - Anderson, Shamika M
AU  - Snyder, Ryan J
AU  - Marshburn, Jamie D
AU  - Rice, Annette B
AU  - Bonner, James C
AU  - Garantziotis, Stavros
AD  - Clinical Research Unit, National Institute of Environmental Health Sciences (NIEHS)/National Institute of Health (NIH), Research Triangle Park, Durham, NC, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 28
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 11
IS  - 1
SN  - 1743-8977, 1743-8977
KW  - Toxicology Abstracts
KW  - Multi-walled carbon nanotubes
KW  - Nanotoxicity
KW  - Fibrosis
KW  - Pyroptosis
KW  - NLRP3 inflammasome
KW  - Human bronchial epithelia
KW  - Epithelial cells
KW  - Antioxidants
KW  - Injuries
KW  - Cathepsin B
KW  - Asthma
KW  - Chronic obstructive pulmonary disease
KW  - Fibroblasts
KW  - Gene expression
KW  - Flow cytometry
KW  - Tissue inhibitor of metalloproteinase 1
KW  - Antibodies
KW  - Carbon
KW  - siRNA
KW  - Transforming growth factor- beta
KW  - Interleukin 18
KW  - Cytokines
KW  - Polymerase chain reaction
KW  - Caspase-1
KW  - Respiratory tract
KW  - X 24490:Other
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544018790?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Particle+and+Fibre+Toxicology&rft.atitle=Inflammasome+activation+in+airway+epithelial+cells+after+multi-walled+carbon+nanotube+exposure+mediates+a+profibrotic+response+in+lung+fibroblasts&rft.au=Hussain%2C+Salik%3BSangtian%2C+Stacey%3BAnderson%2C+Shamika+M%3BSnyder%2C+Ryan+J%3BMarshburn%2C+Jamie+D%3BRice%2C+Annette+B%3BBonner%2C+James+C%3BGarantziotis%2C+Stavros&rft.aulast=Hussain&rft.aufirst=Salik&rft.date=2014-01-01&rft.volume=11&rft.issue=1&rft.spage=28&rft.isbn=&rft.btitle=&rft.title=Particle+and+Fibre+Toxicology&rft.issn=17438977&rft_id=info:doi/10.1186%2F1743-8977-11-28
L2  - http://www.particleandfibretoxicology.com/content/11/1/28
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-07-01
N1  - Number of references - 73
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Epithelial cells; Antioxidants; Injuries; Cathepsin B; Asthma; Fibroblasts; Chronic obstructive pulmonary disease; Tissue inhibitor of metalloproteinase 1; Flow cytometry; Gene expression; Antibodies; Carbon; siRNA; Interleukin 18; Transforming growth factor- beta; Polymerase chain reaction; Cytokines; Caspase-1; Respiratory tract
DO  - http://dx.doi.org/10.1186/1743-8977-11-28
ER  - 



TY  - JOUR
T1  - A Novel Approach for Enriching Cancer Stem Cells from the Human SW-13 Adrenocortical Carcinoma Cell Line
AN  - 1543999215; 19656128
AB  - The present study was undertaken to develop a new method for enriching cancer stem cells (CSCs) from the human adrenal cortical carcinoma (ACC) cell line SW-13. Given that the existence of CSCs in ACC causes resistance to conventional chemotherapies, treatment with cyclophosphamide was used for in vivo selection of CSCs in a BALB/c nude mouse tumor xenograft model established using the ACC cell line SW-13. The characteristics of CSCs in three generations of tumor xenografts were assessed for single-cell colony formation, flat colony formation, and cell sphere formation in serum-free suspension culture. The formation rates of single-cell colonies, flat colonies, and cell spheres were significantly higher for tumor xenograft cells treated with cyclophosphamide than for untreated engrafted tumor cells. Flow cytometry to examine expression of the CSC markers C-X-C chemokine receptor type-4 (CXCR4; CD184) and ATP-binding cassette sub-family G member-2 (ABCG2; CDw338) revealed markedly higher levels of CXCR4 and ABCG2 in cyclophosphamide-treated xenograft tumor cells compared to untreated tumor cells. Together, these results indicate that cyclophosphamide treatment of tumor xenograft cells caused enrichment of CSCs with a strong capability for self-renewal and proliferation. In this method, the administration of cyclophosphamide selectively kills cancer cells without toxicity to CSCs and thereby provides a practical approach for achieving the enrichment of CSCs in ACC.
JF  - Anticancer Research
AU  - Zeng, Wenqing
AU  - Chen, Xiaozhou
AU  - Ma, Yan
AU  - Huang, Zhenxing
AU  - Qin, Yuan
AU  - WU, FENGPING
AU  - Wu, Lili
AU  - LIANG, XINGHUAN
AU  - QIN, YINGFEN
AU  - Zhou, Jia
AU  - Lu, Decheng
AU  - Kuang, Xiaocong
AU  - Li, Qingdi Quentin
AU  - LUO, ZUOJIE
AD  - Department of Endocrinology, liquenti@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 117
EP  - 123
PB  - International Institute of Anticancer Research, 1st km Kapandritiou-Kalamou Road Kapandriti Attiki 19014 Greece
VL  - 34
IS  - 1A
SN  - 0250-7005, 0250-7005
KW  - Biotechnology and Bioengineering Abstracts
KW  - Adrenocortical carcinoma
KW  - cancer stem cell
KW  - chemotherapy
KW  - CXCR4
KW  - ABCG2
KW  - cyclophosphamide
KW  - CXC chemokine receptors
KW  - CXCR4 protein
KW  - Chemotherapy
KW  - Animal models
KW  - Suspension culture
KW  - Toxicity
KW  - Cyclophosphamide
KW  - Tumors
KW  - CD18 antigen
KW  - Tumor cells
KW  - Carcinoma
KW  - Flow cytometry
KW  - Stem cells
KW  - Tumor cell lines
KW  - Colonies
KW  - Cortex
KW  - Xenografts
KW  - Cell proliferation
KW  - W 30945:Fermentation & Cell Culture
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1543999215?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anticancer+Research&rft.atitle=A+Novel+Approach+for+Enriching+Cancer+Stem+Cells+from+the+Human+SW-13+Adrenocortical+Carcinoma+Cell+Line&rft.au=Zeng%2C+Wenqing%3BChen%2C+Xiaozhou%3BMa%2C+Yan%3BHuang%2C+Zhenxing%3BQin%2C+Yuan%3BWU%2C+FENGPING%3BWu%2C+Lili%3BLIANG%2C+XINGHUAN%3BQIN%2C+YINGFEN%3BZhou%2C+Jia%3BLu%2C+Decheng%3BKuang%2C+Xiaocong%3BLi%2C+Qingdi+Quentin%3BLUO%2C+ZUOJIE&rft.aulast=Zeng&rft.aufirst=Wenqing&rft.date=2014-01-01&rft.volume=34&rft.issue=1A&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Anticancer+Research&rft.issn=02507005&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-07-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - CXC chemokine receptors; CXCR4 protein; Chemotherapy; Animal models; Suspension culture; Tumors; Cyclophosphamide; Toxicity; Tumor cells; CD18 antigen; Carcinoma; Flow cytometry; Colonies; Tumor cell lines; Stem cells; Cortex; Xenografts; Cell proliferation
ER  - 



TY  - JOUR
T1  - An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: functional, metabolic, and differential network analysis.
AN  - 1543994629; 25000186
AB  - Estrogen exerts diverse biological effects in multiple tissues in both animals and humans. Much of the accumulated knowledge on the role of estrogen receptor (ER) in the heart has been obtained from studies using ovariectomized mice, whole body ER gene knock-out animal models, ex vivo heart studies, or from isolated cardiac myocytes. In light of the wide systemic influence of ER signaling in regulating a host of biological functions in multiple tissues, it is difficult to infer the direct role of ER on the heart. Therefore, we developed a mouse model with a cardiomyocyte-specific deletion of the ERα allele (cs-ERα-/-). Male and female cs-ERα-/- mice with age/sex-matched wild type controls were examined for differences in cardiac structure and function by echocardiogram and differential gene expression microarray analysis. Our study revealed sex-differences in structural parameters in the hearts of cs-ERα-/- mice, with minimal functional differences. Analysis of microarray data revealed differential variations in the expression of 208 genes affecting multiple transcriptional networks. Furthermore, we report sex-specific differences in the expression of 56 genes. Overall, we developed a mouse model with cardiac-specific deletion of ERα to characterize the role of ERα in the heart independent of systemic effects. Our results suggest that ERα is involved in controlling the expression of diverse genes and networks in the cardiomyocyte in a sex-dependent manner.
JF  - PloS one
AU  - Devanathan, Sriram
AU  - Whitehead, Timothy
AU  - Schweitzer, George G
AU  - Fettig, Nicole
AU  - Kovacs, Attila
AU  - Korach, Kenneth S
AU  - Finck, Brian N
AU  - Shoghi, Kooresh I
AD  - Department of Radiology, Washington University in St. Louis, Saint Louis, Missouri, United States of America. ; Division of Geriatrics and Nutritional Science, Department of Medicine, Washington University in St. Louis, Saint Louis, Missouri, United States of America. ; Center for Cardiovascular Research, Department of Medicine, Washington University in St. Louis, Saint Louis, Missouri, United States of America. ; Laboratory of Reproductive and Developmental Toxicology, Receptor Biology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America. ; Department of Radiology, Washington University in St. Louis, Saint Louis, Missouri, United States of America; Department of Biomedical Engineering, Washington University in St. Louis, Saint Louis, Missouri, United States of America; Division of Biology and Biomedical Sciences, Washington University in St. Louis, Saint Louis, Missouri, United States of America.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1
VL  - 9
IS  - 7
KW  - Biomarkers
KW  - 0
KW  - Estrogen Receptor alpha
KW  - Index Medicus
KW  - Gene Ontology
KW  - Animals
KW  - Oligonucleotide Array Sequence Analysis
KW  - Mice, Inbred C57BL
KW  - Mice
KW  - Signal Transduction
KW  - Male
KW  - Female
KW  - Mice, Knockout
KW  - Myocytes, Cardiac -- cytology
KW  - Gene Expression Profiling
KW  - Gene Regulatory Networks
KW  - Disease Models, Animal
KW  - Biomarkers -- metabolism
KW  - Estrogen Receptor alpha -- physiology
KW  - Myocytes, Cardiac -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1543994629?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+animal+model+with+a+cardiomyocyte-specific+deletion+of+estrogen+receptor+alpha%3A+functional%2C+metabolic%2C+and+differential+network+analysis.&rft.au=Devanathan%2C+Sriram%3BWhitehead%2C+Timothy%3BSchweitzer%2C+George+G%3BFettig%2C+Nicole%3BKovacs%2C+Attila%3BKorach%2C+Kenneth+S%3BFinck%2C+Brian+N%3BShoghi%2C+Kooresh+I&rft.aulast=Devanathan&rft.aufirst=Sriram&rft.date=2014-01-01&rft.volume=9&rft.issue=7&rft.spage=e101900&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0101900
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-12-01
N1  - Date created - 2014-07-08
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Hypertension. 2012 Oct;60(4):1070-7 [22892812]
Cell. 2012 Dec 21;151(7):1595-607 [23260145]
Trends Mol Med. 2013 Mar;19(3):197-209 [23348042]
J Cell Biochem. 2013 Jun;114(6):1306-14 [23296636]
Crit Rev Biochem Mol Biol. 2002;37(1):1-28 [11905545]
Science. 2002 Jul 12;297(5579):240-3 [12114623]
Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12729-34 [11070086]
Biochem Biophys Res Commun. 2000 Nov 30;278(3):640-5 [11095962]
Am J Physiol Endocrinol Metab. 2010 Feb;298(2):E304-19 [19920214]
FASEB J. 2010 Dec;24(12):4660-7 [20667977]
J Appl Physiol (1985). 2011 Apr;110(4):1046-53 [21233345]
BMC Syst Biol. 2011;5 Suppl 2:S6 [22784577]
J Pharmacol Exp Ther. 1996 Feb;276(2):652-7 [8632333]
Endocrinology. 1997 Mar;138(3):863-70 [9048584]
Annu Rev Pharmacol Toxicol. 1997;37:477-515 [9131262]
Endocrinology. 1997 Sep;138(9):4030-3 [9275096]
Endocrinology. 1997 Nov;138(11):4613-21 [9348186]
Circ Res. 1997 Nov;81(5):885-92 [9351464]
FEBS Lett. 1997 Oct 13;416(1):107-12 [9369244]
J Biol Chem. 1997 Dec 26;272(52):33360-6 [9407129]
J Endocrinol. 1998 Feb;156(2):R1-7 [9518889]
Am J Physiol Heart Circ Physiol. 2005 Feb;288(2):H469-76 [15374829]
J Mol Cell Cardiol. 2005 Feb;38(2):289-97 [15698835]
Mol Endocrinol. 2005 Jun;19(6):1402-11 [15914709]
Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1605-8 [16423895]
Diabetologia. 2006 Mar;49(3):588-97 [16463047]
Mol Aspects Med. 2006 Aug;27(4):299-402 [16914190]
Cell Metab. 2007 Jan;5(1):59-72 [17189207]
Science. 2007 Mar 2;315(5816):1278-82 [17332414]
Am J Physiol Endocrinol Metab. 2007 Sep;293(3):E726-36 [17578883]
J Endocrinol. 2008 Nov;199(2):267-73 [18753331]
J Endocrinol. 2008 Nov;199(2):275-86 [18757549]
Am J Physiol Regul Integr Comp Physiol. 2009 Apr;296(4):R972-8 [19211725]
Endocrinology. 2009 May;150(5):2109-17 [19164473]
Mol Endocrinol. 2009 Dec;23(12):2111-6 [19812388]
Trends Endocrinol Metab. 2009 Dec;20(10):477-82 [19783454]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0101900
ER  - 



TY  - JOUR
T1  - Dietary acrylamide and human cancer: a systematic review of literature.
AN  - 1539465059; 24875401
AB  - Cancer remains the second leading cause of death in the United States, and the number of cases is expected to continue to rise worldwide. Cancer prevention strategies are crucial for reducing the cancer burden. The carcinogenic potential of dietary acrylamide exposure from cooked foods is unknown. Acrylamide is a by-product of the common Maillard reaction where reducing sugars (i.e., fructose and glucose) react with the amino acid, asparagine. Based on the evidence of acrylamide carcinogenicity in animals, the International Agency for Research on Cancer has classified acrylamide as a group 2A carcinogen for humans. Since the discovery of acrylamide in foods in 2002, a number of studies have explored its potential as a human carcinogen. This article outlines a systematic review of dietary acrylamide and human cancer, acrylamide exposure and internal dose, exposure assessment methods in the epidemiologic studies, existing data gaps, and future directions. A majority of the studies reported no statistically significant association between dietary acrylamide intake and various cancers, and few studies reported increased risk for renal, endometrial, and ovarian cancers; however, the exposure assessment has been inadequate leading to potential misclassification or underestimation of exposure. Future studies with improved dietary acrylamide exposure assessment are encouraged.
JF  - Nutrition and cancer
AU  - Virk-Baker, Mandeep K
AU  - Nagy, Tim R
AU  - Barnes, Stephen
AU  - Groopman, John
AD  - a Division of Cancer Prevention , National Cancer Institute, National Institutes of Health , Rockville , Maryland , USA.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 774
EP  - 790
VL  - 66
IS  - 5
KW  - Carcinogens
KW  - 0
KW  - beta Carotene
KW  - 01YAE03M7J
KW  - Acrylamide
KW  - 20R035KLCI
KW  - alpha-Tocopherol
KW  - H4N855PNZ1
KW  - Index Medicus
KW  - beta Carotene -- administration & dosage
KW  - Animals
KW  - alpha-Tocopherol -- administration & dosage
KW  - Epidemiologic Studies
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Evidence-Based Practice
KW  - Carcinogens -- toxicity
KW  - Disease Models, Animal
KW  - Male
KW  - Female
KW  - Neoplasms -- epidemiology
KW  - Diet
KW  - Acrylamide -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539465059?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+cancer&rft.atitle=Dietary+acrylamide+and+human+cancer%3A+a+systematic+review+of+literature.&rft.au=Virk-Baker%2C+Mandeep+K%3BNagy%2C+Tim+R%3BBarnes%2C+Stephen%3BGroopman%2C+John&rft.aulast=Virk-Baker&rft.aufirst=Mandeep&rft.date=2014-01-01&rft.volume=66&rft.issue=5&rft.spage=774&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+cancer&rft.issn=1532-7914&rft_id=info:doi/10.1080%2F01635581.2014.916323
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-02-24
N1  - Date created - 2014-06-20
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Eur J Clin Nutr. 2000 Jun;54(6):487-9 [10878650]
Int J Cancer. 2001 Feb 1;91(3):283-7 [11169948]
Int J Cancer. 2001 Feb 1;91(3):407-11 [11169967]
Int J Cancer. 2002 Jul 20;100(3):355-60 [12115553]
J Agric Food Chem. 2002 Aug 14;50(17):4998-5006 [12166997]
Nature. 2002 Oct 3;419(6906):448-9 [12368844]
Nature. 2002 Oct 3;419(6906):449-50 [12368845]
Br J Cancer. 2003 Jan 13;88(1):84-9 [12556964]
Cancer Causes Control. 2010 Dec;21(12):2223-9 [20859673]
Ann Oncol. 2011 Jul;22(7):1487-99 [21239401]
Ann Oncol. 2011 Aug;22(8):1910-5 [21285136]
Int J Cancer. 2012 Jul 15;131(2):479-87 [21866549]
PLoS One. 2012;7(6):e38016 [22723843]
Public Health Nutr. 2004 Oct;7(7):871-8 [15482612]
Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):653-60 [23417989]
Eur J Nutr. 2013 Aug;52(5):1503-12 [23114503]
J Clin Epidemiol. 1990;43(3):285-95 [2313318]
Toxicol Appl Pharmacol. 1991 Nov;111(2):352-63 [1957318]
Toxicol Appl Pharmacol. 1993 May;120(1):45-54 [8511782]
Cancer Epidemiol Biomarkers Prev. 1992 Mar-Apr;1(3):213-9 [1306107]
Lancet. 1996 May 18;347(9012):1351-6 [8637339]
Cancer Epidemiol Biomarkers Prev. 1997 Apr;6(4):215-23 [9107425]
Carcinogenesis. 1997 Oct;18(10):1931-5 [9364002]
Int J Cancer. 1997 Nov 14;73(4):525-30 [9389567]
Public Health Nutr. 2002 Dec;5(6B):1113-24 [12639222]
Int J Cancer. 2003 Jul 1;105(4):558-60 [12712450]
Biosci Biotechnol Biochem. 2003 May;67(5):1188-90 [12834309]
Br J Cancer. 2003 Aug 18;89(4):774-5; author reply 775-6 [12915892]
J Agric Food Chem. 2003 Aug 27;51(18):5556-60 [12926914]
Food Chem Toxicol. 2003 Nov;41(11):1569-79 [12963010]
Food Chem Toxicol. 2003 Nov;41(11):1581-6 [12963011]
Int J Cancer. 2004 May 1;109(5):774-6 [14999788]
Int Arch Occup Environ Health. 2004 Apr;77(3):213-6 [14740221]
Int J Cancer. 2006 Jan 15;118(2):467-71 [16003724]
J Agric Food Chem. 2006 Jan 25;54(2):404-8 [16417297]
Adv Exp Med Biol. 2005;561:255-69 [16438303]
Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):266-71 [16492914]
Toxicol Lett. 2006 Jun 20;164(1):1-5 [16337756]
Inhal Toxicol. 2006 Sep;18(10):831-9 [16774873]
Prostate. 2006 Oct 1;66(14):1512-20 [16921512]
Toxicol Sci. 2006 Oct;93(2):256-67 [16870689]
Int J Epidemiol. 2006 Oct;35(5):1146-50 [16926217]
Int J Cancer. 2007 Mar 15;120(6):1376-7 [17187369]
Scand J Public Health. 2007;35(4):432-41 [17786808]
J Food Sci. 2007 Jan;72(1):C033-8 [17995869]
Cancer Epidemiol Biomarkers Prev. 2007 Nov;16(11):2304-13 [18006919]
Am J Respir Crit Care Med. 2008 Mar 1;177(5):524-30 [17989343]
Int J Cancer. 2008 May 1;122(9):2094-100 [18183576]
Cancer Causes Control. 2008 Apr;19(3):273-81 [17985202]
Am J Clin Nutr. 2008 May;87(5):1428-38 [18469268]
J Agric Food Chem. 2008 Aug 13;56(15):6013-9 [18624443]
J Nutr. 2008 Nov;138(11):2229-36 [18936224]
Int J Cancer. 2009 Mar 1;124(5):1196-9 [19048629]
Am J Epidemiol. 2009 Feb 1;169(3):376-81 [19015201]
Eur J Cancer. 2009 Mar;45(4):513-6 [19121931]
Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):994-7 [19223560]
Am J Epidemiol. 2009 Apr 1;169(7):815-28 [19208726]
Am J Epidemiol. 2009 Apr 15;169(8):954-61 [19224978]
Int J Cancer. 2009 May 15;124(10):2384-90 [19142870]
J Natl Cancer Inst. 2009 May 6;101(9):651-62 [19401552]
Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1663-6 [19383886]
Cancer Epidemiol Biomarkers Prev. 2009 Jun;18(6):1939-41 [19505926]
Am J Epidemiol. 2009 Oct 1;170(7):873-84 [19720866]
Environ Health Perspect. 2010 Feb;118(2):278-83 [20123601]
Cancer Prev Res (Phila). 2010 Jun;3(6):745-52 [20484175]
Breast Cancer Res Treat. 2010 Jul;122(1):199-210 [19949857]
Crit Rev Toxicol. 2010 Jul;40(6):485-512 [20170357]
Cancer Epidemiol Biomarkers Prev. 2010 Oct;19(10):2503-15 [20693310]
Br J Cancer. 2010 Nov 23;103(11):1749-54 [20959829]
Int J Cancer. 2011 Feb 1;128(3):676-81 [20715108]
N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844]
Lancet. 1999 Feb 27;353(9154):703-7 [10073512]
Food Chem Toxicol. 2005 Mar;43(3):365-410 [15680675]
Int J Hyg Environ Health. 2004 Dec;207(6):531-9 [15729833]
JAMA. 2005 Mar 16;293(11):1326-7 [15769965]
Toxicol Sci. 2005 May;85(1):447-59 [15625188]
Shokuhin Eiseigaku Zasshi. 2005 Apr;46(2):33-9 [16018588]
Mutat Res. 2005 Oct 15;578(1-2):284-97 [15982677]
Int J Cancer. 2006 Jan 1;118(1):169-73 [16003738]
Chem Res Toxicol. 1999 Nov;12(11):1110-6 [10563837]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1080/01635581.2014.916323
ER  - 



TY  - JOUR
T1  - Neuroimaging findings in Griscelli syndrome type 2 with primary neurological presentation
AN  - 1534850497; 20039201
AB  - We report the radiologic findings in two children with Griscelli syndrome who presented mainly with neurologic findings. Both children were born to consanguineous parents, had normal birth and developmental histories; both had silvery gray hair from the time of birth. The first child presented with symptoms of increased intracranial pressure and cerebellar ataxia; the second child with cerebellar ataxia alone. Microscopic examination of the hair in both the children demonstrated the characteristic melanin clumps suggestive of Griscelli syndrome. Magnetic resonance imaging of the brain in the first child demonstrated multifocal white matter hyperintensities in the cerebrum and diffuse white matter hyperintensities in the cerebellum, with intense contrast enhancement. In the second child, signal changes were confined to the cerebellum and spinal cord. The first child succumbed to rapidly progressive increased intra-cranial pressure; partial autopsy revealed necrotizing lesions involving the cerebellar hemispheres bilaterally which corresponded to the neuroimaging abnormalities. Histology revealed diffuse histiocytic infiltration of the parenchyma. Griscelli syndrome type 2 should be a diagnostic consideration in a child with silvery hair, neurological deterioration and enhancing multifocal white matter signal intensity changes
JF  - Journal of Pediatric Neuroradiology
AU  - Bindu, Parayil S
AU  - Mahadevan, Anita
AU  - Taly, Arun B
AU  - Chickabasaviah, Yasha T
AU  - Bharath, Rose D
AU  - Nagappa, Madhu
AU  - Sinha, Sanjib
AD  - Department of Neurology, National Institute of Mental Health And Neurosciences (NIMHANS), Bangalore, India
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 81
EP  - 86
PB  - Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands
VL  - 3
IS  - 2
SN  - 1309-6680, 1309-6680
KW  - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts
KW  - Griscelli syndrome
KW  - silvery hair
KW  - cerebellar leukoencephalopathy
KW  - melanin clumps
KW  - Parenchyma
KW  - Autopsy
KW  - Melanin
KW  - Neuroimaging
KW  - Cerebrum
KW  - Spinal cord
KW  - Magnetic resonance imaging
KW  - Cerebellum
KW  - Substantia alba
KW  - Children
KW  - Hair
KW  - Pressure
KW  - Cerebellar ataxia
KW  - W 30910:Imaging
KW  - N3 11027:Neurology & neuropathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534850497?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Pediatric+Neuroradiology&rft.atitle=Neuroimaging+findings+in+Griscelli+syndrome+type+2+with+primary+neurological+presentation&rft.au=Bindu%2C+Parayil+S%3BMahadevan%2C+Anita%3BTaly%2C+Arun+B%3BChickabasaviah%2C+Yasha+T%3BBharath%2C+Rose+D%3BNagappa%2C+Madhu%3BSinha%2C+Sanjib&rft.aulast=Bindu&rft.aufirst=Parayil&rft.date=2014-01-01&rft.volume=3&rft.issue=2&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Journal+of+Pediatric+Neuroradiology&rft.issn=13096680&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-06-01
N1  - Last updated - 2014-10-30
N1  - SubjectsTermNotLitGenreText - Parenchyma; Autopsy; Neuroimaging; Melanin; Spinal cord; Cerebrum; Magnetic resonance imaging; Cerebellum; Substantia alba; Children; Hair; Griscelli syndrome; Pressure; Cerebellar ataxia
ER  - 



TY  - JOUR
T1  - Glutamate Receptor Antagonists as Fast-Acting Therapeutic Alternatives for the Treatment of Depression: Ketamine and Other Compounds
AN  - 1534840922; 20030127
AB  - The N-methyl-D-aspartate (NMDA) receptor antagonist ketamine has rapid and potent antidepressant effects in treatment-resistant major depressive disorder and bipolar depression. These effects are in direct contrast to the more modest effects seen after weeks of treatment with classic monoaminergic antidepressants. Numerous open-label and case studies similarly validate ketamine's antidepressant properties. These clinical findings have been reverse-translated into preclinical models in an effort to elucidate ketamine's antidepressant mechanism of action, and three important targets have been identified: mammalian target of rapamycin (mTOR), eukaryotic elongation factor 2 (eEF2), and glycogen synthase kinase-3 (GSK-3). Current clinical and preclinical research is focused on (a) prolonging/maintaining ketamine's antidepressant effects, (b) developing more selective NMDA receptor antagonists free of ketamine's adverse effects, and (c) identifying predictor, mediator/moderator, and treatment response biomarkers of ketamine's antidepressant effects.
JF  - Annual Review of Pharmacology and Toxicology
AU  - Niciu, Mark J
AU  - Henter, Ioline D
AU  - Luckenbaugh, David A
AU  - Zarate, Carlos A, Jr
AU  - Charney, Dennis S
AD  - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institutes of Health/National Institute of Mental Health, Bethesda, Maryland 20814-9692, mark.niciu@nih.gov
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 119
EP  - 139
PB  - Annual Reviews, Inc., 4139 El Camino Way Palo Alto CA 94303-0139 United States
VL  - 54
SN  - 0362-1642, 0362-1642
KW  - Toxicology Abstracts
KW  - NMDA receptor antagonist
KW  - rapid-acting antidepressants
KW  - major depressive disorder
KW  - bipolar depression
KW  - preclinical models of depression
KW  - mammalian target of rapamycin
KW  - mTOR
KW  - N-Methyl-D-aspartic acid receptors
KW  - Depression
KW  - Glycogen synthase kinase 3
KW  - biomarkers
KW  - Glutamic acid receptors
KW  - Glutamic acid receptors (ionotropic)
KW  - Antagonists
KW  - Models
KW  - Elongation
KW  - Antidepressants
KW  - Reviews
KW  - Ketamine
KW  - TOR protein
KW  - Side effects
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534840922?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Review+of+Pharmacology+and+Toxicology&rft.atitle=Glutamate+Receptor+Antagonists+as+Fast-Acting+Therapeutic+Alternatives+for+the+Treatment+of+Depression%3A+Ketamine+and+Other+Compounds&rft.au=Niciu%2C+Mark+J%3BHenter%2C+Ioline+D%3BLuckenbaugh%2C+David+A%3BZarate%2C+Carlos+A%2C+Jr%3BCharney%2C+Dennis+S&rft.aulast=Niciu&rft.aufirst=Mark&rft.date=2014-01-01&rft.volume=54&rft.issue=&rft.spage=119&rft.isbn=9780824304546&rft.btitle=&rft.title=Annual+Review+of+Pharmacology+and+Toxicology&rft.issn=03621642&rft_id=info:doi/10.1146%2Fannurev-pharmtox-011613-135950
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-06-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - N-Methyl-D-aspartic acid receptors; Depression; Glycogen synthase kinase 3; Glutamic acid receptors; biomarkers; Antagonists; Glutamic acid receptors (ionotropic); Models; Antidepressants; Elongation; Reviews; Ketamine; TOR protein; Side effects
DO  - http://dx.doi.org/10.1146/annurev-pharmtox-011613-135950
ER  - 



TY  - JOUR
T1  - A kinetic fluorescence assay reveals unusual features of Ca super(++) uptake in Plasmodium falciparum-infected erythrocytes
AN  - 1534837793; 20047688
AB  - Background: To facilitate development within erythrocytes, malaria parasites increase their host cell uptake of diverse solutes including Ca super(++). The mechanism and molecular basis of increased Ca super(++) permeability remains less well studied than that of other solutes. Methods: Based on an appropriate Ca super(++) affinity and its greater brightness than related fluorophores, Fluo-8 was selected and used to develop a robust fluorescence-based assay for Ca super(++) uptake by human erythrocytes infected with Plasmodium falciparum. Results: Both uninfected and infected cells exhibited a large Ca super(++)-dependent fluorescence signal after loading with the Fluo-8 dye. Probenecid, an inhibitor of erythrocyte organic anion transporters, abolished the fluorescence signal in uninfected cells; in infected cells, this agent increased fluorescence via mechanisms that depend on parasite genotype. Kinetic fluorescence measurements in 384-well microplates revealed that the infected cell Ca super(++) uptake is not mediated by the plasmodial surface anion channel (PSAC), a parasite nutrient channel at the host membrane; it also appears to be distinct from mammalian Ca super(++) channels. Imaging studies confirmed a low intracellular Ca super(++) in uninfected cells and higher levels in both the host and parasite compartments of infected cells. Parasite growth inhibition studies revealed a conserved requirement for extracellular Ca super(++). Conclusions: Nondestructive loading of Fluo-8 into human erythrocytes permits measurement of Ca super(++) uptake kinetics. The greater Ca super(++) permeability of cells infected with malaria parasites is apparent when probenecid is used to inhibit Fluo-8 efflux at the host membrane. This permeability is mediated by a distinct pathway and may be essential for intracellular parasite development. The miniaturized assay presented here should help clarify the precise transport mechanism and may identify inhibitors suitable for antimalarial drug development.
JF  - Malaria Journal
AU  - Zipprer, Elizabeth M
AU  - Neggers, McKinzie
AU  - Kushwaha, Ambuj
AU  - Rayavara, Kempaiah
AU  - Desai, Sanjay A
AD  - The Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 184
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1475-2875, 1475-2875
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Calcium channels
KW  - Malaria parasites
KW  - Human erythrocytes
KW  - Fluo-8
KW  - Fluorescence kinetics
KW  - Antimalarial drug discovery
KW  - Parasites
KW  - Human diseases
KW  - Anions
KW  - Calcium
KW  - Erythrocytes
KW  - Nutrients
KW  - Malaria
KW  - Genotypes
KW  - fluorophores
KW  - Hosts
KW  - Calcium permeability
KW  - Public health
KW  - Permeability
KW  - Solutes
KW  - Anion channels
KW  - Fluorescence
KW  - Brightness
KW  - Membrane permeability
KW  - Drug development
KW  - Plasmodium falciparum
KW  - imaging
KW  - Calcium (extracellular)
KW  - Calcium (intracellular)
KW  - Kinetics
KW  - Uptake
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534837793?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Malaria+Journal&rft.atitle=A+kinetic+fluorescence+assay+reveals+unusual+features+of+Ca+super%28%2B%2B%29+uptake+in+Plasmodium+falciparum-infected+erythrocytes&rft.au=Zipprer%2C+Elizabeth+M%3BNeggers%2C+McKinzie%3BKushwaha%2C+Ambuj%3BRayavara%2C+Kempaiah%3BDesai%2C+Sanjay+A&rft.aulast=Zipprer&rft.aufirst=Elizabeth&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=184&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-13-184
L2  - http://www.malariajournal.com/content/13/1/184
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-06-01
N1  - Number of references - 48
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Solutes; Permeability; Parasites; Human diseases; Erythrocytes; Uptake; Malaria; Hosts; Public health; Calcium; Fluorescence; Anions; Brightness; Membrane permeability; Drug development; Nutrients; fluorophores; Genotypes; imaging; Calcium (extracellular); Calcium (intracellular); Calcium permeability; Kinetics; Calcium channels; Anion channels; Plasmodium falciparum
DO  - http://dx.doi.org/10.1186/1475-2875-13-184
ER  - 



TY  - JOUR
T1  - Association of total adiposity and computed tomographic measures of regional adiposity with incident cancer risk: a prospective population-based study of older adults
AN  - 1534831261; 20046686
AB  - Obesity is associated with increased risk of many types of cancer. Less is known regarding associations between adipose depots and cancer risk. We aimed to explore relationships between adipose depots, risk of cancer, and obesity-related cancer (per NCI definition) in participants initially aged 70-79 years without prevalent cancer (1179 men, 1340 women), and followed for incident cancer for 13 years. Measures included body mass index (BMI), total adipose tissue from dual-energy X-ray absorptiometry, and computed tomography measures of visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue, thigh intermuscular adipose tissue, and thigh muscle attenuation (Hounsfield unit, HU), where low HU indicates fatty infiltration. Hazard ratios (HR) and 95% confidence intervals (CIs) were estimated by Cox proportional hazards models adjusted for demographics, lifestyle variables, and medical conditions. During follow-up, 617 participants developed cancer of which 224 were obesity-related cancers. Total adipose tissue and VAT were positively associated with cancer risk among women (HR 1.14, 95% CI 1.01-1.30 per SD increase; HR 1.15, 95% CI 1.02-1.30 per SD increase). There were no associations with cancer risk among men. Total adipose tissue was positively associated with obesity-related cancer risk among women (HR 1.23, 95% CI 1.03-1.46 per SD increase). VAT was positively associated with obesity-related cancer risk among men (HR 1.30, 95% CI 1.06-1.60 per SD increase) and remained associated even with adjustment for BMI (HR 1.40, 95% CI 1.08-1.82 per SD increase). These findings provide insight into relationships between specific adipose depots and cancer risk and suggest differential relationships among men and women.Original Abstract: L'obesite est associee a un plus haut risque de plusieurs types de cancer. On sait peu de choses concernant l'association entre les reserves adipeuses et le risque de cancer. Cette etude se propose d'explorer la relation entre les reserves de tissus adipeux, le risque de cancer de toute nature et de cancer associe a l'obesite (selon la definition du NCI) chez des participants ages initialement de 70-79 ans exempts de cancer (1179 hommes, 1340 femmes) et suivis durant 13 ans pour une incidence de cancer. On evalue l'indice de masse corporelle (IMC), la quantite totale de tissus adipeux par absorptiometrie a rayons X en double energie et on enregistre par tomographie assistee par ordinateur les mesures suivantes : la quantite de tissu adipeux visceral (>), de tissu adipeux sous-cutane a l'abdomen (>), de tissu adipeux entre les muscles de la cuisse et le degre d'attenuation des muscles de la cuisse (en unites Hounsfield, >), une HU faible indiquant l'infiltration de gras. On evalue indirectement les > et les intervalles de confiance a 95% (IC) par l'analyse de Cox (modele a risque proportionnel) ajustee d'apres les variables demographiques, du mode de vie et de la condition medicale. Durant le suivi, 617 participants developpent un cancer dont 224 sont des cancers associes a l'obesite. La quantite totale de tissu adipeux et la quantite de VAT sont positivement associees a un risque de cancer chez les femmes (HR : 1,14, IC 95% : 1,01-1,30 par ecart-type, HR : 1,15, IC 95% : 1,02-1,30 par ecart-type). Chez les hommes, on n'observe pas d'associations avec le risque de cancer. Chez les femmes, la quantite totale de tissu adipeux est positivement reliee au risque de cancer associe a l'obesite (HR : 1,23, IC 95% : 1,03-1,46 par ecart-type). Chez les hommes, la quantite de VAT est positivement reliee au risque de cancer associe a l'obesite (HR : 1,30, IC 95% : 1,06-1,60 par ecart-type) et le demeure meme apres la prise en compte du IMC (HR: 1,40, IC 95% : 1,08-1,82 par ecart-type). Ces observations procurent un eclairage sur les relations entre les reserves specifiques de tissu adipeux et le risque de cancer et suggerent des relations differentes chez les hommes et les femmes. [Traduit par la Redaction]
JF  - Applied Physiology, Nutrition, and Metabolism
AU  - Murphy, Rachel A
AU  - Bureyko, Taylor F
AU  - Miljkovic, Iva
AU  - Cauley, Jane A
AU  - Satterfield, Suzanne
AU  - Hue, Trisha F
AU  - Klepin, Heidi D
AU  - Cummings, Steven R
AU  - Newman, Anne B
AU  - Harris, Tamara B
AD  - Laboratory of Epidemiology, and Population Sciences, Intramural Research Program, National Institute on Aging, 7201 Wisconsin Ave, 3C-309, Bethesda, MD 20814, USA., Rachel.murphy@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 687
EP  - 692
PB  - NRC Research Press
VL  - 39
IS  - 6
SN  - 1715-5312, 1715-5312
KW  - Physical Education Index
KW  - obesity
KW  - weight
KW  - adipose
KW  - body fat
KW  - cancer incidence
KW  - cancer risk
KW  - aging
KW  - obesite
KW  - poids
KW  - adipeux
KW  - gras corporel
KW  - incidence de cancer
KW  - risque de cancer
KW  - vieillissement
KW  - X-Ray
KW  - Men
KW  - Body mass
KW  - Women
KW  - Fats
KW  - Legs
KW  - Cancer
KW  - Demographics
KW  - Lifestyle
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534831261?accountid=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=Applied+Physiology%2C+Nutrition%2C+and+Metabolism&rft.atitle=Association+of+total+adiposity+and+computed+tomographic+measures+of+regional+adiposity+with+incident+cancer+risk%3A+a+prospective+population-based+study+of+older+adults&rft.au=Murphy%2C+Rachel+A%3BBureyko%2C+Taylor+F%3BMiljkovic%2C+Iva%3BCauley%2C+Jane+A%3BSatterfield%2C+Suzanne%3BHue%2C+Trisha+F%3BKlepin%2C+Heidi+D%3BCummings%2C+Steven+R%3BNewman%2C+Anne+B%3BHarris%2C+Tamara+B&rft.aulast=Murphy&rft.aufirst=Rachel&rft.date=2014-01-01&rft.volume=39&rft.issue=6&rft.spage=687&rft.isbn=&rft.btitle=&rft.title=Applied+Physiology%2C+Nutrition%2C+and+Metabolism&rft.issn=17155312&rft_id=info:doi/10.1139%2Fapnm-2013-0360
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2014-06-01
N1  - Number of references - 19
N1  - Last updated - 2014-09-18
N1  - SubjectsTermNotLitGenreText - X-Ray; Men; Body mass; Women; Fats; Legs; Demographics; Cancer; Lifestyle
DO  - http://dx.doi.org/10.1139/apnm-2013-0360
ER  - 



TY  - JOUR
T1  - Continued circulation of a single genotype of dengue virus serotype 2 in the Philippines
AN  - 1529952080; 19765464
AB  - Objective: To obtain descriptive information of behavioral pattern in Chinese school-aged children with cleft lip and palate. Methods: A total of 93 cleft lip and palate patients between the age of 6-11 year-old and treated at West China Stomatology Hospital were selected. And another 100 unaffected controls, matched for age and gender, were recruited randomly from a common primary school in Chengdu. Chart review of medical records was used to obtain psychosocial checklists. Scores were compared with published norms and controls to evaluate the risk of problems, separately for three diagnostic groups. Results: The patients group had lower scores of social and academic competencies, especially those with facial deformity or speech problem. No difference was found in the aspect of activity competency. All patients showed elevations in behavior problems. But the type of behavior problems varied in different genders. Conclusions: Chinese school-aged children with cleft lip and palate are at raised risk for social and academic difficulties. Specific pattern of behavior problems displays differently depending on gender of the patient.
JF  - Asian Pacific Journal of Tropical Medicine
AU  - Petronio, Joy Ann G
AU  - Vinarao, Ricky B
AU  - Flores, Kristine Marie G
AU  - Destura, Raul V
AD  - Institute of Molecular Biology and Biotechnology, National Institutes of Health-University of the Philippines, Manila, raul.destura@biotechmanila.uptn.edu.ph
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 30
EP  - 33
PB  - Elsevier
VL  - 7
IS  - 1
SN  - 1995-7645, 1995-7645
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Risk Abstracts; Virology & AIDS Abstracts; Health & Safety Science Abstracts
KW  - Cleft lip and palate
KW  - CBCL
KW  - Psychosocial
KW  - Behavior problems
KW  - Dengue virus
KW  - Age
KW  - Serotypes
KW  - medical records
KW  - Check lists
KW  - Genotypes
KW  - Children
KW  - Education establishments
KW  - Cleft lip/palate
KW  - speech
KW  - Schools
KW  - ISEW, Philippines
KW  - Dengue
KW  - Reviews
KW  - Gender
KW  - China, People's Rep.
KW  - Hospitals
KW  - Sex
KW  - H 13000:Medical Safety
KW  - Q1 08423:Behaviour
KW  - Q5 08524:Public health, medicines, dangerous organisms
KW  - R2 23110:Psychological aspects
KW  - V 22400:Human Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529952080?accountid=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=Asian+Pacific+Journal+of+Tropical+Medicine&rft.atitle=Continued+circulation+of+a+single+genotype+of+dengue+virus+serotype+2+in+the+Philippines&rft.au=Petronio%2C+Joy+Ann+G%3BVinarao%2C+Ricky+B%3BFlores%2C+Kristine+Marie+G%3BDestura%2C+Raul+V&rft.aulast=Petronio&rft.aufirst=Joy+Ann&rft.date=2014-01-01&rft.volume=7&rft.issue=1&rft.spage=30&rft.isbn=&rft.btitle=&rft.title=Asian+Pacific+Journal+of+Tropical+Medicine&rft.issn=19957645&rft_id=info:doi/10.1016%2FS1995-7645%2813%2960187-X
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-05-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Genotypes; Education establishments; Sex; Age; speech; Serotypes; medical records; Check lists; Children; Hospitals; Cleft lip/palate; Schools; Dengue; Reviews; Gender; Dengue virus; ISEW, Philippines; China, People's Rep.
DO  - http://dx.doi.org/10.1016/S1995-7645(13)60187-X
ER  - 



TY  - JOUR
T1  - The effects of oviposition-site deprivation on longevity and bloodfeeding rate in Anopheles gambiae
AN  - 1529932857; 19753188
AB  - Background: The African malaria mosquito, Anopheles gambiae, needs surface water in order to lay their eggs. In many parts of Africa, there are dry periods varying from days to months in length when suitable larval sites are not available and female mosquitoes experience oviposition-site deprivation (OSD). Previous studies have shown that egg-laying and egg-hatching rates were reduced due to OSD. Here, we assessed its effect on longevity and bloodfeeding rate of Anopheles gambiae. We predicted that OSD will increase mosquito longevity and the aptitude of mosquitoes to take additional blood meals; importantly, these changes will increase its vectorial capacity. Methods: To measure the effect of OSD, four treatments were utilized: two oviposition-deprived groups, one of which was bloodfed once (OBOD) and one that was bloodfed weekly (MBOD); a non-oviposition-deprived, weekly bloodfed control group (MBC); and a blood-deprived age-control group (BD). Mortality was assessed daily and bloodfeeding rate was measured at weekly intervals. Results: Under OSD, survival of female A. gambiae was reduced by 10-20%, reflecting reduction of the MBOD and OBOD groups from the MBC group, respectively. Likewise, bloodfeeding response during three weeks of OSD was reduced but the reduction varied as a function of time from the last blood meal. Conclusions: These results indicate that OSD is expected to reduce A. gambiae vectorial capacity and that OSD alone does not act as cue used by female mosquitoes to switch into a dormant state of extended survivorship with reproductive quiescence.
JF  - Parasites & Vectors
AU  - Artis, Monica L
AU  - Huestis, Diana L
AU  - Lehmann, Tovi
AD  - Laboratory of Malaria and Vector Research, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014///0,
PY  - 2014
DA  - 0, 2014
SP  - 163
PB  - BioMed Central Ltd., Floor 6 London WC1X 8HL United Kingdom
VL  - 7
IS  - 1
SN  - 1756-3305, 1756-3305
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Entomology Abstracts; Ecology Abstracts
KW  - Aestivation
KW  - African malaria mosquito
KW  - Dry season
KW  - Drought
KW  - Vectorial capacity
KW  - Mortality
KW  - Parasites
KW  - Feeding
KW  - Surface water
KW  - Vectors
KW  - Survival
KW  - Malaria
KW  - Pest control
KW  - Blood meals
KW  - Anopheles gambiae
KW  - Eggs
KW  - Longevity
KW  - Public health
KW  - Blood
KW  - Africa
KW  - Survivorship
KW  - Aquatic insects
KW  - Mortality causes
KW  - D 04040:Ecosystem and Ecology Studies
KW  - Z 05350:Medical, Veterinary, and Agricultural Entomology
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/1529932857?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parasites+%26+Vectors&rft.atitle=The+effects+of+oviposition-site+deprivation+on+longevity+and+bloodfeeding+rate+in+Anopheles+gambiae&rft.au=Artis%2C+Monica+L%3BHuestis%2C+Diana+L%3BLehmann%2C+Tovi&rft.aulast=Artis&rft.aufirst=Monica&rft.date=2014-01-01&rft.volume=7&rft.issue=1&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Parasites+%26+Vectors&rft.issn=17563305&rft_id=info:doi/10.1186%2F1756-3305-7-163
L2  - http://www.parasitesandvectors.com/content/7/1/163
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-05-01
N1  - Number of references - 29
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Blood; Feeding; Survival; Survivorship; Pest control; Aquatic insects; Mortality causes; Longevity; Public health; Parasites; Mortality; Surface water; Vectors; Malaria; Blood meals; Eggs; Anopheles gambiae; Africa
DO  - http://dx.doi.org/10.1186/1756-3305-7-163
ER  - 



TY  - JOUR
T1  - Risk estimation using probability machines
AN  - 1524419348; 19753073
AB  - Background: Logistic regression has been the de facto, and often the only, model used in the description and analysis of relationships between a binary outcome and observed features. It is widely used to obtain the conditional probabilities of the outcome given predictors, as well as predictor effect size estimates using conditional odds ratios. Results: We show how statistical learning machines for binary outcomes, provably consistent for the nonparametric regression problem, can be used to provide both consistent conditional probability estimation and conditional effect size estimates. Effect size estimates from learning machines leverage our understanding of counterfactual arguments central to the interpretation of such estimates. We show that, if the data generating model is logistic, we can recover accurate probability predictions and effect size estimates with nearly the same efficiency as a correct logistic model, both for main effects and interactions. We also propose a method using learning machines to scan for possible interaction effects quickly and efficiently. Simulations using random forest probability machines are presented. Conclusions: The models we propose make no assumptions about the data structure, and capture the patterns in the data by just specifying the predictors involved and not any particular model structure. So they do not run the same risks of model mis-specification and the resultant estimation biases as a logistic model. This methodology, which we call a "risk machine", will share properties from the statistical machine that it is derived from.
JF  - BioData Mining
AU  - Dasgupta, Abhijit
AU  - Szymczak, Silke
AU  - Moore, Jason H
AU  - Bailey-Wilson, Joan E
AU  - Malley, James D
AD  - Clinical Trials and Outcomes Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Room 4-1350, Bldg 10 CRC, 10 Center Drive, Bethesda, MD 20892-1468, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 2
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 7
IS  - 1
SN  - 1756-0381, 1756-0381
KW  - Biotechnology and Bioengineering Abstracts
KW  - Consistent nonparametric regression
KW  - Logistic regression
KW  - Probability machine
KW  - Odds ratio
KW  - Counterfactuals
KW  - Interactions
KW  - Learning
KW  - Data processing
KW  - Statistics
KW  - Regression analysis
KW  - Forests
KW  - Models
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524419348?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioData+Mining&rft.atitle=Risk+estimation+using+probability+machines&rft.au=Dasgupta%2C+Abhijit%3BSzymczak%2C+Silke%3BMoore%2C+Jason+H%3BBailey-Wilson%2C+Joan+E%3BMalley%2C+James+D&rft.aulast=Dasgupta&rft.aufirst=Abhijit&rft.date=2014-01-01&rft.volume=7&rft.issue=1&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=BioData+Mining&rft.issn=17560381&rft_id=info:doi/10.1186%2F1756-0381-7-2
L2  - http://www.biodatamining.org/content/7/1/2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-05-01
N1  - Number of references - 8
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Learning; Statistics; Data processing; Regression analysis; Forests; Models
DO  - http://dx.doi.org/10.1186/1756-0381-7-2
ER  - 



TY  - JOUR
T1  - 3,4-Methylenedioxymethamphetamine (MDMA) and metabolites disposition in blood and plasma following controlled oral administration
AN  - 1524415080; 19716348
AB  - 3,4-Methylenedioxymethamphetamine (MDMA) is an illicit phenethylamine ingested for entactogenic and euphoric effects. Although blood is more commonly submitted for forensic analysis, previous human MDMA pharmacokinetics research focused on plasma data; no direct blood-plasma comparisons were drawn. Blood and plasma specimens from 50 healthy adult volunteers (33 males, 17 females, 36 African-American) who ingested recreational 1.0 and 1.6 mg/kg MDMA doses were quantified for MDMA and metabolites 4-hydroxy-3-methoxymethamphetamine (HMMA), 3,4-methylenedioxyamphetamine (MDA), and 4-hydroxy-3-methoxyamphetamine (HMA) by two-dimensional gas chromatography-mass spectrometry. Specimens were collected up to 3 h post-dose and evaluated for maximum concentration (C sub(max)), first detection time (t sub(first)), time of C sub(max) (t sub(max)), and 3-h area under the curve (AUC sub(0-3 h)); as well as blood metabolite ratios and blood/plasma ratios. Median blood MDMA and MDA C sub(max) were significantly greater (p <0.0005) than in plasma, but HMMA was significantly less (p <0.0005). HMA was detected in few blood specimens, at low concentrations. Nonlinear pharmacokinetics were not observed for MDMA or MDA in this absorptive phase, but HMMA and AUC sub(0-3 h) were similar for both doses despite the 1.6-fold dose difference. Blood MDA/ MDMA and MDA/HMMA significantly increased (p <0.0001) over the 3-h time course, and HMMA/MDMA significantly decreased (p <0.0001). Blood MDMA was significantly greater in females (p =0.010) after the low dose only. Low-dose HMMA AUC sub(0-3h) was significantly decreased in females' blood and plasma (p =0.027) and in African-Americans' plasma (p =0.035). These data provide valuable insight into MDMA blood-plasma relationships for forensic interpretation and evidence of sex- and race-based differential metabolism and risk profiles.
JF  - Analytical and Bioanalytical Chemistry
AU  - Hartman, Rebecca L
AU  - Desrosiers, Nathalie A
AU  - Barnes, Allan J
AU  - Yun, Keming
AU  - Scheidweiler, Karl B
AU  - Kolbrich-Spargo, Erin A
AU  - Gorelick, David A
AU  - Goodwin, Robert S
AU  - Huestis, Marilyn A
AD  - Chemistry and Drug Metabolism Section, Clinical Pharmacology and Therapeutic Research Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Boulevard, Suite 200 Room 05A721, Baltimore, MD 21224, USA; Program in Toxicology, University of Maryland Baltimore, 660 West Redwood Street, Baltimore, MD 21201, USA, mhuestis@intra.nida.nih.gov
PY  - 2014
SP  - 587
EP  - 599
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 406
IS  - 2
SN  - 1618-2642, 1618-2642
KW  - Aqualine Abstracts; Water Resources Abstracts
KW  - MDMA
KW  - Ecstasy
KW  - Pharmacokinetics
KW  - Metabolites
KW  - Blood
KW  - Plasma
KW  - Detection Times
KW  - Risk
KW  - Profiles
KW  - Administration
KW  - Metabolism
KW  - AQ 00001:Water Resources and Supplies
KW  - SW 5010:Network design
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524415080?accountid=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=3%2C4-Methylenedioxymethamphetamine+%28MDMA%29+and+metabolites+disposition+in+blood+and+plasma+following+controlled+oral+administration&rft.au=Hartman%2C+Rebecca+L%3BDesrosiers%2C+Nathalie+A%3BBarnes%2C+Allan+J%3BYun%2C+Keming%3BScheidweiler%2C+Karl+B%3BKolbrich-Spargo%2C+Erin+A%3BGorelick%2C+David+A%3BGoodwin%2C+Robert+S%3BHuestis%2C+Marilyn+A&rft.aulast=Hartman&rft.aufirst=Rebecca&rft.date=2014-01-01&rft.volume=406&rft.issue=2&rft.spage=587&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-013-7468-y
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-05-01
N1  - Number of references - 36
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Risk; Blood; Profiles; Administration; Metabolites; Detection Times; Metabolism
DO  - http://dx.doi.org/10.1007/s00216-013-7468-y
ER  - 



TY  - JOUR
T1  - Transcriptome analysis identifies Bacillus anthracis genes that respond to CO sub(2) through an AtxA-dependent mechanism
AN  - 1524412713; 19753570
AB  - Background: Upon infection of a mammalian host, Bacillus anthracis responds to host cues, and particularly to elevated temperature (37 degree C) and bicarbonate/CO sub(2) concentrations, with increased expression of virulence factors that include the anthrax toxins and extracellular capsular layer. This response requires the presence of the pXO1 virulence plasmid-encoded pleiotropic regulator AtxA. To better understand the genetic basis of this response, we utilized a controlled in vitro system and Next Generation sequencing to determine and compare RNA expression profiles of the parental strain and an isogenic AtxA-deficient strain in a 2 2 factorial design with growth environments containing or lacking carbon dioxide. Results: We found 15 pXO1-encoded genes and 3 chromosomal genes that were strongly regulated by the separate or synergistic actions of AtxA and carbon dioxide. The majority of the regulated genes responded to both AtxA and carbon dioxide rather than to just one of these factors. Interestingly, we identified two previously unrecognized small RNAs that are highly expressed under physiological carbon dioxide concentrations in an AtxA-dependent manner. Expression levels of the two small RNAs were found to be higher than that of any other gene differentially expressed in response to these conditions. Secondary structure and small RNA-mRNA binding predictions for the two small RNAs suggest that they may perform important functions in regulating B. anthracis virulence. Conclusions: A majority of genes on the virulence plasmid pXO1 that are regulated by the presence of either CO sub(2) or AtxA separately are also regulated synergistically in the presence of both. These results also elucidate novel pXO1-encoded small RNAs that are associated with virulence conditions.
JF  - BMC Genomics
AU  - McKenzie, Andrew T
AU  - Pomerantsev, Andrei P
AU  - Sastalla, Inka
AU  - Martens, Craig
AU  - Ricklefs, Stacy M
AU  - Virtaneva, Kimmo
AU  - Anzick, Sarah
AU  - Porcella, Stephen F
AU  - Leppla, Stephen H
AD  - Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 229
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 15
IS  - 1
SN  - 1471-2164, 1471-2164
KW  - Genetics Abstracts; Toxicology Abstracts
KW  - Temperature effects
KW  - virulence factors
KW  - Secondary structure
KW  - Bicarbonate
KW  - Bacillus anthracis
KW  - Plasmids
KW  - Infection
KW  - Toxins
KW  - Gene expression
KW  - Protein structure
KW  - RNA
KW  - Anthrax
KW  - Carbon dioxide
KW  - X 24370:Natural Toxins
KW  - G 07870:Mammals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524412713?accountid=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=BMC+Genomics&rft.atitle=Transcriptome+analysis+identifies+Bacillus+anthracis+genes+that+respond+to+CO+sub%282%29+through+an+AtxA-dependent+mechanism&rft.au=McKenzie%2C+Andrew+T%3BPomerantsev%2C+Andrei+P%3BSastalla%2C+Inka%3BMartens%2C+Craig%3BRicklefs%2C+Stacy+M%3BVirtaneva%2C+Kimmo%3BAnzick%2C+Sarah%3BPorcella%2C+Stephen+F%3BLeppla%2C+Stephen+H&rft.aulast=McKenzie&rft.aufirst=Andrew&rft.date=2014-01-01&rft.volume=15&rft.issue=1&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=BMC+Genomics&rft.issn=14712164&rft_id=info:doi/10.1186%2F1471-2164-15-229
L2  - http://www.biomedcentral.com/1471-2164/15/229
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-05-01
N1  - Number of references - 60
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Protein structure; Temperature effects; Gene expression; virulence factors; RNA; Secondary structure; Anthrax; Bicarbonate; Infection; Plasmids; Carbon dioxide; Toxins; Bacillus anthracis
DO  - http://dx.doi.org/10.1186/1471-2164-15-229
ER  - 



TY  - JOUR
T1  - TFP5, a Peptide Derived from p35, a Cdk5 Neuronal Activator, Rescues Cortical Neurons from Glucose Toxicity
AN  - 1520387257; 19680536
AB  - Multiple lines of evidence link the incidence of diabetes to the development of Alzheimers disease (AD). Patients with diabetes have a 50 to 75% increased risk of developing AD. Cyclin dependent kinase 5 (Cdk5) is a serine/threonine protein kinase, which forms active complexes with p35 or p39, found principally in neurons and in pancreatic cells. Recent studies suggest that Cdk5 hyperactivity is a possible link between neuropathology seen in AD and diabetes. Previously, we identified P5, a truncated 24-aa peptide derived from the Cdk5 activator p35, later modified as TFP5, so as to penetrate the blood-brain barrier after intraperitoneal injections in AD model mice. This treatment inhibited abnormal Cdk5 hyperactivity and significantly rescued AD pathology in these mice. The present study explores the potential of TFP5 peptide to rescue high glucose (HG)-mediated toxicity in rat embryonic cortical neurons. HG exposure leads to Cdk5-p25 hyperactivity and oxidative stress marked by increased reactive oxygen species production, and decreased glutathione levels and superoxide dismutase activity. It also induces hyperphosphorylation of tau, neuroinflammation as evident from the increased expression of inflammatory cytokines like TNF-, IL-1, and IL-6, and apoptosis. Pretreatment of cortical neurons with TFP5 before HG exposure inhibited Cdk5-p25 hyperactivity and significantly attenuated oxidative stress by decreasing reactive oxygen species levels, while increasing superoxide dismutase activity and glutathione. Tau hyperphosphorylation, inflammation, and apoptosis induced by HG were also considerably reduced by pretreatment with TFP5. These results suggest that TFP5 peptide may be a novel candidate for type 2 diabetes therapy.
JF  - Journal of Alzheimer's Disease
AU  - Zheng, Ya-Li
AD  - Laboratory of Neuronal Cytoskeletal protein Regulation Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 899
EP  - 909
PB  - IOS Press, Nieuwe Hemweg 6B Amsterdam 1013 BG Netherlands
VL  - 39
IS  - 4
SN  - 1387-2877, 1387-2877
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - Apoptosis
KW  - Glutathione
KW  - Pancreas
KW  - Alzheimer's disease
KW  - Glucose
KW  - Toxicity
KW  - Inflammation
KW  - Cyclin-dependent kinase 5
KW  - Diabetes mellitus
KW  - Neurodegenerative diseases
KW  - Cortex
KW  - Phosphorylation
KW  - Reactive oxygen species
KW  - Oxidative stress
KW  - Superoxide dismutase
KW  - Tau protein
KW  - Embryos
KW  - Threonine
KW  - Hyperactivity
KW  - X 24360:Metals
KW  - N3 11027:Neurology & neuropathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520387257?accountid=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+Alzheimer%27s+Disease&rft.atitle=TFP5%2C+a+Peptide+Derived+from+p35%2C+a+Cdk5+Neuronal+Activator%2C+Rescues+Cortical+Neurons+from+Glucose+Toxicity&rft.au=Zheng%2C+Ya-Li&rft.aulast=Zheng&rft.aufirst=Ya-Li&rft.date=2014-01-01&rft.volume=39&rft.issue=4&rft.spage=899&rft.isbn=&rft.btitle=&rft.title=Journal+of+Alzheimer%27s+Disease&rft.issn=13872877&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Apoptosis; Glutathione; Pancreas; Alzheimer's disease; Glucose; Toxicity; Cyclin-dependent kinase 5; Inflammation; Diabetes mellitus; Neurodegenerative diseases; Cortex; Reactive oxygen species; Phosphorylation; Superoxide dismutase; Oxidative stress; Tau protein; Embryos; Threonine; Hyperactivity
ER  - 



TY  - JOUR
T1  - Production of recombinant protein by a novel oxygen-induced system in Escherichia coli
AN  - 1520374005; 19715861
AB  - Background: The SoxRS regulon of E. coli is activated in response to elevated dissolved oxygen concentration likely to protect the bacteria from possible oxygen damage. The soxS expression can be increased up to 16 fold, making it a possible candidate for recombinant protein expression. Compared with the existing induction approaches, oxygen induction is advantageous because it does not involve addition or depletion of growth factors or nutrients, addition of chemical inducers or temperature changes that can affect growth and metabolism of the producing bacteria. It also does not affect the composition of the growth medium simplifying the recovery and purification processes. Results: The soxS promoter was cloned into the commercial pGFPmut3.1 plasmid creating pAB49, an expression vector that can be induced by increasing oxygen concentration. The efficiency and the regulatory properties of the soxS promoter were characterized by measuring the GFP expression when the culture dissolved oxygen concentration was increased from 30% to 300% air saturation. The expression level of recombinant GFP was proportional to the oxygen concentration, demonstrating that pAB49 is a controllable expression vector. A possible harmful effect of elevated oxygen concentration on the recombinant product was found to be negligible by determining the protein-carbonyl content and its specific fluorescence. By performing high density growth in modified LB medium, the cells were induced by increasing the oxygen concentration. After 3 hours at 300% air saturation, GFP fluorescence reached 109000 FU (494 mg of GFP/L), representing 3.4% of total protein, and the cell concentration reached 29.1 g/L (DW). Conclusions: Induction of recombinant protein expression by increasing the dissolved oxygen concentration was found to be a simple and efficient alternative expression strategy that excludes the use of chemical, nutrient or thermal inducers that have a potential negative effect on cell growth or the product recovery.
JF  - Microbial Cell Factories
AU  - Baez, Antonino
AU  - Majdalani, Nadim
AU  - Shiloach, Joseph
AD  - Biotechnology Core Laboratory, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 50
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1475-2859, 1475-2859
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts
KW  - Temperature effects
KW  - Fluorescence
KW  - Nutrients
KW  - Cell culture
KW  - Plasmids
KW  - Dissolved oxygen
KW  - Expression vectors
KW  - Oxygen
KW  - Promoters
KW  - Protein folding
KW  - Escherichia coli
KW  - Growth factors
KW  - Metabolism
KW  - W 30905:Medical Applications
KW  - J 02320:Cell Biology
KW  - A 01300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520374005?accountid=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=Microbial+Cell+Factories&rft.atitle=Production+of+recombinant+protein+by+a+novel+oxygen-induced+system+in+Escherichia+coli&rft.au=Baez%2C+Antonino%3BMajdalani%2C+Nadim%3BShiloach%2C+Joseph&rft.aulast=Baez&rft.aufirst=Antonino&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=50&rft.isbn=&rft.btitle=&rft.title=Microbial+Cell+Factories&rft.issn=14752859&rft_id=info:doi/10.1186%2F1475-2859-13-50
L2  - http://www.microbialcellfactories.com/content/13/1/50
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Number of references - 23
N1  - Last updated - 2014-06-26
N1  - SubjectsTermNotLitGenreText - Temperature effects; Expression vectors; Promoters; Oxygen; Fluorescence; Protein folding; Cell culture; Nutrients; Growth factors; Plasmids; Metabolism; Dissolved oxygen; Escherichia coli
DO  - http://dx.doi.org/10.1186/1475-2859-13-50
ER  - 



TY  - JOUR
T1  - The multifork Escherichia coli chromosome is a self-duplicating and self-segregating thermodynamic ring polymer
AN  - 1520360906; 19716386
AB  - At all but the slowest growth rates, Escherichia coli cell cycles overlap, and its nucleoid is segregated to daughter cells as a forked DNA circle with replication ongoing--a state fundamentally different from eukaryotes. We have solved the chromosome organization, structural dynamics, and segregation of this constantly replicating chromosome. It is locally condensed to form a branched donut, compressed so that the least replicated DNA spans the cell center and the newest DNA extends toward the cell poles. Three narrow zones at the cell center and quarters contain both the replication forks and nascent DNA and serve to segregate the duplicated chromosomal information as it flows outward. The overall pattern is smoothly self-replicating, except when the duplicated terminus region is released from the septum and recoils to the center of a sister nucleoid. In circular cross-section of the cell, the left and right arms of the chromosome form separate, parallel structures that lie in each cell half along the radial cell axis. In contrast, replication forks and origin and terminus regions are found mostly at the center of the cross section, balanced by the parallel chromosome arms. The structure is consistent with the model in which the nucleoid is a constrained ring polymer that develops by spontaneous thermodynamics. The ring polymer pattern extrapolates to higher growth rates and also provides a structural basis for the form of the chromosome during very slow growth.
JF  - Genes & Development
AU  - Youngren, Brenda
AU  - Nielsen, Henrik Jork
AU  - Jun, Suckjoon
AU  - Austin, Stuart
AD  - Gene Regulation and Chromosome Biology Laboratory, NCI-Frederick, National Cancer Institute, Frederick, Maryland 21702, USA, stuart.austin66@gmail.tom
Y1  - 2014/01/01/
PY  - 2014
DA  - 2014 Jan 01
SP  - 71
EP  - 84
PB  - Cold Spring Harbor Laboratory Press, Fulfillment & Distribution Dept. Woodbury NY 11797-2924 United States
VL  - 28
IS  - 1
SN  - 0890-9369, 0890-9369
KW  - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology; Genetics Abstracts
KW  - bacterial cell cycle
KW  - bacterial chromosome
KW  - chromosome organization
KW  - chromosome segregation multifork replication
KW  - Growth rate
KW  - DNA biosynthesis
KW  - Chromosomes
KW  - Replication forks
KW  - Thermodynamics
KW  - Replication
KW  - Escherichia coli
KW  - DNA
KW  - Nucleoids
KW  - Septum
KW  - J 02320:Cell Biology
KW  - N 14845:Miscellaneous
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520360906?accountid=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=Genes+%26+Development&rft.atitle=The+multifork+Escherichia+coli+chromosome+is+a+self-duplicating+and+self-segregating+thermodynamic+ring+polymer&rft.au=Youngren%2C+Brenda%3BNielsen%2C+Henrik+Jork%3BJun%2C+Suckjoon%3BAustin%2C+Stuart&rft.aulast=Youngren&rft.aufirst=Brenda&rft.date=2014-01-01&rft.volume=28&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Genes+%26+Development&rft.issn=08909369&rft_id=info:doi/10.1101%2Fgad.231050.113
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Growth rate; DNA biosynthesis; Chromosomes; Thermodynamics; Replication forks; Replication; DNA; Nucleoids; Septum; Escherichia coli
DO  - http://dx.doi.org/10.1101/gad.231050.113
ER  - 



TY  - JOUR
T1  - Impairments in hearing and vision impact on mortality in older people: the AGES-Reykjavik Study
AN  - 1520327077; 201409319
AB  - Objective: to examine the relationships between impairments in hearing and vision and mortality from all-causes and cardiovascular disease (CVD) among older people. Design: population-based cohort study. Participants: the study population included 4,926 Icelandic individuals, aged >=67 years, 43.4% male, who completed vision and hearing examinations between 2002 and 2006 in the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-RS) and were followed prospectively for mortality through 2009. Methods: participants were classified as having 'moderate or greater' degree of impairment for vision only (VI), hearing only (HI), and both vision and hearing (dual sensory impairment, DSI). Cox proportional hazard regression, with age as the time scale, was used to calculate hazard ratios (HR) associated with impairment and mortality due to all-causes and specifically CVD after a median follow-up of 5.3 years. Results: the prevalence of HI, VI and DSI were 25.4, 9.2 and 7.0%, respectively. After adjusting for age, significantly (P < 0.01) increased mortality from all causes, and CVD was observed for HI and DSI, especially among men. After further adjustment for established mortality risk factors, people with HI remained at higher risk for CVD mortality [HR: 1.70 (1.27-2.27)], whereas people with DSI remained at higher risk of all-cause mortality [HR: 1.43 (1.11-1.85)] and CVD mortality [HR: 1.78 (1.18-2.69)]. Mortality rates were significantly higher in men with HI and DSI and were elevated, although not significantly, among women with HI. Conclusions: older men with HI or DSI had a greater risk of dying from any cause and particularly cardiovascular causes within a median 5-year follow-up. Women with hearing impairment had a non-significantly elevated risk. Vision impairment alone was not associated with increased mortality. Adapted from the source document.
JF  - Age and Ageing
AU  - Fisher, Diana
AU  - Li, Chuan-Ming
AU  - Chiu, May S
AU  - Themann, Christa L
AU  - Petersen, Hannes
AU  - Jonasson, Fri(eth)bert
AU  - Jonsson, Palmi V
AU  - Sverrisdottir, Johanna Eyrun
AU  - Garcia, Melissa
AU  - Harris, Tamara B
AU  - Launer, Lenore J
AU  - Eiriksdottir, Gudny
AU  - Gudnason, Vilmundur
AU  - Hoffman, Howard J
AU  - Cotch, Mary Frances
AD  - Division of Epidemiology and Clinical Applications, National Eye Institute, National Institutes of Health, Bethesda, MD, USA diana.fisher@nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 69
EP  - 76
PB  - Oxford University Press, UK
VL  - 43
IS  - 1
SN  - 0002-0729, 0002-0729
KW  - AGES-Reykjavik study hearing vision dual sensory impairment all-cause mortality cardiovascular disease mortality older people
KW  - Hazards
KW  - Mortality
KW  - Men
KW  - Cardiovascular diseases
KW  - Hearing
KW  - Hearing impairment
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520327077?accountid=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=Age+and+Ageing&rft.atitle=Impairments+in+hearing+and+vision+impact+on+mortality+in+older+people%3A+the+AGES-Reykjavik+Study&rft.au=Fisher%2C+Diana%3BLi%2C+Chuan-Ming%3BChiu%2C+May+S%3BThemann%2C+Christa+L%3BPetersen%2C+Hannes%3BJonasson%2C+Fri%28eth%29bert%3BJonsson%2C+Palmi+V%3BSverrisdottir%2C+Johanna+Eyrun%3BGarcia%2C+Melissa%3BHarris%2C+Tamara+B%3BLauner%2C+Lenore+J%3BEiriksdottir%2C+Gudny%3BGudnason%2C+Vilmundur%3BHoffman%2C+Howard+J%3BCotch%2C+Mary+Frances&rft.aulast=Fisher&rft.aufirst=Diana&rft.date=2014-01-01&rft.volume=43&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Age+and+Ageing&rft.issn=00020729&rft_id=info:doi/10.1093%2Fageing%2Faft122
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-05-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Mortality; Cardiovascular diseases; Hearing; Hearing impairment; Hazards; Men
DO  - http://dx.doi.org/10.1093/ageing/aft122
ER  - 



TY  - JOUR
T1  - Does Loop Electrosurgical Excision Procedure of the Uterine Cervix Affect Anti-Muellerian Hormone Levels?
AN  - 1516752231; 19627302
AB  - Background . A delayed time to pregnancy was recently reported for women who had a loop electrosurgical excision procedure (LEEP) to remove cervical intraepithelial neoplasia (CIN) grade 2 or 3. The objective of the current study was to determine if treatment of CIN with LEEP is associated with decreased levels of anti-Muellerian hormone (AMH), a marker of ovarian reserve. Methods . AMH levels were measured in 18 women treated with LEEP and 18 age-matched controls, who had colposcopy only and did not require LEEP. Cases and controls had their blood drawn at study entry time zero and again 6 months later. Results . The mean AMH level decreased significantly from baseline to follow-up; however, no significant differences were observed when stratifying by LEEP status, suggesting that both groups experienced a similar decrease in AMH levels during the follow-up period. Although women treated with LEEP had lower overall AMH levels than controls at both baseline and follow-up, these differences were not statistically significant. Conclusion . Overall, the delayed time to pregnancy observed in women treated with LEEP is likely not due to a LEEP-associated decrease in ovarian reserve as measured by AMH; thus, other mechanism are responsible for the delayed time to pregnancy associated with LEEP.
JF  - BioMed Research International
AU  - Sklavos, Martha M
AU  - Spracklen, Cassandra N
AU  - Saftlas, Audrey F
AU  - Pinto, Ligia A
AD  - Human Papillomavirus Immunology Laboratory, Leidos Biomedical Research, Incorporated, Frederick National Laboratory for Cancer Research, Building 469, Room 111, 1050 Boyles Street, Frederick, MD 21702, USA, pintol@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Blood
KW  - Uterus
KW  - Statistical analysis
KW  - Cervix
KW  - Hormones
KW  - Neoplasia
KW  - Colposcopy
KW  - Pregnancy
KW  - W 30940:Products
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516752231?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Does+Loop+Electrosurgical+Excision+Procedure+of+the+Uterine+Cervix+Affect+Anti-Muellerian+Hormone+Levels%3F&rft.au=Sklavos%2C+Martha+M%3BSpracklen%2C+Cassandra+N%3BSaftlas%2C+Audrey+F%3BPinto%2C+Ligia+A&rft.aulast=Sklavos&rft.aufirst=Martha&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F875438
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Blood; Uterus; Statistical analysis; Cervix; Hormones; Colposcopy; Neoplasia; Pregnancy
DO  - http://dx.doi.org/10.1155/2014/875438
ER  - 



TY  - JOUR
T1  - Impact of Immunogenetic IL28B Polymorphism on Natural Outcome of HCV Infection
AN  - 1516751706; 19627295
AB  - With the aim of investigating whether interleukin 28B gene (IL28B) rs1297860 polymorphism is associated with different hepatitis C (HCV) infection statuses, we compared IL28B allelic distribution in an Italian case series of 1050 patients with chronic infection and different outcomes, 47 individuals who spontaneously cleared HCV, and 178 blood donors. Furthermore, we compared IL28B variants among 3882 Caucasian patients with chronic infection, 397 with spontaneous clearance, and 1366 blood donors reported in PubMed. Overall data confirmed a relation between IL28B C allele and HCV spontaneous clearance. Furthermore, we found that IL28B T allele had a weak relation with chronic HCV progression to hepatocellular carcinoma. Study findings are in accordance with the hepatocellular carcinogenic model where IL28B TT genotype, by promoting a persistent chronic hepatitis which leads to both hepatocyte injury and chronic inflammation, could facilitate HCC development. Conversely, patients with lymphoproliferative disorders had not any significantly different IL28B rs1297860 allelic distribution than those with chronic HCV, but, like all chronic HCV-related diseases, they showed a lower CC frequency than patients who spontaneously cleared HCV. Study results confirmed the model of persistent HCV infection as a risk factor for the pathogenesis of both liver and lymphoproliferative disorders.
JF  - BioMed Research International
AU  - De Re, Valli
AU  - Gragnani, Laura
AU  - Fognani, Elisa
AU  - Piluso, Alessia
AU  - Izzo, Francesco
AU  - Mangia, Alessandra
AU  - Crovatto, Marina
AU  - Gava, Graziella
AU  - Casarin, Pietro
AU  - Sansonno, Domenico
AU  - Racanelli, Vito
AU  - De Vita, Salvatore
AU  - Pioltelli, Pietro
AU  - Caggiari, Laura
AU  - De Zorzi, Mariangela
AU  - Berretta, Massimiliano
AU  - Gini, Andrea
AU  - Zucchetto, Antonella
AU  - Buonaguro, Franco Maria
AU  - De Paoli, Paolo
AU  - Zignego, Anna Linda
AD  - Bio-Proteomics Facility, Department of Translational Research, CRO, National Cancer Institute, 33081 Aviano, Italy, vdere@cro.it
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2014
SN  - 2314-6133, 2314-6133
KW  - Genetics Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Blood donors
KW  - Data processing
KW  - Liver diseases
KW  - Injuries
KW  - Hepatocytes
KW  - Gene polymorphism
KW  - Inflammation
KW  - Models
KW  - Immunoproliferative diseases
KW  - Immunogenetics
KW  - Hepatitis C virus
KW  - Risk factors
KW  - Chronic infection
KW  - Hepatitis C
KW  - Hepatocellular carcinoma
KW  - W 30940:Products
KW  - F 06915:Cancer Immunology
KW  - G 07730:Development & Cell Cycle
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516751706?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Impact+of+Immunogenetic+IL28B+Polymorphism+on+Natural+Outcome+of+HCV+Infection&rft.au=De+Re%2C+Valli%3BGragnani%2C+Laura%3BFognani%2C+Elisa%3BPiluso%2C+Alessia%3BIzzo%2C+Francesco%3BMangia%2C+Alessandra%3BCrovatto%2C+Marina%3BGava%2C+Graziella%3BCasarin%2C+Pietro%3BSansonno%2C+Domenico%3BRacanelli%2C+Vito%3BDe+Vita%2C+Salvatore%3BPioltelli%2C+Pietro%3BCaggiari%2C+Laura%3BDe+Zorzi%2C+Mariangela%3BBerretta%2C+Massimiliano%3BGini%2C+Andrea%3BZucchetto%2C+Antonella%3BBuonaguro%2C+Franco+Maria%3BDe+Paoli%2C+Paolo%3BZignego%2C+Anna+Linda&rft.aulast=De+Re&rft.aufirst=Valli&rft.date=2014-01-01&rft.volume=2014&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2014%2F710642
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Number of references - 2
N1  - Last updated - 2014-07-24
N1  - SubjectsTermNotLitGenreText - Blood donors; Liver diseases; Data processing; Injuries; Hepatocytes; Gene polymorphism; Models; Inflammation; Immunoproliferative diseases; Immunogenetics; Risk factors; Chronic infection; Hepatitis C; Hepatocellular carcinoma; Hepatitis C virus
DO  - http://dx.doi.org/10.1155/2014/710642
ER  - 



TY  - JOUR
T1  - Validation of a previous day recall for measuring the location and purpose of active and sedentary behaviors compared to direct observation
AN  - 1505340427; 19323419
AB  - Purpose: Gathering contextual information (i.e., location and purpose) about active and sedentary behaviors is an advantage of self-report tools such as previous day recalls (PDR). However, the validity of PDR's for measuring context has not been empirically tested. The purpose of this paper was to compare PDR estimates of location and purpose to direct observation (DO). Methods: Fifteen adult (18-75 y) and 15 adolescent (12-17 y) participants were directly observed during at least one segment of the day (i.e., morning, afternoon or evening). Participants completed their normal daily routine while trained observers recorded the location (i.e., home, community, work/school), purpose (e.g., leisure, transportation) and whether the behavior was sedentary or active. The day following the observation, participants completed an unannounced PDR. Estimates of time in each context were compared between PDR and DO. Intra-class correlations (ICC), percent agreement and Kappa statistics were calculated. Results: For adults, percent agreement was 85% or greater for each location and ICC values ranged from 0.71 to 0.96. The PDR-reported purpose of adults' behaviors were highly correlated with DO for household activities and work (ICCs of 0.84 and 0.88, respectively). Transportation was not significantly correlated with DO (ICC = -0.08). For adolescents, reported classification of activity location was 80.8% or greater. The ICCs for purpose of adolescents' behaviors ranged from 0.46 to 0.78. Participants were most accurate in classifying the location and purpose of the behaviors in which they spent the most time. Conclusions: This study suggests that adults and adolescents can accurately report where and why they spend time in behaviors using a PDR. This information on behavioral context is essential for translating the evidence for specific behavior-disease associations to health interventions and public policy.
JF  - International Journal of Behavioral Nutrition and Physical Activity
AU  - Keadle, Sarah Kozey
AU  - Lyden, Kate
AU  - Hickey, Amanda
AU  - Ray, Evan L
AU  - Fowke, Jay H
AU  - Freedson, Patty S
AU  - Matthews, Charles E
AD  - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 12
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 11
IS  - 1
SN  - 1479-5868, 1479-5868
KW  - Physical Education Index
KW  - Statistics
KW  - Home
KW  - Behavior
KW  - Adolescence
KW  - Work
KW  - Observation
KW  - Adults
KW  - Activities
KW  - Public health
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505340427?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.atitle=Validation+of+a+previous+day+recall+for+measuring+the+location+and+purpose+of+active+and+sedentary+behaviors+compared+to+direct+observation&rft.au=Keadle%2C+Sarah+Kozey%3BLyden%2C+Kate%3BHickey%2C+Amanda%3BRay%2C+Evan+L%3BFowke%2C+Jay+H%3BFreedson%2C+Patty+S%3BMatthews%2C+Charles+E&rft.aulast=Keadle&rft.aufirst=Sarah&rft.date=2014-01-01&rft.volume=11&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.issn=14795868&rft_id=info:doi/10.1186%2F1479-5868-11-12
L2  - http://www.ijbnpa.org/content/11/1/12
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2014-03-01
N1  - Number of references - 40
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Home; Statistics; Behavior; Adolescence; Work; Observation; Adults; Activities; Public health
DO  - http://dx.doi.org/10.1186/1479-5868-11-12
ER  - 



TY  - JOUR
T1  - Urban sprawl, obesity, and cancer mortality in the United States: cross-sectional analysis and methodological challenges
AN  - 1505334022; 19030510
AB  - Background: Urban sprawl has the potential to influence cancer mortality via direct and indirect effects on obesity, access to health services, physical activity, transportation choices and other correlates of sprawl and urbanization. Methods: This paper presents a cross-sectional analysis of associations between urban sprawl and cancer mortality in urban and suburban counties of the United States. This ecological analysis was designed to examine whether urban sprawl is associated with total and obesity-related cancer mortality and to what extent these associations differed in different regions of the US. A major focus of our analyses was to adequately account for spatial heterogeneity in mortality. Therefore, we fit a series of regression models, stratified by gender, successively testing for the presence of spatial heterogeneity. Our resulting models included county level variables related to race, smoking, obesity, access to health services, insurance status, socioeconomic position, and broad geographic region as well as a measure of urban sprawl and several interactions. Our most complex models also included random effects to account for any county-level spatial autocorrelation that remained unexplained by these variables. Results: Total cancer mortality rates were higher in less sprawling areas and contrary to our initial hypothesis; this was also true of obesity related cancers in six of seven U.S. regions (census divisions) where there were statistically significant associations between the sprawl index and mortality. We also found significant interactions (p < 0.05) between region and urban sprawl for total and obesity related cancer mortality in both sexes. Thus, the association between urban sprawl and cancer mortality differs in different regions of the US. Conclusions: Despite higher levels of obesity in more sprawling counties in the US, mortality from obesity related cancer was not greater in such counties. Identification of disparities in cancer mortality within and between geographic regions is an ongoing public health challenge and an opportunity for further analytical work identifying potential causes of these disparities. Future analyses of urban sprawl and health outcomes should consider exploring regional and international variation in associations between sprawl and health.
JF  - International Journal of Health Geographics
AU  - Berrigan, David
AU  - Tatalovich, Zaria
AU  - Pickle, Linda W
AU  - Ewing, Reid
AU  - Ballard-Barbash, Rachel
AD  - Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 3
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1476-072X, 1476-072X
KW  - Health & Safety Science Abstracts; Sustainability Science Abstracts
KW  - Census
KW  - Mortality
KW  - USA
KW  - M3 1010:Issues in Sustainable Development
KW  - H 2000:Transportation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505334022?accountid=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=International+Journal+of+Health+Geographics&rft.atitle=Urban+sprawl%2C+obesity%2C+and+cancer+mortality+in+the+United+States%3A+cross-sectional+analysis+and+methodological+challenges&rft.au=Berrigan%2C+David%3BTatalovich%2C+Zaria%3BPickle%2C+Linda+W%3BEwing%2C+Reid%3BBallard-Barbash%2C+Rachel&rft.aulast=Berrigan&rft.aufirst=David&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Health+Geographics&rft.issn=1476072X&rft_id=info:doi/10.1186%2F1476-072X-13-3
L2  - http://www.ij-healthgeographics.com/content/13/1/3
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 - Mortality; USA
DO  - http://dx.doi.org/10.1186/1476-072X-13-3
ER  - 



TY  - JOUR
T1  - Seasonal Variation in Spatial Distributions of Anopheles gambiae in a Sahelian Village: Evidence for Aestivation
AN  - 1500766944; 19157907
AB  - Changes in spatial distribution of mosquitoes over time in a Sahelian village werestudied to understand the sources of the mosquitoes during the dry season when no larval sites are found. At that time, the sources of Anopheles gambiae Giles may be local shelters used by aestivating mosquitoes or migrants from distant populations. The mosquito distribution was more aggregated during the dry season, when few houses had densities 7- to 24-fold higher than expected. The high-density houses during the dry season differed from those of the wet season. Most high-density houses during the dry season changed between years, yet their vicinity was rather stable. Scan statistics confirmed the presence of one or two adjacent hotspots in the dry season, usually found on one edge of the village. These hotspots shifted between the early and late dry season. During the wet season, the hotspots were relatively stable near the main larval site. The locations of the hotspots in the wet season and early and late dry season were similar between years. Season-specific, stable, and focal hotspots are inconsistent with the predictions based on the arrival of migrants from distant localities during the dry season, but are consistent with the predictions based on local shelters used by aestivating mosquitoes. Targeting hotspots in Sahelian villages for vector control may not be effective because the degree of aggregation is moderate, the hotspots are not easily predicted, and they are not the sources of the population. However, targeting the dry-season shelters may be highly cost-effective, once they can be identified and predicted.
JF  - Journal of Medical Entomology
AU  - Lehmann, Tovi
AU  - Dao, A
AU  - Yaro, A S
AU  - Diallo, M
AU  - Timbine, S
AU  - Huestis, D L
AU  - Adamou, A
AU  - Kassogue, Y
AU  - Traore, AI
AD  - Laboratory of Malaria and Vector Research, NIAID, NIH, Rockville, MD 20852., tlehmann@niaid.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 27
EP  - 38
PB  - Entomological Society of America, 9301 Annapolis Rd. Lanham MD 20706 United States
VL  - 51
IS  - 1
SN  - 0022-2585, 0022-2585
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Entomology Abstracts
KW  - spatial aggregation
KW  - dry-season diapause
KW  - hotspot
KW  - malaria
KW  - long-distance migration
KW  - Houses
KW  - Statistics
KW  - Spatial distribution
KW  - Hot spots
KW  - Vectors
KW  - Shelter
KW  - Pest control
KW  - Hosts
KW  - Anopheles gambiae
KW  - Rainy season
KW  - Aestivation
KW  - Shelters
KW  - Dry season
KW  - Aquatic insects
KW  - Seasonal variations
KW  - Q1 08302:Geographical distribution
KW  - Z 05350:Medical, Veterinary, and Agricultural Entomology
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500766944?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medical+Entomology&rft.atitle=Seasonal+Variation+in+Spatial+Distributions+of+Anopheles+gambiae+in+a+Sahelian+Village%3A+Evidence+for+Aestivation&rft.au=Lehmann%2C+Tovi%3BDao%2C+A%3BYaro%2C+A+S%3BDiallo%2C+M%3BTimbine%2C+S%3BHuestis%2C+D+L%3BAdamou%2C+A%3BKassogue%2C+Y%3BTraore%2C+AI&rft.aulast=Lehmann&rft.aufirst=Tovi&rft.date=2014-01-01&rft.volume=51&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Entomology&rft.issn=00222585&rft_id=info:doi/10.1603%2FME12131
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Number of references - 53
N1  - Last updated - 2014-12-11
N1  - SubjectsTermNotLitGenreText - Rainy season; Hot spots; Aestivation; Shelters; Pest control; Hosts; Dry season; Seasonal variations; Aquatic insects; Houses; Statistics; Spatial distribution; Vectors; Shelter; Anopheles gambiae
DO  - http://dx.doi.org/10.1603/ME12131
ER  - 



TY  - JOUR
T1  - Using single cell sequencing data to model the evolutionary history of a tumor
AN  - 1500759373; 19053761
AB  - Background: The introduction of next-generation sequencing (NGS) technology has made it possible to detect genomic alterations within tumor cells on a large scale. However, most applications of NGS show the genetic content of mixtures of cells. Recently developed single cell sequencing technology can identify variation within a single cell. Characterization of multiple samples from a tumor using single cell sequencing can potentially provide information on the evolutionary history of that tumor. This may facilitate understanding how key mutations accumulate and evolve in lineages to form a heterogeneous tumor. Results: We provide a computational method to infer an evolutionary mutation tree based on single cell sequencing data. Our approach differs from traditional phylogenetic tree approaches in that our mutation tree directly describes temporal order relationships among mutation sites. Our method also accommodates sequencing errors. Furthermore, we provide a method for estimating the proportion of time from the earliest mutation event of the sample to the most recent common ancestor of the sample of cells. Finally, we discuss current limitations on modeling with single cell sequencing data and possible improvements under those limitations. Conclusions: Inferring the temporal ordering of mutational sites using current single cell sequencing data is a challenge. Our proposed method may help elucidate relationships among key mutations and their role in tumor progression.
JF  - BMC Bioinformatics
AU  - Kim, Kyung In
AU  - Simon, Richard
AD  - Biometric Research Branch, National Cancer Institute, 9609 Medical Center Dr., MSC 9735 Bethesda, MD 20892, USA
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 27
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 15
IS  - 1
SN  - 1471-2105, 1471-2105
KW  - Biotechnology and Bioengineering Abstracts
KW  - Phylogeny
KW  - Data processing
KW  - Temporal variations
KW  - Tumors
KW  - Bioinformatics
KW  - genomics
KW  - Computer applications
KW  - Mutation
KW  - Tumor cells
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500759373?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=Using+single+cell+sequencing+data+to+model+the+evolutionary+history+of+a+tumor&rft.au=Kim%2C+Kyung+In%3BSimon%2C+Richard&rft.aulast=Kim&rft.aufirst=Kyung&rft.date=2014-01-01&rft.volume=15&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-15-27
L2  - http://www.biomedcentral.com/1471-2105/15/27
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Number of references - 27
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Phylogeny; Data processing; Temporal variations; genomics; Bioinformatics; Tumors; Computer applications; Tumor cells; Mutation
DO  - http://dx.doi.org/10.1186/1471-2105-15-27
ER  - 



TY  - JOUR
T1  - A rat RNA-Seq transcriptomic BodyMap across 11 organs and 4 developmental stages.
AN  - 1499143095; 24510058
AB  - The rat has been used extensively as a model for evaluating chemical toxicities and for understanding drug mechanisms. However, its transcriptome across multiple organs, or developmental stages, has not yet been reported. Here we show, as part of the SEQC consortium efforts, a comprehensive rat transcriptomic BodyMap created by performing RNA-Seq on 320 samples from 11 organs of both sexes of juvenile, adolescent, adult and aged Fischer 344 rats. We catalogue the expression profiles of 40,064 genes, 65,167 transcripts, 31,909 alternatively spliced transcript variants and 2,367 non-coding genes/non-coding RNAs (ncRNAs) annotated in AceView. We find that organ-enriched, differentially expressed genes reflect the known organ-specific biological activities. A large number of transcripts show organ-specific, age-dependent or sex-specific differential expression patterns. We create a web-based, open-access rat BodyMap database of expression profiles with crosslinks to other widely used databases, anticipating that it will serve as a primary resource for biomedical research using the rat model.
JF  - Nature communications
AU  - Yu, Ying
AU  - Fuscoe, James C
AU  - Zhao, Chen
AU  - Guo, Chao
AU  - Jia, Meiwen
AU  - Qing, Tao
AU  - Bannon, Desmond I
AU  - Lancashire, Lee
AU  - Bao, Wenjun
AU  - Du, Tingting
AU  - Luo, Heng
AU  - Su, Zhenqiang
AU  - Jones, Wendell D
AU  - Moland, Carrie L
AU  - Branham, William S
AU  - Qian, Feng
AU  - Ning, Baitang
AU  - Li, Yan
AU  - Hong, Huixiao
AU  - Guo, Lei
AU  - Mei, Nan
AU  - Shi, Tieliu
AU  - Wang, Kevin Y
AU  - Wolfinger, Russell D
AU  - Nikolsky, Yuri
AU  - Walker, Stephen J
AU  - Duerksen-Hughes, Penelope
AU  - Mason, Christopher E
AU  - Tong, Weida
AU  - Thierry-Mieg, Jean
AU  - Thierry-Mieg, Danielle
AU  - Shi, Leming
AU  - Wang, Charles
AD  - 1] Center for Pharmacogenomics, State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Schools of Life Sciences and Pharmacy, Fudan University, Shanghai 201203, China [2]. ; 1] National Center for Toxicological Research, Food and Drug Administration, Jefferson, Arkansas 92079, USA [2]. ; Center for Pharmacogenomics, State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Schools of Life Sciences and Pharmacy, Fudan University, Shanghai 201203, China. ; Functional Genomics Core, Beckman Research Institute, City of Hope, Duarte, California 91010, USA. ; Army Institute of Public Health, U.S. Army Public Health Command, Aberdeen Proving Ground, Maryland 21010, USA. ; Computation Biology and Bioinformatics, IP & Science, Thomson Reuters, London EC1N 8JS, UK. ; SAS Institute Inc., Cary, North Carolina 27513, USA. ; National Center for Toxicological Research, Food and Drug Administration, Jefferson, Arkansas 92079, USA. ; Expression Analysis Inc., Durham, North Carolina 27713, USA. ; The Center for Bioinformatics and The Institute of Biomedical Sciences, College of Life Science, Shanghai 200241, China. ; Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Wake Forest Institute for Regenerative Medicine, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157, USA. ; Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, California 92350, USA. ; Department of Physiology & Biophysics and the Institute for Computational Biomedicine, Cornell University, New York, New York 10021, USA. ; National Center for Biotechnology Information, National Institutes of Health, Bethesda, Maryland 20894, USA. ; 1] Center for Pharmacogenomics, State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Schools of Life Sciences and Pharmacy, Fudan University, Shanghai 201203, China [2] National Center for Toxicological Research, Food and Drug Administration, Jefferson, Arkansas 92079, USA [3] Fudan-Zhangjiang Center for Clinical Genomics and Zhangjiang Center for Translational Medicine, Shanghai 201203, China. ; Center for Genomics and Division of Microbiology & Molecular Genetics, School of Medicine, Loma Linda University, Loma Linda, California 92350, USA.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 3230
VL  - 5
KW  - Protein Isoforms
KW  - 0
KW  - Index Medicus
KW  - Gene Expression Profiling
KW  - Animals
KW  - Sex Characteristics
KW  - Alternative Splicing
KW  - Protein Isoforms -- metabolism
KW  - Sequence Analysis, RNA
KW  - Male
KW  - Female
KW  - Rats, Inbred F344 -- growth & development
KW  - Transcriptome
KW  - Rats, Inbred F344 -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499143095?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+rat+RNA-Seq+transcriptomic+BodyMap+across+11+organs+and+4+developmental+stages.&rft.au=Yu%2C+Ying%3BFuscoe%2C+James+C%3BZhao%2C+Chen%3BGuo%2C+Chao%3BJia%2C+Meiwen%3BQing%2C+Tao%3BBannon%2C+Desmond+I%3BLancashire%2C+Lee%3BBao%2C+Wenjun%3BDu%2C+Tingting%3BLuo%2C+Heng%3BSu%2C+Zhenqiang%3BJones%2C+Wendell+D%3BMoland%2C+Carrie+L%3BBranham%2C+William+S%3BQian%2C+Feng%3BNing%2C+Baitang%3BLi%2C+Yan%3BHong%2C+Huixiao%3BGuo%2C+Lei%3BMei%2C+Nan%3BShi%2C+Tieliu%3BWang%2C+Kevin+Y%3BWolfinger%2C+Russell+D%3BNikolsky%2C+Yuri%3BWalker%2C+Stephen+J%3BDuerksen-Hughes%2C+Penelope%3BMason%2C+Christopher+E%3BTong%2C+Weida%3BThierry-Mieg%2C+Jean%3BThierry-Mieg%2C+Danielle%3BShi%2C+Leming%3BWang%2C+Charles&rft.aulast=Yu&rft.aufirst=Ying&rft.date=2014-01-01&rft.volume=5&rft.issue=&rft.spage=3230&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms4230
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-10-26
N1  - Date created - 2014-02-10
N1  - Date revised - 2017-01-14
N1  - Genetic sequence - GSE53960; GEO
N1  - SuppNotes - Cited By:
Nature. 2009 Jun 18;459(7249):927-30 [19536255]
Bioinformatics. 2013 Jul 1;29(13):i108-16 [23812974]
Genome Res. 2009 Sep;19(9):1639-45 [19541911]
Nat Rev Genet. 2010 Jan;11(1):31-46 [19997069]
Nat Biotechnol. 2010 Aug;28(8):827-38 [20676074]
Nat Methods. 2010 Dec;7(12):1009-15 [21057496]
BMC Genomics. 2010;11:675 [21118493]
Science. 2010 Dec 24;330(6012):1787-97 [21177974]
Science. 2010 Dec 24;330(6012):1775-87 [21177976]
Nature. 2011 Mar 24;471(7339):473-9 [21179090]
Nucleic Acids Res. 2000 Jan 1;28(1):136-8 [10592203]
J Biol Chem. 2000 Aug 11;275(32):24333-40 [10811639]
Genome Res. 2000 Nov;10(11):1817-27 [11076866]
J Biol Chem. 2001 Nov 9;276(45):42108-15 [11546782]
N Engl J Med. 2003 Sep 18;349(12):1157-67 [13679531]
J Biol. 2004;3(5):21 [15588312]
Drug Metab Dispos. 2005 Oct;33(10):1466-76 [16006569]
Drug Metab Dispos. 2006 Mar;34(3):351-3 [16339353]
Genome Biol. 2006;7 Suppl 1:S12.1-14 [16925834]
Nat Biotechnol. 2006 Sep;24(9):1151-61 [16964229]
Toxicol Pathol. 2007 Feb;35(2):242-51 [17366318]
Nat Genet. 2007 Jun;39(6):715-20 [17534367]
J Biol Chem. 2007 Sep 14;282(37):26707-16 [17613526]
Nat Methods. 2008 Jul;5(7):621-8 [18516045]
Annu Rev Genomics Hum Genet. 2008;9:387-402 [18576944]
Toxicol Sci. 2008 Nov;106(1):263-83 [18653662]
Nature. 2008 Nov 27;456(7221):470-6 [18978772]
Bioinformatics. 2009 May 1;25(9):1105-11 [19289445]
Clin Pharmacol Ther. 2011 Jun;89(6):793-7 [21490594]
Wiley Interdiscip Rev RNA. 2012 Jan-Feb;3(1):133-43 [21898829]
Nat Protoc. 2012 Mar;7(3):562-78 [22383036]
Bioinformatics. 2012 Apr 15;28(8):1184-5 [22345621]
Nucleic Acids Res. 2012 Jul;40(Web Server issue):W622-7 [22684630]
Genome Res. 2012 Sep;22(9):1775-89 [22955988]
Nature. 2012 Sep 6;489(7414):57-74 [22955616]
Nature. 2012 Sep 6;489(7414):101-8 [22955620]
Mamm Genome. 2012 Oct;23(9-10):539-49 [22832508]
Mamm Genome. 2012 Oct;23(9-10):514-24 [22847374]
Sci China Life Sci. 2013 Feb;56(2):134-42 [23393029]
Nat Rev Mol Cell Biol. 2013 Mar;14(3):153-65 [23385723]
Physiol Genomics. 2013 Apr 16;45(8):301-11 [23429212]
Annu Rev Genomics Hum Genet. 2009;10:135-51 [19715439]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1038/ncomms4230
ER  - 



TY  - JOUR
T1  - Linking HIV-positive adolescents to care in 15 different clinics across the United States: creating solutions to address structural barriers for linkage to care
AN  - 1496957565; 4522618
AB  - Linkage to care is a critical corollary to expanded HIV testing, but many adolescents are not successfully linked to care, in part due to fragmented care systems. Through a collaboration of the National Institutes of Health (NIH), Centers for Disease Control and Prevention (CDC) and the Adolescent Trials Network (ATN), a linkage to care outreach worker was provided to ATN clinics. Factors related to linkage were explored to better understand how to improve retention rates and health outcomes for HIV- positive adolescents. We conducted 124 interviews with staff at 15 Adolescent Trials Network clinics to better understand linkage to care processes, barriers, and facilitators. Content analysis was conducted focusing on structural barriers to care and potential solutions, specifically at the macro-, meso-, and micro-levels. Macro- level barriers included navigating health insurance policies, transportation to appointments, and ease of collecting and sharing client-level contact information between testing agencies, local health departments and clinics; meso-level barriers included lack of youth friendliness within clinic space and staff, and duplication of linkage services; micro-level barriers included adolescents' readiness for care and adolescent developmental capacity. Staff initiated solutions included providing transportation for appointments and funding clinic visits and tests with a range of grants and clinic funds while waiting for insurance approval. However, such solutions were often ad hoc and partial, using micro-level solutions to address macro-level barriers. Comprehensive initiatives to improve linkage to care are needed to address barriers to HIV-care for adolescents, whose unique developmental needs make accessing care particularly challenging. Matching the level of structural solution to the level of structural barriers (i.e., macro-level with macro-level), such as creating policy to address needed youth healthcare entitlements versus covering uninsured patients with clinic funds is imperative to achieving the goal of increasing linkage to care rates for newly diagnosed adolescents. Reprinted by permission of Routledge, Taylor & Francis Ltd.
JF  - AIDS care
AU  - Philbin, Morgan M
AU  - Tanner, Amanda E
AU  - DuVal, Anna
AU  - Ellen, Jonathan
AU  - Kapogiannis, Bill
AU  - Fortenberry, J Dennis
AD  - Johns Hopkins Bloomberg School of Public Health ; University of North Carolina, Greensboro ; National Institutes of Health ; Indiana University
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 12
EP  - 19
VL  - 26
IS  - 1
SN  - 0954-0121, 0954-0121
KW  - Sociology
KW  - Qualitative analysis
KW  - Health care
KW  - U.S.A.
KW  - HIV
KW  - Adolescents
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496957565?accountid=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=Linking+HIV-positive+adolescents+to+care+in+15+different+clinics+across+the+United+States%3A+creating+solutions+to+address+structural+barriers+for+linkage+to+care&rft.au=Philbin%2C+Morgan+M%3BTanner%2C+Amanda+E%3BDuVal%2C+Anna%3BEllen%2C+Jonathan%3BKapogiannis%2C+Bill%3BFortenberry%2C+J+Dennis&rft.aulast=Philbin&rft.aufirst=Morgan&rft.date=2014-01-01&rft.volume=26&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2013.808730
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2014-01-23
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - 593; 10519 3279 971 3286; 5703 3617 6220; 5775 13521; 433 293 14
DO  - http://dx.doi.org/10.1080/09540121.2013.808730
ER  - 



TY  - JOUR
T1  - Relationship between viral load and self-report measures of medication adherence among youth with perinatal HIV infection
AN  - 1496951083; 4522608
AB  - Poor adherence to antiretroviral therapy (ART) contributes to disease progression and emergence of drug-resistant HIV in youth with perinatally acquired HIV infection (PHIV +), necessitating reliable measures of adherence. Although electronic monitoring devices have often been considered the gold-standard assessment in HIV research, they are costly, can overestimate nonadherence and are not practical for routine care. Thus, the development of valid, easily administered self-report adherence measures is crucial for adherence monitoring. PHIV+youth aged 7-16 (n = 289) and their caregivers, enrolled in a multisite cohort study, were interviewed to assess several reported indicators of adherence. HIV-1 RNA viral load (VL) was dichotomized into >/≤400 copies/mL. Lower adherence was significantly associated with VL >400 copies/mL across most indicators, including ≥1 missed dose in past seven days [youth report: OR = 2.78 (95% CI, 1.46-5.27)]. Caregiver and combined youth/caregiver reports yielded similar results. Within-rater agreement between various adherence indicators was high for both youth and caregivers. Inter-rater agreement on adherence was moderate across most indicators. Age ≥13 years and living with biological mother or relative were associated with VL >400 copies/mL. Findings support the validity of caregiver and youth adherence reports and identify youth at risk of poor adherence. Reprinted by permission of Routledge, Taylor & Francis Ltd.
JF  - AIDS care
AU  - Usitalo, Ann
AU  - Leister, Erin
AU  - Tassiopoulos, Katherine
AU  - Allison, Susannah
AU  - Malee, Kathleen
AU  - Paul, Mary E
AU  - Smith, Renee
AU  - Dyke, Russell B. Van
AU  - Seage, George R
AU  - Mellins, Claude A
AD  - University of Florida ; Harvard University ; US National Institute of Mental Health ; Ann and Robert H. Lurie Children's Hospital of Chicago ; Baylor College of Medicine ; University of Illinois, Chicago ; Tulane University ; Columbia University
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 107
EP  - 115
VL  - 26
IS  - 1
SN  - 0954-0121, 0954-0121
KW  - Sociology
KW  - Pediatrics
KW  - HIV
KW  - Youth
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496951083?accountid=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=Relationship+between+viral+load+and+self-report+measures+of+medication+adherence+among+youth+with+perinatal+HIV+infection&rft.au=Usitalo%2C+Ann%3BLeister%2C+Erin%3BTassiopoulos%2C+Katherine%3BAllison%2C+Susannah%3BMalee%2C+Kathleen%3BPaul%2C+Mary+E%3BSmith%2C+Renee%3BDyke%2C+Russell+B.+Van%3BSeage%2C+George+R%3BMellins%2C+Claude+A&rft.aulast=Usitalo&rft.aufirst=Ann&rft.date=2014-01-01&rft.volume=26&rft.issue=1&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2013.802280
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2014-01-23
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - 5703 3617 6220; 9345 7894; 13779 652 5676 646 6091; 10449 5772
DO  - http://dx.doi.org/10.1080/09540121.2013.802280
ER  - 



TY  - JOUR
T1  - Correlates of perceived health related quality of life in obese, overweight and normal weight older adults: an observational study
AN  - 1496897372; 19024657
AB  - Background: Obesity is a complex multifactorial disease, which also has an impact on quality of life. The aim of this paper is to identify the correlates of perceived health related quality of life in obese, overweight and normal weight Italians older adults. Methods: 205 subjects at the age greater than or equal to 60 yrs. were recruited into the Division of Endocrinology of the Polytechnic University of Marche Region, Ancona (Italy). A protocol of questionnaires was constructed for data collection, and included domains such as physical activity, quality of life, socio-psychological aspects. The association of the latter variables with SF-36 Health Survey physical component (PCS-36) were evaluated in the whole sample. Multiple linear regression models were used to assess the effect of independent variables on PCS-36 and the physical subscales of SF-36. Results: PCS-36 showed a lower score in the obese and overweight subjects than the normal weight group (post-hoc test, p < 0.001 and p < 0.05 respectively). Age, gender (male), Body Mass Index, years of education, Physical Activity Scale for the Elderly (PASE) total score, Hospital Anxiety and Depression Scale anxiety, Hospital Anxiety and Depression Scale depression, number of medications prescribed and number of diseases were included in the model. Negative and significant PCS-associated variables included depression (p = 0.009), BMI (p = 0.001), age in years (p = 0.007), whereas positive and significant PCS-associated independent variables were years of education (p = 0.022), physical activity (p = 0.026). BMI was negatively associated with all the physical subscales of SF-36 (p < 0.05). Conclusions: Research funding should be invested in the study of the benefits accruing from reducing obesity in the elderly.
JF  - BMC Public Health
AU  - Giuli, Cinzia
AU  - Papa, Roberta
AU  - Bevilacqua, Roberta
AU  - Felici, Elisa
AU  - Gagliardi, Cristina
AU  - Marcellini, Fiorella
AU  - Boscaro, Marco
AU  - De Robertis, Marco
AU  - Mocchegiani, Eugenio
AU  - Faloia, Emanuela
AU  - Tirabassi, Giacomo
AD  - Unit of Geriatrics, INRCA (Italian National Institute on Aging), Fermo, Italy
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 35
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2458, 1471-2458
KW  - Health & Safety Science Abstracts
KW  - Obesity
KW  - Data collection
KW  - Age
KW  - Depression
KW  - Body mass
KW  - Physical activity
KW  - Elderly
KW  - Italy
KW  - Education
KW  - Perception
KW  - Gender
KW  - Italy, Marche
KW  - Italy, Marche, Ancona
KW  - Drugs
KW  - Hospitals
KW  - Quality of life
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496897372?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Public+Health&rft.atitle=Correlates+of+perceived+health+related+quality+of+life+in+obese%2C+overweight+and+normal+weight+older+adults%3A+an+observational+study&rft.au=Giuli%2C+Cinzia%3BPapa%2C+Roberta%3BBevilacqua%2C+Roberta%3BFelici%2C+Elisa%3BGagliardi%2C+Cristina%3BMarcellini%2C+Fiorella%3BBoscaro%2C+Marco%3BDe+Robertis%2C+Marco%3BMocchegiani%2C+Eugenio%3BFaloia%2C+Emanuela%3BTirabassi%2C+Giacomo&rft.aulast=Giuli&rft.aufirst=Cinzia&rft.date=2014-01-01&rft.volume=14&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-14-35
L2  - http://www.biomedcentral.com/1471-2458/14/35
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Number of references - 60
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Obesity; Age; Data collection; Depression; Physical activity; Body mass; Elderly; Education; Perception; Gender; Drugs; Quality of life; Hospitals; Italy, Marche, Ancona; Italy, Marche; Italy
DO  - http://dx.doi.org/10.1186/1471-2458-14-35
ER  - 



TY  - JOUR
T1  - Using a composite index of socioeconomic status to investigate health disparities while protecting the confidentiality of cancer registry data
AN  - 1496887885; 18984868
AB  - Purpose: The lack of individual socioeconomic status (SES) information in cancer registry data necessitates the use of area-based measures to investigate health disparities. Concerns about confidentiality, however, prohibit publishing patients' residential locations at the subcounty level. We developed a census tract-based composite SES index to be released in place of individual census tracts to minimize the risk of disclosure. Methods: Two SES indices based on the measures identified in the literature were constructed using factor analysis. The analyses were repeated using the data from the 2000 decennial census and 2005-2009 American Community Survey to create the indices at two time points, which were linked to 2000-2009 Surveillance, Epidemiology, and End Results registry data to estimate incidence and survival rates. Results: The two indices performed similarly in stratifying census tracts and detecting socioeconomic gradients in cancer incidence and survival. The gradient in the incidence is positive for breast and prostate, and negative for lung cancers, in all races, although the level varies. The positive gradient in survival is more salient for regional-staged breast, colorectal, and lung cancers. Conclusions: The census tract-based SES index provides a valuable tool for monitoring the disparities in cancer burdens while avoiding potential identity disclosure. This index, divided into tertiles and quintiles, is now available to the researchers on request.
JF  - Cancer Causes & Control
AU  - Yu, Mandi
AU  - Tatalovich, Zaria
AU  - Gibson, James T
AU  - Cronin, Kathleen A
AD  - Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Rockville, MD, USA, yum3@mail.nih.gov
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 81
EP  - 92
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 25
IS  - 1
SN  - 0957-5243, 0957-5243
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Census
KW  - Health risks
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/1496887885?accountid=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=Using+a+composite+index+of+socioeconomic+status+to+investigate+health+disparities+while+protecting+the+confidentiality+of+cancer+registry+data&rft.au=Yu%2C+Mandi%3BTatalovich%2C+Zaria%3BGibson%2C+James+T%3BCronin%2C+Kathleen+A&rft.aulast=Yu&rft.aufirst=Mandi&rft.date=2014-01-01&rft.volume=25&rft.issue=1&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-013-0310-1
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Health risks
DO  - http://dx.doi.org/10.1007/s10552-013-0310-1
ER  - 



TY  - JOUR
T1  - Effectiveness of Using the Modified Checklist for Autism in Toddlers in Two-Stage Screening of Autism Spectrum Disorder at the 18-Month Health Check-Up in Japan
AN  - 1496665439; 201402721
AB  - To determine whether the Modified Checklist for Autism in Toddlers (M-CHAT) in conjunction with the routine 18-month health check-up identifies Japanese toddlers with autism spectrum disorder (ASD). Two-stage screening using the M-CHAT was conducted with 1,851 children attending the check-up. Final ASD diagnosis was confirmed at age >=3 years. Screening identified 20/51 children with ASD: 12/20 true positives were developmentally delayed, whereas 16/22 false negatives were high-functioning. Sensitivity was 0.476, specificity 0.986, positive predictive value 0.455, and likelihood ratio 33.4 for children with ASD. With a few modifications, M-CHAT screening successfully detected toddlers with ASD with and without developmental delay and is a promising screening tool to complement existing community surveillance. Adapted from the source document.
JF  - Journal of Autism and Developmental Disorders
AU  - Kamio, Yoko
AU  - Inada, Naoko
AU  - Koyama, Tomonori
AU  - Inokuchi, Eiko
AU  - Tsuchiya, Kenji
AU  - Kuroda, Miho
AD  - Department of Child and Adolescent Mental Health, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi, Kodaira, Tokyo, 187-8553, Japan kamio@ncnp.go.jp
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 194
EP  - 203
PB  - Springer, Dordrecht The Netherlands
VL  - 44
IS  - 1
SN  - 0162-3257, 0162-3257
KW  - Screening
KW  - Young children
KW  - Health
KW  - Children
KW  - Japan
KW  - Autistic spectrum disorders
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496665439?accountid=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=Effectiveness+of+Using+the+Modified+Checklist+for+Autism+in+Toddlers+in+Two-Stage+Screening+of+Autism+Spectrum+Disorder+at+the+18-Month+Health+Check-Up+in+Japan&rft.au=Kamio%2C+Yoko%3BInada%2C+Naoko%3BKoyama%2C+Tomonori%3BInokuchi%2C+Eiko%3BTsuchiya%2C+Kenji%3BKuroda%2C+Miho&rft.aulast=Kamio&rft.aufirst=Yoko&rft.date=2014-01-01&rft.volume=44&rft.issue=1&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Journal+of+Autism+and+Developmental+Disorders&rft.issn=01623257&rft_id=info:doi/10.1007%2Fs10803-013-1864-1
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-02-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JADDDQ
N1  - SubjectsTermNotLitGenreText - Autistic spectrum disorders; Screening; Young children; Children; Japan; Health
DO  - http://dx.doi.org/10.1007/s10803-013-1864-1
ER  - 



TY  - JOUR
T1  - Critical dose and toxicity index of organs at risk in radiotherapy: analyzing the calculated effects of modified dose fractionation in non-small cell lung cancer.
AN  - 1494301607; 24239409
AB  - To increase the efficacy of radiotherapy for non-small cell lung cancer (NSCLC), many schemes of dose fractionation were assessed by a new "toxicity index" (I), which allows one to choose the fractionation schedules that produce less toxic treatments. Thirty-two patients affected by non resectable NSCLC were treated by standard 3-dimensional conformal radiotherapy (3DCRT) with a strategy of limited treated volume. Computed tomography datasets were employed to re plan by simultaneous integrated boost intensity-modulated radiotherapy (IMRT). The dose distributions from plans were used to test various schemes of dose fractionation, in 3DCRT as well as in IMRT, by transforming the dose-volume histogram (DVH) into a biological equivalent DVH (BDVH) and by varying the overall treatment time. The BDVHs were obtained through the toxicity index, which was defined for each of the organs at risk (OAR) by a linear quadratic model keeping an equivalent radiobiological effect on the target volume. The less toxic fractionation consisted in a severe/moderate hyper fractionation for the volume including the primary tumor and lymph nodes, followed by a hypofractionation for the reduced volume of the primary tumor. The 3DCRT and IMRT resulted, respectively, in 4.7% and 4.3% of dose sparing for the spinal cord, without significant changes for the combined-lungs toxicity (p < 0.001). Schedules with reduced overall treatment time (accelerated fractionations) led to a 12.5% dose sparing for the spinal cord (7.5% in IMRT), 8.3% dose sparing for V20 in the combined lungs (5.5% in IMRT), and also significant dose sparing for all the other OARs (p < 0.001). The toxicity index allows to choose fractionation schedules with reduced toxicity for all the OARs and equivalent radiobiological effect for the tumor in 3DCRT, as well as in IMRT, treatments of NSCLC. 
          Copyright © 2014 American Association of Medical Dosimetrists. Published by Elsevier Inc. All rights reserved.
JF  - Medical dosimetry : official journal of the American Association of Medical Dosimetrists
AU  - Pedicini, Piernicola
AU  - Strigari, Lidia
AU  - Benassi, Marcello
AU  - Caivano, Rocchina
AU  - Fiorentino, Alba
AU  - Nappi, Antonio
AU  - Salvatore, Marco
AU  - Storto, Giovanni
AD  - Service of Medical Physics, I.R.C.C.S. Regional Cancer Hospital C.R.O.B, Rionero in Vulture, Italy. Electronic address: ppiern@libero.it. ; Laboratory of Medical Physics and Expert Systems, Regina Elena National Cancer Institute, Rome, Italy. ; Service of Medical Physics, Scientific Institute of Tumours of Romagna I.R.S.T., Meldola, Italy. ; Service of Medical Physics, I.R.C.C.S. Regional Cancer Hospital C.R.O.B, Rionero in Vulture, Italy. ; U.O. of Radiotherapy, I.R.C.C.S. Regional Cancer Hospital C.R.O.B., Rionero in Vulture, Italy. ; U.O. of Nuclear Medicine, I.R.C.C.S. Regional Cancer Hospital C.R.O.B., Rionero in Vulture, Italy. ; U.O. of Nuclear Medicine, I.R.C.C.S. SDN Foundation, Naples, Italy.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 23
EP  - 30
VL  - 39
IS  - 1
KW  - Index Medicus
KW  - LQ model
KW  - BED
KW  - DVH
KW  - Dose fractionation
KW  - SIB-IMRT
KW  - Sensitivity and Specificity
KW  - Reproducibility of Results
KW  - Aged, 80 and over
KW  - Humans
KW  - Treatment Outcome
KW  - Aged
KW  - Middle Aged
KW  - Radiography
KW  - Male
KW  - Female
KW  - Organs at Risk -- radiation effects
KW  - Lung Neoplasms -- complications
KW  - Lung Neoplasms -- radiotherapy
KW  - Carcinoma, Non-Small-Cell Lung -- diagnostic imaging
KW  - Dose Fractionation
KW  - Radiotherapy Planning, Computer-Assisted -- methods
KW  - Radiation Injuries -- prevention & control
KW  - Carcinoma, Non-Small-Cell Lung -- complications
KW  - Lung Neoplasms -- diagnostic imaging
KW  - Radiotherapy, Conformal -- adverse effects
KW  - Radiation Injuries -- etiology
KW  - Carcinoma, Non-Small-Cell Lung -- radiotherapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1494301607?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+dosimetry+%3A+official+journal+of+the+American+Association+of+Medical+Dosimetrists&rft.atitle=Critical+dose+and+toxicity+index+of+organs+at+risk+in+radiotherapy%3A+analyzing+the+calculated+effects+of+modified+dose+fractionation+in+non-small+cell+lung+cancer.&rft.au=Pedicini%2C+Piernicola%3BStrigari%2C+Lidia%3BBenassi%2C+Marcello%3BCaivano%2C+Rocchina%3BFiorentino%2C+Alba%3BNappi%2C+Antonio%3BSalvatore%2C+Marco%3BStorto%2C+Giovanni&rft.aulast=Pedicini&rft.aufirst=Piernicola&rft.date=2014-01-01&rft.volume=39&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Medical+dosimetry+%3A+official+journal+of+the+American+Association+of+Medical+Dosimetrists&rft.issn=1873-4022&rft_id=info:doi/10.1016%2Fj.meddos.2013.08.009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-09-28
N1  - Date created - 2014-02-03
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.meddos.2013.08.009
ER  - 



TY  - JOUR
T1  - Functional Screening Assays with Neurons Generated from Pluripotent Stem Cell-Derived Neural Stem Cells
AN  - 1492649912; 18938828
AB  - Rapid and effective drug discovery for neurodegenerative disease is currently impeded by an inability to source primary neural cells for high-throughput and phenotypic screens. This limitation can be addressed through the use of pluripotent stem cells (PSCs), which can be derived from patient-specific samples and differentiated to neural cells for use in identifying novel compounds for the treatment of neurodegenerative diseases. We have developed an efficient protocol to culture pure populations of neurons, as confirmed by gene expression analysis, in the 96-well format necessary for screens. These differentiated neurons were subjected to viability assays to illustrate their potential in future high-throughput screens. We have also shown that organelles such as nuclei and mitochondria could be live-labeled and visualized through fluorescence, suggesting that we should be able to monitor subcellular phenotypic changes. Neurons derived from a green fluorescent protein-expressing reporter line of PSCs were live-imaged to assess markers of neuronal maturation such as neurite length and co-cultured with astrocytes to demonstrate further maturation. These studies confirm that PSC-derived neurons can be used effectively in viability and functional assays and pave the way for high-throughput screens on neurons derived from patients with neurodegenerative disorders.
JF  - Journal of Biomolecular Screening
AU  - Efthymiou, Anastasia
AU  - Shaltouki, Atossa
AU  - Steiner, Joseph P
AU  - Jha, Balendu
AU  - Heman-Ackah, Sabrina M
AU  - Swistowski, Andrzej
AU  - Zeng, Xianmin
AU  - Rao, Mahendra S
AU  - Malik, Nasir
AD  - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 32
EP  - 43
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 19
IS  - 1
SN  - 1087-0571, 1087-0571
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Astrocytes
KW  - Neurons
KW  - N3 11028:Neuropharmacology & toxicology
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492649912?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Functional+Screening+Assays+with+Neurons+Generated+from+Pluripotent+Stem+Cell-Derived+Neural+Stem+Cells&rft.au=Efthymiou%2C+Anastasia%3BShaltouki%2C+Atossa%3BSteiner%2C+Joseph+P%3BJha%2C+Balendu%3BHeman-Ackah%2C+Sabrina+M%3BSwistowski%2C+Andrzej%3BZeng%2C+Xianmin%3BRao%2C+Mahendra+S%3BMalik%2C+Nasir&rft.aulast=Efthymiou&rft.aufirst=Anastasia&rft.date=2014-01-01&rft.volume=19&rft.issue=1&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113501869
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 1
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Neurons
DO  - http://dx.doi.org/10.1177/1087057113501869
ER  - 



TY  - JOUR
T1  - A Phenotypic Compound Screening Assay for Lysosomal Storage Diseases
AN  - 1492644659; 18938826
AB  - The lysosome is a vital cellular organelle that primarily functions as a recycling center for breaking down unwanted macromolecules through a series of hydrolases. Functional deficiencies in lysosomal proteins due to genetic mutations have been found in more than 50 lysosomal storage diseases that exhibit characteristic lipid/macromolecule accumulation and enlarged lysosomes. Recently, the lysosome has emerged as a new therapeutic target for drug development for the treatment of lysosomal storage diseases. However, a suitable assay for compound screening against the diseased lysosomes is currently unavailable. We have developed a Lysotracker staining assay that measures the enlarged lysosomes in patient-derived cells using both fluorescence intensity readout and fluorescence microscopic measurement. This phenotypic assay has been tested in patient cells obtained from several lysosomal storage diseases and validated using a known compound, methyl- beta -cyclodextrin, in primary fibroblast cells derived from Niemann Pick C disease patients. The results demonstrate that the Lysotracker assay can be used in compound screening for the identification of lead compounds that are capable of reducing enlarged lysosomes for drug development.
JF  - Journal of Biomolecular Screening
AU  - Xu, Miao
AU  - Liu, Ke
AU  - Swaroop, Manju
AU  - Sun, Wei
AU  - Dehdashti, Seameen J
AU  - McKew, John C
AU  - Zheng, Wei
AD  - Therapeutics for Rare and Neglected Disease, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, USA, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 168
EP  - 175
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 19
IS  - 1
SN  - 1087-0571, 1087-0571
KW  - Biotechnology and Bioengineering Abstracts
KW  - Drug development
KW  - Lysosomes
KW  - W 30935:Food Biotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492644659?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Phenotypic+Compound+Screening+Assay+for+Lysosomal+Storage+Diseases&rft.au=Xu%2C+Miao%3BLiu%2C+Ke%3BSwaroop%2C+Manju%3BSun%2C+Wei%3BDehdashti%2C+Seameen+J%3BMcKew%2C+John+C%3BZheng%2C+Wei&rft.aulast=Xu&rft.aufirst=Miao&rft.date=2014-01-01&rft.volume=19&rft.issue=1&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113501197
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Lysosomes
DO  - http://dx.doi.org/10.1177/1087057113501197
ER  - 



TY  - JOUR
T1  - Brominated Flame Retardants in Breast Milk and Behavioural and Cognitive Development at 36 Months
AN  - 1492637495; 18923863
AB  - Polybrominated diphenyl ethers (PBDEs) are persistent flame retardants found in the environment, in household dust, and in humans. Breast feeding is a prominent route of exposure in infancy. PBDEs adversely affect neurodevelopment in animals. Here, we estimate associations between PBDEs in breast milk and behaviour and cognitive skills in children at 36 months of age. We prospectively studied 304 mothers and their children. We measured PBDEs in breast milk collected at 3 months postpartum. At 36 months, we measured child behaviour with the parent-rated Behavioral Assessment System for Children 2 (n = 192), and cognitive skills with the Mullen Scales of Early Learning (n = 184). We analysed data with robust regression. We detected BDE-28, -47, -99, -100, and -153 in >70% of milk samples. For each congener, the highest quartile of breast milk PBDE concentration, vs. the lowest, was associated with more anxious behaviour, after confounder adjustment. Select congeners were associated with increased withdrawal (BDE-28) and improved activity of daily living skills (BDE-153). Cognitive skills tended to be positively associated with PBDEs, especially language and fine motor skills. However, most estimates were imprecise. Here, lactational PBDE exposure was modestly and imprecisely associated with anxiety and withdrawal, but was also associated with improved adaptive and cognitive skills. Positive factors associated with breast feeding may have mitigated some of the hypothesised adverse neurodevelopmental outcomes associated with PBDEs. Further research is needed to inform our understanding of PBDE neurotoxicity and how sources of exposure might confound neurodevelopmental studies.
JF  - Paediatric and Perinatal Epidemiology
AU  - Adgent, Margaret A
AU  - Hoffman, Kate
AU  - Goldman, Barbara Davis
AU  - Sjodin, Andreas
AU  - Daniels, Julie L
AD  - National Institute of Environmental Health Sciences
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 48
EP  - 57
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 28
IS  - 1
SN  - 0269-5022, 0269-5022
KW  - Health & Safety Science Abstracts
KW  - Polybrominated diphenyl ethers
KW  - Age
KW  - Milk
KW  - Cognitive ability
KW  - Households
KW  - Neurotoxicity
KW  - Breast milk
KW  - Breast feeding
KW  - Fire retardants
KW  - Children
KW  - Dust
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492637495?accountid=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=Paediatric+and+Perinatal+Epidemiology&rft.atitle=Brominated+Flame+Retardants+in+Breast+Milk+and+Behavioural+and+Cognitive+Development+at+36+Months&rft.au=Adgent%2C+Margaret+A%3BHoffman%2C+Kate%3BGoldman%2C+Barbara+Davis%3BSjodin%2C+Andreas%3BDaniels%2C+Julie+L&rft.aulast=Adgent&rft.aufirst=Margaret&rft.date=2014-01-01&rft.volume=28&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+Perinatal+Epidemiology&rft.issn=02695022&rft_id=info:doi/10.1111%2Fppe.12078
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Polybrominated diphenyl ethers; Age; Milk; Cognitive ability; Households; Neurotoxicity; Breast milk; Breast feeding; Fire retardants; Children; Dust
DO  - http://dx.doi.org/10.1111/ppe.12078
ER  - 



TY  - JOUR
T1  - Detection of Phospholipidosis Induction: A Cell-Based Assay in High-Throughput and High-Content Format
AN  - 1492624513; 18938829
AB  - Drug-induced phospholipidosis is characterized by the accumulation of intracellular phospholipids in cells exposed to cationic amphiphilic drugs. The appearance of unicentric or multicentric multilamellar bodies viewed under an electron microscope (EM) is the morphological hallmark of phospholipidosis. Although the EM method is the gold standard for detecting cellular phospholipidosis, this method has its drawbacks, including low throughput, high cost, and unsuitability for screening a large chemical library. In this study, a cell-based phospholipidosis assay has been developed using the LipidTOX Red reagent in HepG2 cells and miniaturized into a 1536-well plate format. To validate this assay for high-throughput screening (HTS), the LOPAC library of 1280 compounds was screened using a quantitative HTS platform. A group of known phospholipidosis inducers, such as amiodarone, propranolol, chlorpromazine, desipramine, promazine, clomipramine, and amitriptyline, was identified by the screen, consistent with previous reports. Several novel phospholipidosis inducers, including NAN-190, ebastine, GR127935, and cis-(Z)-flupentixol, were identified in this study and confirmed using the EM method. These results demonstrate that this assay can be used to evaluate and profile large numbers of chemicals for drug-induced phospholipidosis.
JF  - Journal of Biomolecular Screening
AU  - Shahane, Sampada A
AU  - Huang, Ruili
AU  - Gerhold, David
AU  - Baxa, Ulrich
AU  - Austin, Christopher P
AU  - Xia, Menghang
AD  - National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, USA
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 66
EP  - 76
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 19
IS  - 1
SN  - 1087-0571, 1087-0571
KW  - Biotechnology and Bioengineering Abstracts
KW  - Amiodarone
KW  - Propranolol
KW  - W 30935:Food Biotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492624513?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Detection+of+Phospholipidosis+Induction%3A+A+Cell-Based+Assay+in+High-Throughput+and+High-Content+Format&rft.au=Shahane%2C+Sampada+A%3BHuang%2C+Ruili%3BGerhold%2C+David%3BBaxa%2C+Ulrich%3BAustin%2C+Christopher+P%3BXia%2C+Menghang&rft.aulast=Shahane&rft.aufirst=Sampada&rft.date=2014-01-01&rft.volume=19&rft.issue=1&rft.spage=66&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113502851
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Propranolol
DO  - http://dx.doi.org/10.1177/1087057113502851
ER  - 



TY  - JOUR
T1  - Primaquine for Prophylaxis of Malaria: Has the CYP Sailed?
AN  - 1492617285; 18988839
JF  - Journal of Travel Medicine
AU  - Deye, Gregory A
AU  - Magill, Alan J
AD  - Division of Microbiology and Infectious Diseases. National Institutes of Health
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 67
EP  - 69
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 21
IS  - 1
SN  - 1195-1982, 1195-1982
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW  - Travel
KW  - Human diseases
KW  - Primaquine
KW  - Prophylaxis
KW  - Malaria
KW  - K 03410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492617285?accountid=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+Travel+Medicine&rft.atitle=Primaquine+for+Prophylaxis+of+Malaria%3A+Has+the+CYP+Sailed%3F&rft.au=Deye%2C+Gregory+A%3BMagill%2C+Alan+J&rft.aulast=Deye&rft.aufirst=Gregory&rft.date=2014-01-01&rft.volume=21&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Journal+of+Travel+Medicine&rft.issn=11951982&rft_id=info:doi/10.1111%2Fjtm.12080
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 14
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Human diseases; Prophylaxis; Malaria; Travel; Primaquine
DO  - http://dx.doi.org/10.1111/jtm.12080
ER  - 



TY  - JOUR
T1  - The Annexin A2/p11 complex is required for efficient invasion of SalmonellaTyphimurium in epithelial cells
AN  - 1492604483; 18921170
AB  - The facultative intracellular pathogen, Salmonella enterica, triggers its own uptake into non-phagocytic epithelial cells. Invasion is dependent on a type 3 secretion system (T3SS), which delivers a cohort of effector proteins across the plasma membrane where they induce dynamic actin-driven ruffling of the membrane and ultimately, internalization of the bacteria into a modified phagosome. In eukaryotic cells, the calcium- and phospholipid-binding protein Annexin A2 (AnxA2) functions as a platform for actin remodelling in the vicinity of dynamic cellular membranes. AnxA2 is mostly found in a stable heterotetramer, with p11, which can interact with other proteins such as the giant phosphoprotein AHNAK. We show here that AnxA2, p11 and AHNAK are required for T3SS-mediated Salmonella invasion of cultured epithelial cells and that the T3SS effector SopB is required for recruitment of AnxA2 and AHNAK to Salmonella invasion sites. Altogether this work shows that, in addition to targeting Rho-family GTPases, Salmonella can intersect the host cell actin pathway via AnxA2.
JF  - Cellular Microbiology
AU  - Jolly, Carrie
AU  - Winfree, Seth
AU  - Hansen, Bryan
AU  - Steele-Mortimer, Olivia
AD  - Salmonella Host-Cell Interactions Section Laboratory of Intracellular Parasites National Institute of Allergy and Infectious Disease. National Institutes of Health
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 64
EP  - 77
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 16
IS  - 1
SN  - 1462-5814, 1462-5814
KW  - Microbiology Abstracts B: Bacteriology
KW  - Epithelial cells
KW  - Annexins
KW  - Phosphoproteins
KW  - Plasma membranes
KW  - Salmonella enterica
KW  - Secretion
KW  - Phagosomes
KW  - Actin
KW  - Pathogens
KW  - Guanosinetriphosphatase
KW  - J 02330:Biochemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492604483?accountid=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=Cellular+Microbiology&rft.atitle=The+Annexin+A2%2Fp11+complex+is+required+for+efficient+invasion+of+SalmonellaTyphimurium+in+epithelial+cells&rft.au=Jolly%2C+Carrie%3BWinfree%2C+Seth%3BHansen%2C+Bryan%3BSteele-Mortimer%2C+Olivia&rft.aulast=Jolly&rft.aufirst=Carrie&rft.date=2014-01-01&rft.volume=16&rft.issue=1&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=Cellular+Microbiology&rft.issn=14625814&rft_id=info:doi/10.1111%2Fcmi.12180
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-04-17
N1  - SubjectsTermNotLitGenreText - Epithelial cells; Plasma membranes; Phosphoproteins; Annexins; Secretion; Phagosomes; Actin; Pathogens; Guanosinetriphosphatase; Salmonella enterica
DO  - http://dx.doi.org/10.1111/cmi.12180
ER  - 



TY  - JOUR
T1  - Chemotherapy-induced ovarian toxicity in patients affected by endocrine-responsive early breast cancer.
AN  - 1490786426; 23953684
AB  - Cytotoxic chemotherapy may variably affect ovarian function depending on age and ovarian reserve at diagnosis, type of chemotherapy and use of tamoxifen. Ascertaining whether a premenopausal patient with endocrine-responsive early breast cancer and chemotherapy-induced amenorrhea has reached menopause is essential not only in order to provide accurate information on residual fertility, but also to appropriately prescribe endocrine therapy. Indeed, aromatase inhibitors are contraindicated in women with residual ovarian reserve. However, the diagnosis of menopause in patients with chemotherapy-induced amenorrhea is challenging, since clinical features, follicle-stimulating hormone and estradiol levels may be inaccurate to this aim. Recent studies demonstrated that the anti-müllerian hormone may improve the assessment of ovarian reserve residual to chemotherapy in women with early breast cancer. Herein, we review the incidence of amenorrhea and menopause induced by cytotoxic chemotherapy in women affected by early breast cancer and the suggested mechanisms that sustain these side-effects. Furthermore, it has been scrutinized the potential of new markers of ovarian reserve that may facilitate the selection of appropriate endocrine treatment for premenopausal women who develop amenorrhea following adjuvant chemotherapy for early breast cancer.
          Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
JF  - Critical reviews in oncology/hematology
AU  - Torino, Francesco
AU  - Barnabei, Agnese
AU  - De Vecchis, Liana
AU  - Sini, Valentina
AU  - Schittulli, Francesco
AU  - Marchetti, Paolo
AU  - Corsello, Salvatore Maria
AD  - Department of Systems Medicine, Chair of Medical Oncology, Tor Vergata University of Rome, Italy. ; Endocrinology Unit, Regina Elena National Cancer Institute, Rome, Italy. ; Surgical and Medical Department of Clinical Sciences, Biomedical Technologies and Translational Medicine, "Sapienza" University of Rome, Italy. ; Department of Women's Health, Cancer Institute of Bari, Italy. ; Department of Clinical and Molecular Medicine, Medical Oncology Division, Sant'Andrea Hospital, "Sapienza" University of Rome and IDI-IRCCS, Rome, Italy. ; Endocrinology Unit, Università Cattolica, Rome, Italy. Electronic address: corsello.sm@mclink.it.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 27
EP  - 42
VL  - 89
IS  - 1
KW  - Antineoplastic Agents, Hormonal
KW  - 0
KW  - Biomarkers
KW  - Index Medicus
KW  - Ovarian reserve
KW  - Chemotherapy-induced menopause
KW  - Breast cancer
KW  - Chemotherapy-induced amenorrhea
KW  - Aromatase inhibitors
KW  - Ovarian Diseases -- metabolism
KW  - Humans
KW  - Prognosis
KW  - Biomarkers -- metabolism
KW  - Ovarian Diseases -- chemically induced
KW  - Female
KW  - Chemotherapy, Adjuvant
KW  - Fertility Preservation
KW  - Menopause, Premature -- metabolism
KW  - Breast Neoplasms -- drug therapy
KW  - Antineoplastic Agents, Hormonal -- administration & dosage
KW  - Amenorrhea -- metabolism
KW  - Amenorrhea -- chemically induced
KW  - Breast Neoplasms -- complications
KW  - Antineoplastic Agents, Hormonal -- therapeutic use
KW  - Antineoplastic Agents, Hormonal -- adverse effects
KW  - Menopause, Premature -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490786426?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+multifork+Escherichia+coli+chromosome+is+a+self-duplicating+and+self-segregating+thermodynamic+ring+polymer&rft.au=Youngren%2C+Brenda%3BNielsen%2C+Henrik+Jork%3BJun%2C+Suckjoon%3BAustin%2C+Stuart&rft.aulast=Youngren&rft.aufirst=Brenda&rft.date=2014-01-01&rft.volume=28&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Genes+%26+Development&rft.issn=08909369&rft_id=info:doi/10.1101%2Fgad.231050.113
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-08
N1  - Date created - 2013-12-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.critrevonc.2013.07.007
ER  - 



TY  - JOUR
T1  - Comparison of the toxicity of fluoridation compounds in the nematode Caenorhabditis elegans.
AN  - 1490778648; 24105802
AB  - Fluorides are commonly added to drinking water in the United States to decrease the incidence of dental caries. Silicofluorides, such as sodium hexafluorosilicate (Na2 SiF6 ) and fluorosilicic acid (H2 SiF6 ), are mainly used for fluoridation, although fluoride salts such as sodium fluoride (NaF) are also used. Interestingly, only the toxicity of NaF has been examined and not that of the more often used silicofluorides. In the present study, the toxicities of NaF, Na2 SiF6 , and H2 SiF6 were compared. The toxicity of these fluorides on the growth, feeding, and reproduction in the alternative toxicological testing organism Caenorhabditis elegans was examined. Exposure to these compounds produced classic concentration-response toxicity profiles. Although the effects of the fluoride compounds varied among the 3 biological endpoints, no differences were found between the 3 compounds, relative to the fluoride ion concentration, in any of the assays. This suggests that silicofluorides have similar toxicity to NaF.
          © 2013 SETAC.
JF  - Environmental toxicology and chemistry
AU  - Rice, Julie R
AU  - Boyd, Windy A
AU  - Chandra, Dave
AU  - Smith, Marjolein V
AU  - Den Besten, Pamela K
AU  - Freedman, Jonathan H
AD  - Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 82
EP  - 88
VL  - 33
IS  - 1
KW  - Cariostatic Agents
KW  - 0
KW  - Silicic Acid
KW  - 1343-98-2
KW  - hexafluorosilicate
KW  - 17084-08-1
KW  - hexafluorosilicic acid
KW  - 53V4OQG6U1
KW  - Sodium Fluoride
KW  - 8ZYQ1474W7
KW  - Fluorides
KW  - Q80VPU408O
KW  - Index Medicus
KW  - Caenorhabditis elegans
KW  - Silicofluoride
KW  - Fluoride toxicity
KW  - Drinking water
KW  - Toxicity testing
KW  - Eating -- drug effects
KW  - Animals
KW  - Reproduction -- drug effects
KW  - Fluoridation
KW  - Fluorides -- toxicity
KW  - Caenorhabditis elegans -- drug effects
KW  - Caenorhabditis elegans -- physiology
KW  - Cariostatic Agents -- toxicity
KW  - Silicic Acid -- toxicity
KW  - Sodium Fluoride -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490778648?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology+and+chemistry&rft.atitle=Comparison+of+the+toxicity+of+fluoridation+compounds+in+the+nematode+Caenorhabditis+elegans.&rft.au=Rice%2C+Julie+R%3BBoyd%2C+Windy+A%3BChandra%2C+Dave%3BSmith%2C+Marjolein+V%3BDen+Besten%2C+Pamela+K%3BFreedman%2C+Jonathan+H&rft.aulast=Rice&rft.aufirst=Julie&rft.date=2014-01-01&rft.volume=33&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Environmental+toxicology+and+chemistry&rft.issn=1552-8618&rft_id=info:doi/10.1002%2Fetc.2394
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-06
N1  - Date created - 2013-12-20
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1002/etc.2394
ER  - 



TY  - JOUR
T1  - Palladium nanosheets as highly stable and effective contrast agents for in vivo photoacoustic molecular imaging.
AN  - 1490776874; 24317132
AB  - A stable and efficient contrast agent is highly desirable for photoacoustic (PA) imaging applications. Recently gold nanostructures have been widely reported and studied for PA imaging and photothermal therapy. However, the structures of the nonspherical gold nanoparticles are easily destroyed after laser irradiation and thus may fail to complete the intended tasks. In this study, we propose to apply palladium nanosheets (PNSs), with strong optical absorption in the near-infrared (NIR) region, as a new class of exogenous PA contrast agents. PA and ultrasound (US) images were acquired sequentially by a portable and fast photoacoustic tomography (PAT) system with a hand-held transducer. Significant and long-lasting imaging enhancement in SCC7 head and neck squamous cell carcinoma was successfully observed in mice by PAT over time after tail vein administration of PNSs. The morphology and functional perfusion of the tumors were delineated in PA images due to the nanoparticle accumulation. PAT of the main organs was also conducted ex vivo to trace the fate of PNSs, which was further validated by inductively coupled plasma atomic emission spectrometry (ICP-AES). No obvious toxic effect was observed by in vitro MTT assay and ex vivo histological examination 7 days after PNS administration. With the combination of a portable imaging instrument and signal specificity, PNSs might be applied as stable and effective agents for photoacoustic cancer detection, diagnosis and treatment guidance.
JF  - Nanoscale
AU  - Nie, Liming
AU  - Chen, Mei
AU  - Sun, Xiaolian
AU  - Rong, Pengfei
AU  - Zheng, Nanfeng
AU  - Chen, Xiaoyuan
AD  - Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA. shawn.chen@nih.gov.
Y1  - 2014
PY  - 2014
DA  - 2014
SP  - 1271
EP  - 1276
VL  - 6
IS  - 3
KW  - Contrast Media
KW  - 0
KW  - Tetrazolium Salts
KW  - Thiazoles
KW  - Palladium
KW  - 5TWQ1V240M
KW  - Gold
KW  - 7440-57-5
KW  - thiazolyl blue
KW  - EUY85H477I
KW  - Index Medicus
KW  - Thiazoles -- chemistry
KW  - Animals
KW  - Perfusion
KW  - Transducers
KW  - Metal Nanoparticles -- chemistry
KW  - Optics and Photonics
KW  - Acoustics
KW  - Cell Line, Tumor
KW  - Mice
KW  - Tissue Distribution
KW  - Cell Survival
KW  - Neoplasm Transplantation
KW  - Neoplasms -- diagnosis
KW  - Gold -- chemistry
KW  - Tetrazolium Salts -- chemistry
KW  - Palladium -- chemistry
KW  - Photochemistry -- methods
KW  - Tomography -- methods
KW  - Nanostructures -- chemistry
KW  - Contrast Media -- chemistry
KW  - Tomography -- instrumentation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490776874?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanoscale&rft.atitle=Palladium+nanosheets+as+highly+stable+and+effective+contrast+agents+for+in+vivo+photoacoustic+molecular+imaging.&rft.au=Nie%2C+Liming%3BChen%2C+Mei%3BSun%2C+Xiaolian%3BRong%2C+Pengfei%3BZheng%2C+Nanfeng%3BChen%2C+Xiaoyuan&rft.aulast=Nie&rft.aufirst=Liming&rft.date=2014-01-01&rft.volume=6&rft.issue=3&rft.spage=1271&rft.isbn=&rft.btitle=&rft.title=Nanoscale&rft.issn=2040-3372&rft_id=info:doi/10.1039%2Fc3nr05468c
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-09-17
N1  - Date created - 2014-01-17
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1039/c3nr05468c
ER  - 



TY  - JOUR
T1  - In vivo molecular markers for pro-inflammatory cytokine M1 stage and resident microglia in trimethyltin-induced hippocampal injury.
AN  - 1490738656; 24002884
AB  - Microglia polarization to the classical M1 activation state is characterized by elevated pro-inflammatory cytokines; however, a full profile has not been generated in the early stages of a sterile inflammatory response recruiting only resident microglia. We characterized the initial M1 state in a hippocampal injury model dependent upon tumor necrosis factor (TNF) receptor signaling for dentate granule cell death. Twenty-one-day-old CD1 male mice were injected with trimethyltin (TMT 2.3 mg/kg, i.p.) and the hippocampus was examined at an early stage (24-h post-dosing) of neuronal death. Glia activation was assessed using a custom quantitative nuclease protection assay. We report elevated mRNA levels for glia response such as ionizing calcium-binding adapter molecule-1 and glial fibrillary acidic protein (Gfap); Fas, hypoxia inducible factor alpha, complement component 1qb, TNF-related genes (Tnf, Tnfaip3, Tnfrsfla); interleukin-1 alpha, Cd44, chemokine (C-C motif) ligand (Ccl)2, Cc14, integrin alpha M, lipocalin (Lcn2), and secreted phosphoprotein 1 (Spp1). These changes occurred in the absence of changes in matrix metalloproteinase 9 and 12, neural cell adhesion molecule, metabotropic glutamate receptor (Grm)3, and Ly6/neurotoxin 1 (Lynx1), as well as, a decrease in neurotrophin 3, glutamate receptor subunit epsilon (Grin)-2b, and neurotrophic tyrosine kinase receptor, type 3. The M2 anti-inflammatory marker, transforming growth factor beta-1 (Tgfb1) was elevated. mRNAs associated with early stage of injury-induced neurogenesis including fibroblast growth factor 21 and Mki67 were elevated. In the "non-injured" temporal cortex receiving projections from the hippocampus, Lynx1, Grm3, and Grin2b were decreased and Gfap increased. Formalin fixed-paraffin-embedded tissue did not generate a comparable profile.
JF  - Neurotoxicity research
AU  - McPherson, C A
AU  - Merrick, B A
AU  - Harry, G J
AD  - Neurotoxicology Group, Division of National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, P.O. Box 12233, MD E1-07, Research Triangle Park, NC, 27709, USA.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 45
EP  - 56
VL  - 25
IS  - 1
KW  - Biomarkers
KW  - 0
KW  - Cytokines
KW  - RNA, Messenger
KW  - Trimethyltin Compounds
KW  - trimethyltin
KW  - 1631-73-8
KW  - Index Medicus
KW  - Temporal Lobe -- drug effects
KW  - Animals
KW  - Temporal Lobe -- metabolism
KW  - RNA, Messenger -- metabolism
KW  - Cell Death
KW  - Inflammation -- genetics
KW  - Mice
KW  - Inflammation -- metabolism
KW  - Trimethyltin Compounds -- toxicity
KW  - Male
KW  - Hippocampus -- metabolism
KW  - Cytokines -- metabolism
KW  - Hippocampus -- pathology
KW  - Microglia -- drug effects
KW  - Microglia -- metabolism
KW  - Hippocampus -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490738656?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicity+research&rft.atitle=In+vivo+molecular+markers+for+pro-inflammatory+cytokine+M1+stage+and+resident+microglia+in+trimethyltin-induced+hippocampal+injury.&rft.au=McPherson%2C+C+A%3BMerrick%2C+B+A%3BHarry%2C+G+J&rft.aulast=McPherson&rft.aufirst=C&rft.date=2014-01-01&rft.volume=25&rft.issue=1&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Neurotoxicity+research&rft.issn=1476-3524&rft_id=info:doi/10.1007%2Fs12640-013-9422-3
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-28
N1  - Date created - 2014-01-03
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Cancer Res. 2011 Jun 1;17(11):3727-32 [21364035]
Physiol Rev. 2011 Apr;91(2):461-553 [21527731]
Neurotoxicol Teratol. 2011 May-Jun;33(3):415-21 [21371552]
Brain Behav Immun. 2011 Aug;25(6):1063-77 [21435392]
Neurochem Int. 2011 Oct;59(5):591-9 [21683107]
J Neuroinflammation. 2011;8:84 [21777430]
Proc Natl Acad Sci U S A. 2011 Nov 8;108(45):18436-41 [21969573]
Neurotoxicol Teratol. 2012 Jan-Feb;34(1):72-82 [22108043]
Glia. 2012 May;60(5):717-27 [22290798]
Endocrinology. 2012 Sep;153(9):4317-27 [22778218]
Cytokine. 2013 Feb;61(2):491-8 [23199812]
FASEB J. 2013 Mar;27(3):1176-90 [23207546]
Neuro Endocrinol Lett. 2012;33(7):689-96 [23391880]
Brain Behav Immun. 2013 Aug;32:70-85 [23454862]
J Neurosci Res. 2000 Oct 1;62(1):146-55 [11002296]
Neurochem Res. 2000 Oct;25(9-10):1439-51 [11059815]
Stroke. 2001 Apr;32(4):1020-7 [11283406]
Toxicol Appl Pharmacol. 2001 Apr 15;172(2):93-7 [11298495]
J Neurosci Res. 2001 Nov 1;66(3):464-74 [11746364]
Neuron. 2002 Mar 14;33(6):893-903 [11906696]
Exp Neurol. 2002 May;175(1):152-60 [12009767]
Toxicol Appl Pharmacol. 2002 May 1;180(3):205-18 [12009860]
Mol Cells. 2002 Jun 30;13(3):429-35 [12132583]
Neuroscience. 2002;115(1):307-20 [12401343]
Neurotoxicology. 2003 Jun;24(3):343-56 [12782100]
Neurotox Res. 2004;5(8):623-7 [15111239]
Neurotoxicology. 1984 Summer;5(2):187-204 [6390263]
J Histochem Cytochem. 1990 Nov;38(11):1683-6 [2212623]
Neuroscience. 1990;39(1):151-70 [2089275]
J Neuroimmunol. 1995 Jun;59(1-2):65-75 [7797621]
Trends Neurosci. 1996 Aug;19(8):312-8 [8843599]
J Neurochem. 1998 Oct;71(4):1577-87 [9751191]
Neuron. 1999 May;23(1):105-14 [10402197]
J Biol Chem. 2005 Jan 14;280(2):1336-45 [15485828]
Glia. 2005 Jun;50(4):287-98 [15846806]
Expert Opin Drug Saf. 2005 May;4(3):433-42 [15934851]
J Immunol. 2005 Jul 1;175(1):342-9 [15972667]
Neuroscientist. 2005 Oct;11(5):400-7 [16151042]
Neurol Res. 2005 Oct;27(7):685-91 [16197805]
Immunity. 2005 Oct;23(4):344-6 [16226499]
J Neurosci Res. 2005 Dec 1;82(5):609-21 [16273549]
Brain Res. 2007 Feb 2;1131(1):17-28 [17161388]
Brain Res. 2007 Jun 2;1151:195-202 [17395166]
Neuroscience. 2008 Jun 2;153(4):1135-45 [18440706]
J Neurochem. 2008 Jul;106(1):281-98 [18373618]
Blood. 2008 Oct 15;112(8):3425-33 [18544678]
J Neurosci. 2009 Jan 7;29(1):234-49 [19129400]
Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3913-8 [19237579]
Nat Biotechnol. 2009 Nov;27(11):1038-42 [19838197]
Trends Neurosci. 2009 Dec;32(12):638-47 [19782411]
Anat Rec (Hoboken). 2009 Dec;292(12):1882-92 [19943341]
Trends Neurosci. 2010 Feb;33(2):67-75 [19963289]
CNS Neurol Disord Drug Targets. 2010 Apr;9(2):174-91 [20205642]
Mol Neurobiol. 2010 Jun;41(2-3):232-41 [20148316]
Eur J Neurosci. 2010 Jul;32(2):191-7 [20646056]
Science. 2010 Nov 5;330(6005):783-8 [21051630]
Nat Rev Immunol. 2010 Dec;10(12):826-37 [21088683]
Brain Behav Immun. 2011 Jul;25(5):850-62 [20833246]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s12640-013-9422-3
ER  - 



TY  - JOUR
T1  - Comparison of human papillomavirus detections in urine, vulvar, and cervical samples from women attending a colposcopy clinic.
AN  - 1490733132; 24197879
AB  - While urine-based sampling for human papillomavirus (HPV) is being explored as a simple and noninvasive approach for cervical cancer screening, data comparing HPV genotyping in urine and those in cellular sampling of the cervix and vulva, and their correlation with rigorously confirmed cervical disease status, are sparse. We performed HPV genotyping on voided-urine and clinician-collected vulvar and cervical samples from 72 women undergoing colposcopy. Although urine-based HPV carcinogenic HPV detection was lower (58.3%) than cervical (73.6%) and vulvar (72.1%) detection (P = 0.05 and 0.07, respectively), the agreement of urine HPV with cervical and vulvar HPV was moderate (kappa = 0.55) and substantial (kappa = 0.62), respectively. Urine-based carcinogenic HPV detection had a clinical sensitivity of 80.8% (95% confidence interval [CI] = 60.7 to 93.5) and a specificity of 53.3% (95% CI = 37.9 to 68.3) for diagnosing cervical intraepithelial neoplasia grades 2/3 (CIN2/3) on histology; 90.0% of CIN3 was positive for urine HPV. The corresponding sensitivity and specificity values for vulvar sampling were 92% (95% CI = 74 to 99) and 40.5% (95% CI = 25.6 to 56.7), and those for cervical sampling were 96.2% (95% CI = 80.4 to 99.9) and 40% (95% CI = 25.7 to 55.7), respectively. HPV16 was the most common carcinogenic genotype detectable in 25% of urine, 33.8% of vulvar, and 31.9% of cervical samples overall, with prevalence increasing with cervical disease grade, regardless of the sampling method. Stronger cervical HPV PCR signal strengths were associated with increased frequency of urine HPV detection. In summary, the relatively lower detection rates but comparable clinical performance of urine-based HPV sampling underscore the need for larger studies to evaluate urine-based sampling for cervical cancer screening, epidemiologic studies, and postvaccination HPV disease surveillance.
JF  - Journal of clinical microbiology
AU  - Sahasrabuddhe, Vikrant V
AU  - Gravitt, Patti E
AU  - Dunn, S Terence
AU  - Brown, David
AU  - Allen, Richard A
AU  - Eby, Yolanda J
AU  - Smith, Katie
AU  - Zuna, Rosemary E
AU  - Zhang, Roy R
AU  - Gold, Michael A
AU  - Schiffman, Mark
AU  - Walker, Joan L
AU  - Castle, Philip E
AU  - Wentzensen, Nicolas
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, USA.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 187
EP  - 192
VL  - 52
IS  - 1
KW  - Index Medicus
KW  - Sensitivity and Specificity
KW  - Young Adult
KW  - Humans
KW  - Adult
KW  - Early Detection of Cancer -- methods
KW  - Female
KW  - Papillomavirus Infections -- diagnosis
KW  - Papillomaviridae -- isolation & purification
KW  - Urine -- virology
KW  - Papillomavirus Infections -- virology
KW  - Cervix Uteri -- virology
KW  - Specimen Handling -- methods
KW  - Vulva -- virology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490733132?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+microbiology&rft.atitle=Comparison+of+human+papillomavirus+detections+in+urine%2C+vulvar%2C+and+cervical+samples+from+women+attending+a+colposcopy+clinic.&rft.au=Sahasrabuddhe%2C+Vikrant+V%3BGravitt%2C+Patti+E%3BDunn%2C+S+Terence%3BBrown%2C+David%3BAllen%2C+Richard+A%3BEby%2C+Yolanda+J%3BSmith%2C+Katie%3BZuna%2C+Rosemary+E%3BZhang%2C+Roy+R%3BGold%2C+Michael+A%3BSchiffman%2C+Mark%3BWalker%2C+Joan+L%3BCastle%2C+Philip+E%3BWentzensen%2C+Nicolas&rft.aulast=Sahasrabuddhe&rft.aufirst=Vikrant&rft.date=2014-01-01&rft.volume=52&rft.issue=1&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+microbiology&rft.issn=1098-660X&rft_id=info:doi/10.1128%2FJCM.01623-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-25
N1  - Date created - 2013-12-23
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Pediatr Infect Dis J. 2000 Aug;19(8):722-8 [10959740]
CMAJ. 2000 Sep 5;163(5):513-8 [11006761]
Pediatr Dermatol. 2003 May-Jun;20(3):191-4 [12787264]
J Med Virol. 2003 Sep;71(1):110-4 [12858416]
J Clin Virol. 2004 Apr;29(4):230-40 [15018850]
J Clin Microbiol. 1993 Aug;31(8):1975-9 [8396581]
New Microbiol. 1995 Apr;18(2):143-9 [7603341]
Eur J Epidemiol. 1999 Jul;15(6):537-43 [10485346]
Int J Gynaecol Obstet. 2005 Sep;90(3):223-7 [16043176]
J Clin Virol. 2006 Jul;36(3):189-93 [16690350]
J Korean Med Sci. 2007 Feb;22(1):99-104 [17297259]
J Clin Microbiol. 2007 Mar;45(3):897-901 [17229868]
Asian J Androl. 2007 Sep;9(5):705-10 [17712490]
Sex Transm Dis. 2007 Nov;34(11):849-55 [17621246]
J Clin Virol. 2008 Feb;41(2):111-5 [18354821]
Gynecol Oncol. 2008 Apr;109(1):59-64 [18255129]
Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494]
J Obstet Gynaecol. 2009 Oct;29(7):583-9 [19757259]
Cancer. 2010 Jun 1;116(11):2531-42 [20310056]
Rev Med Virol. 2011 May;21(3):139-53 [21538664]
J Med Virol. 2011 Oct;83(10):1744-51 [21837790]
J Med Virol. 2011 Nov;83(11):1983-7 [21915874]
J Clin Microbiol. 2012 May;50(5):1564-70 [22337992]
CA Cancer J Clin. 2012 May-Jun;62(3):147-72 [22422631]
Int J Cancer. 2012 Sep 15;131(6):E946-53 [22419273]
Clin Cancer Res. 2012 Aug 1;18(15):4154-62 [22675168]
Cancer Epidemiol Biomarkers Prev. 2013 Feb;22(2):242-50 [23221127]
Diagn Mol Pathol. 2013 Jun;22(2):85-90 [23628819]
J Infect Dis. 2004 Aug 1;190(3):458-67 [15243917]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1128/JCM.01623-13
ER  - 



TY  - JOUR
T1  - Calibrating a population-based job-exposure matrix using inspection measurements to estimate historical occupational exposure to lead for a population-based cohort in Shanghai, China.
AN  - 1490731114; 22910004
AB  - The epidemiologic evidence for the carcinogenicity of lead is inconsistent and requires improved exposure assessment to estimate risk. We evaluated historical occupational lead exposure for a population-based cohort of women (n=74,942) by calibrating a job-exposure matrix (JEM) with lead fume (n=20,084) and lead dust (n=5383) measurements collected over four decades in Shanghai, China. Using mixed-effect models, we calibrated intensity JEM ratings to the measurements using fixed-effects terms for year and JEM rating. We developed job/industry-specific estimates from the random-effects terms for job and industry. The model estimates were applied to subjects' jobs when the JEM probability rating was high for either job or industry; remaining jobs were considered unexposed. The models predicted that exposure increased monotonically with JEM intensity rating and decreased 20-50-fold over time. The cumulative calibrated JEM estimates and job/industry-specific estimates were highly correlated (Pearson correlation=0.79-0.84). Overall, 5% of the person-years and 8% of the women were exposed to lead fume; 2% of the person-years and 4% of the women were exposed to lead dust. The most common lead-exposed jobs were manufacturing electronic equipment. These historical lead estimates should enhance our ability to detect associations between lead exposure and cancer risk in the future epidemiologic analyses.
JF  - Journal of exposure science & environmental epidemiology
AU  - Koh, Dong-Hee
AU  - Bhatti, Parveen
AU  - Coble, Joseph B
AU  - Stewart, Patricia A
AU  - Lu, Wei
AU  - Shu, Xiao-Ou
AU  - Ji, Bu-Tian
AU  - Xue, Shouzheng
AU  - Locke, Sarah J
AU  - Portengen, Lutzen
AU  - Yang, Gong
AU  - Chow, Wong-Ho
AU  - Gao, Yu-Tang
AU  - Rothman, Nathaniel
AU  - Vermeulen, Roel
AU  - Friesen, Melissa C
AD  - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, North Bethesda, Maryland, USA. ; Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA. ; 1] Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, North Bethesda, Maryland, USA [2] Formerly Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, now Stewart Exposure Assessments, LLC, Arlington, Virginia, USA. ; Shanghai Municipal Center for Disease Control, Shanghai, People's Republic of China. ; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt University School of Medicine, Nashville, Tennessee. ; Environmental and Occupational Health Division, Institute for Risk Assessment Sciences, University of Utrecht, Utrecht, The Netherlands. ; Department of Epidemiology, Shanghai Cancer Institute, Shanghai, People's Republic of China.
PY  - 2014
SP  - 9
EP  - 16
VL  - 24
IS  - 1
KW  - Air Pollutants, Occupational
KW  - 0
KW  - Dust
KW  - Lead
KW  - 2P299V784P
KW  - Index Medicus
KW  - Humans
KW  - Cohort Studies
KW  - Adult
KW  - Retrospective Studies
KW  - Calibration
KW  - Aged
KW  - Middle Aged
KW  - Occupations
KW  - Female
KW  - China
KW  - Industry
KW  - Dust -- analysis
KW  - Air Pollutants, Occupational -- analysis
KW  - Lead -- analysis
KW  - Occupational Exposure -- analysis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490731114?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+exposure+science+%26+environmental+epidemiology&rft.atitle=Calibrating+a+population-based+job-exposure+matrix+using+inspection+measurements+to+estimate+historical+occupational+exposure+to+lead+for+a+population-based+cohort+in+Shanghai%2C+China.&rft.au=Koh%2C+Dong-Hee%3BBhatti%2C+Parveen%3BCoble%2C+Joseph+B%3BStewart%2C+Patricia+A%3BLu%2C+Wei%3BShu%2C+Xiao-Ou%3BJi%2C+Bu-Tian%3BXue%2C+Shouzheng%3BLocke%2C+Sarah+J%3BPortengen%2C+Lutzen%3BYang%2C+Gong%3BChow%2C+Wong-Ho%3BGao%2C+Yu-Tang%3BRothman%2C+Nathaniel%3BVermeulen%2C+Roel%3BFriesen%2C+Melissa+C&rft.aulast=Koh&rft.aufirst=Dong-Hee&rft.date=2014-01-01&rft.volume=24&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Journal+of+exposure+science+%26+environmental+epidemiology&rft.issn=1559-064X&rft_id=info:doi/10.1038%2Fjes.2012.86
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-07
N1  - Date created - 2013-12-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Am J Epidemiol. 2007 Nov 1;166(9):1005-14 [17690218]
Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2514-20 [17164378]
Scand J Urol Nephrol. 2009;43(6):467-70 [19707952]
Occup Environ Med. 2010 Sep;67(9):636-8 [20798029]
Am J Ind Med. 2011 May;54(5):356-65 [21246587]
PLoS One. 2011;6(7):e20432 [21799727]
Occup Environ Med. 2011 Oct;68(10):723-8 [21217163]
Ann Occup Hyg. 2012 Jan;56(1):80-91 [21976309]
Am J Ind Med. 2000 Sep;38(3):295-9 [10940967]
Epidemiology. 2001 Mar;12(2):222-8 [11246584]
Environ Health Perspect. 2002 Apr;110(4):325-9 [11940448]
Ann Occup Hyg. 2002 Mar;46(2):237-43 [12074033]
Am J Ind Med. 2003 Dec;44(6):576-83 [14635234]
Am J Public Health. 1984 Jan;74(1):58-64 [6228153]
Ecotoxicol Environ Saf. 1984 Dec;8(6):526-30 [6391901]
Scand J Work Environ Health. 1985;11 Suppl 4:16-9 [3832430]
Scand J Work Environ Health. 1985;11 Suppl 4:20-5 [3832431]
Am J Ind Med. 1986;9(3):227-37 [3963005]
Ann Occup Hyg. 1991 Feb;35(1):61-121 [2035954]
J Occup Med. 1991 Dec;33(12):1265-73 [1800687]
Occup Environ Med. 1995 Feb;52(2):73-81 [7757170]
Biomed Environ Sci. 1995 Mar;8(1):23-9 [7605596]
Am Ind Hyg Assoc J. 1997 Sep;58(9):650-6 [9291563]
J Occup Environ Med. 1998 Oct;40(10):855-61 [9800169]
Environ Health Perspect. 2004 Dec;112(17):1691-6 [15579415]
Am J Epidemiol. 2005 Dec 1;162(11):1123-31 [16236996]
Int J Cancer. 2006 Sep 1;119(5):1136-44 [16570286]
Regul Toxicol Pharmacol. 2006 Nov;46(2):157-62 [16782249]
Cancer Epidemiol Biomarkers Prev. 2009 Jun;18(6):1841-8 [19505917]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/jes.2012.86
ER  - 



TY  - JOUR
T1  - Minor antigen distribution predicts site-specific graft-versus-tumor activity of adoptively transferred, minor antigen-specific CD8 T Cells.
AN  - 1490730056; 24141010
AB  - The clinical success of allogeneic T cell therapy for cancer relies on the selection of antigens that can effectively elicit antitumor responses with minimal toxicity toward nonmalignant tissues. Although minor histocompatibility antigens (MiHA) represent promising targets, broad expression of these antigens has been associated with poor responses and T cell dysfunction that may not be prevented by targeting MiHA with limited expression. In this study, we hypothesized that antitumor activity of MiHA-specific CD8 T cells after allogeneic bone marrow transplantation (BMT) is determined by the distribution of antigen relative to the site of tumor growth. To test this hypothesis, we utilized the clinically relevant male-specific antigen HY and studied the fate of adoptively transferred, HY-CD8(+) T cells (HY-CD8) against a HY-expressing epithelial tumor (MB49) and pre-B cell leukemia (HY-E2APBX ALL) in BMT recipients. Transplants were designed to produce broad HY expression in nonhematopoietic tissues (female → male BMT, [F → M]), restricted HY expression in hematopoietic tissues (male → female BMT, [M → F]) tissues, and no HY tissue expression (female → female BMT, [F → F]). Broad HY expression induced poor responses to MB49 despite sublethal graft-versus-host disease and accumulation of HY-CD8 in secondary lymphoid tissues. Antileukemia responses, however, were preserved. In contrast, restriction of HY expression to hematopoietic tissues restored MB49 responses but resulted in a loss of antileukemia responses. We concluded that target alloantigen expression in the same compartment of tumor growth impairs CD8 responses to both solid and hematologic tumors. Copyright © 2014 American Society for Blood and Marrow Transplantation. All rights reserved.
JF  - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
AU  - Shand, Jessica C
AU  - Qin, Haiying
AU  - Nasholm, Nicole
AU  - Capitini, Christian M
AU  - Fry, Terry J
AD  - Blood and Marrow Transplant Section, Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Electronic address: Jessica_Shand@URMC.Rochester.edu. ; Blood and Marrow Transplant Section, Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Department of Pediatrics and UW Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 26
EP  - 36
VL  - 20
IS  - 1
KW  - H-Y Antigen
KW  - 0
KW  - Index Medicus
KW  - Adoptive T cell therapy
KW  - Allogeneic transplantation
KW  - Acute lymphoblastic leukemia
KW  - CD8 T cell function
KW  - Minor histocompatibility antigens
KW  - Precursor Cells, B-Lymphoid -- immunology
KW  - Animals
KW  - Dendritic Cells -- pathology
KW  - Dendritic Cells -- immunology
KW  - Precursor Cells, B-Lymphoid -- pathology
KW  - Humans
KW  - Mice
KW  - Mice, Transgenic
KW  - Cell Proliferation
KW  - Alleles
KW  - Gene Expression -- immunology
KW  - Adoptive Transfer
KW  - Lymphocyte Depletion
KW  - Immunophenotyping
KW  - Female
KW  - Male
KW  - Survival Analysis
KW  - Graft vs Host Disease -- immunology
KW  - H-Y Antigen -- genetics
KW  - Graft vs Leukemia Effect
KW  - CD8-Positive T-Lymphocytes -- transplantation
KW  - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- mortality
KW  - CD8-Positive T-Lymphocytes -- cytology
KW  - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- genetics
KW  - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- therapy
KW  - Graft vs Host Disease -- pathology
KW  - CD8-Positive T-Lymphocytes -- immunology
KW  - H-Y Antigen -- immunology
KW  - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- immunology
KW  - Graft vs Host Disease -- genetics
KW  - Bone Marrow Transplantation
KW  - Graft vs Host Disease -- mortality
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490730056?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Minor+antigen+distribution+predicts+site-specific+graft-versus-tumor+activity+of+adoptively+transferred%2C+minor+antigen-specific+CD8+T+Cells.&rft.au=Shand%2C+Jessica+C%3BQin%2C+Haiying%3BNasholm%2C+Nicole%3BCapitini%2C+Christian+M%3BFry%2C+Terry+J&rft.aulast=Shand&rft.aufirst=Jessica&rft.date=2014-01-01&rft.volume=20&rft.issue=1&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.issn=1523-6536&rft_id=info:doi/10.1016%2Fj.bbmt.2013.10.009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-08
N1  - Date created - 2013-12-30
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nat Med. 2001 Jul;7(7):789-94 [11433342]
Biol Blood Marrow Transplant. 2013 Feb;19(2):171-2 [23151493]
Blood. 2003 Jan 15;101(2):766-70 [12393700]
Blood. 2004 Jan 1;103(1):347-52 [12969970]
J Immunother. 2004 Sep-Oct;27(5):329-38 [15314541]
Blood. 1990 Feb 1;75(3):555-62 [2297567]
Blood. 1996 Oct 15;88(8):3230-9 [8963063]
Genes Dev. 2005 Jan 15;19(2):224-33 [15655112]
J Clin Invest. 2005 May;115(5):1177-87 [15841203]
Nat Med. 2005 Nov;11(11):1222-9 [16227989]
Nature. 2006 Feb 9;439(7077):682-7 [16382236]
J Virol. 2007 Jun;81(11):5819-28 [17376899]
Biol Blood Marrow Transplant. 2008 Jan;14(1 Suppl 1):129-35 [18162233]
Eur J Immunol. 2008 May;38(5):1435-45 [18389475]
Blood. 2008 Dec 1;112(12):4371-83 [19029455]
Trends Immunol. 2008 Dec;29(12):624-32 [18952501]
Blood. 2009 May 14;113(20):5002-9 [19258593]
Cancer Immunol Immunother. 2009 Aug;58(8):1257-64 [19139888]
Transplantation. 2009 Jul 27;88(2):188-97 [19623013]
Pediatr Clin North Am. 2010 Feb;57(1):47-66 [20307711]
Biol Blood Marrow Transplant. 2010 May;16(5):565-86 [20152921]
Blood. 2010 May 13;115(19):3869-78 [20071660]
Curr Opin Immunol. 2010 Jun;22(3):397-401 [20427170]
J Clin Invest. 2010 Jul;120(7):2370-8 [20530875]
J Clin Invest. 2010 Nov;120(11):3855-68 [20978352]
Blood. 2011 Apr 28;117(17):4501-10 [21385853]
Cancer Res. 2011 Aug 1;71(15):5111-22 [21659460]
J Immunol. 2011 Aug 15;187(4):1653-63 [21768400]
Blood. 2011 Nov 24;118(22):5965-76 [21917752]
Blood. 2011 Dec 1;118(23):6209-19 [21768295]
Blood. 2012 Jan 5;119(1):273-84 [22072555]
Biol Blood Marrow Transplant. 2012 Mar;18(3):381-7 [22062805]
Biol Blood Marrow Transplant. 2012 Mar;18(3):480-6 [22155141]
Blood. 2012 Apr 19;119(16):3844-53 [22101894]
Blood. 2012 Jul 26;120(4):728-36 [22563087]
Eur J Immunol. 2012 Sep;42(9):2290-304 [22653665]
Eur J Immunol. 2012 Sep;42(9):2285-9 [22949327]
J Immunol. 2013 Feb 1;190(3):1351-9 [23275602]
Biol Blood Marrow Transplant. 2013 Feb;19(2):274-82 [23022467]
Nat Immunol. 2002 Sep;3(9):844-51 [12172545]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.bbmt.2013.10.009
ER  - 



TY  - JOUR
T1  - The effect of St John's wort on the pharmacokinetics of docetaxel.
AN  - 1490723432; 24068654
AB  - St John's wort (SJW), a herbal antidepressant, is commonly used by cancer patients, and its component hyperforin is a known inducer of the cytochrome P450 (CYP) isoenzyme 3A4. Here, the potential pharmacokinetic interaction between SJW and the sensitive CYP3A4 substrate docetaxel was investigated.
          In ten evaluable cancer patients, the pharmacokinetics of docetaxel (135 mg administered intravenously over 60 min) were compared before and after 14 days of supplementation with SJW (300 mg extract [Hyperiplant(®)] three times daily).
          SJW supplementation resulted in a statistically significant decrease in the mean area under the docetaxel plasma concentration-time curve extrapolated to infinity (AUC∞) from 3,035 ± 756 to 2,682 ± 717 ng · h/mL (P = 0.045). Furthermore, docetaxel clearance significantly increased from 47.2 to 53.7 L/h (P = 0.045) after SJW intake. The maximum plasma concentration and elimination half-life of docetaxel were (non-significantly) decreased after SJW supplementation. In addition, the incidence of docetaxel-related toxicities was lower after SJW supplementation. These results suggest that concomitant use of docetaxel and the applied SJW product should be avoided to prevent potential undertreatment of cancer patients.
JF  - Clinical pharmacokinetics
AU  - Goey, Andrew K L
AU  - Meijerman, Irma
AU  - Rosing, Hilde
AU  - Marchetti, Serena
AU  - Mergui-Roelvink, Marja
AU  - Keessen, Marianne
AU  - Burgers, Jacobus A
AU  - Beijnen, Jos H
AU  - Schellens, Jan H M
AD  - Division of Pharmacoepidemiology and Clinical Pharmacology, Department of Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands, andrew.goey@nih.gov.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 103
EP  - 110
VL  - 53
IS  - 1
KW  - Antidepressive Agents
KW  - 0
KW  - Antineoplastic Agents
KW  - Plant Extracts
KW  - Taxoids
KW  - docetaxel
KW  - 15H5577CQD
KW  - CYP3A4 protein, human
KW  - EC 1.14.13.67
KW  - Cytochrome P-450 CYP3A
KW  - EC 1.14.14.1
KW  - Index Medicus
KW  - Area Under Curve
KW  - Humans
KW  - Cytochrome P-450 CYP3A -- metabolism
KW  - Adult
KW  - Cross-Over Studies
KW  - Aged
KW  - Middle Aged
KW  - Male
KW  - Female
KW  - Taxoids -- pharmacokinetics
KW  - Plant Extracts -- pharmacology
KW  - Antidepressive Agents -- pharmacology
KW  - Antineoplastic Agents -- pharmacokinetics
KW  - Hypericum
KW  - Taxoids -- adverse effects
KW  - Taxoids -- blood
KW  - Herb-Drug Interactions
KW  - Antineoplastic Agents -- blood
KW  - Antineoplastic Agents -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490723432?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacokinetics&rft.atitle=The+effect+of+St+John%27s+wort+on+the+pharmacokinetics+of+docetaxel.&rft.au=Goey%2C+Andrew+K+L%3BMeijerman%2C+Irma%3BRosing%2C+Hilde%3BMarchetti%2C+Serena%3BMergui-Roelvink%2C+Marja%3BKeessen%2C+Marianne%3BBurgers%2C+Jacobus+A%3BBeijnen%2C+Jos+H%3BSchellens%2C+Jan+H+M&rft.aulast=Goey&rft.aufirst=Andrew+K&rft.date=2014-01-01&rft.volume=53&rft.issue=1&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Clinical+pharmacokinetics&rft.issn=1179-1926&rft_id=info:doi/10.1007%2Fs40262-013-0102-5
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-21
N1  - Date created - 2014-01-03
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - 2008-000886-41; EudraCT
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s40262-013-0102-5
ER  - 



TY  - JOUR
T1  - Antitumor effects of immunotoxins are enhanced by lowering HCK or treatment with SRC kinase inhibitors.
AN  - 1490710402; 24145282
AB  - Recombinant immunotoxins (RIT) are agents being developed for cancer treatment. They are composed of an Fv that binds to a cancer cell, fused to a 38-kDa fragment of Pseudomonas exotoxin A. SS1P is a RIT that targets mesothelin, a protein expressed on mesothelioma as well as pancreatic, ovarian, lung, and other cancers. Because the protein tyrosine kinase family regulates a variety of cellular processes and pathways, we hypothesized that tyrosine kinases might regulate susceptibility to immunotoxin killing. To investigate their role, we used siRNAs to lower the level of expression of the 88 known tyrosine kinases. We identified five tyrosine kinases, INSR, HCK, SRC, PDGFRβ, and BMX that enhance the activity of SS1P when their level of expression is lowered by siRNAs. We further investigated the Src family member HCK in this study. Knocking down of SRC slightly increased SS1P killing in A431/H9 cells, but knocking down HCK substantially enhanced killing by SS1P. We investigated the mechanism of enhancement and found that HCK knockdown enhanced SS1P cleavage by furin and lowered levels of Mcl-1 and raised Bax. We then found that Src inhibitors mimic the stimulatory effect of HCK knockdown; both SU6656 and SKI-606 (bosutinib) enhanced immunotoxin killing of mesothelin-expressing cells by SS1P and CD22-expressing cells by HA22 (moxetumomab pasudotox). SU6656 also enhanced the antitumor effects of SS1P and HA22 in mouse xenograft tumor models. Our data suggest that the combination of immunotoxin with tyrosine kinase inhibitors may be an effective way to treat some cancers.
JF  - Molecular cancer therapeutics
AU  - Liu, Xiu-Fen
AU  - Xiang, Laiman
AU  - FitzGerald, David J
AU  - Pastan, Ira
AD  - Corresponding Author: Ira Pastan, Laboratory of Molecular Biology, 37 Convent Drive, Room 5106, National Cancer Institute, Bethesda, MD 20892-4264. pastani@mail.nih.gov.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 82
EP  - 89
VL  - 13
IS  - 1
KW  - Aniline Compounds
KW  - 0
KW  - Antibodies, Monoclonal
KW  - Bacterial Toxins
KW  - Exotoxins
KW  - Immunotoxins
KW  - Indoles
KW  - Nitriles
KW  - Quinolines
KW  - SU 6656
KW  - Sulfonamides
KW  - immunotoxin HA22
KW  - bosutinib
KW  - 5018V4AEZ0
KW  - src-Family Kinases
KW  - EC 2.7.10.2
KW  - Index Medicus
KW  - Animals
KW  - Exotoxins -- administration & dosage
KW  - Aniline Compounds -- administration & dosage
KW  - Nitriles -- administration & dosage
KW  - Cell Line, Tumor
KW  - Mice
KW  - Sulfonamides -- administration & dosage
KW  - Bacterial Toxins -- administration & dosage
KW  - Gene Expression Regulation, Neoplastic -- drug effects
KW  - Quinolines -- administration & dosage
KW  - Indoles -- administration & dosage
KW  - Xenograft Model Antitumor Assays
KW  - Drug Synergism
KW  - src-Family Kinases -- genetics
KW  - Neoplasms -- drug therapy
KW  - Neoplasms -- pathology
KW  - Immunotoxins -- administration & dosage
KW  - src-Family Kinases -- antagonists & inhibitors
KW  - Neoplasms -- genetics
KW  - src-Family Kinases -- biosynthesis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490710402?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antitumor+effects+of+immunotoxins+are+enhanced+by+lowering+HCK+or+treatment+with+SRC+kinase+inhibitors.&rft.au=Liu%2C+Xiu-Fen%3BXiang%2C+Laiman%3BFitzGerald%2C+David+J%3BPastan%2C+Ira&rft.aulast=Liu&rft.aufirst=Xiu-Fen&rft.date=2014-01-01&rft.volume=13&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-13-0726
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-09-29
N1  - Date created - 2014-01-15
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638]
Nat Biotechnol. 2005 Sep;23(9):1137-46 [16151407]
Mol Cancer Ther. 2007 Jul;6(7):1962-72 [17620427]
Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569]
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17099-104 [17940013]
Eur J Cell Biol. 2008 Sep;87(8-9):527-42 [18538446]
Curr Opin Drug Discov Devel. 2010 Jan;13(1):86-95 [20047149]
Mol Cancer. 2009;8:132 [20043832]
Mol Cell Biol. 2010 Jul;30(14):3444-52 [20457813]
Mol Cancer Ther. 2010 Jul;9(7):2007-15 [20587662]
Cell Death Differ. 2010 Sep;17(9):1381-91 [20300113]
Expert Rev Hematol. 2009 Oct;2(5):489-97 [21083014]
Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010]
FEBS J. 2011 Dec;278(23):4683-700 [21585657]
Oncogene. 2012 Mar 29;31(13):1673-82 [21822313]
Carcinogenesis. 2012 May;33(5):969-75 [22354875]
J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053]
Cancer Res. 2013 Apr 1;73(7):2281-8 [23348423]
Mol Cell Biol. 2000 Dec;20(23):9018-27 [11074000]
Methods Mol Biol. 2004;248:503-18 [14970517]
Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):3937-42 [15217923]
Oncogene. 2004 Oct 18;23(48):7906-9 [15489908]
Mol Cell Biol. 1987 Jun;7(6):2267-75 [3496523]
J Cell Biol. 1996 May;133(4):895-910 [8666673]
J Biol Chem. 1997 Dec 12;272(50):31707-11 [9395513]
Annu Rev Cell Dev Biol. 1997;13:513-609 [9442882]
Stat Med. 2005 Jan 15;24(1):109-19 [15523707]
J Biol Chem. 2006 Oct 13;281(41):30383-92 [16882656]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/1535-7163.MCT-13-0726
ER  - 



TY  - JOUR
T1  - Childhood height and body mass index were associated with risk of adult thyroid cancer in a large cohort study.
AN  - 1490703525; 24247722
AB  - Taller stature and obesity in adulthood have been consistently associated with an increased risk of thyroid cancer, but few studies have investigated the role of childhood body size. Using data from a large prospective cohort, we examined associations for height and body mass index (BMI) at ages 7 to 13 years with risk of thyroid cancer in later life. The study population included 321,085 children from the Copenhagen School Health Records Register, born between 1930 and 1989 in Copenhagen, Denmark, with measurements of height and weight from 7 to 13 years of age. These data were linked with the Danish Cancer Registry to identify incident thyroid cancer cases (1968-2010). Hazard ratios (HR) and 95% confidence intervals (CI) were calculated for age- and sex-specific height and BMI SD scores (SDS) using proportional hazards models stratified by birth cohort and sex. During follow-up (median = 38.6 years), 171 women and 64 men were diagnosed with thyroid cancer. Both height and BMI were positively associated with thyroid cancer risk, and these associations were similar by age at measurement. Using age 10 as an example, HRs per 1 unit increase in SDS for height (~6-7 cm) and BMI (~1.5-2 kg/m(2)) were 1.22 (95% CI, 1.07-1.40) and 1.15 (95% CI, 1.00-1.34), respectively. These results, together with the relatively young ages at which thyroid cancers are diagnosed compared with other malignancies, suggest a potential link between early-life factors related to growth and body weight and thyroid carcinogenesis.
JF  - Cancer research
AU  - Kitahara, Cari M
AU  - Gamborg, Michael
AU  - Berrington de González, Amy
AU  - Sørensen, Thorkild I A
AU  - Baker, Jennifer L
AD  - Authors' Affiliations: Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, Maryland; Institute of Preventive Medicine; Bispebjerg and Frederiksberg Hospitals, The Capital Region, Copenhagen; and Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Y1  - 2014/01/01/
PY  - 2014
DA  - 2014 Jan 01
SP  - 235
EP  - 242
VL  - 74
IS  - 1
KW  - Index Medicus
KW  - Risk Factors
KW  - Humans
KW  - Cohort Studies
KW  - Denmark -- epidemiology
KW  - Child
KW  - Adolescent
KW  - Male
KW  - Female
KW  - Thyroid Neoplasms -- epidemiology
KW  - Body Height
KW  - Thyroid Neoplasms -- etiology
KW  - Body Mass Index
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490703525?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Childhood+height+and+body+mass+index+were+associated+with+risk+of+adult+thyroid+cancer+in+a+large+cohort+study.&rft.au=Kitahara%2C+Cari+M%3BGamborg%2C+Michael%3BBerrington+de+Gonz%C3%A1lez%2C+Amy%3BS%C3%B8rensen%2C+Thorkild+I+A%3BBaker%2C+Jennifer+L&rft.aulast=Kitahara&rft.aufirst=Cari&rft.date=2014-01-01&rft.volume=74&rft.issue=1&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-2228
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-27
N1  - Date created - 2014-01-07
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Cancer Causes Control. 2000 Feb;11(2):137-44 [10710197]
Thyroid. 2013 Nov;23(11):1470-8 [23488941]
Int J Cancer. 2001 Sep 1;93(5):745-50 [11477590]
JAMA. 2002 Oct 9;288(14):1728-32 [12365956]
Stat Med. 1992 Jul;11(10):1305-19 [1518992]
Cancer Epidemiol Biomarkers Prev. 1997 Nov;6(11):863-73 [9367058]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078]
Obes Rev. 2005 May;6(2):123-32 [15836463]
J Clin Oncol. 2005 Jul 20;23(21):4742-54 [16034050]
Br J Cancer. 2006 Aug 7;95(3):366-70 [16832414]
Obesity (Silver Spring). 2007 Apr;15(4):977-85 [17426333]
Int J Pediatr Obes. 2006;1(1):11-25 [17902211]
Am J Epidemiol. 2007 Nov 15;166(10):1140-9 [17855390]
PLoS One. 2008;3(7):e2728 [18628945]
Cancer Causes Control. 2008 Dec;19(10):1233-42 [18618280]
Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):784-91 [19240234]
Cancer Causes Control. 2009 Jul;20(5):525-31 [19016336]
Cancer Causes Control. 2009 Jul;20(5):581-90 [19043789]
Int J Epidemiol. 2009 Jun;38(3):656-62 [18719090]
Am J Epidemiol. 2009 Jul 1;170(1):53-64 [19403842]
Econ Hum Biol. 2009 Jul;7(2):137-52 [19628438]
Am J Epidemiol. 2010 Jan 15;171(2):242-52 [19951937]
Int J Cancer. 2010 Apr 1;126(7):1702-15 [19810099]
Int J Cancer. 2010 Jun 15;126(12):2947-56 [19795465]
Int J Cancer. 2010 Jun 15;126(12):2984-90 [19950225]
Lancet Oncol. 2010 Jun;11(6):530-42 [20472501]
Phys Med Biol. 2010 Nov 7;55(21):N507-19 [20952815]
Thyroid. 2010 Dec;20(12):1333-9 [21114382]
Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520]
Scand J Public Health. 2011 Jul;39(7 Suppl):42-5 [21775350]
Int J Cancer. 2012 Sep 15;131(6):E1004-14 [22511178]
Cancer Epidemiol Biomarkers Prev. 2012 Sep;21(9):1531-41 [22761305]
Eur J Epidemiol. 2012 Aug;27(8):615-22 [22760704]
Int J Cancer. 2012 Nov 15;131(10):2360-6 [22337133]
World Rev Nutr Diet. 2013;106:135-41 [23428692]
Chronic Dis Inj Can. 2013 Mar;33(2):69-80 [23470172]
Endocr Relat Cancer. 2013 Apr;20(2):263-71 [23447568]
Thyroid. 2013 Jun;23(6):748-57 [23410185]
Thyroid. 2013 Jul;23(7):885-91 [23517343]
Proc Nutr Soc. 2000 May;59(2):317-24 [10946801]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/0008-5472.CAN-13-2228
ER  - 



TY  - JOUR
T1  - 6-C-(E-phenylethenyl)-naringenin suppresses colorectal cancer growth by inhibiting cyclooxygenase-1.
AN  - 1490703325; 24220240
AB  - Recent clinical trials raised concerns regarding the cardiovascular toxicity of selective cyclooxygenase-2 (COX-2) inhibitors and cyclooxygenase-1 (COX-1) is now being reconsidered as a target for chemoprevention. Our aims were to determine whether selective COX-1 inhibition could delay or prevent cancer development and also clarify the underlying mechanisms. Data clearly showed that COX-1 was required for maintenance of malignant characteristics of colon cancer cells or tumor promoter-induced transformation of preneoplastic cells. We also successfully applied a ligand-docking computational method to identify a novel selective COX-1 inhibitor, 6-C-(E-phenylethenyl)-naringenin (designated herein as 6CEPN). 6CEPN could bind to COX-1 and specifically inhibited its activity both in vitro and ex vivo. In colorectal cancer cells, it potently suppressed anchorage-independent growth by inhibiting COX-1 activity. 6CEPN also effectively suppressed tumor growth in a 28-day colon cancer xenograft model without any obvious systemic toxicity. Taken together, COX-1 plays a critical role in human colorectal carcinogenesis, and this specific COX-1 inhibitor merits further investigation as a potential preventive agent against colorectal cancer.
JF  - Cancer research
AU  - Li, Haitao
AU  - Zhu, Feng
AU  - Chen, Hanyong
AU  - Cheng, Ka Wing
AU  - Zykova, Tatyana
AU  - Oi, Naomi
AU  - Lubet, Ronald A
AU  - Bode, Ann M
AU  - Wang, Mingfu
AU  - Dong, Zigang
AD  - Authors' Affiliations: The Hormel Institute, University of Minnesota, Austin, Minnesota; The National Institutes of Health, National Cancer Institute, Bethesda, Maryland; and School of Biological Sciences, The University of Hong Kong, Hong Kong, China.
Y1  - 2014/01/01/
PY  - 2014
DA  - 2014 Jan 01
SP  - 243
EP  - 252
VL  - 74
IS  - 1
KW  - Cyclooxygenase Inhibitors
KW  - 0
KW  - Flavanones
KW  - Cyclooxygenase 1
KW  - EC 1.14.99.1
KW  - naringenin
KW  - HN5425SBF2
KW  - Index Medicus
KW  - Animals
KW  - Transfection
KW  - Humans
KW  - Xenograft Model Antitumor Assays
KW  - Disease Models, Animal
KW  - Mice, Nude
KW  - Mice
KW  - HT29 Cells
KW  - Male
KW  - Female
KW  - Cyclooxygenase 1 -- metabolism
KW  - Colorectal Neoplasms -- pathology
KW  - Colorectal Neoplasms -- enzymology
KW  - Colorectal Neoplasms -- prevention & control
KW  - Colorectal Neoplasms -- drug therapy
KW  - Flavanones -- pharmacology
KW  - Cyclooxygenase Inhibitors -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490703325?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=6-C-%28E-phenylethenyl%29-naringenin+suppresses+colorectal+cancer+growth+by+inhibiting+cyclooxygenase-1.&rft.au=Li%2C+Haitao%3BZhu%2C+Feng%3BChen%2C+Hanyong%3BCheng%2C+Ka+Wing%3BZykova%2C+Tatyana%3BOi%2C+Naomi%3BLubet%2C+Ronald+A%3BBode%2C+Ann+M%3BWang%2C+Mingfu%3BDong%2C+Zigang&rft.aulast=Li&rft.aufirst=Haitao&rft.date=2014-01-01&rft.volume=74&rft.issue=1&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-2245
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-27
N1  - Date created - 2014-01-07
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biochem Biophys Res Commun. 1999 Nov;265(1):205-10 [10548515]
CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087]
Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10197-202 [10963682]
Gastroenterology. 2000 Sep;119(3):706-14 [10982765]
Cancer Res. 2000 Sep 1;60(17):4705-8 [10987272]
Cancer Res. 2001 Feb 15;61(4):1733-40 [11245490]
Circulation. 2001 Nov 13;104(20):2453-8 [11705824]
Nat Med. 2002 Mar;8(3):289-93 [11875501]
Cancer Res. 2002 Jun 15;62(12):3395-401 [12067981]
Br J Pharmacol. 2002 Dec;137(7):1031-8 [12429575]
N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133]
Cancer Res. 2003 Aug 15;63(16):4872-7 [12941808]
Cancer Res. 2004 May 15;64(10):3694-700 [15150130]
N Engl J Med. 1984 Nov 8;311(19):1206-11 [6436696]
Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):609-13 [8290571]
Cancer Res. 1995 Sep 1;55(17):3785-9 [7641194]
Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):657-62 [9012840]
J Biol Chem. 1997 Apr 11;272(15):9962-70 [9092536]
Gastroenterology. 1998 May;114(5):873-7 [9558273]
Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):272-7 [9874808]
N Engl J Med. 2005 Mar 17;352(11):1092-102 [15713943]
N Engl J Med. 2005 Mar 17;352(11):1071-80 [15713944]
N Engl J Med. 2005 Mar 31;352(13):1293-304 [15753114]
Cancer Res. 2005 May 1;65(9):3735-44 [15867369]
Curr Med Chem. 2006;13(6):659-78 [16529558]
N Engl J Med. 2006 Aug 31;355(9):885-95 [16943401]
J Med Chem. 2007 Apr 5;50(7):1425-41 [17341061]
Chem Res Toxicol. 2008 Oct;21(10):2026-34 [18702534]
J Mol Cell Cardiol. 2009 Feb;46(2):160-8 [19084534]
Proc Natl Acad Sci U S A. 2009 May 5;106(18):7548-52 [19376970]
Oncogene. 2010 Feb 25;29(8):1214-26 [19935697]
Curr Med Chem. 2010;17(32):3769-805 [20858219]
Cell. 2011 Mar 4;144(5):646-74 [21376230]
Cancer Prev Res (Phila). 2011 Nov;4(11):1728-35 [21778329]
N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/0008-5472.CAN-13-2245
ER  - 



TY  - JOUR
T1  - Effects of 3,4-methylenedioxymethamphetamine (MDMA) and its main metabolites on cardiovascular function in conscious rats.
AN  - 1477553087; 24328722
AB  - The cardiovascular effects produced by 3,4-methylenedioxymethamphetamine (MDMA; 'Ecstasy') contribute to its acute toxicity, but the potential role of its metabolites in these cardiovascular effects is not known. Here we examined the effects of MDMA metabolites on cardiovascular function in rats.
          Radiotelemetry was employed to evaluate the effects of s.c. administration of racemic MDMA and its phase I metabolites on BP, heart rate (HR) and locomotor activity in conscious male rats. MDMA (1-20 mg·kg(-1)) produced dose-related increases in BP, HR and activity. The peak effects on HR occurred at a lower dose than peak effects on BP or activity. The N-demethylated metabolite, 3,4-methylenedioxyamphetamine (MDA), produced effects that mimicked those of MDMA. The metabolite 3,4-dihydroxymethamphetamine (HHMA; 1-10 mg·kg(-1)) increased HR more potently and to a greater extent than MDMA, whereas 3,4-dihydroxyamphetamine (HHA) increased HR, but to a lesser extent than HHMA. Neither dihydroxy metabolite altered motor activity. The metabolites 4-hydroxy-3-methoxymethamphetamine (HMMA) and 4-hydroxy-3-methoxyamphetamine (HMA) did not affect any of the parameters measured. The tachycardia produced by MDMA and HHMA was blocked by the β-adrenoceptor antagonist propranolol.
          Our results demonstrate that HHMA may contribute significantly to the cardiovascular effects of MDMA in vivo. As such, determining the molecular mechanism of action of HHMA and the other hydroxyl metabolites of MDMA warrants further study. Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
JF  - British journal of pharmacology
AU  - Schindler, Charles W
AU  - Thorndike, Eric B
AU  - Blough, Bruce E
AU  - Tella, Srihari R
AU  - Goldberg, Steven R
AU  - Baumann, Michael H
AD  - Preclinical Pharmacology, National Institutes of Health, National Institute on Drug Abuse, Intramural Research Program, Baltimore, MD, USA.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 83
EP  - 91
VL  - 171
IS  - 1
KW  - Adrenergic beta-Antagonists
KW  - 0
KW  - Hallucinogens
KW  - 4-hydroxy-3-methoxymethamphetamine
KW  - 117652-28-5
KW  - 3-O-methyl-alpha-methyldopamine
KW  - 13026-44-3
KW  - alpha-methylepinine
KW  - 15398-87-5
KW  - Methamphetamine
KW  - 44RAL3456C
KW  - 3,4-Methylenedioxyamphetamine
KW  - 4764-17-4
KW  - N-Methyl-3,4-methylenedioxyamphetamine
KW  - KE1SEN21RM
KW  - Deoxyepinephrine
KW  - R7339QLN1C
KW  - Dopamine
KW  - VTD58H1Z2X
KW  - Index Medicus
KW  - noradrenergic
KW  - heart rate
KW  - telemetry
KW  - BP
KW  - MDMA metabolites
KW  - Dopamine -- analogs & derivatives
KW  - Animals
KW  - Metabolic Detoxication, Phase I
KW  - Dopamine -- pharmacology
KW  - Dose-Response Relationship, Drug
KW  - Deoxyepinephrine -- pharmacology
KW  - Deoxyepinephrine -- analogs & derivatives
KW  - 3,4-Methylenedioxyamphetamine -- metabolism
KW  - Rats
KW  - Rats, Sprague-Dawley
KW  - Consciousness
KW  - Telemetry
KW  - Methamphetamine -- metabolism
KW  - Methamphetamine -- pharmacology
KW  - 3,4-Methylenedioxyamphetamine -- pharmacology
KW  - Deoxyepinephrine -- metabolism
KW  - Motor Activity -- drug effects
KW  - Methamphetamine -- analogs & derivatives
KW  - Time Factors
KW  - Adrenergic beta-Antagonists -- pharmacology
KW  - Male
KW  - Heart Rate -- drug effects
KW  - N-Methyl-3,4-methylenedioxyamphetamine -- metabolism
KW  - Hallucinogens -- pharmacology
KW  - Cardiovascular System -- drug effects
KW  - N-Methyl-3,4-methylenedioxyamphetamine -- pharmacology
KW  - Hallucinogens -- metabolism
KW  - Blood Pressure -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1477553087?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+pharmacology&rft.atitle=Effects+of+3%2C4-methylenedioxymethamphetamine+%28MDMA%29+and+its+main+metabolites+on+cardiovascular+function+in+conscious+rats.&rft.au=Schindler%2C+Charles+W%3BThorndike%2C+Eric+B%3BBlough%2C+Bruce+E%3BTella%2C+Srihari+R%3BGoldberg%2C+Steven+R%3BBaumann%2C+Michael+H&rft.aulast=Schindler&rft.aufirst=Charles&rft.date=2014-01-01&rft.volume=171&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=British+journal+of+pharmacology&rft.issn=1476-5381&rft_id=info:doi/10.1111%2Fbph.12423
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-19
N1  - Date created - 2013-12-16
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Eur J Pharmacol. 1999 Oct 21;383(1):57-68 [10556682]
Clin Pharmacol Ther. 2011 Aug;90(2):246-55 [21677639]
Eur Neuropsychopharmacol. 2000 Jul;10(4):289-95 [10871712]
Physiol Behav. 2000 Jul 1-15;70(1-2):141-8 [10978489]
J Psychopharmacol. 2000;14(3):269-74 [11106307]
Ann Intern Med. 2000 Dec 19;133(12):969-73 [11119398]
Neuropsychopharmacology. 2001 Mar;24(3):240-52 [11166515]
Psychopharmacology (Berl). 2001 Mar 1;154(2):161-8 [11314678]
J Pharmacol Exp Ther. 2001 Jun;297(3):846-52 [11356903]
Br J Pharmacol. 2001 Jun;133(3):429-37 [11375260]
Chem Res Toxicol. 2001 Sep;14(9):1203-8 [11559034]
Neuropsychopharmacology. 2002 Jan;26(1):40-52 [11751031]
J Pharmacol Exp Ther. 2002 Sep;302(3):898-907 [12183645]
Eur J Pharmacol. 2002 Dec 13;457(1):45-9 [12460642]
Pharmacol Rev. 2003 Sep;55(3):463-508 [12869661]
Ther Drug Monit. 2004 Apr;26(2):137-44 [15228154]
Trends Pharmacol Sci. 2004 Oct;25(10):505-8 [15380932]
Am J Forensic Med Pathol. 1988 Dec;9(4):339-41 [3239555]
BMJ. 1990 Jan 27;300(6719):230-5 [2106931]
J Pharmacol Exp Ther. 1990 Oct;255(1):154-60 [2213551]
Life Sci. 1992;51(9):653-60 [1354322]
Pharmacol Biochem Behav. 1992 Aug;42(4):791-6 [1325059]
J Pharmacol Exp Ther. 1992 Nov;263(2):742-51 [1359113]
J Pharm Pharmacol. 1994 Oct;46(10):826-32 [7699571]
Neuropsychopharmacology. 1998 Oct;19(4):241-51 [9718588]
J Pharmacol Exp Ther. 1999 Jul;290(1):136-45 [10381769]
Br J Pharmacol. 2005 Jan;144(2):231-41 [15665862]
Br J Pharmacol. 2006 Apr;147(8):926-34 [16491100]
Psychopharmacology (Berl). 2007 Jan;189(4):565-73 [17047932]
Ther Drug Monit. 2008 Jun;30(3):320-32 [18520604]
Pharmacol Biochem Behav. 2008 Aug;90(2):208-17 [18403002]
J Clin Psychopharmacol. 2008 Aug;28(4):432-40 [18626271]
Drug Metab Dispos. 2009 Oct;37(10):2079-86 [19628751]
Drug Metab Dispos. 2009 Nov;37(11):2163-70 [19679675]
Int Rev Neurobiol. 2009;88:257-96 [19897081]
Toxicol Appl Pharmacol. 2009 Dec 15;241(3):339-47 [19781562]
Neurotox Res. 2010 Aug;18(2):200-9 [19851718]
Br J Pharmacol. 2010 Aug;160(7):1573-6 [20649560]
Br J Pharmacol. 2010 Aug;160(7):1577-9 [20649561]
Curr Pharm Biotechnol. 2010 Aug;11(5):470-5 [20420571]
Emerg Med J. 2010 Aug;27(8):586-9 [20378736]
Neurochem Int. 2011 Jan;58(1):92-101 [21074589]
Hum Exp Toxicol. 2011 Apr;30(4):259-66 [20488845]
Toxicol Lett. 2000 Mar 15;112-113:133-42 [10720722]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/bph.12423
ER  - 



TY  - JOUR
T1  - Smoldering multiple myeloma: present position and potential promises.
AN  - 1477552714; 24112232
AB  - Since smoldering multiple myeloma (SMM) was first described over three decades ago based on a case series of six patients, its definition and our understanding of the entity have evolved considerably. The risk of progression to symptomatic myeloma (MM) varies greatly among individuals diagnosed with myeloma precursor disease. Epidemiologic, molecular, flow cytometric and radiological techniques have demonstrated that this transformation to MM from precursor states is not sudden but rather a continuous overlapping series of events with evidence of end-organ damage that could manifest in the earliest stages of disease. Contemporary antimyeloma therapies can yield rapid, deep, and durable responses with manageable toxicities, and molecular-cell-based measures are now available to rule out minimal residual disease. With this information, clinical studies with correlative measures can now be developed to test the fundamental hypothesis that intervention in early myeloma may provide a measurable clinical benefit to patients by either delaying progression or eradicating plasma cell clones. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
JF  - European journal of haematology
AU  - Tageja, Nishant
AU  - Manasanch, Elisabet E
AU  - Korde, Neha
AU  - Kwok, Mary
AU  - Mailankody, Sham
AU  - Bhutani, Manisha
AU  - Roschewski, Mark
AU  - Landgren, Ola
AD  - Multiple Myeloma Section, Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 1
EP  - 12
VL  - 92
IS  - 1
KW  - Index Medicus
KW  - lenalidomide
KW  - smoldering myeloma
KW  - multiple myeloma
KW  - plasma cell dyscrasia
KW  - flow cytometry
KW  - carfilzomib
KW  - Bone Marrow -- pathology
KW  - Precancerous Conditions
KW  - Bone and Bones -- pathology
KW  - Risk Factors
KW  - Humans
KW  - Monoclonal Gammopathy of Undetermined Significance -- etiology
KW  - Diagnostic Imaging
KW  - Disease Progression
KW  - Flow Cytometry
KW  - Monoclonal Gammopathy of Undetermined Significance -- diagnosis
KW  - Multiple Myeloma -- diagnosis
KW  - Multiple Myeloma -- etiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1477552714?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+haematology&rft.atitle=Smoldering+multiple+myeloma%3A+present+position+and+potential+promises.&rft.au=Tageja%2C+Nishant%3BManasanch%2C+Elisabet+E%3BKorde%2C+Neha%3BKwok%2C+Mary%3BMailankody%2C+Sham%3BBhutani%2C+Manisha%3BRoschewski%2C+Mark%3BLandgren%2C+Ola&rft.aulast=Tageja&rft.aufirst=Nishant&rft.date=2014-01-01&rft.volume=92&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=European+journal+of+haematology&rft.issn=1600-0609&rft_id=info:doi/10.1111%2Fejh.12205
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-31
N1  - Date created - 2013-12-16
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/ejh.12205
ER  - 



TY  - JOUR
T1  - Neurodevelopmental outcomes of extremely low birth weight infants with spontaneous intestinal perforation or surgical necrotizing enterocolitis
AN  - 1471544115; 24135709
AB  - To determine if extremely low birth weight infants with surgical necrotizing enterocolitis have a higher risk of death or neurodevelopmental impairment and neurodevelopmental impairment among survivors (secondary outcome) at 18-22 months corrected age compared with infants with spontaneous intestinal perforation and infants without necrotizing enterocolitis or spontaneous intestinal perforation.  
Retrospective analysis of the Neonatal Research Network very low birth weight registry, evaluating extremely low birth weight infants born between 2000 and 2005. The study infants were designated into three groups: (1) spontaneous intestinal perforation without necrotizing enterocolitis; (2) surgical necrotizing enterocolitis (Bell's stage III); and (3) neither spontaneous intestinal perforation nor necrotizing enterocolitis. Multivariate logistic regression analysis was performed to evaluate the association between the clinical group and death or neurodevelopmental impairment, controlling for multiple confounding factors including center.  
Infants with surgical necrotizing enterocolitis had the highest rate of death before hospital discharge (53.5%) and death or neurodevelopmental impairment (82.3%) compared with infants in the spontaneous intestinal perforation group (39.1 and 79.3%) and no necrotizing enterocolitis/no spontaneous intestinal perforation group (22.1 and 53.3%; P<0.001). Similar results were observed for neurodevelopmental impairment among survivors. On logistic regression analysis, both spontaneous intestinal perforation and surgical necrotizing enterocolitis were associated with increased risk of death or neurodevelopmental impairment (adjusted odds ratio 2.21, 95% confidence interval (CI): 1.5, 3.2 and adjusted OR 2.11, 95% CI: 1.5, 2.9, respectively) and neurodevelopmental impairment among survivors (adjusted OR 2.17, 95% CI: 1.4, 3.2 and adjusted OR 1.70, 95% CI: 1.2, 2.4, respectively).  
Spontaneous intestinal perforation and surgical necrotizing enterocolitis are associated with a similar increase in the risk of death or neurodevelopmental impairment and neurodevelopmental impairment among extremely low birth weight survivors at 18-22 months corrected age.
JF  - Journal of Perinatology
AU  - Wadhawan, R
AU  - Oh, W
AU  - Hintz, S R
AU  - Blakely, M L
AU  - Das, A
AU  - Bell, E F
AU  - Saha, S
AU  - Laptook, A R
AU  - Shankaran, S
AU  - Stoll, B J
AU  - Walsh, M C
AU  - Higgins, R D
Y1  - 2014/01//
PY  - 2014
DA  - Jan 2014
SP  - 64
EP  - 70
CY  - New York
PB  - Nature Publishing Group
VL  - 34
IS  - 1
SN  - 07438346
KW  - Medical Sciences--Pediatrics
KW  - Steroids
KW  - Steroids -- therapeutic use
KW  - Socioeconomic Factors
KW  - Infant
KW  - Young Adult
KW  - Logistic Models
KW  - Humans
KW  - Enterocolitis, Necrotizing -- surgery
KW  - Retrospective Studies
KW  - Infant, Newborn
KW  - Child Development
KW  - Follow-Up Studies
KW  - Female
KW  - Pregnancy
KW  - Enterocolitis, Necrotizing -- complications
KW  - Developmental Disabilities -- etiology
KW  - Intestinal Perforation -- complications
KW  - Infant, Extremely Low Birth Weight
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1471544115?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthcompleteshell&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Perinatology&rft.atitle=Neurodevelopmental+outcomes+of+extremely+low+birth+weight+infants+with+spontaneous+intestinal+perforation+or+surgical+necrotizing+enterocolitis&rft.au=Wadhawan%2C+R%3BOh%2C+W%3BHintz%2C+S+R%3BBlakely%2C+M+L%3BDas%2C+A%3BBell%2C+E+F%3BSaha%2C+S%3BLaptook%2C+A+R%3BShankaran%2C+S%3BStoll%2C+B+J%3BWalsh%2C+M+C%3BHiggins%2C+R+D&rft.aulast=Wadhawan&rft.aufirst=R&rft.date=2014-01-01&rft.volume=34&rft.issue=1&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=Journal+of+Perinatology&rft.issn=07438346&rft_id=info:doi/10.1038%2Fjp.2013.128
LA  - English
DB  - ProQuest Central
N1  - Copyright - Copyright Nature Publishing Group Jan 2014
N1  - Last updated - 2014-08-14
DO  - http://dx.doi.org/10.1038/jp.2013.128
ER  - 



TY  - JOUR
T1  - Binge-like ethanol consumption increases corticosterone levels and neurodegneration whereas occupancy of type II glucocorticoid receptors with mifepristone is neuroprotective.
AN  - 1469639284; 22500955
AB  - Excessive ethanol (EtOH) use leads to impaired memory and cognition. Using a rat model of binge-like intoxication, we tested whether elevated corticosterone (Cort) levels contribute to the neurotoxic consequences of EtOH exposure. Rats were adrenalectomized (Adx) and implanted with cholesterol pellets, or cholesterol pellets containing Cort in order to achieve basal, medium, or high blood concentrations of Cort. Intragastric EtOH or an isocaloric control solution was given three times daily for 4 days to achieve blood alcohol levels ranging between 200 and 350 mg/dl. Mean 24-hour plasma levels of Cort were ∼110 and ∼40 ng/ml in intact EtOH-treated and intact control animals, respectively. Basal Cort replacement concentrations in EtOH-treated Adx animals did not exacerbate alcohol-induced neurodegeneration in the hippocampal dentate gyrus (DG) or the entorhinal cortex (EC) as observed by amino-cupric silver staining. In contrast, Cort replacement pellets resulting in plasma Cort levels twofold higher (medium) than normal, or greater than twofold higher (high) in Adx-Cort-EtOH animals increased neurodegeneration. In separate experiments, pharmacological blockade of the Type II glucocorticoid (GC) receptor was initiated with mifepristone (RU38486; 0, 5, 15 mg/kg/day, i.p.). At the higher dose, mifepristone decreased the number of degenerating hippocampal DG cells in binge-EtOH-treated intact animals, whereas, only a trend for reduction was observed in 15 mg/kg/day mifepristone-treated animals in the EC, as determined by fluoro-jade B staining. These results suggest that elevated circulating Cort in part mediates EtOH-induced neurotoxicity in the brain through activation of Type II GC receptors.
          Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
JF  - Addiction biology
AU  - Cippitelli, Andrea
AU  - Damadzic, Ruslan
AU  - Hamelink, Carol
AU  - Brunnquell, Michael
AU  - Thorsell, Annika
AU  - Heilig, Markus
AU  - Eskay, Robert L
AD  - Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, USA Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health (NIMH), National Institutes of Health (NIH), Bethesda, MD, USA.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 27
EP  - 36
VL  - 19
IS  - 1
KW  - Drug Implants
KW  - 0
KW  - Fluoresceins
KW  - Hormone Antagonists
KW  - Neuroprotective Agents
KW  - Receptors, Glucocorticoid
KW  - fluoro jade
KW  - Mifepristone
KW  - 320T6RNW1F
KW  - Ethanol
KW  - 3K9958V90M
KW  - Cholesterol
KW  - 97C5T2UQ7J
KW  - Corticosterone
KW  - W980KJ009P
KW  - Index Medicus
KW  - ethanol
KW  - mifepristone
KW  - corticosterone
KW  - hippocampus
KW  - neurodegeneration
KW  - FJ-B
KW  - Stress, Physiological -- physiology
KW  - Alcoholic Intoxication -- pathology
KW  - Hypothalamo-Hypophyseal System -- drug effects
KW  - Animals
KW  - Analysis of Variance
KW  - Random Allocation
KW  - Dose-Response Relationship, Drug
KW  - Cholesterol -- administration & dosage
KW  - Drug Implants -- administration & dosage
KW  - Stress, Physiological -- drug effects
KW  - Disease Models, Animal
KW  - Binge Drinking -- complications
KW  - Adrenalectomy
KW  - Rats
KW  - Rats, Sprague-Dawley
KW  - Alcoholic Intoxication -- physiopathology
KW  - Alcohol-Induced Disorders, Nervous System -- etiology
KW  - Silver Staining
KW  - Pituitary-Adrenal System -- drug effects
KW  - Male
KW  - Alcoholic Intoxication -- metabolism
KW  - Entorhinal Cortex -- metabolism
KW  - Receptors, Glucocorticoid -- antagonists & inhibitors
KW  - Dentate Gyrus -- metabolism
KW  - Ethanol -- administration & dosage
KW  - Mifepristone -- pharmacology
KW  - Corticosterone -- metabolism
KW  - Entorhinal Cortex -- pathology
KW  - Ethanol -- blood
KW  - Dentate Gyrus -- drug effects
KW  - Dentate Gyrus -- pathology
KW  - Ethanol -- toxicity
KW  - Hormone Antagonists -- administration & dosage
KW  - Corticosterone -- pharmacology
KW  - Mifepristone -- administration & dosage
KW  - Entorhinal Cortex -- drug effects
KW  - Corticosterone -- administration & dosage
KW  - Hormone Antagonists -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1469639284?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+biology&rft.atitle=Binge-like+ethanol+consumption+increases+corticosterone+levels+and+neurodegneration+whereas+occupancy+of+type+II+glucocorticoid+receptors+with+mifepristone+is+neuroprotective.&rft.au=Cippitelli%2C+Andrea%3BDamadzic%2C+Ruslan%3BHamelink%2C+Carol%3BBrunnquell%2C+Michael%3BThorsell%2C+Annika%3BHeilig%2C+Markus%3BEskay%2C+Robert+L&rft.aulast=Cippitelli&rft.aufirst=Andrea&rft.date=2014-01-01&rft.volume=19&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Addiction+biology&rft.issn=1369-1600&rft_id=info:doi/10.1111%2Fj.1369-1600.2012.00451.x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-18
N1  - Date created - 2013-12-18
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Brain Res Bull. 1989 Feb;22(2):411-22 [2650808]
Neuroendocrinology. 1989 Oct;50(4):427-32 [2554177]
J Neurochem. 1992 May;58(5):1730-5 [1560229]
Behav Neurosci. 1992 Aug;106(4):613-22 [1503656]
Brain Res. 1992 Aug 21;588(2):341-5 [1393587]
Biol Psychiatry. 1992 Nov 1;32(9):756-65 [1450290]
Brain Cogn. 1993 May;22(1):51-62 [8499112]
J Neurosci. 1993 Jul;13(7):2939-45 [7687281]
Behav Neural Biol. 1993 Jul;60(1):9-26 [8216164]
Prog Neurobiol. 1994 May;43(1):1-36 [7526416]
Neurotoxicol Teratol. 1994 Nov-Dec;16(6):545-61 [7532272]
Alcohol Clin Exp Res. 1996 Apr;20(2):284-92 [8730219]
Alcohol Clin Exp Res. 1996 Nov;20(8):1406-11 [8947317]
Neurotoxicology. 1996 Fall-Winter;17(3-4):873-82 [9086511]
Alcohol Clin Exp Res. 1998 Feb;22(1):217-24 [9514310]
J Pharmacol Exp Ther. 2005 Aug;314(2):780-8 [15878999]
Neuroscience. 2005;136(1):259-67 [16182452]
Brain Res. 2006 Apr 12;1082(1):165-72 [16510135]
Biol Psychiatry. 2010 May 1;67(9):823-30 [20132926]
Neurobiol Learn Mem. 2010 Nov;94(4):538-46 [20849966]
Biol Psychiatry. 1999 Dec 1;46(11):1472-9 [10599477]
Toxicol Pathol. 2000 Jan-Feb;28(1):70-83 [10668992]
Brain Res. 2000 Aug 25;874(2):123-30 [10960596]
Alcohol Clin Exp Res. 2000 Nov;24(11):1712-23 [11104119]
Alcohol Clin Exp Res. 2002 Apr;26(4):547-57 [11981132]
Pharmacol Biochem Behav. 2002 Jun;72(3):521-32 [12175448]
Psychoneuroendocrinology. 2004 Sep;29(8):999-1003 [15219650]
Psychopharmacologia. 1975 Sep 17;43(3):245-54 [1237914]
Science. 1981 Oct 30;214(4520):581-4 [6270791]
J Pharmacol Exp Ther. 1984 Apr;229(1):127-31 [6323684]
Science. 1985 Sep 27;229(4720):1397-400 [4035356]
Am J Physiol. 1985 Nov;249(5 Pt 2):R527-32 [2998210]
Brain Res. 1985 Dec 16;359(1-2):300-5 [4075151]
Endocr Rev. 1986 Aug;7(3):284-301 [3527687]
Physiol Rev. 1986 Oct;66(4):1121-88 [3532143]
Horm Metab Res. 1987 Mar;19(3):105-9 [3570145]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/j.1369-1600.2012.00451.x
ER  - 



TY  - JOUR
T1  - Substance use disorders among treatment naïve first-episode psychosis patients.
AN  - 1466374630; 24183888
AB  - To examine the prevalence of substance use among treatment naïve patients with first episode psychosis presenting to a psychiatry outpatient clinic in India.
          The study sample consisted of 139 first episode treatment naïve patients with psychosis from in and around Bangalore, a city in South India. Self as well as informant-reported data on type, use and duration of substance use as well as the severity of psychotic symptoms were collected using structured instruments. Urine toxicology screen was also conducted for six common drugs of abuse. Breath alcohol analysis was performed in all patients. Acute and transient psychosis was the most common diagnosis (42.4%). Overall, 20% of the population reported current substance use disorder (excluding nicotine). Current alcohol dependence was diagnosed among 17.3%, whereas cannabis dependence in 3.6%. Life time as well as current use of cannabis was less than 6%. While one patient reported inhalant abuse none reported use of amphetamine or opioids. There was very high concordance between reported drug use and urine toxicology screen.
          The use of illicit drugs is substantially less among first episode drug naïve patients with psychosis in an Indian urban clinical setting compared to rates reported from developed countries like North America, Canada and UK. © 2014.
JF  - Comprehensive psychiatry
AU  - Chand, Prabhat
AU  - Thirthalli, Jagadisha
AU  - Murthy, Pratima
AD  - Department of Psychiatry, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. Electronic address: prabhatkumarchand@gmail.com.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 165
EP  - 169
VL  - 55
IS  - 1
KW  - Index Medicus
KW  - India -- epidemiology
KW  - Humans
KW  - Adult
KW  - Middle Aged
KW  - Male
KW  - Female
KW  - Comorbidity
KW  - Prevalence
KW  - Pregnancy
KW  - Psychotic Disorders -- epidemiology
KW  - Substance-Related Disorders -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1466374630?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Comprehensive+psychiatry&rft.atitle=Substance+use+disorders+among+treatment+na%C3%AFve+first-episode+psychosis+patients.&rft.au=Chand%2C+Prabhat%3BThirthalli%2C+Jagadisha%3BMurthy%2C+Pratima&rft.aulast=Chand&rft.aufirst=Prabhat&rft.date=2014-01-01&rft.volume=55&rft.issue=1&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Comprehensive+psychiatry&rft.issn=1532-8384&rft_id=info:doi/10.1016%2Fj.comppsych.2013.07.075
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-08-11
N1  - Date created - 2013-12-09
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.comppsych.2013.07.075
ER  - 



TY  - JOUR
T1  - Combining the antimesothelin immunotoxin SS1P with the BH3-mimetic ABT-737 induces cell death in SS1P-resistant pancreatic cancer cells.
AN  - 1466372414; 24316551
AB  - SS1P is an antimesothelin recombinant immunotoxin (RIT). Pancreatic ductal adenocarcinoma (PDAC) cell lines are resistant to SS1P, despite high mesothelin expression. The aim of this study is to examine whether combining SS1P and BH3-mimetic ABT-737 induces cell death in a panel of PDAC cell lines. ABT-737 binds and neutralizes several antiapoptotic BCL2 family proteins, but has a low affinity for the short-lived MCL1 and BCL2A1. SS1P inhibits protein synthesis, which has shown to downregulate MCL1. PDAC cell lines KLM-1, BxPc-3, and Panc 3.014 were resistant to SS1P or ABT-737 alone. Combining both compounds led to a significant increase in cell death. After 48 hours of treatment, cell death was observed in 92% of KLM-1, 55% of BxPc-3, and 23% of Panc 3.014 cells. Panc 3.014 had the highest number of mesothelin-binding sites (92×10(3)), followed by KLM-1 (58×10(3)) and BxPc-3 (3×10(3)). ABT-737 had no effect on SS1P internalization, but enhanced SS1P-induced protein synthesis inhibition significantly in KLM-1, to a lesser extent in BxPc-3, and very little in Panc 3.014. SS1P alone or in combination with ABT-737 downregulated MCL1 in KLM-1 and BxPc-3, but not in Panc 3.014. Similar observations were made for BCL2A1, which had the highest levels in Panc 3.014. Compared with KLM-1, Panc 3.014, and BxPc-3 also had lower proapoptotic BAK and a trend toward higher MCL1. Proapoptotic BAX was similar in KLM-1 and BxPc-3, but lower in Panc 3.014. In conclusion, combining SS1P with ABT-737 overcomes SS1P-resistance in PDAC, although to a variable extent. The efficacy of the combination is mainly associated with the RIT-associated inhibition of protein synthesis and the ability to downregulate MCL1 and BCL2A1, while levels of other key apoptotic proteins may also be important. Our data support the combination of an RIT and a BH3-mimetic, and identify factors that potentially limit the efficacy of such therapeutic approach.
JF  - Journal of immunotherapy (Hagerstown, Md. : 1997)
AU  - Hollevoet, Kevin
AU  - Antignani, Antonella
AU  - Fitzgerald, David J
AU  - Pastan, Ira
AD  - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Y1  - 2014/01//
PY  - 2014
DA  - January 2014
SP  - 8
EP  - 15
VL  - 37
IS  - 1
KW  - ABT-737
KW  - 0
KW  - Antibodies, Monoclonal
KW  - Antigens, Neoplasm
KW  - Biphenyl Compounds
KW  - GPI-Linked Proteins
KW  - Immunotoxins
KW  - Nitrophenols
KW  - Piperazines
KW  - Proto-Oncogene Proteins c-bcl-2
KW  - SS1(dsFv)PE38
KW  - Sulfonamides
KW  - mesothelin
KW  - Index Medicus
KW  - Cell Proliferation -- drug effects
KW  - Protein Biosynthesis -- drug effects
KW  - Proto-Oncogene Proteins c-bcl-2 -- antagonists & inhibitors
KW  - Humans
KW  - Proto-Oncogene Proteins c-bcl-2 -- metabolism
KW  - Cell Line, Tumor
KW  - Cytotoxicity, Immunologic -- drug effects
KW  - Piperazines -- pharmacology
KW  - Drug Synergism
KW  - Cell Death -- drug effects
KW  - Antigens, Neoplasm -- immunology
KW  - Protein Binding -- immunology
KW  - Pancreatic Neoplasms -- metabolism
KW  - Nitrophenols -- pharmacology
KW  - Biphenyl Compounds -- pharmacology
KW  - Drug Resistance, Neoplasm
KW  - Antibodies, Monoclonal -- pharmacology
KW  - Antibodies, Monoclonal -- immunology
KW  - Pancreatic Neoplasms -- therapy
KW  - Sulfonamides -- pharmacology
KW  - Immunotoxins -- immunology
KW  - GPI-Linked Proteins -- antagonists & inhibitors
KW  - Immunotoxins -- pharmacology
KW  - GPI-Linked Proteins -- immunology
KW  - Pancreatic Neoplasms -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1466372414?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunotherapy+%28Hagerstown%2C+Md.+%3A+1997%29&rft.atitle=Combining+the+antimesothelin+immunotoxin+SS1P+with+the+BH3-mimetic+ABT-737+induces+cell+death+in+SS1P-resistant+pancreatic+cancer+cells.&rft.au=Hollevoet%2C+Kevin%3BAntignani%2C+Antonella%3BFitzgerald%2C+David+J%3BPastan%2C+Ira&rft.aulast=Hollevoet&rft.aufirst=Kevin&rft.date=2014-01-01&rft.volume=37&rft.issue=1&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%28Hagerstown%2C+Md.+%3A+1997%29&rft.issn=1537-4513&rft_id=info:doi/10.1097%2FCJI.0000000000000010
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-18
N1  - Date created - 2013-12-09
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/CJI.0000000000000010
ER  - 



TY  - JOUR
T1  - The burden of human papillomavirus infections and related diseases in sub-saharan Africa.
AN  - 1469215524; 24331746
AB  - Despite the scarcity of high quality cancer registries and lack of reliable mortality data, it is clear that human papillomavirus (HPV)-associated diseases, particularly cervical cancer, are major causes of morbidity and mortality in sub-Saharan Africa (SSA). Cervical cancer incidence rates in SSA are the highest in the world and the disease is the most common cause of cancer death among women in the region. The high incidence of cervical cancer is a consequence of the inability of most countries to either initiate or sustain cervical cancer prevention services. In addition, it appears that the prevalence of HPV in women with normal cytology is higher than in more developed areas of the world, at an average of 24%. There is, however, significant regional variation in SSA, with the highest incidence of HPV infection and cervical cancer found in Eastern and Western Africa. It is expected that, due to aging and growth of the population, but also to lack of access to appropriate prevention services and the concomitant human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) epidemic, cervical cancer incidence and mortality rates in SSA will rise over the next 20 years. HPV16 and 18 are the most common genotypes in cervical cancer in SSA, although other carcinogenic HPV types, such as HPV45 and 35, are also relatively more frequent compared with other world regions. Data on other HPV-related anogenital cancers including those of the vulva, vagina, anus, and penis, are limited. Genital warts are common and associated with HPV types 6 and 11. HIV infection increases incidence and prevalence of all HPV-associated diseases. Sociocultural determinants of HPV-related disease, as well as the impact of forces that result in social destabilization, demand further study. Strategies to reduce the excessive burden of HPV-related diseases in SSA include age-appropriate prophylactic HPV vaccination, cervical cancer prevention services for women of the reproductive ages, and control of HIV/AIDS. This article forms part of a regional report entitled "Comprehensive Control of HPV Infections and Related Diseases in the Sub-Saharan Africa Region" Vaccine Volume 31, Supplement 5, 2013. Updates of the progress in the field are presented in a separate monograph entitled "Comprehensive Control of HPV Infections and Related Diseases" Vaccine Volume 30, Supplement 5, 2012.
          Copyright © 2013. Published by Elsevier Ltd.
JF  - Vaccine
AU  - De Vuyst, Hugo
AU  - Alemany, Laia
AU  - Lacey, Charles
AU  - Chibwesha, Carla J
AU  - Sahasrabuddhe, Vikrant
AU  - Banura, Cecily
AU  - Denny, Lynette
AU  - Parham, Groesbeck P
AD  - Infection and Cancer Epidemiology Group, International Agency for Research on Cancer (WHO-IARC), Lyon, France. ; Unit of Infections and Cancer (UNIC), Cancer Epidemiology Research Program (CERP), Institut Català d'Oncologia - Catalan Institute of Oncology (ICO), L'Hospitalet de Llobregat (Barcelona), Spain; CIBER en Epidemiología y Salud Pública (CIBERESP), Spain. ; Centre for Immunology and Infection, Hull York Medical School, University of York, York, UK. ; University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, U.S.A and Centre for Infectious Disease Research in Zambia, Lusaka, Zambia. ; Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Department of Child Health and Development Centre, Makerere University College of Health Sciences, Kampala, Uganda. ; Department of Obstetrics and Gynaecology and Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Groote Schuur Hospital, Observatory, Cape Town, South Africa. ; Department of Obstetrics and Gynecology, UNC Global Women's Health, University of North Carolina - Chapel Hill, North Carolina, USA. Electronic address: groesbeck.parham@cidrz.org.
Y1  - 2013/12/29/
PY  - 2013
DA  - 2013 Dec 29
SP  - F32
EP  - F46
VL  - 31 Suppl 5
KW  - Index Medicus
KW  - Anogenital cancers
KW  - HPV epidemiology
KW  - Cervical cancer
KW  - Sub-Saharan Africa
KW  - Genital warts
KW  - Africa South of the Sahara -- epidemiology
KW  - Humans
KW  - Topography, Medical
KW  - Papillomaviridae
KW  - Incidence
KW  - Alphapapillomavirus
KW  - HIV
KW  - Male
KW  - Female
KW  - Prevalence
KW  - Papillomavirus Infections -- epidemiology
KW  - Uterine Cervical Neoplasms -- epidemiology
KW  - Papillomavirus Infections -- complications
KW  - Anus Neoplasms -- epidemiology
KW  - Condylomata Acuminata -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1469215524?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=The+burden+of+human+papillomavirus+infections+and+related+diseases+in+sub-saharan+Africa.&rft.au=De+Vuyst%2C+Hugo%3BAlemany%2C+Laia%3BLacey%2C+Charles%3BChibwesha%2C+Carla+J%3BSahasrabuddhe%2C+Vikrant%3BBanura%2C+Cecily%3BDenny%2C+Lynette%3BParham%2C+Groesbeck+P&rft.aulast=De+Vuyst&rft.aufirst=Hugo&rft.date=2013-12-29&rft.volume=31+Suppl+5&rft.issue=&rft.spage=F32&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=1873-2518&rft_id=info:doi/10.1016%2Fj.vaccine.2012.07.092
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-30
N1  - Date created - 2013-12-16
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Lancet. 2011 Jul 16;378(9787):247-55 [21763937]
Sex Transm Dis. 2011 Apr;38(4):253-9 [20966828]
Sex Transm Dis. 2011 Apr;38(4):308-15 [21150817]
J Acquir Immune Defic Syndr. 2011 Aug;57 Suppl 3:S217-24 [21857322]
Intervirology. 1999;42(4):221-7 [10567840]
Int J Cancer. 2000 Jan 15;85(2):206-10 [10629079]
JAMA. 2000 Jan 5;283(1):81-6 [10632284]
J Med Virol. 2000 May;61(1):65-9 [10745234]
Am J Pathol. 2001 Oct;159(4):1211-8 [11583947]
Cancer Epidemiol Biomarkers Prev. 2001 Oct;10(10):1037-45 [11588129]
Lancet. 2001 Oct 27;358(9291):1429-30 [11705494]
Dev Biol (Basel). 2001;106:443-51; discussion 452-3, 465-75 [11761260]
Int J Epidemiol. 2002 Feb;31(1):202-9 [11914322]
Int J Gynecol Cancer. 2002 Jul-Aug;12(4):383-8 [12144687]
Int J Cancer. 2003 Mar 1;103(6):803-9 [12516102]
Sex Transm Dis. 2003 Feb;30(2):137-42 [12567172]
Acta Obstet Gynecol Scand. 2003 Aug;82(8):762-6 [12848649]
J Med Virol. 2003 Oct;71(2):265-73 [12938202]
Br J Cancer. 2004 Feb 9;90(3):638-45 [14760378]
J Gen Virol. 2004 Aug;85(Pt 8):2189-90 [15269357]
Br J Vener Dis. 1981 Jun;57(3):181-3 [6894561]
IARC Sci Publ. 1984;(63):413-31 [6399280]
Int J Cancer. 1992 Jun 19;51(4):515-21 [1318265]
J Med Virol. 1994 Jul;43(3):231-7 [7931183]
J Natl Cancer Inst. 1995 Jun 7;87(11):796-802 [7791229]
Int J Cancer. 1998 May 18;76(4):480-6 [9590121]
Int J Cancer. 2005 Sep 10;116(4):606-16 [15825185]
Br J Cancer. 2005 Oct 31;93(9):1068-76 [16106268]
Ethiop Med J. 2005 Jul;43(3):151-8 [16370546]
J Med Virol. 2006 Oct;78(10):1341-6 [16927292]
AIDS. 2006 Nov 28;20(18):2337-44 [17117020]
Br J Cancer. 2007 May 7;96(9):1480-3 [17437020]
J Clin Microbiol. 2007 Jun;45(6):1679-83 [17409209]
Clin Infect Dis. 2007 Aug 15;45(4):510-3 [17638204]
Int J Cancer. 2008 Jan 1;122(1):244-6 [17764116]
BJOG. 2008 Feb;115(3):301-3 [18190365]
Sex Transm Infect. 2008 Feb;84(1):62-6 [17991686]
J Clin Microbiol. 2008 Feb;46(2):740-2 [17977997]
Int J Cancer. 2008 Apr 15;122(8):1901-4 [18076064]
J Womens Health (Larchmt). 2008 Mar;17(2):279-85 [18321179]
Int J Cancer. 2008 Sep 1;123(5):1224-5 [18537158]
BMC Infect Dis. 2008;8:85 [18577214]
Cancer Epidemiol Biomarkers Prev. 2008 Jul;17(7):1611-22 [18628412]
Cancer Lett. 2008 Sep 28;269(1):159-64 [18513854]
J Infect Dis. 2009 Jan 1;199(1):14-9 [19086814]
Int J Cancer. 2009 Apr 1;124(7):1626-36 [19115209]
Acta Virol. 2009;53(1):43-8 [19301950]
N Engl J Med. 2009 Mar 26;360(13):1298-309 [19321868]
Br J Cancer. 2009 Jul 7;101(1):202-8 [19536089]
J Clin Pathol. 2009 Oct;62(10):870-8 [19706632]
Int J Cancer. 2010 Jan 15;126(2):572-7 [19626601]
Disasters. 2011 Oct;35(4):661-79 [21913930]
Disasters. 2011 Oct;35(4):680-700 [21913931]
Int J Cancer. 2011 Dec 15;129(12):2970-5 [21462185]
J Gen Virol. 2011 Dec;92(Pt 12):2784-91 [21900420]
Sex Transm Infect. 2011 Dec;87(7):544-7 [21970896]
Virol J. 2011;8:514 [22074103]
Int J Cancer. 2012 May 1;130(9):2111-7 [21630264]
Int J Cancer. 2012 Aug 15;131(4):949-55 [21960453]
Trop Med Int Health. 2011 Nov;16(11):1432-8 [21749583]
Cancer. 2012 Sep 15;118(18):4372-84 [22252462]
Int J Cancer. 2012 Nov 15;131(10):2349-59 [22323075]
Vaccine. 2012 Nov 20;30 Suppl 5:F168-74 [23199960]
Int J Cancer. 2010 Mar 1;126(5):1187-95 [19688826]
Lancet. 2010 Jan 23;375(9711):341-5 [20109961]
AIDS Behav. 2010 Feb;14(1):11-6; dicussion 34-7 [18648926]
AIDS Behav. 2010 Feb;14(1):17-24; discussion 25-8 [19488848]
J Infect Dis. 2010 Mar;201(5):681-90 [20105077]
Lancet Oncol. 2010 Feb;11(2):165-73 [20005175]
J Adolesc Health. 2010 Apr;46(4 Suppl):S12-9 [20307839]
PLoS One. 2010;5(4):e10094 [20386706]
J Infect Dis. 2010 Jun 1;201(11):1677-85 [20415595]
BMJ. 2010;340:c3270 [20576708]
Trop Med Int Health. 2010 Aug;15(8):890-3 [20545913]
Sex Health. 2010 Sep;7(3):244-52 [20719211]
BMC Infect Dis. 2010;10:242 [20716343]
Lancet. 2010 Oct 16;376(9749):1329-37 [20851460]
Lancet Oncol. 2010 Nov;11(11):1048-56 [20952254]
Health Technol Assess. 2010 Nov;14(53):iii-iv, ix-x, 1-101 [21083999]
J Infect Dis. 2010 Dec 15;202(12):1789-99 [21067372]
Cancer Causes Control. 2010 Dec;21(12):2309-13 [20938733]
Int J Cancer. 2011 Feb 15;128(4):927-35 [20473886]
Lancet. 2011 Jan 15;377(9761):209-18 [21216000]
BMC Infect Dis. 2011;11:20 [21251265]
Int J STD AIDS. 2011 Feb;22(2):107-9 [21427434]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.vaccine.2012.07.092
ER  - 



TY  - JOUR
T1  - Prediction of the location and size of the stomach using patient characteristics for retrospective radiation dose estimation following radiotherapy
AN  - 1827911141; PQ0001754217
AB  - Following cancer radiotherapy, reconstruction of doses to organs, other than the target organ, is of interest for retrospective health risk studies. The stomach location and size are known to be highly variable between individuals, but have been little studied. In light of the poor information available to locate the stomach in historical dose reconstructions, the purpose of this work was to investigate the variability of stomach location and size among adult male patients and to develop prediction models for the stomach location and size using predictor variables generally available in medical records of radiotherapy patients treated in the past. To collect data on stomach size and position, we segmented the contours of the stomach and of the skeleton on contemporary computed tomography (CT) images for 30 male patients in supine position. Those stomachs compared with doses derived from a reference model of the body that might be used in the absence of individual CT scan data.
JF  - Physics in Medicine & Biology
AU  - Lamart, Stephanie
AU  - Imran, Rebecca
AU  - Simon, Steven L
AU  - Doi, Kazutaka
AU  - Morton, Lindsay M
AU  - Curtis, Rochelle E
AU  - Lee, Choonik
AU  - Drozdovitch, Vladimir
AU  - Maass-Moreno, Roberto
AU  - Chen, Clara C
AU  - Whatley, Millie
AU  - Miller, Donald L
AU  - Pacak, Karel
AU  - Lee, Choonsik
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, leechoonsik@mail.nih.gov
Y1  - 2013/12/21/
PY  - 2013
DA  - 2013 Dec 21
SP  - 8739
EP  - 8753
PB  - IOP Publishing, The Public Ledger Building, Suite 929 Philadelphia PA 19106 United States
VL  - 58
IS  - 24
SN  - 0031-9155, 0031-9155
KW  - Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - Radiation
KW  - medical records
KW  - Computed tomography
KW  - Radiotherapy
KW  - Stomach
KW  - Cancer
KW  - Models
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827911141?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Physics+in+Medicine+%26+Biology&rft.atitle=Prediction+of+the+location+and+size+of+the+stomach+using+patient+characteristics+for+retrospective+radiation+dose+estimation+following+radiotherapy&rft.au=Lamart%2C+Stephanie%3BImran%2C+Rebecca%3BSimon%2C+Steven+L%3BDoi%2C+Kazutaka%3BMorton%2C+Lindsay+M%3BCurtis%2C+Rochelle+E%3BLee%2C+Choonik%3BDrozdovitch%2C+Vladimir%3BMaass-Moreno%2C+Roberto%3BChen%2C+Clara+C%3BWhatley%2C+Millie%3BMiller%2C+Donald+L%3BPacak%2C+Karel%3BLee%2C+Choonsik&rft.aulast=Lamart&rft.aufirst=Stephanie&rft.date=2013-12-21&rft.volume=58&rft.issue=24&rft.spage=8739&rft.isbn=&rft.btitle=&rft.title=Physics+in+Medicine+%26+Biology&rft.issn=00319155&rft_id=info:doi/10.1088%2F0031-9155%2F58%2F24%2F8739
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-10-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Data processing; Radiation; medical records; Computed tomography; Radiotherapy; Cancer; Stomach; Models
DO  - http://dx.doi.org/10.1088/0031-9155/58/24/8739
ER  - 



TY  - JOUR
T1  - Circulating inflammation markers and prospective risk for lung cancer.
AN  - 1469649225; 24249745
AB  - Despite growing recognition of an etiologic role for inflammation in lung carcinogenesis, few prospective epidemiologic studies have comprehensively investigated the association of circulating inflammation markers with lung cancer.
          We conducted a nested case-control study (n = 526 lung cancer patients and n = 592 control subjects) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Control subjects were matched to lung cancer case patients on age, sex, follow-up time (median = 2.9 years), randomization year, and smoking (pack-years and time since quitting). Serum levels of 77 inflammation markers were measured using a Luminex bead-based assay. Conditional logistic regression and weighted Cox models were used to estimate odds ratios (ORs) and cumulative risks, respectively. Of 68 evaluable markers, 11 were statistically significantly associated with lung cancer risk (P trend across marker categories < .05), including acute-phase proteins (C-reactive protein [CRP], serum amyloid A [SAA]), proinflammatory cytokines (soluble tumor necrosis factor receptor 2 [sTNFRII]), anti-inflammatory cytokines (interleukin 1 receptor antagonist [IL-1RA]), lymphoid differentiation cytokines (interleukin 7 [IL-7]), growth factors (transforming growth factor alpha [TGF-A]), and chemokines (epithelial neutrophil-activating peptide 78 [ENA 78/CXCL5], monokine induced by gamma interferon [MIG/CXCL9], B cell-attracting chemokine 1 [BCA-1/CXCL13], thymus activation regulated chemokine [TARC/CCL17], macrophage-derived chemokine [MDC/CCL22]). Elevated marker levels were associated with increased lung cancer risk, with odds ratios comparing the highest vs the lowest group ranging from 1.47 (IL-7) to 2.27 (CRP). For IL-1RA, elevated levels were associated with decreased lung cancer risk (OR = 0.71; 95% confidence interval = 0.51 to 1.00). Associations did not differ by smoking, lung cancer histology, or latency. A cross-validated inflammation score using four independent markers (CRP, BCA-1/CXCL13, MDC/CCL22, and IL-1RA) provided good separation in 10-year lung cancer cumulative risks among former smokers (quartile [Q] 1 = 1.1% vs Q4 = 3.1%) and current smokers (Q1 = 2.3% vs Q4 = 7.9%) even after adjustment for smoking.
          Some circulating inflammation marker levels are associated with prospective lung cancer risk.
JF  - Journal of the National Cancer Institute
AU  - Shiels, Meredith S
AU  - Pfeiffer, Ruth M
AU  - Hildesheim, Allan
AU  - Engels, Eric A
AU  - Kemp, Troy J
AU  - Park, Ju-Hyun
AU  - Katki, Hormuzd A
AU  - Koshiol, Jill
AU  - Shelton, Gloriana
AU  - Caporaso, Neil E
AU  - Pinto, Ligia A
AU  - Chaturvedi, Anil K
AD  - Affiliations of authors: Infections and Immunoepidemiology Branch (MSS, AH, EAE, JK, AKC), Biostatistics Branch (RMP, HAK), and Genetic Epidemiology Branch (NEC), Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; HPV Immunology Laboratory, SAIC-Frederick Inc., Frederick, MD (TJK, GS, LAP); Department of Statistics, Dongguk University, Seoul, Korea (J-HP).
Y1  - 2013/12/18/
PY  - 2013
DA  - 2013 Dec 18
SP  - 1871
EP  - 1880
VL  - 105
IS  - 24
KW  - Biomarkers
KW  - 0
KW  - Biomarkers, Tumor
KW  - Chemokines
KW  - Cytokines
KW  - Serum Amyloid A Protein
KW  - Transforming Growth Factor alpha
KW  - C-Reactive Protein
KW  - 9007-41-4
KW  - Index Medicus
KW  - Cytokines -- blood
KW  - Odds Ratio
KW  - Serum Amyloid A Protein -- metabolism
KW  - Humans
KW  - Aged
KW  - Predictive Value of Tests
KW  - Risk Assessment
KW  - Transforming Growth Factor alpha -- blood
KW  - Prospective Studies
KW  - Logistic Models
KW  - Risk Factors
KW  - Case-Control Studies
KW  - Middle Aged
KW  - Biomarkers -- blood
KW  - C-Reactive Protein -- metabolism
KW  - Female
KW  - Male
KW  - Chemokines -- blood
KW  - Lung Neoplasms -- diagnosis
KW  - Lung Neoplasms -- blood
KW  - Inflammation -- blood
KW  - Biomarkers, Tumor -- blood
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1469649225?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Circulating+inflammation+markers+and+prospective+risk+for+lung+cancer.&rft.au=Shiels%2C+Meredith+S%3BPfeiffer%2C+Ruth+M%3BHildesheim%2C+Allan%3BEngels%2C+Eric+A%3BKemp%2C+Troy+J%3BPark%2C+Ju-Hyun%3BKatki%2C+Hormuzd+A%3BKoshiol%2C+Jill%3BShelton%2C+Gloriana%3BCaporaso%2C+Neil+E%3BPinto%2C+Ligia+A%3BChaturvedi%2C+Anil+K&rft.aulast=Shiels&rft.aufirst=Meredith&rft.date=2013-12-18&rft.volume=105&rft.issue=24&rft.spage=1871&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjt309
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-17
N1  - Date created - 2013-12-18
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Int J Cancer. 2007 Jan 1;120(1):1-6 [17058200]
Cancer Immunol Immunother. 2006 Nov;55(11):1320-9 [16453150]
J Natl Cancer Inst. 2007 May 2;99(9):715-26 [17470739]
Cancer Res. 2007 Jul 1;67(13):6520-7 [17596594]
Cancer Res. 2007 Oct 15;67(20):10019-26 [17942936]
Respir Med. 2007 Dec;101(12):2534-40 [17870458]
Int J Cancer. 2009 Mar 1;124(5):1183-7 [19058197]
Clin Chem. 2009 Feb;55(2):305-12 [19095726]
J Thorac Oncol. 2009 Mar;4(3):291-9 [19190518]
J Clin Oncol. 2009 May 1;27(13):2217-24 [19289618]
PLoS One. 2009;4(10):e7380 [19812684]
Thorax. 2010 Jan;65(1):70-6 [19996344]
Cancer Res. 2011 Oct 15;71(20):6391-9 [21900403]
JAMA. 2011 Nov 2;306(17):1865-73 [22031728]
J Thorac Oncol. 2012 Apr;7(4):698-708 [22425918]
Cancer Discov. 2011 Oct;1(5):420-9 [22586632]
PLoS One. 2012;7(8):e43075 [22912790]
Cancer. 2012 Nov 15;118(22):5630-6 [23044494]
Cell. 2010 Mar 19;140(6):883-99 [20303878]
J Clin Oncol. 2010 Jun 1;28(16):2719-26 [20421535]
Cancer Epidemiol Biomarkers Prev. 2010 Jun;19(6):1498-505 [20501758]
Cancer Epidemiol Biomarkers Prev. 2011 Apr;20(4):672-8 [21335509]
J Natl Cancer Inst. 2011 Jul 6;103(13):1058-68 [21606442]
J Natl Cancer Inst. 2011 Jul 20;103(14):1112-22 [21685357]
N Engl J Med. 2011 Aug 4;365(5):395-409 [21714641]
Cancer Epidemiol Biomarkers Prev. 2011 Sep;20(9):1902-11 [21715603]
Cancer Epidemiol Biomarkers Prev. 2011 Oct;20(10):2262-72 [21828236]
Am J Respir Crit Care Med. 2000 Jan;161(1):5-8 [10619790]
Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684]
Int J Epidemiol. 2001 Feb;30(1):118-24 [11171871]
Nature. 2002 Dec 19-26;420(6917):860-7 [12490959]
J Natl Cancer Inst. 2003 Mar 19;95(6):470-8 [12644540]
Clin Lung Cancer. 2003 Jul;5(1):46-62 [14596704]
Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1624-30 [15466979]
Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2413-8 [16214925]
Nat Clin Pract Oncol. 2005 Feb;2(2):90-7; quiz 1 p following 113 [16264881]
Am J Respir Crit Care Med. 2006 Mar 1;173(5):535-9 [16339918]
Contrib Microbiol. 2006;13:118-37 [16627962]
J Clin Oncol. 2007 Feb 10;25(5):561-70 [17290066]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/jnci/djt309
ER  - 



TY  - JOUR
T1  - The Janus Kinases Inhibitor AZD1480 Attenuates Growth of Small Cell Lung Cancers In Vitro and In Vivo
AN  - 1668253614; 20333171
AB  - Purpose: The prognosis of small cell lung cancer (SCLC) is poor, and there has been very little progress in the medical treatment of SCLC in the past two decades. We investigated the potential of Janus-activated kinases (JAK) inhibitor, AZD1480, for treatment of SCLC in vitro and in vivo.Experimental Design: JAK1 and JAK2 were inhibited by AZD1480 or siRNAs, and the effect of inhibition of JAK gene family on SCLC cell viability was evaluated. The effect of AZD1480 on cell-cycle distribution and apoptosis induction was studied. Antitumor effects of AZD1480 in tumor xenografts were assessed.Results: AZD1480 significantly inhibited growth of six out of 13 SCLC cells with IC50s ranging from 0.73 to 3.08 mu mol/L. Knocking down of JAK2 and JAK1 inhibited proliferation of Jak2-positive/Jak1-negative H82 cells and Jak1-positive/Jak2-negative GLC4 cells, respectively. Treatment of SCLC cells with AZD1480 for 24 hours resulted in an increase of 4N DNA content and histone 3 serine 10 phosphorylation, indicative of G2-M phase arrest. Moreover, SCLCs underwent apoptosis after AZD1480 treatment as exemplified by the downregulation of MCL1, the accumulation of cleaved caspase 3, cleaved PARP, and increase of annexin-V-positive cells. Finally, xenograft experiments showed that AZD1480 attenuated the growth of H82 and GLC4 tumors in mice, and we observed stronger apoptosis as well as decreased CD31-positive endothelial cells in H82 and GLC4 xenografts upon AZD1480 treatment.Conclusions: JAK inhibitor AZD1480 attenuated growth of SCLC cells in vitro and in vivo. Clinical development of anti-JAKs therapies in SCLC warrants further investigation. Clin Cancer Res; 19(24); 6777-86. [copy2013 AACR.
JF  - Clinical Cancer Research
AU  - Lee, Jih-Hsiang
AU  - Park, Kang-Seo
AU  - Alberobello, Anna Teresa
AU  - Kallakury, Bhaskar
AU  - Weng, Meng-Tzu
AU  - Wang, Yisong
AU  - Giaccone, Giuseppe
AD  - Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland; and Lombardi Comprehensive Cancer Center, Georgetown University, Washington, District of Columbia
Y1  - 2013/12/15/
PY  - 2013
DA  - 2013 Dec 15
SP  - 6777
EP  - 6786
PB  - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL  - 19
IS  - 24
SN  - 1078-0432, 1078-0432
KW  - Biotechnology and Bioengineering Abstracts
KW  - Histones
KW  - Apoptosis
KW  - Prognosis
KW  - Tumors
KW  - Gene families
KW  - Janus kinase
KW  - Endothelial cells
KW  - Phosphorylation
KW  - siRNA
KW  - Mcl-1 protein
KW  - Poly(ADP-ribose) polymerase
KW  - Janus kinase 2
KW  - Caspase-3
KW  - DNA
KW  - Xenografts
KW  - Cell proliferation
KW  - Serine
KW  - Antitumor activity
KW  - Lung cancer
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668253614?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=The+Janus+Kinases+Inhibitor+AZD1480+Attenuates+Growth+of+Small+Cell+Lung+Cancers+In+Vitro+and+In+Vivo&rft.au=Lee%2C+Jih-Hsiang%3BPark%2C+Kang-Seo%3BAlberobello%2C+Anna+Teresa%3BKallakury%2C+Bhaskar%3BWeng%2C+Meng-Tzu%3BWang%2C+Yisong%3BGiaccone%2C+Giuseppe&rft.aulast=Lee&rft.aufirst=Jih-Hsiang&rft.date=2013-12-15&rft.volume=19&rft.issue=24&rft.spage=6777&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-13-1110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Apoptosis; Histones; Prognosis; Tumors; Gene families; Janus kinase; Endothelial cells; siRNA; Phosphorylation; Poly(ADP-ribose) polymerase; Mcl-1 protein; Janus kinase 2; DNA; Caspase-3; Xenografts; Cell proliferation; Serine; Lung cancer; Antitumor activity
DO  - http://dx.doi.org/10.1158/1078-0432.CCR-13-1110
ER  - 



TY  - JOUR
T1  - Staphylococcus aureus Leukotoxin GH Promotes Formation of Neutrophil Extracellular Traps
AN  - 1551614490; 20360344
AB  - Staphylococcus aureus secretes numerous virulence factors that facilitate evasion of the host immune system. Among these molecules are pore-forming cytolytic toxins, including Panton-Valentine leukocidin (PVL), leukotoxin GH (LukGH; also known as LukAB), leukotoxin DE, and gamma -hemolysin. PVL and LukGH have potent cytolytic activity in vitro, and both toxins are proinflammatory in vivo. Although progress has been made toward elucidating the role of these toxins in S. aureus virulence, our understanding of the mechanisms that underlie the proinflammatory capacity of these toxins, as well as the associated host response toward them, is incomplete. To address this deficiency in knowledge, we assessed the ability of LukGH to prime human PMNs for enhanced bactericidal activity and further investigated the impact of the toxin on neutrophil function. We found that, unlike PVL, LukGH did not prime human neutrophils for increased production of reactive oxygen species nor did it enhance binding and/or uptake of S. aureus. Unexpectedly, LukGH promoted the release of neutrophil extracellular traps (NETs), which, in turn, ensnared but did not kill S. aureus. Furthermore, we found that electropermeabilization of human neutrophils, used as a separate means to create pores in the neutrophil plasma membrane, similarly induced formation of NETs, a finding consistent with the notion that NETs can form during nonspecific cytolysis. We propose that the ability of LukGH to promote formation of NETs contributes to the inflammatory response and host defense against S. aureus infection.
JF  - Journal of Immunology
AU  - Malachowa, Natalia
AU  - Kobayashi, Scott D
AU  - Freedman, Brett
AU  - Dorward, David W
AU  - DeLeo, Frank R
AD  - Laboratory of Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; and
Y1  - 2013/12/15/
PY  - 2013
DA  - 2013 Dec 15
SP  - 6022
EP  - 6029
PB  - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States
VL  - 191
IS  - 12
SN  - 0022-1767, 0022-1767
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Growth hormone
KW  - leukocidin
KW  - virulence factors
KW  - Immune system
KW  - Leukocytes (neutrophilic)
KW  - Infection
KW  - Toxins
KW  - Inflammation
KW  - Pores
KW  - Cytolytic activity
KW  - Reactive oxygen species
KW  - Plasma membranes
KW  - Cytolysis
KW  - Staphylococcus aureus
KW  - Bactericidal activity
KW  - F 06910:Microorganisms & Parasites
KW  - J 02340:Antibiotics & Antimicrobials
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551614490?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=Staphylococcus+aureus+Leukotoxin+GH+Promotes+Formation+of+Neutrophil+Extracellular+Traps&rft.au=Malachowa%2C+Natalia%3BKobayashi%2C+Scott+D%3BFreedman%2C+Brett%3BDorward%2C+David+W%3BDeLeo%2C+Frank+R&rft.aulast=Malachowa&rft.aufirst=Natalia&rft.date=2013-12-15&rft.volume=191&rft.issue=12&rft.spage=6022&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1301821
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-10-02
N1  - SubjectsTermNotLitGenreText - Growth hormone; virulence factors; leukocidin; Immune system; Leukocytes (neutrophilic); Infection; Toxins; Inflammation; Pores; Cytolytic activity; Plasma membranes; Reactive oxygen species; Cytolysis; Bactericidal activity; Staphylococcus aureus
DO  - http://dx.doi.org/10.4049/jimmunol.1301821
ER  - 



TY  - CPAPER
T1  - Mechanical and structural properties of nonmuscle myosin II molecules and a novel interacting protein
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510100616; 6279426
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Billington, Neil
AU  - Sellers, James
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Myosin
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510100616?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Mechanical+and+structural+properties+of+nonmuscle+myosin+II+molecules+and+a+novel+interacting+protein&rft.au=Billington%2C+Neil%3BSellers%2C+James&rft.aulast=Billington&rft.aufirst=Neil&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Dynamic clonal analysis of murine hematopoietic stem and progenitor cells marked by 5 fluorescent proteins using confocal and multiphoton microscopy
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510100150; 6279688
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Malide, D
AU  - Metais, J-Y
AU  - Dunbar, C
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Microscopy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510100150?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Dynamic+clonal+analysis+of+murine+hematopoietic+stem+and+progenitor+cells+marked+by+5+fluorescent+proteins+using+confocal+and+multiphoton+microscopy&rft.au=Malide%2C+D%3BMetais%2C+J-Y%3BDunbar%2C+C&rft.aulast=Malide&rft.aufirst=D&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - A novel M2-like macrophage mediated intracellular collagen degradation pathway identified by intravital imaging
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510099750; 6279692
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Madsen, D
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Degradation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510099750?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=A+novel+M2-like+macrophage+mediated+intracellular+collagen+degradation+pathway+identified+by+intravital+imaging&rft.au=Madsen%2C+D&rft.aulast=Madsen&rft.aufirst=D&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Mitophagy: how autophagosomes recogize and engulf damaged mitochondria
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510097005; 6279415
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Youle, Richard
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Mitochondria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510097005?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Mitophagy%3A+how+autophagosomes+recogize+and+engulf+damaged+mitochondria&rft.au=Youle%2C+Richard&rft.aulast=Youle&rft.aufirst=Richard&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Pericentrin regulates centrosome asymmetry in neuroblasts by suppressing interphase centrosome function
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510095900; 6279444
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Lerit, Dorothy
AU  - Rusan, Nasser
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Centrosomes
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095900?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Pericentrin+regulates+centrosome+asymmetry+in+neuroblasts+by+suppressing+interphase+centrosome+function&rft.au=Lerit%2C+Dorothy%3BRusan%2C+Nasser&rft.aulast=Lerit&rft.aufirst=Dorothy&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Nuclear architecture, chromatin and epigenetics/ career paths
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510095685; 6279648
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Misteli, Tom
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Careers
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095685?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Nuclear+architecture%2C+chromatin+and+epigenetics%2F+career+paths&rft.au=Misteli%2C+Tom&rft.aulast=Misteli&rft.aufirst=Tom&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Epigenetics of chromosomal breakage sites and translocations
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510095545; 6279586
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Burman, B
AU  - Burgess, R
AU  - Zhang, Z
AU  - Lieb, J
AU  - Misteli, T
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Translocation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095545?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Epigenetics+of+chromosomal+breakage+sites+and+translocations&rft.au=Burman%2C+B%3BBurgess%2C+R%3BZhang%2C+Z%3BLieb%2C+J%3BMisteli%2C+T&rft.aulast=Burman&rft.aufirst=B&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Generation of compartmentalized pressure by a nuclear piston drives 3D cell motility
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510095346; 6279669
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Petrie, R
AU  - Koo, H
AU  - Doyle, A
AU  - Yamada, K
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Cell migration
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095346?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Generation+of+compartmentalized+pressure+by+a+nuclear+piston+drives+3D+cell+motility&rft.au=Petrie%2C+R%3BKoo%2C+H%3BDoyle%2C+A%3BYamada%2C+K&rft.aulast=Petrie&rft.aufirst=R&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - A novel matrix-specific mechanism of active RhoA suppression is required for 3D collagen migration
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510095176; 6279615
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Kutys, M
AU  - Yamada, K
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Migration
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095176?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=A+novel+matrix-specific+mechanism+of+active+RhoA+suppression+is+required+for+3D+collagen+migration&rft.au=Kutys%2C+M%3BYamada%2C+K&rft.aulast=Kutys&rft.aufirst=M&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Two distinct populations of vinculin molecules interact with paxillin and talin at focal adhesions
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510095148; 6279501
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Case, L
AU  - Shtengel, G
AU  - Baird, M
AU  - Davidson, M
AU  - Campbell, S
AU  - Hess, H
AU  - Waterman, C
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Adhesion
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095148?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Two+distinct+populations+of+vinculin+molecules+interact+with+paxillin+and+talin+at+focal+adhesions&rft.au=Case%2C+L%3BShtengel%2C+G%3BBaird%2C+M%3BDavidson%2C+M%3BCampbell%2C+S%3BHess%2C+H%3BWaterman%2C+C&rft.aulast=Case&rft.aufirst=L&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Physics and the future of cell biology
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510094983; 6279336
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Lippincott-Schwartz, Jennifer
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Cytology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094983?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Physics+and+the+future+of+cell+biology&rft.au=Lippincott-Schwartz%2C+Jennifer&rft.aulast=Lippincott-Schwartz&rft.aufirst=Jennifer&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - TFE3 is activated in response to nutrient deprivation and regulates autophagy, lysosomal biogenesis, and cellular clearance
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510094934; 6279522
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Martina, J
AU  - Diab, H
AU  - Li, L.
AU  - Lim, J-A
AU  - Patange, S
AU  - Raben, N
AU  - Puertollano, R
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Biogenesis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094934?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=TFE3+is+activated+in+response+to+nutrient+deprivation+and+regulates+autophagy%2C+lysosomal+biogenesis%2C+and+cellular+clearance&rft.au=Martina%2C+J%3BDiab%2C+H%3BLi%2C+L.%3BLim%2C+J-A%3BPatange%2C+S%3BRaben%2C+N%3BPuertollano%2C+R&rft.aulast=Martina&rft.aufirst=J&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Secretory pathways, Golgi, mitochondria, autophagy, super resolution imaging, HIV budding, actin cytoskeleton
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510094931; 6279479
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Lippincott-Schwartz, Jennifer
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Human immunodeficiency virus
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094931?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Secretory+pathways%2C+Golgi%2C+mitochondria%2C+autophagy%2C+super+resolution+imaging%2C+HIV+budding%2C+actin+cytoskeleton&rft.au=Lippincott-Schwartz%2C+Jennifer&rft.aulast=Lippincott-Schwartz&rft.aufirst=Jennifer&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - A novel splice isoform of the actin-regulatory protein Spire1 regulates mitochondria morphology
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510094877; 6279517
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Manor, U
AU  - Bartholomew, S
AU  - Higgs, H
AU  - Spudich, J
AU  - Lippincott-Schwartz, J
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Morphology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094877?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=A+novel+splice+isoform+of+the+actin-regulatory+protein+Spire1+regulates+mitochondria+morphology&rft.au=Manor%2C+U%3BBartholomew%2C+S%3BHiggs%2C+H%3BSpudich%2C+J%3BLippincott-Schwartz%2C+J&rft.aulast=Manor&rft.aufirst=U&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Endocytic machinery regulates viral replication through remodeling the host cell cholesterol landscape
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510091879; 6279489
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Altan-Bonnet, N
AU  - Ilnytska, O
AU  - Santiana, M
AU  - Chen, Y-H
AU  - Hsu, N-Y
AU  - Du, W-L
AU  - Belov, G
AU  - Viktorova, E
AU  - Moore, C
AU  - Dixon, J
AU  - Brinker, A
AU  - Storch, J
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Cholesterol
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091879?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=Endocytic+machinery+regulates+viral+replication+through+remodeling+the+host+cell+cholesterol+landscape&rft.au=Altan-Bonnet%2C+N%3BIlnytska%2C+O%3BSantiana%2C+M%3BChen%2C+Y-H%3BHsu%2C+N-Y%3BDu%2C+W-L%3BBelov%2C+G%3BViktorova%2C+E%3BMoore%2C+C%3BDixon%2C+J%3BBrinker%2C+A%3BStorch%2C+J&rft.aulast=Altan-Bonnet&rft.aufirst=N&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - A Coxiella burnetii effector protein subverts clathrin-mediated vesicular trafficking for pathogen vacuole biogenesis
T2  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AN  - 1510091778; 6279492
JF  - 2013 Annual Meeting of The American Society for Cell Biology (ASCB 2013)
AU  - Larson, C
AU  - Beare, P
AU  - Howe, D
AU  - Heinzen, R
Y1  - 2013/12/14/
PY  - 2013
DA  - 2013 Dec 14
KW  - Pathogens
KW  - Coxiella burnetii
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091778?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.atitle=A+Coxiella+burnetii+effector+protein+subverts+clathrin-mediated+vesicular+trafficking+for+pathogen+vacuole+biogenesis&rft.au=Larson%2C+C%3BBeare%2C+P%3BHowe%2C+D%3BHeinzen%2C+R&rft.aulast=Larson&rft.aufirst=C&rft.date=2013-12-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+The+American+Society+for+Cell+Biology+%28ASCB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ascb.org/meetings/program/web/files/assets/common/downloads/2013%20Complete%20Annual%20Meeting%20Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - JOUR
T1  - Personal history of prostate cancer and increased risk of incident melanoma in the United States.
AN  - 1466372146; 24190118
AB  - Steroid hormones, particularly androgens, play a major role in prostatic carcinogenesis. Personal history of severe acne, a surrogate for higher androgen activity, has been associated with an increased risk of prostate cancer (PCa), and one recent study indicated that severe teenage acne was a novel risk factor for melanoma. These findings suggest a possible relationship between PCa and risk of melanoma. We prospectively evaluated this association among US men.
          A total of 42,372 participants in the Health Professionals' Follow-Up Study (HPFS; 1986 to 2010) were included. Biennially self-reported PCa diagnosis was confirmed using pathology reports. Diagnosis of melanoma and nonmelanoma skin cancer (NMSC) was self-reported biennially, and diagnosis of melanoma was pathologically confirmed. We sought to confirm the association in 18,603 participants from the Physicians' Health Study (PHS; 1982 to 1998). We identified 539 melanomas in the HPFS. Personal history of PCa was associated with an increased risk of melanoma (multivariate-adjusted hazard ratio [HR], 1.83; 95% CI, 1.32 to 2.54). Although we also detected a marginally increased risk of NMSC associated with PCa (HR, 1.08; 95% CI, 0.995 to 1.16), the difference in the magnitude of the association between melanoma and NMSC was significant (P for heterogeneity = .002). We did not find an altered risk of melanoma associated with personal history of other cancers. The association between PCa and risk of incident melanoma was confirmed in the PHS (HR, 2.17; 95% CI, 1.12 to 4.21). Personal history of PCa is associated with an increased risk of melanoma, which may not be entirely a result of greater medical scrutiny.
JF  - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU  - Li, Wen-Qing
AU  - Qureshi, Abrar A
AU  - Ma, Jing
AU  - Goldstein, Alisa M
AU  - Giovannucci, Edward L
AU  - Stampfer, Meir J
AU  - Han, Jiali
AD  - Wen-Qing Li and Alisa M. Goldstein, National Cancer Institute, National Institutes of Health, Rockville, MD; Wen-Qing Li, Abrar A. Qureshi, Jing Ma, Edward L. Giovannucci, Meir J. Stampfer, and Jiali Han, Brigham and Women's Hospital, Harvard Medical School; Edward L. Giovannucci and Meir J. Stampfer, Harvard School of Public Health, Boston, MA; Jiali Han, Richard M. Fairbanks School of Public Health, Simon Cancer Center, Indiana University, Indianapolis, IN; and Jiali Han, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Y1  - 2013/12/10/
PY  - 2013
DA  - 2013 Dec 10
SP  - 4394
EP  - 4399
VL  - 31
IS  - 35
KW  - Index Medicus
KW  - Humans
KW  - Aged
KW  - Risk Assessment -- statistics & numerical data
KW  - Acne Vulgaris -- epidemiology
KW  - Risk Assessment -- methods
KW  - Comorbidity
KW  - Health Personnel -- statistics & numerical data
KW  - Risk Factors
KW  - Adult
KW  - Surveys and Questionnaires
KW  - Incidence
KW  - Follow-Up Studies
KW  - Middle Aged
KW  - United States -- epidemiology
KW  - Male
KW  - Prostatic Neoplasms -- epidemiology
KW  - Skin Neoplasms -- epidemiology
KW  - Melanoma -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1466372146?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Personal+history+of+prostate+cancer+and+increased+risk+of+incident+melanoma+in+the+United+States.&rft.au=Li%2C+Wen-Qing%3BQureshi%2C+Abrar+A%3BMa%2C+Jing%3BGoldstein%2C+Alisa+M%3BGiovannucci%2C+Edward+L%3BStampfer%2C+Meir+J%3BHan%2C+Jiali&rft.aulast=Li&rft.aufirst=Wen-Qing&rft.date=2013-12-10&rft.volume=31&rft.issue=35&rft.spage=4394&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.2013.51.1915
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-14
N1  - Date created - 2013-12-09
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Natl Cancer Inst. 1993 Oct 6;85(19):1571-9 [8105097]
Am J Epidemiol. 1986 May;123(5):894-900 [3962971]
J Natl Cancer Inst. 1996 Aug 21;88(16):1118-26 [8757191]
Int J Cancer. 2007 Dec 15;121(12):2688-92 [17724724]
J Natl Cancer Inst. 2008 Feb 6;100(3):170-83 [18230794]
Med Chem. 2008 Mar;4(2):100-5 [18336327]
Blood. 2009 Sep 10;114(11):2236-43 [19561322]
Lancet Oncol. 2010 Feb;11(2):155-64 [20004617]
J Biol Chem. 2010 Apr 2;285(14):10472-6 [20110352]
J Am Acad Dermatol. 2010 May;62(5):757-67 [20223559]
Nat Med. 2010 Jul;16(7):793-8 [20526349]
J Natl Cancer Inst. 2011 Jun 8;103(11):876-84 [21586702]
J Clin Oncol. 2011 Sep 20;29(27):3677-85 [21825260]
Urology. 2011 Oct;78(4):970.e15-20 [21820706]
Cancer Res. 2011 Nov 1;71(21):6758-63 [22028319]
JAMA. 2011 Dec 7;306(21):2359-66 [22147380]
Arch Dermatol. 2011 Dec;147(12):1395-402 [22184761]
Lancet. 2012 Jan 28;379(9813):361-72 [21880356]
Nat Rev Cancer. 2012 Apr;12(4):289-97 [22378189]
Cancer Epidemiol Biomarkers Prev. 2012 Aug;21(8):1319-29 [22828207]
Eur J Cancer Prev. 2012 Nov;21(6):552-9 [22433633]
CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087]
Aging (Albany NY). 2013 Jan;5(1):3-17 [23363843]
Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):528-32 [23549396]
Nat Rev Clin Oncol. 2013 May;10(5):289-301 [23529000]
N Engl J Med. 1989 Jul 20;321(3):129-35 [2664509]
Am J Clin Nutr. 2000 Jan;71(1):135-41 [10617958]
J Natl Cancer Inst Monogr. 2000;(27):39-66 [10963619]
Cancer Res. 2002 Jul 15;62(14):3992-6 [12124332]
J Surg Res. 2003 Apr;110(2):393-8 [12788670]
Physiol Rev. 2004 Oct;84(4):1155-228 [15383650]
Lancet. 1980 Mar 15;1(8168 Pt 1):562-4 [6102285]
Ann Epidemiol. 1992 May;2(3):231-9 [1342273]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1200/JCO.2013.51.1915
ER  - 



TY  - JOUR
T1  - Prediction of nanoparticle prodrug metabolism by pharmacokinetic modeling of biliary excretion.
AN  - 1448221607; 23664969
AB  - Pharmacokinetic modeling and simulation is a powerful tool for the prediction of drug concentrations in the absence of analytical techniques that allow for direct quantification. The present study applied this modeling approach to determine active drug release from a nanoparticle prodrug formulation. A comparative pharmacokinetic study of a nanoscale micellar docetaxel (DTX) prodrug, Procet 8, and commercial DTX formulation, Taxotere, was conducted in bile duct cannulated rats. The nanoscale (~40nm) size of the Procet 8 formulation resulted in confinement within the plasma space and high prodrug plasma concentrations. Ex vivo prodrug hydrolysis during plasma sample preparation resulted in unacceptable error that precluded direct measurement of DTX concentrations. Pharmacokinetic modeling of Taxotere and Procet 8 plasma concentrations, and their associated biliary metabolites, allowed for prediction of the DTX concentration profile and DTX bioavailability, and thereby evaluation of Procet 8 metabolism. Procet 8 plasma decay and in vitro plasma hydrolytic rates were identical, suggesting that systemic clearance of the prodrug was primarily metabolic. The Procet 8 and Taxotere plasma profiles, and associated docetaxel hydroxy-tert-butyl carbamate (HDTX) metabolite biliary excretion, were best fit by a two compartment model, with both linear and non-linear DTX clearance, and first order Procet 8 hydrolysis. The model estimated HDTX clearance rate agreed with in vitro literature values, supporting the predictability of the proposed model. Model simulation at the 10mg DTX equivalent/kg dose level predicted DTX formation rate-limited kinetics and a peak plasma DTX concentration of 39ng/mL at 4h for Procet 8, in comparison to 2826ng/mL for Taxotere. As a result of nonlinear DTX clearance, the DTX AUCinf for the Procet 8 formulation was predicted to be 2.6 times lower than Taxotere (775 vs. 2017h×ng/mL, respectively), resulting in an absolute bioavailability estimate of 38%. As DTX clearance in man is considered linear, this low bioavailability is likely species-dependent. These data support the use of pharmacokinetic modeling and simulation in cases of complex formulations, where analytical methods for direct measurement of free (released) drug concentrations are unavailable. Uses of such models may include interpretation of preclinical toxicology studies, selection of first in man dosing regimens, and PK/PD model development. 
          Copyright © 2013 Elsevier B.V. All rights reserved.
JF  - Journal of controlled release : official journal of the Controlled Release Society
AU  - Stern, Stephan T
AU  - Zou, Peng
AU  - Skoczen, Sarah
AU  - Xie, Sherwin
AU  - Liboiron, Barry
AU  - Harasym, Troy
AU  - Tardi, Paul
AU  - Mayer, Lawrence D
AU  - McNeil, Scott E
AD  - Nanotechnology Characterization Laboratory, Advanced Technology Program, SAIC-Frederick Inc., Frederick National Lab for Cancer Research, Frederick, 21702, USA. Electronic address: sternstephan@mail.nih.gov.
Y1  - 2013/12/10/
PY  - 2013
DA  - 2013 Dec 10
SP  - 558
EP  - 567
VL  - 172
IS  - 2
KW  - Antineoplastic Agents
KW  - 0
KW  - Micelles
KW  - Prodrugs
KW  - Taxoids
KW  - docetaxel
KW  - 15H5577CQD
KW  - Index Medicus
KW  - Biliary clearance
KW  - Pharmacokinetic modeling and simulation
KW  - Nanomicellar prodrug
KW  - Rats
KW  - Animals
KW  - Rats, Sprague-Dawley
KW  - Computer Simulation
KW  - Kinetics
KW  - Models, Biological
KW  - Hydrolysis
KW  - Male
KW  - Female
KW  - Taxoids -- pharmacokinetics
KW  - Nanoparticles -- metabolism
KW  - Antineoplastic Agents -- pharmacokinetics
KW  - Taxoids -- metabolism
KW  - Antineoplastic Agents -- metabolism
KW  - Prodrugs -- pharmacokinetics
KW  - Bile -- metabolism
KW  - Prodrugs -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448221607?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.atitle=Prediction+of+nanoparticle+prodrug+metabolism+by+pharmacokinetic+modeling+of+biliary+excretion.&rft.au=Stern%2C+Stephan+T%3BZou%2C+Peng%3BSkoczen%2C+Sarah%3BXie%2C+Sherwin%3BLiboiron%2C+Barry%3BHarasym%2C+Troy%3BTardi%2C+Paul%3BMayer%2C+Lawrence+D%3BMcNeil%2C+Scott+E&rft.aulast=Stern&rft.aufirst=Stephan&rft.date=2013-12-10&rft.volume=172&rft.issue=2&rft.spage=558&rft.isbn=&rft.btitle=&rft.title=Journal+of+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.issn=1873-4995&rft_id=info:doi/10.1016%2Fj.jconrel.2013.04.025
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-30
N1  - Date created - 2013-11-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Chemother Pharmacol. 1999;44(6):469-74 [10550567]
Ther Deliv. 2011 May;2(5):643-72 [21837267]
Drug Metab Dispos. 2004 Jun;32(6):666-74 [15155559]
Eur J Pharm Biopharm. 2004 Jul;58(1):151-9 [15207549]
Cancer Res. 1993 Mar 1;53(5):1037-42 [8094996]
Anal Biochem. 1995 Dec 10;232(2):149-57 [8747469]
Clin Pharmacokinet. 1999 Feb;36(2):99-114 [10092957]
Bioconjug Chem. 2004 Nov-Dec;15(6):1364-75 [15546204]
Cancer Chemother Pharmacol. 2005 May;55(5):497-501 [15711828]
Cancer Chemother Pharmacol. 2005 Sep;56(3):299-306 [15864592]
J Control Release. 2005 Dec 10;110(1):90-102 [16271793]
Bioconjug Chem. 2006 Nov-Dec;17(6):1432-40 [17105221]
Toxicol Appl Pharmacol. 2008 May 15;229(1):121-34 [18355886]
Cancer Chemother Pharmacol. 2009 May;63(6):1035-48 [18791717]
Cancer Chemother Pharmacol. 2009 May;63(6):1049-63 [18791718]
Biol Pharm Bull. 2009 May;32(5):921-7 [19420765]
AAPS J. 2009 Jun;11(2):262-76 [19408130]
Biomaterials. 2010 Apr;31(11):3043-53 [20122727]
J Control Release. 2010 Sep 1;146(2):164-74 [20385183]
Cancer Res. 2011 Apr 15;71(8):3018-28 [21363913]
Sci Transl Med. 2012 Apr 4;4(128):128ra39 [22491949]
J Control Release. 2001 Jul 6;74(1-3):243-7 [11489501]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.jconrel.2013.04.025
ER  - 



TY  - JOUR
T1  - Understanding the correlation between in vitro and in vivo immunotoxicity tests for nanomedicines.
AN  - 1448221331; 23742883
AB  - Preclinical characterization of novel nanotechnology-based formulations is often challenged by physicochemical characteristics, sterility/sterilization issues, safety and efficacy. Such challenges are not unique to nanomedicine, as they are common in the development of small and macromolecular drugs. However, due to the lack of a general consensus on critical characterization parameters, a shortage of harmonized protocols to support testing, and the vast variety of engineered nanomaterials, the translation of nanomedicines into clinic is particularly complex. Understanding the immune compatibility of nanoformulations has been identified as one of the important factors in (pre)clinical development and requires reliable in vitro and in vivo immunotoxicity tests. The generally low sensitivity of standard in vivo toxicity tests to immunotoxicities, inter-species variability in the structure and function of the immune system, high costs and relatively low throughput of in vivo tests, and ethical concerns about animal use underscore the need for trustworthy in vitro assays. Here, we consider the correlation (or lack thereof) between in vitro and in vivo immunotoxicity tests as a mean to identify useful in vitro assays. We review literature examples and case studies from the experience of the NCI Nanotechnology Characterization Lab, and highlight assays where predictability has been demonstrated for a variety of nanomaterials and assays with high potential for predictability in vivo. Copyright © 2013 Elsevier B.V. All rights reserved.
JF  - Journal of controlled release : official journal of the Controlled Release Society
AU  - Dobrovolskaia, Marina A
AU  - McNeil, Scott E
AD  - Nanotechnology Characterization Laboratory, Advanced Technology Program, SAIC-Frederick Inc., NCI-Frederick, Frederick, MD 21702, USA.
Y1  - 2013/12/10/
PY  - 2013
DA  - 2013 Dec 10
SP  - 456
EP  - 466
VL  - 172
IS  - 2
KW  - Cytokines
KW  - 0
KW  - Index Medicus
KW  - Disseminated intravascular coagulation
KW  - Coagulopathy
KW  - Anaphylaxis
KW  - Complement activation
KW  - Hemolysis
KW  - Phagocytosis
KW  - Nanoparticles
KW  - Thrombosis
KW  - Procoagulant activity
KW  - Thrombosis -- chemically induced
KW  - Animals
KW  - Humans
KW  - Nanomedicine -- methods
KW  - Cytokines -- immunology
KW  - Complement Activation -- drug effects
KW  - Phagocytosis -- drug effects
KW  - Drug Evaluation, Preclinical -- methods
KW  - Cytotoxicity Tests, Immunologic -- methods
KW  - Nanostructures -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448221331?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.atitle=Understanding+the+correlation+between+in+vitro+and+in+vivo+immunotoxicity+tests+for+nanomedicines.&rft.au=Dobrovolskaia%2C+Marina+A%3BMcNeil%2C+Scott+E&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2013-12-10&rft.volume=172&rft.issue=2&rft.spage=456&rft.isbn=&rft.btitle=&rft.title=Journal+of+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.issn=1873-4995&rft_id=info:doi/10.1016%2Fj.jconrel.2013.05.025
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-30
N1  - Date created - 2013-11-01
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.jconrel.2013.05.025
ER  - 



TY  - JOUR
T1  - Perinatal toxicity and carcinogenicity studies of styrene-acrylonitrile trimer, a ground water contaminant.
AN  - 1459561326; 24060431
AB  - Styrene acrylonitrile (SAN) trimer is a by-product in the production of acrylonitrile styrene plastics. Following a report of a childhood cancer cluster in the Toms River section of Dover Township, New Jersey, SAN Trimer was identified as one of the groundwater contaminants at Reich Farm Superfund site in the township. The contaminants from the Reich Farm site's ground water plume impacted two wells at the Parkway well field. The National Toxicology Program (NTP) studied the toxicity and carcinogenicity of SAN Trimer in rats exposed during their perinatal developmental period and adulthood. The chronic toxicity and carcinogenicity studies in F344/N rats were preceded by 7- and 18-week perinatal toxicity studies to determine the exposure concentrations for the 2-year studies. Subsequently, Fisher 344 pregnant dams were exposed to SAN Trimer containing diet at 400, 800, or 1600ppm concentrations during gestation, nursing and weaning periods of offspring followed by two year of adult exposures to both male and female pups. There was no statistically significant evidence of carcinogenic activity following SAN-Trimer exposure; however, rare neoplasms in the brain and spinal cord were observed in males and to lesser extent in female rats. These incidences were considered within the range of historical background in the animal model used in the current studies. Therefore, the presence of a few rarely occurring CNS tumors in the treated groups were not judged to be associated with the SAN Trimer exposure. The major finding was a dose-related peripheral neuropathy associated with the sciatic nerves in females and spinal nerve roots in males and females thereby suggesting that SAN Trimer is potentially a nervous system toxicant. Published by Elsevier Ireland Ltd.
JF  - Toxicology
AU  - Behl, Mamta
AU  - Elmore, Susan A
AU  - Malarkey, David E
AU  - Hejtmancik, Milton R
AU  - Gerken, Diane K
AU  - Chhabra, Rajendra S
AD  - Kelly Government Solutions, Research Triangle Park, NC, USA; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: behlmv@niehs.nih.gov.
Y1  - 2013/12/06/
PY  - 2013
DA  - 2013 Dec 06
SP  - 84
EP  - 94
VL  - 314
IS  - 1
KW  - Mutagens
KW  - 0
KW  - Water Pollutants, Chemical
KW  - Styrene
KW  - 44LJ2U959V
KW  - Acrylonitrile
KW  - MP1U0D42PE
KW  - Index Medicus
KW  - Rats
KW  - Developmental
KW  - Styrene acrylonitrile trimer
KW  - Toxicity
KW  - Cancer
KW  - Eating -- drug effects
KW  - Animals
KW  - Pregnancy
KW  - Prenatal Exposure Delayed Effects -- pathology
KW  - Spinal Nerve Roots -- pathology
KW  - Rats, Inbred F344
KW  - Body Weight -- drug effects
KW  - Diet
KW  - Sciatic Nerve -- pathology
KW  - Female
KW  - Growth -- drug effects
KW  - Male
KW  - Survival Analysis
KW  - Groundwater -- chemistry
KW  - Water Pollutants, Chemical -- toxicity
KW  - Acrylonitrile -- toxicity
KW  - Styrene -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1459561326?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Perinatal+toxicity+and+carcinogenicity+studies+of+styrene-acrylonitrile+trimer%2C+a+ground+water+contaminant.&rft.au=Behl%2C+Mamta%3BElmore%2C+Susan+A%3BMalarkey%2C+David+E%3BHejtmancik%2C+Milton+R%3BGerken%2C+Diane+K%3BChhabra%2C+Rajendra+S&rft.aulast=Behl&rft.aufirst=Mamta&rft.date=2013-12-06&rft.volume=314&rft.issue=1&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2013.09.006
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-14
N1  - Date created - 2013-11-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Ann N Y Acad Sci. 1982;381:304-19 [6953796]
J Gerontol. 1985 Nov;40(6):657-70 [4056321]
J Gerontol. 1985 Nov;40(6):671-88 [4056322]
J Natl Cancer Inst. 1986 Feb;76(2):283-9 [3456066]
Biometrics. 1988 Jun;44(2):417-31 [3390507]
J Expo Anal Environ Epidemiol. 1999 May-Jun;9(3):200-16 [10412669]
Int J Hyg Environ Health. 2005;208(1-2):45-54 [15881978]
Toxicol Lett. 2008 Apr 21;178(1):1-8 [18384980]
Environ Mol Mutagen. 2012 Apr;53(3):227-38 [22351108]
Natl Toxicol Program Tech Rep Ser. 2012 Jul;(573):1-155 [22837102]
Toxicol Pathol. 2000 Jan-Feb;28(1):202-14 [10669008]
Biometrics. 1971 Mar;27(1):103-17 [5547548]
Biometrics. 1972 Jun;28(2):519-31 [5037867]
Vet Pathol. 1981 Jan;18(1):110-3 [7467059]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.tox.2013.09.006
ER  - 



TY  - JOUR
T1  - Role of the bed nucleus of the stria terminalis in cardiovascular changes following chronic treatment with cocaine and testosterone: a role beyond drug seeking in addiction?
AN  - 1448216269; 23994153
AB  - Neural plasticity has been observed in the bed nucleus of the stria terminalis (BNST) following exposure to both cocaine and androgenic-anabolic steroids. Here we investigated the involvement of the BNST on changes in cardiovascular function and baroreflex activity following either single or combined administration of cocaine and testosterone for 10 consecutive days in rats. Single administration of testosterone increased values of arterial pressure, evoked rest bradycardia and reduced baroreflex-mediated bradycardia. These effects of testosterone were not affected by BNST inactivation caused by local bilateral microinjections of the nonselective synaptic blocker CoCl2. The single administration of cocaine as well as the combined treatment with testosterone and cocaine increased both bradycardiac and tachycardiac responses of the baroreflex. Cocaine-evoked baroreflex changes were totally reversed after BNST inactivation. However, BNST inhibition in animals subjected to combined treatment with cocaine and testosterone reversed only the increase in reflex tachycardia, whereas facilitation of reflex bradycardia was not affected by local BNST treatment with CoCl2. In conclusion, the present study provides the first direct evidence that the BNST play a role in cardiovascular changes associated with drug abuse. Our findings suggest that alterations in cardiovascular function following subchronic exposure to cocaine are mediated by neural plasticity in the BNST. The single treatment with cocaine and the combined administration of testosterone and cocaine had similar effects on baroreflex activity, however the association with testosterone inhibited cocaine-induced changes in the BNST control of reflex bradycardia. Testosterone-induced cardiovascular changes seem to be independent of the BNST. Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
JF  - Neuroscience
AU  - Cruz, F C
AU  - Alves, F H F
AU  - Leão, R M
AU  - Planeta, C S
AU  - Crestani, C C
AD  - Laboratory of Pharmacology, Department of Natural Active Principles and Toxicology, School of Pharmaceutical Sciences, Univ. Estadual Paulista - UNESP, Araraquara, SP 14801-902, Brazil; Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, US National Institutes of Health, Department of Health and Human Services, Baltimore, MD, USA.
Y1  - 2013/12/03/
PY  - 2013
DA  - 2013 Dec 03
SP  - 29
EP  - 39
VL  - 253
KW  - Androgens
KW  - 0
KW  - Dopamine Uptake Inhibitors
KW  - Testosterone
KW  - 3XMK78S47O
KW  - Cocaine
KW  - I5Y540LHVR
KW  - Index Medicus
KW  - testosterone
KW  - cocaine
KW  - vehicle
KW  - BNST
KW  - AAS
KW  - HR
KW  - bed nucleus of the stria terminalis
KW  - mean arterial pressure
KW  - androgenic-anabolic steroids
KW  - steroids
KW  - MAP
KW  - baroreflex
KW  - T
KW  - veh
KW  - ANOVA
KW  - heart rate
KW  - addiction
KW  - analysis of variance
KW  - coc
KW  - extended amygdala
KW  - Rats
KW  - Animals
KW  - Heart Rate -- drug effects
KW  - Analysis of Variance
KW  - Baroreflex -- drug effects
KW  - Dose-Response Relationship, Drug
KW  - Rats, Wistar
KW  - Blood Pressure -- drug effects
KW  - Male
KW  - Testosterone -- pharmacology
KW  - Septal Nuclei -- physiology
KW  - Cardiovascular System -- drug effects
KW  - Androgens -- pharmacology
KW  - Septal Nuclei -- drug effects
KW  - Cocaine -- pharmacology
KW  - Dopamine Uptake Inhibitors -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448216269?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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&rft.atitle=Role+of+the+bed+nucleus+of+the+stria+terminalis+in+cardiovascular+changes+following+chronic+treatment+with+cocaine+and+testosterone%3A+a+role+beyond+drug+seeking+in+addiction%3F&rft.au=Cruz%2C+F+C%3BAlves%2C+F+H+F%3BLe%C3%A3o%2C+R+M%3BPlaneta%2C+C+S%3BCrestani%2C+C+C&rft.aulast=Cruz&rft.aufirst=F&rft.date=2013-12-03&rft.volume=253&rft.issue=&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=1873-7544&rft_id=info:doi/10.1016%2Fj.neuroscience.2013.08.034
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-19
N1  - Date created - 2013-11-01
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.neuroscience.2013.08.034
ER  - 



TY  - JOUR
T1  - Safety and tolerability of a live oral Salmonella typhimurium vaccine candidate in SIV-infected nonhuman primates
AN  - 1732836287; 19722948
AB  - Nontyphoidal Salmonella (NTS) serovars are a common cause of acute food-borne gastroenteritis worldwide and can cause invasive systemic disease in young infants, the elderly, and immunocompromised hosts, accompanied by high case fatality. Vaccination against invasive NTS disease is warranted where the disease incidence and mortality are high and multidrug resistance is prevalent, as in sub-Saharan Africa. Live-attenuated vaccines that mimic natural infection constitute one strategy to elicit protection. However, they must particularly be shown to be adequately attenuated for consideration of immunocompromised subjects. Accordingly, we examined the safety and tolerability of an oral live attenuated Salmonella typhimurium vaccine candidate, CVD 1921, in an established chronic simian immunodeficiency virus (SIV)-infected rhesus macaque model. We evaluated clinical parameters, histopathology, and measured differences in mucosal permeability to wild-type and vaccine strains. Compared to the wild-type S. typhimurium strain 177 in both SIV-infected and SIV-uninfected nonhuman primate hosts, this live-attenuated vaccine shows reduced shedding and systemic spread, exhibits limited pathological disease manifestations in the digestive tract, and induces low levels of cellular infiltration in tissues. Furthermore, wild-type S. typhimurium induces increased intestinal epithelial damage and permeability, with infiltration of neutrophils and macrophages in both SIV-infected and SIV-uninfected nonhuman primates compared to the vaccine strain. Based on shedding, systemic spread, and histopathology, the live-attenuated S. typhimurium strain CVD 1921 appears to be safe and well-tolerated in the nonhuman primate model, including chronically SIV-infected rhesus macaques.
JF  - Vaccine
AU  - Ault, Alida
AU  - Tennant, Sharon M
AU  - Gorres, J Patrick
AU  - Eckhaus, Michael
AU  - Sandler, Netanya G
AU  - Roque, Annelys
AU  - Livio, Sofie
AU  - Bao, Saran
AU  - Foulds, Kathryn E
AU  - Kao, Shing-Fen
AU  - Roederer, Mario
AU  - Schmidlein, Patrick
AU  - Boyd, Mary Adetinuke
AU  - Pasetti, Marcela F
AU  - Douek, Daniel C
AU  - Estes, Jacob D
AU  - Nabel, Gary J
AU  - Levine, Myron M
AU  - Rao, Srinivas S
AD  - Laboratory Animal Medicine, Vaccine Research Center, NIAID, NIH, Bethesda, MD 20892, United States, sraol@mail.nih.gov
Y1  - 2013/12/02/
PY  - 2013
DA  - 2013 Dec 02
SP  - 5879
EP  - 5888
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 31
IS  - 49
SN  - 0264-410X, 0264-410X
KW  - Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Nontyphoidal Salmonella
KW  - Live oral vaccine
KW  - Nonhuman primates
KW  - Simian immunodeficiency virus
KW  - Human immunodeficiency virus
KW  - Macrophages
KW  - Mortality
KW  - Food
KW  - Mucosa
KW  - Leukocytes (neutrophilic)
KW  - Animal models
KW  - Membrane permeability
KW  - Salmonella typhimurium
KW  - Primates
KW  - Permeability
KW  - Digestive tract
KW  - Immunocompromised hosts
KW  - Intestine
KW  - Geriatrics
KW  - Macaca mulatta
KW  - Multidrug resistance
KW  - Vaccines
KW  - Solitary tract nucleus
KW  - Gastroenteritis
KW  - Infants
KW  - V 22360:AIDS and HIV
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732836287?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Safety+and+tolerability+of+a+live+oral+Salmonella+typhimurium+vaccine+candidate+in+SIV-infected+nonhuman+primates&rft.au=Ault%2C+Alida%3BTennant%2C+Sharon+M%3BGorres%2C+J+Patrick%3BEckhaus%2C+Michael%3BSandler%2C+Netanya+G%3BRoque%2C+Annelys%3BLivio%2C+Sofie%3BBao%2C+Saran%3BFoulds%2C+Kathryn+E%3BKao%2C+Shing-Fen%3BRoederer%2C+Mario%3BSchmidlein%2C+Patrick%3BBoyd%2C+Mary+Adetinuke%3BPasetti%2C+Marcela+F%3BDouek%2C+Daniel+C%3BEstes%2C+Jacob+D%3BNabel%2C+Gary+J%3BLevine%2C+Myron+M%3BRao%2C+Srinivas+S&rft.aulast=Ault&rft.aufirst=Alida&rft.date=2013-12-02&rft.volume=31&rft.issue=49&rft.spage=5879&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2013.09.041
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-11-01
N1  - Last updated - 2015-11-13
N1  - SubjectsTermNotLitGenreText - Macrophages; Mortality; Food; Mucosa; Animal models; Leukocytes (neutrophilic); Membrane permeability; Permeability; Digestive tract; Immunocompromised hosts; Geriatrics; Intestine; Multidrug resistance; Vaccines; Gastroenteritis; Solitary tract nucleus; Infants; Macaca mulatta; Salmonella typhimurium; Primates; Simian immunodeficiency virus
DO  - http://dx.doi.org/10.1016/j.vaccine.2013.09.041
ER  - 



TY  - JOUR
T1  - Insulin and extremity muscle mass in overweight and obese women
AN  - 1837322765; 18890503
AB  - Background: Obesity disproportionately affects women, especially those of African descent, and is associated with increases in both fat and muscle masses. Objective: Although increased extremity muscle mass may be compensatory to fat mass load, we propose that elevated insulin levels resulting from diminished insulin sensitivity may additionally contribute to extremity muscle mass in overweight or obese women. Methods: The following measurements were performed in 197 non-diabetic women (57% black, 35% white; age 46 plus or minus 11 years (mean plus or minus s.d.), body mass index (BMI) range 25.0-57.7 kg m super(-2)): dual-energy X-ray absorptiometry for fat and extremity muscle masses; exercise performance by duration and peak oxygen consumption (VO sub(2) peak) during graded treadmill exercise; fasting insulin and, in 183 subjects, insulin sensitivity index (S sub(I)) calculated from the minimal model. Results: S sub(I) (range 0.5-14.1 l mU super(-1 )min super(-1)) was negatively, and fasting insulin (range 1.9-35.6 mu U ml super(-1)) positively associated with extremity muscle mass (both P<0.001), independent of age and height. Sixty-seven percent of women completed 6 months of participation in a weight loss and exercise program: we found a significant association between reduction in fasting insulin and a decrease in extremity muscle mass (P=0.038), independent of reduction in fat mass or improvement in exercise performance by VO sub(2) peak and exercise duration, and without association with change in S sub(I) or interaction by race. Conclusions: Hyperinsulinemia in overweight or obese women is associated with increased extremity muscle mass, which is partially reversible with reduction in fasting insulin concentration, consistent with the stimulatory effects of insulin on skeletal muscle.
JF  - International Journal of Obesity
AU  - Leon, B
AU  - Jenkins, S
AU  - Pepin, K
AU  - Chaudhry, H
AU  - Smith, K
AU  - Zalos, G
AU  - Miller, B V
AU  - Chen, K Y
AU  - Remaley, A T
AU  - Waclawiw, M A
AU  - Sumner, A E
AU  - Cannon, R O
AD  - Cardiovascular and Pulmonary Branch, National Institute of Diabetes, Digestive Diseases and Kidney Diseases; National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1560
EP  - 1564
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 37
IS  - 12
SN  - 0307-0565, 0307-0565
KW  - Physical Education Index
KW  - Obesity
KW  - Muscles (function)
KW  - Muscles (size)
KW  - Exercise (duration)
KW  - Body mass
KW  - Women
KW  - Hormones
KW  - Maximum oxygen consumption
KW  - Treadmill ergometry
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837322765?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medical+Internet+Research&rft.atitle=Collaborative+Biomedicine+in+the+Age+of+Big+Data%3A+The+Case+of+Cancer&rft.au=Shaikh%2C+Abdul+R%3BButte%2C+Atul+J%3BSchully%2C+Sheri+D%3BDalton%2C+William+S%3BKhoury%2C+Muin+J%3BHesse%2C+Bradford+W&rft.aulast=Shaikh&rft.aufirst=Abdul&rft.date=2014-01-01&rft.volume=16&rft.issue=4&rft.spage=%5Bnp%5D&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Internet+Research&rft.issn=14388871&rft_id=info:doi/10.2196%2Fjmir.2496
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Muscles (function); Obesity; Muscles (size); Exercise (duration); Body mass; Women; Maximum oxygen consumption; Hormones; Treadmill ergometry
DO  - http://dx.doi.org/10.1038/ijo.2013.45
ER  - 



TY  - JOUR
T1  - Characterization of fast-decaying PET radiotracers solely through LC-MS/MS of constituent radioactive and carrier isotopologues
AN  - 1732836926; PQ0002204272
AB  - Background: The characterization of fast-decaying radiotracers that are labeled with carbon-11 (t sub(1/2)=20.38 min), including critical measurement of specific radioactivity (activity per mole at a specific time) before release for use in positron-emission tomography (PET), has relied heavily on chromatographic plus radiometric measurements, each of which may be vulnerable to significant errors. Thus, we aimed to develop a mass-specific detection method using sensitive liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) for identifying super(11)C-labeled tracers and for verifying their specific radioactivities. Methods: The LC-MS/MS was tuned and set up with methods to generate and measure the product ions specific for carbon-11 species and M+1 carrier (predominantly the carbon-13 isotopologue) in four super(11)C-labeled tracers. These radiotracers were synthesized and then analyzed before extensive carbon-11 decay. The peak areas of carbon-11 species and M+1 carrier from the LC-MS/MS measurement and the calculated abundances of carbon-12 carrier and M+1 radioactive species gave the mole fraction of carbon-11 species in each sample. This value upon multiplication with the theoretical specific radioactivity of carbon-11 gave the specific radioactivity of the radiotracer. Results: LC-MS/MS of each super(11)C-labeled tracer generated the product ion peaks for carbon-11 species and M+1 carrier at the expected LC retention time. The intensity of the radioactive peak diminished as time elapsed and was undetectable after six half-lives of carbon-11. Measurements of radiotracer-specific radioactivity determined solely by LC-MS/MS at timed intervals gave a half-life for carbon-11 (20.43 min) in excellent agreement with the value obtained radiometrically. Additionally, the LC-MS/MS measurement gave specific radioactivity values (83 to 505 GBq/ mu mol) in good agreement with those from conventional radiometric methods. Conclusions: super(11)C-Labeled tracers were characterized at a fundamental level involving isolation and mass detection of extremely low-abundance carbon-11 species along with the M+1 carrier counterpart. This LC-MS/MS method for characterizing fast-decaying radiotracers is valuable in both the development and production of PET radiopharmaceuticals.
JF  - EJNMMI Research
AU  - Shetty, H Umesha
AU  - Morse, Cheryl L
AU  - Zhang, Yi
AU  - Pike, Victor W
AD  - Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Building 10, Room B3 C351, 10 Center Drive, MSC 1003, Bethesda, MD, 20892-1003, USA, shettyu@mail.nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1
EP  - 8
PB  - Springer Science & Business Media, Berlin/Heidelberg
VL  - 3
IS  - 1
KW  - Oncogenes & Growth Factors Abstracts; Toxicology Abstracts
KW  - Tracers
KW  - Ions
KW  - Radioisotopes
KW  - Positron emission tomography
KW  - Pharmaceuticals
KW  - Radioactivity
KW  - Mass spectroscopy
KW  - X 24390:Radioactive Materials
KW  - B 26660:Miscellaneous Oncogenes & Growth Factors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732836926?accountid=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=EJNMMI+Research&rft.atitle=Characterization+of+fast-decaying+PET+radiotracers+solely+through+LC-MS%2FMS+of+constituent+radioactive+and+carrier+isotopologues&rft.au=Shetty%2C+H+Umesha%3BMorse%2C+Cheryl+L%3BZhang%2C+Yi%3BPike%2C+Victor+W&rft.aulast=Shetty&rft.aufirst=H&rft.date=2013-12-01&rft.volume=3&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=EJNMMI+Research&rft.issn=2191-219X&rft_id=info:doi/10.1186%2F2191-219X-3-3
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-11-01
N1  - Number of references - 26
N1  - Last updated - 2016-04-13
N1  - SubjectsTermNotLitGenreText - Ions; Tracers; Positron emission tomography; Radioisotopes; Pharmaceuticals; Radioactivity; Mass spectroscopy
DO  - http://dx.doi.org/10.1186/2191-219X-3-3
ER  - 



TY  - JOUR
T1  - super(11)C-LY2428703, a positron emission tomographic radioligand for the metabotropic glutamate receptor 1, is unsuitable for imaging in monkey and human brains
AN  - 1732836505; PQ0002204310
AB  - Background: A recent study from our laboratory demonstrated that super(11)C-LY2428703, a new positron emission tomographic radioligand for metabotropic glutamate receptor 1 (mGluR1), has promising in vitro properties and excellent in vivo performance for imaging rat brain. The present study evaluated super(11)C-LY2428703 for imaging mGluR1 in monkey and human brains. Methods: Rhesus monkeys were imaged at baseline and after administration of an mGluR1 blocking agent to calculate nonspecific binding, as well as after the administration of permeability glycoprotein (P-gp) and breast cancer resistance protein (BCRP) blockers to assess whether super(11)C-LY2428703 is a substrate for efflux transporters at the blood-brain barrier. Human imaging was performed at baseline in three healthy volunteers, and arterial input function was measured. Results: Overall brain uptake was low in monkeys, though slightly higher in the cerebellum, where mGluR1s are concentrated. However, the uptake was not clearly displaceable in the scans after mGluR1 blockade. Brain penetration of the ligand did not increase after P-gp and BCRP blockade. Brain uptake was similarly low in all human subjects (mean V sub(T) with a two-tissue compartment model, 0.093 plus or minus 0.012 mL/cm super(3)) and for all regions, including the cerebellum. Conclusions: Despite promising in vitro and in vivo results in rodents, super(11)C-LY2428703 was unsuitable for imaging mGluR1s in monkey or human brain because of low brain uptake, which was likely caused by high binding to plasma proteins.
JF  - EJNMMI Research
AU  - Zanotti-Fregonara, Paolo
AU  - Barth, Vanessa N
AU  - Zoghbi, Sami S
AU  - Liow, Jeih-San
AU  - Nisenbaum, Eric
AU  - Siuda, Edward
AU  - Gladding, Robert L
AU  - Rallis-Frutos, Denise
AU  - Morse, Cheryl
AU  - Tauscher, Johannes
AU  - Pike, Victor W
AU  - Innis, Robert B
AD  - Molecular Imaging Branch, National Institute of Mental Health, 10 Center Drive, Bethesda, MD, 20892, USA, innisr@mail.nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1
EP  - 9
PB  - Springer Science & Business Media, Berlin/Heidelberg
VL  - 3
IS  - 1
KW  - CSA Neurosciences Abstracts; Toxicology Abstracts
KW  - Glutamic acid receptors (metabotropic)
KW  - Neuroimaging
KW  - Blood-brain barrier
KW  - Brain
KW  - Cerebellum
KW  - Animal models
KW  - Membrane permeability
KW  - Models
KW  - Plasma proteins
KW  - Radioisotopes
KW  - Breast cancer
KW  - Macaca mulatta
KW  - Glycoproteins
KW  - N3 11008:Neurochemistry
KW  - X 24300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732836505?accountid=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=EJNMMI+Research&rft.atitle=super%2811%29C-LY2428703%2C+a+positron+emission+tomographic+radioligand+for+the+metabotropic+glutamate+receptor+1%2C+is+unsuitable+for+imaging+in+monkey+and+human+brains&rft.au=Zanotti-Fregonara%2C+Paolo%3BBarth%2C+Vanessa+N%3BZoghbi%2C+Sami+S%3BLiow%2C+Jeih-San%3BNisenbaum%2C+Eric%3BSiuda%2C+Edward%3BGladding%2C+Robert+L%3BRallis-Frutos%2C+Denise%3BMorse%2C+Cheryl%3BTauscher%2C+Johannes%3BPike%2C+Victor+W%3BInnis%2C+Robert+B&rft.aulast=Zanotti-Fregonara&rft.aufirst=Paolo&rft.date=2013-12-01&rft.volume=3&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=EJNMMI+Research&rft.issn=2191-219X&rft_id=info:doi/10.1186%2F2191-219X-3-47
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-11-01
N1  - Number of references - 29
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Plasma proteins; Neuroimaging; Glutamic acid receptors (metabotropic); Blood-brain barrier; Animal models; Radioisotopes; Cerebellum; Brain; Membrane permeability; Breast cancer; Glycoproteins; Models; Macaca mulatta
DO  - http://dx.doi.org/10.1186/2191-219X-3-47
ER  - 



TY  - JOUR
T1  - 077 PBMC gene expression profiles: Impact of sample handling
AN  - 1722180186; PQ0002106032
AB  - Background: Previously, we showed that human peripheral blood mononuclear cells (PBMCs) that were cryopreserved, stored for 14 months at: (1) -150 degree C; (2) -150 degree C except temperature cycled for 104h; and (3) -80 degree C and then thawed had numerous genes that were differentially regulated compared to freshly isolated cells. Study Design and Methods: We have expanded our initial report to include a 6.5 year time point with aliquots from the same 10 donors in order to determine the effect of longer storage time on gene expression from these samples. We also collected another 10 donors (4 donors were identical from the 1st collection). Identical processing and storage methodology was done as previously, except we decreased the initial storage interval to 3 months and cultured aliquots for 24h to more precisely determine when gene expression changes occur and if they are reversible, respectively. We also performed flow cytometry and viability analysis on samples to monitor changes in cell phenotype and apoptosis/necrosis that occurred during sample handling. Significantly modulated genes (p 2-fold change) were selected based on ANVOVA with contrast analysis for comparison of difference storage conditions and storage time. Genes that correlated with cell viability values were selected based on r 2 >0.3 (p 2-fold difference in the gene expression value. Results: Gene expression analysis indicated little difference at 3 months between fresh and the 3 storage conditions which was consistent with no significant differences in cell viability between fresh and the 3 storage conditions. At 6 years nearly 600 genes were differentially modulated in the -80 degree C stored samples and a couple of hundred genes were altered in the LN2 and LN2-cycled condition; the mean percent of recovered viable cells was 98% for fresh, 78% LN2, 68% LN2-cycled and 9% for -80 degree C. Culturing of fresh cells and stored cells consistently modulated a set of the same 1800 genes that where highly enriched in various aspects of immune activation, most likely the result of stimulation by serum. To better understand the biological pathways involved in poor cell recovery following cryopreservation, we correlated cell viability with gene expression levels across all storage conditions and times. In uncultured samples, the percentage of dead cells correlated with genes significantly enriched in apoptosis, MAP kinase, c-jun, heat shock and stress response pathways. When these same samples were cultured for 24h, the percentage of dead cells correlated with genes significantly for enriched cytokine, inflammation and immune response pathways. Our presentation will also discuss and relate our current findings to how storage conditions and time in storage also influence cell subset frequency, apoptosis level and necrosis level and could lead to candidate biomarkers of quality for cryopreserved human PBMC samples. Conclusion: Expression profiling identified genes involved in apoptosis and stress-response pathways that are associated with poor cell viability caused by suboptimal handling; and provides candidate pathways to target with inhibitors of cell death to improve cellular recovery and function. Culturing of low quality samples results in increased expression of cytokines and immune response genes which may severely skew the interpretation of functional assays. Source of funding: Funded by NCI Contract No. HHSN261200800001E. Conflict of interest: None declar
JF  - Cryobiology
AU  - Lempicki, Richard A
AU  - Diaz, Norma
AU  - Yang, Jun
AU  - Adelsberger, Joseph
AU  - Metcalf, Julia A
AU  - Stevens, Randy
AU  - Rupert, Adam
AU  - Baseler, Michael
AU  - Cosentino, Mark
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 419
EP  - 420
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 67
IS  - 3
SN  - 0011-2240, 0011-2240
KW  - Biotechnology and Bioengineering Abstracts
KW  - Temperature effects
KW  - MAP kinase
KW  - Apoptosis
KW  - Stress
KW  - c-Jun protein
KW  - biomarkers
KW  - Cryopreservation
KW  - Inflammation
KW  - Flow cytometry
KW  - Gene expression
KW  - Necrosis
KW  - Peripheral blood mononuclear cells
KW  - Transcription factors
KW  - Storage conditions
KW  - Cytokines
KW  - Heat shock
KW  - Immune response
KW  - W 30945:Fermentation & Cell Culture
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722180186?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cryobiology&rft.atitle=077+PBMC+gene+expression+profiles%3A+Impact+of+sample+handling&rft.au=Lempicki%2C+Richard+A%3BDiaz%2C+Norma%3BYang%2C+Jun%3BAdelsberger%2C+Joseph%3BMetcalf%2C+Julia+A%3BStevens%2C+Randy%3BRupert%2C+Adam%3BBaseler%2C+Michael%3BCosentino%2C+Mark&rft.aulast=Lempicki&rft.aufirst=Richard&rft.date=2013-12-01&rft.volume=67&rft.issue=3&rft.spage=419&rft.isbn=&rft.btitle=&rft.title=Cryobiology&rft.issn=00112240&rft_id=info:doi/10.1016%2Fj.cryobiol.2013.09.083
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-10-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Temperature effects; MAP kinase; Apoptosis; Stress; c-Jun protein; Cryopreservation; biomarkers; Inflammation; Gene expression; Flow cytometry; Peripheral blood mononuclear cells; Necrosis; Storage conditions; Transcription factors; Heat shock; Cytokines; Immune response
DO  - http://dx.doi.org/10.1016/j.cryobiol.2013.09.083
ER  - 



TY  - JOUR
T1  - Discordant minimum inhibitory concentration analysis: A new path to licensure for anti-infective drugs
AN  - 1705063393; 20498192
AB  - BACKGROUND: Evaluation of anti-infective drugs for licensure often relies on a noninferiority (NI) design where new drug B is noninferior to comparator drug A if the difference in success rates is reliably not worse than some fixed margin. The margin must be based on historical studies that estimate the magnitude of the benefit of drug A over placebo. This approach hampers drug development because the obligatory evidence for margin determination is often nonexistent. PURPOSE: To develop a new method for licensure of anti-infective drugs when there is no historical evidence for reliable construction of the NI margin. METHODS: The minimum inhibitory concentration (MIC) measures the minimum amount of drug that it takes to inhibit growth of bacteria in vitro. Patients who are infected with bacteria that have a low MIC to a given drug are expected to have good outcomes when treated with that drug. Thus, a differential effect of drug B versus drug A, if it exists, is likely to occur in patients whose pathogens have discordant MICs (e.g., low MIC for drug B, high MIC for drug A, or vice versa). A new paradigm for licensure of anti-infective drugs is proposed where a clinically acceptable NI margin is selected and licensure supported if the NI margin is met and B is reliably demonstrated superior to A in a subset of patients whose paired MICs favor B. The requirement for some evidence of superiority encourages a study that is carefully designed and executed. RESULTS: Simulations indicate that the approach shows promise in realistic settings, provided adequate data are available. A simulated example illustrates use of the methods. LIMITATIONS: If the data have small sample size, weak MIC/success relationship, or high correlation between MIC-A, MIC-B, this procedure will have poor power. CONCLUSION: Discordant MIC analysis may offer a novel path to licensure for certain anti-infective drugs.
JF  - Clinical Trials
AU  - Follmann, Dean
AU  - Brittain, Erica
AU  - Powers, John H
AD  - Biostatistics Research Branch, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 876
EP  - 885
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 10
IS  - 6
SN  - 1740-7745, 1740-7745
KW  - Toxicology Abstracts
KW  - Data processing
KW  - Drug development
KW  - Pathogens
KW  - Drugs
KW  - Minimum inhibitory concentration
KW  - Clinical trials
KW  - X 24360:Metals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705063393?accountid=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=Clinical+Trials&rft.atitle=Discordant+minimum+inhibitory+concentration+analysis%3A+A+new+path+to+licensure+for+anti-infective+drugs&rft.au=Follmann%2C+Dean%3BBrittain%2C+Erica%3BPowers%2C+John+H&rft.aulast=Follmann&rft.aufirst=Dean&rft.date=2013-12-01&rft.volume=10&rft.issue=6&rft.spage=876&rft.isbn=&rft.btitle=&rft.title=Clinical+Trials&rft.issn=17407745&rft_id=info:doi/10.1177%2F1740774513507503
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-08-01
N1  - Number of references - 17
N1  - Last updated - 2015-09-03
N1  - SubjectsTermNotLitGenreText - Data processing; Drug development; Pathogens; Clinical trials; Minimum inhibitory concentration; Drugs
DO  - http://dx.doi.org/10.1177/1740774513507503
ER  - 



TY  - JOUR
T1  - The Complex Relationship between Weather and Dengue Virus Transmission in Thailand
AN  - 1647022893; 21172310
AB  - Using a novel analytical approach, weather dynamics and seasonal dengue virus transmission cycles were profiled for each Thailand province, 1983-2001, using monthly assessments of cases, temperature, humidity, and rainfall. We observed systematic differences in the structure of seasonal transmission cycles of different magnitude, the role of weather in regulating seasonal cycles, necessary versus optimal transmission "weather-space," basis of large epidemics, and predictive indicators that estimate risk. Larger epidemics begin earlier, develop faster, and are predicted at Onset change-point when case counts are low. Temperature defines a viable range for transmission; humidity amplifies the potential within that range. This duality is central to transmission. Eighty percent of 1.2 million severe dengue cases occurred when mean temperature was 27-29.5[degrees]C and mean humidity was > 75%. Interventions are most effective when applied early. Most cases occur near Peak, yet small reductions at Onset can substantially reduce epidemic magnitude. Monitoring the Quiet-Phase is fundamental in effectively targeting interventions pre-emptively.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Campbell, Karen M
AU  - Lin, C D
AU  - Iamsirithaworn, Sopon
AU  - Scott, Thomas W
AD  - Department of Mathematics and Statistics, San Diego State University, San Diego, California; Office of Disease Prevention and Control 1, Bangkok, Thailand; Department of Entomology, University of California, Davis, California; Fogarty International Center, National Institutes of Health, Bethesda, Maryland; Computational Science Research Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-1245, kmca@roadrunner.com
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1066
EP  - 1080
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
IS  - 6
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Risk Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Health & Safety Science Abstracts
KW  - Dengue virus
KW  - Risk assessment
KW  - Temperature effects
KW  - Prediction
KW  - Weather
KW  - Epidemics
KW  - Thailand
KW  - Rainfall
KW  - Temperature
KW  - Intervention
KW  - Humidity
KW  - Sulfur dioxide
KW  - Dengue
KW  - Hygiene
KW  - Seasonal variations
KW  - Weather forecasting
KW  - J 02310:Genetics & Taxonomy
KW  - V 22490:Miscellaneous
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - K 03450:Ecology
KW  - R2 23050:Environment
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022893?accountid=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=The+Complex+Relationship+between+Weather+and+Dengue+Virus+Transmission+in+Thailand&rft.au=Campbell%2C+Karen+M%3BLin%2C+C+D%3BIamsirithaworn%2C+Sopon%3BScott%2C+Thomas+W&rft.aulast=Campbell&rft.aufirst=Karen&rft.date=2013-12-01&rft.volume=89&rft.issue=6&rft.spage=1066&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0321
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Prediction; Epidemics; Humidity; Hygiene; Weather forecasting; Temperature effects; Weather; Dengue; Rainfall; Risk assessment; Sulfur dioxide; Temperature; Intervention; Seasonal variations; Dengue virus; Thailand
DO  - http://dx.doi.org/10.4269/ajtmh.13-0321
ER  - 



TY  - JOUR
T1  - Evaluation of propargyl alcohol toxicity and carcinogenicity in F344/N rats and B6C3F1/N mice following whole-body inhalation exposure
AN  - 1647007822; 21278296
AB  - Propargyl alcohol (PA) is a high production volume chemical used in synthesis of many industrial chemicals and agricultural products. Despite the potential for prolonged or accidental exposure to PA in industrial settings, the toxicity potential of PA was not well characterized. To address the knowledge gaps relevant to the toxicity profile of PA, the National Toxicology Program (NTP) conducted 2-week, 14-week and 2-year studies in male and female F344/N rats and B6C3F1/N mice. For the 2-week inhalation study, the rats and mice were exposed to 0, 31.3, 62.5, 125, 250 or 500ppm. Significant mortality was observed in both rats and mice exposed to greater than or equal to 125ppm of PA. The major target organ of toxicity in both mice and rats was the liver with exposure-related histopathological changes (250 and 500ppm). Based on the decreased survival in the 2-week study, the rats and mice were exposed to 0, 4, 8, 16, 32 or 64ppm of PA in the 14-week study. No treatment-related mortality was observed. Mean body weights of male ( greater than or equal to 8ppm) and female mice (32 and 64ppm) were significantly decreased (7-16%). Histopathological changes were noted in the nasal cavity, and included suppurative inflammation, squamous metaplasia, hyaline droplet accumulation, olfactory epithelium atrophy, and necrosis. In the 2-year inhalation studies, the rats were exposed to 0, 16, 32 and 64ppm of PA and the mice were exposed to 0, 8, 16 and 32ppm of PA. Survival of male rats was significantly reduced (32 and 64ppm). Mean body weights of 64ppm male rats were significantly decreased relative to the controls. Both mice and rats showed a spectrum of non-neoplastic changes in the nose. Increased neoplastic incidences of nasal respiratory/transitional epithelial adenoma were observed in both rats and mice. The incidence of mononuclear cell leukemia was significantly increased in male rats and was considered to be treatment-related. In conclusion, the key findings from this study indicated that the nose was the primary target organ of toxicity for PA. Long term inhalation exposure to PA led to nonneoplastic changes in the nose, and increased incidences of respiratory/transitional epithelial adenomas in both mice and rats. Increased incidences of harderian gland adenoma may also have been related to exposure to PA in male mice.
JF  - Toxicology
AU  - Thakur, Sheetal A
AU  - Flake, Gordon P
AU  - Travlos, Greg S
AU  - Dill, Jeffrey A
AU  - Grumbein, Sondra L
AU  - Harbo, Sam J
AU  - Hooth, Michelle J
AD  - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, PO Box 12233, MD: K2-07, NIH, NTP, Research Triangle Park, NC 27709, United States
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 100
EP  - 111
PB  - Elsevier B.V., P.O. Box 85 Limerick Ireland
VL  - 314
IS  - 1
SN  - 0300-483X, 0300-483X
KW  - Toxicology Abstracts
KW  - Propargyl alcohol
KW  - Toxicity
KW  - Carcinogenicity
KW  - Chronic
KW  - Occupational
KW  - Respiratory
KW  - Inhalation
KW  - Leukocytes (mononuclear)
KW  - Mortality
KW  - Harderian gland
KW  - Agricultural products
KW  - Survival
KW  - Inflammation
KW  - Leukemia
KW  - Necrosis
KW  - Olfactory epithelium
KW  - Body weight
KW  - Metaplasia
KW  - alcohols
KW  - Liver
KW  - Atrophy
KW  - Nose
KW  - Adenoma
KW  - X 24380:Social Poisons & Drug Abuse
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647007822?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Evaluation+of+propargyl+alcohol+toxicity+and+carcinogenicity+in+F344%2FN+rats+and+B6C3F1%2FN+mice+following+whole-body+inhalation+exposure&rft.au=Thakur%2C+Sheetal+A%3BFlake%2C+Gordon+P%3BTravlos%2C+Greg+S%3BDill%2C+Jeffrey+A%3BGrumbein%2C+Sondra+L%3BHarbo%2C+Sam+J%3BHooth%2C+Michelle+J&rft.aulast=Thakur&rft.aufirst=Sheetal&rft.date=2013-12-01&rft.volume=314&rft.issue=1&rft.spage=100&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/10.1016%2Fj.tox.2013.09.002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Number of references - 41
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Inhalation; Mortality; Leukocytes (mononuclear); Harderian gland; Agricultural products; Survival; Toxicity; Inflammation; Leukemia; Olfactory epithelium; Necrosis; Body weight; Carcinogenicity; Metaplasia; Liver; alcohols; Nose; Atrophy; Adenoma
DO  - http://dx.doi.org/10.1016/j.tox.2013.09.002
ER  - 



TY  - JOUR
T1  - Liver-directed adeno-associated virus serotype 8 gene transfer rescues a lethal murine model of citrullinemia type 1
AN  - 1554946811; 20501237
AB  - Citrullinemia type 1 (CTLN1) is an autosomal recessive disorder of metabolism caused by a deficiency of argininosuccinate synthetase. Despite optimal management, CTLN1 patients still suffer from lethal metabolic instability and experience life-threatening episodes of acute hyperammonemia. A murine model of CTLN1 (fold/fold) that displays lethality within the first 21 days of life was used to determine the efficacy of adeno-associated viral (AAV) gene transfer as a potential therapy. An AAV serotype 8 (AAV8) vector was engineered to express the human ASS1 cDNA under the control of a liver-specific promoter (thyroxine-binding globulin, TBG), AAV8-TBG-hASS1, and delivered to 7-10 days old mice via intraperitoneal injection. Greater than 95% of the mice were rescued from lethality and survival was extended beyond 100 days after receiving a single dose of vector. AAV8-TBG-hASS1 treatment resulted in liver-specific expression of hASS1, increased ASS1 enzyme activity, reduction in plasma ammonia and citrulline concentrations and significant phenotypic improvement of the fold/fold growth and skin phenotypes. These experiments highlight a gene transfer approach using AAV8 vector for liver-targeted gene therapy that could serve as a treatment for CTLN1.
JF  - Gene Therapy
AU  - Chandler, R J
AU  - Tarasenko, T N
AU  - Cusmano-Ozog, K
AU  - Sun, Q
AU  - Sutton, V R
AU  - Venditti, C P
AU  - McGuire, P J
AD  - Organic Acid Research Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 1188
EP  - 1191
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 20
IS  - 12
SN  - 0969-7128, 0969-7128
KW  - Virology & AIDS Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Skin
KW  - Hereditary diseases
KW  - Serotypes
KW  - Gene therapy
KW  - Ammonia
KW  - citrulline
KW  - Animal models
KW  - Enzymes
KW  - Survival
KW  - Globulins
KW  - Adeno-associated virus
KW  - Expression vectors
KW  - Promoters
KW  - Lethality
KW  - hyperammonemia
KW  - Metabolism
KW  - W 30905:Medical Applications
KW  - V 22410:Animal Diseases
KW  - G 07870:Mammals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554946811?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Liver-directed+adeno-associated+virus+serotype+8+gene+transfer+rescues+a+lethal+murine+model+of+citrullinemia+type+1&rft.au=Chandler%2C+R+J%3BTarasenko%2C+T+N%3BCusmano-Ozog%2C+K%3BSun%2C+Q%3BSutton%2C+V+R%3BVenditti%2C+C+P%3BMcGuire%2C+P+J&rft.aulast=Chandler&rft.aufirst=R&rft.date=2013-12-01&rft.volume=20&rft.issue=12&rft.spage=1188&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2013.53
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-12-11
N1  - SubjectsTermNotLitGenreText - Serotypes; Hereditary diseases; Skin; Gene therapy; Ammonia; citrulline; Animal models; Survival; Enzymes; Globulins; Expression vectors; Promoters; Lethality; hyperammonemia; Metabolism; Adeno-associated virus
DO  - http://dx.doi.org/10.1038/gt.2013.53
ER  - 



TY  - JOUR
T1  - Altered brain activity for phonological manipulation in dyslexic Japanese children
AN  - 1541992744; 201410066
AB  - Because of unique linguistic characteristics, the prevalence rate of developmental dyslexia is relatively low in the Japanese language. Paradoxically, Japanese children have serious difficulty analysing phonological processes when they have dyslexia. Neurobiological deficits in Japanese dyslexia remain unclear and need to be identified, and may lead to better understanding of the commonality and diversity in the disorder among different linguistic systems. The present study investigated brain activity that underlies deficits in phonological awareness in Japanese dyslexic children using functional magnetic resonance imaging. We developed and conducted a phonological manipulation task to extract phonological processing skills and to minimize the influence of auditory working memory on healthy adults, typically developing children, and dyslexic children. Current experiments revealed that several brain regions participated in manipulating the phonological information including left inferior and middle frontal gyrus, left superior temporal gyrus, and bilateral basal ganglia. Moreover, dyslexic children showed altered activity in two brain regions. They showed hyperactivity in the basal ganglia compared with the two other groups, which reflects inefficient phonological processing. Hypoactivity in the left superior temporal gyrus was also found, suggesting difficulty in composing and processing phonological information. The altered brain activity shares similarity with those of dyslexic children in countries speaking alphabetical languages, but disparity also occurs between these two populations. These are initial findings concerning the neurobiological impairments in dyslexic Japanese children. Adapted from the source document
JF  - Brain
AU  - Kita, Yosuke
AU  - Yamamoto, Hisako
AU  - Oba, Kentaro
AU  - Terasawa, Yuri
AU  - Moriguchi, Yoshiya
AU  - Uchiyama, Hitoshi
AU  - Seki, Ayumi
AU  - Koeda, Tatsuya
AU  - Inagaki, Masumi
AD  - Department of Developmental Disorders, National Institute of Mental Health, National Centre of Neurology and Psychiatry (NCNP), Tokyo, Japan kitay@ncnp.go.jp
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 3696
EP  - 3708
VL  - 136
IS  - 12
SN  - 0006-8950, 0006-8950
KW  - Functional Magnetic Resonance Imaging (fMRI) (26525)
KW  - Phonological Awareness (64970)
KW  - Disorders (19450)
KW  - Phonological Processing (65110)
KW  - Language Acquisition (41600)
KW  - Brain (09350)
KW  - Dyslexia (20250)
KW  - Japanese (39500)
KW  - Children (11850)
KW  - article
KW  - 4018: psycholinguistics; neurolinguistics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541992744?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain&rft.atitle=Altered+brain+activity+for+phonological+manipulation+in+dyslexic+Japanese+children&rft.au=Kita%2C+Yosuke%3BYamamoto%2C+Hisako%3BOba%2C+Kentaro%3BTerasawa%2C+Yuri%3BMoriguchi%2C+Yoshiya%3BUchiyama%2C+Hitoshi%3BSeki%2C+Ayumi%3BKoeda%2C+Tatsuya%3BInagaki%2C+Masumi&rft.aulast=Kita&rft.aufirst=Yosuke&rft.date=2013-12-01&rft.volume=136&rft.issue=12&rft.spage=3696&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/
LA  - English
DB  - Linguistics and Language Behavior Abstracts (LLBA)
N1  - Date revised - 2014-07-01
N1  - Last updated - 2016-09-27
N1  - CODEN - BRAIAK
N1  - SubjectsTermNotLitGenreText - Dyslexia (20250); Phonological Awareness (64970); Functional Magnetic Resonance Imaging (fMRI) (26525); Children (11850); Japanese (39500); Brain (09350); Phonological Processing (65110); Disorders (19450); Language Acquisition (41600)
ER  - 



TY  - JOUR
T1  - Photobiomodulation and implants: implications for dentistry
AN  - 1534823594; 19928836
AB  - The use of dental implants has become a mainstay of rehabilitative and restorative dentistry. With an impressive clinical success rate, mere remain a few minor clinical issues with the use of implants such as peri-implant mucositis and peri-implantitis. The use of laser technology with implants has a fascinating breadth of applications, beginning from their precision manufacturing to clinical uses for surgical site preparation, reducing pain and inflammation, and promoting osseointegration and tissue regeneration. This latter aspect is the focus of this review, which outlines various studies of implants and laser therapy in animal models. The use of low level light therapy or photobiomodulation has demonstrated its efficacy in these studies. Besides more research studies to understand its molecular mechanisms, significant efforts are needed to standardize the clinical dosing and delivery protocols for laser therapy to ensure the maximal efficacy and safety of this potent clinical tool for photobiomodulation.
JF  - Journal of Periodontal & Implant Science
AU  - Tang, Elieza
AU  - Arany, Praveen
AD  - Cell Regulation and Control Unit, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA, praveen.arany@nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 262
EP  - 268
PB  - Korean Academy of Periodontology, Shinchon-dong, Seodaemun-gu Seoul 120-752, Korea Korea, Republic of
VL  - 43
IS  - 6
SN  - 2093-2278, 2093-2278
KW  - Biotechnology and Bioengineering Abstracts; Calcium & Calcified Tissue Abstracts
KW  - Dental implants
KW  - Low-level laser therapy
KW  - Peri-implantitis
KW  - Phototherapy
KW  - Molecular modelling
KW  - Dental restorative materials
KW  - Mucositis
KW  - Animal models
KW  - Lasers
KW  - Osseointegration
KW  - Pain
KW  - Dentistry
KW  - Inflammation
KW  - Light effects
KW  - T 2065:General and Miscellaneous Topics
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534823594?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Periodontal+%26+Implant+Science&rft.atitle=Photobiomodulation+and+implants%3A+implications+for+dentistry&rft.au=Tang%2C+Elieza%3BArany%2C+Praveen&rft.aulast=Tang&rft.aufirst=Elieza&rft.date=2013-12-01&rft.volume=43&rft.issue=6&rft.spage=262&rft.isbn=&rft.btitle=&rft.title=Journal+of+Periodontal+%26+Implant+Science&rft.issn=20932278&rft_id=info:doi/10.5051%2Fjpis.2013.43.6-262
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-06-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Dental restorative materials; Molecular modelling; Mucositis; Animal models; Pain; Osseointegration; Lasers; Dentistry; Light effects; Inflammation
DO  - http://dx.doi.org/10.5051/jpis.2013.43.6-262
ER  - 



TY  - JOUR
T1  - The altered landscape of the human skin microbiome in patients with primary immunodeficiencies
AN  - 1512329993; 19411209
AB  - While landmark studies have shown that microbiota activate and educate host immunity, how immune systems shape microbiomes and contribute to disease is incompletely characterized. Primary immunodeficiency (PID) patients suffer recurrent microbial infections, providing a unique opportunity to address this issue. To investigate the potential influence of host immunity on the skin microbiome, we examined skin microbiomes in patients with rare monogenic PIDs: hyper-IgE (STAT3-deficient), Wiskott-Aldrich, and dedicator of cytokinesis 8 syndromes. While specific immunologic defects differ, a shared hallmark is atopic dermatitis (AD)-like eczema. We compared bacterial and fungal skin microbiomes (41 PID, 13 AD, 49 healthy controls) at four clinically relevant sites representing the major skin microenvironments. PID skin displayed increased ecological permissiveness with altered population structures, decreased site specificity and temporal stability, and colonization with microbial species not observed in controls, including Clostridium species and Serratia marcescens. Elevated fungal diversity and increased representation of opportunistic fungi (Candida, Aspergillus) supported increased PID skin permissiveness, suggesting that skin may serve as a reservoir for the recurrent fungal infections observed in these patients. The overarching theme of increased ecological permissiveness in PID skin was counterbalanced by the maintenance of a phylum barrier in which colonization remained restricted to typical human-associated phyla. Clinical parameters, including markers of disease severity, were positively correlated with prevalence of Staphylococcus, Corynebacterium, and other less abundant taxa. This study examines differences in microbial colonization and community stability in PID skin and informs our understanding of host-microbiome interactions, suggesting a bidirectional dialogue between skin commensals and the host organism.
JF  - Genome Research
AU  - Oh, Julia
AU  - Freeman, Alexandra F
AU  - Park, Morgan
AU  - Sokolic, Robert
AU  - Candotti, Fabio
AU  - Holland, Steven M
AU  - Segre, Julia A
AU  - Kong, Heidi H
AD  - Genetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA, jsegre@mail.nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 2103
EP  - 2114
PB  - Cold Spring Harbor Laboratory Press, Fulfillment & Distribution Dept. Woodbury NY 11797-2924 United States
VL  - 23
IS  - 12
SN  - 1088-9051, 1088-9051
KW  - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts; Genetics Abstracts
KW  - Clostridium
KW  - Skin
KW  - Stat3 protein
KW  - Immune system
KW  - Fungi
KW  - Staphylococcus
KW  - Landscape
KW  - Candida
KW  - Commensals
KW  - Immunodeficiency
KW  - Aspergillus
KW  - Eczema
KW  - Immunity
KW  - Corynebacterium
KW  - Colonization
KW  - Cytokinesis
KW  - Serratia marcescens
KW  - Microenvironments
KW  - Population structure
KW  - Recurrent infection
KW  - Atopic dermatitis
KW  - A 01490:Miscellaneous
KW  - N 14845:Miscellaneous
KW  - K 03450:Ecology
KW  - F 06950:Immunogenetics, MHC, HLA
KW  - G 07780:Fungi
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512329993?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+Research&rft.atitle=The+altered+landscape+of+the+human+skin+microbiome+in+patients+with+primary+immunodeficiencies&rft.au=Oh%2C+Julia%3BFreeman%2C+Alexandra+F%3BPark%2C+Morgan%3BSokolic%2C+Robert%3BCandotti%2C+Fabio%3BHolland%2C+Steven+M%3BSegre%2C+Julia+A%3BKong%2C+Heidi+H&rft.aulast=Oh&rft.aufirst=Julia&rft.date=2013-12-01&rft.volume=23&rft.issue=12&rft.spage=2103&rft.isbn=&rft.btitle=&rft.title=Genome+Research&rft.issn=10889051&rft_id=info:doi/10.1101%2Fgr.159467.113
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Skin; Stat3 protein; Fungi; Immune system; Landscape; Immunodeficiency; Commensals; Immunity; Eczema; Colonization; Cytokinesis; Microenvironments; Recurrent infection; Population structure; Atopic dermatitis; Clostridium; Staphylococcus; Candida; Serratia marcescens; Aspergillus; Corynebacterium
DO  - http://dx.doi.org/10.1101/gr.159467.113
ER  - 



TY  - JOUR
T1  - Telomere length and risk of glioma
AN  - 1500788057; 19047137
AB  - Background Telomere length in blood or buccal cell DNA has been associated with risk of various cancers. Glioma can be a highly malignant brain tumor and has few known risk factors. Genetic variants in or near and , key components of telomere biology, are associated with glioma risk. Therefore, we evaluated the association between relative telomere length (RTL) and glioma in a prospective study. Materials and methods We performed a nested case-control study within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. RTL was determined by quantitative PCR on blood or buccal cell DNA obtained at least 2 years prior to diagnosis from 101 individuals with glioma cases. Healthy controls (=198) were matched to cases (2:1) on age, gender, smoking status, calendar year, and DNA source. Conditional logistic regression was used to investigate the association between RTL and glioma. Results As expected, RTL declined with increasing age in both cases and controls. There was no statistically significant association between RTL and glioma overall. An analysis stratified by gender suggested that short RTL (1st tertile) in males was associated with glioma (odds ratio, [OR]=2.29, 95% confidence interval [CI] 1.02-5.11); this association was not observed for females (OR=0.41, 95% CI 0.14-1.17). Conclusions This prospective study did not identify significant associations between RTL and glioma risk, but there may be gender-specific differences. Larger, prospective studies are needed to evaluate these findings.
JF  - Cancer Epidemiology
AU  - Walcott, Farzana
AU  - Rajaraman, Preetha
AU  - Gadalla, Shahinaz M
AU  - Inskip, Peter D
AU  - Purdue, Mark P
AU  - Albanes, Demetrius
AU  - Orr, Esther
AU  - De Vivo, Immaculata
AU  - Savage, Sharon A
AD  - Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, MD 20892, United States
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 935
EP  - 938
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 37
IS  - 6
SN  - 1877-7821, 1877-7821
KW  - Health & Safety Science Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Risk Abstracts
KW  - Ovarian cancer
KW  - Age
KW  - Phospholipase C
KW  - Statistical analysis
KW  - Cancer
KW  - Brain tumors
KW  - Health risks
KW  - Telomeres
KW  - Blood
KW  - Smoking
KW  - Lung
KW  - Risk factors
KW  - Gender
KW  - DNA
KW  - Polymerase chain reaction
KW  - Glioma
KW  - Prostate
KW  - H 11000:Diseases/Injuries/Trauma
KW  - N 14820:DNA Metabolism & Structure
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500788057?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology&rft.atitle=Telomere+length+and+risk+of+glioma&rft.au=Walcott%2C+Farzana%3BRajaraman%2C+Preetha%3BGadalla%2C+Shahinaz+M%3BInskip%2C+Peter+D%3BPurdue%2C+Mark+P%3BAlbanes%2C+Demetrius%3BOrr%2C+Esther%3BDe+Vivo%2C+Immaculata%3BSavage%2C+Sharon+A&rft.aulast=Walcott&rft.aufirst=Farzana&rft.date=2013-12-01&rft.volume=37&rft.issue=6&rft.spage=935&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2013.10.002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2014-06-26
N1  - SubjectsTermNotLitGenreText - Brain tumors; Smoking; Ovarian cancer; Blood; Telomeres; Age; Risk factors; Phospholipase C; Statistical analysis; Polymerase chain reaction; Glioma; Prostate; Health risks; Lung; Gender; DNA; Cancer
DO  - http://dx.doi.org/10.1016/j.canep.2013.10.002
ER  - 



TY  - JOUR
T1  - Information-seeking trends of medical professionals and students from middle-income countries: a focus on the Philippines
AN  - 1496969863; 201401568
AB  - Background: Increased emphasis has been given to the practice of evidence-based medicine (EBM) worldwide. Access to quality health information is essential to the practice of EBM in developing countries. Objectives: To understand the information needs and sources of information of physicians from low- and middle-income countries (LMICs). Methods: Medical doctors and students participated in an 18-question online or paper study. Results: Of the 156 respondents from six LMICs, 146 (94%) came from the Philippines. Eighty-eight per cent encountered at least one clinical question daily, while 58% were very likely to search for answers. A basic mobile phone was the most used device at home (94%) and at work (82%). More than half had Internet connectivity at home (62%) and just under half at work (46%). In decreasing order, short messaging services (SMS), email, instant messaging and multimedia messaging services (MMS) were the most commonly used messaging tools at home and at work. The primary source for medication questions was a formulary, but for diagnostic dilemmas, colleagues were consulted first. PubMed use was high for therapy and management questions. Conclusion: The use of health information from the Internet through mobile devices may be increasing. Access to health information was higher at home than at work. These results may be useful when planning resources for healthcare givers in resource-poor settings. Adapted from the source document.
JF  - Health Information and Libraries Journal
AU  - Gavino, Alex I
AU  - Ho, Beverly Lorraine C
AU  - Wee, Pura Angela A
AU  - Marcelo, Alvin B
AU  - Fontelo, Paul
AD  - National Library of Medicine, Bethesda, MD, USA gavinoai@mail.nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 303
EP  - 317
PB  - Blackwell Publishing, Oxford UK
VL  - 30
IS  - 4
SN  - 1471-1834, 1471-1834
KW  - information seeking behaviour
KW  - students
KW  - medical
KW  - doctors
KW  - Asia
KW  - South East
KW  - Medline
KW  - Doctors
KW  - Information seeking behaviour
KW  - Southeast Asia
KW  - Developing countries
KW  - Evidence based medicine
KW  - article
KW  - 12.22: SEARCHING
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496969863?accountid=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=Health+Information+and+Libraries+Journal&rft.atitle=Information-seeking+trends+of+medical+professionals+and+students+from+middle-income+countries%3A+a+focus+on+the+Philippines&rft.au=Gavino%2C+Alex+I%3BHo%2C+Beverly+Lorraine+C%3BWee%2C+Pura+Angela+A%3BMarcelo%2C+Alvin+B%3BFontelo%2C+Paul&rft.aulast=Gavino&rft.aufirst=Alex&rft.date=2013-12-01&rft.volume=30&rft.issue=4&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Health+Information+and+Libraries+Journal&rft.issn=14711834&rft_id=info:doi/10.1111%2Fhir.12032
LA  - English
DB  - Library & Information Science Abstracts (LISA)
N1  - Date revised - 2014-02-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Evidence based medicine; Southeast Asia; Doctors; Information seeking behaviour; Developing countries
DO  - http://dx.doi.org/10.1111/hir.12032
ER  - 



TY  - JOUR
T1  - Biodegradable Gold Nanovesicles with an Ultrastrong Plasmonic Coupling Effect for Photoacoustic Imaging and Photothermal Therapy
AN  - 1496890469; 18925890
AB  - The hierarchical assembly of gold nanoparticles (GNPs) allows the localized surface plasmon resonance peaks to be engineered to the near-infrared (NIR) region for enhanced photothermal therapy (PTT). Herein we report a novel theranostic platform based on biodegradable plasmonic gold nanovesicles for photoacoustic (PA) imaging and PTT. The disulfide bond at the terminus of a PEG-b-PCL block-copolymer graft enables dense packing of GNPs during the assembly process and induces ultrastrong plasmonic coupling between adjacent GNPs. The strong NIR absorption induced by plasmon coupling and very high photothermal conversion efficiency ( eta =37%) enable simultaneous thermal/PA imaging and enhanced PTT efficacy with improved clearance of the dissociated particles after the completion of PTT. The assembly of various nanocrystals with tailored optical, magnetic, and electronic properties into vesicle architectures opens new possibilities for the construction of multifunctional biodegradable platforms for biomedical applications. They do their job and clear out: A disulfide-terminated copolymer graft enabled the dense packing of gold nanoparticles (GNPs) into biodegradable plasmonic gold vesicles for simultaneous thermal/photoacoustic cancer imaging and photothermal therapy (PTT; see picture). The ultrastrong plasmonic coupling effect between adjacent GNPs led to a strong near-infrared (NIR) absorption and very high photothermal conversion efficiency ( eta =37%).
JF  - Angewandte Chemie (International Edition)
AU  - Huang, Peng
AU  - Lin, Jing
AU  - Li, Wanwan
AU  - Rong, Pengfei
AU  - Wang, Zhe
AU  - Wang, Shouju
AU  - Wang, Xiaoping
AU  - Sun, Xiaolian
AU  - Aronova, Maria
AU  - Niu, Gang
AU  - Leapman, Richard D
AU  - Nie, Zhihong
AU  - Chen, Xiaoyuan
AD  - Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (USA).
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 13958
EP  - 13964
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 52
IS  - 52
SN  - 1433-7851, 1433-7851
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts
KW  - biodegradable block copolymers
KW  - gold nanovesicles
KW  - photoacoustic imaging
KW  - photothermal therapy
KW  - plasmonic coupling
KW  - I.R. radiation
KW  - Disulfide bonds
KW  - Crystals
KW  - Packing
KW  - Biodegradability
KW  - imaging
KW  - Cancer
KW  - surface plasmon resonance
KW  - Copolymers
KW  - Photoacoustics
KW  - Gold
KW  - Vesicles
KW  - nanoparticles
KW  - W 30910:Imaging
KW  - A 01320:Microbial Degradation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496890469?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Angewandte+Chemie+%28International+Edition%29&rft.atitle=Biodegradable+Gold+Nanovesicles+with+an+Ultrastrong+Plasmonic+Coupling+Effect+for+Photoacoustic+Imaging+and+Photothermal+Therapy&rft.au=Huang%2C+Peng%3BLin%2C+Jing%3BLi%2C+Wanwan%3BRong%2C+Pengfei%3BWang%2C+Zhe%3BWang%2C+Shouju%3BWang%2C+Xiaoping%3BSun%2C+Xiaolian%3BAronova%2C+Maria%3BNiu%2C+Gang%3BLeapman%2C+Richard+D%3BNie%2C+Zhihong%3BChen%2C+Xiaoyuan&rft.aulast=Huang&rft.aufirst=Peng&rft.date=2013-12-01&rft.volume=52&rft.issue=52&rft.spage=13958&rft.isbn=&rft.btitle=&rft.title=Angewandte+Chemie+%28International+Edition%29&rft.issn=14337851&rft_id=info:doi/10.1002%2Fanie.201308986
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-07-23
N1  - SubjectsTermNotLitGenreText - I.R. radiation; Disulfide bonds; Packing; Crystals; imaging; Biodegradability; Cancer; surface plasmon resonance; Photoacoustics; Copolymers; Gold; Vesicles; nanoparticles
DO  - http://dx.doi.org/10.1002/anie.201308986
ER  - 



TY  - JOUR
T1  - Biodegradable Gold Nanovesicles with an Ultrastrong Plasmonic Coupling Effect for Photoacoustic Imaging and Photothermal Therapy
AN  - 1496888701; 18925876
AB  - The hierarchical assembly of gold nanoparticles (GNPs) allows the localized surface plasmon resonance peaks to be engineered to the near-infrared (NIR) region for enhanced photothermal therapy (PTT). Herein we report a novel theranostic platform based on biodegradable plasmonic gold nanovesicles for photoacoustic (PA) imaging and PTT. The disulfide bond at the terminus of a PEG-b-PCL block-copolymer graft enables dense packing of GNPs during the assembly process and induces ultrastrong plasmonic coupling between adjacent GNPs. The strong NIR absorption induced by plasmon coupling and very high photothermal conversion efficiency ( eta =37%) enable simultaneous thermal/PA imaging and enhanced PTT efficacy with improved clearance of the dissociated particles after the completion of PTT. The assembly of various nanocrystals with tailored optical, magnetic, and electronic properties into vesicle architectures opens new possibilities for the construction of multifunctional biodegradable platforms for biomedical applications.Original Abstract: Ein Disulfid-terminiertes Copolymer ermoglicht die dichte Packung von Gold-Nanopartikeln (GNPs) zu biologisch abbaubaren plasmonischen Goldvesikeln fuer simultane thermische/photoakustische Krebsbildgebung und Photothermaltherapie (PTT; siehe Bild). Die starke plasmonische Kopplung zwischen benachbarten GNPs fuehrte zu einer starken NIR-Absorption und einer sehr hohen photothermischen Umwandlungseffizienz ( eta =37%).
JF  - Angewandte Chemie (English Edition)
AU  - Huang, Peng
AU  - Lin, Jing
AU  - Li, Wanwan
AU  - Rong, Pengfei
AU  - Wang, Zhe
AU  - Wang, Shouju
AU  - Wang, Xiaoping
AU  - Sun, Xiaolian
AU  - Aronova, Maria
AU  - Niu, Gang
AU  - Leapman, Richard D
AU  - Nie, Zhihong
AU  - Chen, Xiaoyuan
AD  - Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (USA).
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 14208
EP  - 14214
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 125
IS  - 52
SN  - 0044-8249, 0044-8249
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts
KW  - Biologisch abbaubare Blockcopolymere
KW  - Gold-Nanovesikel
KW  - Photoakustische Bildgebung
KW  - Photothermaltherapie
KW  - Plasmonenkopplung
KW  - surface plasmon resonance
KW  - I.R. radiation
KW  - Photoacoustics
KW  - Disulfide bonds
KW  - Gold
KW  - Vesicles
KW  - Crystals
KW  - Packing
KW  - imaging
KW  - Biodegradability
KW  - nanoparticles
KW  - W 30910:Imaging
KW  - A 01320:Microbial Degradation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496888701?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Angewandte+Chemie+%28English+Edition%29&rft.atitle=Biodegradable+Gold+Nanovesicles+with+an+Ultrastrong+Plasmonic+Coupling+Effect+for+Photoacoustic+Imaging+and+Photothermal+Therapy&rft.au=Huang%2C+Peng%3BLin%2C+Jing%3BLi%2C+Wanwan%3BRong%2C+Pengfei%3BWang%2C+Zhe%3BWang%2C+Shouju%3BWang%2C+Xiaoping%3BSun%2C+Xiaolian%3BAronova%2C+Maria%3BNiu%2C+Gang%3BLeapman%2C+Richard+D%3BNie%2C+Zhihong%3BChen%2C+Xiaoyuan&rft.aulast=Huang&rft.aufirst=Peng&rft.date=2013-12-01&rft.volume=125&rft.issue=52&rft.spage=14208&rft.isbn=&rft.btitle=&rft.title=Angewandte+Chemie+%28English+Edition%29&rft.issn=00448249&rft_id=info:doi/10.1002%2Fange.201308986
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-07-23
N1  - SubjectsTermNotLitGenreText - I.R. radiation; surface plasmon resonance; Disulfide bonds; Photoacoustics; Gold; Vesicles; Packing; Crystals; nanoparticles; Biodegradability; imaging
DO  - http://dx.doi.org/10.1002/ange.201308986
ER  - 



TY  - JOUR
T1  - Smoking behaviours and attitudes toward tobacco control among assistant environmental health officer trainees
AN  - 1496887424; 19031357
AB  - Assistant environmental health officers (AEHO) are health care providers (HCPs) who act as enforcers, educators and trusted role models for the public. This is the first study to explore smoking behaviour and attitudes toward tobacco control among future HCPs. Almost 30% of AEHO trainees did not know the role of AEHOs in counselling smokers to stop smoking, but 91% agreed they should not smoke before advising others not to do so. The majority agreed that tobacco control regulations may be used as a means of reducing the prevalence of smoking. Future AEHOs had positive attitudes toward tobacco regulations but lacked understanding of their responsibility in tobacco control measures.
JF  - International Journal of Tuberculosis and Lung Disease
AU  - Tee, G H
AU  - Gurpreet, K
AU  - Hairi, N N
AU  - Zarihah, Z
AU  - Fadzilah, K
AD  - Institute for Public Health, National Institutes of Health, Ministry of Health Malaysia, Jalan Bangsar, 50590 Kuala Lumpur, Malaysia, helentee.gh@moh.gov.my
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 1652
EP  - 1655
PB  - International Union Against Tuberculosis and Lung Disease, 68 bvd Saint-Michel Paris 75006 France
VL  - 17
IS  - 12
SN  - 1027-3719, 1027-3719
KW  - Health & Safety Science Abstracts
KW  - allied health science trainees
KW  - smoking
KW  - attitudes
KW  - tobacco control
KW  - Malaysia
KW  - Smoke
KW  - Smoking
KW  - Attitudes
KW  - Health care
KW  - Mycobacterium
KW  - Responsibility
KW  - Lung
KW  - Tobacco
KW  - Environmental health
KW  - Tuberculosis
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496887424?accountid=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=International+Journal+of+Tuberculosis+and+Lung+Disease&rft.atitle=Smoking+behaviours+and+attitudes+toward+tobacco+control+among+assistant+environmental+health+officer+trainees&rft.au=Tee%2C+G+H%3BGurpreet%2C+K%3BHairi%2C+N+N%3BZarihah%2C+Z%3BFadzilah%2C+K&rft.aulast=Tee&rft.aufirst=G&rft.date=2013-12-01&rft.volume=17&rft.issue=12&rft.spage=1652&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Tuberculosis+and+Lung+Disease&rft.issn=10273719&rft_id=info:doi/10.5588%2Fijtld.13.0241
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-04-16
N1  - SubjectsTermNotLitGenreText - Smoke; Smoking; Attitudes; Health care; Lung; Responsibility; Tobacco; Environmental health; Tuberculosis; Mycobacterium
DO  - http://dx.doi.org/10.5588/ijtld.13.0241
ER  - 



TY  - JOUR
T1  - Physicians' attitudes about communicating and managing scientific uncertainty differ by perceived ambiguity aversion of their patients
AN  - 1496666442; 201403326
AB  - Background Medical interventions are often characterized by substantial scientific uncertainty regarding their benefits and harms. Physicians must communicate to their patients as part of the process of shared decision making, yet they may not always communicate scientific uncertainty for several reasons. One suggested by past research is individual differences in physicians' tolerance of uncertainty. Relatedly, an unexplored explanation is physicians' beliefs about their patients' tolerance of uncertainty. Design To test this possibility, we surveyed a sample of primary care physicians (N=1500) and examined the association between their attitudes about communicating and managing scientific uncertainty and their perceptions of negative reactions to uncertainty by their patients. Physician perceptions were measured by their propensity towards pessimistic appraisals of risk information and avoidance of decision making when risk information is ambiguous -- of uncertain reliability, credibility or adequacy, known as 'ambiguity aversion'. Results Confirming past studies, physician demographics (e.g. medical specialty) predicted attitudes toward communicating scientific uncertainty. Additionally, physicians' beliefs about their patients' ambiguity aversion significantly predicted these preferences. Physicians who thought that more of their patients would have negative reactions to ambiguous information were more likely to think that they should decide what is best for their patients (Beta=0.065, P=0.013), and to withhold an intervention that had uncertainty associated with it (Beta=0.170, P<0.001). Discussion When faced with the task of communicating scientific uncertainty about medical tests and treatments, physicians' perceptions of their patients' ambiguity aversion may be related to their attitudes towards communicating uncertainty. Adapted from the source document.
JF  - Health Expectations
AU  - Portnoy, David B
AU  - Han, Paul K J
AU  - Ferrer, Rebecca A
AU  - Klein, William M P
AU  - Clauser, Steven B
AD  - Cancer Prevention Fellow, Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, Bethesda, MD
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 362
EP  - 372
PB  - Blackwell Publishing, Oxford UK
VL  - 16
IS  - 4
SN  - 1369-6513, 1369-6513
KW  - Uncertainty
KW  - Perceptions
KW  - Attitudes
KW  - Doctors
KW  - Interventions
KW  - Ambiguity
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496666442?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Expectations&rft.atitle=Physicians%27+attitudes+about+communicating+and+managing+scientific+uncertainty+differ+by+perceived+ambiguity+aversion+of+their+patients&rft.au=Portnoy%2C+David+B%3BHan%2C+Paul+K+J%3BFerrer%2C+Rebecca+A%3BKlein%2C+William+M+P%3BClauser%2C+Steven+B&rft.aulast=Portnoy&rft.aufirst=David&rft.date=2013-12-01&rft.volume=16&rft.issue=4&rft.spage=362&rft.isbn=&rft.btitle=&rft.title=Health+Expectations&rft.issn=13696513&rft_id=info:doi/10.1111%2Fj.1369-7625.2011.00717.x
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-02-01
N1  - Last updated - 2016-09-27
N1  - CODEN - HEHPFM
N1  - SubjectsTermNotLitGenreText - Uncertainty; Doctors; Ambiguity; Attitudes; Interventions; Perceptions
DO  - http://dx.doi.org/10.1111/j.1369-7625.2011.00717.x
ER  - 



TY  - JOUR
T1  - What Should Be Disclosed to Research Participants?
AN  - 1494297043; 2011-551742
AB  - Debate surrounding the SUPPORT study highlights the absence of consensus regarding what information should be disclosed to potential research participants. Some commentators endorse the view that clinical research should be subject to high disclosure standards, even when it is testing standard-of-care interventions. Others argue that trials assessing standard-of-care interventions need to disclose only the information that is disclosed in the clinical care setting. To resolve this debate, it is important to identify the ethical concerns raised by clinical research and determine what consent process is needed to address them. Adapted from the source document.
JF  - The American Journal of Bioethics
AU  - Wendler, David
AD  - Department of Bioethics, NIH Clinical Center dwendler@nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 3
EP  - 8
PB  - Taylor & Francis, Philadelphia PA
VL  - 13
IS  - 12
SN  - 1526-5161, 1526-5161
KW  - Health conditions and policy - Medicine and health care
KW  - Health conditions and policy - Health and health policy
KW  - Medical research Experimentation on humans
KW  - Standards
KW  - Health policy
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1494297043?accountid=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=The+American+Journal+of+Bioethics&rft.atitle=What+Should+Be+Disclosed+to+Research+Participants%3F&rft.au=Wendler%2C+David&rft.aulast=Wendler&rft.aufirst=David&rft.date=2013-12-01&rft.volume=13&rft.issue=12&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2013.851578
LA  - English
DB  - PAIS Index
N1  - Date revised - 2014-02-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Health policy; Standards; Medical research Experimentation on humans
DO  - http://dx.doi.org/10.1080/15265161.2013.851578
ER  - 



TY  - JOUR
T1  - Assessment of diffusion parameters by intravoxel incoherent motion MRI in head and neck squamous cell carcinoma
AN  - 1492659647; 18920006
AB  - The objectives of this study were to assess the diffusion parameters derived from intravoxel incoherent motion (IVIM) MRI in head and neck squamous cell carcinoma (HNSCC) and to investigate the agreement between different methods of tumor delineation and two numerical methods to extract the perfusion fraction f. Thirty-seven untreated patients with histopathologically confirmed primary HNSCC were included retrospectively in the study. The entire volume of the primary tumor was outlined on diffusion-weighted images using co-registered morphological images as a guide to the tumor location. Apparent diffusion coefficient (ADC) and IVIM diffusion parameters were estimated considering the largest tumor section as well as the entire tumor volume. A bi-exponential fit was implemented to extract f, D (pure diffusion coefficient) and D* (pseudo-diffusion coefficient). A second simplified method, based on an asymptotic extrapolation, was used to determine f. The agreement between ADC and IVIM diffusion parameters derived from the delineation of single and multiple slices, and between the two f estimations, was assessed by Bland-Altman plots. The inter-slice variability of ADC and IVIM diffusion parameters was evaluated. The Kruskal-Wallis test was used to investigate whether the tumor location had a statistically significant influence on the values of the parameters. Comparing the tumor delineation methods, a better accordance was found for ADC and D, with a mean percentage difference of less than 2%. Larger discrepancies were found for f and D*, with mean differences of 4.5% and 5.5%, respectively. When comparing the two f estimation methods, small mean differences were found (<3.5%), suggesting that the two methods may be considered as equivalent for the assessment of f in our patient population. The observed ADC and IVIM diffusion parameters were dependent on the anatomic site of the lesion, carcinoma of the nasopharynx showing more homogeneous and dissimilar estimations than other HNSCCs. Copyright copyright 2013 John Wiley & Sons, Ltd. Different approaches to the tumor region of interest selection and different numerical methods to extract intravoxel incoherent motion (IVIM) diffusion parameters were implemented and compared in a group of patients with head and neck squamous cell carcinoma. The largest tumor section was found to be representative of the entire tumor volume. Our results suggest that a simplified IVIM acquisition protocol could be defined, with a reduced number of b values in the low b value range, to assess the perfusion fraction. The apparent diffusion coefficient and IVIM diffusion parameters were dependent on the anatomic site of the lesion.
JF  - NMR in Biomedicine
AU  - Marzi, Simona
AU  - Piludu, Francesca
AU  - Vidiri, Antonello
AD  - Medical Physics Laboratory, Regina Elena National Cancer Institute, Rome, Italy.
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 1806
EP  - 1814
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 26
IS  - 12
SN  - 0952-3480, 0952-3480
KW  - Biotechnology and Bioengineering Abstracts
KW  - Diffusion coefficient
KW  - Tumors
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492659647?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Assessment+of+diffusion+parameters+by+intravoxel+incoherent+motion+MRI+in+head+and+neck+squamous+cell+carcinoma&rft.au=Marzi%2C+Simona%3BPiludu%2C+Francesca%3BVidiri%2C+Antonello&rft.aulast=Marzi&rft.aufirst=Simona&rft.date=2013-12-01&rft.volume=26&rft.issue=12&rft.spage=1806&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3020
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Tumors
DO  - http://dx.doi.org/10.1002/nbm.3020
ER  - 



TY  - JOUR
T1  - PAVIS: a tool for Peak Annotation and Visualization
AN  - 1492631766; 18891095
AB  - Summary: We introduce a web-based tool, Peak Annotation and Visualization (PAVIS), for annotating and visualizing ChIP-seq peak data. PAVIS is designed with non-bioinformaticians in mind and presents a straightforward user interface to facilitate biological interpretation of ChIP-seq peak or other genomic enrichment data. PAVIS, through association with annotation, provides relevant genomic context for each peak, such as peak location relative to genomic features including transcription start site, intron, exon or 5'/3'-untranslated region. PAVIS reports the relative enrichment P-values of peaks in these functionally distinct categories, and provides a summary plot of the relative proportion of peaks in each category. PAVIS, unlike many other resources, provides a peak-oriented annotation and visualization system, allowing dynamic visualization of tens to hundreds of loci from one or more ChIP-seq experiments, simultaneously. PAVIS enables rapid, and easy examination and cross-comparison of the genomic context and potential functions of the underlying genomic elements, thus supporting downstream hypothesis generation.
JF  - Bioinformatics
AU  - Huang, Weichun
AU  - Loganantharaj, Rasiah
AU  - Schroeder, Bryce
AU  - Fargo, David
AU  - Li, Leping
AD  - super(1)Biostatistics Branch and super(2)the Integrative Bioinformatics Group, National Institute of Environmental Health Sciences, Durham, NC 27709, USA
Y1  - 2013/12/01/
PY  - 2013
DA  - 2013 Dec 01
SP  - 3097
EP  - 3099
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 23
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - 3' Untranslated regions
KW  - Exons
KW  - Introns
KW  - Transcription
KW  - genomics
KW  - Bioinformatics
KW  - Internet
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492631766?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=PAVIS%3A+a+tool+for+Peak+Annotation+and+Visualization&rft.au=Huang%2C+Weichun%3BLoganantharaj%2C+Rasiah%3BSchroeder%2C+Bryce%3BFargo%2C+David%3BLi%2C+Leping&rft.aulast=Huang&rft.aufirst=Weichun&rft.date=2013-12-01&rft.volume=29&rft.issue=23&rft.spage=3097&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt520
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Data processing; 3' Untranslated regions; Exons; Introns; Transcription; Bioinformatics; genomics; Internet
DO  - http://dx.doi.org/10.1093/bioinformatics/btt520
ER  - 



TY  - JOUR
T1  - JC viruria and kidney disease in APOL1 risk genotype individuals: is this a clue to a gene environment interaction?
AN  - 1492627219; 18855374
AB  - APOL1 nephropathy occurs in a minority of genetically at-risk individuals, suggesting that other factors, such as other genes or environmental factors, contribute. Divers and colleagues report that among individuals with two APOL1 risk alleles, those with JC viruria are less likely to manifest kidney disease compared with those lacking JC viruria. These data might suggest that JC virus infection confers protection against glomerular injury, perhaps by altering cell function or generating immunity against a related polyomavirus.
JF  - Kidney International
AU  - Kopp, Jeffrey B
AD  - Kidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 1069
EP  - 1072
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 84
IS  - 6
SN  - 0085-2538, 0085-2538
KW  - Genetics Abstracts; Risk Abstracts
KW  - Data processing
KW  - Injuries
KW  - Kidney diseases
KW  - Polyomavirus
KW  - Immunity
KW  - Genotypes
KW  - Infection
KW  - Environmental factors
KW  - JC virus
KW  - Risk factors
KW  - Nephropathy
KW  - Kidney
KW  - Viruria
KW  - R2 23060:Medical and environmental health
KW  - G 07730:Development & Cell Cycle
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492627219?accountid=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=Kidney+International&rft.atitle=JC+viruria+and+kidney+disease+in+APOL1+risk+genotype+individuals%3A+is+this+a+clue+to+a+gene+environment+interaction%3F&rft.au=Kopp%2C+Jeffrey+B&rft.aulast=Kopp&rft.aufirst=Jeffrey&rft.date=2013-12-01&rft.volume=84&rft.issue=6&rft.spage=1069&rft.isbn=&rft.btitle=&rft.title=Kidney+International&rft.issn=00852538&rft_id=info:doi/10.1038%2Fki.2013.299
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Data processing; Injuries; Nephropathy; Kidney diseases; Viruria; Genotypes; Immunity; Infection; Environmental factors; Risk factors; Kidney; Polyomavirus; JC virus
DO  - http://dx.doi.org/10.1038/ki.2013.299
ER  - 



TY  - JOUR
T1  - Subconjunctival Palomid 529 in the treatment of neovascular age-related macular degeneration.
AN  - 1477563710; 23689994
AB  - Recent evidence suggests that neovascular age-related macular degeneration (AMD) may have an immune mediated component. Palomid 529, an investigational medication involving the immune Akt/mTOR pathway, is unique in dissociating both targets of rapamycin complexes TORC1 and TORC2. This small short-term pilot study assesses the safety of subconjunctival Palomid 529 in the treatment of neovascular AMD, with some limited efficacy information.
          In this 12-week phase I open-label prospective pilot study, five participants with neovascular age-related macular degeneration that were refractory to intravitreal anti-vascular endothelial growth factor (VEGF) received three serial monthly subconjunctival doses of 1.9 mg Palomid 529. All participants were also offered concomitant monthly intravitreal anti-VEGF injections. Safety was monitored via adverse events recording. Additional outcome measures included visual acuity, optical coherence tomography, fluorescein angiography, indocyanine green angiography and fundus photography. The study drug was well-tolerated by all participants. There were no drug-related adverse events and no serious adverse events. A depot formed at the injection site, which persisted at the end of the study. In these anti-VEGF refractory patients, no clinically important changes in best-corrected visual acuity, fluorescein leakage pattern, choroidal neovascularization size on indocyanine green angiography, or autofluorescence pattern on fundus autofluorescence were observed compared to baseline. The fluid status, assessed with optical coherence tomography showed that central retinal thickness and macular volume remained stable in three participants, while the other two participants clinically progressed.
          Serial subconjunctival injections of Palomid 529 were well-tolerated and resulted in depot formation. There were no concerns for any ocular or systemic toxicity during this small short-term study. Larger randomized studies are required to determine efficacy.
JF  - Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
AU  - Dalal, Monica
AU  - Jacobs-El, Naima
AU  - Nicholson, Benjamin
AU  - Tuo, Jingsheng
AU  - Chew, Emily
AU  - Chan, Chi-Chao
AU  - Nussenblatt, Robert
AU  - Ferris, Frederick
AU  - Meyerle, Catherine
AD  - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 2705
EP  - 2709
VL  - 251
IS  - 12
KW  - Benzopyrans
KW  - 0
KW  - Coloring Agents
KW  - Enzyme Inhibitors
KW  - Multiprotein Complexes
KW  - TOR complex 2
KW  - mechanistic target of rapamycin complex 1
KW  - TOR Serine-Threonine Kinases
KW  - EC 2.7.1.1
KW  - Indocyanine Green
KW  - IX6J1063HV
KW  - palomid 529
KW  - XV9409EWG4
KW  - Index Medicus
KW  - TOR Serine-Threonine Kinases -- antagonists & inhibitors
KW  - Humans
KW  - Fluorescein Angiography
KW  - Aged
KW  - Conjunctiva
KW  - Pilot Projects
KW  - Multiprotein Complexes -- antagonists & inhibitors
KW  - Visual Acuity -- physiology
KW  - Prospective Studies
KW  - Aged, 80 and over
KW  - Treatment Outcome
KW  - Tomography, Optical Coherence
KW  - Female
KW  - Male
KW  - Enzyme Inhibitors -- therapeutic use
KW  - Benzopyrans -- therapeutic use
KW  - Wet Macular Degeneration -- diagnosis
KW  - Wet Macular Degeneration -- drug therapy
KW  - Wet Macular Degeneration -- physiopathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1477563710?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Graefe%27s+archive+for+clinical+and+experimental+ophthalmology+%3D+Albrecht+von+Graefes+Archiv+fur+klinische+und+experimentelle+Ophthalmologie&rft.atitle=Subconjunctival+Palomid+529+in+the+treatment+of+neovascular+age-related+macular+degeneration.&rft.au=Dalal%2C+Monica%3BJacobs-El%2C+Naima%3BNicholson%2C+Benjamin%3BTuo%2C+Jingsheng%3BChew%2C+Emily%3BChan%2C+Chi-Chao%3BNussenblatt%2C+Robert%3BFerris%2C+Frederick%3BMeyerle%2C+Catherine&rft.aulast=Dalal&rft.aufirst=Monica&rft.date=2013-12-01&rft.volume=251&rft.issue=12&rft.spage=2705&rft.isbn=&rft.btitle=&rft.title=Graefe%27s+archive+for+clinical+and+experimental+ophthalmology+%3D+Albrecht+von+Graefes+Archiv+fur+klinische+und+experimentelle+Ophthalmologie&rft.issn=1435-702X&rft_id=info:doi/10.1007%2Fs00417-013-2375-7
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-12
N1  - Date created - 2013-12-16
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - NCT01271270; ClinicalTrials.gov
N1  - SuppNotes - Cited By:
Am J Ophthalmol. 2007 Oct;144(4):618-26 [17698021]
J Clin Invest. 2005 Aug;115(8):2119-27 [16075056]
Cancer Res. 2008 Nov 15;68(22):9551-7 [19010932]
Lancet. 2008 Nov 22;372(9652):1835-45 [19027484]
Curr Opin Investig Drugs. 2009 May;10(5):434-42 [19431076]
Cell Cycle. 2009 Dec;8(23):3831-7 [19901542]
Nat Med. 2010 Feb;16(2):205-13 [20072130]
Mol Vis. 2010;16:184-93 [20157617]
Arch Ophthalmol. 2010 Jun;128(6):750-8 [20547953]
Eye (Lond). 2011 Feb;25(2):127-39 [21183941]
Cell. 2012 May 11;149(4):847-59 [22541070]
Nat Med. 2012 May;18(5):791-8 [22484808]
N Engl J Med. 2012 Aug 23;367(8):768-70 [22913688]
FASEB J. 2002 Jun;16(8):771-80 [12039858]
Nature. 1999 Jun 10;399(6736):597-601 [10376602]
Mol Vis. 2004 Dec 22;10:964-72 [15623986]
Semin Immunopathol. 2008 Apr;30(2):97-110 [18299834]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s00417-013-2375-7
ER  - 



TY  - JOUR
T1  - Childhood height and birth weight in relation to future prostate cancer risk: a cohort study based on the copenhagen school health records register.
AN  - 1466375071; 24089459
AB  - Adult height has been positively associated with prostate cancer risk. However, the exposure window of importance is currently unknown and assessments of height during earlier growth periods are scarce. In addition, the association between birth weight and prostate cancer remains undetermined. We assessed these relationships in a cohort of the Copenhagen School Health Records Register (CSHRR).
          The CSHRR comprises 372,636 school children. For boys born between the 1930s and 1969, birth weight and annual childhood heights-measured between ages 7 and 13 years-were analyzed in relation to prostate cancer risk. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI). There were 125,211 males for analysis, 2,987 of who were subsequently diagnosed with prostate cancer during 2.57 million person-years of follow-up. Height z-score was significantly associated with prostate cancer risk at all ages (HRs, 1.13 to 1.14). Height at age 13 years was more important than height change (P = 0.024) and height at age 7 years (P = 0.024), when estimates from mutually adjusted models were compared. Adjustment of birth weight did not alter the estimates. Birth weight was not associated with prostate cancer risk.
          The association between childhood height and prostate cancer risk was driven by height at age 13 years. Our findings implicate late childhood, adolescence, and adulthood growth periods as containing the exposure window(s) of interest that underlies the association between height and prostate cancer. The causal factor may not be singular given the complexity of both human growth and carcinogenesis.
          ©2013 AACR.
JF  - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
AU  - Cook, Michael B
AU  - Gamborg, Michael
AU  - Aarestrup, Julie
AU  - Sørensen, Thorkild I A
AU  - Baker, Jennifer L
AD  - Authors' Affiliations: Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland; Institute of Preventive Medicine, Bispebjerg and Frederiksberg Hospital, The Capital Region; and The Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 2232
EP  - 2240
VL  - 22
IS  - 12
KW  - Index Medicus
KW  - School Health Services
KW  - Registries
KW  - Risk Factors
KW  - Humans
KW  - Cohort Studies
KW  - Denmark -- epidemiology
KW  - Child
KW  - Adolescent
KW  - Male
KW  - Proportional Hazards Models
KW  - Birth Weight
KW  - Prostatic Neoplasms -- epidemiology
KW  - Body Height
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1466375071?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Childhood+height+and+birth+weight+in+relation+to+future+prostate+cancer+risk%3A+a+cohort+study+based+on+the+copenhagen+school+health+records+register.&rft.au=Cook%2C+Michael+B%3BGamborg%2C+Michael%3BAarestrup%2C+Julie%3BS%C3%B8rensen%2C+Thorkild+I+A%3BBaker%2C+Jennifer+L&rft.aulast=Cook&rft.aufirst=Michael&rft.date=2013-12-01&rft.volume=22&rft.issue=12&rft.spage=2232&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-13-0712
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-10-02
N1  - Date created - 2013-12-09
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Causes Control. 2010 Jul;21(7):1071-80 [20333462]
Scand J Public Health. 2011 Jul;39(7 Suppl):22-5 [21775345]
Lancet. 1999 Oct 30;354(9189):1526-7 [10551505]
Cancer Epidemiol Biomarkers Prev. 2000 Feb;9(2):221-3 [10698486]
Am J Epidemiol. 2001 Sep 15;154(6):530-7 [11549558]
Int J Cancer. 2001 Dec 20;96(6):363-71 [11745507]
Int J Epidemiol. 2002 Apr;31(2):383-90 [11980800]
Best Pract Res Clin Endocrinol Metab. 2002 Jun;16(2):225-41 [12064890]
J Natl Cancer Inst. 2002 Jul 3;94(13):981-90 [12096083]
Urol Clin North Am. 2002 Feb;29(1):173-81 [12109343]
Cancer Causes Control. 2003 May;14(4):335-8 [12846364]
Nutr Cancer. 2003;47(1):34-9 [14769535]
Scand J Public Health. 2011 Jul;39(7 Suppl):42-5 [21775350]
Endocrinol Metab Clin North Am. 2011 Sep;40(3):577-90, ix [21889722]
Hum Mol Genet. 2011 Oct 15;20(20):4069-75 [21757498]
World J Urol. 2012 Apr;30(2):143-8 [22116601]
Am J Hum Biol. 2012 Jul-Aug;24(4):406-10 [22287160]
Cancer Causes Control. 2012 Aug;23(8):1377-85 [22706676]
Am J Phys Anthropol. 2012 Aug;148(4):487-94 [22552747]
Cancer Epidemiol Biomarkers Prev. 2012 Sep;21(9):1531-41 [22761305]
Int J Epidemiol. 2012 Oct;41(5):1419-33 [22825588]
Prostate. 2013 Feb 15;73(3):261-6 [22851289]
Cancer Prev Res (Phila). 2013 Feb;6(2):91-9 [23315596]
Nat Rev Cancer. 2013 Mar;13(3):208-518 [23363989]
Nat Genet. 2013 Apr;45(4):385-91, 391e1-2 [23535732]
Cancer Causes Control. 2013 Jun;24(6):1129-35 [23519640]
Int J Cancer. 2013 Jul 15;133(2):495-504 [23341348]
J Natl Cancer Inst. 2013 Jul 17;105(14):1050-8 [23847245]
Cancer Chemother Rep. 1966 Mar;50(3):125-8 [5948714]
Br J Prev Soc Med. 1972 Nov;26(4):224-30 [4658268]
Hum Biol. 1978 Feb;50(1):69-72 [649106]
J Natl Cancer Inst. 1988 Jul 20;80(10):772-4 [3385783]
Eur J Clin Nutr. 1990 Jan;44(1):45-60 [2354692]
Crit Rev Oncol Hematol. 1990;10(3):283-303 [2257089]
J Urol. 1993 Aug;150(2 Pt 1):379-85 [8326560]
J Urol. 1994 May;151(5):1427-32 [8158800]
Int J Cancer. 1994 May 1;57(3):313-7 [8168989]
Eur J Clin Nutr. 1994 Feb;48 Suppl 1:S25-43; discussion S43-4 [8005089]
J Clin Endocrinol Metab. 1995 Aug;80(8):2534-42 [7543116]
Acta Paediatr. 1995 May;84(5):532-5 [7633149]
BMJ. 1996 Aug 10;313(7053):337-41 [8760741]
J Clin Lab Anal. 1996;10(6):468-9 [8951622]
Am J Epidemiol. 1998 Jun 15;147(12):1140-4 [9645792]
Br J Nutr. 1951;5(1):142-51 [14886531]
J Pathol Bacteriol. 1954 Oct;68(2):603-16 [14354564]
Int J Cancer. 2005 Mar 1;113(6):1002-4 [15514943]
Epidemiology. 2005 Mar;16(2):175-81 [15703531]
Obes Res. 2005 Dec;13(12):2187-94 [16421354]
Food Nutr Bull. 2006 Dec;27(4 Suppl Growth Standard):S279-94 [17361663]
Prostate. 2007 Aug 1;67(11):1247-54 [17570499]
Cancer. 2007 Jul 15;110(2):412-9 [17538980]
CA Cancer J Clin. 2007 Jul-Aug;57(4):190-205 [17626117]
Can J Urol. 2008 Feb;15(1):3866-71 [18304396]
Differentiation. 2008 Jul;76(6):565-77 [18462432]
Cancer Epidemiol Biomarkers Prev. 2008 Sep;17(9):2325-36 [18768501]
Ann Hum Biol. 2008 Sep-Oct;35(5):518-34 [18821329]
Cancer Causes Control. 2009 Mar;20(2):243-51 [18855108]
Eur J Clin Nutr. 2009 Mar;63(3):375-81 [18301438]
Int J Epidemiol. 2009 Jun;38(3):656-62 [18719090]
Econ Hum Biol. 2009 Jul;7(2):137-52 [19628438]
Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2422-6 [19690187]
J Natl Cancer Inst. 2009 Oct 7;101(19):1325-9 [19720969]
Obes Facts. 2009;2(3):179-86 [20054223]
J Forensic Leg Med. 2010 Feb;17(2):78-83 [20129426]
Ugeskr Laeger. 2010 Mar 1;172(9):696-700 [20199746]
Cancer Causes Control. 2009 Oct;20(8):1431-40 [19526319]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/1055-9965.EPI-13-0712
ER  - 



TY  - JOUR
T1  - DNA methylation profiling in human B cells reveals immune regulatory elements and epigenetic plasticity at Alu elements during B-cell activation.
AN  - 1464893833; 24013550
AB  - Memory is a hallmark of adaptive immunity, wherein lymphocytes mount a superior response to a previously encountered antigen. It has been speculated that epigenetic alterations in memory lymphocytes contribute to their functional distinction from their naive counterparts. However, the nature and extent of epigenetic alterations in memory compartments remain poorly characterized. Here we profile the DNA methylome and the transcriptome of B-lymphocyte subsets representing stages of the humoral immune response before and after antigen exposure in vivo from multiple humans. A significant percentage of activation-induced losses of DNA methylation mapped to transcription factor binding sites. An additional class of demethylated loci mapped to Alu elements across the genome and accompanied repression of DNA methyltransferase 3A. The activation-dependent DNA methylation changes were largely retained in the progeny of activated B cells, generating a similar epigenetic signature in downstream memory B cells and plasma cells with distinct transcriptional programs. These findings provide insights into the methylation dynamics of the genome during cellular differentiation in an immune response.
JF  - Genome research
AU  - Lai, Anne Y
AU  - Mav, Deepak
AU  - Shah, Ruchir
AU  - Grimm, Sara A
AU  - Phadke, Dhiral
AU  - Hatzi, Katerina
AU  - Melnick, Ari
AU  - Geigerman, Cissy
AU  - Sobol, Steve E
AU  - Jaye, David L
AU  - Wade, Paul A
AD  - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 2030
EP  - 2041
VL  - 23
IS  - 12
KW  - Transcription Factors
KW  - 0
KW  - DNA (Cytosine-5-)-Methyltransferase
KW  - EC 2.1.1.37
KW  - DNA methyltransferase 3A
KW  - Index Medicus
KW  - Plasma Cells -- metabolism
KW  - Genome, Human
KW  - Transcription Factors -- metabolism
KW  - Humans
KW  - Plasma Cells -- immunology
KW  - Cell Differentiation -- genetics
KW  - DNA (Cytosine-5-)-Methyltransferase -- metabolism
KW  - Epigenesis, Genetic
KW  - Transcription Factors -- genetics
KW  - DNA (Cytosine-5-)-Methyltransferase -- genetics
KW  - Gene Expression Profiling
KW  - Immunologic Memory -- genetics
KW  - Adaptive Immunity -- genetics
KW  - Gene Expression Regulation
KW  - Binding Sites -- genetics
KW  - Adaptive Immunity -- immunology
KW  - Lymphocyte Activation -- genetics
KW  - Regulatory Elements, Transcriptional -- genetics
KW  - DNA Methylation
KW  - Alu Elements
KW  - B-Lymphocytes -- immunology
KW  - B-Lymphocytes -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464893833?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+research&rft.atitle=DNA+methylation+profiling+in+human+B+cells+reveals+immune+regulatory+elements+and+epigenetic+plasticity+at+Alu+elements+during+B-cell+activation.&rft.au=Lai%2C+Anne+Y%3BMav%2C+Deepak%3BShah%2C+Ruchir%3BGrimm%2C+Sara+A%3BPhadke%2C+Dhiral%3BHatzi%2C+Katerina%3BMelnick%2C+Ari%3BGeigerman%2C+Cissy%3BSobol%2C+Steve+E%3BJaye%2C+David+L%3BWade%2C+Paul+A&rft.aulast=Lai&rft.aufirst=Anne&rft.date=2013-12-01&rft.volume=23&rft.issue=12&rft.spage=2030&rft.isbn=&rft.btitle=&rft.title=Genome+research&rft.issn=1549-5469&rft_id=info:doi/10.1101%2Fgr.155473.113
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-09
N1  - Date created - 2013-12-03
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - GSE42386; GEO; GSE24919
N1  - SuppNotes - Cited By:
Curr Opin Immunol. 2010 Jun;22(3):341-7 [20226645]
Nature. 2008 Aug 7;454(7205):766-70 [18600261]
Nat Rev Mol Cell Biol. 2010 Sep;11(9):607-20 [20683471]
J Exp Med. 2010 Aug 30;207(9):1939-50 [20733034]
Nature. 2010 Sep 16;467(7313):285-90 [20644535]
Nature. 2010 Sep 16;467(7313):338-42 [20720541]
Nat Immunol. 2011 Jan;12(1):62-9 [21113164]
Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21931-6 [21106759]
PLoS Biol. 2011 Apr;9(4):e1001046 [21526222]
Nucleic Acids Res. 2011 May;39(10):4099-108 [21278160]
Blood. 2011 Sep 29;118(13):3559-69 [21828137]
Mol Cell. 2011 Oct 7;44(1):17-28 [21924933]
Nature. 2011 Dec 22;480(7378):490-5 [22170606]
Annu Rev Immunol. 2012;30:429-57 [22224772]
Nat Chem Biol. 2012 Sep;8(9):751-8 [22772155]
Mol Cell. 2012 Aug 24;47(4):633-47 [22841485]
Nature. 2012 Sep 6;489(7414):75-82 [22955617]
Cell. 1999 Oct 29;99(3):247-57 [10555141]
Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14412-7 [10588719]
Nature. 1999 Nov 11;402(6758):187-91 [10647011]
Cell. 2000 Jan 7;100(1):157-68 [10647940]
Nat Immunol. 2003 Jan;4(1):78-86 [12447360]
Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2639-44 [12604779]
Blood. 2004 Apr 1;103(7):2683-90 [14645008]
Cell. 2004 Oct 1;119(1):75-86 [15454082]
Cell. 1992 Jun 12;69(6):915-26 [1606615]
Cell. 1992 Nov 27;71(5):865-73 [1423634]
Mol Cell Biol. 1993 Aug;13(8):4523-30 [8336699]
J Biol Chem. 1993 Sep 15;268(26):19565-73 [8366099]
Genes Dev. 1994 Feb 15;8(4):481-90 [8125260]
J Exp Med. 1994 Jul 1;180(1):329-39 [8006591]
Immunity. 1995 Mar;2(3):239-48 [7535180]
J Biol Chem. 1995 Apr 28;270(17):10091-6 [7730313]
Nat Rev Immunol. 2005 Mar;5(3):230-42 [15738953]
Annu Rev Immunol. 2005;23:487-513 [15771579]
Nat Rev Immunol. 2005 Jun;5(6):497-508 [15928681]
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517]
Proc Natl Acad Sci U S A. 2009 Jan 20;106(3):671-8 [19139413]
Curr Opin Immunol. 2009 Jun;21(3):298-304 [19497721]
Genome Res. 2009 Sep;19(9):1639-45 [19541911]
Mol Cell Biol. 2009 Oct;29(19):5366-76 [19620278]
Nat Rev Genet. 2009 Nov;10(11):805-11 [19789556]
Nat Genet. 2009 Nov;41(11):1207-15 [19801979]
Nature. 2009 Nov 19;462(7271):315-22 [19829295]
Nucleic Acids Res. 2010 Jan;38(2):391-9 [19906696]
Curr Opin Genet Dev. 2010 Apr;20(2):149-55 [20176473]
Immunity. 2006 Mar;24(3):269-81 [16546096]
J Immunol. 2006 Apr 1;176(7):4083-93 [16547244]
Cancer Res. 2006 Aug 15;66(16):7939-47 [16912168]
Cell. 2006 Aug 25;126(4):663-76 [16904174]
Biostatistics. 2007 Jan;8(1):118-27 [16632515]
BMC Genomics. 2007;8:23 [17239240]
Nat Genet. 2007 Apr;39(4):457-66 [17334365]
J Exp Med. 2007 Apr 16;204(4):715-22 [17420264]
Nat Immunol. 2007 Jul;8(7):705-14 [17558410]
Nature. 2007 Jul 19;448(7151):318-24 [17554336]
Nature. 2007 Aug 2;448(7153):553-60 [17603471]
J Pathol. 2007 Sep;213(1):106-15 [17573669]
Proc Natl Acad Sci U S A. 2007 Aug 14;104(33):13420-5 [17673551]
Nucleic Acids Res. 2008 Jun;36(10):e58 [18450815]
Nature. 2008 Jul 3;454(7200):49-55 [18509334]
Science. 2010 Jul 23;329(5990):444-8 [20651149]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1101/gr.155473.113
ER  - 



TY  - JOUR
T1  - Comparison of super(18)F-labeled CXCR4 antagonist peptides for PET imaging of CXCR4 expression
AN  - 1464511024; 18809675
AB  - Purpose: CXCR4 is overexpressed on tumor cells from many types of human cancers. A high level of CXCR4 expression often correlates with poor prognosis, chemotherapy resistance, and metastasis. The development of CXCR4-specific radiotracers for positron emission tomography (PET) imaging will allow in vivo evaluation of receptor expression level for diagnosis or therapeutic evaluation. Procedures: Two new super(18)F-labeled radiotracers based on an Ac-TC14012 peptide, [ super(18)F]FP-Ac-TC14012 and [ super(18)F]FB-Ac-TC14012, were synthesized and characterized. The affinities of the 2-fluoropropionate (FP)-conjugated or 4-fluorobenzoate (FB)-conjugated peptides to CXCR4-transfected Chinese hamster ovarian (CHO) cells were evaluated in a competitive binding assay with [ super(125)I]CXCL12 radioligand. The cell uptake and retention of [ super(18)F]FP-labeled and [ super(18)F]FB-labeled peptides were measured. The tumor targetability and pharmacokinetics of these two tracers were also evaluated by microPET imaging and biodistribution studies. Results: The labeled peptides retained high binding affinity to CXCR4 and showed much higher uptake in CXCR4-positive CHO cells than in CXCR4-negative cells in vitro. The smaller and more hydrophilic [ super(18)F]FP prosthetic group resulted in higher affinity and lower nonspecific cell uptake compared to the [ super(18)F]FB-labeled peptide. Both radiotracers showed much higher accumulation in CXCR4-positive than CXCR4-negative tumor xenografts in mice and allowed clear visualization of CXCR4 expression by PET. Among the two, [ super(18)F]FP-Ac-TC14012 showed higher tumor uptake and better tumor-to-background contrast. Unlike their N-terminal 4-F-benzoate analogs, these two tracers had minimal blood retention, likely due to reduced red blood cell binding. Metabolic organs, such as the liver and kidney, also showed high uptake. When blocked with low-dose cold peptide (10 mu g), the tumor uptake was significantly increased, most likely due to the increased concentration in blood circulation, as evidenced by decreased liver uptake. Conclusion: These results demonstrate that the [ super(18)F]FP-labeled Ac-TC14012 peptide with high tumor uptake, low nonspecific binding, and good tumor-to-background contrast promises [ super(18)F]FP-Ac-TC14012 as a PET tracer for in vivo PET imaging of CXCR4 expression.
JF  - Molecular Imaging and Biology
AU  - Zhang, Xiao-Xiang
AU  - Sun, Zhongchan
AU  - Guo, Jinxia
AU  - Wang, Zhe
AU  - Wu, Chenxi
AU  - Niu, Gang
AU  - Ma, Ying
AU  - Kiesewetter, Dale O
AU  - Chen, Xiaoyuan
AD  - Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD, 20892, USA, dkiesewetter@mail.nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 758
EP  - 767
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 15
IS  - 6
SN  - 1536-1632, 1536-1632
KW  - Biotechnology and Bioengineering Abstracts
KW  - Blood circulation
KW  - CXCR4 protein
KW  - Chemotherapy
KW  - Erythrocytes
KW  - Prognosis
KW  - Tumors
KW  - Tumor cells
KW  - Pharmacokinetics
KW  - Cancer
KW  - Metastases
KW  - Tracers
KW  - Prosthetic groups
KW  - Kidney
KW  - Liver
KW  - Positron emission tomography
KW  - Radioisotopes
KW  - Xenografts
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464511024?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Imaging+and+Biology&rft.atitle=Comparison+of+super%2818%29F-labeled+CXCR4+antagonist+peptides+for+PET+imaging+of+CXCR4+expression&rft.au=Zhang%2C+Xiao-Xiang%3BSun%2C+Zhongchan%3BGuo%2C+Jinxia%3BWang%2C+Zhe%3BWu%2C+Chenxi%3BNiu%2C+Gang%3BMa%2C+Ying%3BKiesewetter%2C+Dale+O%3BChen%2C+Xiaoyuan&rft.aulast=Zhang&rft.aufirst=Xiao-Xiang&rft.date=2013-12-01&rft.volume=15&rft.issue=6&rft.spage=758&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-013-0640-0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 41
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - CXCR4 protein; Blood circulation; Chemotherapy; Erythrocytes; Prognosis; Tumors; Tumor cells; Cancer; Pharmacokinetics; Metastases; Prosthetic groups; Tracers; Radioisotopes; Positron emission tomography; Liver; Kidney; Xenografts
DO  - http://dx.doi.org/10.1007/s11307-013-0640-0
ER  - 



TY  - JOUR
T1  - Immunochemical characterization of synthetic hexa-, octa- and decasaccharide conjugate vaccines for Vibrio cholerae O:1 Serotype Ogawa with emphasis on antigenic density and chain length
AN  - 1464510069; 18751319
AB  - Cholera remains to be a global health problem without suitable vaccines for endemic control or outbreak relief. Here we describe a new parenteral vaccine based on neoglyco-conjugate of synthetic fragments of O-specific polysaccharide (O-SP) of Vibrio cholerae O1, serotype Ogawa. Hexa-, octa- and decasaccharides of the O-SP with carboxylic acid at the reducing end were chemically synthesized and conjugated to tetanus toxoid (TT). The conjugates prepared by a novel linking scheme consisted of 17-atom linker of hydrazide and alkyl bonds elicited robust serum IgG anti-LPS responses with vibriocidal activities in mice. There is a length dependence in immune response with decasaccharide conjugates elicited the highest anti-LPS IgG. There seems to be an indication that regardless of the carbohydrate chain length, a molar ratio of 230 plus or minus 10 monosaccharide units per TT induced high antibody response. The conjugates also elicited cross-reactive antibodies to serotype Inaba. The formulation of the proposed cholera conjugate vaccine, similar to other licensed polysaccharide vaccine, is suitable for children immunization. A parenteral cholera vaccine could overcome the diminishing immunogenicity in most of oral vaccines due to the gastrointestinal complexity and environmental enteropathy in children living in impoverished environment and could be considered for global cholera immunization.
JF  - Glycoconjugate Journal
AU  - Ftacek, Peter
AU  - Nelson, Victor
AU  - Szu, Shousun C
AD  - Eunice Kennedy Shriver National Institute of Child Health & Human Development, National Institutes of Health, Bldg. 6, Room 1A06, 9000 Rockville Pike, Bethesda, MD, 20892, USA, szunih@gmail.com
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 871
EP  - 880
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 30
IS  - 9
SN  - 0282-0080, 0282-0080
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Serotypes
KW  - Disease control
KW  - monosaccharides
KW  - Tetanus
KW  - Polysaccharides
KW  - Defence mechanisms
KW  - Endemic species
KW  - carboxylic acids
KW  - Cholera
KW  - Carbohydrates
KW  - Pathogenic bacteria
KW  - Bacterial diseases
KW  - Antibody response
KW  - Children
KW  - Immunization
KW  - Vibrio cholerae
KW  - glycoconjugates
KW  - Antibodies
KW  - Immunogenicity
KW  - Immunoglobulin G
KW  - Immune response
KW  - Vaccines
KW  - F 06905:Vaccines
KW  - Q1 08423:Behaviour
KW  - J 02350:Immunology
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464510069?accountid=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=Glycoconjugate+Journal&rft.atitle=Immunochemical+characterization+of+synthetic+hexa-%2C+octa-+and+decasaccharide+conjugate+vaccines+for+Vibrio+cholerae+O%3A1+Serotype+Ogawa+with+emphasis+on+antigenic+density+and+chain+length&rft.au=Ftacek%2C+Peter%3BNelson%2C+Victor%3BSzu%2C+Shousun+C&rft.aulast=Ftacek&rft.aufirst=Peter&rft.date=2013-12-01&rft.volume=30&rft.issue=9&rft.spage=871&rft.isbn=&rft.btitle=&rft.title=Glycoconjugate+Journal&rft.issn=02820080&rft_id=info:doi/10.1007%2Fs10719-013-9491-9
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 72
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Endemic species; Antibodies; Pathogenic bacteria; Bacterial diseases; Disease control; Vaccines; Defence mechanisms; Polysaccharides; Immunization; Serotypes; Antibody response; monosaccharides; Children; Tetanus; glycoconjugates; Immunogenicity; Immunoglobulin G; carboxylic acids; Cholera; Carbohydrates; Immune response; Vibrio cholerae
DO  - http://dx.doi.org/10.1007/s10719-013-9491-9
ER  - 



TY  - JOUR
T1  - Complex Histopathologic Response in Rat Kidney to Oral beta -myrcene: An Unusual Dose-related Nephrosis and Low-dose Alpha2u-Globulin Nephropathy
AN  - 1464505313; 18799064
AB  - Oral gavage studies with beta -myrcene in male F344 rats showed a complex renal pathology comprising both alpha2u-globulin ( alpha 2u-g) nephropathy, an unusual nephrosis involving the outer stripe of outer medulla (OSOM), and an increased incidence of renal tubule tumors by 2 years. In the 90-day and 2-year studies, respectively, alpha 2u-g nephropathy and linear papillary mineralization were observed in males at the two lower doses but were absent from the high dose. Nephrosis was characterized by dilation of the S3 tubules, nuclear enlargement (including karyomegaly), and luminal pyknotic cells, all in the outermost OSOM. Nephrosis was minimal at the higher doses in the 90-day study, but progressed to a severe grade in males dosed with 1,000 mg/kg for 2 years. Renal tubule tumors developed in treated groups with incidences up to 30% in the 250 and 500 mg/kg male dose groups. Tumors at the lower doses in males may have been associated with alpha 2u-g nephropathy, while those at higher doses in both sexes may have been due to the nephrosis. Because beta -myrcene induced a complex spectrum of renal pathology, the alpha 2u-g nephropathy mechanism cannot be the sole mechanism of carcinogenesis in these rats.
JF  - Toxicologic Pathology
AU  - Cesta, Mark F
AU  - Hard, Gordon C
AU  - Boyce, John T
AU  - Ryan, Michael J
AU  - Chan, Po C
AU  - Sills, Robert C
AD  - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, cesta@niehs.nih.gov
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1068
EP  - 1077
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 41
IS  - 8
SN  - 0192-6233, 0192-6233
KW  - Toxicology Abstracts
KW  - kidney
KW  - nephropathy
KW  - beta -myrcene
KW  - alpha2u-globulin
KW  - rat.
KW  - renal tubules
KW  - Nephropathy
KW  - Carcinogenesis
KW  - Kidney
KW  - Myrcene
KW  - Tumors
KW  - Mineralization
KW  - Sex
KW  - X 24490:Other
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464505313?accountid=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=Complex+Histopathologic+Response+in+Rat+Kidney+to+Oral+beta+-myrcene%3A+An+Unusual+Dose-related+Nephrosis+and+Low-dose+Alpha2u-Globulin+Nephropathy&rft.au=Cesta%2C+Mark+F%3BHard%2C+Gordon+C%3BBoyce%2C+John+T%3BRyan%2C+Michael+J%3BChan%2C+Po+C%3BSills%2C+Robert+C&rft.aulast=Cesta&rft.aufirst=Mark&rft.date=2013-12-01&rft.volume=41&rft.issue=8&rft.spage=1068&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313482057
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 16
N1  - Last updated - 2016-08-03
N1  - SubjectsTermNotLitGenreText - renal tubules; Carcinogenesis; Nephropathy; Kidney; Tumors; Myrcene; Mineralization; Sex
DO  - http://dx.doi.org/10.1177/0192623313482057
ER  - 



TY  - JOUR
T1  - Functional Role of Methylation of G518 of the 16S rRNA 530 Loop by GidB in Mycobacterium tuberculosis
AN  - 1464504907; 18808460
AB  - Posttranscriptional modifications of bacterial rRNA serve a variety of purposes, from stabilizing ribosome structure to preserving its functional integrity. Here, we investigated the functional role of one rRNA modification in particular-the methylation of guanosine at position 518 (G518) of the 16S rRNA in Mycobacterium tuberculosis. Based on previously reported evidence that G518 is located 5 Aa; from proline 44 of ribosomal protein S12, which interacts directly with the mRNA wobble position of the codon:anticodon helix at the A site during translation, we speculated that methylation of G518 affects protein translation. We transformed reporter constructs designed to probe the effect of functional lesions at one of the three codon positions on translational fidelity into the wild-type strain, H37Rv, and into a Delta gidB mutant, which lacks the methyltransferase (GidB) that methylates G518. We show that mistranslation occurs less in the Delta gidB mutant only in the construct bearing a lesion in the wobble position compared to H37Rv. Thus, the methylation of G518 allows mistranslation to occur at some level in order for translation to proceed smoothly and efficiently. We also explored the role of methylation at G518 in altering the susceptibility of M. tuberculosis to streptomycin (SM). Using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), we confirmed that G518 is not methylated in the Delta gidB mutant. Furthermore, isothermal titration calorimetry experiments performed on 70S ribosomes purified from wild-type and Delta gidB mutant strains showed that methylation significantly enhances SM binding. These results provide a mechanistic explanation for the low-level, SM-resistant phenotype observed in M. tuberculosis strains that contain a gidB mutation.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Wong, Sharon Y
AU  - Javid, Babak
AU  - Addepalli, Balasubrahmanyam
AU  - Piszczek, Grzegorz
AU  - Strader, Michael Brad
AU  - Limbach, Patrick A
AU  - Barry, Clifton E, III
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 6311
EP  - 6318
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 12
SN  - 0066-4804, 0066-4804
KW  - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Translation
KW  - Proline
KW  - ribosomal protein S12
KW  - Probes
KW  - Ribosomes
KW  - Streptomycin
KW  - Mass spectroscopy
KW  - rRNA
KW  - Fidelity
KW  - Methyltransferase
KW  - RNA modification
KW  - Titration
KW  - Codons
KW  - Calorimetry
KW  - Tuberculosis
KW  - Guanosine
KW  - Post-transcription
KW  - rRNA 16S
KW  - Methylation
KW  - Mutation
KW  - Mycobacterium tuberculosis
KW  - J 02310:Genetics & Taxonomy
KW  - A 01340:Antibiotics & Antimicrobials
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464504907?accountid=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=Functional+Role+of+Methylation+of+G518+of+the+16S+rRNA+530+Loop+by+GidB+in+Mycobacterium+tuberculosis&rft.au=Wong%2C+Sharon+Y%3BJavid%2C+Babak%3BAddepalli%2C+Balasubrahmanyam%3BPiszczek%2C+Grzegorz%3BStrader%2C+Michael+Brad%3BLimbach%2C+Patrick+A%3BBarry%2C+Clifton+E%2C+III&rft.aulast=Wong&rft.aufirst=Sharon&rft.date=2013-12-01&rft.volume=57&rft.issue=12&rft.spage=6311&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00905-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 31
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Translation; Proline; ribosomal protein S12; Probes; Ribosomes; Streptomycin; Mass spectroscopy; rRNA; Fidelity; Methyltransferase; Titration; RNA modification; Codons; Calorimetry; Tuberculosis; Guanosine; Post-transcription; Mutation; Methylation; rRNA 16S; Mycobacterium tuberculosis
DO  - http://dx.doi.org/10.1128/AAC.00905-13
ER  - 



TY  - JOUR
T1  - Functional Comparison of Plasmodium falciparum Transmission-Blocking Vaccine Candidates by the Standard Membrane-Feeding Assay
AN  - 1464504574; 18808552
AB  - Recently, there has been a renewed interest in the development of transmission-blocking vaccines (TBV) against Plasmodium falciparum malaria. While several candidate TBVs have been reported, studies directly comparing them in functional assays are limited. To this end, recombinant proteins of TBV candidates Pfs25, Pfs230, and PfHAP2 were expressed in the wheat germ cell-free expression system. Outbred CD-1 mice were immunized twice with the antigens. Two weeks after the second immunization, IgG levels were measured by enzyme-linked immunosorbent assay (ELISA), and IgG functionality was assessed by the standard membrane-feeding assay (SMFA) using cultured P. falciparum NF54 gametocytes and Anopheles stephensi mosquitoes. All three recombinant proteins elicited similar levels of antigen-specific IgG judged by ELISA. When IgGs purified from pools of immune serum were tested at 0.75 mg/ml in the SMFA, all three IgGs showed 97 to 100% inhibition in oocyst intensity compared to control IgG. In two additional independent SMFA evaluations, anti-Pfs25, anti-Pfs230, and anti-PfHAP2 IgGs inhibited oocyst intensity in a dose-dependent manner. When all three data sets were analyzed, anti-Pfs25 antibody showed significantly higher inhibition than the other two antibodies (P < 0.001 for both), while there was no significant difference between the other two (P = 0.15). A proportion of plasma samples collected from adults living in an area of malaria endemicity in Mali recognized Pfs230 and PfHAP2. This is the first study showing that the HAP2 protein of P. falciparum can induce transmission-blocking antibody. The current study supports the possibility of using this system for a comparative study with multiple TBV candidates.
JF  - Infection and Immunity
AU  - Miura, Kazutoyo
AU  - Takashima, Eizo
AU  - Deng, Bingbing
AU  - Tullo, Gregory
AU  - Diouf, Ababacar
AU  - Moretz, Samuel E
AU  - Nikolaeva, Daria
AU  - Diakite, Mahamadou
AU  - Fairhurst, Rick M
AU  - Fay, Michael P
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 4377
EP  - 4382
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 12
SN  - 0019-9567, 0019-9567
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts
KW  - Parasites
KW  - Human diseases
KW  - Mali
KW  - Wheat germ
KW  - Anopheles stephensi
KW  - Disease control
KW  - Malaria
KW  - Triticum aestivum
KW  - ELISA
KW  - Enzyme-linked immunosorbent assay
KW  - Data processing
KW  - Immune serum
KW  - Oocysts
KW  - Gametocytes
KW  - Pest control
KW  - Plasmodium falciparum
KW  - Immunization
KW  - Recombinants
KW  - Antibodies
KW  - Immunoglobulin G
KW  - Vaccines
KW  - Hap2 protein
KW  - K 03410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464504574?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Functional+Comparison+of+Plasmodium+falciparum+Transmission-Blocking+Vaccine+Candidates+by+the+Standard+Membrane-Feeding+Assay&rft.au=Miura%2C+Kazutoyo%3BTakashima%2C+Eizo%3BDeng%2C+Bingbing%3BTullo%2C+Gregory%3BDiouf%2C+Ababacar%3BMoretz%2C+Samuel+E%3BNikolaeva%2C+Daria%3BDiakite%2C+Mahamadou%3BFairhurst%2C+Rick+M%3BFay%2C+Michael+P&rft.aulast=Miura&rft.aufirst=Kazutoyo&rft.date=2013-12-01&rft.volume=81&rft.issue=12&rft.spage=4377&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01056-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 22
N1  - Last updated - 2016-04-29
N1  - SubjectsTermNotLitGenreText - Recombinants; Parasites; Human diseases; Antibodies; Disease control; ELISA; Malaria; Pest control; Vaccines; Enzyme-linked immunosorbent assay; Immune serum; Data processing; Gametocytes; Oocysts; Wheat germ; Immunoglobulin G; Hap2 protein; Immunization; Triticum aestivum; Anopheles stephensi; Plasmodium falciparum; Mali
DO  - http://dx.doi.org/10.1128/IAI.01056-13
ER  - 



TY  - JOUR
T1  - Methamphetamine alters reference gene expression in nigra and striatum of adult rat brain.
AN  - 1464497314; 24042092
AB  - The nigrostriatal dopaminergic system is a major lesion target for methamphetamine (MA), one of the most addictive and neurotoxic drugs of abuse. High doses of MA alter the expression of a large number of genes. Reference genes (RGs) are considered relatively stable and are often used as standards for quantitative real-time PCR (qRT-PCR) reactions. The purpose of this study was to determine whether MA altered the expression of RGs and to identify the appropriate RGs for gene expression studies in animals receiving MA. Adult male Sprague-Dawley rats were treated with high doses of MA or saline. Striatum and substantia nigra were harvested at 2h or 24h after MA administration. The expression and stability of 10 commonly used RGs were examined using qRT-PCR and then evaluated by geNorm and Normfinder. We found that MA altered the expression of selected RGs. These candidate RGs presented differential stability in the striatum and in substantia nigra at both 2h and 24h after MA injection. Selection of an unstable RG as a standard altered the significance of tyrosine hydroxylase (TH) mRNA expression after MA administration. In conclusion, our data show that MA site- and time-dependently altered the expression of RGs in nigrostriatal dopaminergic system. These temporal and spatial factors should be considered when selecting appropriate RGs for interpreting the expression of target genes in animals receiving MA. 
          Published by Elsevier B.V.
JF  - Neurotoxicology
AU  - He, Yi
AU  - Yu, Seongjin
AU  - Bae, Eunkyung
AU  - Shen, Hui
AU  - Wang, Yun
AD  - Neural Protection and Regeneration Section, National Institute on Drug Abuse, Intramural Research Program, NIH, Baltimore, MD 21224, USA. Electronic address: yi.he2@nih.gov.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 138
EP  - 145
VL  - 39
KW  - Central Nervous System Stimulants
KW  - 0
KW  - Nerve Tissue Proteins
KW  - RNA, Messenger
KW  - Methamphetamine
KW  - 44RAL3456C
KW  - Tyrosine 3-Monooxygenase
KW  - EC 1.14.16.2
KW  - Index Medicus
KW  - Real-time PCR
KW  - Housekeeping genes
KW  - Nigra
KW  - Reference genes
KW  - Striatum
KW  - Rats
KW  - Animals
KW  - Rats, Sprague-Dawley
KW  - RNA, Messenger -- metabolism
KW  - Nerve Tissue Proteins -- metabolism
KW  - Nerve Tissue Proteins -- genetics
KW  - Male
KW  - Tyrosine 3-Monooxygenase -- metabolism
KW  - Central Nervous System Stimulants -- pharmacology
KW  - Tyrosine 3-Monooxygenase -- genetics
KW  - Methamphetamine -- pharmacology
KW  - Substantia Nigra -- drug effects
KW  - Corpus Striatum -- drug effects
KW  - Gene Expression Regulation -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464497314?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Methamphetamine+alters+reference+gene+expression+in+nigra+and+striatum+of+adult+rat+brain.&rft.au=He%2C+Yi%3BYu%2C+Seongjin%3BBae%2C+Eunkyung%3BShen%2C+Hui%3BWang%2C+Yun&rft.aulast=He&rft.aufirst=Yi&rft.date=2013-12-01&rft.volume=39&rft.issue=&rft.spage=138&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=1872-9711&rft_id=info:doi/10.1016%2Fj.neuro.2013.08.009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-23
N1  - Date created - 2013-11-29
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Stroke. 2001 Mar;32(3):775-82 [11239201]
PLoS One. 2012;7(6):e38909 [22715419]
Parkinsonism Relat Disord. 2003 Mar;9(4):213-9 [12618056]
Folia Biol (Praha). 2003;49(6):211-6 [14748434]
Cancer Res. 2004 Aug 1;64(15):5245-50 [15289330]
Eur J Pharmacol. 1976 Apr;36(2):363-71 [6286]
Brain Res Bull. 1985 Dec;15(6):569-77 [2867819]
Neuropsychopharmacology. 2006 Nov;31(11):2359-67 [16855532]
Addict Biol. 2007 Mar;12(1):69-80 [17407499]
Genome Biol. 2007;8(2):R19 [17291332]
J Mol Neurosci. 2007;32(1):38-46 [17873286]
Synapse. 2008 Apr;62(4):302-9 [18241047]
Neurosci Lett. 2008 Sep 5;442(1):15-8 [18598737]
FEBS J. 2008 Dec;275(23):5947-59 [19021769]
Clin Chem. 2009 Apr;55(4):611-22 [19246619]
Neurotoxicology. 2009 May;30(3):436-44 [19442829]
Int J Neuropsychopharmacol. 2009 Jul;12(6):805-22 [19149911]
BMC Mol Biol. 2009;10:57 [19531214]
PLoS One. 2010;5(12):e15193 [21151937]
PLoS One. 2010;5(12):e15208 [21179435]
PLoS One. 2011;6(4):e19179 [21547080]
Neuroscience. 2011 Oct 27;194:170-80 [21867746]
Mol Biol Rep. 2012 Jan;39(1):569-76 [21633896]
PLoS One. 2012;7(3):e34236 [22470541]
Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.neuro.2013.08.009
ER  - 



TY  - JOUR
T1  - Gambling experiences, problems and policy in India: a historical analysis
AN  - 1463032546; 4508327
AB  - This paper seeks to provide a historical overview of gambling and contemporary anti-gambling legislation in India. Based on a review of available literature, including historical sources, publications in the lay press and internet sources, this paper draws together evidence to present a synopsis of gambling and anti-gambling measures from antiquity to present times. Gambling is a popular pastime and has been a ubiquitous part of daily life from antiquity until the present. Archaic laws, framed in the 19th century, still regulate gambling in India, with a formal ban on most forms of gambling. This has created a huge illegal gambling market, with its attendant problems. Recent developments, including an explosion of sports betting operations (especially in cricket) and internet betting sites, are challenging the status quo and leading to calls for legalizing gambling. Concern for the consequences of pathological/ problem gambling is conspicuous by its absence in popular discourse and academic research. Despite the importance and longevity of the practice of gambling in the daily life of India, and the opposition to it, due to the potential for individual and societal harm there is a surprising lack of contemporary curiosity and scholarly literature on pathological gambling from the region. The prohibitions against gambling are being increasingly challenged to change to a system of legalized gambling. To inform and guide public policy and future legislation, there is a serious need to initiate rational, scientific enquiries into the nature and impact of gambling in India. Reprinted by permission of Blackwell Publishing
JF  - Addiction
AU  - Benegal, Vivek
AD  - National Institute of Mental Health and Neurosciences, Bangalore
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 2062
EP  - 2067
VL  - 108
IS  - 12
SN  - 0965-2140, 0965-2140
KW  - Political Science
KW  - Gambling
KW  - 19th century
KW  - Everyday life
KW  - Policy making
KW  - Regulation
KW  - Public policy
KW  - Legislation
KW  - India
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463032546?accountid=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=Gambling+experiences%2C+problems+and+policy+in+India%3A+a+historical+analysis&rft.au=Benegal%2C+Vivek&rft.aulast=Benegal&rft.aufirst=Vivek&rft.date=2013-12-01&rft.volume=108&rft.issue=12&rft.spage=2062&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fj.1360-0443.2012.04068.x
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-12-02
N1  - Last updated - 2013-12-03
N1  - SubjectsTermNotLitGenreText - 5401 7336 3198; 9625 9628; 7321; 4559; 10742; 475 8168 5889; 10472; 175 387 30
DO  - http://dx.doi.org/10.1111/j.1360-0443.2012.04068.x
ER  - 



TY  - JOUR
T1  - MicroRNA Involvement in Human Cancers.
AN  - 1462764463; 23462030
JF  - Clinical chemistry
AU  - Yanaihara, Nozomu
AU  - Harris, Curtis C
AD  - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD;
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1811
EP  - 1812
VL  - 59
IS  - 12
KW  - Biomarkers, Tumor
KW  - 0
KW  - MicroRNAs
KW  - Index Medicus
KW  - Humans
KW  - Male
KW  - Female
KW  - Biomarkers, Tumor -- genetics
KW  - Lung Neoplasms -- genetics
KW  - Adenocarcinoma -- genetics
KW  - MicroRNAs -- analysis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1462764463?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+chemistry&rft.atitle=MicroRNA+Involvement+in+Human+Cancers.&rft.au=Yanaihara%2C+Nozomu%3BHarris%2C+Curtis+C&rft.aulast=Yanaihara&rft.aufirst=Nozomu&rft.date=2013-12-01&rft.volume=59&rft.issue=12&rft.spage=1811&rft.isbn=&rft.btitle=&rft.title=Clinical+chemistry&rft.issn=1530-8561&rft_id=info:doi/10.1373%2Fclinchem.2012.198176
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-23
N1  - Date created - 2013-11-29
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Comment On:
Cancer Cell. 2006 Mar;9(3):189-98 [16530703]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1373/clinchem.2012.198176
ER  - 



TY  - JOUR
T1  - Probiotic bacteria in cancer patients undergoing chemotherapy and radiation therapy.
AN  - 1462370734; 24280481
AB  - Probiotics are live microorganisms, which as drugs or food supplements help to maintain health beneficial microbial balance in the digestive tract of a human or other host. Probiotics by their properties may help strengthen homeostasis and thus reduce side effects associated with cancer treatment. Experimental evidence suggests that probiotics might have beneficial effect on the toxicity of anticancer therapy.
          A computer-based literature search was carried out using PubMed (keywords: "probiotic" and "lactic acid bacteria" in association with the search terms "cancer" or "oncology" or "chemotherapy" or "radiation"); data reported at international meetings were included. Probiotics might have beneficial effects on some aspects of toxicity related to anticancer treatment especially radiation therapy. However, reported trials vary in utilized probiotic strains, dose of probiotics and vast majority of them are small trials with substantial risk of bias. Despite limited data, it seems that probiotic bacteria as live microorganisms could be safely administered even in the setting of neutropenia.
          Current evidence supporting probiotic use as adjunctive therapy to anticancer treatment is limited, especially in cancer patients treated with chemotherapy. Well designed clinical trials are needed to find true role of probiotics in oncology. Copyright © 2013 Elsevier Ltd. All rights reserved.
JF  - Complementary therapies in medicine
AU  - Mego, Michal
AU  - Holec, Vladimir
AU  - Drgona, Lubos
AU  - Hainova, Katarina
AU  - Ciernikova, Sona
AU  - Zajac, Vladimir
AD  - Department of Medical Oncology, Faculty of Medicine, Comenius University and National Cancer Institute, Klenova 1, 833 10 Bratislava, Slovak Republic. Electronic address: misomego@gmail.com.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 712
EP  - 723
VL  - 21
IS  - 6
KW  - Index Medicus
KW  - Radiation therapy
KW  - Probiotics
KW  - Chemotherapy
KW  - Cancer
KW  - Bacterial Infections -- prevention & control
KW  - Humans
KW  - Clinical Trials as Topic
KW  - Chemoradiotherapy
KW  - Bacterial Infections -- drug therapy
KW  - Neoplasms -- drug therapy
KW  - Neoplasms -- radiotherapy
KW  - Probiotics -- therapeutic use
KW  - Neoplasms -- therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1462370734?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Complementary+therapies+in+medicine&rft.atitle=Probiotic+bacteria+in+cancer+patients+undergoing+chemotherapy+and+radiation+therapy.&rft.au=Mego%2C+Michal%3BHolec%2C+Vladimir%3BDrgona%2C+Lubos%3BHainova%2C+Katarina%3BCiernikova%2C+Sona%3BZajac%2C+Vladimir&rft.aulast=Mego&rft.aufirst=Michal&rft.date=2013-12-01&rft.volume=21&rft.issue=6&rft.spage=712&rft.isbn=&rft.btitle=&rft.title=Complementary+therapies+in+medicine&rft.issn=1873-6963&rft_id=info:doi/10.1016%2Fj.ctim.2013.08.018
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-15
N1  - Date created - 2013-11-27
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.ctim.2013.08.018
ER  - 



TY  - JOUR
T1  - Preclinical evaluation of a new liposomal formulation of cisplatin, lipoplatin, to treat cisplatin-resistant cervical cancer.
AN  - 1461885535; 24029417
AB  - Cisplatin-based chemotherapy has been shown to improve survival in cervical cancer; however, treatment is associated with tumor resistance and significant toxicity. Lipoplatin is a new liposomal formulation of cisplatin, developed to reduce cisplatin toxicity, to improve drug accumulation at tumor sites and to overcome drug resistance. The aim of this study is to analyze the antitumoral activity of lipoplatin against cisplatin-resistant cervical cancer cells and to investigate its mechanism of action.
          The activity and mechanism of action of lipoplatin were studied in the ME-180 cervical cancer cell line and its cisplatin-resistant clone R-ME-180 and HeLa cells using cell proliferation assays, flow cytometry, ELISA assay, cell migration, spheroids and tumor xenograft. We demonstrated that lipoplatin exhibited a potent antitumoral activity on HeLa, ME-180 cells and its cisplatin-resistant clone R-ME-180. Lipoplatin inhibited cell proliferation in a dose-dependent manner and was more active than the reference drug cisplatin in R-ME-180 cells and induced apoptosis, as evaluated by Annexin-V staining and DNA fragmentation, caspases 9 and 3 activation, Bcl-2, and Bcl-xL down-regulation, but Bax up-regulation inhibited thioredoxin reductase (TrxR) enzymatic activity and increased reactive oxygen species (ROS) accumulation; reduced EGFR expression and inhibited both migration and invasion. R-ME-180, but not ME-180 cells, generated three-dimensional (3D)-multicellular spheroids expressing the cancer stem cell marker ALDH. The ability of R-ME-180 cells to form spheroids in vitro and tumors in nude mice was also remarkably decreased by lipoplatin.
          Overall, our results suggest that lipoplatin has potential for the treatment of cisplatin-resistant cervical cancer. © 2013.
JF  - Gynecologic oncology
AU  - Casagrande, Naike
AU  - De Paoli, Monica
AU  - Celegato, Marta
AU  - Borghese, Cinzia
AU  - Mongiat, Maurizio
AU  - Colombatti, Alfonso
AU  - Aldinucci, Donatella
AD  - Experimental Oncology 2, Centro di Riferimento Oncologico, IRCCS, National Cancer Institute, Aviano, PN, Italy.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 744
EP  - 752
VL  - 131
IS  - 3
KW  - Liposomes
KW  - 0
KW  - Reactive Oxygen Species
KW  - lipoplatin
KW  - Aldehyde Dehydrogenase
KW  - EC 1.2.1.3
KW  - Thioredoxin-Disulfide Reductase
KW  - EC 1.8.1.9
KW  - Receptor, Epidermal Growth Factor
KW  - EC 2.7.10.1
KW  - Cisplatin
KW  - Q20Q21Q62J
KW  - Index Medicus
KW  - Spheroids
KW  - Liposomal cisplatin
KW  - Cervical cancer
KW  - Cisplatin-resistance
KW  - Migration
KW  - Cancer stem cells
KW  - Reactive Oxygen Species -- metabolism
KW  - Animals
KW  - Spheroids, Cellular
KW  - HeLa Cells
KW  - Neoplastic Stem Cells -- pathology
KW  - Humans
KW  - Cell Line, Tumor
KW  - Drug Resistance, Neoplasm
KW  - Mice
KW  - Mice, Nude
KW  - Receptor, Epidermal Growth Factor -- biosynthesis
KW  - Neoplastic Stem Cells -- drug effects
KW  - Cell Growth Processes -- drug effects
KW  - Thioredoxin-Disulfide Reductase -- antagonists & inhibitors
KW  - Mitochondria -- drug effects
KW  - Apoptosis -- drug effects
KW  - Thioredoxin-Disulfide Reductase -- metabolism
KW  - Cell Movement -- drug effects
KW  - Xenograft Model Antitumor Assays
KW  - Mitochondria -- metabolism
KW  - Aldehyde Dehydrogenase -- metabolism
KW  - Female
KW  - Uterine Cervical Neoplasms -- drug therapy
KW  - Liposomes -- administration & dosage
KW  - Uterine Cervical Neoplasms -- metabolism
KW  - Cisplatin -- pharmacology
KW  - Uterine Cervical Neoplasms -- pathology
KW  - Cisplatin -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1461885535?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preclinical+evaluation+of+a+new+liposomal+formulation+of+cisplatin%2C+lipoplatin%2C+to+treat+cisplatin-resistant+cervical+cancer.&rft.au=Casagrande%2C+Naike%3BDe+Paoli%2C+Monica%3BCelegato%2C+Marta%3BBorghese%2C+Cinzia%3BMongiat%2C+Maurizio%3BColombatti%2C+Alfonso%3BAldinucci%2C+Donatella&rft.aulast=Casagrande&rft.aufirst=Naike&rft.date=2013-12-01&rft.volume=131&rft.issue=3&rft.spage=744&rft.isbn=&rft.btitle=&rft.title=Gynecologic+oncology&rft.issn=1095-6859&rft_id=info:doi/10.1016%2Fj.ygyno.2013.08.041
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-23
N1  - Date created - 2013-11-25
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.ygyno.2013.08.041
ER  - 



TY  - JOUR
T1  - Chronic cadmium exposure in vitro induces cancer cell characteristics in human lung cells.
AN  - 1461880633; 23811327
AB  - Cadmium is a known human lung carcinogen. Here, we attempt to develop an in vitro model of cadmium-induced human lung carcinogenesis by chronically exposing the peripheral lung epithelia cell line, HPL-1D, to a low level of cadmium. Cells were chronically exposed to 5 μM cadmium, a noncytotoxic level, and monitored for acquired cancer characteristics. By 20 weeks of continuous cadmium exposure, these chronic cadmium treated lung (CCT-LC) cells showed marked increases in secreted MMP-2 activity (3.5-fold), invasion (3.4-fold), and colony formation in soft agar (2-fold). CCT-LC cells were hyperproliferative, grew well in serum-free media, and overexpressed cyclin D1. The CCT-LC cells also showed decreased expression of the tumor suppressor genes p16 and SLC38A3 at the protein levels. Also consistent with an acquired cancer cell phenotype, CCT-LC cells showed increased expression of the oncoproteins K-RAS and N-RAS as well as the epithelial-to-mesenchymal transition marker protein Vimentin. Metallothionein (MT) expression is increased by cadmium, and is typically overexpressed in human lung cancers. The major MT isoforms, MT-1A and MT-2A were elevated in CCT-LC cells. Oxidant adaptive response genes HO-1 and HIF-1A were also activated in CCT-LC cells. Expression of the metal transport genes ZNT-1, ZNT-5, and ZIP-8 increased in CCT-LC cells culminating in reduced cadmium accumulation, suggesting adaptation to the metal. Overall, these data suggest that exposure of human lung epithelial cells to cadmium causes acquisition of cancer cell characteristics. Furthermore, transformation occurs despite the cell's ability to adapt to chronic cadmium exposure.
          © 2013.
JF  - Toxicology and applied pharmacology
AU  - Person, Rachel J
AU  - Tokar, Erik J
AU  - Xu, Yuanyuan
AU  - Orihuela, Ruben
AU  - Ngalame, Ntube N Olive
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, NC, USA.
Y1  - 2013/12/01/
PY  - 2013
DA  - 2013 Dec 01
SP  - 281
EP  - 288
VL  - 273
IS  - 2
KW  - Cadmium
KW  - 00BH33GNGH
KW  - Index Medicus
KW  - Transformation
KW  - HIF-1A
KW  - lung cancer
KW  - DMPO
KW  - MT-2A
KW  - IST
KW  - Human lung cells
KW  - Epithelial-to-mesenchymal transition
KW  - chronic cadmium treated-lung cells
KW  - HO-1
KW  - PBS
KW  - 4′,6-diamidino-2-phenylindole
KW  - metallothionein-2A
KW  - matrix metalloproteinase-2
KW  - ZIP
KW  - CCT-LC
KW  - INT
KW  - 5,5-dimethyl-1-pyrroline N-oxide
KW  - human peripheral lung
KW  - heme oxygenase-1
KW  - Adaptation
KW  - Zinc Transporter
KW  - Lung cancer
KW  - qRT-PCR
KW  - HPL
KW  - quantitative real time reverse transcription polymerase chain reaction
KW  - LUCA
KW  - MMP-2
KW  - BSA
KW  - MT-1A
KW  - bovine serum albumin
KW  - DAPI
KW  - lethal concentration 50
KW  - phosphate buffered saline
KW  - p-iodonitro-tetrazolium violet
KW  - metallothionein-1A
KW  - immuno-spin trapping
KW  - LC50
KW  - hypoxia inducible factor-1 alpha
KW  - Zrt/Irt-like Proteins
KW  - ZNT
KW  - Oxidative Stress -- physiology
KW  - DNA Damage -- physiology
KW  - Tumor Cells, Cultured
KW  - Humans
KW  - Oxidative Stress -- drug effects
KW  - Time Factors
KW  - DNA Damage -- drug effects
KW  - Respiratory Mucosa -- metabolism
KW  - Cell Transformation, Neoplastic -- pathology
KW  - Cadmium -- administration & dosage
KW  - Cell Transformation, Neoplastic -- metabolism
KW  - Respiratory Mucosa -- drug effects
KW  - Lung -- drug effects
KW  - Cell Transformation, Neoplastic -- chemically induced
KW  - Cadmium -- toxicity
KW  - Lung Neoplasms -- chemically induced
KW  - Lung -- pathology
KW  - Lung -- metabolism
KW  - Respiratory Mucosa -- pathology
KW  - Lung Neoplasms -- pathology
KW  - Lung Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1461880633?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+cadmium+exposure+in+vitro+induces+cancer+cell+characteristics+in+human+lung+cells.&rft.au=Person%2C+Rachel+J%3BTokar%2C+Erik+J%3BXu%2C+Yuanyuan%3BOrihuela%2C+Ruben%3BNgalame%2C+Ntube+N+Olive%3BWaalkes%2C+Michael+P&rft.aulast=Person&rft.aufirst=Rachel&rft.date=2013-12-01&rft.volume=273&rft.issue=2&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2013.06.013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-20
N1  - Date created - 2013-11-25
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Drug Discov Ther. 2012 Feb;6(1):24-30 [22460425]
Toxicol Sci. 2012 Feb;125(2):412-7 [22112500]
Environ Health Perspect. 2012 Sep;120(9):1265-71 [22626610]
Tumour Biol. 2012 Dec;33(6):1819-28 [22718017]
Arch Toxicol. 2013 Feb;87(2):311-21 [22914987]
Biochim Biophys Acta. 2000 May 1;1465(1-2):190-8 [10748254]
Cancer Res. 2001 Jan 15;61(2):455-8 [11212230]
Toxicology. 2001 Mar 7;160(1-3):65-70 [11246125]
Lung Cancer. 2001 Nov;34(2):207-18 [11679179]
J Clin Oncol. 2002 Jan 1;20(1):254-62 [11773177]
Science. 2002 Mar 29;295(5564):2387-92 [11923519]
Free Radic Biol Med. 2002 Mar 15;32(6):525-35 [11958953]
J Toxicol Environ Health B Crit Rev. 2003 May-Jun;6(3):227-55 [12746140]
Pflugers Arch. 2004 Feb;447(5):744-51 [12748859]
Pflugers Arch. 2004 Feb;447(5):796-800 [12748861]
Annu Rev Nutr. 2004;24:151-72 [15189117]
Epidemiology. 1990 Mar;1(2):107-15 [2073496]
Semin Cancer Biol. 1996 Jun;7(3):147-54 [8773300]
Am J Respir Crit Care Med. 1996 Oct;154(4 Pt 1):1067-75 [8887609]
Cancer Res. 1997 Nov 1;57(21):4898-904 [9354455]
J Clin Oncol. 1998 Mar;16(3):1197-206 [9508208]
Int J Cancer. 2005 Apr 10;114(3):346-55 [15551354]
Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3401-6 [15722412]
Histol Histopathol. 2005 Oct;20(4):1037-44 [16136485]
Int J Cancer. 2006 Jul 1;119(1):99-107 [16432833]
Biochim Biophys Acta. 2006 Jul;1763(7):711-22 [16675045]
Mol Carcinog. 2006 Aug;45(8):561-71 [16568437]
Prostate. 2007 Feb 1;67(2):135-45 [17075824]
Nat Protoc. 2007;2(3):512-22 [17406615]
Int J Occup Environ Health. 2007 Apr-Jun;13(2):202-12 [17718178]
Mol Med. 2007 Jul-Aug;13(7-8):337-43 [17622322]
J Reprod Dev. 2008 Apr;54(2):129-34 [17420618]
Nat Protoc. 2008;3(6):1101-8 [18546601]
Chem Res Toxicol. 2008 Jul;21(7):1375-83 [18512965]
Nature. 2008 Oct 23;455(7216):1069-75 [18948947]
Methods Mol Biol. 2009;472:3-23 [19107427]
Prog Histochem Cytochem. 2009;44(1):29-64 [19348910]
J Clin Invest. 2009 Jun;119(6):1420-8 [19487818]
Toxicol Appl Pharmacol. 2009 Aug 1;238(3):250-7 [19265717]
Toxicol Appl Pharmacol. 2009 Aug 1;238(3):215-20 [19362100]
Curr Protein Pept Sci. 2009 Aug;10(4):360-75 [19689357]
Biochimie. 2009 Oct;91(10):1218-22 [19375483]
Future Oncol. 2009 Oct;5(8):1169-79 [19852728]
Cell. 2009 Nov 25;139(5):871-90 [19945376]
Environ Health Perspect. 2009 Dec;117(12):1847-52 [20049202]
Cell Physiol Biochem. 2010;25(1):159-68 [20054154]
Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578]
Toxicol In Vitro. 2010 Mar;24(2):370-4 [19900532]
Am J Ind Med. 2010 May;53(5):476-85 [20187007]
Cancer Epidemiol. 2010 Aug;34(4):472-7 [20444664]
Anticancer Res. 2011 Sep;31(9):2833-9 [21868526]
Toxicol Sci. 2012 Jan;125(1):10-9 [21984483]
Metallomics. 2012 Jul;4(7):700-8 [22534978]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.taap.2013.06.013
ER  - 



TY  - JOUR
T1  - Trace elements and endometriosis: the ENDO study.
AN  - 1461343680; 23892002
AB  - There has been limited study of trace elements and endometriosis. Using a matched cohort design, 473 women aged 18-44 years were recruited into an operative cohort, along with 131 similarly aged women recruited into a population cohort. Endometriosis was defined as surgically visualized disease in the operative cohort, and magnetic resonance imaging diagnosed disease in the population cohort. Twenty trace elements in urine and three in blood were quantified using inductively coupled plasma mass spectrometry. Logistic regression estimated the adjusted odds (aOR) of endometriosis diagnosis for each element by cohort. No association was observed between any element and endometriosis in the population cohort. In the operative cohort, blood cadmium was associated with a reduced odds of diagnosis (aOR=0.55; 95% CI: 0.31, 0.98), while urinary chromium and copper reflected an increased odds (aOR=1.97; 95% CI: 1.21, 3.19; aOR=2.66; 95% CI: 1.26, 5.64, respectively). The varied associations underscore the need for continued research. 
          Published by Elsevier Inc.
JF  - Reproductive toxicology (Elmsford, N.Y.)
AU  - Pollack, Anna Z
AU  - Louis, Germaine M Buck
AU  - Chen, Zhen
AU  - Peterson, C Matthew
AU  - Sundaram, Rajeshwari
AU  - Croughan, Mary S
AU  - Sun, Liping
AU  - Hediger, Mary L
AU  - Stanford, Joseph B
AU  - Varner, Michael W
AU  - Palmer, Christopher D
AU  - Steuerwald, Amy J
AU  - Parsons, Patrick J
AD  - Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Health, 6100 Executive Blvd. Rockville, Maryland 20852, United States. Electronic address: pollacka@mail.nih.gov.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 41
EP  - 48
VL  - 42
KW  - Environmental Pollutants
KW  - 0
KW  - Metals, Heavy
KW  - Arsenic
KW  - N712M78A8G
KW  - Index Medicus
KW  - NIST
KW  - adjusted odds ratio
KW  - magnetic resonance imaging
KW  - lead
KW  - body mass index
KW  - National Institute of Standards and Technology
KW  - Endometriosis
KW  - internal quality control
KW  - Lead
KW  - LOD
KW  - Trace elements
KW  - endometriosis: Natural History, Diagnosis and Outcomes Study
KW  - cadmium
KW  - Cd
KW  - BMI
KW  - Cadmium
KW  - limits of detection
KW  - Hg
KW  - aOR
KW  - mercury
KW  - ENDO
KW  - Metals
KW  - Chromium
KW  - 95% confidence interval
KW  - Pb
KW  - NHANES
KW  - OR
KW  - CI
KW  - IQC
KW  - MRI
KW  - odds ratio
KW  - Mercury
KW  - National Health and Nutrition Examination Survey
KW  - Environmental Monitoring
KW  - Young Adult
KW  - Odds Ratio
KW  - Humans
KW  - Utah -- epidemiology
KW  - Cohort Studies
KW  - Adult
KW  - California -- epidemiology
KW  - Female
KW  - Arsenic -- urine
KW  - Endometriosis -- epidemiology
KW  - Endometriosis -- blood
KW  - Metals, Heavy -- blood
KW  - Metals, Heavy -- urine
KW  - Environmental Pollutants -- urine
KW  - Environmental Pollutants -- blood
KW  - Endometriosis -- urine
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1461343680?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Trace+elements+and+endometriosis%3A+the+ENDO+study.&rft.au=Pollack%2C+Anna+Z%3BLouis%2C+Germaine+M+Buck%3BChen%2C+Zhen%3BPeterson%2C+C+Matthew%3BSundaram%2C+Rajeshwari%3BCroughan%2C+Mary+S%3BSun%2C+Liping%3BHediger%2C+Mary+L%3BStanford%2C+Joseph+B%3BVarner%2C+Michael+W%3BPalmer%2C+Christopher+D%3BSteuerwald%2C+Amy+J%3BParsons%2C+Patrick+J&rft.aulast=Pollack&rft.aufirst=Anna&rft.date=2013-12-01&rft.volume=42&rft.issue=&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2013.05.009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-08
N1  - Date created - 2013-11-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Akush Ginekol (Sofiia). 2000;39(2):36-7 [10948620]
Am J Obstet Gynecol. 2013 Jun;208(6):451.e1-11 [23454253]
Am J Epidemiol. 2003 Feb 15;157(4):355-63 [12578806]
Fertil Steril. 2003 May;79(5):1078-85 [12738499]
Semin Reprod Med. 2003 May;21(2):243-54 [12917793]
Abdom Imaging. 2003 Sep-Oct;28(5):733-42 [14628887]
Toxicol Lett. 2004 Dec 1;154(1-2):89-93 [15475182]
N Engl J Med. 1982 Oct 21;307(17):1062-5 [7121516]
Fertil Steril. 1982 Dec;38(6):667-72 [6216124]
JAMA. 1986 Apr 11;255(14):1904-8 [3951117]
Fertil Steril. 1997 May;67(5):817-21 [9130884]
Obstet Gynecol Clin North Am. 1997 Jun;24(2):235-58 [9163765]
Fertil Steril. 1999 Jul;72(1):129-34 [10428161]
Lancet. 2004 Nov 13-19;364(9447):1789-99 [15541453]
Hum Reprod. 2005 Jan;20(1):279-85 [15513976]
Hum Reprod. 2005 Jul;20(7):2014-20 [15817589]
Hum Reprod. 2005 Oct;20(10):2698-704 [15980014]
Am J Epidemiol. 2006 Feb 15;163(4):374-83 [16394206]
J Appl Toxicol. 2006 May-Jun;26(3):191-7 [16489580]
Hum Reprod. 2006 Nov;21(11):2810-6 [16849816]
Int Arch Occup Environ Health. 2006 Nov;80(2):149-53 [16688463]
Clin Exp Pharmacol Physiol. 2007 May-Jun;34(5-6):467-74 [17439417]
Environ Health Perspect. 2007 Oct;115(10):1435-41 [17938732]
Hum Reprod. 2008 Mar;23(3):679-87 [18192673]
Fertil Steril. 2008 Apr;89(4):934-42 [17582405]
Mol Hum Reprod. 2008 Jul;14(7):377-85 [18508952]
Sci Total Environ. 2008 Sep 1;402(2-3):171-5 [18558423]
Reprod Toxicol. 2009 Jun;27(3-4):212-30 [19429401]
Reprod Toxicol. 2010 Jun;29(3):298-305 [20096775]
N Engl J Med. 2010 Jun 24;362(25):2389-98 [20573927]
Environ Health Perspect. 2010 Sep;118(9):1280-5 [20423815]
J Proteome Res. 2010 Sep 3;9(9):4443-53 [20681587]
J Assist Reprod Genet. 2010 Aug;27(8):463-8 [20508982]
Occup Environ Med. 2011 Apr;68(4):250-6 [20974743]
Fertil Steril. 2011 Aug;96(2):360-5 [21719000]
J Environ Monit. 2011 Sep;13(9):2413-9 [21773592]
J Environ Monit. 2012 Mar;14(3):1035-43 [22334237]
Environ Sci Technol. 2012 Apr 17;46(8):4624-32 [22417702]
Environ Health Perspect. 2012 Jun;120(6):811-6 [22417635]
Obstet Gynecol. 2012 Jul;120(1):104-12 [22914398]
Reprod Biol Endocrinol. 2012;10:49 [22748101]
BMC Res Notes. 2013;6:13 [23317102]
Ann N Y Acad Sci. 2002 Mar;955:11-22; discussion 34-6, 396-406 [11949940]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.reprotox.2013.05.009
ER  - 



TY  - JOUR
T1  - Effect of nitric oxide on the anticancer activity of the topoisomerase-active drugs etoposide and adriamycin in human melanoma cells.
AN  - 1459979333; 24049059
AB  - Nitric oxide (·NO) was originally identified as an innate cytotoxin. However, in tumors it can enhance resistance to chemotherapy and exacerbate cancer progression. Our previous studies indicated that (·NO/·NO-derived species react with etoposide (VP-16) in vitro and form products that show significantly reduced activity toward HL60 cells and lipopolysaccharide (LPS)-induced macrophages. Here, we further confirm the hypothesis that (÷)NO generation contributes to VP-16 resistance by examining interactions of ·NO with VP-16 in inducible nitric-oxide synthase (iNOS)-expressing human melanoma A375 cells. Inhibition of iNOS catalysis by N(6)-(1-iminoethyl)-L-lysine dihydrochloride (L-NIL) in human melanoma A375 cells reversed VP-16 resistance, leading to increased DNA damage and apoptosis. Furthermore, we found that coculturing A375 melanoma cells with LPS-induced macrophage RAW cells also significantly reduced VP-16 cytotoxicity and DNA damage in A375 cells. We also examined the interactions of (·)NO with another topoisomerase active drug, Adriamycin, in A375 cells. In contrast, to VP-16, (·)NO caused no significant modulation of cytotoxicity or Adriamycin-dependent apoptosis, suggesting that (⋅)NO does not interact with Adriamycin. Our studies support the hypothesis that (·)NO oxidative chemistry can detoxify VP-16 through direct nitrogen oxide radical attack. Our results provide insights into the pharmacology and anticancer mechanisms of VP-16 that may ultimately contribute to increased resistance, treatment failure, and induction of secondary leukemia in VP-16-treated patients.
JF  - The Journal of pharmacology and experimental therapeutics
AU  - Sinha, Birandra K
AU  - Kumar, Ashutosh
AU  - Bhattacharjee, Suchandra
AU  - Espey, Michael G
AU  - Mason, Ronald P
AD  - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina (B.K.S., A.K., S.B., R.P.M.); and National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland (M.G.E.).
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 607
EP  - 614
VL  - 347
IS  - 3
KW  - Antibiotics, Antineoplastic
KW  - 0
KW  - Antineoplastic Agents
KW  - Antineoplastic Agents, Phytogenic
KW  - Enzyme Inhibitors
KW  - N(6)-(1-iminoethyl)lysine
KW  - Nitric Oxide
KW  - 31C4KY9ESH
KW  - Etoposide
KW  - 6PLQ3CP4P3
KW  - Doxorubicin
KW  - 80168379AG
KW  - Nitric Oxide Synthase
KW  - EC 1.14.13.39
KW  - Caspase 3
KW  - EC 3.4.22.-
KW  - DNA Topoisomerases
KW  - EC 5.99.1.-
KW  - Lysine
KW  - K3Z4F929H6
KW  - Index Medicus
KW  - Lysine -- pharmacology
KW  - Blotting, Western
KW  - Electrophoresis, Polyacrylamide Gel
KW  - Nitric Oxide Synthase -- antagonists & inhibitors
KW  - Humans
KW  - Lysine -- analogs & derivatives
KW  - Enzyme Inhibitors -- pharmacology
KW  - Cell Line, Tumor
KW  - Macrophages -- drug effects
KW  - Cell Survival
KW  - Caspase 3 -- metabolism
KW  - Etoposide -- pharmacology
KW  - DNA Topoisomerases -- drug effects
KW  - Doxorubicin -- pharmacology
KW  - Antibiotics, Antineoplastic -- pharmacology
KW  - Melanoma -- drug therapy
KW  - Antineoplastic Agents, Phytogenic -- pharmacology
KW  - Nitric Oxide -- pharmacology
KW  - Antineoplastic Agents -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1459979333?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+nitric+oxide+on+the+anticancer+activity+of+the+topoisomerase-active+drugs+etoposide+and+adriamycin+in+human+melanoma+cells.&rft.au=Sinha%2C+Birandra+K%3BKumar%2C+Ashutosh%3BBhattacharjee%2C+Suchandra%3BEspey%2C+Michael+G%3BMason%2C+Ronald+P&rft.aulast=Sinha&rft.aufirst=Birandra&rft.date=2013-12-01&rft.volume=347&rft.issue=3&rft.spage=607&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.207928
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-23
N1  - Date created - 2013-11-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Res. 1988 Sep 1;48(17):4766-9 [2842038]
Cancer Res. 1988 Feb 1;48(3):589-601 [3335022]
Biochemistry. 1989 May 30;28(11):4839-46 [2548593]
Annu Rev Biochem. 1989;58:351-75 [2549853]
Nitric Oxide. 1997 Feb;1(1):88-94 [9701048]
Biochemistry (Mosc). 1998 Jul;63(7):802-9 [9721332]
Cancer Res. 2006 Jan 15;66(2):605-12 [16423985]
Cancer Res. 2006 Jun 15;66(12):6353-60 [16778213]
Chem Res Toxicol. 2006 Jul;19(7):937-43 [16841962]
Chem Res Toxicol. 2007 Apr;20(4):709-14 [17388608]
Cancer. 2008 Jan 15;112(2):372-81 [18008356]
J Biol Chem. 2008 Jul 4;283(27):18513-21 [18445594]
Nitric Oxide. 2008 Sep;19(2):133-7 [18472017]
J Leukoc Biol. 2008 Sep;84(3):623-30 [18467655]
Biochemistry. 2008 Oct 28;47(43):11377-85 [18831539]
J Immunol. 2009 Sep 15;183(6):4055-66 [19717511]
Clin Cancer Res. 2010 Mar 15;16(6):1834-44 [20215556]
Curr Pharm Des. 2010;16(4):381-91 [20236067]
Nitric Oxide. 2010 Dec 15;23(4):319-26 [20854923]
Cell Cycle. 2011 Feb 15;10(4):619-24 [21293193]
Mol Pharmacol. 2011 Mar;79(3):479-87 [21097707]
Chem Res Toxicol. 2013 Mar 18;26(3):379-87 [23402364]
Drugs. 1990 Mar;39(3):438-90 [2184009]
Eur J Cancer. 1990;26(5):590-3 [2169277]
J Biol Chem. 1994 Aug 26;269(34):21891-7 [7520445]
Drugs. 1995 Jan;49(1):11-9 [7705211]
Proc Natl Acad Sci U S A. 1995 May 9;92(10):4392-6 [7538668]
Biochem Biophys Res Commun. 1996 Jul 25;224(3):696-702 [8713109]
Arch Biochem Biophys. 1996 Nov 15;335(2):369-76 [8914934]
Br J Cancer. 1997;76(3):325-34 [9252199]
Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2175-9 [9482858]
Mol Pharmacol. 1998 Mar;53(3):422-8 [9495807]
Free Radic Res. 1999 Dec;31(6):597-606 [10630683]
Nitric Oxide. 2000 Apr;4(2):147-56 [10835295]
Biochemistry. 2001 Feb 6;40(5):1159-70 [11170441]
J Biol Chem. 2001 Aug 10;276(32):30085-91 [11404354]
Cancer Res. 2001 Nov 1;61(21):7777-84 [11691792]
Cancer Res. 2002 Apr 15;62(8):2227-31 [11956073]
Cell Res. 2002 Dec;12(5-6):311-20 [12528889]
J Biol Chem. 2004 Jan 2;279(1):288-98 [14576150]
Nitric Oxide. 2004 May;10(3):119-29 [15158691]
Biochemistry. 1976 Dec 14;15(25):5443-8 [999819]
Chem Biol Interact. 1980 Apr;30(1):67-77 [7379206]
Biochim Biophys Acta. 1980 Jun 5;630(1):119-30 [6248123]
Cancer Res. 1983 Oct;43(10):4543-51 [6309369]
J Biol Chem. 1983 Dec 25;258(24):15365-70 [6317692]
Biochemistry. 1984 Mar 13;23(6):1183-8 [6712942]
Cancer Res. 1984 Jul;44(7):2892-6 [6327028]
Cancer Res. 1986 Apr;46(4 Pt 2):1934-8 [3004711]
Biochem Biophys Res Commun. 1986 Feb 26;135(1):215-20 [3006680]
Biochem Pharmacol. 1987 Feb 15;36(4):527-36 [3030329]
Cancer Res. 1987 Sep 1;47(17):4658-62 [3621161]
Chem Biol Interact. 1987;62(3):237-47 [3040275]
Biochemistry. 1987 Jun 30;26(13):3776-81 [2820475]
Cancer Res. 1987 Nov 15;47(22):5835-40 [3117357]
Cancer Res. 1988 Sep 15;48(18):5096-100 [2842045]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1124/jpet.113.207928
ER  - 



TY  - JOUR
T1  - Phase 1 oncology trials and informed consent.
AN  - 1459562751; 23161617
AB  - Ethical concerns have been raised about the quality of informed consent by participants in phase 1 oncology trials. Interview surveys indicate that substantial proportions of trial participants do not understand the purpose of these trials-evaluating toxicity and dosing for subsequent efficacy studies-and overestimate the prospect of therapeutic benefit that they offer. In this article we argue that although these data suggest the desirability of enhancing the process of information disclosure and assessment of comprehension of the implications of study participation, they do not necessarily invalidate consent by phase 1 trial participants.
JF  - Journal of medical ethics
AU  - Miller, Franklin G
AU  - Joffe, Steven
AD  - Department of Bioethics, National Institutes of Health, , Bethesda, Maryland, USA.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 761
EP  - 764
VL  - 39
IS  - 12
KW  - Bioethics
KW  - Index Medicus
KW  - Informed Consent
KW  - Humans
KW  - Ethics, Medical
KW  - Comprehension
KW  - Decision Making
KW  - Disclosure
KW  - Informed Consent -- ethics
KW  - Clinical Trials, Phase I as Topic -- ethics
KW  - Informed Consent -- standards
KW  - Research Subjects -- psychology
KW  - Nontherapeutic Human Experimentation -- ethics
KW  - Ethics, Research
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1459562751?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medical+ethics&rft.atitle=Phase+1+oncology+trials+and+informed+consent.&rft.au=Miller%2C+Franklin+G%3BJoffe%2C+Steven&rft.aulast=Miller&rft.aufirst=Franklin&rft.date=2013-12-01&rft.volume=39&rft.issue=12&rft.spage=761&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+ethics&rft.issn=1473-4257&rft_id=info:doi/10.1136%2Fmedethics-2012-100832
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-03-31
N1  - Date created - 2013-11-18
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1136/medethics-2012-100832
ER  - 



TY  - JOUR
T1  - Label-retaining liver cancer cells are relatively resistant to sorafenib.
AN  - 1449764339; 23411027
AB  - The standard therapy for advanced hepatocellular carcinoma (HCC) is sorafenib, with most patients experiencing disease progression within 6 months. Label-retaining cancer cells (LRCC) represent a novel subpopulation of cancer stem cells (CSC). The objective was to test whether LRCC are resistant to sorafenib.
          We tested human HCC derived LRCC and non-LRCC before and after treatment with sorafenib. LRCC derived from human HCC are relatively resistant to sorafenib. The proportion of LRCC in HCC cell lines is increased after sorafenib while the general population of cancer cells undergoes growth suppression. We show that LRCC demonstrate improved viability and toxicity profiles, and reduced apoptosis, over non-LRCC. We show that after treatment with sorafenib, LRCC upregulate the CSC marker aldehyde dehydrogenase 1 family, wingless-type MMTV-integration-site family, cell survival and proliferation genes, and downregulate apoptosis, cell cycle arrest, cell adhesion and stem cells differentiation genes. This phenomenon was accompanied by non-uniform activation of specific isoforms of the sorafenib target proteins extracellular-signal-regulated kinases and v-akt-murine-thymoma-viral-oncogene homologue (AKT) in LRCC but not in non-LRCC. A molecular pathway map for sorafenib treated LRCC is proposed.
          Our results suggest that HCC derived LRCC are relatively resistant to sorafenib. Since LRCC can generate tumours with as few as 10 cells, our data suggest a potential role for these cells in disease recurrence. Further investigation of this phenomenon might provide novel insights into cancer biology, cancer recurrence and drug resistance with important implications for the development of novel cancer therapies based on targeting LRCC.
JF  - Gut
AU  - Xin, Hong-Wu
AU  - Ambe, Chenwi M
AU  - Hari, Danielle M
AU  - Wiegand, Gordon W
AU  - Miller, Tyler C
AU  - Chen, Jin-Qiu
AU  - Anderson, Andrew J
AU  - Ray, Satyajit
AU  - Mullinax, John E
AU  - Koizumi, Tomotake
AU  - Langan, Russell C
AU  - Burka, Douglas
AU  - Herrmann, Michelle A
AU  - Goldsmith, Paul K
AU  - Stojadinovic, Alexander
AU  - Rudloff, Udo
AU  - Thorgeirsson, Snorri S
AU  - Avital, Itzhak
AD  - Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, , Bethesda, Maryland, USA.
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 1777
EP  - 1786
VL  - 62
IS  - 12
KW  - Antineoplastic Agents
KW  - 0
KW  - Phenylurea Compounds
KW  - Niacinamide
KW  - 25X51I8RD4
KW  - sorafenib
KW  - 9ZOQ3TZI87
KW  - Oncogene Protein v-akt
KW  - EC 2.7.11.1
KW  - Extracellular Signal-Regulated MAP Kinases
KW  - EC 2.7.11.24
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Drug Resistance
KW  - Stem Cells
KW  - Hepatocellular Carcinoma
KW  - Cell Proliferation
KW  - Cancer
KW  - Stem Cells -- drug effects
KW  - Real-Time Polymerase Chain Reaction
KW  - Gene Expression Profiling
KW  - Oncogene Protein v-akt -- metabolism
KW  - Humans
KW  - Cell Line, Tumor -- cytology
KW  - Apoptosis -- drug effects
KW  - Drug Resistance, Neoplasm
KW  - Cell Line, Tumor -- drug effects
KW  - Extracellular Signal-Regulated MAP Kinases -- metabolism
KW  - Niacinamide -- therapeutic use
KW  - Carcinoma, Hepatocellular -- drug therapy
KW  - Liver Neoplasms -- drug therapy
KW  - Phenylurea Compounds -- therapeutic use
KW  - Niacinamide -- analogs & derivatives
KW  - Antineoplastic Agents -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449764339?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gut&rft.atitle=Label-retaining+liver+cancer+cells+are+relatively+resistant+to+sorafenib.&rft.au=Xin%2C+Hong-Wu%3BAmbe%2C+Chenwi+M%3BHari%2C+Danielle+M%3BWiegand%2C+Gordon+W%3BMiller%2C+Tyler+C%3BChen%2C+Jin-Qiu%3BAnderson%2C+Andrew+J%3BRay%2C+Satyajit%3BMullinax%2C+John+E%3BKoizumi%2C+Tomotake%3BLangan%2C+Russell+C%3BBurka%2C+Douglas%3BHerrmann%2C+Michelle+A%3BGoldsmith%2C+Paul+K%3BStojadinovic%2C+Alexander%3BRudloff%2C+Udo%3BThorgeirsson%2C+Snorri+S%3BAvital%2C+Itzhak&rft.aulast=Xin&rft.aufirst=Hong-Wu&rft.date=2013-12-01&rft.volume=62&rft.issue=12&rft.spage=1777&rft.isbn=&rft.btitle=&rft.title=Gut&rft.issn=1468-3288&rft_id=info:doi/10.1136%2Fgutjnl-2012-303261
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-06
N1  - Date created - 2013-11-08
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Comment In:
Gut. 2013 Dec;62(12):1674-5 [23481262]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1136/gutjnl-2012-303261
ER  - 



TY  - JOUR
T1  - A single glycine in extracellular loop 1 is the critical determinant for pharmacological specificity of dopamine D2 and D3 receptors.
AN  - 1449275822; 24061855
AB  - Subtype-selective agents for the dopamine D3 receptor (D3R) have been considered as potential medications for drug addiction and other neuropsychiatric disorders. Medicinal chemistry efforts have led to the discovery of 4-phenylpiperazine derivatives that are >100-fold selective for the dopamine D3 receptor over dopamine D2 receptor (D2R), despite high sequence identity (78% in the transmembrane domain). Based on the recent crystal structure of D3R, we demonstrated that the 4-phenylpiperazine moiety in this class of D3R-selective compounds binds to the conserved orthosteric binding site, whereas the extended aryl amide moiety is oriented toward a divergent secondary binding pocket (SBP). In an effort to further characterize molecular determinants of the selectivity of these compounds, we modeled their binding modes in D3R and D2R by comparative ligand docking and molecular dynamics simulations. We found that the aryl amide moiety in the SBP differentially induces conformational changes in transmembrane segment 2 and extracellular loop 1 (EL1), which amplify the divergence of the SBP in D3R and D2R. Receptor chimera and site-directed mutagenesis studies were used to validate these binding modes and to identify a divergent glycine in EL1 as critical to D3R over D2R subtype selectivity. A better understanding of drug-dependent receptor conformations such as these is key to the rational design of compounds targeting a specific receptor among closely related homologs, and may also lead to discovery of novel chemotypes that exploit subtle differences in protein conformations.
JF  - Molecular pharmacology
AU  - Michino, Mayako
AU  - Donthamsetti, Prashant
AU  - Beuming, Thijs
AU  - Banala, Ashwini
AU  - Duan, Lihua
AU  - Roux, Thomas
AU  - Han, Yang
AU  - Trinquet, Eric
AU  - Newman, Amy Hauck
AU  - Javitch, Jonathan A
AU  - Shi, Lei
AD  - Department of Physiology and Biophysics, Institute for Computational Biomedicine, Weill Medical College of Cornell University, New York, New York (M.M., L.S.); Departments of Psychiatry and Pharmacology, Columbia University College of Physicians and Surgeons, New York, New York (P.D., L.D., Y.H., J.A.J.); Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, New York (P.D., L.D., Y.H., J.A.J.); Schrödinger, Inc., New York, New York (T.B.); Medicinal Chemistry Section, Molecular Targets and Medications Discovery Branch, Intramural Research Program of the National Institutes of Health National Institute on Drug Abuse, Baltimore, Maryland (A.B., A.H.N.); and Cisbio Bioassays, Codolet, France (T.R., E.T.).
Y1  - 2013/12//
PY  - 2013
DA  - December 2013
SP  - 854
EP  - 864
VL  - 84
IS  - 6
KW  - Ligands
KW  - 0
KW  - Piperazines
KW  - Receptors, Dopamine D2
KW  - Receptors, Dopamine D3
KW  - Recombinant Fusion Proteins
KW  - Glycine
KW  - TE7660XO1C
KW  - Index Medicus
KW  - Mutagenesis, Site-Directed
KW  - Molecular Docking Simulation
KW  - Humans
KW  - HEK293 Cells
KW  - Binding, Competitive
KW  - Radioligand Assay
KW  - Molecular Dynamics Simulation
KW  - Recombinant Fusion Proteins -- chemistry
KW  - Protein Conformation
KW  - Binding Sites
KW  - Glycine -- chemistry
KW  - Piperazines -- chemistry
KW  - Receptors, Dopamine D3 -- metabolism
KW  - Receptors, Dopamine D2 -- chemistry
KW  - Receptors, Dopamine D3 -- genetics
KW  - Receptors, Dopamine D3 -- chemistry
KW  - Receptors, Dopamine D2 -- genetics
KW  - Piperazines -- metabolism
KW  - Receptors, Dopamine D2 -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449275822?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+single+glycine+in+extracellular+loop+1+is+the+critical+determinant+for+pharmacological+specificity+of+dopamine+D2+and+D3+receptors.&rft.au=Michino%2C+Mayako%3BDonthamsetti%2C+Prashant%3BBeuming%2C+Thijs%3BBanala%2C+Ashwini%3BDuan%2C+Lihua%3BRoux%2C+Thomas%3BHan%2C+Yang%3BTrinquet%2C+Eric%3BNewman%2C+Amy+Hauck%3BJavitch%2C+Jonathan+A%3BShi%2C+Lei&rft.aulast=Michino&rft.aufirst=Mayako&rft.date=2013-12-01&rft.volume=84&rft.issue=6&rft.spage=854&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.113.087833
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-06
N1  - Date created - 2013-11-05
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Pharmacol Ther. 2006 Oct;112(1):281-333 [16905195]
J Med Chem. 2006 Jan 26;49(2):534-53 [16420040]
J Med Chem. 2007 Aug 23;50(17):4135-46 [17672446]
J Am Chem Soc. 2008 Mar 5;130(9):2817-31 [18266362]
Nature. 2008 Jul 24;454(7203):486-91 [18594507]
Phys Chem Chem Phys. 2008 Apr 21;10(15):2073-7 [18688361]
J Med Chem. 2009 Apr 23;52(8):2559-70 [19331412]
Protein Sci. 2009 Aug;18(8):1609-19 [19569188]
J Med Chem. 2009 Aug 13;52(15):4923-35 [19606869]
Ann N Y Acad Sci. 2010 Feb;1187:4-34 [20201845]
Nat Chem Biol. 2010 Aug;6(8):587-94 [20622858]
Science. 2010 Nov 19;330(6007):1091-5 [21097933]
Trends Pharmacol Sci. 2010 Dec;31(12):567-74 [20870300]
Nature. 2011 Jan 13;469(7329):236-40 [21228876]
Nature. 2011 Jan 13;469(7329):241-4 [21228877]
J Med Chem. 2011 May 26;54(10):3581-94 [21495689]
Proc Natl Acad Sci U S A. 2011 Aug 9;108(32):13118-23 [21778406]
Trends Pharmacol Sci. 2012 Jan;33(1):17-27 [22032986]
Proteins. 2012 Mar;80(3):871-83 [22223256]
J Med Chem. 2012 Feb 23;55(4):1424-44 [22239221]
Nature. 2012 Feb 23;482(7386):552-6 [22358844]
Nat Rev Drug Discov. 2012 May;11(5):355-65 [22543468]
Trends Pharmacol Sci. 2012 May;33(5):249-60 [22465153]
Structure. 2012 May 9;20(5):841-9 [22579251]
J Med Chem. 2012 May 24;55(10):4847-60 [22559880]
J Phys Chem B. 2012 Jun 14;116(23):6952-9 [22424156]
J Med Chem. 2012 Aug 9;55(15):6689-99 [22632094]
J Med Chem. 2012 Aug 23;55(16):7141-53 [22845053]
Biochem Pharmacol. 2012 Oct 1;84(7):882-90 [22781742]
Subcell Biochem. 2012;63:113-29 [23161136]
J Comput Chem. 2005 Jul 15;26(9):915-31 [15841474]
Mol Pharmacol. 1999 Dec;56(6):1116-26 [10570038]
Protein Eng. 2000 Sep;13(9):603-6 [11054453]
Trends Pharmacol Sci. 2000 Nov;21(11):445-51 [11121576]
Mol Pharmacol. 2001 Jul;60(1):1-19 [11408595]
J Med Chem. 2001 Sep 13;44(19):3175-86 [11543687]
Biochemistry. 2001 Oct 16;40(41):12339-48 [11591153]
Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):14931-6 [11752441]
J Biol Chem. 2003 Feb 14;278(7):4385-8 [12496294]
J Mol Graph Model. 2004 May;22(5):377-95 [15099834]
Proteins. 2004 Aug 1;56(2):310-21 [15211514]
Biochem Pharmacol. 1973 Dec 1;22(23):3099-108 [4202581]
J Recept Res. 1988;8(1-4):533-46 [3385692]
Biochemistry. 1995 Dec 19;34(50):16433-9 [8845371]
Neuropharmacology. 2004 Dec;47(8):1117-34 [15567422]
Annu Rev Biophys Biomol Struct. 2007;36:21-42 [17201676]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1124/mol.113.087833
ER  - 



TY  - JOUR
T1  - Risk factors for anal HPV infection and anal precancer in HIV-infected men who have sex with men.
AN  - 1449274266; 23908478
AB  - Carcinogenic human papillomaviruses (HPVs) cause a large proportion of anal cancers. Human immunodeficiency virus (HIV)-infected men who have sex with men (MSM) are at increased risk of HPV infection and anal cancer compared with HIV-negative men. We evaluated risk factors for HPV infection and anal precancer in a population of HIV-infected MSM.
          Our study included 305 MSM at an HIV/AIDS clinic in the Kaiser Permanente Northern California Health Maintenance Organization. Logistic regression was used to estimate associations of risk factors comparing men without anal HPV infection; men with anal HPV infection, but no precancer; and men with anal precancer. Low CD4 count (<350 cells/mm(3)) and previous chlamydia infection were associated with an increased risk of carcinogenic HPV infection (odds ratio [OR], 3.65; 95% confidence interval [CI], 1.28-10.40 and OR, 4.24; 95% CI, 1.16-15.51, respectively). History of smoking (OR, 2.71 95% CI, 1.43-5.14), duration, recency, and dose of smoking increased the risk of anal precancer among carcinogenic HPV-positive men but had no association with HPV infection.
          We found distinct risk factors for anal HPV infection and anal precancer. Risk factors for HPV infection and anal precancer are similar to established risk factors for cervical cancer progression.
JF  - The Journal of infectious diseases
AU  - Schwartz, Lauren M
AU  - Castle, Philip E
AU  - Follansbee, Stephen
AU  - Borgonovo, Sylvia
AU  - Fetterman, Barbara
AU  - Tokugawa, Diane
AU  - Lorey, Thomas S
AU  - Sahasrabuddhe, Vikrant V
AU  - Luhn, Patricia
AU  - Gage, Julia C
AU  - Darragh, Teresa M
AU  - Wentzensen, Nicolas
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville.
Y1  - 2013/12/01/
PY  - 2013
DA  - 2013 Dec 01
SP  - 1768
EP  - 1775
VL  - 208
IS  - 11
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - men who have sex with men (MSM)
KW  - human immunodeficiency virus (HIV)
KW  - human papillomavirus (HPV)
KW  - anal intraepithelial neoplasia (AIN)
KW  - anal cancer
KW  - Young Adult
KW  - Papillomaviridae -- pathogenicity
KW  - Humans
KW  - Anal Canal -- virology
KW  - Smoking -- adverse effects
KW  - CD4 Lymphocyte Count
KW  - Demography
KW  - Sexual Behavior
KW  - HIV Seropositivity
KW  - Logistic Models
KW  - Risk Factors
KW  - Chlamydia Infections -- complications
KW  - Adult
KW  - Confidence Intervals
KW  - Middle Aged
KW  - Adolescent
KW  - California -- epidemiology
KW  - Male
KW  - HIV Infections -- virology
KW  - Papillomavirus Infections -- complications
KW  - Papillomavirus Infections -- virology
KW  - Anus Neoplasms -- complications
KW  - Precancerous Conditions -- complications
KW  - Precancerous Conditions -- epidemiology
KW  - Precancerous Conditions -- virology
KW  - Papillomavirus Infections -- epidemiology
KW  - HIV Infections -- complications
KW  - Homosexuality, Male -- statistics & numerical data
KW  - Anus Neoplasms -- epidemiology
KW  - HIV Infections -- epidemiology
KW  - Anus Neoplasms -- virology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449274266?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Risk+factors+for+anal+HPV+infection+and+anal+precancer+in+HIV-infected+men+who+have+sex+with+men.&rft.au=Schwartz%2C+Lauren+M%3BCastle%2C+Philip+E%3BFollansbee%2C+Stephen%3BBorgonovo%2C+Sylvia%3BFetterman%2C+Barbara%3BTokugawa%2C+Diane%3BLorey%2C+Thomas+S%3BSahasrabuddhe%2C+Vikrant+V%3BLuhn%2C+Patricia%3BGage%2C+Julia+C%3BDarragh%2C+Teresa+M%3BWentzensen%2C+Nicolas&rft.aulast=Schwartz&rft.aufirst=Lauren&rft.date=2013-12-01&rft.volume=208&rft.issue=11&rft.spage=1768&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjit374
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-03
N1  - Date created - 2013-11-04
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer. 2004 Jul 15;101(2):270-80 [15241823]
JAMA. 2002 Apr 24;287(16):2114-9 [11966386]
J Infect Dis. 1998 Feb;177(2):361-7 [9466522]
J Natl Cancer Inst Monogr. 1998;(23):15-20 [9709296]
J Natl Cancer Inst. 2005 Jun 15;97(12):896-905 [15956651]
Am J Epidemiol. 2005 Oct 1;162(7):668-75 [16120706]
Am J Epidemiol. 2007 May 15;165(10):1143-53 [17344204]
Ann Intern Med. 2008 May 20;148(10):728-36 [18490686]
J Acquir Immune Defic Syndr. 2008 Aug 1;48(4):491-9 [18614927]
Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):113-20 [19124488]
Int J Cancer. 2009 Apr 1;124(7):1626-36 [19115209]
Int J STD AIDS. 2009 Apr;20(4):262-4 [19304972]
Obstet Gynecol Clin North Am. 2009 Mar;36(1):187-200 [19344856]
Cancer Cytopathol. 2011 Feb 25;119(1):5-19 [21319310]
AIDS Patient Care STDS. 2011 Apr;25(4):213-9 [21366437]
Clin Infect Dis. 2011 May;52(9):1174-81 [21364075]
J Natl Cancer Inst. 2011 May 4;103(9):753-62 [21483021]
Gynecol Endocrinol. 2011 Aug;27(8):597-604 [21438669]
J Acquir Immune Defic Syndr. 2011 Aug;57 Suppl 3:S217-24 [21857322]
J Infect Dis. 2011 Dec 1;204(11):1711-22 [21964400]
J Clin Microbiol. 2012 Jan;50(1):61-5 [22075592]
Cancer Epidemiol Biomarkers Prev. 2012 Jan;21(1):111-21 [22028398]
CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781]
Clin Infect Dis. 2012 Apr;54(7):1026-34 [22291097]
Int J STD AIDS. 2012 Feb;23(2):77-82 [22422679]
Lancet Oncol. 2012 May;13(5):438-40 [22445258]
Lancet Oncol. 2012 May;13(5):487-500 [22445259]
Int J Cancer. 2012 Aug 15;131(4):949-55 [21960453]
PLoS One. 2012;7(6):e38731 [22723879]
Lancet Oncol. 2012 Jul;13(7):e279-80; author rreply e280 [22748261]
AIDS. 2012 Nov 13;26(17):2185-92 [23018436]
AIDS Res Hum Retroviruses. 2012 Dec;28(12):1734-8 [22519744]
Cancer Epidemiol Biomarkers Prev. 2013 Jan;22(1):42-9 [23155136]
J Infect Dis. 2013 Feb 1;207(3):392-401 [23162133]
Cancer Cytopathol. 2013 Feb;121(2):72-8 [22811048]
AIDS Behav. 2013 Mar;17(3):1211-8 [22419454]
J Acquir Immune Defic Syndr. 2013 Aug 1;63(4):472-9 [23514956]
Am J Med. 1997 May 5;102(5A):3-8 [9217656]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/infdis/jit374
ER  - 



TY  - JOUR
T1  - Safety, tolerability, and immunogenicity of repeated doses of dermavir, a candidate therapeutic HIV vaccine, in HIV-infected patients receiving combination antiretroviral therapy: results of the ACTG 5176 trial.
AN  - 1447496727; 24169120
AB  - HIV-specific cellular immune responses are associated with control of viremia and delayed disease progression. An effective therapeutic vaccine could mimic these effects and reduce the need for continued antiretroviral therapy. DermaVir, a topically administered plasmid DNA-nanomedicine expressing HIV (CladeB) virus-like particles consisting of 15 antigens, induces predominantly central memory T-cell responses.
          Treated HIV-infected adults (HIV RNA 350) were randomized to placebo or escalating DermaVir doses (0.1 or 0.4 mg of plasmid DNA at weeks 1, 7, and 13 in the low- and intermediate-dose groups and 0.8 mg at weeks 0, 1, 6, 7, 12, and 13 in the high-dose group), n = 5-6 evaluable subjects per group. Immunogenicity was assessed by a 12-day cultured interferon-γ enzyme-linked immunosorbent spot assay at baseline and at weeks 9, 17, and 37 using 1 Tat/Rev and 3 overlapping Gag peptide pools (p17, p24, and p15).
          Groups were comparable at baseline. The study intervention was well tolerated, without dose-limiting toxicities. Most responses were highest at week 17 (4 weeks after last vaccination) when Gag p24 responses were significantly greater among intermediate-dose group compared with control subjects [median (IQR): 67,600 (5633-74,368) versus 1194 (9-1667)] net spot-forming units per million cells, P = 0.032. In the intermediate-dose group, there was also a marginal Gag p15 response increase from baseline to week 17 [2859 (1867-56,933), P = 0.06], and this change was significantly greater than in the placebo group [0 (-713 to 297), P = 0.016].
          DermaVir administration was associated with a trend toward greater HIV-specific, predominantly central memory T-cell responses. The intermediate DermaVir dose tended to show the greatest immunogenicity, consistent with previous studies in different HIV-infected patient populations.
JF  - Journal of acquired immune deficiency syndromes (1999)
AU  - Rodriguez, Benigno
AU  - Asmuth, David M
AU  - Matining, Roy M
AU  - Spritzler, John
AU  - Jacobson, Jeffrey M
AU  - Mailliard, Robbie B
AU  - Li, Xiao-Dong
AU  - Martinez, Ana I
AU  - Tenorio, Allan R
AU  - Lori, Franco
AU  - Lisziewicz, Julianna
AU  - Yesmin, Suria
AU  - Rinaldo, Charles R
AU  - Pollard, Richard B
AD  - *Division of Infectious Diseases and Center for AIDS Research, Case Western Reserve University/University Hospitals of Cleveland, Cleveland, OH; †Division of Infectious Diseases, University of California Davis Medical Center, Sacramento, CA; ‡Statistical and Data Analysis Center, Harvard School of Public Health, Boston, MA; §Division of Infectious Diseases and HIV Medicine, Drexel University College of Medicine, Philadelphia, PA; ‖University of Pittsburgh, Pittsburgh, PA; ¶Division of AIDS, National Institute of Allergy and Infectious Diseases, Bethesda, MD; #Department of Medicine, Rush University Medical Center, Chicago, IL; **ViroStatics srl, Sassari, Italy; ††Genetic Immunity, Budapest, Hungary; ‡‡Genetic Immunity, McLean, VA; and §§Social & Scientific Systems, Inc, Silver Spring, MD.
Y1  - 2013/12/01/
PY  - 2013
DA  - 2013 Dec 01
SP  - 351
EP  - 359
VL  - 64
IS  - 4
KW  - AIDS Vaccines
KW  - 0
KW  - Anti-HIV Agents
KW  - DermaVir
KW  - RNA, Viral
KW  - Index Medicus
KW  - AIDS/HIV
KW  - Viral Load
KW  - Drug Therapy, Combination
KW  - Humans
KW  - CD8-Positive T-Lymphocytes
KW  - Viremia
KW  - Immunization Schedule
KW  - CD4 Lymphocyte Count
KW  - CD4-Positive T-Lymphocytes
KW  - AIDS Vaccines -- administration & dosage
KW  - Anti-HIV Agents -- therapeutic use
KW  - AIDS Vaccines -- immunology
KW  - Anti-HIV Agents -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447496727?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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%2C+tolerability%2C+and+immunogenicity+of+repeated+doses+of+dermavir%2C+a+candidate+therapeutic+HIV+vaccine%2C+in+HIV-infected+patients+receiving+combination+antiretroviral+therapy%3A+results+of+the+ACTG+5176+trial.&rft.au=Rodriguez%2C+Benigno%3BAsmuth%2C+David+M%3BMatining%2C+Roy+M%3BSpritzler%2C+John%3BJacobson%2C+Jeffrey+M%3BMailliard%2C+Robbie+B%3BLi%2C+Xiao-Dong%3BMartinez%2C+Ana+I%3BTenorio%2C+Allan+R%3BLori%2C+Franco%3BLisziewicz%2C+Julianna%3BYesmin%2C+Suria%3BRinaldo%2C+Charles+R%3BPollard%2C+Richard+B&rft.aulast=Rodriguez&rft.aufirst=Benigno&rft.date=2013-12-01&rft.volume=64&rft.issue=4&rft.spage=351&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.0b013e3182a99590
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-24
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Expert Opin Biol Ther. 2009 Jan;9(1):55-69 [19063693]
PLoS Med. 2008 Oct 21;5(10):e203 [18942885]
AIDS. 2009 Jul 17;23(11):1329-40 [19528789]
AIDS. 2009 Aug 24;23(13):1743-53 [19571723]
Immunology. 2009 Sep;128(1):83-91 [19689738]
Clin Immunol. 2010 Feb;134(2):140-7 [19889582]
J Virol. 2010 May;84(9):4461-8 [20147397]
Int J Pharm. 2010 Jun 15;392(1-2):261-7 [20347027]
J Infect Dis. 2010 Jun 15;201(12):1788-95 [20446848]
PLoS One. 2010;5(6):e11068 [20548786]
J Infect Dis. 2010 Sep 1;202(5):705-16 [20662716]
Science. 2010 Dec 10;330(6010):1551-7 [21051598]
PLoS One. 2010;5(12):e14330 [21179404]
Vaccine. 2011 Jan 17;29(4):744-53 [21109034]
J Infect Dis. 2011 Feb 15;203(4):473-8 [21233310]
Curr Opin HIV AIDS. 2011 May;6(3):197-201 [21502922]
N Engl J Med. 2011 Aug 11;365(6):493-505 [21767103]
J Infect Dis. 2011 Oct 15;204(8):1217-26 [21917895]
Expert Rev Vaccines. 2011 Oct;10(10):1371-84 [21988301]
J Acquir Immune Defic Syndr. 2011 Nov 1;58(3):248-52 [21709567]
AIDS. 2012 Feb 20;26(4):F1-12 [22156965]
Immunity. 2012 Mar 23;36(3):491-501 [22406268]
Nanomedicine. 2012 May;8(4):497-506 [21839051]
PLoS One. 2012;7(5):e35416 [22590502]
J Virol. 2012 Jun;86(12):6959-69 [22514340]
Clin Diagn Lab Immunol. 2000 Mar;7(2):279-87 [10702505]
Eur J Immunol. 2000 Mar;30(3):883-91 [10741405]
J Virol. 2001 Aug;75(16):7621-8 [11462034]
J Immunol. 2002 Nov 1;169(9):4778-87 [12391187]
J Exp Med. 1995 Apr 1;181(4):1365-72 [7699324]
J Virol. 1995 Sep;69(9):5838-42 [7637030]
Proc Natl Acad Sci U S A. 1997 Jan 7;94(1):254-8 [8990195]
Science. 1997 Nov 14;278(5341):1291-5 [9360926]
N Engl J Med. 1998 Mar 26;338(13):853-60 [9516219]
AIDS. 1998 Dec 3;12(17):2261-70 [9863867]
Science. 1999 Feb 5;283(5403):857-60 [9933172]
J Virol. 1999 Oct;73(10):8356-63 [10482586]
AIDS. 2005 Jan 3;19(1):35-43 [15627031]
J Invest Dermatol. 2005 Jan;124(1):160-9 [15654970]
Virology. 2005 Mar 15;333(2):226-38 [15721357]
Vaccine. 2005 Mar 18;23(17-18):2030-4 [15755566]
J Immunol. 2005 Nov 1;175(9):5675-80 [16237057]
Curr Drug Deliv. 2006 Jan;3(1):83-8 [16472097]
J Virol. 2006 May;80(10):4717-28 [16641265]
J Immunol. 2006 May 15;176(10):6130-46 [16670322]
Blood. 2006 Jun 15;107(12):4781-9 [16467198]
J Infect Dis. 2006 Sep 1;194(5):623-32 [16897661]
N Engl J Med. 2006 Nov 30;355(22):2283-96 [17135583]
J Virol. 2007 Apr;81(7):3465-76 [17251286]
Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6776-81 [17428922]
Clin Vaccine Immunol. 2008 Feb;15(2):284-92 [17942609]
J Immunol. 2008 May 1;180(9):5907-15 [18424710]
J Exp Med. 2008 Oct 27;205(11):2537-50 [18838548]
BMJ. 2009;338:b1649 [19406887]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/QAI.0b013e3182a99590
ER  - 



TY  - JOUR
T1  - Physical chemistry of nucleic acids and their complexes
AN  - 1443376381; 18643925
AB  - Studies of the physical properties of nucleic acids began almost immediately following the discovery of the DNA structure. Early investigations focused on the stability and specificity of multi-strand polynucleotide complexes, then gradually on their interaction with other molecules, particularly proteins. As molecular and structural biology expanded to provide detailed information about biochemical mechanisms, physical studies eventually acquired the additional constraint that they should be relevant to functioning biological systems. We describe work in our laboratory that began with investigations of relatively simple questions about the role of electrostatic interactions in the stabilization of multi-strand nucleic acid structures, and evolved to studies of chromatin structure in vitro and within the nucleus. Published 2013 Wiley Periodicals, Inc*. Biopolymers 99: 910-915, 2013.
JF  - Biopolymers
AU  - Ghirlando, Rodolfo
AU  - Felsenfeld, Gary
AD  - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892.
Y1  - 2013/12//
PY  - 2013
DA  - Dec 2013
SP  - 910
EP  - 915
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 99
IS  - 12
SN  - 0006-3525, 0006-3525
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - DNA
KW  - chromatin
KW  - polynucleotide structures
KW  - nucleic acids
KW  - DNA structure
KW  - Chromatin
KW  - Biopolymers
KW  - Electrostatic properties
KW  - polynucleotides
KW  - Nuclei
KW  - N 14820:DNA Metabolism & Structure
KW  - W 30935:Food Biotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443376381?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Physical+chemistry+of+nucleic+acids+and+their+complexes&rft.au=Ghirlando%2C+Rodolfo%3BFelsenfeld%2C+Gary&rft.aulast=Ghirlando&rft.aufirst=Rodolfo&rft.date=2013-12-01&rft.volume=99&rft.issue=12&rft.spage=910&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22311
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - DNA structure; nucleic acids; Chromatin; Biopolymers; Electrostatic properties; polynucleotides; Nuclei
DO  - http://dx.doi.org/10.1002/bip.22311
ER  - 



TY  - JOUR
T1  - Novel structural and functional insights into M3 muscarinic receptor dimer/oligomer formation.
AN  - 1464491549; 24133207
AB  - Class A G protein-coupled receptors (GPCRs) are able to form homodimers and/or oligomeric arrays. We recently proposed, based on bioluminescence resonance energy transfer studies with the M3 muscarinic receptor (M3R), a prototypic class A GPCR, that the M3R is able to form multiple, structurally distinct dimers that are probably transient in nature (McMillin, S. M., Heusel, M., Liu, T., Costanzi, S., and Wess, J. (2011) J. Biol. Chem. 286, 28584-28598). To provide more direct experimental support for this concept, we employed a disulfide cross-linking strategy to trap various M3R dimeric species present in a native lipid environment (transfected COS-7 cells). Disulfide cross-linking studies were carried out with many mutant M3Rs containing single cysteine (Cys) substitutions within two distinct cytoplasmic M3R regions, the C-terminal portion of the second intracellular loop (i2) and helix H8 (H8). The pattern of cross-links that we obtained, in combination with molecular modeling studies, was consistent with the existence of two structurally distinct M3R dimer interfaces, one involving i2/i2 contacts (TM4-TM5-i2 interface) and the other one characterized by H8-H8 interactions (TM1-TM2-H8 interface). Specific H8-H8 disulfide cross-links led to significant impairments in M3R-mediated G protein activation, suggesting that changes in the structural orientation or mobility of H8 are critical for efficient receptor-G protein coupling. Our findings provide novel structural and functional insights into the mechanisms involved in M3R dimerization (oligomerization). Because the M3R shows a high degree of sequence similarity with many other class A GPCRs, our findings should be of considerable general interest.
JF  - The Journal of biological chemistry
AU  - Hu, Jianxin
AU  - Hu, Kelly
AU  - Liu, Tong
AU  - Stern, Matthew K
AU  - Mistry, Rajendra
AU  - Challiss, R A John
AU  - Costanzi, Stefano
AU  - Wess, Jürgen
AD  - From the Molecular Signaling Section, Laboratory of Bioorganic Chemistry, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Y1  - 2013/11/29/
PY  - 2013
DA  - 2013 Nov 29
SP  - 34777
EP  - 34790
VL  - 288
IS  - 48
KW  - Phosphatidylinositols
KW  - 0
KW  - Receptor, Muscarinic M3
KW  - Cysteine
KW  - K848JZ4886
KW  - Index Medicus
KW  - Site-directed Mutagenesis
KW  - Receptor Structure-function
KW  - G Protein-coupled Receptors (GPCR)
KW  - Cholinergic Receptor
KW  - Neurotransmitter Receptors
KW  - Phosphatidylinositols -- chemistry
KW  - Mutagenesis, Site-Directed
KW  - Phosphatidylinositols -- metabolism
KW  - Animals
KW  - Protein Structure, Secondary
KW  - Cysteine -- chemistry
KW  - COS Cells
KW  - Cercopithecus aethiops
KW  - Amino Acid Sequence
KW  - Protein Structure, Tertiary
KW  - Binding Sites
KW  - Receptor, Muscarinic M3 -- metabolism
KW  - Protein Multimerization
KW  - Receptor, Muscarinic M3 -- chemistry
KW  - Receptor, Muscarinic M3 -- genetics
KW  - Protein Conformation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464491549?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Novel+structural+and+functional+insights+into+M3+muscarinic+receptor+dimer%2Foligomer+formation.&rft.au=Hu%2C+Jianxin%3BHu%2C+Kelly%3BLiu%2C+Tong%3BStern%2C+Matthew+K%3BMistry%2C+Rajendra%3BChalliss%2C+R+A+John%3BCostanzi%2C+Stefano%3BWess%2C+J%C3%BCrgen&rft.aulast=Hu&rft.aufirst=Jianxin&rft.date=2013-11-29&rft.volume=288&rft.issue=48&rft.spage=34777&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M113.503714
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-21
N1  - Date created - 2013-12-02
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biochemistry. 1996 Nov 12;35(45):14040-6 [8916888]
EMBO J. 2008 Sep 3;27(17):2293-304 [18668123]
J Biol Chem. 1999 Jun 4;274(23):16629-40 [10347230]
Biochemistry. 1999 Jun 22;38(25):7925-30 [10387034]
J Biol Chem. 1999 Jul 2;274(27):19487-97 [10383466]
J Biol Chem. 2006 Feb 17;281(7):4109-16 [16354660]
J Biol Chem. 2006 Mar 3;281(9):5416-25 [16368694]
Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16123-8 [17060607]
Biochim Biophys Acta. 2007 Apr;1768(4):825-35 [17069751]
Proc Natl Acad Sci U S A. 2007 May 1;104(18):7682-7 [17452637]
Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12199-204 [17620610]
J Biol Chem. 2007 Sep 7;282(36):26284-93 [17623649]
J Biol Chem. 2007 Oct 19;282(42):30363-72 [17726027]
Science. 2007 Nov 23;318(5854):1258-65 [17962520]
J Biol Chem. 2008 Feb 15;283(7):4387-94 [18033822]
Nat Rev Drug Discov. 2008 Apr;7(4):339-57 [18382464]
Nat Methods. 2009 Mar;6(3):225-30 [19234451]
Mol Pharmacol. 2009 Jun;75(6):1296-9 [19273553]
Proc Natl Acad Sci U S A. 2010 Feb 9;107(6):2693-8 [20133736]
Sci Signal. 2010;3(115):pe12 [20354223]
Nat Chem Biol. 2010 Jul;6(7):541-8 [20512139]
J Biol Chem. 2000 Jan 21;275(3):1937-43 [10636895]
Science. 2000 Mar 17;287(5460):1960-4 [10720314]
Br J Pharmacol. 2001 Feb;132(4):950-8 [11181437]
Annu Rev Pharmacol Toxicol. 2002;42:409-35 [11807178]
Nat Rev Mol Cell Biol. 2002 Sep;3(9):639-50 [12209124]
J Biol Chem. 2003 Jun 13;278(24):21655-62 [12663652]
Mol Pharmacol. 2004 Nov;66(5):1077-82 [15319448]
Biochem J. 1972 Feb;126(3):553-60 [5075266]
Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):3103-7 [8385357]
Crit Rev Neurobiol. 1996;10(1):69-99 [8853955]
Biochemistry. 2010 Aug 10;49(31):6771-6 [20617813]
Regul Pept. 2010 Sep 24;164(2-3):113-9 [20541569]
Trends Biochem Sci. 2010 Nov;35(11):595-600 [20538466]
Science. 2010 Nov 19;330(6007):1066-71 [20929726]
J Cell Biol. 2011 Feb 7;192(3):463-80 [21300851]
J Biol Chem. 2011 Aug 12;286(32):28584-98 [21685385]
Nature. 2011 Sep 29;477(7366):549-55 [21772288]
FASEB J. 2012 Feb;26(2):604-16 [22031716]
Nature. 2012 Feb 23;482(7386):552-6 [22358844]
Biochemistry. 2012 Mar 6;51(9):1819-21 [22352709]
Nature. 2012 May 17;485(7398):321-6 [22437502]
Nature. 2012 May 17;485(7398):327-32 [22437504]
Annu Rev Pharmacol Toxicol. 2013;53:531-56 [23140243]
Proc Natl Acad Sci U S A. 2013 Jan 8;110(2):743-8 [23267088]
J Mol Cell Cardiol. 2013 Apr;57:129-36 [23357106]
Nat Struct Mol Biol. 2013 Apr;20(4):419-25 [23435379]
J Struct Biol. 2013 May;182(2):164-72 [23458690]
Mol Pharmacol. 2013 Jul;84(1):158-69 [23632086]
Pharmacol Ther. 1998 Dec;80(3):231-64 [9888696]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1074/jbc.M113.503714
ER  - 



TY  - JOUR
T1  - On stand by: host genetics of HIV control
AN  - 1765971880; PQ0002559351
AB  - The impact of host genetic variation on determining the differential outcomes after HIV infection has been studied by two approaches: targeting of candidate genes and genome-wide association studies (GWASs). The overlap in genetic variants that has been identified by these two means has essentially been restricted to variants near to the human leukocyte antigen (HLA) class I genes, although variation in the CCR5 locus, which was first shown to have an effect on HIV outcomes using the candidate gene approach, does reach significance genome-wide when very large samples sizes (i.e. thousands) are used in GWAS. Overall, many of the variants identified by the candidate gene approach are likely to be spurious, as no additional variants apart from a novel variant near the HLA-C gene have been consistently identified by GWAS. Variants with low frequency and/or low impact on HIV outcomes are likely to exist in the genome and there could be many of them, but these are not identifiable, given current GWAS sample sizes. Several loci centrally involved in the immune response, including the immunoglobulin genes, T-cell receptor loci, or leukocyte receptor complex, are either poorly covered on the GWAS chips or difficult to interpret due to their repetitive nature and/or the presence of insertion/deletion polymorphisms in the region. These loci warrant further interrogation, but genetic characterization of these regions across a range of individuals will first be required. Finally, synergistic interactions between loci may affect outcome after infection, as suggested by associations of specific, functionally relevant HLA and killer cell immunoglobulin-like receptor variants with HIV disease outcomes, and these require further consideration as well.
JF  - AIDS
AU  - Carrington, Mary
AU  - Bashirova, Arman A
AU  - McLaren, Paul J
AD  - Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC Frederick Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland, carringm@mail.nih.gov
Y1  - 2013/11/28/
PY  - 2013
DA  - 2013 Nov 28
SP  - 2831
EP  - 2839
PB  - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL  - 27
IS  - 18
SN  - 0269-9370, 0269-9370
KW  - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW  - genome-wide association study
KW  - host genetics
KW  - human leukocyte antigen
KW  - Histocompatibility antigen HLA
KW  - Genomes
KW  - Acquired immune deficiency syndrome
KW  - T-cell receptor
KW  - Gene polymorphism
KW  - Leukocytes
KW  - Genetic diversity
KW  - CCR5 protein
KW  - Infection
KW  - Human immunodeficiency virus
KW  - Insertion
KW  - Killer cell immunoglobulin-like receptors
KW  - Immune response
KW  - Immunoglobulins
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - V 22360:AIDS and HIV
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765971880?accountid=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=On+stand+by%3A+host+genetics+of+HIV+control&rft.au=Carrington%2C+Mary%3BBashirova%2C+Arman+A%3BMcLaren%2C+Paul+J&rft.aulast=Carrington&rft.aufirst=Mary&rft.date=2013-11-28&rft.volume=27&rft.issue=18&rft.spage=2831&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2F01.aids.0000432536.85335.c8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-02-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Genomes; Histocompatibility antigen HLA; T-cell receptor; Insertion; Killer cell immunoglobulin-like receptors; Gene polymorphism; Leukocytes; Genetic diversity; CCR5 protein; Immune response; Infection; Immunoglobulins; Acquired immune deficiency syndrome; Human immunodeficiency virus
DO  - http://dx.doi.org/10.1097/01.aids.0000432536.85335.c8
ER  - 



TY  - JOUR
T1  - Polyfluoroalkyl Chemicals and Menopause among Women 20-65 Years of Age (NHANES)
AN  - 1505348299; 19339719
AB  - Background: Polyfluoroalkyl chemicals (PFCs) such as perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) have been associated with early menopause. However, previous cross-sectional studies have lacked adequate data to investigate possible reverse causality (i.e., higher serum concentrations due to decreased excretion after menopause). Objectives: We investigated the association between PFOS, PFOA, perfluorononanoate (PFNA), and perfluorohexane sulfonate (PFHxS) and age at natural menopause among women 20-65 years of age in NHANES (National Health and Nutrition Examination Survey). Methods: We used proportional hazard models to estimate hazard ratios (HRs) for the onset of natural menopause as a function of age and serum PFC levels, and to investigate reverse causation by estimating associations between PFC levels and the rate of hysterectomy. We also used multivariable linear regression to determine whether time since menopause predicted serum PFC levels. Results: After adjusting for age at survey, race/ethnicity, education, ever smoking, and parity, women with higher levels of PFCs had earlier menopause than did women with the lowest PFC levels. We observed a monotonic association with PFHxS: The HR was 1.42 (95% CI: 1.08, 1.87) for serum concentrations in tertile 2 versus tertile 1, and 1.70 (95% CI: 1.36, 2.12) for tertile 3 versus tertile 1. We also found evidence of reverse causation: PFCs were positively associated with rate of hysterectomy, and time since natural menopause was positively associated with serum PFCs. Conclusions: Our findings suggest a positive association between PFCs and menopause; however, at least part of the association may be due to reverse causation. Regardless of underlying cause, women appear to have higher PFC concentrations after menopause. Citation: Taylor KW, Hoffman K, Thayer KA, Daniels JL. 2014. Polyfluoroalkyl chemicals and menopause among women 20-65 years of age (NHANES). Environ Health Perspect 122:145-150; http://dx.doi.org/10.1289/ehp.1306707
JF  - Environmental Health Perspectives
AU  - Taylor, Kyla W
AU  - Hoffman, Kate
AU  - Thayer, Kristina A
AU  - Daniels, Julie L
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  - 2013/11/26/
PY  - 2013
DA  - 2013 Nov 26
SP  - 145
EP  - 150
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  - Environment Abstracts; Health & Safety Science Abstracts
KW  - Chemicals
KW  - Parity
KW  - Smoking
KW  - Age
KW  - Education
KW  - Sulfonates
KW  - Excretion
KW  - Females
KW  - Nutrition
KW  - Menopause
KW  - Ethnic groups
KW  - H 12000:Epidemiology and Public Health
KW  - ENA 04:Environmental Education
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505348299?accountid=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=Polyfluoroalkyl+Chemicals+and+Menopause+among+Women+20-65+Years+of+Age+%28NHANES%29&rft.au=Taylor%2C+Kyla+W%3BHoffman%2C+Kate%3BThayer%2C+Kristina+A%3BDaniels%2C+Julie+L&rft.aulast=Taylor&rft.aufirst=Kyla&rft.date=2013-11-26&rft.volume=122&rft.issue=2&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306707
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Parity; Chemicals; Smoking; Education; Age; Sulfonates; Excretion; Females; Nutrition; Ethnic groups; Menopause
DO  - http://dx.doi.org/10.1289/ehp.1306707
ER  - 



TY  - JOUR
T1  - Repair of UV photolesions in xeroderma pigmentosum group C cells induced by translational readthrough of premature termination codons.
AN  - 1462370474; 24218596
AB  - About 12% of human genetic disorders involve premature termination codons (PTCs). Aminoglycoside antibiotics have been proposed for restoring full-length proteins by readthrough of PTC. To assess the efficiency of readthrough, we selected homozygous and compound heterozygous skin fibroblasts from xeroderma pigmentosum (XP) patients with different PTCs in the XPC DNA repair gene. XP patients have a nucleotide excision repair defect and a 10,000-fold increased risk of UV-induced skin cancer. In six of eight PTC-containing XP-C cells, treatment with Geneticin and gentamicin resulted in (i) stabilized XPC-mRNA, which would have been degraded by nonsense-mediated decay; (ii) increased expression of XPC protein that localized to UV-damaged sites; (iii) recruitment of XPB and XPD proteins to UV DNA damage sites; and (iv) increased repair of 6-4 photoproducts and cyclobutane pyrimidine dimers. Expression of PTC in a transfected vector revealed that readthrough depends on the PTC sequence and its location within the gene. This sensitive DNA repair assay system demonstrates the complexity of response to PTC readthrough inducers. The efficiency of aminoglycoside-mediated readthrough depends on the type and copy number of PTC, the downstream 4+ nucleotide, and the location within the exon. Treatment with small-molecule nonaminoglycoside compounds (PTC124, BZ16, or RTC14) resulted in similarly increased XPC mRNA expression and photoproduct removal with less toxicity than with the aminoglycosides. Characterizing PTC structure and parameters governing effective PTC readthrough may provide a unique prophylactic therapy for skin cancer prevention in XP-C patients.
JF  - Proceedings of the National Academy of Sciences of the United States of America
AU  - Kuschal, Christiane
AU  - DiGiovanna, John J
AU  - Khan, Sikandar G
AU  - Gatti, Richard A
AU  - Kraemer, Kenneth H
AD  - Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892.
Y1  - 2013/11/26/
PY  - 2013
DA  - 2013 Nov 26
SP  - 19483
EP  - 19488
VL  - 110
IS  - 48
KW  - Codon, Nonsense
KW  - 0
KW  - DNA Primers
KW  - Gentamicins
KW  - Oxadiazoles
KW  - ataluren
KW  - antibiotic G 418
KW  - A08F5XTI6G
KW  - Luciferases
KW  - EC 1.13.12.-
KW  - Index Medicus
KW  - UV radiation
KW  - readthrough compounds
KW  - Real-Time Polymerase Chain Reaction
KW  - Immunoblotting
KW  - Fibroblasts -- drug effects
KW  - DNA Primers -- genetics
KW  - Humans
KW  - Enzyme-Linked Immunosorbent Assay
KW  - Fluorescent Antibody Technique
KW  - Codon, Nonsense -- genetics
KW  - DNA Repair -- genetics
KW  - RNA Stability -- drug effects
KW  - Xeroderma Pigmentosum -- genetics
KW  - Xeroderma Pigmentosum -- drug therapy
KW  - Skin Neoplasms -- prevention & control
KW  - DNA Repair -- drug effects
KW  - Gentamicins -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1462370474?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+UV+photolesions+in+xeroderma+pigmentosum+group+C+cells+induced+by+translational+readthrough+of+premature+termination+codons.&rft.au=Kuschal%2C+Christiane%3BDiGiovanna%2C+John+J%3BKhan%2C+Sikandar+G%3BGatti%2C+Richard+A%3BKraemer%2C+Kenneth+H&rft.aulast=Kuschal&rft.aufirst=Christiane&rft.date=2013-11-26&rft.volume=110&rft.issue=48&rft.spage=19483&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.1312088110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-27
N1  - Date created - 2013-11-27
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Res. 2000 Apr 1;60(7):1974-82 [10766188]
Pharmacogenomics. 2005 Jan;6(1):27-36 [15723603]
Pigment Cell Res. 2001 Apr;14(2):94-102 [11310797]
J Invest Dermatol. 2001 Aug;117(2):197-204 [11511294]
Nucleic Acids Res. 2002 Aug 15;30(16):3624-31 [12177305]
J Invest Dermatol. 2002 Nov;119(5):1177-82 [12445209]
Photochem Photobiol Sci. 2002 Apr;1(4):225-36 [12661961]
Biochim Biophys Acta. 2003 May 13;1627(1):1-6 [12759186]
Clin Microbiol Rev. 2003 Jul;16(3):430-50 [12857776]
Acta Myol. 2003 May;22(1):15-21 [12966700]
Hum Mol Genet. 2004 Feb 1;13(3):343-52 [14662655]
Ann Neurol. 2004 Mar;55(3):422-6 [14991821]
Biochim Biophys Acta. 1972 Aug 16;277(1):7-14 [5053775]
Nat Genet. 1993 Dec;5(4):413-7 [8298653]
J Invest Dermatol. 1998 Nov;111(5):791-6 [9804340]
Hum Mutat. 2010 Feb;31(2):167-75 [19953607]
Mutat Res. 2010 Mar 1;685(1-2):21-8 [19686765]
Am J Dermatopathol. 2010 Apr;32(2):109-17 [19915453]
J Biochem. 2010 Apr;147(4):463-70 [19910311]
J Invest Dermatol. 2010 Jun;130(6):1537-42 [20054342]
J Med Genet. 2011 Mar;48(3):168-76 [21097776]
Eur Respir J. 2011 Jul;38(1):59-69 [21233271]
J Invest Dermatol. 2012 Mar;132(3 Pt 2):785-96 [22217736]
Ann N Y Acad Sci. 2012 Feb;1250:33-40 [22364446]
Pharmacol Ther. 2012 Nov;136(2):227-66 [22820013]
Exp Dermatol. 2013 Jan;22(1):24-9 [23173980]
Mol Ther. 2013 Sep;21(9):1653-60 [23774824]
Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2151-6 [10681431]
Am J Respir Crit Care Med. 2000 Mar;161(3 Pt 1):860-5 [10712334]
J Invest Dermatol. 2005 Jan;124(1):87-91 [15654957]
Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15676-81 [15498871]
DNA Repair (Amst). 2005 May 2;4(5):571-82 [15811629]
J Cell Sci. 2005 May 1;118(Pt 9):1773-6 [15860725]
Carcinogenesis. 2006 Jan;27(1):84-94 [16081512]
J Invest Dermatol. 2006 Jan;126(1):229-31 [16417242]
Clin Pharmacol Ther. 2007 Jan;81(1):99-103 [17186006]
J Clin Pharmacol. 2007 Apr;47(4):430-44 [17389552]
DNA Repair (Amst). 2007 Sep 1;6(9):1359-70 [17509950]
Org Biomol Chem. 2008 Jan 21;6(2):227-39 [18174989]
DNA Repair (Amst). 2008 May 3;7(5):744-50 [18329345]
Br J Dermatol. 2008 Sep;159(4):968-73 [18717677]
J Exp Med. 2009 Sep 28;206(10):2285-97 [19770270]
Eur J Hum Genet. 2010 Jan;18(1):130-2 [19603067]
RNA. 2000 Jul;6(7):1044-55 [10917599]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1073/pnas.1312088110
ER  - 



TY  - JOUR
T1  - Commensal Bacteria Control Cancer Response to Therapy by Modulating the Tumor Microenvironment
AN  - 1551635269; 20375040
AB  - The Microbiota Makes for Good TherapyThe gut microbiota has been implicated in the development of some cancers, such as colorectal cancer, but-given the important role our intestinal habitants play in metabolism-they may also modulate the efficacy of certain cancer therapeutics. Iida et al. (p. 967) evaluated the impact of the microbiota on the efficacy of an immunotherapy [CpG (the cytosine, guanosine, phosphodiester link) oligonucleotides] and oxaliplatin, a platinum compound used as a chemotherapeutic. Both therapies were reduced in efficacy in tumor-bearing mice that lacked microbiota, with the microbiota important for activating the innate immune response against the tumors. Viaud et al. (p. 971) found a similar effect of the microbiota on tumor-bearing mice treated with cyclophosphamide, but in this case it appeared that the microbiota promoted an adaptive immune response against the tumors.
JF  - Science
AU  - Iida, Noriho
AU  - Dzutsev, Amiran
AU  - Stewart, CAndrew
AU  - Smith, Loretta
AU  - Bouladoux, Nicolas
AU  - Weingarten, Rebecca A
AU  - Molina, Daniel A
AU  - Salcedo, Rosalba
AU  - Back, Timothy
AU  - Cramer, Sarah
AU  - Dai, Ren-Ming
AU  - Kiu, Hiu
AU  - Cardone, Marco
AU  - Naik, Shruti
AU  - Patri, Anil K
AU  - Wang, Ena
AU  - Marincola, Francesco M
AU  - Frank, Karen M
AU  - Belkaid, Yasmine
AU  - Trinchieri, Giorgio
AU  - Goldszmid, Romina S
AD  - Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA, trinchig@mail.nih.gov
Y1  - 2013/11/22/
PY  - 2013
DA  - 2013 Nov 22
SP  - 967
EP  - 970
PB  - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States
VL  - 342
IS  - 6161
SN  - 0036-8075, 0036-8075
KW  - Ecology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology
KW  - Immunotherapy
KW  - Commensals
KW  - Colorectal cancer
KW  - Cyclophosphamide
KW  - oxaliplatin
KW  - CpG islands
KW  - Tumors
KW  - Oligonucleotides
KW  - Cytosine
KW  - Digestive tract
KW  - Intestine
KW  - Platinum
KW  - Microenvironments
KW  - phosphodiesters
KW  - Guanosine
KW  - Immune response
KW  - D 04040:Ecosystem and Ecology Studies
KW  - A 01490:Miscellaneous
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551635269?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science&rft.atitle=Commensal+Bacteria+Control+Cancer+Response+to+Therapy+by+Modulating+the+Tumor+Microenvironment&rft.au=Iida%2C+Noriho%3BDzutsev%2C+Amiran%3BStewart%2C+CAndrew%3BSmith%2C+Loretta%3BBouladoux%2C+Nicolas%3BWeingarten%2C+Rebecca+A%3BMolina%2C+Daniel+A%3BSalcedo%2C+Rosalba%3BBack%2C+Timothy%3BCramer%2C+Sarah%3BDai%2C+Ren-Ming%3BKiu%2C+Hiu%3BCardone%2C+Marco%3BNaik%2C+Shruti%3BPatri%2C+Anil+K%3BWang%2C+Ena%3BMarincola%2C+Francesco+M%3BFrank%2C+Karen+M%3BBelkaid%2C+Yasmine%3BTrinchieri%2C+Giorgio%3BGoldszmid%2C+Romina+S&rft.aulast=Iida&rft.aufirst=Noriho&rft.date=2013-11-22&rft.volume=342&rft.issue=6161&rft.spage=967&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1240527
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Immunotherapy; Colorectal cancer; Commensals; Tumors; CpG islands; oxaliplatin; Cyclophosphamide; Oligonucleotides; Cytosine; Digestive tract; Platinum; Intestine; Microenvironments; phosphodiesters; Immune response; Guanosine
DO  - http://dx.doi.org/10.1126/science.1240527
ER  - 



TY  - CPAPER
T1  - Poly (ADP-ribose) polymerase-1 is a key mediator of liver inflammation and fibrosis
T2  - 20th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2013)
AN  - 1490510493; 6248820
JF  - 20th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2013)
AU  - Pacher, Pal
Y1  - 2013/11/20/
PY  - 2013
DA  - 2013 Nov 20
KW  - Liver
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490510493?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=20th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2013%29&rft.atitle=Poly+%28ADP-ribose%29+polymerase-1+is+a+key+mediator+of+liver+inflammation+and+fibrosis&rft.au=Pacher%2C+Pal&rft.aulast=Pacher&rft.aufirst=Pal&rft.date=2013-11-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=20th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.sfrbm.org/pdf/SFRBM2013-OralPresentations.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-30
N1  - Last updated - 2014-02-10
ER  - 



TY  - JOUR
T1  - Statistical and practical considerations for clinical evaluation of predictive biomarkers.
AN  - 1461337017; 24136891
AB  - Predictive biomarkers to guide therapy for cancer patients are a cornerstone of precision medicine. Discussed herein are considerations regarding the design and interpretation of such predictive biomarker studies. These considerations are important for both planning and interpreting prospective studies and for using specimens collected from completed randomized clinical trials. Specific issues addressed are differentiation between qualitative and quantitative predictive effects, challenges due to sample size requirements for predictive biomarker assessment, and consideration of additional factors relevant to clinical utility assessment, such as toxicity and cost of new therapies as well as costs and potential morbidities associated with routine use of biomarker-based tests.
JF  - Journal of the National Cancer Institute
AU  - Polley, Mei-Yin C
AU  - Freidlin, Boris
AU  - Korn, Edward L
AU  - Conley, Barbara A
AU  - Abrams, Jeffrey S
AU  - McShane, Lisa M
AD  - Affiliations of authors: Biometric Research Branch (M-YCP, BF, ELK, LMS), Cancer Diagnosis Program (BAC), and Cancer Treatment and Evaluation Program (JSA), Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Y1  - 2013/11/20/
PY  - 2013
DA  - 2013 Nov 20
SP  - 1677
EP  - 1683
VL  - 105
IS  - 22
KW  - Antineoplastic Agents
KW  - 0
KW  - Biomarkers, Tumor
KW  - Interleukin-6
KW  - Pyrimidines
KW  - Quinazolines
KW  - Sulfonamides
KW  - Tumor Suppressor Proteins
KW  - Dacarbazine
KW  - 7GR28W0FJI
KW  - pazopanib
KW  - 7RN5DR86CK
KW  - DNA Modification Methylases
KW  - EC 2.1.1.-
KW  - MGMT protein, human
KW  - EC 2.1.1.63
KW  - Receptor, Epidermal Growth Factor
KW  - EC 2.7.10.1
KW  - DNA Repair Enzymes
KW  - EC 6.5.1.-
KW  - gefitinib
KW  - S65743JHBS
KW  - temozolomide
KW  - YF1K15M17Y
KW  - Index Medicus
KW  - Kidney Neoplasms -- drug therapy
KW  - DNA Modification Methylases -- metabolism
KW  - Glioblastoma -- radiotherapy
KW  - Pyrimidines -- therapeutic use
KW  - Humans
KW  - Lung Neoplasms -- drug therapy
KW  - Glioblastoma -- drug therapy
KW  - Carcinoma, Renal Cell -- drug therapy
KW  - Sulfonamides -- therapeutic use
KW  - Sulfonamides -- pharmacology
KW  - Dacarbazine -- analogs & derivatives
KW  - Dacarbazine -- pharmacology
KW  - Tumor Suppressor Proteins -- metabolism
KW  - Glioblastoma -- metabolism
KW  - DNA Repair Enzymes -- metabolism
KW  - Randomized Controlled Trials as Topic
KW  - Carcinoma, Non-Small-Cell Lung -- genetics
KW  - Interleukin-6 -- metabolism
KW  - Pyrimidines -- pharmacology
KW  - Predictive Value of Tests
KW  - Dacarbazine -- therapeutic use
KW  - Radiotherapy, Adjuvant
KW  - Carcinoma, Renal Cell -- metabolism
KW  - Receptor, Epidermal Growth Factor -- genetics
KW  - Kidney Neoplasms -- metabolism
KW  - Quinazolines -- therapeutic use
KW  - Lung Neoplasms -- genetics
KW  - Carcinoma, Non-Small-Cell Lung -- drug therapy
KW  - Methylation
KW  - Mutation
KW  - Quinazolines -- pharmacology
KW  - Neoplasms -- drug therapy
KW  - Molecular Targeted Therapy
KW  - Sample Size
KW  - Precision Medicine -- trends
KW  - Antineoplastic Agents -- therapeutic use
KW  - Antineoplastic Agents -- pharmacology
KW  - Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1461337017?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Statistical+and+practical+considerations+for+clinical+evaluation+of+predictive+biomarkers.&rft.au=Polley%2C+Mei-Yin+C%3BFreidlin%2C+Boris%3BKorn%2C+Edward+L%3BConley%2C+Barbara+A%3BAbrams%2C+Jeffrey+S%3BMcShane%2C+Lisa+M&rft.aulast=Polley&rft.aufirst=Mei-Yin&rft.date=2013-11-20&rft.volume=105&rft.issue=22&rft.spage=1677&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjt282
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-10
N1  - Date created - 2013-11-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Control Clin Trials. 1993 Dec;14(6):511-22 [8119066]
J Clin Oncol. 2013 Sep 1;31(25):3158-61 [23569306]
N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010]
Oncologist. 2006 Jun;11(6):541-52 [16794234]
J Clin Oncol. 2007 Jan 1;25(1):118-45 [17159189]
J Natl Cancer Inst. 2007 Jul 4;99(13):1036-43 [17596577]
Clin Cancer Res. 2008 Oct 1;14(19):5977-83 [18829476]
Lancet. 2009 May 2;373(9674):1525-31 [19410716]
Lancet Oncol. 2009 May;10(5):459-66 [19269895]
N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680]
J Natl Cancer Inst. 2009 Nov 4;101(21):1446-52 [19815849]
J Natl Cancer Inst. 2009 Nov 4;101(21):1453-63 [19855077]
J Natl Cancer Inst. 2010 Feb 3;102(3):152-60 [20075367]
J Clin Oncol. 2010 Feb 20;28(6):918-27 [20100958]
Future Oncol. 2010 Sep;6(9):1407-14 [20919826]
J Proteome Res. 2011 Aug 5;10(8):3429-38 [21574648]
J Clin Oncol. 2011 Nov 1;29(31):4113-20 [21969500]
J Clin Oncol. 2011 Nov 1;29(31):4068-70 [21969515]
Lancet Oncol. 2012 Jan;13(1):33-42 [22056021]
Cancer Treat Rev. 2012 Oct;38(6):618-25 [22118887]
Lancet Oncol. 2012 Aug;13(8):827-37 [22759480]
Stat Med. 2013 Mar 15;32(6):1027-37 [23413213]
N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/jnci/djt282
ER  - 



TY  - JOUR
T1  - A primate-specific microRNA enters the lung cancer landscape.
AN  - 1461344477; 24191054
JF  - Proceedings of the National Academy of Sciences of the United States of America
AU  - Robles, Ana I
AU  - Harris, Curtis C
AD  - Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892.
Y1  - 2013/11/19/
PY  - 2013
DA  - 2013 Nov 19
SP  - 18748
EP  - 18749
VL  - 110
IS  - 47
KW  - Biomarkers, Tumor
KW  - 0
KW  - MicroRNAs
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Biomarkers, Tumor -- metabolism
KW  - Lung Neoplasms -- diagnosis
KW  - Carcinogenesis -- metabolism
KW  - MicroRNAs -- metabolism
KW  - Respiratory Mucosa -- cytology
KW  - Cell Differentiation -- physiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1461344477?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+primate-specific+microRNA+enters+the+lung+cancer+landscape.&rft.au=Robles%2C+Ana+I%3BHarris%2C+Curtis+C&rft.aulast=Robles&rft.aufirst=Ana&rft.date=2013-11-19&rft.volume=110&rft.issue=47&rft.spage=18748&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.1318740110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-22
N1  - Date created - 2013-11-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cell. 1993 Dec 3;75(5):855-62 [8252622]
Cell. 1993 Dec 3;75(5):843-54 [8252621]
Environ Health Perspect. 1993 Dec;101 Suppl 5:15-26 [7516873]
Lancet Oncol. 2011 Feb;12(2):175-80 [21277552]
Nat Cell Biol. 2011 Jun;13(6):693-9 [21602795]
Cell Cycle. 2011 Sep 1;10(17):2874-82 [21857159]
Hepatology. 2011 Dec;54(6):2137-48 [21809363]
Oncogene. 2012 Mar 29;31(13):1609-22 [21860412]
Oncogene. 2012 Aug 2;31(31):3607-20 [22105365]
Cell. 2012 Sep 14;150(6):1107-20 [22980975]
Cell. 2012 Sep 14;150(6):1121-34 [22980976]
Nat Commun. 2012;3:1145 [23093182]
Nature. 2013 Mar 7;495(7439):103-6 [23395958]
Cell Stem Cell. 2013 May 2;12(5):602-15 [23642368]
Nature. 2013 Aug 22;500(7463):415-21 [23945592]
Am J Respir Cell Mol Biol. 2013 Sep;49(3):384-95 [23590309]
Proc Natl Acad Sci U S A. 2013 Nov 19;110(47):18946-51 [24158479]
Oncogene. 2002 Oct 21;21(48):7298-306 [12379874]
Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020]
Comment On:
Proc Natl Acad Sci U S A. 2013 Nov 19;110(47):18946-51 [24158479]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1073/pnas.1318740110
ER  - 



TY  - JOUR
T1  - Strengths and limitations of microarray-based phenotype prediction: lessons learned from the IMPROVER Diagnostic Signature Challenge
AN  - 1492618197; 18891076
AB  - Motivation: After more than a decade since microarrays were used to predict phenotype of biological samples, real-life applications for disease screening and identification of patients who would best benefit from treatment are still emerging. The interest of the scientific community in identifying best approaches to develop such prediction models was reaffirmed in a competition style international collaboration called IMPROVER Diagnostic Signature Challenge whose results we describe herein.Results: Fifty-four teams used public data to develop prediction models in four disease areas including multiple sclerosis, lung cancer, psoriasis and chronic obstructive pulmonary disease, and made predictions on blinded new data that we generated. Teams were scored using three metrics that captured various aspects of the quality of predictions, and best performers were awarded. This article presents the challenge results and introduces to the community the approaches of the best overall three performers, as well as an R package that implements the approach of the best overall team.The analyses of model performance data submitted in the challenge as well as additional simulations that we have performed revealed that (i) the quality of predictions depends more on the disease endpoint than on the particular approaches used in the challenge; (ii) the most important modeling factor (e.g. data preprocessing, feature selection and classifier type) is problem dependent; and (iii) for optimal results datasets and methods have to be carefully matched. Biomedical factors such as the disease severity and confidence in diagnostic were found to be associated with the misclassification rates across the different teams.Availability: The lung cancer dataset is available from Gene Expression Omnibus (accession, GSE43580). The maPredictDSC R package implementing the approach of the best overall team is available at www.bioconductor.org or http://bioinformaticsprb.med.wayne.edu/.Contact: gustavo super(s).ibm.comSupplementary information: Supplementary data are available at Bioinformatics online.
JF  - Bioinformatics
AU  - Tarca, Adi L
AU  - Lauria, Mario
AU  - Unger, Michael
AU  - Bilal, Erhan
AU  - Boue, Stephanie
AU  - Kumar Dey, Kushal
AU  - Hoeng, Julia
AU  - Koeppl, Heinz
AU  - Martin, Florian
AU  - Meyer, Pablo
AU  - Nandy, Preetam
AU  - Norel, Raquel
AU  - Peitsch, Manuel
AU  - Rice, Jeremy J
AU  - Romero, Roberto
AU  - Stolovitzky, Gustavo
AU  - Talikka, Marja
AU  - Xiang, Yang
AU  - Zechner, Christoph
AD  - super(1)Department of Computer Science, Wayne State University, super(2)Perinatology Research Branch, NICHD/NIH, Detroit, MI 48201, USA, super(3)The Microsoft Research - University of Trento Centre for Computational and Systems Biology, Rovereto 38068, Italy, super(4)ETH Zurich, Zurich 8092, Switzerland, super(5)IBM Thomas J. Watson Research Center, Yorktown Heights, NY 10598, USA and super(6)Philip Morris International, Research & Development, Neuchatel CH-2000, Switzerland
Y1  - 2013/11/15/
PY  - 2013
DA  - 2013 Nov 15
SP  - 2892
EP  - 2899
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 22
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Gene expression
KW  - Data processing
KW  - Psoriasis
KW  - Multiple sclerosis
KW  - Bioinformatics
KW  - DNA microarrays
KW  - Competition
KW  - Internet
KW  - Models
KW  - Lung cancer
KW  - Chronic obstructive pulmonary disease
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492618197?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Strengths+and+limitations+of+microarray-based+phenotype+prediction%3A+lessons+learned+from+the+IMPROVER+Diagnostic+Signature+Challenge&rft.au=Tarca%2C+Adi+L%3BLauria%2C+Mario%3BUnger%2C+Michael%3BBilal%2C+Erhan%3BBoue%2C+Stephanie%3BKumar+Dey%2C+Kushal%3BHoeng%2C+Julia%3BKoeppl%2C+Heinz%3BMartin%2C+Florian%3BMeyer%2C+Pablo%3BNandy%2C+Preetam%3BNorel%2C+Raquel%3BPeitsch%2C+Manuel%3BRice%2C+Jeremy+J%3BRomero%2C+Roberto%3BStolovitzky%2C+Gustavo%3BTalikka%2C+Marja%3BXiang%2C+Yang%3BZechner%2C+Christoph&rft.aulast=Tarca&rft.aufirst=Adi&rft.date=2013-11-15&rft.volume=29&rft.issue=22&rft.spage=2892&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt492
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Gene expression; Data processing; Multiple sclerosis; Psoriasis; Bioinformatics; Competition; DNA microarrays; Internet; Chronic obstructive pulmonary disease; Lung cancer; Models
DO  - http://dx.doi.org/10.1093/bioinformatics/btt492
ER  - 



TY  - JOUR
T1  - A-clustering: a novel method for the detection of co-regulated methylation regions, and regions associated with exposure
AN  - 1492611337; 18891056
AB  - Motivation: DNA methylation is a heritable modifiable chemical process that affects gene transcription and is associated with other molecular markers (e.g. gene expression) and biomarkers (e.g. cancer or other diseases). Current technology measures methylation in hundred of thousands, or millions of CpG sites throughout the genome. It is evident that neighboring CpG sites are often highly correlated with each other, and current literature suggests that clusters of adjacent CpG sites are co-regulated.Results: We develop the Adjacent Site Clustering (A-clustering) algorithm to detect sets of neighboring CpG sites that are correlated with each other. To detect methylation regions associated with exposure, we propose an analysis pipeline for high-dimensional methylation data in which CpG sites within regions identified by A-clustering are modeled as multivariate responses to environmental exposure using a generalized estimating equation approach that assumes exposure equally affects all sites in the cluster. We develop a correlation preserving simulation scheme, and study the proposed methodology via simulations. We study the clusters detected by the algorithm on high dimensional dataset of peripheral blood methylation of pesticide applicators.
JF  - Bioinformatics
AU  - Sofer, Tamar
AU  - Schifano, Elizabeth D
AU  - Hoppin, Jane A
AU  - Hou, Lifang
AU  - Baccarelli, Andrea A
AD  - super(1)Department of Biostatistics, Harvard School of Public Health, 677 Huntington Avenue, SPH2, 4th floor, Boston, MA 02115, USA, super(2)Department of Statistics, University of Connecticut, 215 Glenbrook Road, Storrs, CT 06269, USA, super(3)NIEHS, Epidemiology Branch, MD A3-05, PO Box 12233, Research Triangle Park, NC 27709, USA, super(4)Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, 680 N Lake Shore Drive, Suite 1400 Chicago, IL 60611, USA, super(5)Department of Environmental Health and super(6)Department of Epidemiology, Harvard School of Public Health, 401 Park Drive, Landmark Ctr Room 415E, Boston, MA 02215, USA
Y1  - 2013/11/15/
PY  - 2013
DA  - 2013 Nov 15
SP  - 2884
EP  - 2891
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 22
SN  - 1367-4803, 1367-4803
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - Genomes
KW  - Mathematical models
KW  - Data processing
KW  - Algorithms
KW  - Transcription
KW  - Peripheral blood
KW  - CpG islands
KW  - biomarkers
KW  - Cancer
KW  - Gene expression
KW  - Pesticides
KW  - DNA methylation
KW  - Bioinformatics
KW  - Internet
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/1492611337?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A-clustering%3A+a+novel+method+for+the+detection+of+co-regulated+methylation+regions%2C+and+regions+associated+with+exposure&rft.au=Sofer%2C+Tamar%3BSchifano%2C+Elizabeth+D%3BHoppin%2C+Jane+A%3BHou%2C+Lifang%3BBaccarelli%2C+Andrea+A&rft.aulast=Sofer&rft.aufirst=Tamar&rft.date=2013-11-15&rft.volume=29&rft.issue=22&rft.spage=2884&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt498
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Genomes; Data processing; Mathematical models; Algorithms; Transcription; Peripheral blood; CpG islands; biomarkers; Cancer; Gene expression; Pesticides; DNA methylation; Bioinformatics; Internet
DO  - http://dx.doi.org/10.1093/bioinformatics/btt498
ER  - 



TY  - JOUR
T1  - Bendamustine and rituximab in relapsed and refractory hairy cell leukemia.
AN  - 1459564334; 24097860
AB  - To determine tolerability and for the first time explore efficacy of bendamustine-rituximab (BR) in multiply relapsed/refractory hairy cell leukemia (HCL), using two different dose levels of bendamustine. Patients with HCL with ≥2 prior therapies requiring treatment received rituximab 375 mg/m(2) days 1 and 15 plus bendamustine 70 (n = 6) or 90 (n = 6) mg/m(2), days 1 and 2, for six cycles at 4-week intervals.
          At 70 and 90 mg/m(2)/dose of bendamustine, overall response rate was 100%, with three (50%) and four (67%) complete remissions (CR) in each respective group. Minimal residual disease (MRD) was absent in 67% and 100% of CRs, respectively. All six without MRD remain in CR at 30 to 35 (median, 31) months of follow-up. Soluble CD22 and CD25 levels decreased with all responses, with median values decreasing from 17.7 and 42 ng/mL at baseline to undetectable and 2 ng/mL after CR, respectively (P < 0.001). Of 12 patients receiving 72 cycles of BR, the most common toxicities were hematologic, including thrombocytopenia (83%), lymphopenia (75%), leukopenia (58%), and neutropenia (42%). Grade III and IV hematologic toxicity included lymphopenia and thrombocytopenia (each 75%), leukopenia (58%), and neutropenia (25%). No significant dose-related differences were detected in response or toxicity.
          BR has significant activity in HCL. Bendamustine at either 70 or 90 mg/m(2)/dose was highly effective in multiply relapsed/refractory HCL and could be considered for achieving durable CRs without MRD in patients after failure of standard therapies. As it was not dose-limiting, 90 mg/m(2)/dose was chosen for future testing. ©2013 AACR.
JF  - Clinical cancer research : an official journal of the American Association for Cancer Research
AU  - Burotto, Mauricio
AU  - Stetler-Stevenson, Maryalice
AU  - Arons, Evgeny
AU  - Zhou, Hong
AU  - Wilson, Wyndham
AU  - Kreitman, Robert J
AD  - Authors' Affiliations: Laboratories of Molecular Biology and Pathology, and Metabolism Branch, National Cancer Institute, NIH, Bethesda, Maryland.
Y1  - 2013/11/15/
PY  - 2013
DA  - 2013 Nov 15
SP  - 6313
EP  - 6321
VL  - 19
IS  - 22
SN  - 1078-0432, 1078-0432
KW  - Antibodies, Monoclonal, Murine-Derived
KW  - 0
KW  - Antineoplastic Agents, Alkylating
KW  - Immunologic Factors
KW  - Nitrogen Mustard Compounds
KW  - Rituximab
KW  - 4F4X42SYQ6
KW  - Bendamustine Hydrochloride
KW  - 981Y8SX18M
KW  - Index Medicus
KW  - CD8-Positive T-Lymphocytes -- drug effects
KW  - Drug Administration Schedule
KW  - Blood Platelets -- drug effects
KW  - Humans
KW  - Aged
KW  - Pilot Projects
KW  - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW  - CD4-Positive T-Lymphocytes -- drug effects
KW  - Lymphocyte Count
KW  - Treatment Outcome
KW  - Middle Aged
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Female
KW  - Male
KW  - Remission Induction
KW  - Platelet Count
KW  - Antineoplastic Agents, Alkylating -- therapeutic use
KW  - Nitrogen Mustard Compounds -- therapeutic use
KW  - Antibodies, Monoclonal, Murine-Derived -- therapeutic use
KW  - Nitrogen Mustard Compounds -- adverse effects
KW  - Immunologic Factors -- therapeutic use
KW  - Leukemia, Hairy Cell -- drug therapy
KW  - Antineoplastic Agents, Alkylating -- adverse effects
KW  - Antibodies, Monoclonal, Murine-Derived -- adverse effects
KW  - Immunologic Factors -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1459564334?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bendamustine+and+rituximab+in+relapsed+and+refractory+hairy+cell+leukemia.&rft.au=Burotto%2C+Mauricio%3BStetler-Stevenson%2C+Maryalice%3BArons%2C+Evgeny%3BZhou%2C+Hong%3BWilson%2C+Wyndham%3BKreitman%2C+Robert+J&rft.aulast=Burotto&rft.aufirst=Mauricio&rft.date=2013-11-15&rft.volume=6&rft.issue=3&rft.spage=1271&rft.isbn=&rft.btitle=&rft.title=Nanoscale&rft.issn=2040-3372&rft_id=info:doi/10.1039%2Fc3nr05468c
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-21
N1  - Date created - 2013-11-18
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Leukemia. 1997 Jan;11(1):42-7 [9001417]
Blood. 1994 May 15;83(10):2906-11 [7910051]
Eur J Haematol. 2004 Dec;73(6):412-7 [15522063]
Blood. 2012 May 17;119(20):4608-13 [22451423]
J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053]
Ann Hematol. 2012 Oct;91(10):1579-86 [22752146]
J Clin Oncol. 2012 Sep 10;30(26):3209-16 [22869884]
Br J Haematol. 2012 Oct;159(1):67-77 [22861163]
J Clin Oncol. 2013 Jan 1;31(1):104-10 [23109692]
Br J Haematol. 2013 Feb;160(3):321-30 [23150919]
J Clin Oncol. 2013 Feb 1;31(4):456-60 [23248254]
J Cancer Res Clin Oncol. 2013 Mar;139(3):499-508 [23184429]
Leuk Res. 2013 Apr;37(4):401-9 [23347903]
J Clin Oncol. 2013 Jun 10;31(17):2103-9 [23650408]
J Clin Oncol. 2005 May 20;23(15):3383-9 [15908650]
Clin Cancer Res. 2006 May 1;12(9):2804-11 [16675574]
Blood. 2006 Jun 15;107(12):4658-62 [16497968]
Hematol Oncol Clin North Am. 2006 Oct;20(5):1051-63 [16990106]
Leuk Lymphoma. 2006 Nov;47(11):2301-7 [17107901]
Leuk Lymphoma. 2007 Dec;48(12):2441-3 [18067021]
Blood. 2008 Sep 15;112(6):2272-7 [18596230]
Leuk Lymphoma. 2008 Sep;49(9):1817-20 [18798112]
J Clin Oncol. 2009 Mar 20;27(9):1492-501 [19224851]
J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673]
Br J Haematol. 2009 Jun;145(6):733-40 [19344416]
Cancer. 2010 Jan 1;116(1):106-14 [19890959]
Blood. 2010 Mar 11;115(10):1893-6 [20056789]
Expert Rev Anticancer Ther. 2010 Sep;10(9):1353-65 [20836669]
Cancer Sci. 2010 Sep;101(9):2059-64 [20626754]
Clin Lymphoma Myeloma Leuk. 2010 Dec;10(6):452-7 [21189660]
J Clin Oncol. 2011 Feb 10;29(5):583-90 [21220590]
Blood. 2011 Mar 10;117(10):2807-12 [21239695]
Br J Haematol. 2011 May;153(3):351-7 [21371003]
Semin Hematol. 2011 Apr;48 Suppl 1:S24-36 [21530769]
Leuk Lymphoma. 2011 Jun;52(6):1153-6 [21463128]
Ann Oncol. 2011 Aug;22(8):1839-44 [21257672]
J Clin Oncol. 2011 Sep 10;29(26):3559-66 [21844497]
Blood. 2011 Oct 6;118(14):3818-23 [21821712]
Blood. 2012 Apr 5;119(14):3330-2 [22210875]
Clin Lymphoma Myeloma Leuk. 2012 Jun;12(3):197-200 [22578814]
J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422]
Haematologica. 2001 May;86(5):485-93 [11410411]
Haematologica. 2002 Jan;87(1):33-43 [11801463]
Am J Clin Pathol. 2003 Feb;119(2):213-7 [12579991]
Blood. 2003 Aug 1;102(3):810-3 [12663446]
Blood. 1988 May;71(5):1304-9 [3129046]
Clin Cancer Res. 1999 Jul;5(7):1665-70 [10430066]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/1078-0432.CCR-13-1848
ER  - 



TY  - JOUR
T1  - Prevalence of and risk factors for oral human papillomavirus among young women in Costa Rica.
AN  - 1444860286; 24014882
AB  - Little is known about the epidemiology of oral human papillomavirus (HPV) in Latin America.
          Women (N = 5838) aged 22-29 in the control and vaccine arms of an HPV-16/18 vaccine trial in Costa Rica had oral, cervical, and anal specimens collected. Samples were tested for alpha mucosal HPV types (SPF10/LiPA25 version 1); a subset of oral samples (n = 500) was tested for cutaneous HPV types in the genera alpha, beta, gamma, mu, and nu. In the control arm (n = 2926), 1.9% of women had an oral alpha mucosal HPV detected, 1.3% had carcinogenic HPV, and 0.4% had HPV-16; similar patterns for non-16/18 HPV types were observed in the vaccine arm. Independent risk factors for any oral alpha mucosal HPV among women in the control arm included marital status (adjusted odds ratio [AOR], 3.2; 95% confidence interval [CI], 1.8-5.7 for single compared to married/living as married), number of sexual partners (AOR, 2.4; 95% CI, 1.0-6.1 for ≥4 partners compared to 0-1 partners), chronic sinusitis (AOR, 3.1; 95% CI, 1.5-6.7), and cervical HPV infection (AOR, 2.6; 95% CI, 1.4-4.6). Detection of beta HPV was common (18.6%) and not associated with sexual activity. Unlike cutaneous HPV types, alpha mucosal HPV types were uncommon in the oral region and were predominately associated with sexual behavior. Clinical Trials Registration. NCT00128661.
JF  - The Journal of infectious diseases
AU  - Lang Kuhs, Krystle A
AU  - Gonzalez, Paula
AU  - Struijk, Linda
AU  - Castro, Felipe
AU  - Hildesheim, Allan
AU  - van Doorn, Leen-Jan
AU  - Rodriguez, Ana Cecilia
AU  - Schiffman, Mark
AU  - Quint, Wim
AU  - Lowy, Douglas R
AU  - Porras, Carolina
AU  - Delvecchio, Corey
AU  - Katki, Hormuzd A
AU  - Jimenez, Silvia
AU  - Safaeian, Mahboobeh
AU  - Schiller, John
AU  - Solomon, Diane
AU  - Wacholder, Sholom
AU  - Herrero, Rolando
AU  - Kreimer, Aimée R
AU  - Costa Rica Vaccine Trial Group
AD  - National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Costa Rica Vaccine Trial Group
Y1  - 2013/11/15/
PY  - 2013
DA  - 2013 Nov 15
SP  - 1643
EP  - 1652
VL  - 208
IS  - 10
KW  - Papillomavirus Vaccines
KW  - 0
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - oropharynx cancer
KW  - Guanacaste
KW  - Costa Rica
KW  - HPV
KW  - human papillomavirus vaccine
KW  - oral HPV DNA
KW  - Human papillomavirus 18 -- genetics
KW  - Young Adult
KW  - Papillomavirus Vaccines -- immunology
KW  - Human papillomavirus 18 -- immunology
KW  - Risk Factors
KW  - Humans
KW  - Adult
KW  - Human papillomavirus 16 -- genetics
KW  - Costa Rica -- epidemiology
KW  - Human papillomavirus 16 -- immunology
KW  - Female
KW  - Prevalence
KW  - Papillomavirus Infections -- epidemiology
KW  - Papillomaviridae -- classification
KW  - Stomatitis -- epidemiology
KW  - Papillomaviridae -- genetics
KW  - Papillomavirus Infections -- prevention & control
KW  - Papillomaviridae -- immunology
KW  - Stomatitis -- prevention & control
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1444860286?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prevalence+of+and+risk+factors+for+oral+human+papillomavirus+among+young+women+in+Costa+Rica.&rft.au=Lang+Kuhs%2C+Krystle+A%3BGonzalez%2C+Paula%3BStruijk%2C+Linda%3BCastro%2C+Felipe%3BHildesheim%2C+Allan%3Bvan+Doorn%2C+Leen-Jan%3BRodriguez%2C+Ana+Cecilia%3BSchiffman%2C+Mark%3BQuint%2C+Wim%3BLowy%2C+Douglas+R%3BPorras%2C+Carolina%3BDelvecchio%2C+Corey%3BKatki%2C+Hormuzd+A%3BJimenez%2C+Silvia%3BSafaeian%2C+Mahboobeh%3BSchiller%2C+John%3BSolomon%2C+Diane%3BWacholder%2C+Sholom%3BHerrero%2C+Rolando%3BKreimer%2C+Aim%C3%A9e+R%3BCosta+Rica+Vaccine+Trial+Group&rft.aulast=Lang+Kuhs&rft.aufirst=Krystle&rft.date=2013-11-15&rft.volume=208&rft.issue=10&rft.spage=1643&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjit369
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-19
N1  - Date created - 2013-10-23
N1  - Date revised - 2017-01-14
N1  - Genetic sequence - NCT00128661; ClinicalTrials.gov
N1  - SuppNotes - Cited By:
J Virol. 2000 Dec;74(24):11636-41 [11090162]
Cancer Epidemiol Biomarkers Prev. 2001 Jun;10(6):687-96 [11401920]
J Clin Microbiol. 2003 Jun;41(6):2509-14 [12791874]
J Clin Pathol. 2004 May;57(5):449-55 [15113849]
Virology. 2004 Jun 20;324(1):17-27 [15183049]
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Jul;98(1):91-6 [15243477]
J Forensic Sci. 1992 Mar;37(2):387-95 [1500889]
Cancer Epidemiol Biomarkers Prev. 1998 Aug;7(8):719-24 [9718225]
Jpn J Clin Oncol. 2005 Jan;35(1):45-7 [15681605]
Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):467-75 [15734974]
J Med Virol. 2006 May;78(5):614-8 [16555270]
J Clin Microbiol. 2006 May;44(5):1792-800 [16672409]
Eur J Obstet Gynecol Reprod Biol. 2006 May 1;126(1):104-6 [16324781]
J Clin Microbiol. 2006 Sep;44(9):3292-8 [16954263]
J Gen Virol. 2007 May;88(Pt 5):1489-95 [17412978]
N Engl J Med. 2007 May 10;356(19):1944-56 [17494927]
Nat Med. 2007 Jul;13(7):857-61 [17603495]
Biomarkers. 2007 Sep-Oct;12(5):510-22 [17701749]
J Clin Oncol. 2008 Feb 1;26(4):612-9 [18235120]
Vaccine. 2008 Sep 2;26(37):4795-808 [18640170]
BMC Infect Dis. 2009;9:74 [19473489]
Oral Oncol. 2009 Sep;45(9):e85-9 [19457708]
Braz J Otorhinolaryngol. 2010 Jan-Feb;76(1):78-84 [20339693]
Virology. 2010 May 25;401(1):70-9 [20206957]
J Clin Microbiol. 2010 May;48(5):1706-11 [20237103]
Ann R Coll Surg Engl. 2010 Nov;92(8):655-9 [20615309]
Cancer Epidemiol Biomarkers Prev. 2011 Jan;20(1):172-82 [21148755]
Br J Cancer. 2011 Mar 1;104(5):886-91 [21285981]
Int J Cancer. 2011 Aug 1;129(3):733-41 [20878955]
PLoS One. 2011;6(7):e22529 [21799888]
Am J Rhinol Allergy. 2011 Jul-Aug;25(4):241-4 [21819760]
J Infect Dis. 2011 Sep 1;204(5):787-92 [21844305]
Acta Dermatovenerol Alp Pannonica Adriat. 2011 Sep;20(3):145-54 [22131115]
JAMA. 2012 Feb 15;307(7):693-703 [22282321]
Sex Transm Dis. 2012 Jul;39(7):559-66 [22706220]
Braz J Otorhinolaryngol. 2012 Jul-Aug;78(4):66-70 [22936139]
Vaccine. 2012 Nov 20;30 Suppl 5:F34-54 [23199965]
J Clin Virol. 2013 Jan;56(1):72-6 [23092620]
PLoS One. 2013;8(7):e68329 [23873171]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/infdis/jit369
ER  - 



TY  - JOUR
T1  - Nuclear Industry Meets National Cyber Security Challenges
AN  - 1567090241; 20459993
AB  - Protection and mitigation efforts for cyber security are an important measure within the nuclear industry. Post-911 efforts began in 2002 as the industry implemented a program to protect critical digital assets and information from malicious use or cyber sabotage. The need to incorporate cyber security into the physical protection of the plant was also identified. In 2009, the Nuclear Regulatory Commission (NRC) established extensive regulations for commercial nuclear reactors for cyber security. In February 2013 President Obama signed an Executive Order to improve critical infrastructure cyber security, increase information sharing, and raise standards [1]. The Executive Order directs the Department of Homeland Security (DHS) to identify critical infrastructure. To that end, the industry and regulators have been working together to share information between these two entities. This paper presents some of the areas where industry and regulatory groups are working to provide protection to the industry and ensure the industry is prepared for the ever-changing face of cyber security. In addition, it brings to light the need for continuous training for those within the industry in the area of cyber security.
JF  - Transactions of the American Nuclear Society
AU  - LeClair, Jane
AU  - Abraham, Sherly
AU  - Skinner, Adrian
AD  - National Cybersecurity Institute, Excelsior College, 2000 M Street, Washington, DC; Excelsior College, 7 Columbia Circle, Albany, NY, 12203 jleclair@nci.edu
Y1  - 2013/11/14/
PY  - 2013
DA  - 2013 Nov 14
SP  - 225
PB  - American Nuclear Society, Inc.
VL  - 109
SN  - 0003-018X, 0003-018X
KW  - Mechanical & Transportation Engineering Abstracts (MT); Environmental Engineering Abstracts (EN); Electronics and Communications Abstracts (EA); Computer and Information Systems Abstracts (CI); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - Infrastructure
KW  - Regulatory agencies
KW  - Regulators
KW  - Computer information security
KW  - Standards
KW  - Regulations
KW  - Homeland security
KW  - Digital
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1567090241?accountid=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=Nuclear+Industry+Meets+National+Cyber+Security+Challenges&rft.au=LeClair%2C+Jane%3BAbraham%2C+Sherly%3BSkinner%2C+Adrian&rft.aulast=LeClair&rft.aufirst=Jane&rft.date=2013-11-14&rft.volume=109&rft.issue=&rft.spage=225&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 - 2014-10-01
N1  - Last updated - 2014-11-05
ER  - 



TY  - JOUR
T1  - Discovery of an in vivo chemical probe of the lysine methyltransferases G9a and GLP.
AN  - 1490716516; 24102134
AB  - Among epigenetic "writers", "readers", and "erasers", the lysine methyltransferases G9a and GLP, which catalyze mono- and dimethylation of histone H3 lysine 9 (H3K9me2) and nonhistone proteins, have been implicated in a variety of human diseases. A "toolkit" of well-characterized chemical probes will allow biological and disease hypotheses concerning these proteins to be tested in cell-based and animal models with high confidence. We previously discovered potent and selective G9a/GLP inhibitors including the cellular chemical probe UNC0638, which displays an excellent separation of functional potency and cell toxicity. However, this inhibitor is not suitable for animal studies due to its poor pharmacokinetic (PK) properties. Here, we report the discovery of the first G9a and GLP in vivo chemical probe UNC0642, which not only maintains high in vitro and cellular potency, low cell toxicity, and excellent selectivity, but also displays improved in vivo PK properties, making it suitable for animal studies.
JF  - Journal of medicinal chemistry
AU  - Liu, Feng
AU  - Barsyte-Lovejoy, Dalia
AU  - Li, Fengling
AU  - Xiong, Yan
AU  - Korboukh, Victoria
AU  - Huang, Xi-Ping
AU  - Allali-Hassani, Abdellah
AU  - Janzen, William P
AU  - Roth, Bryan L
AU  - Frye, Stephen V
AU  - Arrowsmith, Cheryl H
AU  - Brown, Peter J
AU  - Vedadi, Masoud
AU  - Jin, Jian
AD  - Center for Integrative Chemical Biology and Drug Discovery, Division of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, ‡National Institute of Mental Health Psychoactive Drug Screening Program, §Department of Pharmacology, School of Medicine, and ∥Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill , Chapel Hill, North Carolina 27599, United States.
Y1  - 2013/11/14/
PY  - 2013
DA  - 2013 Nov 14
SP  - 8931
EP  - 8942
VL  - 56
IS  - 21
KW  - Antineoplastic Agents
KW  - 0
KW  - Enzyme Inhibitors
KW  - Histocompatibility Antigens
KW  - EHMT1 protein, human
KW  - EC 2.1.1.-
KW  - EHMT2 protein, human
KW  - EC 2.1.1.43
KW  - Histone-Lysine N-Methyltransferase
KW  - Index Medicus
KW  - Molecular Structure
KW  - Cell Proliferation -- drug effects
KW  - Drug Screening Assays, Antitumor
KW  - Animals
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Histocompatibility Antigens -- metabolism
KW  - Mice
KW  - Cell Line, Tumor
KW  - Male
KW  - Structure-Activity Relationship
KW  - Histone-Lysine N-Methyltransferase -- antagonists & inhibitors
KW  - Drug Discovery
KW  - Enzyme Inhibitors -- chemistry
KW  - Enzyme Inhibitors -- pharmacology
KW  - Antineoplastic Agents -- chemical synthesis
KW  - Enzyme Inhibitors -- chemical synthesis
KW  - Antineoplastic Agents -- chemistry
KW  - Histone-Lysine N-Methyltransferase -- metabolism
KW  - Antineoplastic Agents -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490716516?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Discovery+of+an+in+vivo+chemical+probe+of+the+lysine+methyltransferases+G9a+and+GLP.&rft.au=Liu%2C+Feng%3BBarsyte-Lovejoy%2C+Dalia%3BLi%2C+Fengling%3BXiong%2C+Yan%3BKorboukh%2C+Victoria%3BHuang%2C+Xi-Ping%3BAllali-Hassani%2C+Abdellah%3BJanzen%2C+William+P%3BRoth%2C+Bryan+L%3BFrye%2C+Stephen+V%3BArrowsmith%2C+Cheryl+H%3BBrown%2C+Peter+J%3BVedadi%2C+Masoud%3BJin%2C+Jian&rft.aulast=Liu&rft.aufirst=Feng&rft.date=2013-11-14&rft.volume=56&rft.issue=21&rft.spage=8931&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Fjm401480r
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-18
N1  - Date created - 2014-01-03
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nat Commun. 2012;3:1288 [23250418]
Nature. 2012 Dec 6;492(7427):108-12 [23051747]
Org Lett. 2013 Jan 18;15(2):414-7 [23272941]
Proc Natl Acad Sci U S A. 2013 May 7;110(19):7922-7 [23620515]
Nat Chem Biol. 2013 Apr;9(4):195-9 [23508172]
J Med Chem. 2013 Mar 14;56(5):2110-24 [23445220]
Mol Cell. 2013 May 9;50(3):444-56 [23583077]
Cancer Cell. 2013 May 13;23(5):677-92 [23680150]
ACS Chem Biol. 2013;8(6):1324-34 [23614352]
Genes Dev. 2002 Jul 15;16(14):1779-91 [12130538]
Genes Dev. 2005 Apr 1;19(7):815-26 [15774718]
J Med Chem. 2005 Jul 14;48(14):4511-25 [15999990]
Nat Rev Mol Cell Biol. 2005 Nov;6(11):838-49 [16261189]
Am J Hum Genet. 2006 Aug;79(2):370-7 [16826528]
Nature. 2006 Nov 30;444(7119):629-32 [17108971]
Mol Cell. 2007 Feb 9;25(3):473-81 [17289593]
Cell. 2007 Feb 23;128(4):669-81 [17320505]
Cell. 2007 Feb 23;128(4):693-705 [17320507]
PLoS One. 2008;3(4):e2037 [18446223]
Nat Chem Biol. 2008 Jun;4(6):344-6 [18438403]
Cell Stem Cell. 2008 Jun 5;2(6):525-8 [18522845]
EMBO J. 2008 Oct 22;27(20):2691-701 [18818693]
EMBO J. 2008 Oct 22;27(20):2681-90 [18818694]
Cell Stem Cell. 2008 Nov 6;3(5):568-74 [18983970]
Nat Struct Mol Biol. 2009 Mar;16(3):312-7 [19219047]
Mol Cancer Res. 2009 Jun;7(6):851-62 [19531572]
Nat Rev Drug Discov. 2009 Sep;8(9):724-32 [19721445]
J Med Genet. 2009 Sep;46(9):598-606 [19264732]
Neuron. 2009 Dec 10;64(5):678-91 [20005824]
J Med Chem. 2009 Dec 24;52(24):7950-3 [19891491]
Science. 2010 Jan 8;327(5962):213-6 [20056891]
Leukemia. 2010 Jan;24(1):81-8 [19776757]
PLoS One. 2010;5(1):e8570 [20084102]
J Biol Chem. 2010 Mar 26;285(13):9636-41 [20118233]
J Biol Chem. 2010 May 28;285(22):16538-45 [20335163]
J Mol Biol. 2010 Jul 2;400(1):1-7 [20434463]
Chem Biol. 2010 Jun 25;17(6):561-77 [20609406]
Chem Biol. 2010 Jul 30;17(7):695-704 [20659682]
J Med Chem. 2010 Aug 12;53(15):5844-57 [20614940]
J Chem Inf Model. 2011 Mar 28;51(3):612-23 [21366357]
Cancer Cell. 2011 Jul 12;20(1):53-65 [21741596]
Nat Chem Biol. 2011 Aug;7(8):566-74 [21743462]
Nat Chem Biol. 2011 Aug;7(8):499-500 [21769094]
Neuron. 2011 Aug 25;71(4):656-70 [21867882]
J Med Chem. 2011 Sep 8;54(17):6139-50 [21780790]
Structure. 2011 Sep 7;19(9):1262-73 [21782458]
J Am Chem Soc. 2011 Oct 26;133(42):16746-9 [21936531]
J Am Chem Soc. 2012 Apr 4;134(13):5909-15 [22404544]
Nat Rev Drug Discov. 2012 May;11(5):384-400 [22498752]
ACS Chem Biol. 2012 Jul 20;7(7):1152-7 [22536950]
Structure. 2012 Aug 8;20(8):1425-35 [22795084]
J Med Chem. 2012 Sep 27;55(18):8066-74 [22924785]
Nat Chem Biol. 2012 Nov;8(11):890-6 [23023262]
J Am Chem Soc. 2012 Oct 31;134(43):18004-14 [23043551]
Genes Dev. 2012 Nov 15;26(22):2499-511 [23105005]
Proc Natl Acad Sci U S A. 2012 Dec 26;109(52):21360-5 [23236167]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1021/jm401480r
ER  - 



TY  - CPAPER
T1  - Something fishy: Fish advisory considerations for public health nurses
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433512962; 6233471
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Backus, Ann
AU  - Hewitt, Jeanne
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Nursing
KW  - Fish
KW  - Medical personnel
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433512962?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Something+fishy%3A+Fish+advisory+considerations+for+public+health+nurses&rft.au=Backus%2C+Ann%3BHewitt%2C+Jeanne&rft.aulast=Backus&rft.aufirst=Ann&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - NCI quitpal: An evidence-based app to help people quit smoking
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433512803; 6234399
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Massett, Holly
AU  - Atkinson, Nancy
AU  - Kraiger, Amanda
AU  - Grady, Meredith
AU  - Killam, Bill
AU  - Barry, Barbara
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Smoking
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433512803?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=NCI+quitpal%3A+An+evidence-based+app+to+help+people+quit+smoking&rft.au=Massett%2C+Holly%3BAtkinson%2C+Nancy%3BKraiger%2C+Amanda%3BGrady%2C+Meredith%3BKillam%2C+Bill%3BBarry%2C+Barbara&rft.aulast=Massett&rft.aufirst=Holly&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Preparing public health nurses for population-focused practice
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433511380; 6234261
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Hewitt, Jeanne
AU  - Pasha James, Deborah
AU  - Backus, Ann
AU  - Delgado, Luis
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Nursing
KW  - Medical personnel
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433511380?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Preparing+public+health+nurses+for+population-focused+practice&rft.au=Hewitt%2C+Jeanne%3BPasha+James%2C+Deborah%3BBackus%2C+Ann%3BDelgado%2C+Luis&rft.aulast=Hewitt&rft.aufirst=Jeanne&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Prevalence of secondary task engagement and distraction among novice teen drivers
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433511210; 6233344
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Ehsani, Johnathon
AU  - Perlus, Jessamyn
AU  - Russell, Ashley
AU  - Li, Kaigang
AU  - Simons-Morton, Bruce
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433511210?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Prevalence+of+secondary+task+engagement+and+distraction+among+novice+teen+drivers&rft.au=Ehsani%2C+Johnathon%3BPerlus%2C+Jessamyn%3BRussell%2C+Ashley%3BLi%2C+Kaigang%3BSimons-Morton%2C+Bruce&rft.aulast=Ehsani&rft.aufirst=Johnathon&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Translating the message: Ensuring quality spanish-language oral health information
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433511171; 6232642
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Gonzalez-Flores, Matilde
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433511171?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Translating+the+message%3A+Ensuring+quality+spanish-language+oral+health+information&rft.au=Gonzalez-Flores%2C+Matilde&rft.aulast=Gonzalez-Flores&rft.aufirst=Matilde&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Conducting ethical post-event medical countermeasure trials with children
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433511135; 6232790
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Grady, Christine
AU  - Michael, Nelson
AU  - Lee, Lisa
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Ethics
KW  - Children
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433511135?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Conducting+ethical+post-event+medical+countermeasure+trials+with+children&rft.au=Grady%2C+Christine%3BMichael%2C+Nelson%3BLee%2C+Lisa&rft.aulast=Grady&rft.aufirst=Christine&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Research to reality: A mentorship approach to building cancer control capacity
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433510819; 6232550
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Sanchez, Michael
AU  - Purcell, Peyton
AU  - Vinson, Cynthia
AU  - LaPorta, Madeline
AU  - Gallagher, Alissa
AU  - Farrell, Margaret
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433510819?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Research+to+reality%3A+A+mentorship+approach+to+building+cancer+control+capacity&rft.au=Sanchez%2C+Michael%3BPurcell%2C+Peyton%3BVinson%2C+Cynthia%3BLaPorta%2C+Madeline%3BGallagher%2C+Alissa%3BFarrell%2C+Margaret&rft.aulast=Sanchez&rft.aufirst=Michael&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Development of performance measures for wide-ranging clinical research programs in diverse global settings
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433510800; 6231963
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Weiss, Susanna
AU  - McNay, Laura
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Clinical trials
KW  - Research programs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433510800?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Development+of+performance+measures+for+wide-ranging+clinical+research+programs+in+diverse+global+settings&rft.au=Weiss%2C+Susanna%3BMcNay%2C+Laura&rft.aulast=Weiss&rft.aufirst=Susanna&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Communicating risk to environmental justice communities: Promoting a culturally-fluent, bi-directional conversation enhancing expertise with local knowledge
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433510628; 6231635
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Sullivan, John
AU  - Subra, Wilma
AU  - Croisant, Sharon
AU  - Prochaska, John
AU  - Nolen, Alexandra
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Environmental equity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433510628?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Communicating+risk+to+environmental+justice+communities%3A+Promoting+a+culturally-fluent%2C+bi-directional+conversation+enhancing+expertise+with+local+knowledge&rft.au=Sullivan%2C+John%3BSubra%2C+Wilma%3BCroisant%2C+Sharon%3BProchaska%2C+John%3BNolen%2C+Alexandra&rft.aulast=Sullivan&rft.aufirst=John&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Sustainability, climate resilience, and health: Case studies from the department of health and human services
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433510318; 6234605
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Balbus, John
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Resource management
KW  - Case studies
KW  - Climate
KW  - Sustainability
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433510318?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Sustainability%2C+climate+resilience%2C+and+health%3A+Case+studies+from+the+department+of+health+and+human+services&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Framingham heart study's influence on public health policy
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433510250; 6231943
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Levy, Daniel
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Heart
KW  - Policies
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433510250?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Framingham+heart+study%27s+influence+on+public+health+policy&rft.au=Levy%2C+Daniel&rft.aulast=Levy&rft.aufirst=Daniel&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - How well do intersectoral interventions work to improve health: The research agenda
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433509897; 6234598
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Kaplan, Robert
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Intervention
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433509897?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=How+well+do+intersectoral+interventions+work+to+improve+health%3A+The+research+agenda&rft.au=Kaplan%2C+Robert&rft.aulast=Kaplan&rft.aufirst=Robert&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Impact of dizziness and balance problems and other chronic health conditions on falling risk in United States adults
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433509550; 6232226
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Hoffman, Howard
AU  - Li, Chuan-Ming
AU  - Losonczy, Katalin
AU  - Sklare, Daniel
AU  - Cohen, Helen
AU  - Della Santina, Charley
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - USA
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433509550?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Impact+of+dizziness+and+balance+problems+and+other+chronic+health+conditions+on+falling+risk+in+United+States+adults&rft.au=Hoffman%2C+Howard%3BLi%2C+Chuan-Ming%3BLosonczy%2C+Katalin%3BSklare%2C+Daniel%3BCohen%2C+Helen%3BDella+Santina%2C+Charley&rft.aulast=Hoffman&rft.aufirst=Howard&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - From science to policy: The experimental study used to evaluate proposed corrective statements in US vs. Philip Morris USA, Inc.
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433509545; 6232456
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Blake, Kelly
AU  - Bloch, Michele
AU  - Augustson, Erik
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Policies
KW  - USA
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433509545?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=From+science+to+policy%3A+The+experimental+study+used+to+evaluate+proposed+corrective+statements+in+US+vs.+Philip+Morris+USA%2C+Inc.&rft.au=Blake%2C+Kelly%3BBloch%2C+Michele%3BAugustson%2C+Erik&rft.aulast=Blake&rft.aufirst=Kelly&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Measuring use of health services among working age adults with disabilities with the ACS-6: What constitutes elevated service need and use?
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433509489; 6232215
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Gulley, Stephen
AU  - Rasch, Elizabeth
AU  - Altman, Barbara
AU  - Chan, Leighton
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Age
KW  - Disabilities
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433509489?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Measuring+use+of+health+services+among+working+age+adults+with+disabilities+with+the+ACS-6%3A+What+constitutes+elevated+service+need+and+use%3F&rft.au=Gulley%2C+Stephen%3BRasch%2C+Elizabeth%3BAltman%2C+Barbara%3BChan%2C+Leighton&rft.aulast=Gulley&rft.aufirst=Stephen&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Global environmental health: Using niehs science to help address the major environmental causes of death and disease around the world
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433509041; 6234903
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Balbus, John
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Mortality
KW  - Environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433509041?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Global+environmental+health%3A+Using+niehs+science+to+help+address+the+major+environmental+causes+of+death+and+disease+around+the+world&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - CPAPER
T1  - Harvard worldmap: A tool for visualizing and sharing hydrofracking data
T2  - 141st American Public Health Association Annual Meeting and Exposition
AN  - 1433508498; 6231931
JF  - 141st American Public Health Association Annual Meeting and Exposition
AU  - Backus, Ann
Y1  - 2013/11/02/
PY  - 2013
DA  - 2013 Nov 02
KW  - Data processing
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433508498?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.atitle=Harvard+worldmap%3A+A+tool+for+visualizing+and+sharing+hydrofracking+data&rft.au=Backus%2C+Ann&rft.aulast=Backus&rft.aufirst=Ann&rft.date=2013-11-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=141st+American+Public+Health+Association+Annual+Meeting+and+Exposition&rft.issn=&rft_id=info:doi/
L2  - https://apha.confex.com/apha/141am/webprogram/meeting.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-31
N1  - Last updated - 2013-09-19
ER  - 



TY  - JOUR
T1  - Patientsʼ and family membersʼ views on patient-centered communication during cancer care
AN  - 1665158252
AB  - Objectives To explore patientsʼ and family membersʼ views on communication during cancer care and to identify those aspects of clinician–patient communication which were most important to patients and family members. Methods We conducted a secondary data analysis of qualitative data from 137 patients with cancer and family members of patients with cancer. We used a modified version of the constant comparative method and coding paradigm of grounded theory. Results Patients want sensitive, caring clinicians who provide information that they need, when they need it, in a way that they can understand; who listen and respond to questions and concerns, and who attempt to understand the patientʼs experience. Effective information exchange and a positive interpersonal relationship with the clinician were of fundamental importance to patients and family members. These were interrelated; for instance, failure to provide information a patient needed could damage the relationship, whereas excellent listening could foster the relationship. Information exchange and relationship were also integral to decision-making, managing uncertainty, responding to emotions, and self-management. Clinicians who were responsive to patientsʼ needs beyond the immediate medical encounter were valued. Conclusions The complexity of cancer care today suggests that efforts to improve communication must be multilevel, acknowledging and addressing patient, clinician, organizational and policy barriers, and facilitators. Measurement tools are needed to assess cancer patientsʼ and family membersʼ experiences with communication over the course of cancer care to provide meaningful, actionable feedback to those seeking to optimize their effectiveness in communicating with patients with cancer. Copyright © 2013 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Mazor, Kathleen M
AU  - Beard, Reneé L
AU  - Alexander, Gwen L
AU  - Arora, Neeraj K
AU  - Firneno, Cassandra
AU  - Gaglio, Bridget
AU  - Greene, Sarah M
AU  - Lemay, Celeste A
AU  - Robinson, Brandi E
AU  - Roblin, Douglas W
AU  - Walsh, Kathleen
AU  - Street, Richard L
AU  - Gallagher, Thomas H
AD  - Meyers Primary Care Institute, University of Massachusetts Medical School, Reliant Medical Group, Fallon Community Health Plan, Worcester, MA, USA. ; Department of Sociology and Anthropology, College of the Holy Cross, Worcester, MA, USA. ; Henry Ford Health System, Department of Public Health Sciences, Detroit, MI, USA. ; National Cancer Institute, Division of Cancer Control and Population Sciences, Rockville, MD, USA. ; Mid-Atlantic Permanente, Research Institute, Kaiser Permanente Mid-Atlantic States, Rockville, MD, USA. ; Group Health Cooperative, Seattle, WA, USA. ; Kaiser Permanente Georgia, Center for Health Research, Atlanta, GA, USA. ; University of Massachusetts Medical School, Department of Pediatrics and Meyers Primary Care Institute, Worcester, MA, USA. ; Department of Communication, Texas A&M University, College Station, TX, USA. ; Meyers Primary Care Institute, University of Massachusetts Medical School, Reliant Medical Group, Fallon Community Health Plan, Worcester, MA, USA., Medicine, Bioethics & Humanities, University of Washington, Seattle, WA, USA. ; Meyers Primary Care Institute, University of Massachusetts Medical School, Reliant Medical Group, Fallon Community Health Plan, Worcester, MA, USA.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 2487
EP  - 2495
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 11
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Attitudes
KW  - Relatives
KW  - Selfmanagement
KW  - Uncertainty
KW  - Cancer
KW  - Caring
KW  - Coding
KW  - Communication
KW  - Decision making
KW  - Emotions
KW  - Facilitators
KW  - Feedback
KW  - Grounded theory
KW  - Information sharing
KW  - Listening
KW  - Measurement
KW  - Patient care
KW  - Patient centredness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665158252?accountid=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=Patients%CA%BC+and+family+members%CA%BC+views+on+patient-centered+communication+during+cancer+care&rft.au=Mazor%2C+Kathleen+M%3BBeard%2C+Rene%C3%A9+L%3BAlexander%2C+Gwen+L%3BArora%2C+Neeraj+K%3BFirneno%2C+Cassandra%3BGaglio%2C+Bridget%3BGreene%2C+Sarah+M%3BLemay%2C+Celeste+A%3BRobinson%2C+Brandi+E%3BRoblin%2C+Douglas+W%3BWalsh%2C+Kathleen%3BStreet%2C+Richard+L%3BGallagher%2C+Thomas+H&rft.aulast=Mazor&rft.aufirst=Kathleen&rft.date=2013-11-01&rft.volume=22&rft.issue=11&rft.spage=2487&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3317
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.3317
ER  - 



TY  - JOUR
T1  - Review Article: Malaria Diagnostics in Clinical Trials
AN  - 1647022945; 21172272
AB  - Malaria diagnostics are widely used in epidemiologic studies to investigate natural history of disease and in drug and vaccine clinical trials to exclude participants or evaluate efficacy. The Malaria Laboratory Network (MLN), managed by the Office of HIV/AIDS Network Coordination, is an international working group with mutual interests in malaria disease and diagnosis and in human immunodeficiency virus/acquired immunodeficiency syndrome clinical trials. The MLN considered and studied the wide array of available malaria diagnostic tests for their suitability for screening trial participants and/or obtaining study endpoints for malaria clinical trials, including studies of HIV/malaria co-infection and other malaria natural history studies. The MLN provides recommendations on microscopy, rapid diagnostic tests, serologic tests, and molecular assays to guide selection of the most appropriate test(s) for specific research objectives. In addition, this report provides recommendations regarding quality management to ensure reproducibility across sites in clinical trials. Performance evaluation, quality control, and external quality assessment are critical processes that must be implemented in all clinical trials using malaria tests.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Murphy, Sean C
AU  - Shott, Joseph P
AU  - Parikh, Sunil
AU  - Etter, Paige
AU  - Prescott, William R
AU  - Stewart, V Ann
AD  - Division of Intramural Research, National Institute of Allergy and Infectious Diseases,National Institutes of Health, Bethesda, Maryland; Yale University School of Public Health, New Haven, Connecticut; Office of HIV/AIDS Network Coordination, Fred Hutchinson Cancer Research Center, Seattle, Washington; Hydas World Health, Hershey, Pennsylvania; Uniformed Services University of the Health Sciences, Bethesda, Maryland; Department of Laboratory Medicine, University of Washington Medical Center, Seattle, WA 98195, murphysc@uw.edu
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 824
EP  - 839
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
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  - Screening
KW  - Symptoms
KW  - Acquired immune deficiency syndrome
KW  - Human diseases
KW  - Disease control
KW  - Malaria
KW  - Clinical trials
KW  - Public health
KW  - Human immunodeficiency virus
KW  - Quality control
KW  - Reviews
KW  - Microscopy
KW  - Vaccines
KW  - Hygiene
KW  - Drugs
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - J 02400:Human Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022945?accountid=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=Review+Article%3A+Malaria+Diagnostics+in+Clinical+Trials&rft.au=Murphy%2C+Sean+C%3BShott%2C+Joseph+P%3BParikh%2C+Sunil%3BEtter%2C+Paige%3BPrescott%2C+William+R%3BStewart%2C+V+Ann&rft.aulast=Murphy&rft.aufirst=Sean&rft.date=2013-11-01&rft.volume=89&rft.issue=5&rft.spage=824&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0675
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Screening; Symptoms; Human diseases; Disease control; Malaria; Vaccines; Hygiene; Drugs; Public health; Acquired immune deficiency syndrome; Reviews; Quality control; Microscopy; Clinical trials; Human immunodeficiency virus
DO  - http://dx.doi.org/10.4269/ajtmh.12-0675
ER  - 



TY  - JOUR
T1  - Personality Traits and Chronic Disease: Implications for Adult Personality Development
AN  - 1627731482
AB  - Objective. Personality traits have been associated with chronic disease. Less is known about the longitudinal relation between personality and disease and whether chronic disease is associated with changes in personality. Method. Participants from the Baltimore Longitudinal Study of Aging (N = 2,008) completed the Revised NEO Personality Inventory and a standard medical interview at regularly scheduled visits; the Charlson Comorbidity Index, a weighted sum of 19 serious diseases, was derived from this interview. Using data from 6,685 visits, we tested whether personality increased risk of disease and whether disease was associated with personality change. Results. Measured concurrently, neuroticism and conscientiousness were associated with greater disease burden. The impulsiveness facet of neuroticism was the strongest predictor of developing disease across the follow-up period: For every standard deviation increase in impulsiveness, there was a 26% increased risk of developing disease and a 36% increased risk of getting more ill. Personality traits changed only modestly with disease: As participants developed chronic illnesses, they became more conservative (decreased openness). Discussion. This research indicates that personality traits confer risk for disease, in part, through health-risk behaviors. These traits, however, were relatively resistant to the effect of serious disease.
JF  - The Journals of Gerontology.  Series B, Psychological Sciences and Social Sciences
AU  - Sutin, Angelina R
AU  - Zonderman, Alan B
AU  - Ferrucci, Luigi
AU  - Terracciano, Antonio
AD  - Department of Medical Humanities and Social Sciences, Florida State University College of Medicine, Tallahassee, Florida and National Institute on Aging, National Institutes of Health, Baltimore, Maryland ; Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, Maryland ; Clinical Research Branch, National Institute on Aging, National Institutes of Health,Baltimore, Maryland ; Department of Geriatrics, Florida State University College of Medicine, Tallahassee, Florida and National Institute on Aging, National Institutes of Health, Baltimore Maryland ; Department of Medical Humanities and Social Sciences, Florida State University College of Medicine, Tallahassee, Florida and National Institute on Aging, National Institutes of Health, Baltimore, Maryland
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 912
EP  - 920
CY  - Washington
PB  - Oxford University Press, UK
VL  - 68
IS  - 6
SN  - 1079-5014
KW  - Gerontology And Geriatrics
KW  - Disease burden
KW  - Illness
KW  - Openness
KW  - Personality change
KW  - Personality
KW  - Comorbidity
KW  - Conscientiousness
KW  - Deviation
KW  - Health behaviour
KW  - Health risks
KW  - Neo Personality Inventory
KW  - Personality development
KW  - Personality tests
KW  - Risk behaviour
KW  - Chronic diseases
KW  - Chronic sickness
KW  - Burden
KW  - Neuroticism
KW  - Ageing
KW  - Impulsivity
KW  - Baltimore Maryland
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627731482?accountid=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+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.atitle=Personality+Traits+and+Chronic+Disease%3A+Implications+for+Adult+Personality+Development&rft.au=Sutin%2C+Angelina+R%3BZonderman%2C+Alan+B%3BFerrucci%2C+Luigi%3BTerracciano%2C+Antonio&rft.aulast=Sutin&rft.aufirst=Angelina&rft.date=2013-11-01&rft.volume=68&rft.issue=6&rft.spage=912&rft.isbn=&rft.btitle=&rft.title=The+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.issn=10795014&rft_id=info:doi/10.1093%2Fgeronb%2Fgbt036
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-10-14
N1  - Last updated - 2016-05-16
N1  - SubjectsTermNotLitGenreText - Baltimore Maryland
DO  - http://dx.doi.org/10.1093/geronb/gbt036
ER  - 



TY  - JOUR
T1  - Magnesium sulfate potentiates effect of DigiFab on marinobufagenin-induced Na/K-ATPase inhibition.
AN  - 1612984905; 23878005
AB  - Immunoneutralization of elevated circulating levels of endogenous digitalis-like Na/K-ATPase inhibitors (i.e. cardiotonic steroids (CTS)) represents a novel approach in the treatment of preeclampsia (PE). Recently we demonstrated that DigiFab (Fab fragments of affinity-purified ovine digoxin antibody) restores PE-induced inhibition of Na/K-ATPase in erythrocytes ex vivo. Previously magnesium ions were shown to antagonize digitalis-induced toxicity, which is mediated by Na/K-ATPase inhibition. We hypothesized that magnesium sulfate would potentiate the effect of DigiFab in the reversal of CTS-induced Na/K-ATPase inhibition.
          To test this hypothesis, we studied the ex vivo effect of DigiFab on Na/K-ATPase activity in erythrocytes from patients with PE in the absence and in the presence of 3 mmol/L magnesium sulfate. Compared with 11 normotensive pregnant subjects (29 ± 1 years; gestational age = 39.0 ± 0.2 weeks; blood pressure = 111 ± 2/73 ± 2 mm Hg), the 12 patients with PE (30 ± 1 years; gestational age = 37.9 ± 0.3 weeks; blood pressure = 159 ± 5/99 ± 3 mm Hg) had plasma levels of marino-bufagenin increased 3-fold (1.38 ± 0.40 vs. 0.38 ± 0.10 nmol/L; P < 0.01) and activity of Na/K-ATPase in erythrocytes was inhibited (1.16 ± 0.11 vs. 2.80 ± 0.20 μmol Pi/ml/h; P < 0.01). Ex vivo, DigiFab (1 µg/ml) restored erythrocyte Na/K-ATPase activity (1.72 ± 0.13 µmol Pi/ml/h; P < 0.01), and 3 mmol magnesium sulfate potentiated the effect of DigiFab (2.30 ± 0.20 µmol Pi/ml/h; P < 0.01).
          Magnesium is capable of increasing the efficacy of immunoneutralization of marinobufagenin-induced Na/K-ATPase inhibition. © Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd 2013. This work is written by (a) US Government employee(s) and is in the public domain in the US.
JF  - American journal of hypertension
AU  - Zazerskaya, Irina E
AU  - Ishkaraeva, Valentina V
AU  - Frolova, Elena V
AU  - Solodovnikova, Nelly G
AU  - Grigorova, Yulia N
AU  - David Adair, C
AU  - Fedorova, Olga V
AU  - Bagrov, Alexei Y
AD  - Institutes of Neonatology and Heart and Vessels, Almazov Federal Heart, Blood and Endocrinology Center, St. Petersburg, Russia; ; Sechenov Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia; ; Institutes of Neonatology and Heart and Vessels, Almazov Federal Heart, Blood and Endocrinology Center, St. Petersburg, Russia; National Institute on Aging, National Institutes of Health, Baltimore, MD; ; Department of Obstetrics and Gynecology, University of Tennessee, Chattanooga, Tennessee. ; National Institute on Aging, National Institutes of Health, Baltimore, MD; ; National Institute on Aging, National Institutes of Health, Baltimore, MD; bagrova@mail.nih.gov.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1269
EP  - 1272
VL  - 26
IS  - 11
KW  - Bufanolides
KW  - 0
KW  - Immunoglobulin Fab Fragments
KW  - Tocolytic Agents
KW  - digoxin antibodies Fab fragments
KW  - marinobufagenin
KW  - 470-42-8
KW  - Magnesium Sulfate
KW  - 7487-88-9
KW  - Sodium-Potassium-Exchanging ATPase
KW  - EC 3.6.3.9
KW  - Index Medicus
KW  - magnesium
KW  - blood pressure
KW  - digifab
KW  - hypertension
KW  - NA/K-ATPase
KW  - immunotherapy
KW  - preeclampsia.
KW  - digitalis-like factors
KW  - cardiotonic steroids
KW  - Animals
KW  - Erythrocytes -- enzymology
KW  - Sheep
KW  - Humans
KW  - Adult
KW  - Case-Control Studies
KW  - Drug Synergism
KW  - Drug Evaluation, Preclinical
KW  - Female
KW  - Pregnancy
KW  - Sodium-Potassium-Exchanging ATPase -- metabolism
KW  - Pre-Eclampsia -- blood
KW  - Immunoglobulin Fab Fragments -- therapeutic use
KW  - Bufanolides -- blood
KW  - Tocolytic Agents -- therapeutic use
KW  - Pre-Eclampsia -- drug therapy
KW  - Magnesium Sulfate -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1612984905?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+hypertension&rft.atitle=Magnesium+sulfate+potentiates+effect+of+DigiFab+on+marinobufagenin-induced+Na%2FK-ATPase+inhibition.&rft.au=Zazerskaya%2C+Irina+E%3BIshkaraeva%2C+Valentina+V%3BFrolova%2C+Elena+V%3BSolodovnikova%2C+Nelly+G%3BGrigorova%2C+Yulia+N%3BDavid+Adair%2C+C%3BFedorova%2C+Olga+V%3BBagrov%2C+Alexei+Y&rft.aulast=Zazerskaya&rft.aufirst=Irina&rft.date=2013-11-01&rft.volume=26&rft.issue=11&rft.spage=1269&rft.isbn=&rft.btitle=&rft.title=American+journal+of+hypertension&rft.issn=1941-7225&rft_id=info:doi/10.1093%2Fajh%2Fhpt117
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-06-29
N1  - Date created - 2014-10-15
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biochim Biophys Acta. 1971 Aug 13;241(2):443-61 [4258481]
Ann N Y Acad Sci. 1974;242(0):617-34 [4279610]
Reprod Sci. 2012 Dec;19(12):1260-7 [22649120]
J Hypertens. 2011 Apr;29(4):769-76 [21330936]
Am J Perinatol. 2010 Sep;27(8):655-62 [20232280]
J Hypertens. 2008 Dec;26(12):2414-25 [19008721]
Curr Hypertens Rep. 2008 Aug;10(4):305-12 [18625161]
J Biol Chem. 2008 Jun 27;283(26):17946-53 [18434301]
J Hypertens. 1999 Aug;17(8):1179-87 [10466474]
Am J Cardiol. 1992 Jun 4;69(18):108G-118G; disc. 118G-119G [1626485]
N Engl J Med. 1988 Feb 25;318(8):518-9 [3340135]
J Emerg Med. 1986;4(6):463-9 [3549866]
Am J Obstet Gynecol. 1984 Sep 1;150(1):83-5 [6540989]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/ajh/hpt117
ER  - 



TY  - JOUR
T1  - Guidelines for Exposure Assessment in Health Risk Studies Following a Nuclear Reactor Accident
AN  - 1520375986; 19716848
AB  - Background: Worldwide concerns regarding health effects after the Chernobyl and Fukushima nuclear power plant accidents indicate a clear need to identify short- and long-term health impacts that might result from accidents in the future. Fundamental to addressing this problem are reliable and accurate radiation dose estimates for the affected populations. The available guidance for activities following nuclear accidents is limited with regard to strategies for dose assessment in health risk studies. Objectives: Here we propose a comprehensive systematic approach to estimating radiation doses for the evaluation of health risks resulting from a nuclear power plant accident, reflected in a set of seven guidelines. Discussion: Four major nuclear reactor accidents have occurred during the history of nuclear power production. The circumstances leading to these accidents were varied, as were the magnitude of the releases of radioactive materials, the pathways by which persons were exposed, the data collected afterward, and the lifestyle factors and dietary consumption that played an important role in the associated radiation exposure of the affected populations. Accidents involving nuclear reactors may occur in the future under a variety of conditions. The guidelines we recommend here are intended to facilitate obtaining reliable dose estimations for a range of different exposure conditions. We recognize that full implementation of the proposed approach may not always be feasible because of other priorities during the nuclear accident emergency and because of limited resources in manpower and equipment. Conclusions: The proposed approach can serve as a basis to optimize the value of radiation dose reconstruction following a nuclear reactor accident. Citation: Bouville A, Linet MS, Hatch M, Mabuchi K, Simon SL. 2014. Guidelines for exposure assessment in health risk studies following a nuclear reactor accident. Environ Health Perspect 122:1-5; http://dx.doi.org/10.1289/ehp.1307120
JF  - Environmental Health Perspectives
AU  - Bouville, Andre
AU  - Linet, Martha S
AU  - Hatch, Maureen
AU  - Mabuchi, Kiyohiko
AU  - Simon, Steven L
AD  - National Cancer Institute (retired), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Rockville, Maryland, USA
Y1  - 2013/11/01/
PY  - 2013
DA  - 2013 Nov 01
SP  - 1
EP  - 5
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 122
IS  - 1
SN  - 0091-6765, 0091-6765
KW  - Toxicology Abstracts; Risk Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - Diets
KW  - Risk assessment
KW  - Historical account
KW  - Ukraine, Chernobyl
KW  - Data processing
KW  - Guidelines
KW  - Health risks
KW  - Nuclear power plants
KW  - Accidents
KW  - Nuclear reactors
KW  - Radiation
KW  - Radioactive materials
KW  - Priorities
KW  - X 24390:Radioactive Materials
KW  - H 8000:Radiation Safety/Electrical Safety
KW  - R2 23060:Medical and environmental health
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520375986?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Guidelines+for+Exposure+Assessment+in+Health+Risk+Studies+Following+a+Nuclear+Reactor+Accident&rft.au=Bouville%2C+Andre%3BLinet%2C+Martha+S%3BHatch%2C+Maureen%3BMabuchi%2C+Kiyohiko%3BSimon%2C+Steven+L&rft.aulast=Bouville&rft.aufirst=Andre&rft.date=2013-11-01&rft.volume=122&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1307120
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Risk assessment; Nuclear power plants; Accidents; Data processing; Radiation; Radioactive materials; Diets; Historical account; Health risks; Nuclear reactors; Guidelines; Priorities; Ukraine, Chernobyl
DO  - http://dx.doi.org/10.1289/ehp.1307120
ER  - 



TY  - JOUR
T1  - The role of work status on European older volunteers' motivation
AN  - 1508433188; 4539715
AB  - The article aims to identify differences in motivation between working and nonworking older volunteers, in order to contribute to knowledge on the relationship between work status and volunteering in later life. The study also contributes a cross-European view, given that most literature emanates from the United States. It was conducted utilizing a database of 955 working and nonworking older volunteers in three European countries: the Netherlands, Germany, and Italy. Results showed that work status has a significant impact on the motivation to volunteer, suggesting that voluntary organizations need to consider responding to different motivations between older volunteers still in paid employment and those who are retired. Specifically, those in paid work may be more driven by the desire to improve their career or knowledge, whereas older retired volunteers and those employed part time may consider volunteering as a response to challenges associated with retirement and later life or an unsatisfactory working situation. [Reprinted by permission of Sage Publications Inc., copyright holder.] Reprinted by permission of Sage Publications Ltd
JF  - Research on aging
AU  - Principi, Andrea
AU  - Warburton, Jeni
AU  - Schippers, Joop
AU  - Rosa, Mirko Di
AD  - National Institute on Aging
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 710
EP  - 735
VL  - 35
IS  - 6
SN  - 0164-0275, 0164-0275
KW  - Sociology
KW  - Occupational roles
KW  - Motivation
KW  - Federal Republic of Germany
KW  - Europe
KW  - Employment
KW  - Germany
KW  - Netherlands
KW  - Italy
KW  - Working conditions
KW  - Knowledge
KW  - Retirement
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508433188?accountid=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=Research+on+aging&rft.atitle=The+role+of+work+status+on+European+older+volunteers%27+motivation&rft.au=Principi%2C+Andrea%3BWarburton%2C+Jeni%3BSchippers%2C+Joop%3BRosa%2C+Mirko+Di&rft.aulast=Principi&rft.aufirst=Andrea&rft.date=2013-11-01&rft.volume=35&rft.issue=6&rft.spage=710&rft.isbn=&rft.btitle=&rft.title=Research+on+aging&rft.issn=01640275&rft_id=info:doi/10.1177%2F0164027512460693
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2014-03-18
N1  - Last updated - 2014-03-19
N1  - SubjectsTermNotLitGenreText - 8322; 10984; 7073; 8855 11099; 4843; 13713 4214; 4214; 129; 275 462 129; 144 462 129; 188 396 129
DO  - http://dx.doi.org/10.1177/0164027512460693
ER  - 



TY  - JOUR
T1  - Predictors of response to tiotropium versus salmeterol in asthmatic adults
AN  - 1504841318; 24084072
AB  - Background  
Tiotropium has activity as an asthma controller. However, predictors of a positive response to tiotropium have not been described.  
Objective  
We sought to describe individual and differential responses of asthmatic patients to salmeterol and tiotropium when added to an inhaled corticosteroid, as well as predictors of a positive clinical response.  
Methods  
Data from the double-blind, 3-way, crossover National Heart, Lung, and Blood Institute's Asthma Clinical Research Network's Tiotropium Bromide as an Alternative to Increased Inhaled Glucocorticoid in Patients Inadequately Controlled on a Lower Dose of Inhaled Corticosteroid (ClinicalTrials.govnumber,NCT00565266) trial were analyzed for individual and differential treatment responses to salmeterol and tiotropium and predictors of a positive response to the end points FEV1, morning peak expiratory flow (PEF), and asthma control days (ACDs).  
Results  
Although approximately equal numbers of patients showed a differential response to salmeterol and tiotropium in terms of morning PEF (n = 90 and 78, respectively) and ACDs (n = 49 and 53, respectively), more showed a differential response to tiotropium for FEV1(n = 104) than salmeterol (n = 62). An acute response to a short-acting bronchodilator, especially albuterol, predicted a positive clinical response to tiotropium for FEV1(odds ratio, 4.08; 95% CI, 2.00-8.31;P< .001) and morning PEF (odds ratio, 2.12; 95% CI, 1.12-4.01;P= 0.021), as did a decreased FEV1/forced vital capacity ratio (FEV1response increased 0.39% of baseline for every 1% decrease in FEV1/forced vital capacity ratio). Higher cholinergic tone was also a predictor, whereas ethnicity, sex, atopy, IgE level, sputum eosinophil count, fraction of exhaled nitric oxide, asthma duration, and body mass index were not.  
Conclusion  
Although these results require confirmation, predictors of a positive clinical response to tiotropium include a positive response to albuterol and airway obstruction, factors that could help identify appropriate patients for this therapy.
JF  - Journal of Allergy and Clinical Immunology
AU  - Peters, Stephen P
AU  - Bleecker, Eugene R
AU  - Kunselman, Susan J
AU  - Icitovic, Nikolina
AU  - Moore, Wendy C
AU  - Pascual, Rodolfo
AU  - Ameredes, Bill T
AU  - Boushey, Homer A
AU  - Calhoun, William J
AU  - Castro, Mario
AU  - Cherniack, Reuben M
AU  - Craig, Timothy
AU  - Denlinger, Loren C
AU  - Engle, Linda L
AU  - DiMango, Emily A
AU  - Israel, Elliot
AU  - Kraft, Monica
AU  - Lazarus, Stephen C
AU  - Lemanske, Robert F
AU  - Lugogo, Njira
AU  - Martin, Richard J
AU  - Meyers, Deborah A
AU  - Ramsdell, Joe
AU  - Sorkness, Christine A
AU  - Sutherland, E Rand
AU  - Wasserman, Stephen I
AU  - Walter, Michael J
AU  - Wechsler, Michael E
AU  - Chinchilli, Vernon M
AU  - Szefler, Stanley J
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1068
EP  - 1074.e1
CY  - St. Louis
PB  - Elsevier Science Ltd.
VL  - 132
IS  - 5
SN  - 00916749
KW  - Abstracting And Indexing Services
KW  - Adrenergic beta-2 Receptor Agonists
KW  - Anti-Asthmatic Agents
KW  - Bronchodilator Agents
KW  - Scopolamine Derivatives
KW  - tiotropium
KW  - salmeterol
KW  - Albuterol
KW  - Asthma
KW  - Medical treatment
KW  - Digital divide
KW  - Airway management
KW  - Drug dosages
KW  - Biomarkers
KW  - Patients
KW  - Albuterol -- therapeutic use
KW  - Humans
KW  - Adult
KW  - Treatment Outcome
KW  - Prognosis
KW  - Cross-Over Studies
KW  - Middle Aged
KW  - Male
KW  - Female
KW  - Scopolamine Derivatives -- therapeutic use
KW  - Adrenergic beta-2 Receptor Agonists -- therapeutic use
KW  - Asthma -- drug therapy
KW  - Albuterol -- analogs & derivatives
KW  - Bronchodilator Agents -- therapeutic use
KW  - Anti-Asthmatic Agents -- therapeutic use
KW  - Asthma -- diagnosis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504841318?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthcompleteshell&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Allergy+and+Clinical+Immunology&rft.atitle=Predictors+of+response+to+tiotropium+versus+salmeterol+in+asthmatic+adults&rft.au=Peters%2C+Stephen+P%3BBleecker%2C+Eugene+R%3BKunselman%2C+Susan+J%3BIcitovic%2C+Nikolina%3BMoore%2C+Wendy+C%3BPascual%2C+Rodolfo%3BAmeredes%2C+Bill+T%3BBoushey%2C+Homer+A%3BCalhoun%2C+William+J%3BCastro%2C+Mario%3BCherniack%2C+Reuben+M%3BCraig%2C+Timothy%3BDenlinger%2C+Loren+C%3BEngle%2C+Linda+L%3BDiMango%2C+Emily+A%3BIsrael%2C+Elliot%3BKraft%2C+Monica%3BLazarus%2C+Stephen+C%3BLemanske%2C+Robert+F%3BLugogo%2C+Njira%3BMartin%2C+Richard+J%3BMeyers%2C+Deborah+A%3BRamsdell%2C+Joe%3BSorkness%2C+Christine+A%3BSutherland%2C+E+Rand%3BWasserman%2C+Stephen+I%3BWalter%2C+Michael+J%3BWechsler%2C+Michael+E%3BChinchilli%2C+Vernon+M%3BSzefler%2C+Stanley+J&rft.aulast=Peters&rft.aufirst=Stephen&rft.date=2013-11-01&rft.volume=132&rft.issue=5&rft.spage=1068&rft.isbn=&rft.btitle=&rft.title=Journal+of+Allergy+and+Clinical+Immunology&rft.issn=00916749&rft_id=info:doi/10.1016%2Fj.jaci.2013.08.003
LA  - English
DB  - ProQuest Central
N1  - Copyright - Copyright Elsevier Limited Nov 2013
N1  - Last updated - 2014-11-06
DO  - http://dx.doi.org/10.1016/j.jaci.2013.08.003
ER  - 



TY  - JOUR
T1  - Mirror Artifacts in Obstetric Ultrasound: Case Presentation of a Ghost Twin during the Second-Trimester Ultrasound Scan
AN  - 1496888738; 18885549
AB  - Mirror artifacts are produced by the reflection of ultrasound waves after they propagate through a structure and encounter a strong and smooth interface capable of acting as a mirror. Ultrasound waves bounce back and forth between the mirroring interface and the reflective object and then eventually return to the transducer. The typical display of the mirror artifact consists of two similar structures separated and at similar distances from the reflective interface. We report a mirror artifact in a patient with a singleton gestation at 18 weeks. The image was interpreted as consistent with a twin gestation using transabdominal and transvaginal ultrasound. The differential diagnosis consisted of an abdominal heterotopic pregnancy. The presence of synchronized but opposite movements of both fetuses, and the blurred image of the second fetus, suggested a mirror artifact. The reflective surface was created by the interface located between a distended rectosigmoid filled with gas and the posterior uterine wall. Mirror artifacts can lead to diagnostic errors. This case illustrates how a distended rectosigmoid colon can generate an image that simulates either a twin gestation or an abdominal heterotopic pregnancy. Copyright [copy 2013 S. Karger AG, Basel
JF  - Fetal Diagnosis and Therapy: clinical advances and basic research
AU  - Ahn, Hyunyoung
AU  - Hernndez-Andrade, Edgar
AU  - Romero, Roberto
AU  - Ptwardhan, Manasi
AU  - Goncalves, Luis F
AU  - Aurioles-Garibay, Alma
AU  - Garcia, Maynor
AU  - Hassan, Sonia S
AU  - Yeo, Lami
AD  - Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD, and Detroit, MI
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 248
EP  - 252
PB  - S. Karger AG, P.O. Box Basel CH-4009 Switzerland
VL  - 34
IS  - 4
SN  - 1015-3837, 1015-3837
KW  - Biotechnology and Bioengineering Abstracts
KW  - Colon
KW  - Ultrasound
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496888738?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fetal+Diagnosis+and+Therapy%3A+clinical+advances+and+basic+research&rft.atitle=Mirror+Artifacts+in+Obstetric+Ultrasound%3A+Case+Presentation+of+a+Ghost+Twin+during+the+Second-Trimester+Ultrasound+Scan&rft.au=Ahn%2C+Hyunyoung%3BHernndez-Andrade%2C+Edgar%3BRomero%2C+Roberto%3BPtwardhan%2C+Manasi%3BGoncalves%2C+Luis+F%3BAurioles-Garibay%2C+Alma%3BGarcia%2C+Maynor%3BHassan%2C+Sonia+S%3BYeo%2C+Lami&rft.aulast=Ahn&rft.aufirst=Hyunyoung&rft.date=2013-11-01&rft.volume=34&rft.issue=4&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Fetal+Diagnosis+and+Therapy%3A+clinical+advances+and+basic+research&rft.issn=10153837&rft_id=info:doi/10.1159%2F000353702
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Ultrasound
DO  - http://dx.doi.org/10.1159/000353702
ER  - 



TY  - JOUR
T1  - Use of Novel Technology-Based Techniques to Improve Alcohol-Related Outcomes in Clinical Trials
AN  - 1496663967; 201400621
AB  - With a better understanding of the biologic basis of alcohol dependence and the considerable financial burden of alcohol abuse and dependence, the number of alcohol-related clinical pharmacotherapy trials has been on the rise. Subsequently, the potential to find efficacious treatments is more promising. Unfortunately, alcohol-related trials face a number of challenges, as a result of the difficulties that arise from traditional and outdated methods to collect data and ensure medication adherence. Novel technology-based assessments, such as ecological momentary assessment, interactive voice response, transdermal sensor and medication-event monitoring system provide a prospective solution-albeit not without possible concerns-to the difficulties faced in alcohol-related clinical trials. Clinical trials are meant to define the efficacy of the treatment and to determine an effective and safe dosage. However, due to lack of adherence a drug could inappropriately or mistakenly be judged as ineffective for treating a specific disorder. The described technologies may be important tools to prevent false negatives in validating drug efficacy, to provide consistency in clinical trials and to improve available data regarding the study of pharmacotherapies for alcohol dependence. Adapted from the source document.
JF  - Alcohol and Alcoholism
AU  - Gurvich, Eugenia M
AU  - Kenna, George A
AU  - Leggio, Lorenzo
AD  - Biomedical Engineering Undergraduate Program, Brown University School of Engineering, Providence, RI, USA
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 712
EP  - 719
PB  - Oxford University Press, UK
VL  - 48
IS  - 6
SN  - 0735-0414, 0735-0414
KW  - Efficacy
KW  - Pharmacology
KW  - Adherence
KW  - Alcohol dependence
KW  - Clinical trials
KW  - Alcohol related
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496663967?accountid=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=Alcohol+and+Alcoholism&rft.atitle=Use+of+Novel+Technology-Based+Techniques+to+Improve+Alcohol-Related+Outcomes+in+Clinical+Trials&rft.au=Gurvich%2C+Eugenia+M%3BKenna%2C+George+A%3BLeggio%2C+Lorenzo&rft.aulast=Gurvich&rft.aufirst=Eugenia&rft.date=2013-11-01&rft.volume=48&rft.issue=6&rft.spage=712&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+Alcoholism&rft.issn=07350414&rft_id=info:doi/10.1093%2Falcalc%2Fagt134
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-01-01
N1  - Last updated - 2016-09-27
N1  - CODEN - ALALDD
N1  - SubjectsTermNotLitGenreText - Alcohol related; Clinical trials; Alcohol dependence; Adherence; Pharmacology; Efficacy
DO  - http://dx.doi.org/10.1093/alcalc/agt134
ER  - 



TY  - JOUR
T1  - Triggers for driving treatment of at-risk patients with invasive fungal disease
AN  - 1492646161; 18892496
AB  - Timing of treatment for invasive fungal disease (IFD) is critical for making appropriate clinical decisions. Historically, many centres have treated at-risk patients prior to disease detection to try to prevent fungal colonization or in response to antibiotic-resistant fever. Many studies have indicated that a diagnostic-driven approach, using radiological tests and biomarkers to guide treatment decisions, may be a more clinically relevant and cost-effective approach. The Invasive Fungal Infections Cooperative Group of the European Organization for Research and Treatment of Cancer/Mycoses Study Group (EORTC/MSG) defined host clinical and mycological criteria for proven, probable and possible classes of IFD, to aid diagnosis. However, some patients at risk of IFD do not meet EORTC/MSG criteria and have been termed Groups B (patients with persistent unexplained febrile neutropenia) and C (patients with non-definitive signs of IFD) in a study by Maertens et al. (Haematologica 2012; 97: 325-7). Consequently, we considered the most appropriate triggers (clinical or radiological signs or biomarkers) for treatment of all patient groups, especially the unclassified B and C groups, based on our clinical experience. For Group C patients, additional diagnostic testing is recommended before a decision to treat, including repeat galactomannan tests, radiological scans and analysis of bronchoalveolar lavage fluid. Triggers for stopping antifungal treatment were considered to include resolution of all clinical signs and symptoms. For Group B patients, it was concluded that better definition of risk factors predisposing patients to fungal infection and the use of more sensitive diagnostic tests are required to aid treatment decisions and improve clinical outcomes.
JF  - Journal of Antimicrobial Chemotherapy
AU  - Drgona, Lubos
AU  - Colita, Anca
AU  - Klimko, Nikolay
AU  - Rahav, Galia
AU  - Ozcan, Mehmet A
AU  - Donnelly, J Peter
AD  - 1 Department of Hemato-oncology, National Cancer Institute and Comenius University, Bratislava, Slovakia, lubos.drgona@nou.sk
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - iii17
EP  - iii24
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 68
IS  - suppl_3
SN  - 0305-7453, 0305-7453
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - diagnostic-driven therapy
KW  - immunocompromised patients
KW  - radiological triggers
KW  - galactomannan test
KW  - Fever
KW  - Colonization
KW  - Decision making
KW  - Neutropenia
KW  - Invasiveness
KW  - Bronchus
KW  - Risk factors
KW  - Infection
KW  - biomarkers
KW  - Cancer
KW  - Alveoli
KW  - A 01340:Antibiotics & Antimicrobials
KW  - K 03420:Plant Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492646161?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Antimicrobial+Chemotherapy&rft.atitle=Triggers+for+driving+treatment+of+at-risk+patients+with+invasive+fungal+disease&rft.au=Drgona%2C+Lubos%3BColita%2C+Anca%3BKlimko%2C+Nikolay%3BRahav%2C+Galia%3BOzcan%2C+Mehmet+A%3BDonnelly%2C+J+Peter&rft.aulast=Drgona&rft.aufirst=Lubos&rft.date=2013-11-01&rft.volume=68&rft.issue=suppl_3&rft.spage=iii17&rft.isbn=&rft.btitle=&rft.title=Journal+of+Antimicrobial+Chemotherapy&rft.issn=03057453&rft_id=info:doi/10.1093%2Fjac%2Fdkt391
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Fever; Neutropenia; Decision making; Colonization; Invasiveness; Bronchus; Risk factors; Infection; biomarkers; Alveoli; Cancer
DO  - http://dx.doi.org/10.1093/jac/dkt391
ER  - 



TY  - JOUR
T1  - An embedded four-channel receive-only RF coil array for fMRI experiments of the somatosensory pathway in conscious awake marmosets
AN  - 1492612237; 18894569
AB  - fMRI has established itself as the main research tool in neuroscience and brain cognitive research. The common marmoset (Callithrix jacchus) is a non-human primate model of increasing interest in biomedical research. However, commercial MRI coils for marmosets are not generally available. The present work describes the design and construction of a four-channel receive-only surface RF coil array with excellent signal-to-noise ratio (SNR) specifically optimized for fMRI experiments in awake marmosets in response to somatosensory stimulation. The array was designed as part of a helmet-based head restraint system used to prevent motion during the scans. High SNR was obtained by building the coil array using a thin and flexible substrate glued to the inner surface of the restraint helmet, so as to minimize the distance between the array elements and the somatosensory cortex. Decoupling between coil elements was achieved by partial geometrical overlapping and by connecting them to home-built low-input-impedance preamplifiers. In vivo images show excellent coverage of the brain cortical surface with high sensitivity near the somatosensory cortex. Embedding the coil elements within the restraint helmet allowed fMRI data in response to somatosensory stimulation to be collected with high sensitivity and reproducibility in conscious, awake marmosets. Published 2013. This article is a U.S. Government work and is in the public domain in the USA. An embedded four-channel receive-only RF coil array was constructed and optimized for fMRI experiments of the somatosensory pathway in conscious, awake marmosets. The array was designed as part of a helmet-based head restraint system used to prevent motion during the MRI data acquisition. High SNR was obtained by building the array elements using a thin and flexible substrate glued to the inner surface of the restraint helmet, minimizing the distance between the array elements and the somatosensory cortex.
JF  - NMR in Biomedicine
AU  - Papoti, Daniel
AU  - Yen, Cecil Chern-Chyi
AU  - Mackel, Julie B
AU  - Merkle, Hellmut
AU  - Silva, Afonso C
AD  - Cerebral Microcirculation Unit, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1395
EP  - 1402
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 26
IS  - 11
SN  - 0952-3480, 0952-3480
KW  - Biotechnology and Bioengineering Abstracts
KW  - Brain mapping
KW  - Functional magnetic resonance imaging
KW  - Callithrix jacchus
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492612237?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+embedded+four-channel+receive-only+RF+coil+array+for+fMRI+experiments+of+the+somatosensory+pathway+in+conscious+awake+marmosets&rft.au=Papoti%2C+Daniel%3BYen%2C+Cecil+Chern-Chyi%3BMackel%2C+Julie+B%3BMerkle%2C+Hellmut%3BSilva%2C+Afonso+C&rft.aulast=Papoti&rft.aufirst=Daniel&rft.date=2013-11-01&rft.volume=26&rft.issue=11&rft.spage=1395&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.2965
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Functional magnetic resonance imaging; Callithrix jacchus
DO  - http://dx.doi.org/10.1002/nbm.2965
ER  - 



TY  - JOUR
T1  - Antivirals in the 2009 pandemic - lessons and implications for future strategies
AN  - 1468384642; 18830939
AB  - The World Health Organization's declaration of an imminent swine-origin influenza A pandemic in April 2009 triggered the global launch of national pandemic preparedness plans. An integral component of pandemic preparedness in many countries was the targeted use of antiviral therapy for containment, disease mitigation, and treatment. The 2009 pandemic marked the first pandemic during which influenza antivirals were available for global use. Although most national pandemic plans included provisions for antiviral treatment, these pre-determined protocols required frequent updating as more information became available about the virus, and its susceptibility to antiviral agents, the epidemiology of infection, and the population groups that were most susceptible to severe disease. National public health agencies in countries with both plans for use of antivirals and pre-existing stockpiles, including those in Japan, the United Kingdom, and the United States, operated distinctly different antiviral distribution and treatment programs from one another. In the 3 years following the pandemic, there is still little comparison of the diversity of national antiviral treatment policies and drug distribution mechanisms that were implemented, whether they had any mitigating effects and which might be most efficient. The purpose of this study is to outline roles of antiviral medicines in a pandemic period, provide insights into the diversity of antiviral treatment and distribution policies applied by selected countries between April 2009-July 2010, and to stimulate discussion on whether these policies remain appropriate for implementation in future pandemics.
JF  - Influenza and Other Respiratory Viruses
AU  - Berera, Deeva
AU  - Zambon, Maria
AD  - Division of International Epidemiology and Population Studies, Fogarty International Center. National Institutes of Health
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 72
EP  - 79
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 7
SN  - 1750-2640, 1750-2640
KW  - Virology & AIDS Abstracts; Health & Safety Science Abstracts
KW  - Antiviral agents
KW  - Influenza
KW  - pandemics
KW  - Japan
KW  - V:22400
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468384642?accountid=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=Influenza+and+Other+Respiratory+Viruses&rft.atitle=Antivirals+in+the+2009+pandemic+-+lessons+and+implications+for+future+strategies&rft.au=Berera%2C+Deeva%3BZambon%2C+Maria&rft.aulast=Berera&rft.aufirst=Deeva&rft.date=2013-11-01&rft.volume=7&rft.issue=&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=Influenza+and+Other+Respiratory+Viruses&rft.issn=17502640&rft_id=info:doi/10.1111%2Firv.12172
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - pandemics; Influenza; Japan
DO  - http://dx.doi.org/10.1111/irv.12172
ER  - 



TY  - JOUR
T1  - Noninvasive pulsed focused ultrasound allows spatiotemporal control of targeted homing for multiple stem cell types in murine skeletal muscle and the magnitude of cell homing can be increased through repeated applications
AN  - 1468341383; 18853078
AB  - Abstract Stem cells are promising therapeutics for cardiovascular diseases, and i.v. injection is the most desirable route of administration clinically. Subsequent homing of exogenous stem cells to pathological loci is frequently required for therapeutic efficacy and is mediated by chemoattractants (cell adhesion molecules, cytokines, and growth factors). Homing processes are inefficient and depend on short-lived pathological inflammation that limits the window of opportunity for cell injections. Noninvasive pulsed focused ultrasound (pFUS), which emphasizes mechanical ultrasound-tissue interactions, can be precisely targeted in the body and is a promising approach to target and maximize stem cell delivery by stimulating chemoattractant expression in pFUS-treated tissue prior to cell infusions. We demonstrate that pFUS is nondestructive to murine skeletal muscle tissue (no necrosis, hemorrhage, or muscle stem cell activation) and initiates a largely M2-type macrophage response. We also demonstrate that local upregulation of chemoattractants in pFUS-treated skeletal muscle leads to enhance homing, permeability, and retention of human mesenchymal stem cells (MSC) and human endothelial precursor cells (EPC). Furthermore, the magnitude of MSC or EPC homing was increased when pFUS treatments and cell infusions were repeated daily. This study demonstrates that pFUS defines transient "molecular zip codes" of elevated chemoattractants in targeted muscle tissue, which effectively provides spatiotemporal control and tunability of the homing process for multiple stem cell types. pFUS is a clinically translatable modality that may ultimately improve homing efficiency and flexibility of cell therapies for cardiovascular diseases. Stem Cells 2013; 31:2551-2560
JF  - Stem Cells
AU  - Burks, Scott R
AU  - Ziadloo, Ali
AU  - Kim, Saejeong J
AU  - Nguyen, Ben A
AU  - Frank, Joseph A
AD  - Frank Laboratory, Radiology and Imaging Sciences, Clinical Center, Clinical Center and National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 2551
EP  - 2560
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 11
SN  - 1066-5099, 1066-5099
KW  - Biotechnology and Bioengineering Abstracts
KW  - Cardiovascular diseases
KW  - Stem cells
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468341383?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Noninvasive+pulsed+focused+ultrasound+allows+spatiotemporal+control+of+targeted+homing+for+multiple+stem+cell+types+in+murine+skeletal+muscle+and+the+magnitude+of+cell+homing+can+be+increased+through+repeated+applications&rft.au=Burks%2C+Scott+R%3BZiadloo%2C+Ali%3BKim%2C+Saejeong+J%3BNguyen%2C+Ben+A%3BFrank%2C+Joseph+A&rft.aulast=Burks&rft.aufirst=Scott&rft.date=2013-11-01&rft.volume=31&rft.issue=11&rft.spage=2551&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1495
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Stem cells
DO  - http://dx.doi.org/10.1002/stem.1495
ER  - 



TY  - JOUR
T1  - Using creative problem solving to promote students' performance of concept mapping
AN  - 1464604149; 18785909
AB  - The purpose of the study was to explore that using creative problem solving can promote students' performance of concept mapping (CMPING). Students were encouraged to use creative problem solving (CPS) in constructing nanometer knowledge structure, and then to promote the performance of CMPING. The knowledge structure was visualized through CMPING which helps students to improve their performance. The participants were 42 college juniors who selected the course "Nano-environmental Engineering Technology". Four instruments were used to classify student learning performance (meaningful learning, rote learning and non-learning). This study included three main issues: (1) Student learning quality was determined by the change in concept map construction. (2) In-depth interviews were applied to understand student's CPS process. (3) Student interaction quality in a discussion board on a web-platform was evaluated. The results showed that meaningful high-level learners successfully applied CPS in constructing concept maps and they presented better performance of CMPING. Rote learners' results were in the second place, and non-learners achieved the worse outcomes. It is suggested that a future teaching study can use creative problem solving to promote students' performance of CMPING in other courses.
JF  - International Journal of Technology and Design Education
AU  - Tseng, Kuo-Hung
AU  - Chang, Chi-Cheng
AU  - Lou, Shi-Jer
AU  - Hsu, Pi-Shan
AD  - Graduate Institute of Business and Management, Meiho University, No. 23, Pingguang Road, Meiho Village, Nei-Pu Township, Pingtung, 91202, Pingtung County, Taiwan, ROC
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1093
EP  - 1109
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 23
IS  - 4
SN  - 0957-7572, 0957-7572
KW  - Mechanical & Transportation Engineering Abstracts (MT); Materials Business File (MB); Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - Concept mapping
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464604149?accountid=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=International+Journal+of+Technology+and+Design+Education&rft.atitle=Using+creative+problem+solving+to+promote+students%27+performance+of+concept+mapping&rft.au=Tseng%2C+Kuo-Hung%3BChang%2C+Chi-Cheng%3BLou%2C+Shi-Jer%3BHsu%2C+Pi-Shan&rft.aulast=Tseng&rft.aufirst=Kuo-Hung&rft.date=2013-11-01&rft.volume=23&rft.issue=4&rft.spage=1093&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Technology+and+Design+Education&rft.issn=09577572&rft_id=info:doi/10.1007%2Fs10798-012-9230-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Number of references - 1
N1  - Last updated - 2014-03-12
DO  - http://dx.doi.org/10.1007/s10798-012-9230-8
ER  - 



TY  - JOUR
T1  - Spatially isotropic four-dimensional imaging with dual-view plane illumination microscopy
AN  - 1464513512; 18788071
AB  - Optimal four-dimensional imaging requires high spatial resolution in all dimensions, high speed and minimal photobleaching and damage. We developed a dual-view, plane illumination microscope with improved spatiotemporal resolution by switching illumination and detection between two perpendicular objectives in an alternating duty cycle. Computationally fusing the resulting volumetric views provides an isotropic resolution of 330 nm. As the sample is stationary and only two views are required, we achieve an imaging speed of 200 images/s (i.e., 0.5 s for a 50-plane volume). Unlike spinning-disk confocal or Bessel beam methods, which illuminate the sample outside the focal plane, we maintain high spatiotemporal resolution over hundreds of volumes with negligible photobleaching. To illustrate the ability of our method to study biological systems that require high-speed volumetric visualization and/or low photobleaching, we describe microtubule tracking in live cells, nuclear imaging over 14 h during nematode embryogenesis and imaging of neural wiring during Caenorhabditis elegans brain development over 5 h.
JF  - Nature Biotechnology
AU  - Wu, Yicong
AU  - Wawrzusin, Peter
AU  - Senseney, Justin
AU  - Fischer, Robert S
AU  - Christensen, Ryan
AU  - Santella, Anthony
AU  - York, Andrew G
AU  - Winter, Peter W
AU  - Waterman, Clare M
AU  - Bao, Zhirong
AU  - Colon-Ramos, Daniel A
AU  - McAuliffe, Matthew
AU  - Shroff, Hari
AD  - Section on High Resolution Optical Imaging, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1032
EP  - 1038
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 31
IS  - 11
SN  - 1087-0156, 1087-0156
KW  - Biotechnology and Bioengineering Abstracts
KW  - Neuroimaging
KW  - Microtubules
KW  - Embryogenesis
KW  - Illumination
KW  - Photobleaching
KW  - Microscopes
KW  - Caenorhabditis elegans
KW  - Microscopy
KW  - Brain
KW  - spatial discrimination
KW  - Nematoda
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464513512?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spatially+isotropic+four-dimensional+imaging+with+dual-view+plane+illumination+microscopy&rft.au=Wu%2C+Yicong%3BWawrzusin%2C+Peter%3BSenseney%2C+Justin%3BFischer%2C+Robert+S%3BChristensen%2C+Ryan%3BSantella%2C+Anthony%3BYork%2C+Andrew+G%3BWinter%2C+Peter+W%3BWaterman%2C+Clare+M%3BBao%2C+Zhirong%3BColon-Ramos%2C+Daniel+A%3BMcAuliffe%2C+Matthew%3BShroff%2C+Hari&rft.aulast=Wu&rft.aufirst=Yicong&rft.date=2013-11-01&rft.volume=31&rft.issue=11&rft.spage=1032&rft.isbn=&rft.btitle=&rft.title=Nature+Biotechnology&rft.issn=10870156&rft_id=info:doi/10.1038%2Fnbt.2713
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Embryogenesis; Microtubules; Neuroimaging; Illumination; Microscopes; Photobleaching; Microscopy; Brain; spatial discrimination; Caenorhabditis elegans; Nematoda
DO  - http://dx.doi.org/10.1038/nbt.2713
ER  - 



TY  - JOUR
T1  - Intravenous nicotine injection induces rapid, experience-dependent sensitization of glutamate release in the ventral tegmental area and nucleus accumbens
AN  - 1464513242; 18786984
AB  - Although numerous data suggest that glutamate (GLU) is involved in mediating the neural effects of nicotine, direct data on nicotine-induced changes in GLU release are still lacking. Here, we used high-speed amperometry with enzyme-based GLU and enzyme-free GLU-null biosensors to examine changes in extracellular GLU levels in the ventral tegmental area (VTA) and nucleus accumbens shell (NAcc) induced by intravenous nicotine in a low, behaviorally active dose (30 mu g/kg) in freely moving rats. Using this approach, we found that the initial nicotine injection in drug-naive conditions induces rapid, transient, and relatively small GLU release (~ 90 nM; latency ~ 15 s, duration ~ 60 s) that is correlative in the VTA and NAcc. Following subsequent nicotine injections within the same session, this phasic GLU release was supplemented by stronger tonic increases in GLU levels (100-300 nM) that paralleled increases in drug-induced locomotor activation. GLU responses induced by repeated nicotine injections were more phasic and stronger in the NAcc than in VTA. Therefore, GLU is phasically released within the brain's reinforcement circuit following intravenous nicotine administration. Robust enhancement of nicotine-induced GLU responses following repeated injections suggests this change as an important mediator of sensitized behavioral and neural effects of nicotine. By using high-speed amperometry with glutamate (GLU) biosensors, we show that i.v. nicotine at a low, behaviorally relevant dose induces rapid GLU release in the NAcc and VTA that is enhanced following repeated drug injections. This is the first study reporting second-scale fluctuations in extracellular GLU levels induced by nicotine in two critical structures of the motivation-reinforcement circuit and rapid sensitization of GLU responses coupled with locomotor sensitization. By using high-speed amperometry with glutamate (GLU) biosensors, we show that i.v. nicotine at a low, behaviorally relevant dose induces rapid GLU release in the NAcc and VTA that is enhanced following repeated drug injections. This is the first study reporting second-scale fluctuations in extracellular GLU levels induced by nicotine in two critical structures of the motivation-reinforcement circuit and rapid sensitization of GLU responses coupled with locomotor sensitization.
JF  - Journal of Neurochemistry
AU  - Lenoir, Magalie
AU  - Kiyatkin, Eugene A
AD  - In-Vivo Electrophysiology Unit Behavioral Neuroscience Branch. National Institute on Drug Abuse - Intramural Research ProgramNational Institutes of HealthDHHS
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 541
EP  - 551
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 127
IS  - 4
SN  - 0022-3042, 0022-3042
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - Biosensors
KW  - Nicotine
KW  - X 24380:Social Poisons & Drug Abuse
KW  - N3 11008:Neurochemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464513242?accountid=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+Neurochemistry&rft.atitle=Intravenous+nicotine+injection+induces+rapid%2C+experience-dependent+sensitization+of+glutamate+release+in+the+ventral+tegmental+area+and+nucleus+accumbens&rft.au=Lenoir%2C+Magalie%3BKiyatkin%2C+Eugene+A&rft.aulast=Lenoir&rft.aufirst=Magalie&rft.date=2013-11-01&rft.volume=127&rft.issue=4&rft.spage=541&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurochemistry&rft.issn=00223042&rft_id=info:doi/10.1111%2Fjnc.12450
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Nicotine
DO  - http://dx.doi.org/10.1111/jnc.12450
ER  - 



TY  - JOUR
T1  - Reassessing target antigens for adoptive T-cell therapy
AN  - 1464512458; 18788072
AB  - Adoptive T-cell therapy can target and kill widespread malignant cells thereby inducing durable clinical responses in melanoma and selected other malignances. However, many commonly targeted tumor antigens are also expressed by healthy tissues, and T cells do not distinguish between benign and malignant tissues if both express the target antigen. Autoimmune toxicity from T cell-mediated destruction of normal tissue has limited the development and adoption of this otherwise promising type of cancer therapy. A review of the unique biology of T-cell therapy and of recent clinical experience compels a reassessment of target antigens that traditionally have been viewed from the perspective of weaker immunotherapeutic modalities. It is important that target antigens chosen for adoptive T-cell therapy are expressed by tumors and not by essential healthy tissues. The risk of adverse autoimmune events can be further mitigated by generating antigen receptors using strategies that reduce the chance of cross-reactivity against epitopes in unintended targets. In general, a circumspect approach to target selection and thoughtful preclinical and clinical studies are pivotal to the ongoing advancement of these promising treatments.
JF  - Nature Biotechnology
AU  - Hinrichs, Christian S
AU  - Restifo, Nicholas P
AD  - National Cancer Institute, Surgery Branch, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 999
EP  - 1008
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 31
IS  - 11
SN  - 1087-0156, 1087-0156
KW  - Biotechnology and Bioengineering Abstracts
KW  - Cross-reactivity
KW  - Reviews
KW  - Antigen (tumor-associated)
KW  - Lymphocytes T
KW  - Adoption
KW  - Tumors
KW  - Toxicity
KW  - Epitopes
KW  - Cancer
KW  - Benign
KW  - Melanoma
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464512458?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reassessing+target+antigens+for+adoptive+T-cell+therapy&rft.au=Hinrichs%2C+Christian+S%3BRestifo%2C+Nicholas+P&rft.aulast=Hinrichs&rft.aufirst=Christian&rft.date=2013-11-01&rft.volume=31&rft.issue=11&rft.spage=999&rft.isbn=&rft.btitle=&rft.title=Nature+Biotechnology&rft.issn=10870156&rft_id=info:doi/10.1038%2Fnbt.2725
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2013-12-04
N1  - SubjectsTermNotLitGenreText - Cross-reactivity; Reviews; Antigen (tumor-associated); Lymphocytes T; Adoption; Toxicity; Tumors; Cancer; Epitopes; Melanoma; Benign
DO  - http://dx.doi.org/10.1038/nbt.2725
ER  - 



TY  - JOUR
T1  - The National Lung Screening Trial: Results stratified by demographics, smoking history, and lung cancer histology
AN  - 1464511256; 18811366
AB  - BACKGROUND The National Lung Screening Trial (NLST), which compared lung cancer screening with low-dose computed tomography (LDCT) versus chest radiography (CXR), demonstrated a statistically significant mortality benefit of LDCT screening. In the current study, the authors performed a post hoc analysis to examine whether the benefit was affected by various baseline factors, including age, sex, and smoking status, and whether it differed by tumor histology. METHODS Lung cancer death rates were computed as events over person-years of observation; the mortality risk ratio (RR) was defined as the lung cancer death rate in the LDCT versus CXR trial arms. Poisson regression was used to test for interactions of sex, age (<65 years vs greater than or equal to 65 years), and smoking status (current vs former) with trial arm. Mortality RRs were also computed for specific lung cancer histologies. RESULTS The overall mortality RR was 0.92 in men and 0.73 in women, with a P value for interaction of .08. RRs were similar for individuals aged <65 years versus those aged greater than or equal to 65 years (0.82 vs 0.87), and for current versus former smokers (0.81 vs 0.91). By tumor histology, mortality RRs were 0.75 for adenocarcinoma, 0.71 for all non-small cell lung cancers except squamous, 1.23 for squamous cell carcinoma, and 0.90 for small cell carcinoma. RRs were similar for men and women for nonsquamous non-small cell lung cancers (0.71 and 0.70, respectively); women were found to have lower RRs for small cell and squamous cell carcinoma. CONCLUSIONS A benefit of LDCT did not appear to vary substantially by age or smoking status; there was weak evidence of a differential benefit by sex. A differential benefit across lung cancer histologies may exist. Cancer 2013; 119:3976-3983. Published 2013. This article is a U.S. Government work and is in the public domain in the USA. The benefit of computed tomography screening in the National Lung Screening Trial did not vary substantially by age or smoking status; there was weak evidence of a differential benefit by sex. A differential benefit across lung cancer histologies may exist.
JF  - Cancer
AU  - Pinsky, Paul F
AU  - Church, Timothy R
AU  - Izmirlian, Grant
AU  - Kramer, Barnett S
AD  - Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 3976
EP  - 3983
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 22
SN  - 0008-543X, 0008-543X
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Age
KW  - USA
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/1464511256?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=The+National+Lung+Screening+Trial%3A+Results+stratified+by+demographics%2C+smoking+history%2C+and+lung+cancer+histology&rft.au=Pinsky%2C+Paul+F%3BChurch%2C+Timothy+R%3BIzmirlian%2C+Grant%3BKramer%2C+Barnett+S&rft.aulast=Pinsky&rft.aufirst=Paul&rft.date=2013-11-01&rft.volume=119&rft.issue=22&rft.spage=3976&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.28326
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Lung cancer; USA
DO  - http://dx.doi.org/10.1002/cncr.28326
ER  - 



TY  - JOUR
T1  - Driver mutations among never smoking female lung cancer tissues in China identify unique EGFR and KRAS mutation pattern associated with household coal burning
AN  - 1464509963; 18746767
AB  - Lung cancer in never smokers, which has been partially attributed to household solid fuel use (i.e., coal), is etiologically and clinically different from lung cancer attributed to tobacco smoking. To explore the spectrum of driver mutations among lung cancer tissues from never smokers, specifically in a population where high lung cancer rates have been attributed to indoor air pollution from domestic coal use, multiplexed assays were used to detect >40 point mutations, insertions, and deletions (EGFR, KRAS, BRAF, HER2, NRAS, PIK3CA, MEK1, AKT1, and PT2N) among the lung tumors of confirmed never smoking females from Xuanwei, China [32 adenocarcinomas (ADCs), 7 squamous cell carcinomas (SCCs), 1 adenosquamous carcinoma (ADSC)]. mutations were detected in 35% of tumors. 46% of these involved exon 18 G719X, while 14% were exon 21 L858R mutations. mutations, all of which were G12C_34G>T, were observed in 15% of tumors. and mutations were mutually exclusive, and no mutations were observed in the other tested genes. Most point mutations were transversions and were also found in tumors from patients who used coal in their homes. Our high mutation frequencies in exon 18 and and low mutation frequency in exon 21 are strikingly divergent from those in other smoking and never smoking populations from Asia. Given that our subjects live in a region where coal is typically burned indoors, our findings provide new insights into the pathogenesis of lung cancer among never smoking females exposed to indoor air pollution from coal.
JF  - Respiratory Medicine
AU  - Hosgood, HDean III
AU  - Pao, William
AU  - Rothman, Nathaniel
AU  - Hu, Wei
AU  - Pan, Yumei Helen
AU  - Kuchinsky, Kyle
AU  - Jones, Kirk D
AU  - Xu, Jun
AU  - Vermeulen, Roel
AU  - Simko, Jeff
AU  - Lan, Qing
AD  - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI, NIH, DHHS, Bethesda, MD, USA
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1755
EP  - 1762
PB  - Elsevier B.V., Radarweg 29 Amsterdam 1043 NX Netherlands
VL  - 107
IS  - 11
SN  - 0954-6111, 0954-6111
KW  - Pollution Abstracts; Health & Safety Science Abstracts
KW  - Burning
KW  - China, People's Rep.
KW  - Mutation
KW  - P 0000:AIR POLLUTION
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464509963?accountid=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=Respiratory+Medicine&rft.atitle=Driver+mutations+among+never+smoking+female+lung+cancer+tissues+in+China+identify+unique+EGFR+and+KRAS+mutation+pattern+associated+with+household+coal+burning&rft.au=Hosgood%2C+HDean+III%3BPao%2C+William%3BRothman%2C+Nathaniel%3BHu%2C+Wei%3BPan%2C+Yumei+Helen%3BKuchinsky%2C+Kyle%3BJones%2C+Kirk+D%3BXu%2C+Jun%3BVermeulen%2C+Roel%3BSimko%2C+Jeff%3BLan%2C+Qing&rft.aulast=Hosgood&rft.aufirst=HDean&rft.date=2013-11-01&rft.volume=107&rft.issue=11&rft.spage=1755&rft.isbn=&rft.btitle=&rft.title=Respiratory+Medicine&rft.issn=09546111&rft_id=info:doi/10.1016%2Fj.rmed.2013.08.018
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Mutation; China, People's Rep.
DO  - http://dx.doi.org/10.1016/j.rmed.2013.08.018
ER  - 



TY  - JOUR
T1  - A review of non-cancer effects, especially circulatory and ocular diseases
AN  - 1464509923; 18750892
AB  - There is a well-established association between high doses (>5 Gy) of ionizing radiation exposure and damage to the heart and coronary arteries, although only recently have studies with high-quality individual dosimetry been conducted that would enable quantification of this risk adjusting for concomitant chemotherapy. The association between lower dose exposures and late occurring circulatory disease has only recently begun to emerge in the Japanese atomic bomb survivors and in various occupationally exposed cohorts and is still controversial. Excess relative risks per unit dose in moderate- and low-dose epidemiological studies are somewhat variable, possibly a result of confounding and effect modification by well-known (but unobserved) risk factors. Radiation doses of 1 Gy or more are associated with increased risk of posterior subcapsular cataract. Accumulating evidence from the Japanese atomic bomb survivors, Chernobyl liquidators, US astronauts, and various other exposed groups suggests that cortical cataracts may also be associated with ionizing radiation, although there is little evidence that nuclear cataracts are radiogenic. The dose-response appears to be linear, although modest thresholds (of no more than about 0.6 Gy) cannot be ruled out. A variety of other non-malignant effects have been observed after moderate/low-dose exposure in various groups, in particular respiratory and digestive disease and central nervous system (and in particular neuro-cognitive) damage. However, because these are generally only observed in isolated groups, or because the evidence is excessively heterogeneous, these associations must be treated with caution.
JF  - Radiation and Environmental Biophysics
AU  - Little, Mark P
AD  - Radiation Epidemiology Branch, National Cancer Institute, 9609 Medical Center Drive MSC 9778, Bethesda, MD, 20892-9778, USA, mark.little@nih.gov
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 435
EP  - 449
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 52
IS  - 4
SN  - 0301-634X, 0301-634X
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Central nervous system
KW  - Ukraine, Chernobyl
KW  - Cataracts
KW  - Chemotherapy
KW  - Atomic bombs
KW  - Dosimetry
KW  - Risk factors
KW  - Ionizing radiation
KW  - Reviews
KW  - Dose-response effects
KW  - Japan
KW  - Occupational exposure
KW  - H 1000:Occupational Safety and Health
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464509923?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Family+Violence&rft.atitle=Skin+Lesions+and+Other+Associated+Findings+in+Children+with+Abusive+Head+Trauma&rft.au=Luyet%2C+Francois+M%3BWipperfurth%2C+Jessica%3BPalm%2C+Amanda%3BKnox%2C+Barbara+L&rft.aulast=Luyet&rft.aufirst=Francois&rft.date=2016-10-01&rft.volume=31&rft.issue=7&rft.spage=805&rft.isbn=&rft.btitle=&rft.title=Journal+of+Family+Violence&rft.issn=08857482&rft_id=info:doi/10.1007%2Fs10896-016-9841-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 110
N1  - Last updated - 2015-05-27
N1  - SubjectsTermNotLitGenreText - Central nervous system; Cataracts; Chemotherapy; Dose-response effects; Reviews; Ionizing radiation; Risk factors; Dosimetry; Atomic bombs; Occupational exposure; Ukraine, Chernobyl; Japan
DO  - http://dx.doi.org/10.1007/s00411-013-0484-7
ER  - 



TY  - JOUR
T1  - EHP Paper of the Year, 2013.
AN  - 1462764976; 24284034
JF  - Environmental health perspectives
AU  - Tilson, Hugh A
AD  - Editor-in-Chief, EHP, E-mail: tilsonha@niehs.nih.gov.
PY  - 2013
SP  - 1
VL  - 121
IS  - 11-12
KW  - Index Medicus
KW  - History, 21st Century
KW  - Peer Review, Research -- standards
KW  - Environmental Health -- history
KW  - Environmental Health -- standards
KW  - Periodicals as Topic -- standards
KW  - Awards and Prizes
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1462764976?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=EHP+Paper+of+the+Year%2C+2013.&rft.au=Tilson%2C+Hugh+A&rft.aulast=Tilson&rft.aufirst=Hugh&rft.date=2013-11-01&rft.volume=121&rft.issue=11-12&rft.spage=A322&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1307850
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-28
N1  - Date created - 2013-11-28
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Environ Health Perspect. 2009 Feb;117(2):217-22 [19270791]
Environ Health Perspect. 2013 Sep;121(9):A266 [24004545]
Environ Health Perspect. 2012 Oct;120(10):1425-31 [22851337]
Environ Health Perspect. 2011 Jun;119(6):A238 [21628120]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1289/ehp.1307850
ER  - 



TY  - JOUR
T1  - Misconceptions about coercion and undue influence: reflections on the views of IRB members
AN  - 1459556686; 4503107
AB  - Payment to recruit research subjects is a common practice but raises ethical concerns relating to the potential for coercion or undue influence. We conducted the first national study of IRB members and human subjects protection professionals to explore attitudes as to whether and why payment of research participants constitutes coercion or undue influence. Upon critical evaluation of the cogency of ethical concerns regarding payment, as reflected in our survey results, we found expansive or inconsistent views about coercion and undue influence that may interfere with valuable research. In particular, respondents appear to believe that coercion and undue influence lie on a continuum; by contrast, we argue that they are wholly distinct: whereas undue influence is a cognitive distortion relating to assessment of risks and benefits, coercion is a threat of harm. Because payment is an offer, rather than a threat, payment is never coercive. Reprinted by permission of Blackwell Publishers
JF  - Bioethics
AU  - Largent, Emily
AU  - Grady, Christine
AU  - Miller, Franklin G
AU  - Wertheimer, Alan
AD  - Harvard University ; National Institutes of Health, Maryland ; National Institutes of Health ; University of Vermont
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 500
EP  - 507
VL  - 27
IS  - 9
SN  - 0269-9702, 0269-9702
KW  - Anthropology
KW  - Attitudes
KW  - Critical theory
KW  - Bioethics
KW  - Surveys
KW  - Professionalism
KW  - Payments
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1459556686?accountid=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=Bioethics&rft.atitle=Misconceptions+about+coercion+and+undue+influence%3A+reflections+on+the+views+of+IRB+members&rft.au=Largent%2C+Emily%3BGrady%2C+Christine%3BMiller%2C+Franklin+G%3BWertheimer%2C+Alan&rft.aulast=Largent&rft.aufirst=Emily&rft.date=2013-11-01&rft.volume=27&rft.issue=9&rft.spage=500&rft.isbn=&rft.btitle=&rft.title=Bioethics&rft.issn=02699702&rft_id=info:doi/10.1111%2Fj.1467-8519.2012.01972.x
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-11-18
N1  - Last updated - 2013-11-20
N1  - SubjectsTermNotLitGenreText - 1603 4408 8282 8281 6085; 9295; 1378 10404; 3041 12004 12008; 10300; 12429
DO  - http://dx.doi.org/10.1111/j.1467-8519.2012.01972.x
ER  - 



TY  - JOUR
T1  - Microbial natural products: molecular blueprints for antitumor drugs
AN  - 1458540312; 18733163
AB  - Microbes from two of the three domains of life, the Prokarya, and Eukarya, continue to serve as rich sources of structurally complex chemical scaffolds that have proven to be essential for the development of anticancer therapeutics. This review describes only a handful of exemplary natural products and their derivatives as well as those that have served as elegant blueprints for the development of novel synthetic structures that are either currently in use or in clinical or preclinical trials together with some of their earlier analogs in some cases whose failure to proceed aided in the derivation of later compounds. In every case, a microbe has been either identified as the producer of secondary metabolites or speculated to be involved in the production via symbiotic associations. Finally, rapidly evolving next-generation sequencing technologies have led to the increasing availability of microbial genomes. Relevant examples of genome mining and genetic manipulation are discussed, demonstrating that we have only barely scratched the surface with regards to harnessing the potential of microbes as sources of new pharmaceutical leads/agents or biological probes.
JF  - Journal of Industrial Microbiology & Biotechnology
AU  - Giddings, Lesley-Ann
AU  - Newman, David J
AD  - Natural Products Branch, Developmental Therapeutics Program, DCTD, Frederick National Laboratory for Cancer Research, P.O. Box B, Frederick, MD, 21702, USA, Lesley-Ann.Giddings@nih.gov
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1181
EP  - 1210
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 40
IS  - 11
SN  - 1367-5435, 1367-5435
KW  - Biotechnology and Bioengineering Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Genomes
KW  - DNA probes
KW  - Secondary metabolites
KW  - Pharmaceuticals
KW  - natural products
KW  - Drug development
KW  - Mining
KW  - Clinical trials
KW  - scaffolds
KW  - A 01450:Environmental Pollution & Waste Treatment
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458540312?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=NCI-60+whole+exome+sequencing+and+pharmacological+CellMiner+analyses.&rft.au=Reinhold%2C+William+C%3BVarma%2C+Sudhir%3BSousa%2C+Fabricio%3BSunshine%2C+Margot%3BAbaan%2C+Ogan+D%3BDavis%2C+Sean+R%3BReinhold%2C+Spencer+W%3BKohn%2C+Kurt+W%3BMorris%2C+Joel%3BMeltzer%2C+Paul+S%3BDoroshow%2C+James+H%3BPommier%2C+Yves&rft.aulast=Reinhold&rft.aufirst=William&rft.date=2014-01-01&rft.volume=9&rft.issue=7&rft.spage=e101670&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0101670
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 244
N1  - Last updated - 2015-05-27
N1  - SubjectsTermNotLitGenreText - Genomes; DNA probes; Pharmaceuticals; Secondary metabolites; Drug development; natural products; Mining; Clinical trials; scaffolds
DO  - http://dx.doi.org/10.1007/s10295-013-1331-1
ER  - 



TY  - JOUR
T1  - Mesenteric Vasculature-Guided Small Bowel Segmentation on 3-D CT
AN  - 1458539957; 18778376
AB  - Due to its importance and possible applications in visualization, tumor detection and preoperative planning, automatic small bowel segmentation is essential for computer-aided diagnosis of small bowel pathology. However, segmenting the small bowel directly on computed tomography (CT) scans is very difficult because of the low image contrast on CT scans and high tortuosity of the small bowel and its close proximity to other abdominal organs. Motivated by the intensity characteristics of abdominal CT images, the anatomic relationship between the mesenteric vasculature and the small bowel, and potential usefulness of the mesenteric vasculature for establishing the path of the small bowel, we propose a novel mesenteric vasculature map-guided method for small bowel segmentation on high-resolution CT angiography scans. The major mesenteric arteries are first segmented using a vessel tracing method based on multi-linear subspace vessel model and Bayesian inference. Second, multi-view, multi-scale vesselness enhancement filters are used to segment small vessels, and vessels directly or indirectly connecting to the superior mesenteric artery are classified as mesenteric vessels. Third, a mesenteric vasculature map is built by linking vessel bifurcation points, and the small bowel is segmented by employing the mesenteric vessel map and fuzzy connectness. The method was evaluated on 11 abdominal CT scans of patients suspected of having carcinoid tumors with manually labeled reference standard. The result, 82.5% volume overlap accuracy compared with the reference standard, shows it is feasible to segment the small bowel on CT scans using the mesenteric vasculature as a roadmap.
JF  - IEEE Transactions on Medical Imaging
AU  - Zhang, Weidong
AU  - Liu, Jiamin
AU  - Yao, Jianhua
AU  - Louie, Adeline
AU  - Nguyen, Tan B
AU  - Wank, Stephen
AU  - Nowinski, Wieslaw L
AU  - Summers, Ronald M
AD  - Imaging Biomarkers and Computer-Aided Diagnosis Lab, National Institutes of Health Clinical Center, USA
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 2006
EP  - 2021
PB  - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States
VL  - 32
IS  - 11
SN  - 0278-0062, 0278-0062
KW  - Biotechnology and Bioengineering Abstracts
KW  - Filters
KW  - Angiography
KW  - Mathematical models
KW  - Bayesian analysis
KW  - Arteries
KW  - Computed tomography
KW  - Intestine
KW  - Segmentation
KW  - Image processing
KW  - Tumors
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458539957?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mesenteric+Vasculature-Guided+Small+Bowel+Segmentation+on+3-D+CT&rft.au=Zhang%2C+Weidong%3BLiu%2C+Jiamin%3BYao%2C+Jianhua%3BLouie%2C+Adeline%3BNguyen%2C+Tan+B%3BWank%2C+Stephen%3BNowinski%2C+Wieslaw+L%3BSummers%2C+Ronald+M&rft.aulast=Zhang&rft.aufirst=Weidong&rft.date=2013-11-01&rft.volume=32&rft.issue=11&rft.spage=2006&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Medical+Imaging&rft.issn=02780062&rft_id=info:doi/10.1109%2FTMI.2013.2271487
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Filters; Angiography; Mathematical models; Bayesian analysis; Arteries; Computed tomography; Segmentation; Intestine; Image processing; Tumors
DO  - http://dx.doi.org/10.1109/TMI.2013.2271487
ER  - 



TY  - JOUR
T1  - Role of Yersinia pestis Toxin Complex Family Proteins in Resistance to Phagocytosis by Polymorphonuclear Leukocytes
AN  - 1458539036; 18745937
AB  - Yersinia pestis carries homologues of the toxin complex (Tc) family proteins, which were first identified in other Gram-negative bacteria as having potent insecticidal activity. The Y. pestis Tc proteins are neither toxic to fleas nor essential for survival of the bacterium in the flea, even though tc gene expression is highly upregulated and much more of the Tc proteins YitA and YipA are produced in the flea than when Y. pestis is grown in vitro. We show that Tc+ and Tc- Y. pestis strains are transmitted equivalently from coinfected fleas, further demonstrating that the Tc proteins have no discernible role, either positive or negative, in transmission by the flea vector. Tc proteins did, however, confer Y. pestis with increased resistance to killing by polymorphonuclear leukocytes (PMNs). Resistance to killing was not the result of decreased PMN viability or increased intracellular survival but instead correlated with a Tc protein-dependent resistance to phagocytosis that was independent of the type III secretion system (T3SS). Correspondingly, we did not detect T3SS-dependent secretion of the native Tc proteins YitA and YipA or the translocation of YitA- or YipA- beta -lactamase fusion proteins into CHO-K1 (CHO) cells or human PMNs. Thus, although highly produced by Y. pestis within the flea and related to insecticidal toxins, the Tc proteins do not affect interaction with the flea or transmission. Rather, the Y. pestis Tc proteins inhibit phagocytosis by mouse PMNs, independent of the T3SS, and may be important for subverting the mammalian innate immune response immediately following transmission from the flea.
JF  - Infection and Immunity
AU  - Spinner, Justin L
AU  - Carmody, Aaron B
AU  - Jarrett, Clayton O
AU  - Hinnebusch, B Joseph
AD  - Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, Justin.Spinner@nih.gov.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 4041
EP  - 4052
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 11
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Cell survival
KW  - Leukocytes (polymorphonuclear)
KW  - Gram-negative bacteria
KW  - Yersinia pestis
KW  - Fusion protein
KW  - Immune response
KW  - Phagocytosis
KW  - Translocation
KW  - Toxins
KW  - Disease transmission
KW  - double prime tc gene
KW  - J 02350:Immunology
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458539036?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Role+of+Yersinia+pestis+Toxin+Complex+Family+Proteins+in+Resistance+to+Phagocytosis+by+Polymorphonuclear+Leukocytes&rft.au=Spinner%2C+Justin+L%3BCarmody%2C+Aaron+B%3BJarrett%2C+Clayton+O%3BHinnebusch%2C+B+Joseph&rft.aulast=Spinner&rft.aufirst=Justin&rft.date=2013-11-01&rft.volume=81&rft.issue=11&rft.spage=4041&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00648-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 53
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Cell survival; Gram-negative bacteria; Leukocytes (polymorphonuclear); Immune response; Fusion protein; Phagocytosis; Translocation; Toxins; double prime tc gene; Disease transmission; Yersinia pestis
DO  - http://dx.doi.org/10.1128/IAI.00648-13
ER  - 



TY  - JOUR
T1  - Alcohol use and alcohol-use disorders among older adults in India: a literature review
AN  - 1449942689; 4502087
AB  - Objectives: With changing attitudes to alcohol and an increasing life span in India, the prevalence of alcohol use and misuse in successive cohorts of older people is likely to increase. In this paper, we attempt to review the most recent evidence covering alcohol use and alcohol-use disorders in the Indian elderly. Reprinted by permission of Taylor and Francis Ltd.
JF  - Aging and mental health
AU  - Nadkarni, Abhijit
AU  - Murthy, Pratima
AU  - Crome, Ilana B
AU  - Rao, Rahul
AD  - London School of Hygiene and Tropical Medicine ; National Institute of Mental Health and Neurosciences, Bangalore ; Keele University ; King's College London
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 979
EP  - 991
VL  - 17
IS  - 8
SN  - 1360-7863, 1360-7863
KW  - Sociology
KW  - Review articles
KW  - Alcohol
KW  - Attitudes
KW  - Alcoholism
KW  - Aged
KW  - Adults
KW  - Life expectancy
KW  - Evidence
KW  - India
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449942689?accountid=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=Aging+and+mental+health&rft.atitle=Alcohol+use+and+alcohol-use+disorders+among+older+adults+in+India%3A+a+literature+review&rft.au=Nadkarni%2C+Abhijit%3BMurthy%2C+Pratima%3BCrome%2C+Ilana+B%3BRao%2C+Rahul&rft.aulast=Nadkarni&rft.aufirst=Abhijit&rft.date=2013-11-01&rft.volume=17&rft.issue=8&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=Aging+and+mental+health&rft.issn=13607863&rft_id=info:doi/10.1080%2F13607863.2013.793653
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-11-11
N1  - Last updated - 2013-11-12
N1  - SubjectsTermNotLitGenreText - 10999; 909; 603; 654; 4560; 7397 8291 3409 6306; 1378 10404; 913 561 6220; 175 387 30
DO  - http://dx.doi.org/10.1080/13607863.2013.793653
ER  - 



TY  - JOUR
T1  - A phase 2 study of oxaliplatin combined with continuous infusion topotecan for patients with previously treated ovarian cancer.
AN  - 1448220317; 24172094
AB  - Phase 2 trials suggest that prolonged intravenous (IV) infusion of the topoisomerase 1 inhibitor topotecan may be less toxic than when given by standard IV bolus 5-day administration. Oxaliplatin exhibits efficacy in platinum-pretreated disease and shows preclinical synergy with topoisomerase 1 inhibitors. We sought to determine the efficacy and safety of oxaliplatin plus infusion topotecan in recurrent platinum-pretreated ovarian cancer.
          Patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancers previously treated with 1 to 2 prior regimens including platinum and taxane received oxaliplatin (85 mg/m(2) day 1 and day 15) and topotecan (0.4 mg/m(2) per day) by continuous IV infusion over 14 days every 4 weeks. The primary objective of the trial was to estimate the objective response rate in platinum-resistant disease (stratum 1) and in platinum-sensitive disease (stratum 2). Toxicities were assessed in all patients. Thirty-eight patients received 144 cycles of therapy (median, 4; range, 1-6). The most common grade 3 and grade 4 toxicities included thrombocytopenia (grade 3, 37%; and grade 4, 19%), neutropenia (grade 3, 37%; grade 4, 11%), and anemia (grade 3, 15%). Response occurred in 4 of 19 patients in stratum I (21%; 95% confidence intervals, 6%-46%) and 9 of 19 patients in stratum 2 (47%; 95% CI, 24%-71%). Three in each stratum had lengthy complete responses.
          Biweekly oxaliplatin plus a 14-day continuous IV infusion of topotecan, given monthly, is an active regimen in platinum-pretreated ovarian cancer and merits additional evaluation.
JF  - International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
AU  - Stein, Stacey M
AU  - Tiersten, Amy
AU  - Hochster, Howard S
AU  - Blank, Stephanie V
AU  - Pothuri, Bhavana
AU  - Curtin, John
AU  - Shapira, Ilan
AU  - Levinson, Benjamin
AU  - Ivy, Percy
AU  - Joseph, Benson
AU  - Guddati, Achuta Kumar
AU  - Muggia, Franco
AD  - *Division of Medical Oncology, Department of Medicine, Yale School of Medicine, New Haven, CT; †Division of Medical Oncology, Department of Medicine, and ‡Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY; §Beth Israel Cancer Center, Albert Einstein College of Medicine, NY; New York University School of Medicine, New York, NY, ∥Division of Biostatistics, Department of Population Health, New York University School of Medicine, New York, NY; ¶Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD; and #Department of Internal Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1577
EP  - 1582
VL  - 23
IS  - 9
KW  - Organoplatinum Compounds
KW  - 0
KW  - oxaliplatin
KW  - 04ZR38536J
KW  - Topotecan
KW  - 7M7YKX2N15
KW  - Index Medicus
KW  - Infusion Pumps
KW  - Aged, 80 and over
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - Female
KW  - Chemotherapy, Adjuvant
KW  - Survival Analysis
KW  - Topotecan -- adverse effects
KW  - Organoplatinum Compounds -- adverse effects
KW  - Organoplatinum Compounds -- administration & dosage
KW  - Neoplasms, Glandular and Epithelial -- drug therapy
KW  - Ovarian Neoplasms -- mortality
KW  - Neoplasms, Glandular and Epithelial -- mortality
KW  - Topotecan -- administration & dosage
KW  - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW  - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW  - Ovarian Neoplasms -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448220317?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+phase+2+study+of+oxaliplatin+combined+with+continuous+infusion+topotecan+for+patients+with+previously+treated+ovarian+cancer.&rft.au=Stein%2C+Stacey+M%3BTiersten%2C+Amy%3BHochster%2C+Howard+S%3BBlank%2C+Stephanie+V%3BPothuri%2C+Bhavana%3BCurtin%2C+John%3BShapira%2C+Ilan%3BLevinson%2C+Benjamin%3BIvy%2C+Percy%3BJoseph%2C+Benson%3BGuddati%2C+Achuta+Kumar%3BMuggia%2C+Franco&rft.aulast=Stein&rft.aufirst=Stacey&rft.date=2013-11-01&rft.volume=23&rft.issue=9&rft.spage=1577&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.0b013e3182a809e0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-01
N1  - Date created - 2013-10-31
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Lancet. 2003 Jun 21;361(9375):2099-106 [12826431]
J Clin Oncol. 2003 May 15;21(10 Suppl):187s-193s [12743133]
Control Clin Trials. 1989 Mar;10(1):1-10 [2702835]
Biochem Pharmacol. 1996 Dec 24;52(12):1855-65 [8951344]
Ann Oncol. 1996 Dec;7(10):1065-70 [9037366]
Semin Oncol. 1998 Apr;25(2 Suppl 5):4-12 [9609103]
Clin Cancer Res. 1997 Aug;3(8):1245-52 [9815806]
N Engl J Med. 2004 Dec 9;351(24):2519-29 [15590954]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078]
Clin Cancer Res. 2005 Aug 15;11(16):5912-9 [16115933]
Gynecol Oncol. 2006 Feb;100(2):324-9 [16253316]
J Clin Oncol. 2006 Oct 10;24(29):4699-707 [16966687]
Gynecol Oncol. 2008 Mar;108(3):500-4 [18191187]
Cancer. 2008 May 15;112(10):2289-300 [18393325]
Br J Cancer. 2009 Feb 24;100(4):601-7 [19190632]
Gynecol Oncol. 2010 May;117(2):152-8 [20056266]
J Clin Oncol. 2010 Jul 10;28(20):3323-9 [20498395]
Int J Gynecol Cancer. 2010 Aug;20(6):953-7 [20683401]
CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300 [20610543]
J Clin Oncol. 2012 Jun 10;30(17):2039-45 [22529265]
Br J Cancer. 2012 Aug 7;107(4):588-91 [22836511]
J Clin Oncol. 1999 Aug;17(8):2553-61 [10561322]
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437]
J Clin Oncol. 2001 Jul 15;19(14):3312-22 [11454878]
Ann Oncol. 2002 Mar;13(3):392-8 [11996469]
Clin Cancer Res. 2004 Jun 1;10(11):3919-26 [15173101]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/IGC.0b013e3182a809e0
ER  - 



TY  - JOUR
T1  - Oxaliplapin and capecitabine (XELOX) based chemotherapy in the treatment of metastatic colorectal cancer: the right choice in elderly patients.
AN  - 1447499478; 24102280
AB  - Elderly patients with metastatic colorectal cancer (mCRC) differ from the general population and are underrepresented in clinical trials. We, retrospectively, analyzed the safety and efficacy of XELOX regimen in the treatment of elderly patients affected by mCRC.
          One-hundred-eleven consecutive patients, aged 70 years or older, were enrolled in the study. All patients were evaluated for safety and efficacy (male/female, 63/48). Median age was 75 years (range 71-85 years). Median Eastern Cooperative Oncology Group Performance Status (ECOG PS) was 0 (range 0-2). Metastatic sites distribution is as follows: liver (44.1%), lung (13.5%), liver plus lung (12.6%) and other (29.7%). A total of 584 cycles were administered (median 6 cycles/patient, range 2-10). Median follow-up time was 14.5 months (range 1-41 months). In an intent-to-treat analysis, objective responses and stable disease were recorded in 41 (40.4%) and 29 (26.6%) patients, respectively. The median response duration was 5.9 months (range 0.5-28.8). The median progression free-survival (PFS) was 7.5 months (range 1-26 months). The median overall survival (OS) was 15 months (range 1-64 months). The grade 3 toxicities were: neutropenia (8.1%), diarrhea and neurotoxicity (5.4% respectively). Most adverse events were mild to moderate; the most common was acute sensory neuropathy (57.6%).
          XELOX is a highly effective first-line treatment for mCRC elderly patients. Response rates, PFS and OS are similar to those observed with fluorouracil/leucovorin/oxaliplatin combinations. XELOX is a convenient regimen, likely to be preferred by both patient and healthcare providers.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Berretta, Massimiliano
AU  - Aprile, Giuseppe
AU  - Nasti, Guglielmo
AU  - Urbani, Martina
AU  - Bearz, Alessandra
AU  - Lutrino, Stefania
AU  - Foltran, Luisa
AU  - Ferrari, Laura
AU  - Talamini, Renato
AU  - Fiorica, Francesco
AU  - Lleshi, Arben
AU  - Canzonieri, Vincenzo
AU  - Lestuzzi, Chiara
AU  - Borsatti, Eugenio
AU  - Fisichella, Rossella
AU  - Tirelli, Umberto
AD  - Department of Medical Oncology, National Cancer Institute, Aviano (PN) Italy, Via Franco Gallini 2, 33081 Aviano (PN), Italy. mberretta@cro.it.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1344
EP  - 1353
VL  - 13
IS  - 9
KW  - Deoxycytidine
KW  - 0W860991D6
KW  - Fluorouracil
KW  - U3P01618RT
KW  - Index Medicus
KW  - Aged, 80 and over
KW  - Neoplasm Metastasis -- drug therapy
KW  - Humans
KW  - Retrospective Studies
KW  - Disease Progression
KW  - Aged
KW  - Male
KW  - Female
KW  - Survival Analysis
KW  - Fluorouracil -- therapeutic use
KW  - Fluorouracil -- adverse effects
KW  - Colorectal Neoplasms -- diagnosis
KW  - Deoxycytidine -- adverse effects
KW  - Colorectal Neoplasms -- pathology
KW  - Deoxycytidine -- analogs & derivatives
KW  - Fluorouracil -- analogs & derivatives
KW  - Deoxycytidine -- therapeutic use
KW  - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Colorectal Neoplasms -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447499478?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oxaliplapin+and+capecitabine+%28XELOX%29+based+chemotherapy+in+the+treatment+of+metastatic+colorectal+cancer%3A+the+right+choice+in+elderly+patients.&rft.au=Berretta%2C+Massimiliano%3BAprile%2C+Giuseppe%3BNasti%2C+Guglielmo%3BUrbani%2C+Martina%3BBearz%2C+Alessandra%3BLutrino%2C+Stefania%3BFoltran%2C+Luisa%3BFerrari%2C+Laura%3BTalamini%2C+Renato%3BFiorica%2C+Francesco%3BLleshi%2C+Arben%3BCanzonieri%2C+Vincenzo%3BLestuzzi%2C+Chiara%3BBorsatti%2C+Eugenio%3BFisichella%2C+Rossella%3BTirelli%2C+Umberto&rft.aulast=Berretta&rft.aufirst=Massimiliano&rft.date=2013-11-01&rft.volume=13&rft.issue=9&rft.spage=1344&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 - 2014-12-28
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - Autologus stem cell transplatation as a care option in elderly patients. A review.
AN  - 1447499267; 24102271
AB  - The ageing population and the increase in life expectancy have put new social and health questions into the public health agenda of western countries. Hematological cancer incidence peaks in older population as a logical consequence of a longer lifespan promoting prolonged exposure to carcinogens and accumulation of genetic alterations. Hematological cancer represents a major cause of mortality in this age group despite recent progress observed in the management of cancer in the general population. Autologous stem cell transplantation (ASCT) represents a therapeutic option in the treatment of a large proportion of lymphomas and multiple myeloma, but their role in the onco-geriatric setting remains an open question, due to the presence of chronic disease. Ageing is characterized by progressive decrements in physiologic reserves and abilities to compensate for physical and/or functional limitations, which increase the risk of developing morbidity and disability. These events explains the extreme diversity of ageing individuals in terms of clinical and functional status. As a consequence, life expectancy in the elderly is influenced not only by the neoplastic diseases itself but also by the various co-morbidities common to this age group. The management of elderly people with hematological diseases potentially curative, should therefore combine both geriatric and tumor assessments. Among the elderly patients identified as being candidates for AHSCT, after the mobilization of progenitor cells from the bone marrow into the peripheral blood, the aphaeresis procedure is the most common method for collecting an adequate number of stem cells. The proper selection of patients may greatly improve the results and the toxicity related to cancer treatment in the elderly. We recommend the adoption of some form of geriatric assessment in the evaluation of any patient who is 70 years and older, this review intends to offer an overview of the state of art in ASCT in elderly patients.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Fratino, Lucia
AU  - Rupolo, Maurizio
AU  - Mazzuccato, Mario
AU  - Berretta, Massimiliano
AU  - Lleshi, Arben
AU  - Tirelli, Umberto
AU  - Michieli, Mariagrazia
AD  - Division of Medical Oncology A, National Cancer Institute, Via Franco Gallini 2, 33081 Aviano (PN), Italy. lfratino@cro.it.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1419
EP  - 1429
VL  - 13
IS  - 9
KW  - Index Medicus
KW  - Aged, 80 and over
KW  - Humans
KW  - Aged
KW  - Transplantation, Autologous
KW  - Quality Assurance, Health Care
KW  - Neoplasms -- therapy
KW  - Hematopoietic Stem Cell Transplantation -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447499267?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Autologus+stem+cell+transplatation+as+a+care+option+in+elderly+patients.+A+review.&rft.au=Fratino%2C+Lucia%3BRupolo%2C+Maurizio%3BMazzuccato%2C+Mario%3BBerretta%2C+Massimiliano%3BLleshi%2C+Arben%3BTirelli%2C+Umberto%3BMichieli%2C+Mariagrazia&rft.aulast=Fratino&rft.aufirst=Lucia&rft.date=2013-11-01&rft.volume=13&rft.issue=9&rft.spage=1419&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 - 2014-12-28
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - BH4 domain of bcl-2 protein is required for its proangiogenic function under hypoxic condition.
AN  - 1447499220; 23836782
AB  - Beyond its classical role as apoptosis inhibitor, bcl-2 protein promotes tumor angiogenesis and the removal of N-terminal bcl-2 homology (BH4) domain abrogates bcl-2-induced hypoxia-inducible factor 1 (HIF-1)-mediated vascular endothelial growth factor (VEGF) expression in hypoxic cancer cells. Using M14 human melanoma cell line and its derivative clones stably overexpressing bcl-2 wild-type or deleted of its BH4 domain, we found that conditioned media (CM) from cells expressing BH4-deleted bcl-2 protein showed a reduced capability to increase in vitro human endothelial cells proliferation and differentiation, and in vivo neovascularization compared with CM from cells overexpressing wild-type bcl-2. Moreover, xenografts derived from cells expressing bcl-2 lacking BH4 domain showed a reduction of metastatic potential compared with tumors derived from wild-type bcl-2 transfectants injection. Stably expressing the Flag-tagged N-terminal sequence of bcl-2 protein, encompassing BH4 domain, we found that this domain is sufficient to enhance the proangiogenic HIF-1/VEGF axis under hypoxic condition. Indeed, lacking of BH4 domain abolishes the interaction between bcl-2 and HIF-1α proteins and the capability of exogenous bcl-2 protein to localize in the nucleus. Moreover, when endoplasmic reticulum-targeted bcl-2 protein is overexpressed in cells, this protein lost the capability to synergize with hypoxia to induce the proangiogenic HIF-1/VEGF axis as shown by wild-type bcl-2 protein. These results demonstrate that BH4 domain of bcl-2 is required for the ability of this protein to increase tumor angiogenesis and progression and indicate that bcl-2 nuclear localization may be required for bcl-2-mediated induction of HIF-1/VEGF axis.
JF  - Carcinogenesis
AU  - Gabellini, Chiara
AU  - De Luca, Teresa
AU  - Trisciuoglio, Daniela
AU  - Desideri, Marianna
AU  - Di Martile, Marta
AU  - Passeri, Daniela
AU  - Candiloro, Antonio
AU  - Biffoni, Mauro
AU  - Rizzo, Maria Giulia
AU  - Orlandi, Augusto
AU  - Del Bufalo, Donatella
AD  - Experimental Chemotherapy Laboratory, Regina Elena National Cancer Institute, Rome 00158, Italy.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 2558
EP  - 2567
VL  - 34
IS  - 11
KW  - Hypoxia-Inducible Factor 1, alpha Subunit
KW  - 0
KW  - Proto-Oncogene Proteins c-bcl-2
KW  - RNA, Messenger
KW  - Vascular Endothelial Growth Factor A
KW  - Index Medicus
KW  - Real-Time Polymerase Chain Reaction
KW  - Heterografts
KW  - Animals
KW  - Apoptosis
KW  - Wound Healing
KW  - Humans
KW  - Immunoprecipitation
KW  - Mice, Nude
KW  - Mice
KW  - Reverse Transcriptase Polymerase Chain Reaction
KW  - RNA, Messenger -- genetics
KW  - Cell Proliferation
KW  - Gene Expression Regulation, Neoplastic
KW  - Blotting, Western
KW  - Cells, Cultured
KW  - Proto-Oncogene Proteins c-bcl-2 -- metabolism
KW  - Proto-Oncogene Proteins c-bcl-2 -- genetics
KW  - Protein Structure, Tertiary
KW  - Protein Interaction Domains and Motifs
KW  - Fluorescent Antibody Technique
KW  - Immunoenzyme Techniques
KW  - Human Umbilical Vein Endothelial Cells -- cytology
KW  - Human Umbilical Vein Endothelial Cells -- metabolism
KW  - Lung Neoplasms -- blood supply
KW  - Lung Neoplasms -- secondary
KW  - Neovascularization, Pathologic -- metabolism
KW  - Hypoxia-Inducible Factor 1, alpha Subunit -- metabolism
KW  - Melanoma -- metabolism
KW  - Neovascularization, Pathologic -- pathology
KW  - Melanoma -- blood supply
KW  - Hypoxia-Inducible Factor 1, alpha Subunit -- genetics
KW  - Melanoma -- pathology
KW  - Hypoxia
KW  - Vascular Endothelial Growth Factor A -- genetics
KW  - Vascular Endothelial Growth Factor A -- metabolism
KW  - Lung Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447499220?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=BH4+domain+of+bcl-2+protein+is+required+for+its+proangiogenic+function+under+hypoxic+condition.&rft.au=Gabellini%2C+Chiara%3BDe+Luca%2C+Teresa%3BTrisciuoglio%2C+Daniela%3BDesideri%2C+Marianna%3BDi+Martile%2C+Marta%3BPasseri%2C+Daniela%3BCandiloro%2C+Antonio%3BBiffoni%2C+Mauro%3BRizzo%2C+Maria+Giulia%3BOrlandi%2C+Augusto%3BDel+Bufalo%2C+Donatella&rft.aulast=Gabellini&rft.aufirst=Chiara&rft.date=2013-11-01&rft.volume=34&rft.issue=11&rft.spage=2558&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt242
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-22
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/carcin/bgt242
ER  - 



TY  - JOUR
T1  - Gastrointestinal non colorectal cancer. Do elderly patients need a specific management?
AN  - 1447499060; 24102272
AB  - Elderly patients (65 years and over) develop often, sometimes predominantly , esophageal, gastro esophageal junction, gastric and pancreatic cancer (gastrointestinal non colorectal cancer). Most clinical trials exclude elderly patients from accrual considering aging a potential risk factor. In fact an elderly patient can develop greater toxicity than a younger patient from oncologic treatments (chemotherapy, radiotherapy, target therapies) due to a worse function of vital organs.
          We analyzed the current scientific literature, searching articles since 1990, about gastrointestinal non colorectal cancer in elderly patients, to establish if they need a specific management, different from younger patients. Data from analyzed studies, both gastro esophageal and pancreatic cancer, are contradictory. In some reports elderly patients don't seem to bring greater toxicity than younger. Other trials consider that dose-adjustment to renal function is need in elderly patients, but these trials are very few. Other trials may include several biases such as accrual of "only fit" elderly patients.
          It is very important in elderly patients with higher risk of toxicity, to distinguish the aim of cancer treatment: is it curative or palliative? Furthermore, in this type of patients the most important target is probably maintaining the quality of life especially in gastric and pancreatic cancer that often started as advanced disease. For these valuation chronological age alone is not sufficient. Another very important factor in elderly cancer patients is the geriatric assessment including not only age but also functional, social and mental status.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Silvestro, Lucrezia
AU  - Nasti, Guglielmo
AU  - Ottaiano, Alessandro
AU  - Montano, Massimo
AU  - Casaretti, Rossana
AU  - Avallone, Antonio
AU  - Berretta, Massimiliano
AU  - Romano, Carmela
AU  - Cassata, Antonio
AU  - Tafuto, Salvatore
AU  - Iaffaioli, Rosario Vincenzo
AD  - Department of Abdominal Oncology, National Cancer Institute "G. Pascale"- Via M.Semmola, 80131 Naples, Italy. l.silvestro@istitutotumori.na.it.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1364
EP  - 1370
VL  - 13
IS  - 9
KW  - Index Medicus
KW  - Humans
KW  - Quality of Life
KW  - Palliative Care
KW  - Aged
KW  - Geriatric Assessment
KW  - Pancreatic Neoplasms -- diagnosis
KW  - Pancreatic Neoplasms -- therapy
KW  - Stomach Neoplasms -- therapy
KW  - Stomach Neoplasms -- diagnosis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447499060?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gastrointestinal+non+colorectal+cancer.+Do+elderly+patients+need+a+specific+management%3F&rft.au=Silvestro%2C+Lucrezia%3BNasti%2C+Guglielmo%3BOttaiano%2C+Alessandro%3BMontano%2C+Massimo%3BCasaretti%2C+Rossana%3BAvallone%2C+Antonio%3BBerretta%2C+Massimiliano%3BRomano%2C+Carmela%3BCassata%2C+Antonio%3BTafuto%2C+Salvatore%3BIaffaioli%2C+Rosario+Vincenzo&rft.aulast=Silvestro&rft.aufirst=Lucrezia&rft.date=2013-11-01&rft.volume=13&rft.issue=9&rft.spage=1364&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 - 2014-12-28
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - Treatment of elderly patients affected by lung cancer: why to treat, when to treat and what we know.
AN  - 1447499022; 24102274
AB  - In the recent years many advances have been achieved in the field of the treatment of lung cancer; with the development of novel therapeutic pathways due to the knowledge of oncologic drivers involved in the carcinogenesis of the lung, as well as the involvement of new radiotherapic and surgical techniques. Nevertheless, the standard treatment for elderly is still debated, mainly because of an underrepresentation of elderly patients in clinical trials. Herein we try to summarize the main guidelines for the treatment of lung cancer, with particular attention for the elderly patients, what we know and what has changed.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Bearz, Alessandra
AU  - Berretta, Massimiliano
AU  - Lleshi, Arben
AU  - Berto, Eleonora
AU  - Tirelli, Umberto
AD  - Department of Medical Oncology, National Cancer Institute of Aviano, via Franco Gallini 2, 33081 Aviano (PN), Italy. abearz@cro.it.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1378
EP  - 1382
VL  - 13
IS  - 9
KW  - Index Medicus
KW  - Aged, 80 and over
KW  - Humans
KW  - Aged
KW  - Lung Neoplasms -- therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447499022?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+of+elderly+patients+affected+by+lung+cancer%3A+why+to+treat%2C+when+to+treat+and+what+we+know.&rft.au=Bearz%2C+Alessandra%3BBerretta%2C+Massimiliano%3BLleshi%2C+Arben%3BBerto%2C+Eleonora%3BTirelli%2C+Umberto&rft.aulast=Bearz&rft.aufirst=Alessandra&rft.date=2013-11-01&rft.volume=13&rft.issue=9&rft.spage=1378&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 - 2014-12-28
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - Innate immunity gene polymorphisms and the risk of colorectal neoplasia.
AN  - 1447498917; 23803696
AB  - Inherited variation in genes that regulate innate immunity and inflammation may contribute to colorectal neoplasia risk. To evaluate this association, we conducted a nested case-control study of 451 colorectal cancer cases, 694 colorectal advanced adenoma cases and 696 controls of European descent within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. A total of 935 tag single-nucleotide polymorphisms (SNPs) in 98 genes were evaluated. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association with colorectal neoplasia. Sixteen SNPs were associated with colorectal neoplasia risk at P < 0.01, but after adjustment for multiple testing, only rs2838732 (ITGB2) remained suggestively associated with colorectal neoplasia (OR(per T allele) = 0.68, 95% CI: 0.57-0.83, P = 7.7 × 10(-5), adjusted P = 0.07). ITGB2 codes for the CD18 protein in the integrin beta chain family. The ITGB2 association was stronger for colorectal cancer (OR(per T allele) = 0.41, 95% CI: 0.30-0.55, P = 2.4 × 10(-) (9)) than for adenoma (OR(per T allele) = 0.84, 95%CI: 0.69-1.03, P = 0.08), but it did not replicate in the validation study. The ITGB2 rs2838732 association was significantly modified by smoking status (P value for interaction = 0.003). Among never and former smokers, it was inversely associated with colorectal neoplasia (OR(per T allele) = 0.5, 95% CI: 0.37-0.69 and OR(per T allele) = 0.72, 95% CI: 0.54-0.95, respectively), but no association was seen among current smokers. Other notable findings were observed for SNPs in BPI/LBP and MYD88. Although the results need to be replicated, our findings suggest that genetic variation in inflammation-related genes may be related to the risk of colorectal neoplasia.
JF  - Carcinogenesis
AU  - Chang, Cindy M
AU  - Chia, Victoria M
AU  - Gunter, Marc J
AU  - Zanetti, Krista A
AU  - Ryan, Bríd M
AU  - Goodman, Julie E
AU  - Harris, Curtis C
AU  - Weissfeld, Joel
AU  - Huang, Wen-Yi
AU  - Chanock, Stephen
AU  - Yeager, Meredith
AU  - Hayes, Richard B
AU  - Berndt, Sonja I
AU  - Genetics and Epidemiology of Colorectal Cancer Consortium
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20892, USA. ; Genetics and Epidemiology of Colorectal Cancer Consortium
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 2512
EP  - 2520
VL  - 34
IS  - 11
KW  - Biomarkers, Tumor
KW  - 0
KW  - Index Medicus
KW  - Prospective Studies
KW  - Neoplasm Staging
KW  - Risk Factors
KW  - Humans
KW  - Prognosis
KW  - Case-Control Studies
KW  - Aged
KW  - Middle Aged
KW  - Follow-Up Studies
KW  - Gene-Environment Interaction
KW  - Male
KW  - Female
KW  - Biomarkers, Tumor -- genetics
KW  - Colorectal Neoplasms -- pathology
KW  - Inflammation -- genetics
KW  - Colorectal Neoplasms -- etiology
KW  - Adenoma -- etiology
KW  - Immunity, Innate -- genetics
KW  - Adenoma -- pathology
KW  - Polymorphism, Single Nucleotide -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447498917?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Innate+immunity+gene+polymorphisms+and+the+risk+of+colorectal+neoplasia.&rft.au=Chang%2C+Cindy+M%3BChia%2C+Victoria+M%3BGunter%2C+Marc+J%3BZanetti%2C+Krista+A%3BRyan%2C+Br%C3%ADd+M%3BGoodman%2C+Julie+E%3BHarris%2C+Curtis+C%3BWeissfeld%2C+Joel%3BHuang%2C+Wen-Yi%3BChanock%2C+Stephen%3BYeager%2C+Meredith%3BHayes%2C+Richard+B%3BBerndt%2C+Sonja+I%3BGenetics+and+Epidemiology+of+Colorectal+Cancer+Consortium&rft.aulast=Chang&rft.aufirst=Cindy&rft.date=2013-11-01&rft.volume=34&rft.issue=11&rft.spage=2512&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt228
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-22
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Int J Cancer. 2010 Dec 15;127(12):2822-30 [21351261]
Cardiovasc Res. 2011 Jun 1;90(3):475-83 [21285293]
World J Gastroenterol. 2011 May 14;17(18):2326-31 [21633598]
Int J Obes (Lond). 2011 Dec;35(12):1530-8 [21343904]
Hum Genet. 2012 Feb;131(2):217-34 [21761138]
Cancer Res. 2012 Mar 15;72(6):1467-77 [22282660]
J Natl Cancer Inst. 2012 Oct 3;104(19):1433-57 [23019048]
Ann Oncol. 2013 Apr;24(4):1079-87 [23211939]
Gastroenterology. 2013 Apr;144(4):799-807.e24 [23266556]
Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684]
Gut. 2001 Apr;48(4):526-35 [11247898]
Am J Hum Genet. 2002 Feb;70(2):425-34 [11791212]
J Natl Cancer Inst. 2002 Feb 20;94(4):252-66 [11854387]
J Clin Invest. 2003 Dec;112(12):1796-808 [14679176]
Am J Hum Genet. 2004 Jan;74(1):106-20 [14681826]
Cell. 2004 Aug 6;118(3):285-96 [15294155]
J Pharmacol Exp Ther. 2004 Oct;311(1):123-30 [15161935]
J Pediatr. 1982 Dec;101(6):932-40 [7143170]
Carcinogenesis. 1993 Aug;14(8):1493-7 [8353834]
J Periodontal Res. 1998 Aug;33(6):359-68 [9777587]
Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300]
Carcinogenesis. 2005 Jul;26(7):1182-95 [15790591]
Nature. 2006 May 25;441(7092):431-6 [16724054]
Gastroenterology. 2006 Dec;131(6):1683-9 [17188959]
Cancer Res. 2007 Feb 1;67(3):1395-404 [17283177]
Lancet. 2007 May 12;369(9573):1603-13 [17499602]
Science. 2007 Jul 6;317(5834):124-7 [17615359]
Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901]
Histol Histopathol. 2007 Dec;22(12):1387-98 [17701919]
Cancer Causes Control. 2007 Dec;18(10):1095-105 [17694420]
Mutat Res. 2007 Nov 1;624(1-2):88-100 [17544013]
Gastroenterology. 2007 Dec;133(6):1869-81 [18054559]
Cancer Res. 2008 Jan 1;68(1):323-8 [18172326]
Lancet. 2008 Feb 16;371(9612):569-78 [18280327]
Science. 2008 Aug 1;321(5889):691-6 [18669862]
JAMA. 2008 Dec 17;300(23):2765-78 [19088354]
J Natl Cancer Inst. 2009 Feb 18;101(4):256-66 [19211452]
Int J Cancer. 2009 May 15;124(10):2406-15 [19142968]
Ann N Y Acad Sci. 2009 Sep;1173:108-23 [19758139]
Cancer Causes Control. 2009 Nov;20(9):1739-51 [19760027]
Lancet Oncol. 2009 Nov;10(11):1033-4 [19891056]
Cancer Res. 2010 Mar 1;70(5):1749-52 [20145153]
Br J Cancer. 2010 Mar 2;102(5):908-15 [20145615]
Gastroenterology. 2010 Jun;138(6):2101-2114.e5 [20420949]
Carcinogenesis. 2010 Sep;31(9):1604-11 [20622004]
Genet Epidemiol. 2010 Dec;34(8):816-34 [21058334]
Lancet. 2010 Nov 20;376(9754):1741-50 [20970847]
Mutat Res. 2011 Jan 10;706(1-2):13-20 [21035469]
Lancet. 2011 Jan 1;377(9759):31-41 [21144578]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/carcin/bgt228
ER  - 



TY  - JOUR
T1  - Management of elderly patients with diffuse large B-cell lymphomas.
AN  - 1447498301; 24102270
AB  - Life expectancy has impressively increased over the past century and the US population over 65 years is rapidly growing, especially those over 80 years. In fact, persons older than 80 years have increased by more than 250% between the years 1960 and 2000, and it is expected that the population aged >75 years will triple by the year 2030. With the increase of the geriatric population, there is a need for the development and validation of treatment strategies for NHL for these patients. Therapy in elderly patients needs special attention because older patients usually suffered of several co-morbidities and their management represents a challenge for physicians. In fact, older patients treated for lymphoma may not tolerate the high-dose therapies used in younger patients and have increased risk of therapy-related toxicity as a result of age-related physiological changes and frequent co-morbidities. The widespread use of a comprehensive geriatric assessment tool might overcome the difficulty to run prospective clinical trial in elderly patients with lymphoma.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Ciancia, Rosanna
AU  - Tirelli, Umberto
AU  - Ribera, Josep- Maria
AU  - Spina, Michele
AD  - Division of Medical Oncology A, National Cancer Institute of Aviano, Via Franco Gallini 2, 33081 Aviano (PN), Italy. mspina@cro.it.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1412
EP  - 1418
VL  - 13
IS  - 9
KW  - Index Medicus
KW  - Aged, 80 and over
KW  - Humans
KW  - Aged
KW  - Lymphoma, Large B-Cell, Diffuse -- drug therapy
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Lymphoma, Large B-Cell, Diffuse -- diagnosis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447498301?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Management+of+elderly+patients+with+diffuse+large+B-cell+lymphomas.&rft.au=Ciancia%2C+Rosanna%3BTirelli%2C+Umberto%3BRibera%2C+Josep-+Maria%3BSpina%2C+Michele&rft.aulast=Ciancia&rft.aufirst=Rosanna&rft.date=2013-11-01&rft.volume=13&rft.issue=9&rft.spage=1412&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 - 2014-12-28
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - Colorectal cancer in elderly patients: from best supportive care to cure.
AN  - 1447498232; 24102277
AB  - Colorectal cancer is one of the major causes of cancer mortality in the elderly population (median age at diagnosis of 71 years) in Western Countries. Moreover patients with metastatic disease are often elderly with significant co- morbidities. Unfortunately, elderly patients are often untreated and under-represented in clinical trials, even if most clinical trials that have included this setting of population have shown similar survival rates and toxicities to younger patients. Age itself should not be considered for candidacy to chemotherapy but it should be taken in consideration the great heterogeneity of co-morbidities present in the elderly population. Therefore, the best treatment strategy for elderly colorectal cancer patients has not yet been defined. Comprehensive Geriatric Assessment is recommended to evaluate the best strategy treatment and to reduce the adverse events. In fact, while fit elderly patients could receive the same therapeutic treatment as the younger counterpart, a palliative approach should be taken in consideration for frail elderly patients and for those with a short life expectancy.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Berretta, Massimiliano
AU  - Di Benedetto, Fabrizio
AU  - Di Francia, Raffaele
AU  - Lo Menzo, Emanuele
AU  - Palmeri, Sergio
AU  - De Paoli, Paolo
AU  - Tirelli, Umberto
AD  - Department of Medical Oncology, National Cancer Institute, Via Franco Gallini 2 - 33081 Aviano (PN) - Italy. mberretta@cro.it.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1332
EP  - 1343
VL  - 13
IS  - 9
KW  - Index Medicus
KW  - Aged, 80 and over
KW  - Humans
KW  - Aged
KW  - Antineoplastic Combined Chemotherapy Protocols -- chemistry
KW  - Quality of Health Care
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Colorectal Neoplasms -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447498232?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Efficient+drug+delivery+of+Paclitaxel+glycoside%3A+a+novel+solubility+gradient+encapsulation+into+liposomes+coupled+with+immunoliposomes+preparation.&rft.au=Shigehiro%2C+Tsukasa%3BKasai%2C+Tomonari%3BMurakami%2C+Masaharu%3BSekhar%2C+Sreeja+C%3BTominaga%2C+Yuki%3BOkada%2C+Masashi%3BKudoh%2C+Takayuki%3BMizutani%2C+Akifumi%3BMurakami%2C+Hiroshi%3BSalomon%2C+David+S%3BMikuni%2C+Katsuhiko%3BMandai%2C+Tadakatsu%3BHamada%2C+Hiroki%3BSeno%2C+Masaharu&rft.aulast=Shigehiro&rft.aufirst=Tsukasa&rft.date=2014-01-01&rft.volume=9&rft.issue=9&rft.spage=e107976&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0107976
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-12-28
N1  - Date created - 2013-10-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - Neuroprotection and lifespan extension in Ppt1(-/-) mice by NtBuHA: therapeutic implications for INCL.
AN  - 1447105530; 24056696
AB  - Infantile neuronal ceroid lipofuscinosis (INCL) is a devastating childhood neurodegenerative lysosomal storage disease (LSD) that has no effective treatment. It is caused by inactivating mutations in the palmitoyl-protein thioesterase-1 (PPT1) gene. PPT1 deficiency impairs the cleavage of thioester linkage in palmitoylated proteins (constituents of ceroid), preventing degradation by lysosomal hydrolases. Consequently, accumulation of lysosomal ceroid leads to INCL. Thioester linkage is cleaved by nucleophilic attack. Hydroxylamine, a potent nucleophilic cellular metabolite, may have therapeutic potential for INCL, but its toxicity precludes clinical application. We found that a hydroxylamine derivative, N-(tert-Butyl) hydroxylamine (NtBuHA), was non-toxic, cleaved thioester linkage in palmitoylated proteins and mediated lysosomal ceroid depletion in cultured cells from INCL patients. In Ppt1(-/-) mice, which mimic INCL, NtBuHA crossed the blood-brain barrier, depleted lysosomal ceroid, suppressed neuronal apoptosis, slowed neurological deterioration and extended lifespan. Our findings provide a proof of concept that thioesterase-mimetic and antioxidant small molecules such as NtBuHA are potential drug targets for thioesterase deficiency diseases such as INCL.
JF  - Nature neuroscience
AU  - Sarkar, Chinmoy
AU  - Chandra, Goutam
AU  - Peng, Shiyong
AU  - Zhang, Zhongjian
AU  - Liu, Aiyi
AU  - Mukherjee, Anil B
AD  - 1] Section on Developmental Genetics, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA. [2].
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1608
EP  - 1617
VL  - 16
IS  - 11
KW  - Carbon Isotopes
KW  - 0
KW  - Hydroxylamines
KW  - N-(tert-butyl)hydroxylamine
KW  - Neuroprotective Agents
KW  - Palmitoyl Coenzyme A
KW  - 1763-10-6
KW  - Thiolester Hydrolases
KW  - EC 3.1.2.-
KW  - palmitoyl-protein thioesterase
KW  - EC 3.1.2.22
KW  - Index Medicus
KW  - Animals
KW  - Neurons -- metabolism
KW  - Dose-Response Relationship, Drug
KW  - Neurons -- drug effects
KW  - Longevity -- drug effects
KW  - Palmitoyl Coenzyme A -- metabolism
KW  - Disease Models, Animal
KW  - Mice
KW  - Neurons -- ultrastructure
KW  - Mice, Knockout
KW  - Gene Expression Regulation -- genetics
KW  - Apoptosis -- genetics
KW  - Palmitoyl Coenzyme A -- drug effects
KW  - Carbon Isotopes -- metabolism
KW  - Cells, Cultured
KW  - Longevity -- genetics
KW  - Cerebral Cortex -- pathology
KW  - Apoptosis -- drug effects
KW  - Mice, Inbred C57BL
KW  - Gene Expression Regulation -- drug effects
KW  - Time Factors
KW  - Neuronal Ceroid-Lipofuscinoses -- pathology
KW  - Neuroprotective Agents -- metabolism
KW  - Neuronal Ceroid-Lipofuscinoses -- genetics
KW  - Neuronal Ceroid-Lipofuscinoses -- drug therapy
KW  - Hydroxylamines -- pharmacology
KW  - Neuroprotective Agents -- therapeutic use
KW  - Hydroxylamines -- metabolism
KW  - Hydroxylamines -- therapeutic use
KW  - Thiolester Hydrolases -- deficiency
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1447105530?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuroscience&rft.atitle=Neuroprotection+and+lifespan+extension+in+Ppt1%28-%2F-%29+mice+by+NtBuHA%3A+therapeutic+implications+for+INCL.&rft.au=Sarkar%2C+Chinmoy%3BChandra%2C+Goutam%3BPeng%2C+Shiyong%3BZhang%2C+Zhongjian%3BLiu%2C+Aiyi%3BMukherjee%2C+Anil+B&rft.aulast=Sarkar&rft.aufirst=Chinmoy&rft.date=2013-11-01&rft.volume=16&rft.issue=11&rft.spage=1608&rft.isbn=&rft.btitle=&rft.title=Nature+neuroscience&rft.issn=1546-1726&rft_id=info:doi/10.1038%2Fnn.3526
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-27
N1  - Date created - 2013-10-29
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Hum Mol Genet. 2008 Feb 15;17(4):469-77 [17989065]
Nat Protoc. 2006;1(5):2315-9 [17406473]
Prog Lipid Res. 2009 May-Jul;48(3-4):117-27 [19233228]
Cell Stem Cell. 2009 Sep 4;5(3):310-9 [19733542]
Nat Med. 2009 Oct;15(10):1215-8 [19749771]
Mol Genet Metab. 2010 Apr;99(4):374-8 [20036592]
Biochem Soc Trans. 2010 Dec;38(6):1484-8 [21118112]
PLoS One. 2010;5(11):e15045 [21152083]
J Cell Biol. 2010 Dec 27;191(7):1229-38 [21187327]
Curr Pharm Biotechnol. 2011 Jun;12(6):867-83 [21235444]
J Neurosci. 2011 Oct 26;31(43):15575-85 [22031903]
J Pathol. 2012 Jan;226(2):241-54 [21990005]
Hum Mutat. 2012 Jan;33(1):42-63 [21990111]
Neurodegener Dis. 2012;9(4):159-69 [22327870]
Nat Rev Neurol. 2012 Jun;8(6):307-18 [22526003]
Mol Genet Metab. 2012 Sep;107(1-2):213-21 [22704978]
J Biol Chem. 2012 Oct 26;287(44):37330-9 [22902780]
Biochim Biophys Acta. 2013 Nov;1832(11):1795-800 [22959893]
Biochim Biophys Acta. 2013 Nov;1832(11):1807-26 [23200925]
Biochim Biophys Acta. 2009 Apr;1793(4):737-45 [18824038]
Brain Res Dev Brain Res. 1999 Dec 10;118(1-2):1-11 [10611498]
Neurology. 2000 May 9;54(9):1828-32 [10802792]
FASEB J. 2001 Oct;15(12):2196-204 [11641246]
Neurology. 2001 Oct 23;57(8):1411-6 [11673581]
Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13566-71 [11717424]
Nat Rev Neurosci. 2002 Oct;3(10):791-802 [12360323]
Annu Rev Biochem. 2004;73:559-87 [15189153]
J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682]
Crit Rev Toxicol. 1985;14(1):87-99 [3882333]
Neurosci Biobehav Rev. 1985 Spring;9(1):37-44 [2858080]
Genomics. 1991 Jan;9(1):170-3 [1672288]
J Biol Chem. 1993 Oct 25;268(30):22566-74 [7901201]
J Biol Chem. 1994 Sep 16;269(37):23212-9 [7916016]
J Neurotrauma. 1994 Apr;11(2):187-96 [7932797]
Nature. 1995 Aug 17;376(6541):584-7 [7637805]
J Biol Chem. 1996 Jun 28;271(26):15831-6 [8663305]
Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10046-50 [8816748]
EMBO J. 1996 Oct 1;15(19):5240-5 [8895569]
J Biol Chem. 1998 Jun 19;273(25):15830-7 [9624183]
Gene. 1999 Apr 29;231(1-2):203-11 [10231585]
Nat Rev Neurosci. 2005 Sep;6(9):713-25 [16049428]
Hum Mol Genet. 2006 Jan 15;15(2):337-46 [16368712]
Mol Ther. 2006 Mar;13(3):538-47 [16364693]
Hum Mol Genet. 2006 May 15;15(10):1580-6 [16571600]
Methods. 2006 Oct;40(2):127-34 [17012024]
Sci STKE. 2006 Oct 31;2006(359):re14 [17077383]
Comment In:
Nat Rev Drug Discov. 2013 Nov;12(11):828 [24136395]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1038/nn.3526
ER  - 



TY  - JOUR
T1  - Behavioral and socioemotional competence problems of extremely low birth weight children
AN  - 1446920033; 23867957
AB  - To examine behavioral and social-emotional problems in extremely low birth weight (ELBW) children and to assess factors associated with behavioral and social competency outcomes at 30 to 36 months adjusted age.  
A total of 696 ELBW (401 to 1000g) children from the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network were included. Behavioral and social-emotional problems were assessed using the Brief Infant-Toddler Social and Emotional Assessment administered to parents. Unadjusted comparisons were performed between children with or without behavioral or social-emotional problems. Logistic regression was used to examine factors associated with behavioral outcomes.  
Parents reported behavioral problems in 46.8%, deficits in social-emotional competence in 20.4% and having both behavioral and social-emotional competence problems in 15.4% of ELBW children. Characteristics associated with behavioral problems in logistic regression included female gender, lower household income and a Bayley Psychomotor Developmental Index (PDI)<70. Deficits in social competence were associated with Bayley Mental Developmental Index (MDI) and PDI scores<70 and Hispanic or Other races compared with White non-Hispanic.  
Half of the (51.9%) ELBW children showed behavioral or social-emotional competence problems at 30 months. Low socioeconomic status and low Bayley MDI and PDI scores were associated with behavioral and socioemotional difficulties.
JF  - Journal of Perinatology
AU  - Peralta-carcelen, M
AU  - Bailey, K
AU  - Rector, R
AU  - Gantz, M
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 887
EP  - 92
CY  - New York
PB  - Nature Publishing Group
VL  - 33
IS  - 11
SN  - 07438346
KW  - Medical Sciences--Pediatrics
KW  - Emotions
KW  - Child Behavior Disorders
KW  - Logistic Models
KW  - Humans
KW  - Social Behavior
KW  - Child
KW  - Male
KW  - Female
KW  - Child, Preschool
KW  - Developmental Disabilities
KW  - Infant, Very Low Birth Weight -- psychology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1446920033?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthcompleteshell&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Perinatology&rft.atitle=Behavioral+and+socioemotional+competence+problems+of+extremely+low+birth+weight+children&rft.au=Peralta-carcelen%2C+M%3BBailey%2C+K%3BRector%2C+R%3BGantz%2C+M&rft.aulast=Peralta-carcelen&rft.aufirst=M&rft.date=2013-11-01&rft.volume=33&rft.issue=11&rft.spage=887&rft.isbn=&rft.btitle=&rft.title=Journal+of+Perinatology&rft.issn=07438346&rft_id=info:doi/10.1038%2Fjp.2013.78
LA  - English
DB  - ProQuest Central
N1  - Copyright - Copyright Nature Publishing Group Nov 2013
N1  - Last updated - 2014-09-08
DO  - http://dx.doi.org/10.1038/jp.2013.78
ER  - 



TY  - JOUR
T1  - The Utility of a Composite Biological Endpoint in HIV/STI Prevention Trials
AN  - 1445256353; 23748863
AB  - A human immunodeficiency virus (HIV) as a biological endpoint in HIV prevention trials may not be feasible, so investigators have used surrogate biological outcomes. In a multisite trial, the epidemiology of STIs may be different across sites and preclude using one STI as the outcome. This study explored using a composite STI outcome to address that problem. The combined biological endpoint was the incidence of any of six new STIs (chlamydia, gonorrhea, trichomonas (women only), syphilis, herpes simplex virus type 2 infection and HIV) during a 24-month follow up period. We investigated how a composite STI outcome would perform compared to single and dual STI outcomes under various conditions. We simulated outcomes for four populations that represented a wide range of sex and age distributions, and STI prevalences. The simulations demonstrated that a combined biologic outcome was superior to single and dual STI outcomes in assessing intervention effects in 82 % of the cases. A composite biological outcome was effective in detecting intervention effects and might allow more investigations to incorporate multiple biological outcomes in the assessment of behavioral intervention trials for HIV prevention.[PUBLICATION ABSTRACT]
JF  - AIDS and Behavior
AU  - Hartwell, Tyler D
AU  - Pequegnat, Willo
AU  - Moore, Janet L
AU  - Parker, Corette B
AU  - Strader, Lisa C
AU  - Green, Annette M
AU  - Quinn, Thomas C
AU  - Wasserheit, Judith N
AU  - Klausner, Jeffrey D
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 2893
EP  - 901
CY  - New York
PB  - Springer Science & Business Media
VL  - 17
IS  - 9
SN  - 10907165
KW  - Psychology
KW  - Human immunodeficiency virus--HIV
KW  - Sexual behavior
KW  - Sexually transmitted diseases--STD
KW  - Disease prevention
KW  - Humans
KW  - Trichomonas Infections -- prevention & control
KW  - Syphilis -- prevention & control
KW  - Gonorrhea -- prevention & control
KW  - Preventive Health Services -- statistics & numerical data
KW  - Adult
KW  - Incidence
KW  - Follow-Up Studies
KW  - Herpes Genitalis -- prevention & control
KW  - HIV Infections -- epidemiology
KW  - Sexually Transmitted Diseases, Bacterial -- epidemiology
KW  - Female
KW  - Male
KW  - Sexual Behavior -- statistics & numerical data
KW  - Chlamydia Infections -- prevention & control
KW  - Prevalence
KW  - Risk Reduction Behavior
KW  - HIV Infections -- prevention & control
KW  - Sexually Transmitted Diseases, Bacterial -- prevention & control
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1445256353?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acriminaljusticeperiodicals&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+and+Behavior&rft.atitle=The+Utility+of+a+Composite+Biological+Endpoint+in+HIV%2FSTI+Prevention+Trials&rft.au=Hartwell%2C+Tyler+D%3BPequegnat%2C+Willo%3BMoore%2C+Janet+L%3BParker%2C+Corette+B%3BStrader%2C+Lisa+C%3BGreen%2C+Annette+M%3BQuinn%2C+Thomas+C%3BWasserheit%2C+Judith+N%3BKlausner%2C+Jeffrey+D&rft.aulast=Hartwell&rft.aufirst=Tyler&rft.date=2013-11-01&rft.volume=17&rft.issue=9&rft.spage=2893&rft.isbn=&rft.btitle=&rft.title=AIDS+and+Behavior&rft.issn=10907165&rft_id=info:doi/10.1007%2Fs10461-013-0501-5
LA  - English
DB  - ProQuest Central
N1  - Copyright - Springer Science+Business Media New York 2013
N1  - Document feature - References
N1  - Last updated - 2014-11-06
N1  - CODEN - AIBEFC
DO  - http://dx.doi.org/10.1007/s10461-013-0501-5
ER  - 



TY  - JOUR
T1  - 3,3'-diindolylmethane rapidly and selectively inhibits hepatocyte growth factor/c-Met signaling in breast cancer cells.
AN  - 1443995597; 23968581
AB  - 3,3'-Diindolylmethane (DIM), an indole derivative from vegetables of the Brassica genus, has antiproliferative activity in breast cancer cells. Part of this activity is thought to be due to DIM inhibition of Akt signaling, but an upstream mechanism of DIM-induced Akt inhibition has not been described. The goals of this study were to investigate the kinetics of inhibition of Akt by physiologically relevant concentrations of DIM and to identify an upstream factor that mediates this effect. Here we report that DIM (5-25 μM) inhibited Akt activation from 30 min to 24h in tumorigenic MDA-MB-231 cells but did not inhibit Akt activation in non-tumorigenic preneoplastic MCF10AT cells. DIM inhibited hepatocyte growth factor (HGF)-induced Akt activation by up to 46%, cell migration by 66% and cell proliferation by up to 54%, but did not inhibit induction of Akt by epidermal growth factor or insulin-like growth factor-1. DIM decreased phosphorylation of the HGF receptor, c-Met, at tyrosines 1234 and 1235, indicating decreased activation of the receptor. This decrease was reversed by pretreatment with inhibitors of p38 or calcineurin. Our results demonstrate the important role of HGF and c-Met in DIM's anti-proliferative effect on breast cancer cells and suggest that DIM could have preventive or clinical value as an inhibitor of c-Met signaling. Copyright © 2013 Elsevier Inc. All rights reserved.
JF  - The Journal of nutritional biochemistry
AU  - Nicastro, Holly L
AU  - Firestone, Gary L
AU  - Bjeldanes, Leonard F
AD  - Department of Nutritional Science & Toxicology, University of California Berkeley, Berkeley, CA 94720-3104. Electronic address: holly.nicastro@nih.gov.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1882
EP  - 1888
VL  - 24
IS  - 11
KW  - Indoles
KW  - 0
KW  - Hepatocyte Growth Factor
KW  - 67256-21-7
KW  - MET protein, human
KW  - EC 2.7.10.1
KW  - Proto-Oncogene Proteins c-met
KW  - Proto-Oncogene Proteins c-akt
KW  - EC 2.7.11.1
KW  - 3,3'-diindolylmethane
KW  - SSZ9HQT61Z
KW  - Index Medicus
KW  - Breast cancer
KW  - c-Met
KW  - 3,3′-diindolylmethane
KW  - Akt
KW  - Cell Proliferation -- drug effects
KW  - Hepatocyte Growth Factor -- physiology
KW  - Tumor Cells, Cultured
KW  - Humans
KW  - Hepatocyte Growth Factor -- pharmacology
KW  - Signal Transduction -- drug effects
KW  - Cell Movement -- drug effects
KW  - Female
KW  - Breast Neoplasms -- drug therapy
KW  - Indoles -- pharmacology
KW  - Proto-Oncogene Proteins c-met -- antagonists & inhibitors
KW  - Proto-Oncogene Proteins c-akt -- antagonists & inhibitors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443995597?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+nutritional+biochemistry&rft.atitle=3%2C3%27-diindolylmethane+rapidly+and+selectively+inhibits+hepatocyte+growth+factor%2Fc-Met+signaling+in+breast+cancer+cells.&rft.au=Nicastro%2C+Holly+L%3BFirestone%2C+Gary+L%3BBjeldanes%2C+Leonard+F&rft.aulast=Nicastro&rft.aufirst=Holly&rft.date=2013-11-01&rft.volume=24&rft.issue=11&rft.spage=1882&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutritional+biochemistry&rft.issn=1873-4847&rft_id=info:doi/10.1016%2Fj.jnutbio.2013.05.004
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-12
N1  - Date created - 2013-10-21
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Oncogene. 2000 Apr 27;19(18):2212-23 [10822371]
Int J Oncol. 2012 Feb;40(2):436-42 [21993423]
JAMA. 2001 Jun 20;285(23):2975-7 [11410091]
FASEB J. 2002 Jan;16(1):108-10 [11729097]
Biochem Pharmacol. 2002 Mar 15;63(6):1085-97 [11931841]
Carcinogenesis. 2002 Aug;23(8):1297-305 [12151347]
Nutr Cancer. 2002;42(1):1-9 [12235639]
Oncogene. 2003 Nov 20;22(52):8498-508 [14627990]
Nat Rev Mol Cell Biol. 2003 Dec;4(12):915-25 [14685170]
Drug Metab Dispos. 2004 Jun;32(6):632-8 [15155555]
J Natl Cancer Inst. 1981 Jun;66(6):1191-308 [7017215]
Int J Cancer. 1991 May 30;48(3):350-4 [2040528]
J Biol Chem. 1991 Aug 25;266(24):16098-104 [1651934]
Oncogene. 1994 Jan;9(1):49-57 [8302603]
Cancer Res. 1994 Apr 1;54(7):1630-3 [8137271]
Proc Natl Acad Sci U S A. 1994 May 24;91(11):4731-5 [8197126]
Cancer. 1998 Apr 15;82(8):1513-20 [9554529]
Carcinogenesis. 1998 Sep;19(9):1631-9 [9771935]
Cancer Res. 2005 Jan 1;65(1):364-71 [15665315]
J Nutr Biochem. 2005 Feb;16(2):65-73 [15681163]
Carcinogenesis. 2005 Apr;26(4):771-8 [15661811]
Oncogene. 2005 Mar 31;24(14):2343-53 [15735741]
Anticancer Drugs. 2005 Sep;16(8):797-803 [16096426]
Carcinogenesis. 2006 Mar;27(3):541-50 [16199440]
Oncogene. 2006 Mar 23;25(13):1922-30 [16449979]
Cancer Res. 2006 May 1;66(9):4880-7 [16651444]
Cancer Res. 2007 Apr 1;67(7):3475-82 [17389758]
Pharmacol Res. 2007 Mar;55(3):224-36 [17317210]
Acta Pharmacol Sin. 2007 Sep;28(9):1274-304 [17723163]
Nat Med. 2007 Sep;13(9):1114-9 [17694068]
Mol Cancer Ther. 2007 Oct;6(10):2757-65 [17913854]
Mol Cancer Ther. 2008 Feb;7(2):341-9 [18281517]
In Vivo. 2008 Jul-Aug;22(4):441-5 [18712169]
J Nutr. 2009 Apr;139(4):646-52 [19244381]
Cancer Lett. 2009 Jul 18;280(1):1-14 [19100682]
Biochem Pharmacol. 2009 Sep 1;78(5):469-76 [19433067]
Mol Cancer. 2009;8:81 [19796390]
J Nutr. 2010 Jan;140(1):1-6 [19889811]
Mutat Res. 2011 Jul-Oct;728(1-2):47-66 [21703360]
Immunopharmacol Immunotoxicol. 2011 Dec;33(4):603-8 [21428708]
Semin Cancer Biol. 2001 Apr;11(2):153-65 [11322834]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.jnutbio.2013.05.004
ER  - 



TY  - JOUR
T1  - Metabolomics reveals trichloroacetate as a major contributor to trichloroethylene-induced metabolic alterations in mouse urine and serum.
AN  - 1443418167; 23575800
AB  - Trichloroethylene (TCE)-induced liver toxicity and carcinogenesis is believed to be mediated in part by activation of the peroxisome proliferator-activated receptor α (PPARα). However, the contribution of the two TCE metabolites, dichloroacetate (DCA) and trichloroacetate (TCA) to the toxicity of TCE, remains unclear. The aim of the present study was to determine the metabolite profiles in serum and urine upon exposure of mice to TCE, to aid in determining the metabolic response to TCE exposure and the contribution of DCA and TCA to TCE toxicity. C57BL/6 mice were administered TCE, TCA, or DCA, and urine and serum subjected to ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight mass spectrometry (UPLC-ESI-QTOFMS)-based global metabolomics analysis. The ions were identified through searching metabolomics databases and by comparison with authentic standards, and quantitated using multiple reactions monitoring. Quantitative polymerase chain reaction of mRNA, biochemical analysis, and liver histology were also performed. TCE exposure resulted in a decrease in urine of metabolites involved in fatty acid metabolism, resulting from altered expression of PPARα target genes. TCE treatment also induced altered phospholipid homeostasis in serum, as revealed by increased serum lysophosphatidylcholine 18:0 and 18:1, and phosphatidylcholine metabolites. TCA administration revealed similar metabolite profiles in urine and serum upon TCE exposure, which correlated with a more robust induction of PPARα target gene expression associated with TCA than DCA treatment. These data show the metabolic response to TCE exposure and demonstrate that TCA is the major contributor to TCE-induced metabolite alterations observed in urine and serum.
JF  - Archives of toxicology
AU  - Fang, Zhong-Ze
AU  - Krausz, Kristopher W
AU  - Tanaka, Naoki
AU  - Li, Fei
AU  - Qu, Aijuan
AU  - Idle, Jeffrey R
AU  - Gonzalez, Frank J
AD  - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 3106, Bethesda, MD, 20892, USA.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1975
EP  - 1987
VL  - 87
IS  - 11
KW  - Fatty Acids
KW  - 0
KW  - Phospholipids
KW  - Trichloroethylene
KW  - 290YE8AR51
KW  - Trichloroacetic Acid
KW  - 5V2JDO056X
KW  - Dichloroacetic Acid
KW  - 9LSH52S3LQ
KW  - Aspartate Aminotransferases
KW  - EC 2.6.1.1
KW  - Alanine Transaminase
KW  - EC 2.6.1.2
KW  - Index Medicus
KW  - Hepatomegaly -- metabolism
KW  - Spectrometry, Mass, Electrospray Ionization
KW  - Animals
KW  - Dichloroacetic Acid -- toxicity
KW  - Phospholipids -- metabolism
KW  - Mice
KW  - Homeostasis -- drug effects
KW  - Chromatography, High Pressure Liquid
KW  - Multivariate Analysis
KW  - Fatty Acids -- metabolism
KW  - Polymerase Chain Reaction
KW  - Aspartate Aminotransferases -- blood
KW  - Alanine Transaminase -- blood
KW  - Dichloroacetic Acid -- metabolism
KW  - Mice, Inbred C57BL
KW  - Hepatomegaly -- chemically induced
KW  - Male
KW  - Chemical and Drug Induced Liver Injury -- blood
KW  - Trichloroethylene -- metabolism
KW  - Metabolism -- drug effects
KW  - Chemical and Drug Induced Liver Injury -- urine
KW  - Trichloroacetic Acid -- metabolism
KW  - Trichloroethylene -- toxicity
KW  - Metabolomics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443418167?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Metabolomics+reveals+trichloroacetate+as+a+major+contributor+to+trichloroethylene-induced+metabolic+alterations+in+mouse+urine+and+serum.&rft.au=Fang%2C+Zhong-Ze%3BKrausz%2C+Kristopher+W%3BTanaka%2C+Naoki%3BLi%2C+Fei%3BQu%2C+Aijuan%3BIdle%2C+Jeffrey+R%3BGonzalez%2C+Frank+J&rft.aulast=Fang&rft.aufirst=Zhong-Ze&rft.date=2013-11-01&rft.volume=87&rft.issue=11&rft.spage=1975&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-013-1053-1
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-15
N1  - Date created - 2013-10-15
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/s00204-013-1053-1
ER  - 



TY  - JOUR
T1  - A novel gadolinium-based trimetasphere metallofullerene for application as a magnetic resonance imaging contrast agent.
AN  - 1443406283; 23748228
AB  - Macromolecular contrast agents for magnetic resonance imaging (MRI) are useful blood-pool agents because of their long systemic half-life and have found applications in monitoring tumor vasculature and angiogenesis. Macromolecular contrast agents have been able to overcome some of the disadvantages of the conventional small-molecule contrast agent Magnevist (gadolinium-diethylenetriaminepentaacetic acid), such as rapid extravasation and quick renal clearance, which limits the viable MRI time. There is an urgent need for new MRI contrast agents that increase the sensitivity of detection with a higher relaxivity, longer blood half-life, and reduced toxicity from free Gd3+ ions. Here, we report on the characterization of a novel water-soluble, derivatized, gadolinium-enclosed metallofullerene nanoparticle (Hydrochalarone-1) in development as an MRI contrast agent.
          The physicochemical properties of Hydrochalarone-1 were characterized by dynamic light scattering (hydrodynamic diameter), atomic force microscopy (particle height), ζ potential analysis (surface charge), and inductively coupled plasma-mass spectrometry (gadolinium concentration). The blood compatibility of Hydrochalarone-1 was also assessed in vitro through analysis of hemolysis, platelet aggregation, and complement activation of human blood. In vitro relaxivities, in vivo pharmacokinetics, and a pilot in vivo acute toxicity study were also performed. An extensive in vitro and in vivo characterization of Hydrochalarone-1 is described here. The hydrodynamic size of Hydrochalarone-1 was 5 to 7 nm depending on the dispersing media, and it was negatively charged at physiological pH. Hydrochalarone-1 showed compatibility with blood cells in vitro, and no significant hemolysis, platelet aggregation, or complement activation was observed in vitro. In addition, Hydrochalarone-1 had significantly higher r1 and r2 in vitro relaxivities in human plasma in comparison with Magnevist and was not toxic at the doses administered in an in vivo pilot acute-dose toxicity study in mice.In vivo MRI pharmacokinetic analysis after a single intravenous injection of Hydrochalarone-1 (0.2 mmol Gd/kg) showed that the volume of distribution at steady state was approximately 100 mL/kg, suggesting prolonged systemic circulation. Hydrochalarone-1 also had a long blood half-life (88 minutes) and increased relaxivity, suggesting application as a promising blood-pool MRI contrast agent.
          The evidence suggests that Hydrochalarone-1, with its long systemic half-life, may have significant utility as a blood-pool MRI contrast agent.
JF  - Investigative radiology
AU  - Adiseshaiah, Pavan
AU  - Dellinger, Anthony
AU  - MacFarland, Darren
AU  - Stern, Stephan
AU  - Dobrovolskaia, Marina
AU  - Ileva, Lilia
AU  - Patri, Anil K
AU  - Bernardo, Marcelino
AU  - Brooks, D Bradford
AU  - Zhou, Zhiguo
AU  - McNeil, Scott
AU  - Kepley, Christopher
AD  - From the *Nanotechnology Characterization Laboratory, Advanced Technology Program, SAIC-Frederick, Inc, Frederick National Laboratory for Cancer Research, Frederick, MD; †Luna nanoWorks, Luna Innovations, Inc, Danville, VA; ‡Department of Nanoscience, Joint School of Nanoscience and Nanoengineering, Greensboro, NC; §Small Animal Imaging Program, Laboratory Animal Sciences Program, SAIC-Frederick, Inc, Frederick National Laboratory for Cancer Research, Frederick; and ∥Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 745
EP  - 754
VL  - 48
IS  - 11
KW  - Contrast Media
KW  - 0
KW  - Fullerenes
KW  - Macromolecular Substances
KW  - Organometallic Compounds
KW  - hydrochalarone-1
KW  - Gadolinium
KW  - AU0V1LM3JT
KW  - Index Medicus
KW  - Animals
KW  - Platelet Aggregation
KW  - Humans
KW  - Hemolysis
KW  - Microscopy, Atomic Force
KW  - Spectrophotometry, Atomic
KW  - Mice
KW  - Molecular Dynamics Simulation
KW  - Nanoparticles
KW  - Complement Activation
KW  - Gadolinium -- pharmacokinetics
KW  - Magnetic Resonance Imaging
KW  - Contrast Media -- pharmacokinetics
KW  - Contrast Media -- toxicity
KW  - Gadolinium -- chemistry
KW  - Organometallic Compounds -- toxicity
KW  - Fullerenes -- toxicity
KW  - Organometallic Compounds -- chemistry
KW  - Organometallic Compounds -- pharmacokinetics
KW  - Fullerenes -- pharmacokinetics
KW  - Fullerenes -- chemistry
KW  - Contrast Media -- chemistry
KW  - Gadolinium -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443406283?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigative+radiology&rft.atitle=A+novel+gadolinium-based+trimetasphere+metallofullerene+for+application+as+a+magnetic+resonance+imaging+contrast+agent.&rft.au=Adiseshaiah%2C+Pavan%3BDellinger%2C+Anthony%3BMacFarland%2C+Darren%3BStern%2C+Stephan%3BDobrovolskaia%2C+Marina%3BIleva%2C+Lilia%3BPatri%2C+Anil+K%3BBernardo%2C+Marcelino%3BBrooks%2C+D+Bradford%3BZhou%2C+Zhiguo%3BMcNeil%2C+Scott%3BKepley%2C+Christopher&rft.aulast=Adiseshaiah&rft.aufirst=Pavan&rft.date=2013-11-01&rft.volume=48&rft.issue=11&rft.spage=745&rft.isbn=&rft.btitle=&rft.title=Investigative+radiology&rft.issn=1536-0210&rft_id=info:doi/10.1097%2FRLI.0b013e318294de5d
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-10
N1  - Date created - 2013-10-04
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/RLI.0b013e318294de5d
ER  - 



TY  - JOUR
T1  - Fuzzy Group Decision-Making in the Measurement of Ecotourism Sustainability Potential
AN  - 1443379736; 18670388
AB  - Both theoretical and practical efforts to evaluate ecotourism development often neglect alternative characteristics that may interact with and mutually influence the primary indicators. To evaluate the sustainability of an ecotourism site, this study utilizes subjective measures to analyze the relationships among tourism, resources, community, economy and society. Yangshan Ecological Park in Kinmen is examined to demonstrate the implementation of the proposed integrated framework in ecotourism development. First, the Fuzzy Delphi Method was applied to select the critical factors. Local residents, tourists and resource administrators were interviewed to explore each group's perception of relationships. Then, Interpretive Structural Modeling was employed to determine the interrelationship among the critical factors. A Fuzzy Analytic Network process model was constructed to evaluate the potential sustainability of ecotourism and the relative importance the weights of the criteria and sub-criteria. The study provides a valuable integrated tool for sustainable destination management.
JF  - Group Decision and Negotiation
AU  - Lin, Ling-Zhong
AU  - Lu, Chi-Fang
AD  - Department of Marketing Management, Shih Chien University Kaohsiung Campus, Taiwan, 200 University Road, Nei-Men Hsiang, Kaohsiung, Hsien, 845, Taiwan, ling@mail.kh.usc.edu.tw
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 1051
EP  - 1079
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 22
IS  - 6
SN  - 0926-2644, 0926-2644
KW  - Sustainability Science Abstracts
KW  - Economics
KW  - Ecotourism
KW  - M3 1010:Issues in Sustainable Development
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443379736?accountid=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=Group+Decision+and+Negotiation&rft.atitle=Fuzzy+Group+Decision-Making+in+the+Measurement+of+Ecotourism+Sustainability+Potential&rft.au=Lin%2C+Ling-Zhong%3BLu%2C+Chi-Fang&rft.aulast=Lin&rft.aufirst=Ling-Zhong&rft.date=2013-11-01&rft.volume=22&rft.issue=6&rft.spage=1051&rft.isbn=&rft.btitle=&rft.title=Group+Decision+and+Negotiation&rft.issn=09262644&rft_id=info:doi/10.1007%2Fs10726-012-9305-7
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Ecotourism
DO  - http://dx.doi.org/10.1007/s10726-012-9305-7
ER  - 



TY  - JOUR
T1  - Current strategies to minimize toxicity of oxaliplatin: selection of pharmacogenomic panel tests.
AN  - 1438571258; 24025562
AB  - Oxaliplatin is an anticancer drug routinely used to treat colorectal, gastroesophageal, ovarian, breast, head/neck, and genitourinary cancers. Discontinuation of oxaliplatin treatment is mostly because of peripheral neuropathy, more often than for tumor progression, potentially compromising patient benefit. Several strategies to prevent neurotoxicity have so far been investigated. To overcome this life-threatening side effect, while taking advantage of the antineoplastic activities of oxaliplatin, we describe in detail recent findings on the underlying mechanisms of genetic variants associated with toxicity and resistance to oxaliplatin-based chemotherapy in colorectal cancer. A comprehensive panel of eight polymorphisms, previously validated as significant markers related to oxaliplatin toxicity, is proposed and discussed. In addition, the most common available strategies or methods to prevent/minimize the toxicity were described in detail. Moreover, an early outline evaluation of the genotyping costs and methods was taken in consideration. With the availability of individual pharmacogenomic profiles, the oncologists will have new means to make treatment decisions for their patients that maximize benefit and minimize toxicity. With this purpose in mind, the clinician and lab manager should cooperate to evaluate the advantages and limitations, in terms of costs and applicability, of the most appropriate pharmacogenomic tests for routine incorporation into clinical practice.
JF  - Anti-cancer drugs
AU  - Di Francia, Raffaele
AU  - Siesto, Raffaella Stefania
AU  - Valente, Daniela
AU  - Del Buono, Andrea
AU  - Pugliese, Sergio
AU  - Cecere, Sabrina
AU  - Cavaliere, Carla
AU  - Nasti, Guglielmo
AU  - Facchini, Gaetano
AU  - Berretta, Massimiliano
AD  - aHematology-Oncology and Stem Cell Transplantation Unit bUro-Gynaecologic Department cAbdominal Department, Medical Oncology Unit, National Cancer Institute, Fondazione 'G. Pascale' IRCCS dItalian Association of Pharmacogenomics and Molecular Diagnostics eMMG ASL CE1, Medicina del Lavoro fCETAC Research Center, Caserta gDepartment of Medical Oncology, CRO National Cancer Institute, Aviano (PN), Italy.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 1069
EP  - 1078
VL  - 24
IS  - 10
KW  - Antineoplastic Agents
KW  - 0
KW  - Organoplatinum Compounds
KW  - oxaliplatin
KW  - 04ZR38536J
KW  - Index Medicus
KW  - Randomized Controlled Trials as Topic
KW  - Drug Administration Schedule
KW  - Polymorphism, Genetic
KW  - Humans
KW  - Organoplatinum Compounds -- pharmacokinetics
KW  - Organoplatinum Compounds -- administration & dosage
KW  - Antineoplastic Agents -- pharmacokinetics
KW  - Neurotoxicity Syndromes -- prevention & control
KW  - Neurotoxicity Syndromes -- etiology
KW  - Neurotoxicity Syndromes -- enzymology
KW  - Antineoplastic Agents -- toxicity
KW  - Organoplatinum Compounds -- toxicity
KW  - Neurotoxicity Syndromes -- genetics
KW  - Pharmacogenetics -- methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1438571258?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+drugs&rft.atitle=Current+strategies+to+minimize+toxicity+of+oxaliplatin%3A+selection+of+pharmacogenomic+panel+tests.&rft.au=Di+Francia%2C+Raffaele%3BSiesto%2C+Raffaella+Stefania%3BValente%2C+Daniela%3BDel+Buono%2C+Andrea%3BPugliese%2C+Sergio%3BCecere%2C+Sabrina%3BCavaliere%2C+Carla%3BNasti%2C+Guglielmo%3BFacchini%2C+Gaetano%3BBerretta%2C+Massimiliano&rft.aulast=Di+Francia&rft.aufirst=Raffaele&rft.date=2013-11-01&rft.volume=24&rft.issue=10&rft.spage=1069&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+drugs&rft.issn=1473-5741&rft_id=info:doi/10.1097%2FCAD.0000000000000002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-05
N1  - Date created - 2013-09-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/CAD.0000000000000002
ER  - 



TY  - JOUR
T1  - Divergent estrogen receptor-positive and -negative breast cancer trends and etiologic heterogeneity in Denmark
AN  - 1434032917; 18510212
AB  - Long-term breast cancer trends in incidence in the United States (US) show rising estrogen receptor (ER)-positive rates and falling ER-negative rates. We hypothesized that these divergent trends reflect etiologic heterogeneity and that comparable trends should be observed in other countries with similar risk factor profiles. Therefore, we analyzed invasive female breast cancers in Denmark, a country with similar risk factors as the US. We summarized the overall trend in age-standardized rates with the estimated annual percentage change (EAPC) statistic (1993-2010) and used age-period-cohort models to estimate age-specific EAPCs, cohort rate ratios and projections for future time periods (2011-2018). In Denmark, the overall rate of ER-positive cancers rose between 1993 and 2010 by 3.0% per year (95% CI: 2.8-3.3% per year), whereas the overall rate of ER-negative cancers fell by 2.1% per year (95% CI: -2.5 to -1.6% per year). The ER-positive rate increased fastest among postmenopausal women and the ER-negative rate decreased fastest among premenopausal women, reflecting that cohorts born after 1944 were at relatively higher risk of ER-positive tumors and lower risk of ER-negative tumors. If current trends continue, ER-positive cancers will increase at least 13% by 2018 in Denmark, ER-negative cancers will fall 15% by 2018, and breast cancer overall will increase at least 7% by 2018. Divergent ER-specific trends are consistent with distinct etiologic pathways. If trends in known risk factors are responsible, the Danish and US experience may foreshadow a common pattern worldwide. What's new? Estrogen receptor- (ER-)negative breast cancer incidence rates are declining nationwide in Denmark and the United States, whereas rates for ER-positive breast cancers are rising. This report suggests that the divergent trends in ER breast cancers in both countries can be explained by parallel trends in environmental and lifestyle factors that are known to either increase or decrease risk for ER-positive or ER-negative malignancies. The patterns observed in Denmark and the United States may foreshadow a common pattern for many countries worldwide.
JF  - International Journal of Cancer
AU  - Anderson, William F
AU  - Rosenberg, Philip S
AU  - Petito, Lucia
AU  - Katki, Hormuzd A
AU  - Ejlertsen, Bent
AU  - Ewertz, Marianne
AU  - Rasmussen, Birgitte B
AU  - Jensen, Maj-Britt
AU  - Kroman, Niels
AD  - DHHS/NIH/National Cancer Institute/Division of Cancer Epidemiology and Genetics/Biostatistics Branch, Bethesda, MD.
Y1  - 2013/11//
PY  - 2013
DA  - Nov 2013
SP  - 2201
EP  - 2206
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 133
IS  - 9
SN  - 0020-7136, 0020-7136
KW  - Risk Abstracts
KW  - Health risks
KW  - USA
KW  - Estrogens
KW  - Post-menopause
KW  - Risk factors
KW  - Breast cancer
KW  - Denmark
KW  - Tumors
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434032917?accountid=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=Divergent+estrogen+receptor-positive+and+-negative+breast+cancer+trends+and+etiologic+heterogeneity+in+Denmark&rft.au=Anderson%2C+William+F%3BRosenberg%2C+Philip+S%3BPetito%2C+Lucia%3BKatki%2C+Hormuzd+A%3BEjlertsen%2C+Bent%3BEwertz%2C+Marianne%3BRasmussen%2C+Birgitte+B%3BJensen%2C+Maj-Britt%3BKroman%2C+Niels&rft.aulast=Anderson&rft.aufirst=William&rft.date=2013-11-01&rft.volume=133&rft.issue=9&rft.spage=2201&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28222
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Health risks; Estrogens; Post-menopause; Risk factors; Breast cancer; Tumors; USA; Denmark
DO  - http://dx.doi.org/10.1002/ijc.28222
ER  - 



TY  - JOUR
T1  - Natural immune responses against eight oncogenic human papillomaviruses in the ASCUS-LSIL Triage Study.
AN  - 1426751675; 23588935
AB  - Only a subset of women with human papillomavirus (HPV) infections will become seropositive, and the factors influencing seroconversion are not well understood. We used a multiplex serology assay in women with mildly abnormal cytology results to examine seroreactivity to oncogenic HPV genotypes. An unbiased subset of women in the atypical squamous cell of undetermined significance /low-grade squamous intraepithelial lesion Triage Study provided blood samples at trial enrollment for serological testing. A Luminex assay based on glutathione s-transferase-L1 fusion proteins as antigens was used to test seroreactivity against eight carcinogenic HPV genotypes (16, 18, 31, 33, 35, 45, 52 and 58). We analyzed the relationship between seroprevalence in women free of precancer (N = 2,464) and HPV DNA status, age, sexual behavior and other HPV-related risk factors. The overall seroprevalence was 24.5% for HPV16 L1 and ∼20% for 18L1 and 31L1. Among women free of precancer, seroprevalence peaked in women less than 29 years and decreased with age. Type-specific seroprevalence was associated with baseline DNA detection for HPV16 (OR = 1.36, 95%CI: 1.04-1.79) and HPV18 (OR = 2.31, 95%CI: 1.61-3.32), as well as for HPV52 and HPV58. Correlates of sexual exposure were associated with increased seroprevalence across most genotypes. Women who were current or former smokers were less likely to be seropositive for all eight of the tested oncogenic genotypes. The multiplex assay showed associations between seroprevalence and known risk factors for HPV infection across nearly all tested HPV genotypes but associations between DNA- and serostatus were weak, suggesting possible misclassification of the participants' HPV serostatus. 
          Copyright © 2013 UICC.
JF  - International journal of cancer
AU  - Wilson, Lauren E
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, Bethesda, MD, USA.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 2172
EP  - 2181
VL  - 133
IS  - 9
KW  - DNA, Viral
KW  - 0
KW  - Index Medicus
KW  - seroepidemiology
KW  - human papillomavirus
KW  - antibodies
KW  - Cross-Sectional Studies
KW  - Risk Factors
KW  - Humans
KW  - Seroepidemiologic Studies
KW  - Adult
KW  - Prognosis
KW  - Neoplasm Grading
KW  - Middle Aged
KW  - Follow-Up Studies
KW  - United States -- epidemiology
KW  - DNA, Viral -- genetics
KW  - Female
KW  - Neoplasms, Squamous Cell -- immunology
KW  - Neoplasms, Squamous Cell -- virology
KW  - Papillomavirus Infections -- complications
KW  - Papillomavirus Infections -- virology
KW  - Cervical Intraepithelial Neoplasia -- immunology
KW  - Papillomaviridae -- genetics
KW  - Neoplasms, Squamous Cell -- epidemiology
KW  - Papillomavirus Infections -- immunology
KW  - Papillomaviridae -- classification
KW  - Uterine Cervical Neoplasms -- epidemiology
KW  - Papillomaviridae -- isolation & purification
KW  - Cervical Intraepithelial Neoplasia -- virology
KW  - Uterine Cervical Neoplasms -- immunology
KW  - Uterine Cervical Neoplasms -- virology
KW  - Cervical Intraepithelial Neoplasia -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1426751675?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Natural+immune+responses+against+eight+oncogenic+human+papillomaviruses+in+the+ASCUS-LSIL+Triage+Study.&rft.au=Wilson%2C+Lauren+E%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=2013-11-01&rft.volume=133&rft.issue=9&rft.spage=2172&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.28215
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-31
N1  - Date created - 2013-08-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Lancet Oncol. 2005 Apr;6(4):204 [15830458]
Clin Exp Immunol. 1999 Apr;116(1):33-40 [10209502]
Am J Epidemiol. 2006 Jul 15;164(2):176-83 [16775041]
Int J Cancer. 2006 Oct 1;119(7):1623-9 [16646070]
Vaccine. 2006 Aug 31;24 Suppl 3:S3/11-25 [16949997]
J Gen Virol. 2006 Nov;87(Pt 11):3183-93 [17030851]
Lancet. 2007 Sep 8;370(9590):890-907 [17826171]
Cancer Epidemiol Biomarkers Prev. 2007 Sep;16(9):1874-9 [17855708]
J Gen Virol. 2008 Jan;89(Pt 1):117-29 [18089735]
Cancer Res. 2010 Nov 1;70(21):8578-86 [20959485]
J Natl Cancer Inst. 2010 Nov 3;102(21):1653-62 [20944077]
J Infect Dis. 2011 Jul 1;204(1):94-102 [21628663]
J Gen Virol. 2011 Sep;92(Pt 9):2034-46 [21632564]
J Infect Dis. 2012 Feb 1;205(3):498-505 [22147792]
Int J Gynecol Cancer. 2012 Feb;22(2):303-10 [22228426]
Acta Obstet Gynecol Scand. 2008;87(1):81-8 [17943470]
Gynecol Oncol. 2008 May;109(2 Suppl):S15-21 [18474288]
Am J Epidemiol. 2008 Jul 15;168(2):123-37 [18483125]
Scand J Infect Dis. 2008;40(9):745-51 [19086247]
Sex Transm Dis. 2009 Apr;36(4):241-8 [19265732]
Sex Transm Dis. 2009 Nov;36(11):675-9 [19773679]
J Gen Virol. 2010 Jul;91(Pt 7):1840-8 [20181747]
BMC Infect Dis. 2010;10:238 [20698998]
Sex Transm Dis. 2010 Nov;37(11):706-14 [20661178]
Sex Transm Dis. 2010 Nov;37(11):672-80 [20729796]
Toxicol Appl Pharmacol. 2000 Apr 1;164(1):65-72 [10739745]
J Infect Dis. 2000 Jun;181(6):1911-9 [10837170]
Adv Ther. 2000 Sep-Oct;17(5):230-7 [11186143]
J Clin Microbiol. 2001 Dec;39(12):4344-8 [11724843]
Cancer Epidemiol Biomarkers Prev. 2002 Apr;11(4):343-51 [11927494]
J Virol Methods. 2002 Oct;106(1):61-70 [12367730]
Arterioscler Thromb Vasc Biol. 2003 Apr 1;23(4):703-4 [12692011]
Am J Obstet Gynecol. 2003 Jun;188(6):1401-5 [12824969]
Br J Cancer. 2003 Oct 6;89(7):1248-54 [14520455]
Br J Cancer. 2004 Oct 4;91(7):1269-74 [15292929]
Int J Cancer. 1979 May 15;23(5):603-9 [457307]
J Clin Lab Anal. 1995;9(1):37-41 [7722770]
J Immunol. 1996 Apr 1;156(7):2384-90 [8786295]
J Infect Dis. 1996 Jun;173(6):1394-8 [8648211]
J Infect Dis. 1996 Nov;174(5):937-43 [8896493]
J Periodontal Res. 1997 May;32(4):381-7 [9210092]
Adv Exp Med Biol. 1998;437:279-89 [9666281]
Clin Chem. 2005 Oct;51(10):1845-53 [16099939]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ijc.28215
ER  - 



TY  - JOUR
T1  - Microfabricated polymeric vessel mimetics for 3-D cancer cell culture.
AN  - 1426514502; 23911071
AB  - Modeling tumor growth in vitro is essential for cost-effective testing of hypotheses in preclinical cancer research. 3-D cell culture offers an improvement over monolayer culture for studying cellular processes in cancer biology because of the preservation of cell-cell and cell-ECM interactions. Oxygen transport poses a major barrier to mimicking in vivo environments and is not replicated in conventional cell culture systems. We hypothesized that we can better mimic the tumor microenvironment using a bioreactor system for controlling gas exchange in cancer cell cultures with silicone hydrogel synthetic vessels. Soft-lithography techniques were used to fabricate oxygen-permeable silicone hydrogel membranes containing arrays of micropillars. These membranes were inserted into a bioreactor and surrounded by basement membrane extract (BME) within which fluorescent ovarian cancer (OVCAR8) cells were cultured. Cell clusters oxygenated by synthetic vessels showed a ∼100μm drop-off to anoxia, consistent with in vivo studies of tumor nodules fed by the microvasculature. Oxygen transport in the bioreactor system was characterized by experimental testing with a dissolved oxygen probe and finite element modeling of convective flow. Our study demonstrates differing growth patterns associated with controlling gas distributions to better mimic in vivo conditions.
          Published by Elsevier Ltd.
JF  - Biomaterials
AU  - Jaeger, Ashley A
AU  - Das, Chandan K
AU  - Morgan, Nicole Y
AU  - Pursley, Randall H
AU  - McQueen, Philip G
AU  - Hall, Matthew D
AU  - Pohida, Thomas J
AU  - Gottesman, Michael M
AD  - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/11//
PY  - 2013
DA  - November 2013
SP  - 8301
EP  - 8313
VL  - 34
IS  - 33
KW  - Polymers
KW  - 0
KW  - Index Medicus
KW  - Bioreactor
KW  - Carcinogenesis
KW  - Oxygenation
KW  - Hydrogel
KW  - Microstructure
KW  - Silicone
KW  - Humans
KW  - Bioreactors
KW  - Cell Line, Tumor
KW  - Female
KW  - Microtechnology
KW  - Cell Culture Techniques -- methods
KW  - Polymers -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1426514502?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Microfabricated+polymeric+vessel+mimetics+for+3-D+cancer+cell+culture.&rft.au=Jaeger%2C+Ashley+A%3BDas%2C+Chandan+K%3BMorgan%2C+Nicole+Y%3BPursley%2C+Randall+H%3BMcQueen%2C+Philip+G%3BHall%2C+Matthew+D%3BPohida%2C+Thomas+J%3BGottesman%2C+Michael+M&rft.aulast=Jaeger&rft.aufirst=Ashley&rft.date=2013-11-01&rft.volume=34&rft.issue=33&rft.spage=8301&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=1878-5905&rft_id=info:doi/10.1016%2Fj.biomaterials.2013.07.013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-04
N1  - Date created - 2013-08-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Br J Cancer. 1955 Dec;9(4):539-49 [13304213]
J Cell Biol. 1997 Apr 7;137(1):231-45 [9105051]
Nat Rev Cancer. 2005 Sep;5(9):675-88 [16148884]
Nat Rev Mol Cell Biol. 2006 Mar;7(3):211-24 [16496023]
Nat Rev Cancer. 2006 Aug;6(8):583-92 [16862189]
Annu Rev Cell Dev Biol. 2006;22:287-309 [16824016]
FASEB J. 2006 Dec;20(14):2531-3 [17077286]
Biotechnol Bioeng. 2007 Jan 1;96(1):156-66 [16917927]
Biomed Microdevices. 2007 Apr;9(2):123-34 [17160707]
Anticancer Res. 2007 May-Jun;27(3A):1295-300 [17593622]
Cell. 2007 Aug 24;130(4):601-10 [17719539]
Nat Rev Mol Cell Biol. 2007 Oct;8(10):839-45 [17684528]
Nat Methods. 2007 Oct;4(10):855-60 [17767164]
J Natl Cancer Inst. 2007 Oct 3;99(19):1441-54 [17895480]
Biomaterials. 2007 Dec;28(36):5487-97 [17881050]
Int J Radiat Biol. 2007 Nov-Dec;83(11-12):849-71 [18058370]
Biotechnol Bioeng. 2008 Apr 15;99(6):1472-81 [17969156]
Biomaterials. 2008 May;29(14):2259-69 [18289662]
Lab Chip. 2008 Jul;8(7):1042-7 [18584077]
Matrix Biol. 2008 Jul;27(6):573-85 [18411046]
Semin Cancer Biol. 2008 Oct;18(5):311-21 [18455428]
Biotechnol J. 2008 Oct;3(9-10):1172-84 [18566957]
Adv Biochem Eng Biotechnol. 2009;112:1-27 [19290495]
Mol Oncol. 2007 Jun;1(1):84-96 [18516279]
Theor Biol Med Model. 2009;6:5 [19371422]
Assay Drug Dev Technol. 2009 Jun;7(3):233-49 [19548831]
J Cell Physiol. 2009 Oct;221(1):18-25 [19492404]
Biorheology. 2009;46(5):417-37 [19940357]
Nat Mater. 2010 Feb;9(2):90-3 [20094076]
Nanomedicine (Lond). 2010 Apr;5(3):469-84 [20394538]
Biomed Microdevices. 2010 Jun;12(3):465-75 [20174871]
Stem Cells. 2010 Jun;28(6):1019-29 [20506127]
J Biotechnol. 2010 Jul 1;148(1):3-15 [20097238]
Biomaterials. 2010 Nov;31(32):8494-506 [20709389]
J Biomater Sci Polym Ed. 2011;22(11):1509-22 [20626957]
Biomaterials. 2011 Sep;32(26):6052-8 [21640378]
Acta Biomater. 2011 Sep;7(9):3312-24 [21704736]
Biomaterials. 2011 Nov;32(31):7905-12 [21782234]
Proc Natl Acad Sci U S A. 2011 Nov 15;108(46):18708-13 [22068913]
Tissue Eng Part C Methods. 2012 Jan;18(1):54-61 [21902468]
Cancer Cell. 2012 Mar 20;21(3):309-22 [22439926]
Biomaterials. 2012 Nov;33(33):8430-41 [22940219]
Integr Biol (Camb). 2013 Mar;5(3):597-605 [23388834]
J Natl Cancer Inst. 2013 Apr 3;105(7):452-8 [23434901]
Cell Biol Int. 1999;23(3):157-61 [10562436]
Artif Organs. 2000 Apr;24(4):278-88 [10816201]
Biomaterials. 2001 Dec;22(24):3273-83 [11700799]
Curr Opin Biotechnol. 2003 Oct;14(5):526-32 [14580584]
Anal Chem. 2003 Dec 1;75(23):6544-54 [14640726]
Nat Biotechnol. 2004 Feb;22(2):151-2 [14755282]
Trends Biotechnol. 2004 Feb;22(2):80-6 [14757042]
Br J Cancer. 1968 Jun;22(2):258-73 [5660132]
J Cell Biol. 1972 Sep;54(3):626-37 [4339818]
Biochemistry. 1982 Nov 23;21(24):6188-93 [6217835]
J Theor Biol. 1982 Nov 7;99(1):31-68 [6892044]
Cancer Res. 1985 Sep;45(9):4200-5 [4028010]
Science. 1988 Apr 8;240(4849):177-84 [2451290]
J Neurosci Methods. 1991 Apr;37(2):173-82 [1715499]
J Cell Physiol. 1992 May;151(2):386-94 [1572910]
J Surg Res. 1992 Dec;53(6):549-57 [1494286]
J Natl Cancer Inst. 1994 Dec 21;86(24):1846-52 [7990159]
Life Sci. 1995;57(2):131-41 [7603295]
Semin Cancer Biol. 2005 Oct;15(5):378-86 [15975825]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.biomaterials.2013.07.013
ER  - 



TY  - JOUR
T1  - Modulation of Distinct Asthmatic Phenotypes in Mice by Dose-Dependent Inhalation of Microbial Products
AN  - 1500787673; 19052661
AB  - Background: Humans with asthma display considerable heterogeneity with regard to T helper (Th) 2-associated eosinophilic and Th17-associated neutrophilic inflammation, but the impact of the environment on these different forms of asthma is poorly understood. Objective: We studied the nature and longevity of asthma-like responses triggered by inhalation of allergen together with environmentally relevant doses of inhaled lipopolysaccharide (LPS). Methods: Ovalbumin (OVA) was instilled into the airways of mice together with a wide range of LPS doses. Following a single OVA challenge, or multiple challenges, animals were assessed for pulmonary cytokine production, airway inflammation, and airway hyperresponsiveness (AHR). Results: Mice instilled with OVA together with very low doses ( less than or equal to 10-3 mu g) of LPS displayed modest amounts of Th2 cytokines, with associated airway eosinophilia and AHR after a single challenge, and these responses were sustained after multiple OVA challenges. When the higher but still environmentally relevant dose of 10-1 mu g LPS was used, mice initially displayed similar Th2 responses, as well as Th17-associated neutrophilia. After multiple OVA challenges, however, the 10-1 mu g LPS animals also accumulated large numbers of allergen-specific T regulatory (Treg) cells with high levels of inducible co-stimulatory molecule (ICOS). As a result, asthma-like features in these mice were shorter-lived than in mice sensitized using lower doses of LPS. Conclusions: The nature and longevity of Th2, Th17, and Treg immune responses to inhaled allergen are dependent on the quantity of LPS inhaled at the time of allergic sensitization. These findings might account in part for the heterogeneity of inflammatory infiltrates seen in lungs of asthmatics. Citation: Whitehead GS, Thomas SY, Cook DN. 2014. Modulation of distinct asthmatic phenotypes in mice by dose-dependent inhalation of microbial products. Environ Health Perspect 122:34-42; http://dx.doi.org/10.1289/ehp.1307280
JF  - Environmental Health Perspectives
AU  - Whitehead, Gregory S
AU  - Thomas, Seddon Y
AU  - Cook, Donald N
AD  - Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
Y1  - 2013/10/29/
PY  - 2013
DA  - 2013 Oct 29
SP  - 34
EP  - 42
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 122
IS  - 1
SN  - 0091-6765, 0091-6765
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Environment Abstracts; Health & Safety Science Abstracts
KW  - Inhalation
KW  - Ovalbumin
KW  - Helper cells
KW  - Respiratory diseases
KW  - Leukocytes (eosinophilic)
KW  - ICOS protein
KW  - Allergens
KW  - Lymphocytes T
KW  - Cytokines
KW  - Lipopolysaccharides
KW  - Respiratory tract
KW  - Leukocytes (neutrophilic)
KW  - Asthma
KW  - Mice
KW  - Eosinophilia
KW  - Longevity
KW  - Inflammation
KW  - Respiratory tract diseases
KW  - Lung
KW  - Immune response
KW  - Neutrophilia
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - A 01450:Environmental Pollution & Waste Treatment
KW  - ENA 07:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500787673?accountid=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=Environmental+Health+Perspectives&rft.atitle=Modulation+of+Distinct+Asthmatic+Phenotypes+in+Mice+by+Dose-Dependent+Inhalation+of+Microbial+Products&rft.au=Whitehead%2C+Gregory+S%3BThomas%2C+Seddon+Y%3BCook%2C+Donald+N&rft.aulast=Whitehead&rft.aufirst=Gregory&rft.date=2013-10-29&rft.volume=122&rft.issue=1&rft.spage=34&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1307280
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Inhalation; Ovalbumin; Helper cells; Leukocytes (neutrophilic); Asthma; Leukocytes (eosinophilic); Eosinophilia; Longevity; Inflammation; Respiratory tract diseases; ICOS protein; Lung; Allergens; Lymphocytes T; Lipopolysaccharides; Cytokines; Immune response; Neutrophilia; Respiratory tract; Mice; Respiratory diseases
DO  - http://dx.doi.org/10.1289/ehp.1307280
ER  - 



TY  - CPAPER
T1  - Mapping susceptibility QTLs for gene-environment interactions and environmental toxicity
T2  - 63rd Annual Meeting of the American Society of Human Genetics (ASHG 2013)
AN  - 1449784180; 6238065
JF  - 63rd Annual Meeting of the American Society of Human Genetics (ASHG 2013)
AU  - French, J
Y1  - 2013/10/22/
PY  - 2013
DA  - 2013 Oct 22
KW  - Toxicity
KW  - Gene mapping
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449784180?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=63rd+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2013%29&rft.atitle=Mapping+susceptibility+QTLs+for+gene-environment+interactions+and+environmental+toxicity&rft.au=French%2C+J&rft.aulast=French&rft.aufirst=J&rft.date=2013-10-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=63rd+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.ashg.org/cgi-bin/2013/ashg13SOE.pl
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-30
N1  - Last updated - 2013-11-11
ER  - 



TY  - CPAPER
T1  - Brain-directed AAV gene therapy
T2  - 63rd Annual Meeting of the American Society of Human Genetics (ASHG 2013)
AN  - 1449781572; 6238040
JF  - 63rd Annual Meeting of the American Society of Human Genetics (ASHG 2013)
AU  - Kaler, S
Y1  - 2013/10/22/
PY  - 2013
DA  - 2013 Oct 22
KW  - Gene therapy
KW  - Adeno-associated virus
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449781572?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=63rd+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2013%29&rft.atitle=Brain-directed+AAV+gene+therapy&rft.au=Kaler%2C+S&rft.aulast=Kaler&rft.aufirst=S&rft.date=2013-10-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=63rd+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.ashg.org/cgi-bin/2013/ashg13SOE.pl
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-30
N1  - Last updated - 2013-11-11
ER  - 



TY  - JOUR
T1  - Phytotechnologies - Preventing Exposures, Improving Public Health
AN  - 1328513628; 17848478
AB  - Phytotechnologies have potential to reduce the amount or toxicity of deleterious chemicals and agents, and thereby, can reduce human exposures to hazardous substances. As such, phytotechnologies are tools for primary prevention in public health. Recent research demonstrates phytotechnologies can be uniquely tailored for effective exposure prevention in a variety of applications. In addition to exposure prevention, plants can be used as sensors to identify environmental contamination and potential exposures. In this paper, we have presented applications and research developments in a framework to illustrate how phytotechnologies can meet basic public health needs for access to clean water, air, and food. Because communities can often integrate plant-based technologies at minimal cost and with low infrastructure needs, the use of these technologies can be applied broadly to minimize potential contaminant exposure and improve environmental quality. These natural treatment systems also provide valuable ecosystem services to communities and society. In the future, integrating and coordinating phytotechnology activities with public health research will allow technology development focused on prevention of environmental exposures to toxic compounds. Hence, phytotechnologies may provide sustainable solutions to environmental exposure challenges, improving public health and potentially reducing the burden of disease.
JF  - International Journal of Phytoremediation
AU  - Henry, Heather F
AU  - Burken, Joel G
AU  - Maier, Raina M
AU  - Newman, Lee A
AU  - Rock, Steven
AU  - Schnoor, Jerald L
AU  - Suk, William A
AD  - Superfund Research Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, henryh@niehs.nih.gov
Y1  - 2013/10/21/
PY  - 2013
DA  - 2013 Oct 21
SP  - 889
EP  - 899
PB  - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL  - 15
IS  - 9
SN  - 1522-6514, 1522-6514
KW  - Pollution Abstracts
KW  - Chemicals
KW  - Infrastructure
KW  - Prevention
KW  - Sensors
KW  - Phytoremediation
KW  - Environmental quality
KW  - Toxicity
KW  - Public health
KW  - Technology
KW  - P 5000:LAND POLLUTION
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328513628?accountid=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=International+Journal+of+Phytoremediation&rft.atitle=Phytotechnologies+-+Preventing+Exposures%2C+Improving+Public+Health&rft.au=Henry%2C+Heather+F%3BBurken%2C+Joel+G%3BMaier%2C+Raina+M%3BNewman%2C+Lee+A%3BRock%2C+Steven%3BSchnoor%2C+Jerald+L%3BSuk%2C+William+A&rft.aulast=Henry&rft.aufirst=Heather&rft.date=2013-10-21&rft.volume=15&rft.issue=9&rft.spage=889&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Phytoremediation&rft.issn=15226514&rft_id=info:doi/10.1080%2F15226514.2012.760521
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2016-08-03
N1  - SubjectsTermNotLitGenreText - Infrastructure; Chemicals; Prevention; Sensors; Phytoremediation; Environmental quality; Toxicity; Technology; Public health
DO  - http://dx.doi.org/10.1080/15226514.2012.760521
ER  - 



TY  - CPAPER
T1  - Immune Privilege vs. Autoimmunity in the Eye - A Role for Commensal Microbiota in Triggering Disease
T2  - 46th Annual Meeting of the Society for Leukocyte Biology
AN  - 1449781835; 6238584
JF  - 46th Annual Meeting of the Society for Leukocyte Biology
AU  - Caspi, Rachel
Y1  - 2013/10/20/
PY  - 2013
DA  - 2013 Oct 20
KW  - Eye
KW  - Autoimmune diseases
KW  - Commensals
KW  - Immune privilege
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449781835?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=46th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.atitle=Immune+Privilege+vs.+Autoimmunity+in+the+Eye+-+A+Role+for+Commensal+Microbiota+in+Triggering+Disease&rft.au=Caspi%2C+Rachel&rft.aulast=Caspi&rft.aufirst=Rachel&rft.date=2013-10-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=46th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.issn=&rft_id=info:doi/
L2  - http://leukocytebiology.org/PDFS/a3/a34d06b4-11a9-4d37-a574-527da7b0882f.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-30
N1  - Last updated - 2013-11-11
ER  - 



TY  - CPAPER
T1  - Chemokines: Tales from the Clinic
T2  - 46th Annual Meeting of the Society for Leukocyte Biology
AN  - 1449781118; 6238538
JF  - 46th Annual Meeting of the Society for Leukocyte Biology
AU  - Murphy, Phillip
Y1  - 2013/10/20/
PY  - 2013
DA  - 2013 Oct 20
KW  - Chemokines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449781118?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=46th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.atitle=Chemokines%3A+Tales+from+the+Clinic&rft.au=Murphy%2C+Phillip&rft.aulast=Murphy&rft.aufirst=Phillip&rft.date=2013-10-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=46th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.issn=&rft_id=info:doi/
L2  - http://leukocytebiology.org/PDFS/a3/a34d06b4-11a9-4d37-a574-527da7b0882f.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-30
N1  - Last updated - 2013-11-11
ER  - 



TY  - JOUR
T1  - Novel Modeling of Cancer Cell Signaling Pathways Enables Systematic Drug Repositioning for Distinct Breast Cancer Metastases
AN  - 1668253615; 20332233
AB  - A generally applicable modeling method based on integrative cancer biology is used to uncover tactics for repositioning existing drugs, with the potential to immediately improve treatments for advanced cancer.
JF  - Cancer Research
AU  - Zhao, Hong
AU  - Jin, Guangxu
AU  - Cui, Kemi
AU  - Ren, Ding
AU  - Liu, Timothy
AU  - Chen, Peikai
AU  - Wong, Solomon
AU  - Li, Fuhai
AU  - Fan, Yubo
AU  - Rodriguez, Angel
AU  - Chang, Jenny
AU  - Wong, Stephen TC
AD  - Department of Systems Medicine and Bioengineering; NCI Center for Modeling Cancer Development, The Methodist Hospital Research Institute, Weill Cornell Medical College; Methodist Cancer Center, The Methodist Hospital; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston; and The University of Texas at Austin, Austin, Texas
Y1  - 2013/10/15/
PY  - 2013
DA  - 2013 Oct 15
SP  - 6149
EP  - 6163
PB  - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL  - 73
IS  - 20
SN  - 0008-5472, 0008-5472
KW  - Biotechnology and Bioengineering Abstracts
KW  - Metastases
KW  - Breast cancer
KW  - Signal transduction
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668253615?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Novel+Modeling+of+Cancer+Cell+Signaling+Pathways+Enables+Systematic+Drug+Repositioning+for+Distinct+Breast+Cancer+Metastases&rft.au=Zhao%2C+Hong%3BJin%2C+Guangxu%3BCui%2C+Kemi%3BRen%2C+Ding%3BLiu%2C+Timothy%3BChen%2C+Peikai%3BWong%2C+Solomon%3BLi%2C+Fuhai%3BFan%2C+Yubo%3BRodriguez%2C+Angel%3BChang%2C+Jenny%3BWong%2C+Stephen+TC&rft.aulast=Zhao&rft.aufirst=Hong&rft.date=2013-10-15&rft.volume=73&rft.issue=20&rft.spage=6149&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-12-4617
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Metastases; Breast cancer; Signal transduction
DO  - http://dx.doi.org/10.1158/0008-5472.CAN-12-4617
ER  - 



TY  - JOUR
T1  - SPOCS: software for predicting and visualizing orthology/paralogy relationships among genomes
AN  - 1492611706; 18890996
AB  - Summary: At the rate that prokaryotic genomes can now be generated, comparative genomics studies require a flexible method for quickly and accurately predicting orthologs among the rapidly changing set of genomes available. SPOCS implements a graph-based ortholog prediction method to generate a simple tab-delimited table of orthologs and in addition, html files that provide a visualization of the predicted ortholog/paralog relationships to which gene/protein expression metadata may be overlaid.
JF  - Bioinformatics
AU  - Curtis, Darren S
AU  - Phillips, Aaron R
AU  - Callister, Stephen J
AU  - Conlan, Sean
AU  - McCue, Lee Ann
AD  - super(1)Computational & Statistical Analytics Division, Pacific Northwest National Laboratory, super(2)Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA, super(3)Genetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA and super(4)Computational Sciences & Mathematics Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA
Y1  - 2013/10/15/
PY  - 2013
DA  - 2013 Oct 15
SP  - 2641
EP  - 2642
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 20
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Computer programs
KW  - software
KW  - Proteins
KW  - genomics
KW  - Bioinformatics
KW  - orthology
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492611706?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=SPOCS%3A+software+for+predicting+and+visualizing+orthology%2Fparalogy+relationships+among+genomes&rft.au=Curtis%2C+Darren+S%3BPhillips%2C+Aaron+R%3BCallister%2C+Stephen+J%3BConlan%2C+Sean%3BMcCue%2C+Lee+Ann&rft.aulast=Curtis&rft.aufirst=Darren&rft.date=2013-10-15&rft.volume=29&rft.issue=20&rft.spage=2641&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt454
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Computer programs; software; Proteins; Bioinformatics; genomics; orthology
DO  - http://dx.doi.org/10.1093/bioinformatics/btt454
ER  - 



TY  - JOUR
T1  - Synthesis and SAR studies of 5-(pyridin-4-yl)-1,3,4-thiadiazol-2-amine derivatives as potent inhibitors of Bloom helicase.
AN  - 1434010478; 24012121
AB  - Human cells utilize a variety of complex DNA repair mechanisms in order to combat constant mutagenic and cytotoxic threats from both exogenous and endogenous sources. The RecQ family of DNA helicases, which includes Bloom helicase (BLM), plays an important function in DNA repair by unwinding complementary strands of duplex DNA as well as atypical DNA structures such as Holliday junctions. Mutations of the BLM gene can result in Bloom syndrome, an autosomal recessive disorder associated with cancer predisposition. BLM-deficient cells exhibit increased sensitivity to DNA damaging agents indicating that a selective BLM inhibitor could be useful in potentiating the anticancer activity of these agents. In this work, we describe the medicinal chemistry optimization of the hit molecule following a quantitative high-throughput screen of >355,000 compounds. These efforts lead to the identification of ML216 and related analogs, which possess potent BLM inhibition and exhibit selectivity over related helicases. Moreover, these compounds demonstrated cellular activity by inducing sister chromatid exchanges, a hallmark of Bloom syndrome. 
          Published by Elsevier Ltd.
JF  - Bioorganic & medicinal chemistry letters
AU  - Rosenthal, Andrew S
AU  - Dexheimer, Thomas S
AU  - Gileadi, Opher
AU  - Nguyen, Giang H
AU  - Chu, Wai Kit
AU  - Hickson, Ian 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, MD 20850, United States.
Y1  - 2013/10/15/
PY  - 2013
DA  - 2013 Oct 15
SP  - 5660
EP  - 5666
VL  - 23
IS  - 20
KW  - 1-(3-cyano-4-(1H-pyrazol-4-yl)phenyl)-3-(5-(pyridin-4-yl)-1,3,4-thiadiazol-2-yl)urea
KW  - 0
KW  - Amines
KW  - Enzyme Inhibitors
KW  - Phenylurea Compounds
KW  - Thiadiazoles
KW  - RecQ Helicases
KW  - EC 3.6.4.12
KW  - Index Medicus
KW  - PEPPSITM-IPr
KW  - NADPH
KW  - BS
KW  - BLM
KW  - HR
KW  - Inhibitor
KW  - nicotinamide adenine dinucleotide phosphate
KW  - PBS
KW  - DMF
KW  - dimethylformamide
KW  - absorption, distribution, metabolism and excretion
KW  - high throughput screen
KW  - SAR
KW  - Small molecule
KW  - Bloom syndrome
KW  - homologous recombination
KW  - Bloom helicase
KW  - MLM
KW  - SCE
KW  - ADME
KW  - HTS
KW  - phosphate buffered saline
KW  - mouse liver microsomes
KW  - [1,3-Bis(2,6-Diisopropylphenyl)imidazole-2-ylidene](3-chloropyridyl)palladium(II)chloride
KW  - sister chromatid exchanges
KW  - structure activity relationship
KW  - Cell Membrane Permeability -- drug effects
KW  - Humans
KW  - Caco-2 Cells
KW  - Structure-Activity Relationship
KW  - Thiadiazoles -- chemical synthesis
KW  - Thiadiazoles -- chemistry
KW  - Phenylurea Compounds -- chemistry
KW  - Phenylurea Compounds -- chemical synthesis
KW  - Amines -- pharmacology
KW  - RecQ Helicases -- metabolism
KW  - Enzyme Inhibitors -- chemistry
KW  - Amines -- chemistry
KW  - Enzyme Inhibitors -- pharmacology
KW  - Enzyme Inhibitors -- chemical synthesis
KW  - Thiadiazoles -- pharmacology
KW  - RecQ Helicases -- antagonists & inhibitors
KW  - Phenylurea Compounds -- pharmacology
KW  - Amines -- chemical synthesis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434010478?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+letters&rft.atitle=Synthesis+and+SAR+studies+of+5-%28pyridin-4-yl%29-1%2C3%2C4-thiadiazol-2-amine+derivatives+as+potent+inhibitors+of+Bloom+helicase.&rft.au=Rosenthal%2C+Andrew+S%3BDexheimer%2C+Thomas+S%3BGileadi%2C+Opher%3BNguyen%2C+Giang+H%3BChu%2C+Wai+Kit%3BHickson%2C+Ian+D%3BJadhav%2C+Ajit%3BSimeonov%2C+Anton%3BMaloney%2C+David+J&rft.aulast=Rosenthal&rft.aufirst=Andrew&rft.date=2013-10-15&rft.volume=23&rft.issue=20&rft.spage=5660&rft.isbn=&rft.btitle=&rft.title=Bioorganic+%26+medicinal+chemistry+letters&rft.issn=1464-3405&rft_id=info:doi/10.1016%2Fj.bmcl.2013.08.025
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-05
N1  - Date created - 2013-09-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Chem Res Toxicol. 1997 Jul;10(7):733-41 [9250406]
Cell. 1995 Nov 17;83(4):655-66 [7585968]
Mol Biol Cell. 1999 Mar;10(3):665-76 [10069810]
Nucleic Acids Res. 2006;34(8):2269-79 [16670433]
Trends Biochem Sci. 2008 Dec;33(12):609-20 [18926708]
Chem Res Toxicol. 2008 Dec;21(12):2361-9 [19548357]
Nat Rev Cancer. 2009 Sep;9(9):644-54 [19657341]
J Cell Biol. 2010 Mar 22;188(6):779-89 [20308424]
Structure. 2010 Sep 8;18(9):1149-58 [20826341]
Proc Natl Acad Sci U S A. 2011 Jan 25;108(4):1525-30 [21220316]
Bioorg Med Chem Lett. 2011 May 1;21(9):2697-701 [21194936]
Trends Genet. 2012 Jan;28(1):7-13 [22024395]
PLoS One. 2012;7(1):e30189 [22272300]
Nucleic Acids Res. 2012 Aug;40(15):7358-67 [22576367]
Chem Biol. 2013 Jan 24;20(1):55-62 [23352139]
Nucleic Acids Res. 2000 Jun 15;28(12):2420-30 [10871376]
Trends Biochem Sci. 2001 Jan;26(1):47-54 [11165517]
J Biol Chem. 2001 Jun 1;276(22):19375-81 [11278509]
Nucleic Acids Res. 2001 Jul 1;29(13):2843-9 [11433031]
Oncogene. 2002 Apr 11;21(16):2525-33 [11971187]
Int J Biochem Cell Biol. 2002 Nov;34(11):1496-501 [12200042]
Nature. 2003 Dec 18;426(6968):870-4 [14685245]
Proc Natl Acad Sci U S A. 1974 Nov;71(11):4508-12 [4140506]
J Biol Chem. 1998 Oct 16;273(42):27587-92 [9765292]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.bmcl.2013.08.025
ER  - 



TY  - JOUR
T1  - Genetic architecture of retinal and macular degenerative diseases: the promise and challenges of next-generation sequencing
AN  - 1622612650; 20868806
AB  - Inherited retinal degenerative diseases (RDDs) display wide variation in their mode of inheritance, underlying genetic defects, age of onset, and phenotypic severity. Molecular mechanisms have not been delineated for many retinal diseases, and treatment options are limited. In most instances, genotype-phenotype correlations have not been elucidated because of extensive clinical and genetic heterogeneity. Next-generation sequencing (NGS) methods, including exome, genome, transcriptome and epigenome sequencing, provide novel avenues towards achieving comprehensive understanding of the genetic architecture of RDDs. Whole-exome sequencing (WES) has already revealed several new RDD genes, whereas RNA-Seq and ChIP-Seq analyses are expected to uncover novel aspects of gene regulation and biological networks that are involved in retinal development, aging and disease. In this review, we focus on the genetic characterization of retinal and macular degeneration using NGS technology and discuss the basic framework for further investigations. We also examine the challenges of NGS application in clinical diagnosis and management.
JF  - Genome Medicine
AU  - Ratnapriya, Rinki
AU  - Swaroop, Anand
AD  - Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA, rinki.ratnapriya@nih.gov
Y1  - 2013/10/11/
PY  - 2013
DA  - 2013 Oct 11
SP  - 84
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 5
IS  - 10
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - Genomes
KW  - Gene expression
KW  - Molecular modelling
KW  - Retina
KW  - Heredity
KW  - Macular degeneration
KW  - retinal degeneration
KW  - Gene regulation
KW  - Aging
KW  - Transcription
KW  - G 07730:Development & Cell Cycle
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622612650?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+Medicine&rft.atitle=Genetic+architecture+of+retinal+and+macular+degenerative+diseases%3A+the+promise+and+challenges+of+next-generation+sequencing&rft.au=Ratnapriya%2C+Rinki%3BSwaroop%2C+Anand&rft.aulast=Ratnapriya&rft.aufirst=Rinki&rft.date=2013-10-11&rft.volume=5&rft.issue=10&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Genome+Medicine&rft.issn=1756-994X&rft_id=info:doi/10.1186%2Fgm488
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Last updated - 2014-11-12
N1  - SubjectsTermNotLitGenreText - Gene expression; Genomes; Molecular modelling; retinal degeneration; Macular degeneration; Heredity; Retina; Gene regulation; Aging; Transcription
DO  - http://dx.doi.org/10.1186/gm488
ER  - 



TY  - JOUR
T1  - Minimal NF-κB activity in neurons.
AN  - 1431297059; 23872390
AB  - Nuclear factor-kappa B (NF-κB) is a ubiquitous transcription factor that regulates immune and cell-survival signaling pathways. NF-κB has been reported to be present in neurons wherein it reportedly responds to immune and toxic stimuli, glutamate, and synaptic activity. However, because the brain contains many cell types, assays specifically measuring neuronal NF-κB activity are difficult to perform and interpret. To address this, we compared NF-κB activity in cultures of primary neocortical neurons, mixed brain cells, and liver cells, employing Western blot of NF-κB subunits, electrophoretic mobility shift assay (EMSA) of nuclear κB DNA binding, reporter assay of κB DNA binding, immunofluorescence of the NF-κB subunit protein p65, quantitative real-time polymerase chain reaction (PCR) of NF-κB-regulated gene expression, and enzyme-linked immunosorbent assay (ELISA) of produced proteins. Assay of p65 showed its constitutive presence in cytoplasm and nucleus of neurons at levels significantly lower than in mixed brain or liver cells. EMSA and reporter assays showed that constitutive NF-κB activity was nearly absent in neurons. Induced activity was minimal--many fold lower than in other cell types, as measured by phosphorylation and degradation of the inhibitor IκBα, nuclear accumulation of p65, binding to κB DNA consensus sites, NF-κB reporting, or induction of NF-κB-responsive genes. The most efficacious activating stimuli for neurons were the pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin-beta (IL-β). Neuronal NF-κB was not responsive to glutamate in most assays, and it was also unresponsive to hydrogen peroxide, lipopolysaccharide, norepinephrine, ATP, phorbol ester, and nerve growth factor. The chemokine gene transcripts CCL2, CXCL1, and CXCL10 were strongly induced via NF-κB activation by TNFα in neurons, but many candidate responsive genes were not, including the neuroprotective genes SOD2 and Bcl-xL. Importantly, the level of induced neuronal NF-κB activity in response to TNFα or any other stimulus was lower than the level of constitutive activity in non-neuronal cells, calling into question the functional significance of neuronal NF-κB activity. Published by Elsevier Ltd.
JF  - Neuroscience
AU  - Listwak, S J
AU  - Rathore, P
AU  - Herkenham, M
AD  - Section on Functional Neuroanatomy, National Institute of Mental Health, NIH, Bethesda, MD 20892-3724, USA.
Y1  - 2013/10/10/
PY  - 2013
DA  - 2013 Oct 10
SP  - 282
EP  - 299
VL  - 250
KW  - Chemokines
KW  - 0
KW  - DNA Primers
KW  - Interleukin-1beta
KW  - NF-kappa B
KW  - Tumor Necrosis Factor-alpha
KW  - Glutamic Acid
KW  - 3KX376GY7L
KW  - DNA
KW  - 9007-49-2
KW  - Index Medicus
KW  - Tris-Buffered Saline containing 0.05% Tween-20
KW  - lipocalin 2
KW  - IgG
KW  - lipopolysaccharide
KW  - TBP
KW  - TLR
KW  - brain-derived neurotrophic factor
KW  - ISHH
KW  - ethylenediaminetetraacetic acid
KW  - PBS
KW  - nuclear localization signal
KW  - Dulbecco’s modified Eagle’s medium
KW  - transcription factor
KW  - mixed brain cells
KW  - BDNF
KW  - normal goat serum
KW  - Tata binding protein
KW  - quantitative real-time polymerase chain reaction
KW  - in situ hybridization histochemistry
KW  - ELISA
KW  - IL
KW  - NGS
KW  - PDTC
KW  - HRP
KW  - electrophoretic mobility shift assay
KW  - TNFα
KW  - sodium dodecyl sulfate
KW  - SDS
KW  - nerve growth factor
KW  - extracellular signal-regulated kinase
KW  - liver cells
KW  - NGF
KW  - horseradish peroxidase
KW  - IκB kinase
KW  - TNF
KW  - PMA
KW  - EMSA
KW  - immunoglobulin G
KW  - phorbol 12-myristate 13-acetate
KW  - tumor necrosis factor α
KW  - LVR
KW  - toll-like receptor
KW  - phosphate-buffered saline
KW  - glyceraldehyde 3-phosphate dehydrogenase
KW  - AP5
KW  - enzyme-linked immunosorbent assay
KW  - NF-κB
KW  - CNQX
KW  - HBSS
KW  - EDTA
KW  - ethylene glycol tetraacetic acid
KW  - qPCR
KW  - DMEM
KW  - plasticity
KW  - GAPDH
KW  - fetal bovine serum
KW  - EGTA
KW  - nuclear factor-kappa B
KW  - LPS
KW  - ERK
KW  - FBS
KW  - interleukin
KW  - TBST
KW  - cortical neurons
KW  - LCN2
KW  - BRN
KW  - ammonium pyrrolidinedithiocarbamate
KW  - TPCA
KW  - 6-cyano-7-nitroquinoxaline-2,3-dione
KW  - IKK
KW  - CxN
KW  - Hanks balanced salt solution
KW  - 2-amino-5-phosphonopentanoate
KW  - neuroprotection
KW  - 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide
KW  - NLS
KW  - Cerebral Cortex -- cytology
KW  - Animals
KW  - Liver -- cytology
KW  - Cerebral Cortex -- metabolism
KW  - Cell Nucleus -- metabolism
KW  - Electrophoretic Mobility Shift Assay
KW  - Liver -- metabolism
KW  - Primary Cell Culture
KW  - DNA -- biosynthesis
KW  - Enzyme-Linked Immunosorbent Assay
KW  - Fluorescent Antibody Technique
KW  - Microglia -- metabolism
KW  - Real-Time Polymerase Chain Reaction
KW  - Cytosol -- metabolism
KW  - Tumor Necrosis Factor-alpha -- pharmacology
KW  - Chemokines -- biosynthesis
KW  - Mice
KW  - Interleukin-1beta -- pharmacology
KW  - Glutamic Acid -- pharmacology
KW  - Pregnancy
KW  - Blotting, Western
KW  - DNA -- genetics
KW  - Mice, Inbred C57BL
KW  - Immunohistochemistry
KW  - Female
KW  - NF-kappa B -- drug effects
KW  - Neurons -- metabolism
KW  - Neurons -- drug effects
KW  - NF-kappa B -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1431297059?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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&rft.atitle=Minimal+NF-%CE%BAB+activity+in+neurons.&rft.au=Listwak%2C+S+J%3BRathore%2C+P%3BHerkenham%2C+M&rft.aulast=Listwak&rft.aufirst=S&rft.date=2013-10-10&rft.volume=250&rft.issue=&rft.spage=282&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=1873-7544&rft_id=info:doi/10.1016%2Fj.neuroscience.2013.07.013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-04
N1  - Date created - 2013-09-09
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Neurosci Lett. 1995 Jun 2;192(1):41-4 [7675306]
Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9618-22 [7568184]
Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9077-81 [7568076]
J Neuroimmunol. 1995 Dec 31;63(2):113-23 [8550808]
J Neurosci. 2002 Oct 1;22(19):8466-75 [12351721]
Neuroscience. 2003;116(2):425-35 [12559097]
EMBO J. 2003 Jul 1;22(13):3356-66 [12839997]
J Comp Neurol. 2003 Oct 20;465(3):417-30 [12966565]
Nat Neurosci. 2003 Oct;6(10):1072-8 [12947408]
J Neurosci. 2003 Oct 15;23(28):9403-8 [14561868]
Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15983-8 [14668448]
FASEB J. 2004 Apr;18(6):723-4 [14766792]
J Biol Chem. 2004 Jul 30;279(31):32869-81 [15155767]
Cell Res. 2011 Jan;21(1):22-39 [21119682]
Antioxid Redox Signal. 2011 Apr 1;14(7):1245-59 [20836702]
J Neurosci. 2011 Apr 6;31(14):5414-25 [21471377]
Trends Neurosci. 2011 Jun;34(6):316-25 [21459462]
Science. 1996 Apr 26;272(5261):542-5 [8614802]
J Biol Chem. 1996 Jun 21;271(25):15002-7 [8663145]
Development. 1996 Jul;122(7):2117-28 [8681793]
Oncogene. 1996 Jul 18;13(2):445-6 [8710386]
Stroke. 1997 May;28(5):1073-80; discussion 1080-1 [9158652]
J Biol Chem. 1997 Aug 22;272(34):21096-103 [9261113]
Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10985-90 [9380746]
J Neurosci. 1998 May 1;18(9):3224-32 [9547231]
J Neurosci. 1998 Dec 15;18(24):10457-63 [9852583]
J Biol Chem. 1999 Mar 26;274(13):8531-8 [10085086]
Brain Res Mol Brain Res. 1999 Apr 20;67(2):303-15 [10216229]
J Pharmacol Exp Ther. 2005 Jan;312(1):373-81 [15316093]
J Cereb Blood Flow Metab. 2005 Jan;25(1):30-40 [15678110]
J Neurosci. 2005 Feb 16;25(7):1788-96 [15716415]
Development. 2005 Apr;132(7):1713-26 [15743881]
J Biol Chem. 2005 Apr 29;280(17):17435-48 [15722553]
Eur J Neurosci. 2005 May;21(10):2845-52 [15926932]
Cell Death Differ. 2005 Jul;12(7):761-72 [15818410]
Mol Cell Biol. 2006 Apr;26(8):2936-46 [16581769]
Nat Neurosci. 2006 Jul;9(7):917-24 [16732273]
PLoS One. 2007;2(7):e589 [17622342]
J Neurosci Res. 2007 Aug 1;85(10):2120-5 [17510981]
Nat Rev Neurosci. 2007 Nov;8(11):895-903 [17948033]
J Neurosci. 2007 Dec 5;27(49):13436-45 [18057202]
Cell Signal. 2008 Jul;20(7):1338-48 [18436431]
Neuron. 2008 Aug 28;59(4):568-80 [18760694]
J Neuroinflammation. 2009;6:16 [19450264]
Development. 2009 Oct;136(20):3405-12 [19762427]
Antioxid Redox Signal. 2009 Sep;11(9):2223-43 [19496701]
PLoS One. 2009;4(12):e8289 [20011518]
Cold Spring Harb Perspect Biol. 2009 Sep;1(3):a001271 [20066105]
J Clin Invest. 2010 May;120(5):1368-79 [20440079]
J Neurosci Res. 2011 Jan;89(1):58-72 [21046675]
J Neurochem. 1999 Nov;73(5):1851-8 [10537043]
Biochem Pharmacol. 2000 Jan 1;59(1):13-23 [10605930]
Synapse. 2000 Feb;35(2):151-9 [10611641]
J Neurochem. 2000 Jun;74(6):2392-400 [10820200]
J Cell Biol. 2001 Feb 19;152(4):753-64 [11266466]
J Biol Chem. 2001 Apr 13;276(15):11821-9 [11096106]
Lab Invest. 2001 Sep;81(9):1275-88 [11555675]
J Immunol. 2002 Feb 1;168(3):1441-6 [11801687]
J Neurosci. 2002 Feb 1;22(3):854-62 [11826115]
J Neurosci. 2011 Jun 22;31(25):9075-83 [21697358]
Nature. 2011 Sep 1;477(7362):90-4 [21886162]
J Neuroinflammation. 2011;8:141 [21999414]
Proc Natl Acad Sci U S A. 2011 Nov 8;108(45):18436-41 [21969573]
J Biol Chem. 2011 Dec 23;286(51):43855-70 [22030398]
J Neurosci. 2012 Apr 18;32(16):5688-703 [22514330]
FASEB J. 2012 Jul;26(7):2811-23 [22441986]
Nat Neurosci. 2012 Aug;15(8):1096-101 [22837040]
Neuroscientist. 2013 Apr;19(2):175-94 [22785105]
J Neurosci. 2004 Sep 29;24(39):8500-9 [15456824]
Brain Res Bull. 1986 May;16(5):723-31 [2874876]
Mol Cell Biol. 1988 Aug;8(8):3526-31 [3145412]
J Biol Chem. 1991 Jan 5;266(1):252-60 [1985897]
Nature. 1993 Oct 21;365(6448):767-70 [7692309]
Neuron. 1994 Jan;12(1):139-53 [7507336]
Mol Cell Biol. 1994 Jun;14(6):3981-92 [8196637]
Methods Enzymol. 1994;234:151-63 [7808288]
Neurochem Int. 1995 Feb;26(2):173-8 [7599537]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.neuroscience.2013.07.013
ER  - 



TY  - JOUR
T1  - Familial Alzheimer's disease Osaka mutant (ΔE22) β-barrels suggest an explanation for the different Aβ1-40/42 preferred conformational states observed by experiment.
AN  - 1499118217; 24000923
AB  - An unusual ΔE693 mutation in the amyloid precursor protein (APP) producing a β-amyloid (Aβ) peptide lacking glutamic acid at position 22 (Glu22) was recently discovered, and dabbed the Osaka mutant (ΔE22). Previously, several point mutations in the Aβ peptide involving Glu22 substitutions were identified and implicated in the early onset of familial Alzheimer's disease (FAD). Despite the absence of Glu22, the Osaka mutant is also associated with FAD, showing a recessive inheritance in families affected by the disease. To see whether this aggregation-prone Aβ mutant could directly relate to the Aβ ion channel-mediated mechanism as observed for the wild type (WT) Aβ peptide in AD pathology, we modeled Osaka mutant β-barrels in a lipid bilayer. Using molecular dynamics (MD) simulations, two conformer ΔE22 barrels with the U-shaped monomer conformation derived from NMR-based WT Aβ fibrils were simulated in explicit lipid environment. Here, we show that the ΔE22 barrels obtain the lipid-relaxed β-sheet channel topology, indistinguishable from the WT Aβ1-42 barrels, as do the outer and pore dimensions of octadecameric (18-mer) ΔE22 barrels. Although the ΔE22 barrels lose the cationic binding site in the pore which is normally provided by the negatively charged Glu22 side chains, the mutant pores gain a new cationic binding site by Glu11 at the lower bilayer leaflet, and exhibit ion fluctuations similar to the WT barrels. Of particular interest, this deletion mutant suggests that toxic WT Aβ1-42 would preferentially adopt a less C-terminal turn similar to that observed for Aβ17-42, and explains why the solid state NMR data for Aβ1-40 point to a more C-terminal turn conformation. The observed ΔE22 barrels conformational preferences also suggest an explanation for the lower neurotoxicity in rat primary neurons as compared to WT Aβ1-42.
JF  - The journal of physical chemistry. B
AU  - Jang, Hyunbum
AU  - Arce, Fernando Teran
AU  - Ramachandran, Srinivasan
AU  - Kagan, Bruce L
AU  - Lal, Ratnesh
AU  - Nussinov, Ruth
AD  - Basic Science Program, SAIC-Frederick, Inc., Cancer and Inflammation Program, National Cancer Institute , Frederick, Maryland 21702, United States.
Y1  - 2013/10/03/
PY  - 2013
DA  - 2013 Oct 03
SP  - 11518
EP  - 11529
VL  - 117
IS  - 39
KW  - APP protein, human
KW  - 0
KW  - Amyloid
KW  - Amyloid beta-Peptides
KW  - Amyloid beta-Protein Precursor
KW  - Lipid Bilayers
KW  - Peptide Fragments
KW  - Phosphatidylcholines
KW  - amyloid beta-protein (1-40)
KW  - amyloid beta-protein (1-42)
KW  - 1,2-oleoylphosphatidylcholine
KW  - H026DM5V6U
KW  - Index Medicus
KW  - Hydrophobic and Hydrophilic Interactions
KW  - Protein Structure, Secondary
KW  - Alzheimer Disease -- genetics
KW  - Phosphatidylcholines -- chemistry
KW  - Humans
KW  - Amyloid -- chemistry
KW  - Lipid Bilayers -- chemistry
KW  - Amino Acid Sequence
KW  - Molecular Dynamics Simulation
KW  - Protein Conformation
KW  - Binding Sites
KW  - Amyloid beta-Protein Precursor -- chemistry
KW  - Peptide Fragments -- chemistry
KW  - Amyloid beta-Peptides -- chemistry
KW  - Amyloid beta-Protein Precursor -- genetics
KW  - Sequence Deletion
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499118217?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+physical+chemistry.+B&rft.atitle=Familial+Alzheimer%27s+disease+Osaka+mutant+%28%CE%94E22%29+%CE%B2-barrels+suggest+an+explanation+for+the+different+A%CE%B21-40%2F42+preferred+conformational+states+observed+by+experiment.&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=2013-10-03&rft.volume=117&rft.issue=39&rft.spage=11518&rft.isbn=&rft.btitle=&rft.title=The+journal+of+physical+chemistry.+B&rft.issn=1520-5207&rft_id=info:doi/10.1021%2Fjp405389n
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-11-04
N1  - Date created - 2014-02-04
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biophys J. 2007 Sep 15;93(6):1938-49 [17526580]
J Biol Chem. 2003 Nov 14;278(46):46179-87 [12944403]
Ann Neurol. 2008 Mar;63(3):377-87 [18300294]
Biophys J. 2008 Nov 15;95(10):4631-42 [18708452]
J Mol Biol. 2009 Feb 13;386(1):81-96 [19111557]
Am J Pathol. 2009 Mar;174(3):957-69 [19164507]
J Am Chem Soc. 2009 Oct 21;131(41):14938-45 [19824733]
Biophys J. 2009 Dec 2;97(11):3029-37 [19948133]
J Neurosci. 2010 Apr 7;30(14):4845-56 [20371804]
Am J Hum Genet. 1992 Nov;51(5):998-1014 [1415269]
Biophys J. 1993 Dec;65(6):2455-60 [7508762]
Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11631-5 [7526400]
Proteins. 1996 Jan;24(1):92-114 [8628736]
Proteins. 1995 Dec;23(4):566-79 [8749853]
Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10427-32 [16020533]
J Comput Chem. 2005 Dec;26(16):1781-802 [16222654]
Proc Natl Acad Sci U S A. 2005 Nov 29;102(48):17342-7 [16293696]
Biochemistry. 2006 Jan 17;45(2):498-512 [16401079]
J Biol Chem. 2006 Jan 27;281(4):2151-61 [16301322]
J Membr Biol. 2005 Dec;208(3):193-202 [16604469]
Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6538-43 [20308552]
FASEB J. 2010 May;24(5):1311-9 [20032312]
Biophys J. 2010 Jun 2;98(11):2644-52 [20513409]
J Phys Chem B. 2010 Jul 29;114(29):9445-51 [20608696]
Chem Rev. 2010 Aug 11;110(8):4820-38 [20402519]
J Phys Chem B. 2010 Jun 17;114(23):7830-43 [20496934]
J Mol Biol. 2010 Dec 17;404(5):917-34 [20970427]
PLoS One. 2011;6(1):e16248 [21267410]
Biochemistry. 2011 Mar 29;50(12):2026-39 [21291268]
J Mol Biol. 2011 May 13;408(4):780-91 [21402079]
Amyloid. 2011 Sep;18(3):98-107 [21668291]
J Am Chem Soc. 2011 Oct 12;133(40):16013-22 [21882806]
Biochemistry. 2012 Jan 24;51(3):776-85 [22242635]
J Phys Chem B. 2012 Feb 9;116(5):1728-35 [22217000]
Biochemistry. 2012 Apr 10;51(14):3031-8 [22413858]
J Mol Biol. 2012 Aug 10;421(2-3):172-84 [22119878]
J Mol Biol. 2012 Aug 24;421(4-5):572-86 [22281438]
Prion. 2012 Sep-Oct;6(4):339-45 [22874669]
J Mol Biol. 2013 Jan 23;425(2):292-308 [23154165]
Phys Chem Chem Phys. 2013 Jun 21;15(23):8868-77 [23450150]
Science. 1990 Jun 1;248(4959):1124-6 [2111584]
J Biol Chem. 2000 Sep 1;275(35):27110-6 [10821838]
Nat Neurosci. 2001 Sep;4(9):887-93 [11528419]
Annu Rev Genomics Hum Genet. 2002;3:67-99 [12142353]
Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14126-31 [12391326]
Biochim Biophys Acta. 2002 Oct 11;1565(2):308-17 [12409203]
Trends Biochem Sci. 2008 Feb;33(2):91-100 [18182298]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1021/jp405389n
ER  - 



TY  - JOUR
T1  - Role of Type II Pneumocyte Senescence in Radiation-Induced Lung Fibrosis
AN  - 1492627547; 18892597
AB  - Background Radiation is a commonly delivered therapeutic modality for cancer. The causes underlying the chronic, progressive nature of radiation injury in the lung are poorly understood. Methods C57Bl/6NCr mice were exposed to thoracic irradiation (n = 3 per dose and time point for tissue collection). Microarray analysis of gene expression from irradiated murine lung was performed using one-way analysis of variance with post hoc Scheffe analysis. Senescence and type II airway epithelial cell (AECII) count were assayed in irradiated murine lung tissue (n = 3 per condition). Irradiated mice were treated with diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase (NOX), and fibrosis was assessed by collagen assays. All statistical tests were two-tailed. Results Gene expression in lung tissue from mice irradiated to 17.5 Gy clustered with that of aged unirradiated mice. Only fibrogenic exposures led to AECII senescence (0 Gy: 0.66% +/- 0.67%; 5 Gy: 4.5% +/- 1.19%; 17.5 Gy: 18.7% +/- 3.05; P = .007) and depletion (0 Gy: 2.89 per alveolus +/- 0.26; 5 Gy: 2.41 +/- 0.19; 17.5 Gy: 1.6 +/- 0.14; P < .001) at 30 weeks. Treatment of irradiated mice with DPI for 16 weeks markedly reduced collagen accumulation (56 Gy: 57.26 mu g/lung +/- 9.91; 56 Gy +/- DPI: 36.54 mu g/lung +/- 4.39; P = .03) and AECII senescence (56 Gy: 37.61% +/- 4.82%; 56 Gy +/- DPI: 12.38% +/- 2.78; P < .001). Conclusions These studies identify senescence as an important process in AECII in vivo and indicate that NOX is a critical mediator of radiation-induced AECII senescence and pulmonary fibrosis.
JF  - Journal of the National Cancer Institute
AU  - Citrin, Deborah E
AU  - Shankavaram, Uma
AU  - Horton, Jason A
AU  - Shield, William
AU  - Zhao, Shuping
AU  - Asano, Hiroaki
AU  - White, Ayla
AU  - Sowers, Anastasia
AU  - Thetford, Angela
AU  - Chung, Eun Joo
AD  - Affiliations of authors: Radiation Oncology Branch (DEC, US, JAH, WS, SZ, HA, AY, EJC) and Radiation Biology Branch (AS, AT), Center for Cancer Research, National Institutes of Health, Bethesda, MD ., citrind@mail.nih.gov
Y1  - 2013/10/02/
PY  - 2013
DA  - 2013 Oct 02
SP  - 1474
EP  - 1484
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 19
SN  - 0027-8874, 0027-8874
KW  - Toxicology Abstracts
KW  - Alveoli
KW  - Lung
KW  - X 24300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492627547?accountid=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+the+National+Cancer+Institute&rft.atitle=Role+of+Type+II+Pneumocyte+Senescence+in+Radiation-Induced+Lung+Fibrosis&rft.au=Citrin%2C+Deborah+E%3BShankavaram%2C+Uma%3BHorton%2C+Jason+A%3BShield%2C+William%3BZhao%2C+Shuping%3BAsano%2C+Hiroaki%3BWhite%2C+Ayla%3BSowers%2C+Anastasia%3BThetford%2C+Angela%3BChung%2C+Eun+Joo&rft.aulast=Citrin&rft.aufirst=Deborah&rft.date=2013-10-02&rft.volume=105&rft.issue=19&rft.spage=1474&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjt212
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Lung
DO  - http://dx.doi.org/10.1093/jnci/djt212
ER  - 



TY  - JOUR
T1  - Daily temporal patterns of heroin and cocaine use and craving: Relationship with business hours regardless of actual employment status
AN  - 1837316694; 18610171
AB  - Real-time monitoring of behavior using Ecological Momentary Assessment (EMA) has provided detailed data about daily temporal patterns of craving and use in cigarette smokers. We have collected similar data from a sample of cocaine and heroin users. Here we analyzed it in the context of its relationship with a societal construct of daily temporal organization: 9-to-5 business hours. In a 28-week prospective study, 112 methadone-maintained polydrug-abusing individuals initiated an electronic-diary entry and provided data each time they used cocaine, heroin, or both during weeks 4 to 28. EMA data were collected for 10,781 person-days and included: 663 cocaine-craving events, 710 cocaine-use events, 288 heroin-craving events, 66 heroin-use events, 630 craving-both-drugs events, and 282 use-of-both-drugs events. At baseline, 34% of the participants reported full-time employment in the preceding 3-year period. Most participants' current employment status fluctuated throughout the study. In a generalized linear mixed model (SAS Proc Glimmix), cocaine use varied by time of day relative to business hours (p < 0.0001) and there was a significant interaction between Day of the Week and Time Relative to Business Hours (p < 0.002) regardless of current work status. Cocaine craving also varied by time of day relative to business hours (p < 0.0001), however, there was no significant interaction between Day of the Week and Time Relative to Business Hours (p = .57). Heroin craving and use were mostly reported during business hours, but data were sparse. Cocaine craving is most frequent during business hours while cocaine use is more frequent after business hours. Cocaine use during business hours, but not craving, seems suppressed on most weekdays, but not weekends, suggesting that societal conventions reflected in business hours influence drug-use patterns even in individuals whose daily schedules are not necessarily dictated by employment during conventional business hours.
JF  - Addictive Behaviors
AU  - Phillips, KA
AU  - Epstein, D H
AU  - Preston, K L
AD  - National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, 251 Bayview Blvd, BRC Building, Suite 200, Baltimore, MD 21224, USA, phillipsk@nida.nih.gov
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 2485
EP  - 2491
VL  - 38
IS  - 10
SN  - 0306-4603, 0306-4603
KW  - Toxicology Abstracts
KW  - Data processing
KW  - Cigarettes
KW  - Heroin
KW  - Cocaine
KW  - Drug abuse
KW  - Models
KW  - X 24380:Social Poisons & Drug Abuse
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837316694?accountid=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=Addictive+Behaviors&rft.atitle=Daily+temporal+patterns+of+heroin+and+cocaine+use+and+craving%3A+Relationship+with+business+hours+regardless+of+actual+employment+status&rft.au=Phillips%2C+KA%3BEpstein%2C+D+H%3BPreston%2C+K+L&rft.aulast=Phillips&rft.aufirst=KA&rft.date=2013-10-01&rft.volume=38&rft.issue=10&rft.spage=2485&rft.isbn=&rft.btitle=&rft.title=Addictive+Behaviors&rft.issn=03064603&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Data processing; Cigarettes; Heroin; Drug abuse; Cocaine; Models
ER  - 



TY  - JOUR
T1  - Effects of providing personalized feedback of child's obesity risk on mothers' food choices using a virtual reality buffet
AN  - 1680439004; 20501264
AB  - Background: Providing personalized genetic-risk feedback of a child's susceptibility to adult-onset health conditions is a topic of considerable debate. Family health history (FHH), specifically parental overweight/obesity status, is a useful assessment for evaluating a child's genetic and environmental risk of becoming obese. It is unclear whether such risk information may influence parents' efforts to reduce their child's risk of obesity.Purpose:To evaluate whether telling mothers the magnitude of their child's risk of becoming obese based on personal FHH influenced food choices for their young child from a virtual reality-based buffet restaurant. Methods: Overweight/obese mothers of a child aged 4-5 years who met eligibility criteria (N=221) were randomly assigned to one of three experimental arms, which emphasized different health information: arm 1, food safety control (Control); arm 2, behavioral-risk information (BRI) alone or arm 3, behavioral-risk information plus personal FHH-based risk assessment (BRI+FHH). Mothers donned a head-mounted display to be immersed in a virtual restaurant buffet, where they selected virtual food and beverages as a lunch for their child. Results: Mothers who were randomized to BRI+FHH filled the index child's plate with an average of 45 fewer calories than those in the Control arm (P<0.05); those in the BRI arm filled the plate with 35 fewer calories than the Control arm, a non-significant difference. Calorie restriction was greatest among mothers in the BRI+FHH arm who received the weaker-risk message (that is, only one overweight parent). Conclusions: The influence of communicating a child's inherited risk of obesity on mothers' feeding practices may vary by the risk level conveyed. High-risk messages may best be coupled with strategies to increase mother's perceptions that efforts can be undertaken to reduce risk and build requisite behavioral skills to reduce risk.
JF  - International Journal of Obesity
AU  - McBride, C M
AU  - Persky, S
AU  - Wagner, L K
AU  - Faith, M S
AU  - Ward, D S
AD  - Social and Behavioral Research Branch, National Human Genome Research Institute (NHGRI), Bethesda, MD, USA
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1322
EP  - 1327
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 37
IS  - 10
SN  - 0307-0565, 0307-0565
KW  - Physical Education Index
KW  - Evaluation
KW  - Obesity
KW  - Genetics
KW  - Virtual reality
KW  - Restaurants
KW  - Strategy
KW  - Health
KW  - Feedback
KW  - Diet
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680439004?accountid=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=Effects+of+providing+personalized+feedback+of+child%27s+obesity+risk+on+mothers%27+food+choices+using+a+virtual+reality+buffet&rft.au=McBride%2C+C+M%3BPersky%2C+S%3BWagner%2C+L+K%3BFaith%2C+M+S%3BWard%2C+D+S&rft.aulast=McBride&rft.aufirst=C&rft.date=2013-10-01&rft.volume=37&rft.issue=10&rft.spage=1322&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2013.87
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2015-05-01
N1  - Last updated - 2015-06-12
N1  - SubjectsTermNotLitGenreText - Evaluation; Genetics; Obesity; Virtual reality; Restaurants; Strategy; Feedback; Health; Diet
DO  - http://dx.doi.org/10.1038/ijo.2013.87
ER  - 



TY  - JOUR
T1  - The concentration of bisphenol A in urine is affected by specimen collection, a preservative, and handling
AN  - 1664194148; PQ0001195205
AB  - In urine specimens that were collected from pregnant women in a large cohort, 24% contained more than 10ng/ml of total bisphenol A (BPA), suggesting external contamination. Therefore, we conducted an investigation of the source(s) of extraneous BPA in the specimens. We found that under the conditions used to collect urine specimens in the epidemiologic study, contamination with BPA occurred, and by two separate mechanisms.
JF  - Environmental Research
AU  - Longnecker, M P
AU  - Harbak, K
AU  - Kissling, GE
AU  - Hoppin, JA
AU  - Eggesbo, M
AU  - Jusko, T A
AU  - Eide, J
AU  - Koch, H M
AD  - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NIH/DHHS/USA, PO Box 12233, MD A3-05, NC 27709, USA
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 211
EP  - 214
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 126
SN  - 0013-9351, 0013-9351
KW  - Pollution Abstracts; Environment Abstracts
KW  - BPA bisphenol A
KW  - LOD limit of detection
KW  - LOQ limit of quantitation
KW  - MoBa Norwegian Mother and Child Cohort Study
KW  - QC quality control
KW  - SD standard deviation
KW  - Bisphenol A
KW  - Urine specimen collection
KW  - Contamination
KW  - Urine
KW  - Preservatives
KW  - Pregnancy
KW  - P 6000:TOXICOLOGY AND HEALTH
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664194148?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=The+concentration+of+bisphenol+A+in+urine+is+affected+by+specimen+collection%2C+a+preservative%2C+and+handling&rft.au=Longnecker%2C+M+P%3BHarbak%2C+K%3BKissling%2C+GE%3BHoppin%2C+JA%3BEggesbo%2C+M%3BJusko%2C+T+A%3BEide%2C+J%3BKoch%2C+H+M&rft.aulast=Longnecker&rft.aufirst=M&rft.date=2013-10-01&rft.volume=126&rft.issue=&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2013.07.002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2016-07-07
N1  - SubjectsTermNotLitGenreText - Bisphenol A; Urine; Preservatives; Pregnancy
DO  - http://dx.doi.org/10.1016/j.envres.2013.07.002
ER  - 



TY  - JOUR
T1  - The relationship among smoking, sleep, and chronic rheumatic conditions commonly associated with pain in the national health interview survey
AN  - 1558992196; 201432016
AB  - Chronic rheumatic conditions are typically characterized by chronic pain and are uniquely associated with increased rates of cigarette smoking and poor sleep quality. However, no study has examined the possible additive or interactive effects of these two health behaviors in individuals diagnosed with a chronic rheumatic condition. The goal of this study is to examine the relationship between cigarette smoking and sleep in a population sample of individuals diagnosed with a chronic rheumatic condition and related functional impairment. Cross sectional survey data was obtained from the 2007 National Health Interview Survey. Individuals diagnosed with a chronic rheumatic condition were more likely to be a former or current smoker compared to non-diagnosed individuals. Individuals with a chronic rheumatic condition were more likely to report <6 h of sleep per night and endorsed significantly more insomnia and daytime sleepiness. There was no interaction between diagnosis of a chronic rheumatic condition and smoking status on any of the sleep outcomes assessed. Finally, an interaction was observed suggesting individuals with a chronic rheumatic condition who currently smoke are more likely to report averaging <6 h of sleep per night and frequent insomnia compared to individuals with a chronic rheumatic condition who never smoked. These results suggest both a unique and additive relationship between smoking and sleep in individuals with a chronic rheumatic condition. Findings can likely be generalized to other conditions commonly associated with chronic pain. Adapted from the source document.
JF  - Journal of Behavioral Medicine
AU  - Stipelman, Brooke A
AU  - Augustson, Erik
AU  - McNeel, Timothy
AD  - Science of Research and Technology Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 6130 Executive Blvd., MSC 7326, Executive Plaza North, Room 4097, Rockville, MD, 20892-7326, USA stipelmanba@mail.nih.gov
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 539
EP  - 548
PB  - Springer Science+Business Media, Inc., Dordrecht, The Netherlands
VL  - 36
IS  - 5
SN  - 0160-7715, 0160-7715
KW  - Insomnia
KW  - Smoking
KW  - Chronic pain
KW  - Sleep
KW  - Health
KW  - Additives
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558992196?accountid=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=The+relationship+among+smoking%2C+sleep%2C+and+chronic+rheumatic+conditions+commonly+associated+with+pain+in+the+national+health+interview+survey&rft.au=Stipelman%2C+Brooke+A%3BAugustson%2C+Erik%3BMcNeel%2C+Timothy&rft.aulast=Stipelman&rft.aufirst=Brooke&rft.date=2013-10-01&rft.volume=36&rft.issue=5&rft.spage=539&rft.isbn=&rft.btitle=&rft.title=Journal+of+Behavioral+Medicine&rft.issn=01607715&rft_id=info:doi/10.1007%2Fs10865-012-9447-8
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-09-01
N1  - Number of references - 63
N1  - Last updated - 2016-09-27
N1  - CODEN - JBMEDD
N1  - SubjectsTermNotLitGenreText - Sleep; Smoking; Chronic pain; Health; Additives; Insomnia
DO  - http://dx.doi.org/10.1007/s10865-012-9447-8
ER  - 



TY  - JOUR
T1  - Neurofeedback Training as an Intervention in a Silent Epidemic: An Indian Scenario
AN  - 1496665574; 201401278
AB  - Traumatic brain injury (TBI) is a 'silent epidemic' that creates a significant burden on health care resources across the globe. TBI is a dynamic process that involves damage to the brain, thus leading to behavioral, cognitive, and emotional consequences and poor quality of life. Neurofeedback training (NFT) was employed as an intervention to study its efficacy in postconcussion symptoms, cognitive deficits, and quality of life. A pre-post design was adopted in which the intervention group underwent NFT and the other waitlist group served as a control. NFT was found to be efficacious in ameliorating postconcussion symptoms and cognitive dysfunctions and improving quality of life. Adapted from the source document.
JF  - Journal of Neurotherapy
AU  - Reddy, Rajakumari P
AU  - Rajeswaran, Jamuna
AU  - Devi, Bhagavatula Indira
AU  - Kandavel, Thennarasu
AD  - Department of Clinical Psychology, National Institute of Mental Health and Neurosciences, Bangalore, India
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 213
EP  - 225
PB  - Taylor & Francis, Philadelphia PA
VL  - 17
IS  - 4
SN  - 1087-4208, 1087-4208
KW  - Symptoms
KW  - Epidemics
KW  - Brain
KW  - Traumatic brain injury
KW  - Dysfunction
KW  - Quality of life
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496665574?accountid=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+Neurotherapy&rft.atitle=Neurofeedback+Training+as+an+Intervention+in+a+Silent+Epidemic%3A+An+Indian+Scenario&rft.au=Reddy%2C+Rajakumari+P%3BRajeswaran%2C+Jamuna%3BDevi%2C+Bhagavatula+Indira%3BKandavel%2C+Thennarasu&rft.aulast=Reddy&rft.aufirst=Rajakumari&rft.date=2013-10-01&rft.volume=17&rft.issue=4&rft.spage=213&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurotherapy&rft.issn=10874208&rft_id=info:doi/10.1080%2F10874208.2013.847139
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-01-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Quality of life; Symptoms; Epidemics; Dysfunction; Traumatic brain injury; Brain
DO  - http://dx.doi.org/10.1080/10874208.2013.847139
ER  - 



TY  - JOUR
T1  - Maximizing DNA Yield for Epidemiologic Studies: No More Buffy Coats?
AN  - 1492616520; 18890573
AB  - Some molecular analyses require microgram quantities of DNA, yet many epidemiologic studies preserve only the buffy coat. In Frederick, Maryland, in 2010, we estimated DNA yields from 5 mL of whole blood and from equivalent amounts of all-cell-pellet (ACP) fraction, buffy coat, and residual blood cells from fresh blood (n = 10 volunteers) and from both fresh and frozen blood (n = 10). We extracted DNA with the QIAamp DNA Blood Midi Kit (Qiagen Sciences, Germantown, Maryland) for silica spin column capture and measured double-stranded DNA. Yields from frozen blood fractions were not statistically significantly different from those obtained from fresh fractions. ACP fractions yielded 80.6% (95% confidence interval: 66, 97) of the yield of frozen whole blood and 99.3% (95% confidence interval: 86, 100) of the yield of fresh blood. Frozen buffy coat and residual blood cells each yielded only half as much DNA as frozen ACP, and the yields were more variable. Assuming that DNA yield and quality from frozen ACP are stable, we recommend freezing plasma and ACP. Not only does ACP yield twice as much DNA as buffy coat but it is easier to process, and its yield is less variable from person to person. Long-term stability studies are needed. If one wishes to separate buffy coat before freezing, one should also save the residual blood cell fraction, which contains just as much DNA.
JF  - American Journal of Epidemiology
AU  - Gail, Mitchell H
AU  - Sheehy, Tim
AU  - Cosentino, Mark
AU  - Pee, David
AU  - Diaz-Mayoral, Norma A
AU  - Garcia-Closas, Montserrat
AU  - Caporaso, Neil E
AU  - Pitt, Karen
AU  - Ziegler, Regina G
AD  - Correspondence to Dr. Mitchell H. Gail, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room 7-E138, Bethesda, MD 20892-9780, gailm@mail.nih.gov
Y1  - 2013/10/01/
PY  - 2013
DA  - 2013 Oct 01
SP  - 1170
EP  - 1176
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 178
IS  - 7
SN  - 0002-9262, 0002-9262
KW  - Biochemistry Abstracts 2: Nucleic Acids; Health & Safety Science Abstracts
KW  - Silica
KW  - DNA
KW  - Buffy coat
KW  - Freezing
KW  - Blood cells
KW  - USA, Maryland
KW  - N 14845:Miscellaneous
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492616520?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Maximizing+DNA+Yield+for+Epidemiologic+Studies%3A+No+More+Buffy+Coats%3F&rft.au=Gail%2C+Mitchell+H%3BSheehy%2C+Tim%3BCosentino%2C+Mark%3BPee%2C+David%3BDiaz-Mayoral%2C+Norma+A%3BGarcia-Closas%2C+Montserrat%3BCaporaso%2C+Neil+E%3BPitt%2C+Karen%3BZiegler%2C+Regina+G&rft.aulast=Gail&rft.aufirst=Mitchell&rft.date=2013-10-01&rft.volume=178&rft.issue=7&rft.spage=1170&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwt079
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Silica; Freezing; Buffy coat; DNA; Blood cells; USA, Maryland
DO  - http://dx.doi.org/10.1093/aje/kwt079
ER  - 



TY  - JOUR
T1  - Sequential screening for psychosocial and behavioural risk during pregnancy in a population of urban African Americans
AN  - 1492615609; 18736377
AB  - Screening for psychosocial and behavioural risks, such as depression, intimate partner violence, and smoking, during pregnancy is considered to be state of the art in prenatal care. This prospective longitudinal analysis examines the added benefit of repeated screening, compared with a single screening, in identifying such risks during pregnancy. Data were collected as part of a randomised controlled trial to address intimate partner violence, depression, smoking, and environmental tobacco smoke exposure in African American women. Prenatal care sites in the District of Columbia serving mainly women of minority background. A cohort of 1044 African American pregnant women in the District of Columbia. Mothers were classified by their initial response (acknowledgement of risks), and these data were updated during pregnancy. Risks were considered new if they were not previously reported. Standard hypothesis tests and logistic regression were used to predict the acknowledgment of any new risk(s) during pregnancy. New risks: psychosocial variables to understand what factors might help identify the acknowledgement of additional risk(s). Repeated screening identified more mothers acknowledging risk over time. Reported smoking increased by 11%, environmental tobacco smoke exposure increased by 19%, intimate partner violence increased by 9%, and depression increased by 20%. The psychosocial variables collected at the baseline that were entered into the logistic regression model included relationship status, education, Medicaid, illicit drug use, and alcohol use during pregnancy. Among these, only education less than high school was associated with the acknowledgement of new risk in the bivariate analyses, and significantly predicted the identification of new risks (OR 1.39, 95% CI 1.01-1.90). It is difficult to predict early on who will acknowledge new risks over the course of pregnancy, and thus all women should be screened repeatedly to allow for the identification of risks and intervention during prenatal care.
JF  - BJOG
AU  - Kiely, M
AU  - Gantz, M G
AU  - El-Khorazaty, M N
AU  - El-Mohandes, AAE
AD  - Division of Epidemiology, Statistics and Prevention ResearchEunice Kennedy Shriver National Institute of Child Health and Human Development
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1395
EP  - 1402
PB  - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801
VL  - 120
IS  - 11
SN  - 1470-0328, 1470-0328
KW  - Risk Abstracts
KW  - Alcohol
KW  - Risk factors
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492615609?accountid=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=BJOG&rft.atitle=Sequential+screening+for+psychosocial+and+behavioural+risk+during+pregnancy+in+a+population+of+urban+African+Americans&rft.au=Kiely%2C+M%3BGantz%2C+M+G%3BEl-Khorazaty%2C+M+N%3BEl-Mohandes%2C+AAE&rft.aulast=Kiely&rft.aufirst=M&rft.date=2013-10-01&rft.volume=120&rft.issue=11&rft.spage=1395&rft.isbn=&rft.btitle=&rft.title=BJOG&rft.issn=14700328&rft_id=info:doi/10.1111%2F1471-0528.12202
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Risk factors
DO  - http://dx.doi.org/10.1111/1471-0528.12202
ER  - 



TY  - JOUR
T1  - Fertility drugs and endometrial cancer risk: results from an extended follow-up of a large infertility cohort
AN  - 1492613455; 18892069
AB  - STUDY QUESTION Do fertility drugs influence the subsequent risk of endometrial cancer in a manner that is independent of other risk predictors, such as parity? SUMMARY ANSWER In this follow-up of a large cohort of women evaluated for infertility and for whom information was captured on fertility drugs, indications for usage and other risk factors that might influence cancer risk, we found no evidence for a substantial relationship between fertility drug use and endometrial cancer risk. WHAT IS ALREADY KNOWN Although the hormonal etiology of endometrial cancer has been well established, it remains unclear whether the use of fertility drugs has an influence on risk. Results regarding the effects of fertility drugs on endometrial cancer risk have been inconsistent, although several studies have shown some evidence for possible increases in risk. The relationship is of particular interest given that clomiphene, a commonly prescribed drug, is a selective estrogen receptor modulator, with chemical properties similar to tamoxifen, another drug linked to an increase in endometrial cancer risk. STUDY DESIGN, SIZE, DURATION In a retrospective cohort of 12 193 women evaluated for infertility between 1965 and 1988 at five US sites, follow-up was pursued through 2010 via both passive as well as active (questionnaire) means. PARTICIPANTS, SETTING, METHODS Among the 9832 subjects for whom follow-up was allowed and achieved, 259 346 at-risk person-years (i.e. prior to hysterectomy) were accrued, and 118 invasive endometrial cancers identified. Cox regression determined hazard ratios (HRs) and 95% confidence intervals (CIs) for fertility treatments adjusted for endometrial cancer risk factors and causes of infertility. MAIN RESULTS AND THE ROLE OF CHANCE Although we observed slight increases in endometrial cancer risk associated with clomiphene (HR = 1.39, 95% CI: 0.96-2.01) and the less commonly prescribed gonadotrophins (1.34, 0.76-2.37), there were no convincing relationships of risk with either cycles of use or cumulative exposures for either drug. A statistically significant risk associated with the use of clomiphene among women who began use at younger ages (<30) (1.93, 1.24-3.00) may have reflected indications for drug usage rather than the effect of the drug itself. Women who received clomiphene followed by gonadotrophins were at a non-significantly elevated risk (1.77, 0.98-3.19). LIMITATIONS, REASONS FOR CAUTION Like most studies of endometrial cancer, we were limited by sample sizes, particularly for evaluating subgroup associations. We were also unable to follow all women and were not able to obtain complete risk factor information (including hysterectomy status) for the entire cohort. WIDER IMPLICATIONS OF THE FINDINGS Although we found no support for a relationship between fertility drugs and endometrial cancer risk, the association should continue to be monitored given that our study population was still young and had not yet reached the age of peak endometrial cancer incidence. STUDY FUNDING/COMPETING INTEREST(S) This project was supported in part by funds from the intramural research program of the National Cancer Institute, National Institutes of Health. None of the authors has any conflicting interests to declare.
JF  - Human Reproduction
AU  - Brinton, Louise A
AU  - Westhoff, Carolyn L
AU  - Scoccia, Bert
AU  - Lamb, Emmet J
AU  - Trabert, Britton
AU  - Niwa, Shelley
AU  - Moghissi, Kamran S
AD  - 1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA,, brinton@nih.gov
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 2813
EP  - 2821
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 28
IS  - 10
SN  - 0268-1161, 0268-1161
KW  - Risk Abstracts
KW  - Age
KW  - Health risks
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492613455?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+Reproduction&rft.atitle=Fertility+drugs+and+endometrial+cancer+risk%3A+results+from+an+extended+follow-up+of+a+large+infertility+cohort&rft.au=Brinton%2C+Louise+A%3BWesthoff%2C+Carolyn+L%3BScoccia%2C+Bert%3BLamb%2C+Emmet+J%3BTrabert%2C+Britton%3BNiwa%2C+Shelley%3BMoghissi%2C+Kamran+S&rft.aulast=Brinton&rft.aufirst=Louise&rft.date=2013-10-01&rft.volume=28&rft.issue=10&rft.spage=2813&rft.isbn=&rft.btitle=&rft.title=Human+Reproduction&rft.issn=02681161&rft_id=info:doi/10.1093%2Fhumrep%2Fdet323
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Health risks
DO  - http://dx.doi.org/10.1093/humrep/det323
ER  - 



TY  - JOUR
T1  - Illuminating the Black Box of Genome Sequence Assembly: a Free Online Tool to Introduce Students to Bioinformatics
AN  - 1492606137; 18714176
AB  - Next-generation sequencing technologies have greatly reduced the cost of sequencing genomes. With the current sequencing technology, a genome is broken into fragments and sequenced, producing millions of "reads." A computer algorithm pieces these reads together in the genome assembly process. PHAST is a set of online modules (http://gcat.davidson.edu/phast) designed to teach advanced high school and college students the genome assembly process. PHAST allows users to assemble phage genomes in real time and includes tutorials detailing the complexities of genome assembly. With PHAST, students learn concepts behind genome assembly and understand how mathematics solves biological problems such as genome assembly.
JF  - American Biology Teacher
AU  - Taylor, DLeland
AU  - Campbell, AMalcolm
AU  - Heyer, Laurie J
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 572
EP  - 577
PB  - National Association of Biology Teachers
VL  - 75
IS  - 8
SN  - 0002-7685, 0002-7685
KW  - Biotechnology and Bioengineering Abstracts
KW  - Algorithms
KW  - Genomes
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492606137?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Biology+Teacher&rft.atitle=Illuminating+the+Black+Box+of+Genome+Sequence+Assembly%3A+a+Free+Online+Tool+to+Introduce+Students+to+Bioinformatics&rft.au=Taylor%2C+DLeland%3BCampbell%2C+AMalcolm%3BHeyer%2C+Laurie+J&rft.aulast=Taylor&rft.aufirst=DLeland&rft.date=2013-10-01&rft.volume=75&rft.issue=8&rft.spage=572&rft.isbn=&rft.btitle=&rft.title=American+Biology+Teacher&rft.issn=00027685&rft_id=info:doi/10.1525%2Fabt.2013.75.8.9
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Genomes
DO  - http://dx.doi.org/10.1525/abt.2013.75.8.9
ER  - 



TY  - JOUR
T1  - Structure, dynamics and biophysics of the cytoplasmic protein-protein complexes of the bacterial phosphoenolpyruvate: sugar phosphotransferase system
AN  - 1468379089; 18735333
AB  - The bacterial phosphotransferase system (PTS) couples phosphoryl transfer, via a series of bimolecular protein-protein interactions, to sugar transport across the membrane. The multitude of complexes in the PTS provides a paradigm for studying protein interactions, and for understanding how the same binding surface can specifically recognize a diverse array of targets. Fifteen years of work aimed at solving the solution structures of all soluble protein-protein complexes of the PTS has served as a test bed for developing NMR and integrated hybrid approaches to study larger complexes in solution and to probe transient, spectroscopically invisible states, including encounter complexes. We review these approaches, highlighting the problems that can be tank-led with these methods, and summarize the current findings on protein interactions.
JF  - Trends in Biochemical Sciences
AU  - Clore, G M
AU  - Venditti, V
AD  - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0520, USA, mariusc@mail.nih.gov
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 515
EP  - 530
VL  - 38
IS  - 10
SN  - 0968-0004, 0968-0004
KW  - Microbiology Abstracts B: Bacteriology
KW  - Bacteria
KW  - Sugar
KW  - Reviews
KW  - Hybrids
KW  - Probes
KW  - N.M.R.
KW  - phosphotransferase
KW  - Protein interaction
KW  - Biophysics
KW  - J 02330:Biochemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468379089?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Biochemical+Sciences&rft.atitle=Structure%2C+dynamics+and+biophysics+of+the+cytoplasmic+protein-protein+complexes+of+the+bacterial+phosphoenolpyruvate%3A+sugar+phosphotransferase+system&rft.au=Clore%2C+G+M%3BVenditti%2C+V&rft.aulast=Clore&rft.aufirst=G&rft.date=2013-10-01&rft.volume=38&rft.issue=10&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Trends+in+Biochemical+Sciences&rft.issn=09680004&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2015-05-27
N1  - SubjectsTermNotLitGenreText - Sugar; Hybrids; Reviews; Probes; N.M.R.; phosphotransferase; Protein interaction; Biophysics; Bacteria
ER  - 



TY  - JOUR
T1  - A genomic update on clostridial phylogeny: Gram-negative spore formers and other misplaced clostridia
AN  - 1468372082; 18695626
AB  - The class Clostridia in the phylum Firmicutes (formerly low-G+C Gram-positive bacteria) includes diverse bacteria of medical, environmental and biotechnological importance. The Selenomonas-Megasphaera-Sporomusa branch, which unifies members of the Firmicutes with Gram-negative-type cell envelopes, was recently moved from Clostridia to a separate class Negativicutes. However, draft genome sequences of the spore-forming members of the Negativicutes revealed typically clostridial sets of sporulation genes. To address this and other questions in clostridial phylogeny, we have compared a phylogenetic tree for a concatenated set of 50 widespread ribosomal proteins with the trees for beta subunits of the RNA polymerase (RpoB) and DNA gyrase (GyrB) and with the 16S rRNA-based phylogeny. The results obtained by these methods showed remarkable consistency, suggesting that they reflect the true evolutionary history of these bacteria. These data put the Selenomonas-Megasphaera-Sporomusa group back within the Clostridia. They also support placement of Clostridium difficile and its close relatives within the family Peptostreptococcaceae; we suggest resolving the long-standing naming conundrum by renaming it Peptoclostridium difficile. These data also indicate the existence of a group of cellulolytic clostridia that belong to the family Ruminococcaceae. As a tentative solution to resolve the current taxonomical problems, we propose assigning 78 validly described Clostridium species that clearly fall outside the family Clostridiaceae to six new genera: Peptoclostridium, Lachnoclostridium, Ruminiclostridium, Erysipelatoclostridium, Gottschalkia and Tyzzerella. This work reaffirms that 16S rRNA and ribosomal protein sequences are better indicators of evolutionary proximity than phenotypic traits, even such key ones as the structure of the cell envelope and Gram-staining pattern.
JF  - Environmental Microbiology
AU  - Yutin, Natalya
AU  - Galperin, Michael Y
AD  - National Center for Biotechnology Information National Library of Medicine. National Institutes of Health
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 2631
EP  - 2641
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 15
IS  - 10
SN  - 1462-2912, 1462-2912
KW  - Microbiology Abstracts B: Bacteriology
KW  - Genomes
KW  - Phylogeny
KW  - Clostridium
KW  - Data processing
KW  - Cell envelopes
KW  - Gram-positive bacteria
KW  - Sporulation
KW  - DNA topoisomerase
KW  - Firmicutes
KW  - DNA-directed RNA polymerase
KW  - Ribosomal proteins
KW  - Clostridium difficile
KW  - genomics
KW  - New genera
KW  - Spores
KW  - Clostridiaceae
KW  - rRNA 16S
KW  - RpoB protein
KW  - Evolution
KW  - J 02310:Genetics & Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468372082?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Microbiology&rft.atitle=A+genomic+update+on+clostridial+phylogeny%3A+Gram-negative+spore+formers+and+other+misplaced+clostridia&rft.au=Yutin%2C+Natalya%3BGalperin%2C+Michael+Y&rft.aulast=Yutin&rft.aufirst=Natalya&rft.date=2013-10-01&rft.volume=15&rft.issue=10&rft.spage=2631&rft.isbn=&rft.btitle=&rft.title=Environmental+Microbiology&rft.issn=14622912&rft_id=info:doi/10.1111%2F1462-2920.12173
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-08-03
N1  - SubjectsTermNotLitGenreText - Phylogeny; Genomes; Data processing; Gram-positive bacteria; Cell envelopes; DNA topoisomerase; Sporulation; DNA-directed RNA polymerase; Ribosomal proteins; New genera; genomics; Spores; rRNA 16S; Evolution; RpoB protein; Clostridium; Clostridium difficile; Firmicutes; Clostridiaceae
DO  - http://dx.doi.org/10.1111/1462-2920.12173
ER  - 



TY  - JOUR
T1  - Mesenchymal stem cells inhibit cutaneous radiation-induced fibrosis by suppressing chronic inflammation
AN  - 1468352679; 18853056
AB  - Exposure to ionizing radiation (IR) can result in the development of cutaneous fibrosis, for which few therapeutic options exist. We tested the hypothesis that bone marrow-derived mesenchymal stem cells (BMSC) would favorably alter the progression of IR-induced fibrosis. We found that a systemic infusion of BMSC from syngeneic or allogeneic donors reduced skin contracture, thickening, and collagen deposition in a murine model. Transcriptional profiling with a fibrosis-targeted assay demonstrated increased expression of interleukin-10 (IL-10) and decreased expression of IL-1[beta] in the irradiated skin of mice 14 days after receiving BMSC. Similarly, immunoassay studies demonstrated durable alteration of these and several additional inflammatory mediators. Immunohistochemical studies revealed a reduction in infiltration of proinflammatory classically activated CD80 super(+) macrophages and increased numbers of anti-inflammatory regulatory CD163 super(+) macrophages in irradiated skin of BMSC-treated mice. In vitro coculture experiments confirmed that BMSC induce expression of IL-10 by activated macrophages, suggesting polarization toward a regulatory phenotype. Furthermore, we demonstrated that tumor necrosis factor-receptor 2 (TNF-R2) mediates IL-10 production and transition toward a regulatory phenotype during coculture with BMSC. Taken together, these data demonstrate that systemic infusion of BMSC can durably alter the progression of radiation-induced fibrosis by altering macrophage phenotype and suppressing local inflammation in a TNF-R2-dependent fashion. Stem Cells 2013; 31:2231-2241
JF  - Stem Cells
AU  - Horton, Jason A
AU  - Hudak, Kathryn E
AU  - Chung, Eun Joo
AU  - White, Ayla O
AU  - Scroggins, Bradley T
AU  - Burkeen, Jeffrey F
AU  - Citrin, Deborah E
AD  - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 2231
EP  - 2241
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 10
SN  - 1066-5099, 1066-5099
KW  - Biotechnology and Bioengineering Abstracts
KW  - Animal models
KW  - Inflammation
KW  - W 30920:Tissue Engineering
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468352679?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mesenchymal+stem+cells+inhibit+cutaneous+radiation-induced+fibrosis+by+suppressing+chronic+inflammation&rft.au=Horton%2C+Jason+A%3BHudak%2C+Kathryn+E%3BChung%2C+Eun+Joo%3BWhite%2C+Ayla+O%3BScroggins%2C+Bradley+T%3BBurkeen%2C+Jeffrey+F%3BCitrin%2C+Deborah+E&rft.aulast=Horton&rft.aufirst=Jason&rft.date=2013-10-01&rft.volume=31&rft.issue=10&rft.spage=2231&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1483
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Inflammation
DO  - http://dx.doi.org/10.1002/stem.1483
ER  - 



TY  - JOUR
T1  - Epistasis and Complex Neuropsychiatric Phenotypes
AN  - 1463067225; 201325779
AB  - Commentary on an article in the same journal issue by Chieh-Hsin Lin, Yu-Lun Tseng, Chieh-Liang Huang, Yue-Cune Chang, Guochuan E. Tsai, Hsien-Yuan Lane, "Synergistic Effects of COMT and TPH2 on Social Cognition" (p 273-294). Adapted from the source document.
JF  - Psychiatry
AU  - Eisenberg, Daniel Paul
AU  - Kleinman, Joel
AU  - Berman, Karen F
AD  - Section on Integrative Neuroimaging, National Institute of Mental Health, NIH, 9000 Rockville Pike, Building 10, Room 3C209, Bethesda, MD 20892-1365 eisenbergd@mail.nih.gov
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 295
EP  - 297
PB  - The Guilford Press
VL  - 76
IS  - 3
SN  - 0033-2747, 0033-2747
KW  - Phenotypes
KW  - Social cognition
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463067225?accountid=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=Psychiatry&rft.atitle=Epistasis+and+Complex+Neuropsychiatric+Phenotypes&rft.au=Eisenberg%2C+Daniel+Paul%3BKleinman%2C+Joel%3BBerman%2C+Karen+F&rft.aulast=Eisenberg&rft.aufirst=Daniel&rft.date=2013-10-01&rft.volume=76&rft.issue=3&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Psychiatry&rft.issn=00332747&rft_id=info:doi/
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-09-27
N1  - CODEN - PSYCAB
N1  - SubjectsTermNotLitGenreText - Social cognition; Phenotypes
ER  - 



TY  - JOUR
T1  - Resveratrol inhibits proliferation, angiogenesis and induces apoptosis in colon cancer cells: Calorie restriction is the force to the cytotoxicity
AN  - 1458541123; 18732267
AB  - The aim of this study was to examine the antitumour activity of resveratrol in human colorectal cancer cell lines (HCT116 and Caco2) and to explore its mechanism of action assuming that it is by calorie-restriction effect. Resveratrol inhibited the proliferation of colon cancer cells with half maximal inhibitory concentration (IC50) equal to 50 and 130 mu M for HCT116 and Caco2, respectively. Caco2 cells appeared with significant time-dependent increase in the glycolytic pathway, a behaviour that was absent in HCT116 cells. Resveratrol (100 mu M) significantly decreased the glycolytic enzymes (pyruvate kinase and lactate dehydrogenase) in Caco2 cells, while an increase in citrate synthase activity and a decrease in glucose consumption were observed in both cell lines. Moreover, resveratrol downregulated the expressions of leptin and c-Myc, and decreased the content of vascular endothelial growth factor. The apoptotic markers, caspases 3 and 8, were activated and the Bax/BCl2 ratio was increased. The study suggested a promising anticancer activity of resveratrol, calorie-restriction pathway may be one of the driving forces for this activity.
JF  - Human & Experimental Toxicology
AU  - Fouad, MA
AU  - Agha, A M
AU  - Merzabani, MM Al
AU  - Shouman, SA
AD  - Pharmacology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Egypt, samiasshouman@yahoo.com
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1067
EP  - 1080
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 32
IS  - 10
SN  - 0960-3271, 0960-3271
KW  - Toxicology Abstracts
KW  - Angiogenesis
KW  - Resveratrol
KW  - X:24300
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458541123?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+%26+Experimental+Toxicology&rft.atitle=Resveratrol+inhibits+proliferation%2C+angiogenesis+and+induces+apoptosis+in+colon+cancer+cells%3A+Calorie+restriction+is+the+force+to+the+cytotoxicity&rft.au=Fouad%2C+MA%3BAgha%2C+A+M%3BMerzabani%2C+MM+Al%3BShouman%2C+SA&rft.aulast=Fouad&rft.aufirst=MA&rft.date=2013-10-01&rft.volume=32&rft.issue=10&rft.spage=1067&rft.isbn=&rft.btitle=&rft.title=Human+%26+Experimental+Toxicology&rft.issn=09603271&rft_id=info:doi/10.1177%2F0960327113475679
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Resveratrol
DO  - http://dx.doi.org/10.1177/0960327113475679
ER  - 



TY  - JOUR
T1  - Physically developed and exploratory young infants contribute to their own long-term academic achievement
AN  - 1449950926; 4500862
AB  - A developmental cascade defines a longitudinal relation in which one psychological characteristic uniquely affects another psychological characteristic later in time, separately from other intrapersonal and extrapersonal factors. Here, we report results of a large-scale (N = 374), normative, prospective, 14-year longitudinal, multivariate, multisource, controlled study of a developmental cascade from infant motor-exploratory competence at 5 months to adolescent academic achievement at 14 years, through conceptually related and age-appropriate measures of psychometric intelligence at 4 and 10 years and academic achievement at 10 years. This developmental cascade applied equally to girls and boys and was independent of children's behavioral adjustment and social competence; mothers' supportive caregiving, verbal intelligence, education, and parenting knowledge; and the material home environment. Infants who were more motorically mature and who explored more actively at 5 months of age achieved higher academic levels as 14-year-olds. Reprinted by permission of Sage Publications
JF  - Psychological science
AU  - Bornstein, Marc H
AU  - Hahn, Chun-shin
AU  - Suwalsky, Joan T.D.
AD  - National Institutes of Health
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1906
EP  - 1917
VL  - 24
IS  - 10
SN  - 0956-7976, 0956-7976
KW  - Sociology
KW  - Longitudinal studies
KW  - Academic achievement
KW  - Gender
KW  - Cognitive development
KW  - Adolescents
KW  - Infants
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449950926?accountid=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=Pediatrics&rft.atitle=Prevalence+of+Retinal+Hemorrhages+in+Critically+Ill+Children&rft.au=Agrawal%2C+Shruti%2C+MD%2C+MRCPCH%3BPeters%2C+Mark+J%2C+MBChB%2C+PhD%3BAdams%2C+Gillian+GW%2C+FRCS+%28Ed%29%2C+FRCOphthal%3BPierce%2C+Christine+M%2C+MRCP%2C+FRCPCH&rft.aulast=Agrawal&rft.aufirst=Shruti&rft.date=2012-06-01&rft.volume=129&rft.issue=6&rft.spage=e1388&rft.isbn=&rft.btitle=&rft.title=Pediatrics&rft.issn=00314005&rft_id=info:doi/
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-11-11
N1  - Last updated - 2013-11-12
N1  - SubjectsTermNotLitGenreText - 501 542 8322; 2450 6075 3483; 593; 5421 6091; 6495 2212; 7541 7537 971
DO  - http://dx.doi.org/10.1177/0956797613479974
ER  - 



TY  - JOUR
T1  - Association between serum 25(OH) vitamin D, incident liver cancer and chronic liver disease mortality in the Linxian Nutrition Intervention Trials: a nested case-control study
AN  - 1448213597; 18656902
AB  - Background: Although vitamin D deficiency has been noted in cross-sectional studies of chronic liver disease and laboratory studies suggest possible benefits of vitamin D in preventing liver cancer, little epidemiologic data are available. Methods: We performed a nested case-control study in the Linxian Nutrition Intervention Trials on participants developing incident liver cancer or dying from chronic liver disease over 22 years of follow-up. Baseline serum 25(OH) vitamin D was measured for 226 incident liver cancer cases, 282 chronic liver disease deaths and 1063 age-, sex- and trial-matched controls. Unconditional logistical regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results: The median serum vitamin D level in controls was low (20 nmol l super(-1)). Compared with the lowest quartile, subjects in the fourth quartile had lower risk of chronic liver disease death (OR=0.34, 95% CI=0.21-0.55). For liver cancer incidence, risk estimates were below one, but were not statistically significant. Associations, however, were significant among participants with higher serum calcium levels (Q4 vs Q1, OR=0.43, 95% CI=0.21-0.89). Results for chronic liver disease did not vary by serum calcium level. Conclusion: In a low vitamin D population, higher serum 25(OH) vitamin D concentrations were associated with significantly lower risk of chronic liver disease deaths, and among those with higher serum calcium, incident liver cancer. Our results suggest a possible protective role for vitamin D in these diseases.
JF  - British Journal of Cancer
AU  - Wang, J-B
AU  - Abnet, C C
AU  - Chen, W
AU  - Dawsey, S M
AU  - Fan, J-H
AU  - Yin, L-Y
AU  - Yin, J
AU  - Major, J M
AU  - Taylor, P R
AU  - Qiao, Y-L
AU  - Freedman, N D
AD  - 1] Department of Cancer Epidemiology, Cancer Institute/Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China [2] Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20850, USA
Y1  - 2013/10/01/
PY  - 2013
DA  - 2013 Oct 01
SP  - 1997
EP  - 2004
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 109
IS  - 7
SN  - 0007-0920, 0007-0920
KW  - Risk Abstracts
KW  - Indexing in process
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448213597?accountid=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+between+serum+25%28OH%29+vitamin+D%2C+incident+liver+cancer+and+chronic+liver+disease+mortality+in+the+Linxian+Nutrition+Intervention+Trials%3A+a+nested+case-control+study&rft.au=Wang%2C+J-B%3BAbnet%2C+C+C%3BChen%2C+W%3BDawsey%2C+S+M%3BFan%2C+J-H%3BYin%2C+L-Y%3BYin%2C+J%3BMajor%2C+J+M%3BTaylor%2C+P+R%3BQiao%2C+Y-L%3BFreedman%2C+N+D&rft.aulast=Wang&rft.aufirst=J-B&rft.date=2013-10-01&rft.volume=109&rft.issue=7&rft.spage=1997&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.546
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-11-04
DO  - http://dx.doi.org/10.1038/bjc.2013.546
ER  - 



TY  - JOUR
T1  - Protecting a transgene expression from the HAC-based vector by different chromatin insulators
AN  - 1448209904; 18668784
AB  - Human artificial chromosomes (HACs) are vectors that offer advantages of capacity and stability for gene delivery and expression. Several studies have even demonstrated their use for gene complementation in gene-deficient recipient cell lines and animal transgenesis. Recently, we constructed an advance HAC-based vector, alphoid super(tetO)-HAC, with a conditional centromere. In this HAC, a gene-loading site was inserted into a centrochromatin domain critical for kinetochore assembly and maintenance. While by definition this domain is permissive for transcription, there have been no long-term studies on transgene expression within centrochromatin. In this study, we compared the effects of three chromatin insulators, cHS4, gamma-satellite DNA, and tDNA, on the expression of an EGFP transgene inserted into the alphoid super(tetO)-HAC vector. Insulator function was essential for stable expression of the transgene in centrochromatin. In two analyzed host cell lines, a tDNA insulator composed of two functional copies of tRNA genes showed the highest barrier activity. We infer that proximity to centrochromatin does not protect genes lacking chromatin insulators from epigenetic silencing. Barrier elements that prevent gene silencing in centrochromatin would thus help to optimize transgenesis using HAC vectors.
JF  - Cellular and Molecular Life Sciences
AU  - Lee, Nicholas CO
AU  - Kononenko, Artem V
AU  - Lee, Hee-Sheung
AU  - Tolkunova, Elena N
AU  - Liskovykh, Mikhail A
AU  - Masumoto, Hiroshi
AU  - Earnshaw, William C
AU  - Tomilin, Alexey N
AU  - Larionov, Vladimir
AU  - Kouprina, Natalay
AD  - Laboratories of Molecular Pharmacology, National Cancer Institute, Bethesda, MD, 20892, USA, larionov@mail.nih.gov
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 3723
EP  - 3737
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 70
IS  - 19
SN  - 1420-682X, 1420-682X
KW  - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts
KW  - Centromeres
KW  - Transgenes
KW  - W 30905:Medical Applications
KW  - N:14820
KW  - G:07700
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448209904?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+and+Molecular+Life+Sciences&rft.atitle=Protecting+a+transgene+expression+from+the+HAC-based+vector+by+different+chromatin+insulators&rft.au=Lee%2C+Nicholas+CO%3BKononenko%2C+Artem+V%3BLee%2C+Hee-Sheung%3BTolkunova%2C+Elena+N%3BLiskovykh%2C+Mikhail+A%3BMasumoto%2C+Hiroshi%3BEarnshaw%2C+William+C%3BTomilin%2C+Alexey+N%3BLarionov%2C+Vladimir%3BKouprina%2C+Natalay&rft.aulast=Lee&rft.aufirst=Nicholas&rft.date=2013-10-01&rft.volume=70&rft.issue=19&rft.spage=3723&rft.isbn=&rft.btitle=&rft.title=Cellular+and+Molecular+Life+Sciences&rft.issn=1420682X&rft_id=info:doi/10.1007%2Fs00018-013-1362-9
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Transgenes
DO  - http://dx.doi.org/10.1007/s00018-013-1362-9
ER  - 



TY  - JOUR
T1  - Macrophage solubilization and cytotoxicity of indium-containing particles in vitro.
AN  - 1445916101; 23872580
AB  - Indium-containing particles (ICPs) are used extensively in the microelectronics industry. Pulmonary toxicity is observed after inhalation exposure to ICPs; however, the mechanism(s) of pathogenesis is unclear. ICPs are insoluble at physiological pH and are initially engulfed by alveolar macrophages (and likely airway epithelial cells). We hypothesized that uptake of ICPs by macrophages followed by phagolysosomal acidification results in the solubilization of ICPs into cytotoxic indium ions. To address this, we characterized the in vitro cytotoxicity of indium phosphide (InP) or indium tin oxide (ITO) particles with macrophages (RAW cells) and lung-derived epithelial (LA-4) cells at 24h using metabolic (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) and membrane integrity (lactate dehydrogenase) assays. InP and ITO were readily phagocytosed by RAW and LA-4 cells; however, the particles were much more cytotoxic to RAW cells and cytotoxicity was dose dependent. Treatment of RAW cells with cytochalasin D (CytoD) blocked particle phagocytosis and reduced cytotoxicity. Treatment of RAW cells with bafilomycin A1, a specific inhibitor of phagolysosomal acidification, also reduced cytotoxicity but did not block particle uptake. Based on direct indium measurements, the concentration of ionic indium was increased in culture medium from RAW but not LA-4 cells following 24-h treatment with particles. Ionic indium derived from RAW cells was significantly reduced by treatment with CytoD. These data implicate macrophage uptake and solubilization of InP and ITO via phagolysosomal acidification as requisite for particle-induced cytotoxicity and the release of indium ions. This may apply to other ICPs and strongly supports the notion that ICPs require solubilization in order to be toxic.
JF  - Toxicological sciences : an official journal of the Society of Toxicology
AU  - Gwinn, William M
AU  - Qu, Wei
AU  - Shines, Cassandra J
AU  - Bousquet, Ronald W
AU  - Taylor, Genie J
AU  - Waalkes, Michael P
AU  - Morgan, Daniel L
AD  - * NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences and.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 414
EP  - 424
VL  - 135
IS  - 2
KW  - Indium
KW  - 045A6V3VFX
KW  - Index Medicus
KW  - indium
KW  - ITO
KW  - macrophage cytotoxicity.
KW  - solubilization
KW  - InP
KW  - Animals
KW  - Solubility
KW  - Spectrophotometry, Atomic
KW  - Mice
KW  - Phagocytosis
KW  - Cell Line
KW  - Macrophages -- cytology
KW  - Indium -- pharmacology
KW  - Cell Survival -- drug effects
KW  - Macrophages -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1445916101?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Macrophage+solubilization+and+cytotoxicity+of+indium-containing+particles+in+vitro.&rft.au=Gwinn%2C+William+M%3BQu%2C+Wei%3BShines%2C+Cassandra+J%3BBousquet%2C+Ronald+W%3BTaylor%2C+Genie+J%3BWaalkes%2C+Michael+P%3BMorgan%2C+Daniel+L&rft.aulast=Gwinn&rft.aufirst=William&rft.date=2013-10-01&rft.volume=135&rft.issue=2&rft.spage=414&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%2Fkft154
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-17
N1  - Date created - 2013-10-25
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Chin Med J (Engl). 2010 May 20;123(10):1347-50 [20529594]
ACS Nano. 2010 Nov 23;4(11):6767-79 [20949917]
ACS Nano. 2008 Jan;2(1):85-96 [19206551]
J Biol Chem. 2009 Mar 20;284(12):7681-6 [19136560]
Toxicol Sci. 2009 Apr;108(2):472-81 [19176593]
Exp Lung Res. 2009 Dec;35(10):858-82 [19995279]
J Occup Health. 2009;51(6):513-21 [19834281]
Toxicol Sci. 2001 Nov;64(1):28-40 [11606799]
Natl Toxicol Program Tech Rep Ser. 2001 Jul;(499):7-340 [12087422]
J Cell Biochem. 2003 Apr 15;88(6):1256-64 [12647307]
J Occup Health. 2003 May;45(3):137-9 [14646287]
J Occup Health. 2003 Jul;45(4):228-30 [14646281]
J Biol Chem. 1990 Dec 5;265(34):21099-107 [2147429]
Eur Respir J. 2005 Jan;25(1):200-4 [15640342]
Eur Respir J. 2007 Feb;29(2):317-24 [17050566]
Sci Total Environ. 2007 Nov 15;387(1-3):155-65 [17804041]
Occup Environ Med. 2008 Jan;65(1):51-5 [17626138]
Eur J Immunol. 2008 Jan;38(1):204-15 [18085665]
Biotechniques. 2008 May;44(6):799-805 [18476833]
Am J Physiol Cell Physiol. 2008 Jul;295(1):C2-12 [18434619]
J Occup Health. 2010;52(1):14-22 [19940388]
Am J Respir Crit Care Med. 2010 Mar 1;181(5):458-64 [20019344]
Nanoscale. 2011 Jun;3(6):2552-9 [21509403]
J Occup Health. 2011;53(3):175-87 [21471693]
Part Fibre Toxicol. 2011;8:27 [21896169]
Anaerobe. 2012 Feb;18(1):148-56 [22209938]
Int Arch Occup Environ Health. 2012 May;85(4):447-53 [21833746]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/toxsci/kft154
ER  - 



TY  - JOUR
T1  - Adolescent reports of aggression as predictors of perceived parenting behaviors and expectations
AN  - 1443631529; 4492592
AB  - This study examined the associations between adolescent self-report of aggression and adolescents' perceptions of parenting practices in a sample of African American early adolescents living in low-income, urban communities. Sixth graders (N=209) completed questionnaires about their aggressive behaviors and perceptions of caregivers' parenting practices at two time points during the school year. Path model findings reveal that adolescent-reported aggression at Time 1 predicted higher levels of perceived parent psychological control and perceived parent expectations for aggressive solutions to conflicts at Time 2. Findings suggest that early adolescent aggression elicits negative parenting behaviors at a subsequent time point.
JF  - Family relations
AU  - Murray, Kantahyanee W
AU  - Haynie, Denise L
AU  - Howard, Donna E
AU  - Cheng, Tina L
AU  - Simons-Morton, Bruce
AD  - University of Maryland ; Eunice Kennedy Shriver National Institute of Child Health and Human Development ; University of Maryland, College Park ; Johns Hopkins University
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 637
EP  - 648
VL  - 62
IS  - 4
SN  - 0197-6664, 0197-6664
KW  - Sociology
KW  - Parenting
KW  - Behavioural psychology
KW  - Aggression
KW  - Family relations
KW  - Low income
KW  - Adolescents
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443631529?accountid=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=Family+relations&rft.atitle=Adolescent+reports+of+aggression+as+predictors+of+perceived+parenting+behaviors+and+expectations&rft.au=Murray%2C+Kantahyanee+W%3BHaynie%2C+Denise+L%3BHoward%2C+Donna+E%3BCheng%2C+Tina+L%3BSimons-Morton%2C+Bruce&rft.aulast=Murray&rft.aufirst=Kantahyanee&rft.date=2013-10-01&rft.volume=62&rft.issue=4&rft.spage=637&rft.isbn=&rft.btitle=&rft.title=Family+relations&rft.issn=01976664&rft_id=info:doi/10.1111%2Ffare.12025
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-10-21
N1  - Last updated - 2013-10-22
N1  - SubjectsTermNotLitGenreText - 4777 6093; 9183; 593; 662; 7553 6271; 1540 1543 10404
DO  - http://dx.doi.org/10.1111/fare.12025
ER  - 



TY  - JOUR
T1  - TusA (YhhP) and IscS are required for molybdenum cofactor-dependent base-analog detoxification.
AN  - 1443425991; 23894086
AB  - Lack of molybdenum cofactor (Moco) in Escherichia coli leads to hypersensitivity to the mutagenic and toxic effects of N-hydroxylated base analogs, such as 6-N-hydroxylaminopurine (HAP). This phenotype is due to the loss of two Moco-dependent activities, YcbX and YiiM, that are capable of reducing HAP to adenine. Here, we describe two novel HAP-sensitive mutants containing a defect in iscS or tusA (yhhP) gene. IscS is a major L-cysteine desulfurase involved in iron-sulfur cluster synthesis, thiamine synthesis, and tRNA thiomodification. TusA is a small sulfur-carrier protein that interacts with IscS. We show that both IscS and TusA operate within the Moco-dependent pathway. Like other Moco-deficient strains, tusA and iscS mutants are HAP sensitive and resistant to chlorate under anaerobic conditions. The base-analog sensitivity of iscS or tusA strains could be suppressed by supplying exogenous L-cysteine or sulfide or by an increase in endogenous sulfur donors (cysB constitutive mutant). The data suggest that iscS and tusA mutants have a defect in the mobilization of sulfur required for active YcbX/YiiM proteins as well as nitrate reductase, presumably due to lack of functional Moco. Overall, our data imply a novel and indispensable role of the IscS/TusA complex in the activity of several molybdoenzymes.
          © 2013 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.
JF  - MicrobiologyOpen
AU  - Kozmin, Stanislav G
AU  - Stepchenkova, Elena I
AU  - Schaaper, Roel M
AD  - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, 27709.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 743
EP  - 755
VL  - 2
IS  - 5
KW  - Chlorates
KW  - 0
KW  - Coenzymes
KW  - Escherichia coli Proteins
KW  - Metalloproteins
KW  - Mutagens
KW  - Pteridines
KW  - TusA protein, E coli
KW  - 6-N-hydroxylaminopurine
KW  - 5667-20-9
KW  - Sulfur
KW  - 70FD1KFU70
KW  - molybdenum cofactor
KW  - 73508-07-3
KW  - Carbon-Sulfur Lyases
KW  - EC 4.4.-
KW  - cysteine desulfurase
KW  - EC 4.4.1.-
KW  - Adenine
KW  - JAC85A2161
KW  - Cysteine
KW  - K848JZ4886
KW  - chloric acid
KW  - Z0V9L75H3K
KW  - Index Medicus
KW  - chlorate resistance
KW  - 6-N-hydroxylaminopurine (HAP) sensitivity
KW  - molybdenum cofactor (Moco) biosynthesis
KW  - IscS cysteine desulfurase
KW  - TusA sulfur-carrier protein.
KW  - Cysteine -- pharmacology
KW  - Sulfur -- metabolism
KW  - Cysteine -- metabolism
KW  - Chlorates -- pharmacology
KW  - Mutagens -- pharmacology
KW  - Mutation
KW  - Adenine -- analogs & derivatives
KW  - Signal Transduction
KW  - Anaerobiosis
KW  - Adenine -- pharmacology
KW  - Gene Expression Regulation, Bacterial
KW  - Escherichia coli Proteins -- metabolism
KW  - Escherichia coli -- metabolism
KW  - Pteridines -- metabolism
KW  - Carbon-Sulfur Lyases -- metabolism
KW  - Carbon-Sulfur Lyases -- genetics
KW  - Escherichia coli -- drug effects
KW  - Coenzymes -- metabolism
KW  - Escherichia coli -- genetics
KW  - Metalloproteins -- metabolism
KW  - Escherichia coli Proteins -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443425991?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=MicrobiologyOpen&rft.atitle=TusA+%28YhhP%29+and+IscS+are+required+for+molybdenum+cofactor-dependent+base-analog+detoxification.&rft.au=Kozmin%2C+Stanislav+G%3BStepchenkova%2C+Elena+I%3BSchaaper%2C+Roel+M&rft.aulast=Kozmin&rft.aufirst=Stanislav&rft.date=2013-10-01&rft.volume=42&rft.issue=3&rft.spage=284&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Law%2C+Medicine+%26+Ethics&rft.issn=10731105&rft_id=info:doi/10.1111%2Fjlme.12145
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-02
N1  - Date created - 2013-10-10
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Adv Enzymol Relat Areas Mol Biol. 1975;42:287-333 [236639]
FEMS Microbiol Lett. 2002 Jan 22;207(1):55-61 [11886751]
J Bacteriol. 1982 Aug;151(2):788-99 [7047497]
Biochem Pharmacol. 1990 Mar 1;39(5):925-33 [2310418]
Mutat Res. 1991 Aug;253(1):33-46 [1870608]
Mol Microbiol. 1992 Nov;6(22):3452-4 [1484496]
J Bacteriol. 1998 Apr;180(8):2257-61 [9555915]
J Biol Chem. 1998 May 22;273(21):13264-72 [9582371]
Mutat Res. 1998 Jun 18;402(1-2):41-50 [9675240]
Biochem J. 1998 Oct 15;335 ( Pt 2):233-40 [9761719]
J Biol Chem. 1956 Nov;223(1):327-39 [13376602]
J Biol Chem. 1956 Jan;218(1):97-106 [13278318]
Mol Cell. 2006 Jan 6;21(1):97-108 [16387657]
J Biol Chem. 2006 Nov 17;281(46):34796-802 [16973608]
Mutat Res. 2007 Jun 1;619(1-2):9-15 [17349664]
Crit Rev Biochem Mol Biol. 2007 Sep-Oct;42(5):373-97 [17917873]
Mol Microbiol. 2008 Apr;68(1):51-65 [18312271]
J Med Chem. 2008 Dec 25;51(24):8173-7 [19053771]
Nature. 2009 Aug 13;460(7257):839-47 [19675644]
J Biol Chem. 2010 Jan 22;285(4):2302-8 [19946146]
J Bacteriol. 2010 Apr;192(8):2026-33 [20118259]
PLoS Biol. 2010;8(4):e1000354 [20404999]
Drug Metab Dispos. 2010 Nov;38(11):1917-21 [20699408]
J Biol Chem. 2010 Nov 26;285(48):37847-59 [20861021]
Biochem J. 2011 Jan 15;433(2):383-91 [21029045]
Eukaryot Cell. 2011 Oct;10(10):1270-82 [21803866]
J Biol Chem. 2011 Oct 14;286(41):35801-12 [21856748]
Biochemistry. 2011 Oct 18;50(41):8813-22 [21916412]
Mol Syst Biol. 2012;8:567 [22294093]
J Biol Chem. 2012 Feb 24;287(9):6307-17 [22203676]
Chem Res Toxicol. 2012 Nov 19;25(11):2443-50 [22924387]
J Biol Chem. 2012 Dec 14;287(51):42795-803 [23086957]
Dalton Trans. 2013 Mar 7;42(9):3029-42 [23318732]
Biochim Biophys Acta. 2013 Mar;1827(3):455-69 [23298813]
J Biol Chem. 2013 Feb 22;288(8):5426-42 [23281480]
J Bacteriol. 2013 May;195(9):2039-49 [23457245]
Biochim Biophys Acta. 2013 Aug-Sep;1827(8-9):1086-101 [23201473]
Res Microbiol. 2013 Sep;164(7):689-94 [23680484]
Biosci Biotechnol Biochem. 2000 Apr;64(4):799-807 [10830496]
Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6640-5 [10829079]
J Bacteriol. 2000 Jun;182(12):3361-7 [10852865]
J Biol Chem. 2001 Jun 22;276(25):22024-31 [11290749]
Proc Natl Acad Sci U S A. 1981 Sep;78(9):5685-9 [6946507]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1002/mbo3.108
ER  - 



TY  - JOUR
T1  - Prospective evaluation of serum sarcosine and risk of prostate cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.
AN  - 1443400261; 23698636
AB  - Metabolomic profiling has identified, sarcosine, a derivative of the amino acid glycine, as an important metabolite involved in the etiology or natural history of prostate cancer. We examined the association between serum sarcosine levels and risk of prostate cancer in 1122 cases (813 non-aggressive and 309 aggressive) and 1112 controls in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Sarcosine was quantified using high-throughput liquid chromatography-mass spectrometry. A significantly increased risk of prostate cancer was observed with increasing levels of sarcosine (odds ratio [OR] for the highest quartile of exposure [Q4] versus the lowest quartile [Q1] = 1.30, 95% confidence interval [CI]: 1.02, 1.65; P-trend 0.03). When stratified by disease aggressiveness, we observed a stronger association for non-aggressive cases (OR for Q4 versus Q1 = 1.44, 95% CI: 1.11, 1.88; P-trend 0.006) but no association for aggressive prostate cancer (OR for Q4 versus Q1 = 1.03, 95% CI: 0.73, 1.47; P-trend 0.89). Although not statistically significant, temporal analyses showed a stronger association between sarcosine and prostate cancer for serum collected closer to diagnosis, suggesting that sarcosine may be an early biomarker of disease. Interestingly, the association between sarcosine and prostate cancer risk was stronger among men with diabetes (OR = 2.66, 95% CI: 1.04, 6.84) compared with those without reported diabetes (OR = 1.23, 95% CI: 0.95-1.59, P-interaction = 0.01). This study found that elevated levels of serum sarcosine are associated with an increased prostate cancer risk and evidence to suggest that sarcosine may be an early biomarker for this disease.
JF  - Carcinogenesis
AU  - Koutros, Stella
AU  - Meyer, Tamra E
AU  - Fox, Stephen D
AU  - Issaq, Haleem J
AU  - Veenstra, Timothy D
AU  - Huang, Wen-Yi
AU  - Yu, Kai
AU  - Albanes, Demetrius
AU  - Chu, Lisa W
AU  - Andriole, Gerald
AU  - Hoover, Robert N
AU  - Hsing, Ann W
AU  - Berndt, Sonja I
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 2281
EP  - 2285
VL  - 34
IS  - 10
KW  - Biomarkers, Tumor
KW  - 0
KW  - Sarcosine
KW  - Z711V88R5F
KW  - Index Medicus
KW  - Risk
KW  - Odds Ratio
KW  - Prospective Studies
KW  - Aged, 80 and over
KW  - Humans
KW  - Early Detection of Cancer
KW  - Case-Control Studies
KW  - Aged
KW  - Middle Aged
KW  - Male
KW  - Sarcosine -- blood
KW  - Prostatic Neoplasms -- epidemiology
KW  - Prostatic Neoplasms -- blood
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443400261?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prospective+evaluation+of+serum+sarcosine+and+risk+of+prostate+cancer+in+the+Prostate%2C+Lung%2C+Colorectal+and+Ovarian+Cancer+Screening+Trial.&rft.au=Koutros%2C+Stella%3BMeyer%2C+Tamra+E%3BFox%2C+Stephen+D%3BIssaq%2C+Haleem+J%3BVeenstra%2C+Timothy+D%3BHuang%2C+Wen-Yi%3BYu%2C+Kai%3BAlbanes%2C+Demetrius%3BChu%2C+Lisa+W%3BAndriole%2C+Gerald%3BHoover%2C+Robert+N%3BHsing%2C+Ann+W%3BBerndt%2C+Sonja+I&rft.aulast=Koutros&rft.aufirst=Stella&rft.date=2013-10-01&rft.volume=34&rft.issue=10&rft.spage=2281&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt176
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-09
N1  - Date created - 2013-10-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684]
Ann Surg Oncol. 2012 Dec;19(13):4238-43 [22766991]
Diabetologia. 2004 Jun;47(6):1071-8 [15164171]
Cancer. 2006 Jan 1;106(1):79-86 [16323173]
Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2056-62 [17119028]
Int J Cancer. 2008 May 15;122(10):2345-50 [18172860]
Cancer Causes Control. 2008 Sep;19(7):703-10 [18340542]
Cancer Causes Control. 2008 Dec;19(10):1267-76 [18618278]
Nature. 2009 Feb 12;457(7231):910-4 [19212411]
Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2427-35 [19706848]
Ann Clin Biochem. 2010 May;47(Pt 3):282 [20233752]
Eur Urol. 2010 Jul;58(1):12-8; discussion 20-1 [20117878]
Eur Urol. 2010 Jul;58(1):19-20 [20227175]
Eur Urol. 2010 Sep;58(3):e29-30; author reply e31-2 [20537788]
Eur Urol. 2010 Oct;58(4):e39-40; author reply e41-2 [20696519]
Cancer Prev Res (Phila). 2010 Oct;3(10):1334-41 [20858760]
J Urol. 2011 Feb;185(2):706-11 [21168877]
Eur Urol. 2010 Nov;58(5):e51 [20728983]
Nat Med. 2011 Apr;17(4):448-53 [21423183]
Prostate Cancer Prostatic Dis. 2011 Jun;14(2):166-72 [21321584]
JAMA. 2011 Jun 22;305(24):2548-55 [21693743]
Anal Bioanal Chem. 2011 Aug;401(2):635-46 [21626193]
Anal Chem. 2011 Jul 15;83(14):5735-40 [21635006]
PLoS One. 2011;6(7):e21417 [21789170]
PLoS One. 2011;6(8):e22486 [21853037]
Prostate. 2011 May 15;71(7):700-10 [20957673]
PLoS One. 2011;6(11):e27361 [22076155]
J Sep Sci. 2011 Dec;34(24):3619-21 [22009695]
J Natl Cancer Inst. 2012 Jan 18;104(2):125-32 [22228146]
S Afr Med J. 2012 Aug;102(8):677-9 [22831945]
Endocr Relat Cancer. 2012 Oct;19(5):F47-62 [22514110]
Prostate. 2012 Nov;72(15):1611-21 [22430630]
Eur Urol. 2012 Nov;62(5):745-52 [22704366]
Control Clin Trials. 2000 Dec;21(6 Suppl):349S-355S [11189687]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/carcin/bgt176
ER  - 



TY  - JOUR
T1  - The RecQ helicase RECQL5 participates in psoralen-induced interstrand cross-link repair.
AN  - 1443400246; 23715498
AB  - Interstrand cross-links (ICLs) are very severe lesions as they are absolute blocks of replication and transcription. This property of interstrand cross-linking agents has been exploited clinically for the treatment of cancers and other diseases. ICLs are repaired in human cells by specialized DNA repair pathways including components of the nucleotide excision repair pathway, double-strand break repair pathway and the Fanconi anemia pathway. In this report, we identify the role of RECQL5, a member of the RecQ family of helicases, in the repair of ICLs. Using laser-directed confocal microscopy, we demonstrate that RECQL5 is recruited to ICLs formed by trioxalen (a psoralen-derived compound) and ultraviolet irradiation A. Using single-cell gel electrophoresis and proliferation assays, we identify the role of RECQL5 in the repair of ICL lesions. The domain of RECQL5 that recruits to the site of ICL was mapped to the KIX region between amino acids 500 and 650. Inhibition of transcription and of topoisomerases did not affect recruitment, which was inhibited by DNA-intercalating agents, suggesting that the DNA structure itself may be responsible for the recruitment of RECQL5 to the sites of ICLs.
JF  - Carcinogenesis
AU  - Ramamoorthy, Mahesh
AU  - May, Alfred
AU  - Tadokoro, Takashi
AU  - Popuri, Venkateswarlu
AU  - Seidman, Michael M
AU  - Croteau, Deborah L
AU  - Bohr, Vilhelm A
AD  - Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, USA.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 2218
EP  - 2230
VL  - 34
IS  - 10
KW  - Cross-Linking Reagents
KW  - 0
KW  - RECQL5 protein, human
KW  - Topoisomerase Inhibitors
KW  - Exodeoxyribonucleases
KW  - EC 3.1.-
KW  - Bloom syndrome protein
KW  - EC 3.6.1.-
KW  - RecQ Helicases
KW  - EC 3.6.4.12
KW  - WRN protein, human
KW  - Werner Syndrome Helicase
KW  - DNA Topoisomerases
KW  - EC 5.99.1.-
KW  - Ficusin
KW  - KTZ7ZCN2EX
KW  - Index Medicus
KW  - Kinetics
KW  - Humans
KW  - Transcription, Genetic
KW  - DNA Topoisomerases -- metabolism
KW  - Protein Interaction Domains and Motifs
KW  - Protein Binding
KW  - Exodeoxyribonucleases -- metabolism
KW  - Cell Line
KW  - Topoisomerase Inhibitors -- pharmacology
KW  - DNA Repair -- physiology
KW  - RecQ Helicases -- metabolism
KW  - Cross-Linking Reagents -- toxicity
KW  - RecQ Helicases -- chemistry
KW  - Ficusin -- toxicity
KW  - DNA Damage -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443400246?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+RecQ+helicase+RECQL5+participates+in+psoralen-induced+interstrand+cross-link+repair.&rft.au=Ramamoorthy%2C+Mahesh%3BMay%2C+Alfred%3BTadokoro%2C+Takashi%3BPopuri%2C+Venkateswarlu%3BSeidman%2C+Michael+M%3BCroteau%2C+Deborah+L%3BBohr%2C+Vilhelm+A&rft.aulast=Ramamoorthy&rft.aufirst=Mahesh&rft.date=2013-10-01&rft.volume=34&rft.issue=10&rft.spage=2218&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt183
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-09
N1  - Date created - 2013-10-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Am J Clin Dermatol. 2000 Nov-Dec;1(6):337-48 [11702610]
Mol Biol Cell. 2012 Nov;23(21):4273-85 [22973052]
FASEB J. 2002 May;16(7):757-8 [11978740]
J Biol Chem. 2002 Oct 25;277(43):41110-9 [12181313]
Nat Rev Cancer. 2003 Mar;3(3):155-68 [12612651]
Nat Rev Cancer. 2003 Mar;3(3):169-78 [12612652]
RNA. 2003 Apr;9(4):493-501 [12649500]
Mol Cell Biol. 2003 May;23(10):3417-26 [12724401]
Carcinogenesis. 2003 Oct;24(10):1571-80 [12919958]
Cancer Res. 2003 Nov 1;63(21):7136-46 [14612507]
Mol Cell Biol. 2004 Jan;24(1):123-34 [14673148]
World J Gastroenterol. 2004 Jan 15;10(2):155-60 [14716813]
EMBO J. 2004 Jul 21;23(14):2882-91 [15241474]
N Engl J Med. 1974 Dec 5;291(23):1207-11 [4422691]
Biochim Biophys Acta. 1975 Jul 23;395(4):401-12 [1148245]
Annu Rev Biochem. 1985;54:1151-93 [2411210]
Proc Natl Acad Sci U S A. 1990 Jun;87(12):4707-11 [2352945]
Nucleic Acids Res. 1993 Dec 25;21(25):5890-5 [8290349]
N Engl J Med. 1997 Apr 10;336(15):1041-5 [9091799]
J Invest Dermatol. 1997 Jun;108(6):897-900 [9182818]
J Biol Chem. 1998 Mar 6;273(10):5858-68 [9488723]
J Natl Cancer Inst. 1998 Sep 2;90(17):1278-84 [9731734]
Mol Cell. 1998 Aug;2(2):223-32 [9734359]
Science. 2005 Feb 18;307(5712):1098-101 [15718470]
J Biol Chem. 2005 Dec 9;280(49):40559-67 [16223718]
Nucleic Acids Res. 2006;34(9):2751-60 [16714450]
Nucleic Acids Res. 2006;34(18):5217-31 [17003056]
J Cell Sci. 2006 Dec 15;119(Pt 24):5137-46 [17118963]
Oncogene. 2007 Jan 11;26(2):215-23 [16819507]
Bioconjug Chem. 2007 Mar-Apr;18(2):431-7 [17373769]
Nat Rev Genet. 2007 Oct;8(10):735-48 [17768402]
Genes Dev. 2007 Dec 1;21(23):3073-84 [18003859]
Nucleic Acids Res. 2007;35(22):7527-44 [18006573]
Chromosoma. 2008 Jun;117(3):219-33 [18188578]
Proc Natl Acad Sci U S A. 2008 Jun 24;105(25):8580-4 [18562274]
Proc Natl Acad Sci U S A. 2008 Oct 14;105(41):15779-84 [18840688]
Trends Biochem Sci. 2008 Dec;33(12):609-20 [18926708]
Nucleic Acids Res. 2009 May;37(8):2645-57 [19270065]
J Biol Chem. 2009 Oct 9;284(41):27908-17 [19684342]
Structure. 2010 Feb 10;18(2):177-87 [20159463]
Crit Rev Biochem Mol Biol. 2010 Feb;45(1):23-49 [20039786]
Mol Cell Biol. 2010 May;30(10):2460-72 [20231364]
DNA Repair (Amst). 2010 Jul 1;9(7):796-804 [20451470]
Photochem Photobiol. 1979 Jun;29(6):1177-97 [388473]
J Cell Physiol. 1983 Jul;116(1):26-34 [6853610]
Mutat Res. 1984 May-Jun;131(5-6):223-30 [6429525]
J Biol Chem. 2000 Mar 31;275(13):9636-44 [10734115]
Curr Biol. 2000 Jul 27-Aug 10;10(15):886-95 [10959836]
Mol Cell Biol. 2000 Nov;20(21):8283-9 [11027296]
FASEB J. 2001 May;15(7):1224-6 [11344095]
Genes Dev. 2001 Sep 1;15(17):2177-96 [11544175]
Aging Cell. 2010 Jun;9(3):358-71 [20222902]
J Mol Biol. 2010 Jun 11;399(3):397-409 [20399214]
Nucleic Acids Res. 2010 Dec;38(22):8131-40 [20705653]
Cancer Res. 2011 Jan 15;71(2):561-71 [21224348]
Mol Cell Biol. 2011 May;31(10):2090-9 [21402780]
Nat Rev Cancer. 2011 Jul;11(7):467-80 [21701511]
Nucleic Acids Res. 2011 Nov 1;39(20):8752-64 [21764772]
Nucleic Acids Res. 2012 Feb;40(4):1621-35 [22013166]
DNA Repair (Amst). 2012 Jul 1;11(7):624-35 [22633600]
Nucleic Acids Res. 2002 Feb 1;30(3):782-93 [11809892]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/carcin/bgt183
ER  - 



TY  - JOUR
T1  - The human papillomavirus-16 E7 oncoprotein exerts antiapoptotic effects via its physical interaction with the actin-binding protein gelsolin.
AN  - 1443399188; 23729654
AB  - The oncoprotein E7 from human papillomavirus-16 (HPV-16 E7) plays a pivotal role in HPV postinfective carcinogenesis, and its physical interaction with host cell targets is essential to its activity. We identified a novel cellular partner for the viral oncoprotein: the actin-binding protein gelsolin (GSN), a key regulator of actin filament assembly and disassembly. In fact, biochemical analyses, generation of a 3D molecular interaction model and the use of specific HPV-16 E7 mutants provided clear cut evidence supporting the crucial role of HPV-16 E7 in affecting GSN integrity and function in human immortalized keratinocytes. Accordingly, functional analyses clearly suggested that stable HPV-16 E7 expression induced an imbalance between polymeric and monomeric actin in favor of the former. These events also lead to changes of cell cycle (increased S phase), to the inhibition of apoptosis and to the increase of cell survival. These results provide support to the hypotheses generated from the 3D molecular interaction model and encourage the design of small molecules hindering HPV-induced host cell reprogramming by specifically targeting HPV-16 E7-expressing cells.
JF  - Carcinogenesis
AU  - Mileo, Anna M
AU  - Abbruzzese, Claudia
AU  - Vico, Carmen
AU  - Bellacchio, Emanuele
AU  - Matarrese, Paola
AU  - Ascione, Barbara
AU  - Federico, Antonio
AU  - Della Bianca, Stefano
AU  - Mattarocci, Stefano
AU  - Malorni, Walter
AU  - Paggi, Marco G
AD  - Department of Development of Therapeutic Programs, Regina Elena National Cancer Institute, IRCCS, Via Elio Chianesi 53, 00144 Rome, Italy.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 2424
EP  - 2433
VL  - 34
IS  - 10
KW  - Actins
KW  - 0
KW  - Gelsolin
KW  - Papillomavirus E7 Proteins
KW  - oncogene protein E7, Human papillomavirus type 16
KW  - Caspase 3
KW  - EC 3.4.22.-
KW  - Index Medicus
KW  - Protein Interaction Mapping
KW  - Molecular Docking Simulation
KW  - Amino Acid Motifs
KW  - Humans
KW  - Actins -- metabolism
KW  - Cell Line, Tumor
KW  - Amino Acid Sequence
KW  - Protein Interaction Domains and Motifs
KW  - Protein Binding
KW  - Mutation
KW  - Protein Conformation
KW  - Caspase 3 -- metabolism
KW  - Papillomavirus E7 Proteins -- genetics
KW  - Gelsolin -- metabolism
KW  - Apoptosis
KW  - Gelsolin -- chemistry
KW  - Papillomavirus E7 Proteins -- metabolism
KW  - Papillomavirus E7 Proteins -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443399188?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+human+papillomavirus-16+E7+oncoprotein+exerts+antiapoptotic+effects+via+its+physical+interaction+with+the+actin-binding+protein+gelsolin.&rft.au=Mileo%2C+Anna+M%3BAbbruzzese%2C+Claudia%3BVico%2C+Carmen%3BBellacchio%2C+Emanuele%3BMatarrese%2C+Paola%3BAscione%2C+Barbara%3BFederico%2C+Antonio%3BDella+Bianca%2C+Stefano%3BMattarocci%2C+Stefano%3BMalorni%2C+Walter%3BPaggi%2C+Marco+G&rft.aulast=Mileo&rft.aufirst=Anna&rft.date=2013-10-01&rft.volume=34&rft.issue=10&rft.spage=2424&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt192
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-09
N1  - Date created - 2013-10-01
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/carcin/bgt192
ER  - 



TY  - JOUR
T1  - Azole Heteroresistance in Cryptococcus neoformans: Emergence of Resistant Clones with Chromosomal Disomy in the Mouse Brain during Fluconazole Treatment
AN  - 1443379340; 18642371
AB  - We have previously reported that Cryptococcus neoformans strains are innately heteroresistant to fluconazole in vitro, producing minor, highly resistant subpopulations due to adaptive formation of disomic chromosomes. Using a mouse model, we assessed the emergence of heteroresistant clones in the brain during fluconazole treatment and found that the occurrence of heteroresistant clones in vivo with chromosomal disomy is strain dependent. Interestingly, emergence of heteroresistant clones in vivo was unrelated to the strain's MIC to fluconazole.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Sionov, Edward
AU  - Chang, Yun C
AU  - Kwon-Chung, Kyung J
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 5127
EP  - 5130
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 10
SN  - 0066-4804, 0066-4804
KW  - Genetics Abstracts; CSA Neurosciences Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Animal models
KW  - fluconazole
KW  - Cryptococcus neoformans
KW  - K 03410:Animal Diseases
KW  - A 01340:Antibiotics & Antimicrobials
KW  - N3 11027:Neurology & neuropathology
KW  - G 07780:Fungi
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443379340?accountid=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=Azole+Heteroresistance+in+Cryptococcus+neoformans%3A+Emergence+of+Resistant+Clones+with+Chromosomal+Disomy+in+the+Mouse+Brain+during+Fluconazole+Treatment&rft.au=Sionov%2C+Edward%3BChang%2C+Yun+C%3BKwon-Chung%2C+Kyung+J&rft.aulast=Sionov&rft.aufirst=Edward&rft.date=2013-10-01&rft.volume=57&rft.issue=10&rft.spage=5127&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00694-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - fluconazole; Cryptococcus neoformans
DO  - http://dx.doi.org/10.1128/AAC.00694-13
ER  - 



TY  - JOUR
T1  - Antiviral Efficacy of Favipiravir against Two Prominent Etiological Agents of Hantavirus Pulmonary Syndrome
AN  - 1443378773; 18642395
AB  - Hantavirus pulmonary syndrome (HPS) is caused by infection with several Sigmodontinae- and Neotominae-borne hantaviruses and has a case fatality rate of 30 to 50%. Humans often become infected by inhalation of materials contaminated with virus-laden rodent urine or saliva, although human-to-human transmission has also been documented for Andes virus (ANDV). The ability to transmit via aerosolization, coupled with the high mortality rates and lack of therapeutic options, makes the development of medical countermeasures against HPS imperative. In the present study, we evaluated the efficacy of the broad-spectrum antiviral agent favipiravir (T-705) against Sin Nombre virus (SNV) and ANDV, the predominant causes of HPS in North and South America, respectively. In vitro, T-705 potently inhibited SNV and ANDV, as evidenced by decreased detection of viral RNA and reduced infectious titers. For both viruses, the 90% effective concentration was estimated at less than or equal to 5 mu g/ml ( less than or equal to 31.8 mu M). In the lethal ANDV hamster model, daily administration of oral T-705 at 50 or 100 mg/kg of body weight diminished the detection of viral RNA and antigen in tissue specimens and significantly improved survival rates. Oral T-705 therapy remained protective against HPS when treatment was initiated prior to the onset of viremia. No disease model for SNV exists; however, using a hamster-adapted SNV, we found that daily administration of oral T-705 significantly reduced the detection of SNV RNA and antigen in tissue specimens, suggesting that the compound would also be effective against HPS in North America. Combined, these results suggest that T-705 treatment is beneficial for postexposure prophylaxis against HPS-causing viruses and should be considered for probable exposures.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Safronetz, David
AU  - Falzarano, Darryl
AU  - Scott, Dana P
AU  - Furuta, Yousuke
AU  - Feldmann, Heinz
AU  - Gowen, Brian B
AD  - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, brian.gowen@usu.edu.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 4673
EP  - 4680
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 10
SN  - 0066-4804, 0066-4804
KW  - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Animal models
KW  - RNA
KW  - Hantavirus
KW  - A:01340
KW  - V:22410
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443378773?accountid=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=Antiviral+Efficacy+of+Favipiravir+against+Two+Prominent+Etiological+Agents+of+Hantavirus+Pulmonary+Syndrome&rft.au=Safronetz%2C+David%3BFalzarano%2C+Darryl%3BScott%2C+Dana+P%3BFuruta%2C+Yousuke%3BFeldmann%2C+Heinz%3BGowen%2C+Brian+B&rft.aulast=Safronetz&rft.aufirst=David&rft.date=2013-10-01&rft.volume=57&rft.issue=10&rft.spage=4673&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00886-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - RNA; Hantavirus
DO  - http://dx.doi.org/10.1128/AAC.00886-13
ER  - 



TY  - JOUR
T1  - P2' Benzene Carboxylic Acid Moiety Is Associated with Decrease in Cellular Uptake: Evaluation of Novel Nonpeptidic HIV-1 Protease Inhibitors Containing P2 bis-Tetrahydrofuran Moiety
AN  - 1443377820; 18642394
AB  - GRL007 and GRL008, two structurally related nonpeptidic human immunodeficiency virus type 1 (HIV-1) protease inhibitors (PIs) containing 3(R),3a(S),6a(R)-bis-tetrahydrofuranylurethane (bis-THF) as the P2 moiety and a sulfonamide isostere consisting of benzene carboxylic acid and benzene carboxamide as the P2' moiety, respectively, were evaluated for their antiviral activity and interactions with wild-type protease (PRWT). Both GRL007 (Ki of 12.7 pM with PRWT) and GRL008 (Ki of 8.9 pM) inhibited PRWT with high potency in vitro. X-ray crystallographic analysis of PRWT in complex with GRL007 or GRL008 showed that the bis-THF moiety of both compounds has three direct polar contacts with the backbone amide nitrogen atoms of Asp29 and Asp30 of PRWT. The P2' moiety of both compounds showed one direct contact with the backbone of Asp30' and a bridging polar contact with Gly48' through a water molecule. Cell-based antiviral assays showed that GRL007 was inactive (50% effective concentration [EC50] of >1 mu M) while GRL008 was highly active (EC50 of 0.04 mu M) against wild-type HIV-1. High-performance liquid chromatography (HPLC)/mass spectrometry-based cellular uptake assays showed 8.1- and 84-fold higher intracellular concentrations of GRL008 than GRL007 in human MT-2 and MT-4 cell extracts, respectively. Thus, GRL007, in spite of its favorable enzyme-inhibitory activity and protease binding profile, exhibited a lack of antiviral activity in cell-based assays, most likely due to its compromised cellular uptake associated with its P2' benzene carboxylic acid moiety. The anti-HIV-1 potency, favorable toxicity, and binding profile of GRL008 suggest that further optimization of the P2' moiety may improve its antiretroviral features.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Yedidi, Ravikiran S
AU  - Maeda, Kenji
AU  - Fyvie, W Sean
AU  - Steffey, Melinda
AU  - Davis, David A
AU  - Palmer, Ira
AU  - Aoki, Manabu
AU  - Kaufman, Joshua D
AU  - Stahl, Stephen J
AU  - Garimella, Harisha
AD  - HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA, hmitsuya@helix.nih.gov.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 4920
EP  - 4927
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 10
SN  - 0066-4804, 0066-4804
KW  - Toxicology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Antiviral activity
KW  - Human immunodeficiency virus 1
KW  - Benzene
KW  - A 01340:Antibiotics & Antimicrobials
KW  - X 24350:Industrial Chemicals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443377820?accountid=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=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=P2%27+Benzene+Carboxylic+Acid+Moiety+Is+Associated+with+Decrease+in+Cellular+Uptake%3A+Evaluation+of+Novel+Nonpeptidic+HIV-1+Protease+Inhibitors+Containing+P2+bis-Tetrahydrofuran+Moiety&rft.au=Yedidi%2C+Ravikiran+S%3BMaeda%2C+Kenji%3BFyvie%2C+W+Sean%3BSteffey%2C+Melinda%3BDavis%2C+David+A%3BPalmer%2C+Ira%3BAoki%2C+Manabu%3BKaufman%2C+Joshua+D%3BStahl%2C+Stephen+J%3BGarimella%2C+Harisha&rft.aulast=Yedidi&rft.aufirst=Ravikiran&rft.date=2013-10-01&rft.volume=57&rft.issue=10&rft.spage=4920&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00868-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Benzene; Human immunodeficiency virus 1
DO  - http://dx.doi.org/10.1128/AAC.00868-13
ER  - 



TY  - JOUR
T1  - Lipids Derived from Virulent Francisella tularensis Broadly Inhibit Pulmonary Inflammation via Toll-Like Receptor 2 and Peroxisome Proliferator-Activated Receptor alpha
AN  - 1443376860; 18681631
AB  - Francisella tularensis is a Gram-negative facultative intracellular pathogen that causes an acute lethal respiratory disease in humans. The heightened virulence of the pathogen is linked to its unique ability to inhibit Toll-like receptor (TLR)-mediated inflammatory responses. The bacterial component and mechanism of this inhibition are unknown. Here we show that lipids isolated from virulent but not attenuated strains of F. tularensis are not detected by host cells, inhibit production of proinflammatory cytokines by primary macrophages in response to known TLR ligands, and suppress neutrophil recruitment in vivo. We further show that lipid-mediated inhibition of inflammation is dependent on TLR2, MyD88, and the nuclear hormone and fatty acid receptor peroxisome proliferator-activated receptor alpha (PPAR alpha ). Pathogen lipid-mediated interference with inflammatory responses through the engagement of TLR2 and PPAR alpha represents a novel manipulation of host signaling pathways consistent with the ability of highly virulent F. tularensis to efficiently evade host immune responses.
JF  - Clinical and Vaccine Immunology
AU  - Crane, Deborah D
AU  - Ireland, Robin
AU  - Alinger, Joshua B
AU  - Small, Pamela
AU  - Bosio, Catharine M
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1531
EP  - 1540
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 20
IS  - 10
SN  - 1556-679X, 1556-679X
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Cytokines
KW  - Francisella tularensis
KW  - Inflammation
KW  - F:06905
KW  - J:02350
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443376860?accountid=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=Lipids+Derived+from+Virulent+Francisella+tularensis+Broadly+Inhibit+Pulmonary+Inflammation+via+Toll-Like+Receptor+2+and+Peroxisome+Proliferator-Activated+Receptor+alpha&rft.au=Crane%2C+Deborah+D%3BIreland%2C+Robin%3BAlinger%2C+Joshua+B%3BSmall%2C+Pamela%3BBosio%2C+Catharine+M&rft.aulast=Crane&rft.aufirst=Deborah&rft.date=2013-10-01&rft.volume=20&rft.issue=10&rft.spage=1531&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=1556679X&rft_id=info:doi/10.1128%2FCVI.00319-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Inflammation; Francisella tularensis
DO  - http://dx.doi.org/10.1128/CVI.00319-13
ER  - 



TY  - JOUR
T1  - Mov10 and APOBEC3G Localization to Processing Bodies Is Not Required for Virion Incorporation and Antiviral Activity
AN  - 1443366636; 18651936
AB  - Mov10 and APOBEC3G (A3G) localize to cytoplasmic granules called processing bodies (P bodies), incorporate into human immunodeficiency virus type 1 (HIV-1) virions, and inhibit viral replication. The functional relevance of Mov10/A3G P-body localization to virion incorporation and antiviral activity has not been fully explored. We found that a helicase V mutant of Mov10 exhibits significantly reduced localization to P bodies but still efficiently inhibits viral infectivity via virion incorporation. Disruption of the P bodies by DDX6 knockdown also confirmed Mov10 antiviral activity without P-body localization. In addition, overexpression of SRP19, which binds to 7SL RNA, depleted A3G from P bodies but did not affect its virion incorporation. Sucrose gradient sedimentation assays revealed that the majority of Mov10, A3G, HIV-1 RNA, and Gag formed high-molecular-mass (HMM) complexes that are converted to low-molecular-mass (LMM) complexes after RNase A treatment. In contrast, the P-body markers DCP2, LSM1, eIF4e, DDX6, and AGO1 were in LMM complexes, whereas AGO2, an effector protein of the RNA-induced silencing complex that localizes to P bodies, was present in both LMM and HMM complexes. Depletion of AGO2 indicated that RNA-induced silencing function is required for Mov10's ability to reduce Gag expression upon overexpression, but not its virion incorporation or effect on virus infectivity. We conclude that the majority of Mov10 and A3G are in HMM complexes, whereas most of the P-body markers are in LMM complexes, and that virion incorporation and the antiviral activities of Mov10 and A3G do not require their localization to P bodies.
JF  - Journal of Virology
AU  - Izumi, Taisuke
AU  - Burdick, Ryan
AU  - Shigemi, Mayu
AU  - Plisov, Sergey
AU  - Hu, Wei-Shau
AU  - Pathak, Vinay K
AD  - HIV Drug Resistance Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA, vinay.pathak@nih.gov.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 11047
EP  - 11062
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 87
IS  - 20
SN  - 0022-538X, 0022-538X
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts
KW  - Granules
KW  - Virions
KW  - Replication
KW  - Antiviral activity
KW  - Initiation factor eIF-4E
KW  - Gag protein
KW  - Argonaute 2 protein
KW  - ribonuclease A
KW  - Infectivity
KW  - RNA
KW  - Sucrose
KW  - Human immunodeficiency virus 1
KW  - RNA-induced silencing complex
KW  - Sedimentation
KW  - DNA helicase
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22360:AIDS and HIV
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443366636?accountid=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+Virology&rft.atitle=Mov10+and+APOBEC3G+Localization+to+Processing+Bodies+Is+Not+Required+for+Virion+Incorporation+and+Antiviral+Activity&rft.au=Izumi%2C+Taisuke%3BBurdick%2C+Ryan%3BShigemi%2C+Mayu%3BPlisov%2C+Sergey%3BHu%2C+Wei-Shau%3BPathak%2C+Vinay+K&rft.aulast=Izumi&rft.aufirst=Taisuke&rft.date=2013-10-01&rft.volume=87&rft.issue=20&rft.spage=11047&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.02070-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 68
N1  - Last updated - 2015-09-03
N1  - SubjectsTermNotLitGenreText - Virions; Granules; Replication; Antiviral activity; Argonaute 2 protein; Gag protein; Initiation factor eIF-4E; ribonuclease A; Infectivity; RNA; Sucrose; RNA-induced silencing complex; Sedimentation; DNA helicase; Human immunodeficiency virus 1
DO  - http://dx.doi.org/10.1128/JVI.02070-13
ER  - 



TY  - JOUR
T1  - Effects of ethnic targeting on the perceived effectiveness of cancer prevention messages among Latinas and Non-Latina white women
AN  - 1440228364; 4489148
AB  - In general, efforts to target Latinos are made through Spanish-language messages, yet 75% of U.S. Latinos are bilingual or English dominant. Acculturation (adapting mainstream traits) is associated with increased lifestyle-related risk behaviors. Latinos maintain cultural traits and ethnic identification even as they appear to acculturate (e.g., through language). This raises questions about how to communicate health information to more-acculturated Latinos who are not reached by traditional Spanish outreach yet may not identify with general-market messages. This study tested the relative efficacy of English-language messages targeted to Latinas, compared with general-market messages, among highly acculturated Latina women and non-Latina White women. In this pair of online experiments, Latinas (n = 715) and non-Latina White women (n = 704) rated the perceived effectiveness of general-market versus Latina-targeted Pap smear and mammogram public service announcements. In 1 of 2 experiments ethnically targeted messages were rated relatively more effective for the intended audience and equally effective for the general audience. The author discusses implications for how campaigns reach U.S. Latinos across the acculturation spectrum. Reprinted by permission of Taylor & Francis Ltd.
JF  - Journal of health communication
AU  - Ramírez, A Susana
AD  - National Institutes of Health, Bethesda
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1256
EP  - 1273
VL  - 18
IS  - 10
SN  - 1081-0730, 1081-0730
KW  - Anthropology
KW  - Information
KW  - Spanish language
KW  - Public services
KW  - Women
KW  - English language
KW  - U.S.A.
KW  - Life styles
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1440228364?accountid=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=Effects+of+ethnic+targeting+on+the+perceived+effectiveness+of+cancer+prevention+messages+among+Latinas+and+Non-Latina+white+women&rft.au=Ram%C3%ADrez%2C+A+Susana&rft.aulast=Ram%C3%ADrez&rft.aufirst=A&rft.date=2013-10-01&rft.volume=18&rft.issue=10&rft.spage=1256&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2013.778362
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-10-08
N1  - Last updated - 2013-10-09
N1  - SubjectsTermNotLitGenreText - 12101 4535 7226 11132 6331; 13598 5421 6091; 1939 3617 6220; 4290 4535 7226 5492 6331; 7404; 6515; 10484; 433 293 14
DO  - http://dx.doi.org/10.1080/10810730.2013.778362
ER  - 



TY  - JOUR
T1  - A prospective validation pharmacogenomic study in the adjuvant setting of colorectal cancer patients treated with the 5-fluorouracil/leucovorin/oxaliplatin (FOLFOX4) regimen
AN  - 1439219369; 18617844
AB  - The discovery of pharmacogenomic markers in colorectal cancer (CRC) could be setting-specific. FOLFOX4 is employed in the adjuvant and metastatic setting in CRC. This prospective study is aimed to validate in the adjuvant setting the pharmacogenomic markers of toxicity reported in the metastatic setting (that is, GSTP1-rs947894, and -rs1138272; GSTM1-null genotype; AGXT-rs4426527, -rs34116584 and del-74 bp), and to discover additional markers. CRC patients (n=144) treated with adjuvant FOLFOX4 were genotyped for 57 polymorphisms in 29 genes. Grade greater than or equal to 2 neurotoxicity was associated (false discovery rate-adjusted q-value <0.1) with single-nucleotide polymorphisms in ABCC1 (rs2074087: odds ratio=0.43(0.22-0.86)), and ABCC2 (rs3740066: 2.99(1.16-7.70); rs1885301: 3.06(1.35-6.92); rs4148396: 4.69(1.60-13.74); rs717620: 14.39(1.63-127.02)). hMSH6-rs3136228 was associated with grade 3-4 neutropenia (3.23(1.38-7.57), q-value=0.0937). XRCC3-rs1799794 was associated with grade 3-4 non-hematological toxicity (8.90(2.48-31.97), q-value=0.0150). The markers previously identified in metastatic CRC were not validated. We have identified new markers of toxicity in genes of transport and DNA repair. If validated in other studies, they could help to identify patients at risk of toxicity.
JF  - Pharmacogenomics Journal
AU  - Cecchin, E
AU  - D'Andrea, M
AU  - Lonardi, S
AU  - Zanusso, C
AU  - Pella, N
AU  - Errante, D
AU  - De Mattia, E
AU  - Polesel, J
AU  - Innocenti, F
AU  - Toffoli, G
AD  - Experimental and Clinical Pharmacology Unit, 'Centro di Riferimento Oncologico'- National Cancer Institute, Aviano, Italy
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 403
EP  - 409
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 13
IS  - 5
SN  - 1470-269X, 1470-269X
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - Metastases
KW  - Neutropenia
KW  - 5-Fluorouracil
KW  - pharmacogenomics
KW  - Single-nucleotide polymorphism
KW  - Gene polymorphism
KW  - Neurotoxicity
KW  - Colorectal cancer
KW  - Adjuvants
KW  - oxaliplatin
KW  - DNA repair
KW  - G 07880:Human Genetics
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439219369?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenomics+Journal&rft.atitle=A+prospective+validation+pharmacogenomic+study+in+the+adjuvant+setting+of+colorectal+cancer+patients+treated+with+the+5-fluorouracil%2Fleucovorin%2Foxaliplatin+%28FOLFOX4%29+regimen&rft.au=Cecchin%2C+E%3BD%27Andrea%2C+M%3BLonardi%2C+S%3BZanusso%2C+C%3BPella%2C+N%3BErrante%2C+D%3BDe+Mattia%2C+E%3BPolesel%2C+J%3BInnocenti%2C+F%3BToffoli%2C+G&rft.aulast=Cecchin&rft.aufirst=E&rft.date=2013-10-01&rft.volume=13&rft.issue=5&rft.spage=403&rft.isbn=&rft.btitle=&rft.title=Pharmacogenomics+Journal&rft.issn=1470269X&rft_id=info:doi/10.1038%2Ftpj.2012.31
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Metastases; Neutropenia; 5-Fluorouracil; Single-nucleotide polymorphism; pharmacogenomics; Gene polymorphism; Neurotoxicity; Colorectal cancer; oxaliplatin; Adjuvants; DNA repair
DO  - http://dx.doi.org/10.1038/tpj.2012.31
ER  - 



TY  - JOUR
T1  - Pharmacogenetically driven patient selection for a first-in-human phase I trial of batracylin in patients with advanced solid tumors and lymphomas.
AN  - 1437578306; 23912694
AB  - Batracylin (daniquidone), an ATP-insensitive topoisomerase I/II inhibitor, demonstrated wide interspecies variation in preclinical models consistent with formation of a toxic metabolite, N-acetyl-batracylin, following metabolism by N-acetyl-transferase 2 (NAT2). To minimize exposure to this toxic metabolite, this first-in-human study was conducted in patients with advanced refractory solid tumors or lymphomas demonstrated to have a slow NAT2 acetylator genotype. The objectives were to determine the safety, maximum tolerated dose (MTD), and pharmacokinetics of batracylin and its metabolites.
          Based on the MTD for rats, the most sensitive species, the starting dose was 5 mg/day for 7 days in 28-day cycles. Dose escalation followed accelerated titration design 4B, with restaging performed every 2 cycles. Thirty-one patients were enrolled. Treatment was well tolerated; one patient experienced grade 3 toxicity (lymphopenia). Dose escalation was stopped at 400 mg/day due to grade 1 and 2 hemorrhagic cystitis. No objective responses were observed, but prolonged disease stabilization was observed in 2 patients, one with peritoneal mesothelioma (8 cycles) and another with adrenocortical cancer (18 cycles). Across an 80-fold range of doses, the ratios of systemic exposures for batracylin and N-acetyl batracylin were near 1.
          Pharmacogenetically selected patients reached a dose that was 20-fold higher than the MTD in rats and 70 % of the MTD in mice. This genotype-guided strategy was successful in safely delivering batracylin to patients. However, due to unexpected cystitis, not preventable by hydration, and in the absence of a stronger signal for antitumor activity, further development of batracylin has been stopped.
JF  - Cancer chemotherapy and pharmacology
AU  - Kummar, Shivaani
AU  - Gutierrez, Martin E
AU  - Anderson, Lawrence W
AU  - Klecker, Raymond W
AU  - Chen, Alice
AU  - Murgo, Anthony J
AU  - Doroshow, James H
AU  - Collins, Jerry M
AD  - Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 917
EP  - 923
VL  - 72
IS  - 4
KW  - Antineoplastic Agents
KW  - 0
KW  - Quinazolines
KW  - batracylin
KW  - 67199-66-0
KW  - Arylamine N-Acetyltransferase
KW  - EC 2.3.1.5
KW  - NAT2 protein, human
KW  - Index Medicus
KW  - Genotype
KW  - Young Adult
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - Maximum Tolerated Dose
KW  - Patient Selection
KW  - Species Specificity
KW  - Pharmacogenetics
KW  - Male
KW  - Female
KW  - Quinazolines -- pharmacokinetics
KW  - Quinazolines -- administration & dosage
KW  - Neoplasms -- drug therapy
KW  - Neoplasms -- pathology
KW  - Antineoplastic Agents -- administration & dosage
KW  - Antineoplastic Agents -- pharmacokinetics
KW  - Lymphoma -- drug therapy
KW  - Quinazolines -- adverse effects
KW  - Lymphoma -- pathology
KW  - Arylamine N-Acetyltransferase -- genetics
KW  - Antineoplastic Agents -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1437578306?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacogenetically+driven+patient+selection+for+a+first-in-human+phase+I+trial+of+batracylin+in+patients+with+advanced+solid+tumors+and+lymphomas.&rft.au=Kummar%2C+Shivaani%3BGutierrez%2C+Martin+E%3BAnderson%2C+Lawrence+W%3BKlecker%2C+Raymond+W%3BChen%2C+Alice%3BMurgo%2C+Anthony+J%3BDoroshow%2C+James+H%3BCollins%2C+Jerry+M&rft.aulast=Kummar&rft.aufirst=Shivaani&rft.date=2013-10-01&rft.volume=72&rft.issue=4&rft.spage=917&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=1432-0843&rft_id=info:doi/10.1007%2Fs00280-013-2244-4
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-28
N1  - Date created - 2013-09-26
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s00280-013-2244-4
ER  - 



TY  - JOUR
T1  - Characteristics of extremely low-birth-weight infant survivors with unimpaired outcomes at 30 months of age
AN  - 1437152614; 23807719
AB  - To evaluate characteristics of unimpaired outcome in extremely low-birth-weight (ELBW) survivors.  
ELBW infants (n=714) with 30 months' assessments were analyzed. Logistic regression was used to develop a model for the binary outcome of unimpaired versus impaired outcome.  
Thirty-three percent of infants had an unimpaired outcome. Seventeen percent of ELBW survivors had a Bayley II Mental Developmental Index score of ≥ 101 and 2% had a score of ≥ 116. Female gender, use of antenatal steroids (ANS), maternal education ≥ high school and the absence of major neonatal morbidities were independent predictors of unimpaired outcome. The likelihood of an unimpaired outcome in the presence of major neonatal morbidities was higher in infants exposed to ANS.  
The majority of unimpaired ELBW survivors had cognitive scores shifted toward the lower end of the normal distribution. Exposure to ANS was associated with higher likelihood of an unimpaired outcome in infants with major neonatal morbidities.
JF  - Journal of Perinatology
AU  - Kumar, P
AU  - Shankaran, S
AU  - Ambalavanan, N
AU  - Kendrick, D E
AU  - Pappas, A
AU  - Vohr, B R
AU  - Poindexter, B B
AU  - Das, A
AU  - Higgins, R D
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 800
EP  - 5
CY  - New York
PB  - Nature Publishing Group
VL  - 33
IS  - 10
SN  - 07438346
KW  - Medical Sciences--Pediatrics
KW  - Logistic Models
KW  - Cognition Disorders -- epidemiology
KW  - Humans
KW  - Infant, Newborn
KW  - Follow-Up Studies
KW  - Infant, Premature, Diseases -- epidemiology
KW  - Infant, Premature
KW  - Cerebral Palsy -- epidemiology
KW  - Male
KW  - Female
KW  - Child Development
KW  - Infant, Extremely Low Birth Weight
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1437152614?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthcompleteshell&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Perinatology&rft.atitle=Characteristics+of+extremely+low-birth-weight+infant+survivors+with+unimpaired+outcomes+at+30+months+of+age&rft.au=Kumar%2C+P%3BShankaran%2C+S%3BAmbalavanan%2C+N%3BKendrick%2C+D+E%3BPappas%2C+A%3BVohr%2C+B+R%3BPoindexter%2C+B+B%3BDas%2C+A%3BHiggins%2C+R+D&rft.aulast=Kumar&rft.aufirst=P&rft.date=2013-10-01&rft.volume=33&rft.issue=10&rft.spage=800&rft.isbn=&rft.btitle=&rft.title=Journal+of+Perinatology&rft.issn=07438346&rft_id=info:doi/10.1038%2Fjp.2013.71
LA  - English
DB  - ProQuest Central
N1  - Copyright - Copyright Nature Publishing Group Oct 2013
N1  - Last updated - 2014-05-31
DO  - http://dx.doi.org/10.1038/jp.2013.71
ER  - 



TY  - JOUR
T1  - Host lymphocyte depletion as a strategy to facilitate early full donor chimerism after reduced-intensity allogeneic stem cell transplantation.
AN  - 1434747090; 23948062
AB  - Reduced-intensity conditioning (RIC) allogeneic hematopoietic stem cell transplantation (RIC-alloHSCT) is associated with lower toxicity but higher rates of prolonged mixed chimerism than myeloablative conditioning. Decreased pretransplantation host T cell numbers are associated with less graft rejection and early full donor chimerism. To compensate for variability in pretransplantation host lymphocyte numbers and facilitate the achievement of rapid full donor chimerism, we tested a strategy of targeted lymphocyte depletion (TLD) using chemotherapy at conventional doses to provide cytoreduction and lymphocyte depletion before RIC-alloHSCT. In our study, 111 patients with advanced hematologic malignancies received 1 to 3 cycles of conventional-dose chemotherapy to reduce circulating lymphocytes to a predetermined level. Patients then underwent RIC-alloHSCT from HLA-matched siblings. Patients received a median of 2 cycles of TLD chemotherapy, resulting in a median 71% decline in CD4(+) count. All patients engrafted; there were no late graft failures. By day +14, median CD3(+) chimerism was 99% donor and was significantly associated with lower post-TLD CD4(+) counts (P = .012). One- and 5-year treatment-related mortality were 15% and 21%, respectively. At 1-year follow-up, 66% of patients had achieved complete remission (CR) of which 92% were not in CR at the time of transplantation. Overall survival at 1 and 5 years post transplantation were 66% and 47%, respectively.
          Copyright © 2013 American Society for Blood and Marrow Transplantation. All rights reserved.
JF  - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
AU  - Salit, Rachel B
AU  - Fowler, Daniel H
AU  - Dean, Robert M
AU  - Pavletic, Steven Z
AU  - Hakim, Frances T
AU  - Steinberg, Seth M
AU  - Hardy, Nancy T
AU  - Sportes, Claude
AU  - Gress, Ronald E
AU  - Bishop, Michael R
AD  - Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland; Fred Hutchinson Cancer Research Center, Clinical Research Division, Seattle, Washington. Electronic address: rsalit@fhcrc.org.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 1509
EP  - 1513
VL  - 19
IS  - 10
KW  - Index Medicus
KW  - Lymphocyte depletion
KW  - Engraftment
KW  - Reduced-intensity transplantation
KW  - Young Adult
KW  - Humans
KW  - Graft Survival -- physiology
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - Transplantation, Homologous
KW  - Graft Rejection -- prevention & control
KW  - Male
KW  - Female
KW  - Transplantation Conditioning -- methods
KW  - Transplantation Chimera
KW  - Lymphocyte Depletion -- methods
KW  - Hematopoietic Stem Cell Transplantation -- methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434747090?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Host+lymphocyte+depletion+as+a+strategy+to+facilitate+early+full+donor+chimerism+after+reduced-intensity+allogeneic+stem+cell+transplantation.&rft.au=Salit%2C+Rachel+B%3BFowler%2C+Daniel+H%3BDean%2C+Robert+M%3BPavletic%2C+Steven+Z%3BHakim%2C+Frances+T%3BSteinberg%2C+Seth+M%3BHardy%2C+Nancy+T%3BSportes%2C+Claude%3BGress%2C+Ronald+E%3BBishop%2C+Michael+R&rft.aulast=Salit&rft.aufirst=Rachel&rft.date=2013-10-01&rft.volume=19&rft.issue=10&rft.spage=1509&rft.isbn=&rft.btitle=&rft.title=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.issn=1523-6536&rft_id=info:doi/10.1016%2Fj.bbmt.2013.08.001
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-24
N1  - Date created - 2013-09-20
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.bbmt.2013.08.001
ER  - 



TY  - JOUR
T1  - Biliary tract cancer incidence in the United States-Demographic and temporal variations by anatomic site
AN  - 1434032996; 18510147
AB  - We evaluated incidence patterns of biliary tract cancers (gallbladder, extrahepatic bile duct, ampulla of Vater and not otherwise specified) to provide potential insight into the etiology of these cancers. Data were obtained from the population-based Surveillance, Epidemiology and End Results program. Rates for cases diagnosed during 1992-2009 were calculated by racial/ethnic, gender and age groups. Temporal trends during 1974-2009 and annual percentage changes (APC) during 1992-2009 were estimated. Age-adjusted rates by site were higher among American Indian/Alaska Natives, Hispanics (white) and Asian/Pacific Islanders (Asian/PI) and lower among whites and blacks. Gallbladder cancer was more common among women in all ethnic groups (female-to-male incidence rate ratio [IRR] ranged from 1.24 to 2.86), but bile duct and ampulla of Vater cancers were more common among men (female-to-male IRR 0.57 to 0.82). Gallbladder cancer rates declined among all racial/ethnic and gender groups except blacks (APC -0.4% to -3.9%). In contrast, extrahepatic bile duct cancer rates rose significantly in most female racial/ethnic groups; the APCs among whites were 0.8 among females and 1.3 among males, both significant. Rates for ampulla of Vater cancer decreased among Asian/PI females (APC -2.7%) but remained stable for the other groups. In addition to confirming that biliary tract cancer incidence patterns differ by gender and site and that the gallbladder cancer incidence rates have been declining, our study provides novel evidence that extrahepatic bile duct cancer rates are rising. These observations may help guide future etiologic studies. What's new? Cancers of the biliary tract are rare but often fatal, and the risk factors for them are not well known. Analysis of data from the U.S. Surveillance, Epidemiology, and End Results (SEER) program revealed elevated rates of biliary tract cancers among American Indian/Alaska Natives, Hispanics, and Asian/Pacific Islanders compared with blacks and whites. Gallbladder cancer rates declined among most ethnic groups, whereas extrahepatic bile duct cancer rates rose, especially among women. These observations suggest that these cancers may differ in their etiology and provide clues for further research.
JF  - International Journal of Cancer
AU  - Castro, Felipe A
AU  - Koshiol, Jill
AU  - Hsing, Ann W
AU  - Devesa, Susan S
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1664
EP  - 1671
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 133
IS  - 7
SN  - 0020-7136, 0020-7136
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Health risks
KW  - Etiology
KW  - Risk factors
KW  - Gender
KW  - INE, USA, Alaska
KW  - Age groups
KW  - Cancer
KW  - Ethnic groups
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/1434032996?accountid=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=Biliary+tract+cancer+incidence+in+the+United+States-Demographic+and+temporal+variations+by+anatomic+site&rft.au=Castro%2C+Felipe+A%3BKoshiol%2C+Jill%3BHsing%2C+Ann+W%3BDevesa%2C+Susan+S&rft.aulast=Castro&rft.aufirst=Felipe&rft.date=2013-10-01&rft.volume=133&rft.issue=7&rft.spage=1664&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28161
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Health risks; Etiology; Risk factors; Gender; Age groups; Ethnic groups; Cancer; INE, USA, Alaska
DO  - http://dx.doi.org/10.1002/ijc.28161
ER  - 



TY  - JOUR
T1  - Congenital malformations and testicular germ cell tumors
AN  - 1434032727; 18510169
AB  - Cryptorchidism is one of the few known risk factors for testicular germ cell tumors (TGCT). It has been postulated that other congenital malformations, in particular hypospadias, are also associated with increased risk; however, associations with birth defects have not been extensively studied. Using Swedish population-based registries we evaluated the relationship between birth defects and risk of TGCT. TGCT cases (n = 6,593) diagnosed between 15 and 65 years of age were identified from the Swedish Cancer Registry between 1964 and 2008. Five controls per case were randomly selected from the population register and matched on birth year and birth county. Congenital malformations were identified via linkage with the Hospital Discharge Register. Odds ratios (ORs) and 95% confidence intervals (CIs) for the association between each group of malformations and TGCT were estimated using conditional logistic regression. In addition to the expected association between cryptorchidism and TGCT risk [OR (95% CI): 3.18 (2.50-4.04)], hypospadias [2.41 (1.27-4.57)], inguinal hernia [1.37 (1.11-1.68)] and other genital malformations [2.19 (1.17-4.10)] were associated with an increased risk of TGCT. Mutual adjustment for cryptorchidism, hypospadias, inguinal hernia and other genital malformations did not appreciably change the associations (ORs: 3.16, 2.25, 1.30 and 1.90, respectively). The other (nongenital) malformations evaluated were not associated with TGCT. These data suggest that developmental urogenital abnormalities, specifically cryptorchidism, hypospadias and inguinal hernia, are associated with an increased risk of TGCT, further supporting the hypothesis that prenatal exposure(s) related to proper genital development are related to this tumor. What's new? While cryptorchidism is a known risk factor for testicular germ cell tumors (TGCT), few studies have evaluated the association between other birth defects and risk of TGCT. Using large, population-based registries in Sweden, the authors evaluated this important question and demonstrate that hypospadias, inguinal hernia, and other genital malformations are associated with an increased risk of TGCT. The findings highlight the importance of prenatal exposures related to proper genital development in the etiology of TGCT.
JF  - International Journal of Cancer
AU  - Trabert, Britton
AU  - Zugna, Daniela
AU  - Richiardi, Lorenzo
AU  - McGlynn, Katherine A
AU  - Akre, Olof
AD  - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 1900
EP  - 1904
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 133
IS  - 8
SN  - 0020-7136, 0020-7136
KW  - Risk Abstracts
KW  - Health risks
KW  - Age
KW  - Etiology
KW  - Prenatal experience
KW  - Risk factors
KW  - Congenital defects
KW  - Tumors
KW  - Cancer
KW  - Sweden
KW  - Hospitals
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434032727?accountid=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=Congenital+malformations+and+testicular+germ+cell+tumors&rft.au=Trabert%2C+Britton%3BZugna%2C+Daniela%3BRichiardi%2C+Lorenzo%3BMcGlynn%2C+Katherine+A%3BAkre%2C+Olof&rft.aulast=Trabert&rft.aufirst=Britton&rft.date=2013-10-01&rft.volume=133&rft.issue=8&rft.spage=1900&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28207
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Health risks; Etiology; Age; Prenatal experience; Risk factors; Congenital defects; Tumors; Cancer; Hospitals; Sweden
DO  - http://dx.doi.org/10.1002/ijc.28207
ER  - 



TY  - JOUR
T1  - Characterizing Carbohydrate-Protein Interactions by Nuclear Magnetic Resonance Spectroscopy
AN  - 1434015997; 18483823
AB  - Interactions between proteins and soluble carbohydrates and/or surface displayed glycans are central to countless recognition, attachment and signaling events in biology. The physical chemical features associated with these binding events vary considerably, depending on the biological system of interest. For example, carbohydrate-protein interactions can be stoichiometric or multivalent, the protein receptors can be monomeric or oligomeric, and the specificity of recognition can be highly stringent or rather promiscuous. Equilibrium dissociation constants for carbohydrate binding are known to vary from micromolar to millimolar, with weak interactions being far more prevalent; and individual carbohydrate-binding sites can be truly symmetrical or merely homologous, and hence, the affinities of individual sites within a single protein can vary, as can the order of binding. Several factors, including the weak affinities with which glycans bind their protein receptors, the dynamic nature of the glycans themselves, and the nonequivalent interactions among oligomeric carbohydrate receptors, have made nuclear magnetic resonance (NMR) an especially powerful tool for studying and defining carbohydrate-protein interactions. Here, we describe those NMR approaches that have proven to be the most robust in characterizing these systems, and explain what type of information can (or cannot) be obtained from each. Our goal is to provide the reader the information necessary for selecting the correct experiment or sets of experiments to characterize their carbohydrate-protein interaction of interest. Published 2013 Wiley Periodicals, Inc.* Biopolymers 99: 796-806, 2013.
JF  - Biopolymers
AU  - Bewley, Carole A
AU  - Shahzad-ul-Hussan, Syed
AD  - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 796
EP  - 806
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 99
IS  - 10
SN  - 0006-3525, 0006-3525
KW  - Biotechnology and Bioengineering Abstracts
KW  - glycan binding
KW  - complex-type glycan
KW  - oligomannose
KW  - multivalent
KW  - Biopolymers
KW  - N.M.R.
KW  - Carbohydrates
KW  - Polysaccharides
KW  - Spectroscopy
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434015997?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterizing+Carbohydrate-Protein+Interactions+by+Nuclear+Magnetic+Resonance+Spectroscopy&rft.au=Bewley%2C+Carole+A%3BShahzad-ul-Hussan%2C+Syed&rft.aulast=Bewley&rft.aufirst=Carole&rft.date=2013-10-01&rft.volume=99&rft.issue=10&rft.spage=796&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22329
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Biopolymers; N.M.R.; Carbohydrates; Spectroscopy; Polysaccharides
DO  - http://dx.doi.org/10.1002/bip.22329
ER  - 



TY  - JOUR
T1  - Mucin-Type Glycopeptide Structure in Solution: Past, Present, and Future
AN  - 1434013349; 18483825
AB  - Mucins are very high molecular weight glycoproteins that form a "mucus" barrier at the surface of epithelial cells. They are heavily glycosylated with O-linked glycans that are involved in myriad cellular functions, including protection from external changes in pH, ion flux and reactive oxygen species. Aberrations in mucin expression and their glycan constitution have been associated with many disease states including gastritis, pulmonary disorders and cancer. High resolution structural information on mucins is lacking due to their complexity, in particular their large size and the many variants of O-linked glycans produced in their biosynthesis. This review discusses the structures of glycopeptides that contain "mucin-type" glycosylation, and concentrates primarily on data obtained by NMR spectroscopy. The effect of the glycan on the peptide backbone, the features that have shown to be common to this type of glycosylation and the differences of glycosylation at serine and threonine residues are the major topics of discussion. Published 2013 Wiley Periodicals, Inc. Biopolymers 99: 713-723, 2013.
JF  - Biopolymers
AU  - Barchi, Joseph J
AD  - Chemical Biology Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702.
Y1  - 2013/10//
PY  - 2013
DA  - Oct 2013
SP  - 713
EP  - 723
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 99
IS  - 10
SN  - 0006-3525, 0006-3525
KW  - Biotechnology and Bioengineering Abstracts
KW  - mucins
KW  - O-linked glycans
KW  - NMR
KW  - conformation
KW  - serine/threonine
KW  - Epithelial cells
KW  - Data processing
KW  - Biopolymers
KW  - Mucus
KW  - Glycosylation
KW  - Polysaccharides
KW  - Cancer
KW  - Glycopeptides
KW  - Reactive oxygen species
KW  - Magnetic resonance spectroscopy
KW  - mucin
KW  - Glycoproteins
KW  - pH effects
KW  - Threonine
KW  - Gastritis
KW  - Serine
KW  - Lung cancer
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434013349?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mucin-Type+Glycopeptide+Structure+in+Solution%3A+Past%2C+Present%2C+and+Future&rft.au=Barchi%2C+Joseph+J&rft.aulast=Barchi&rft.aufirst=Joseph&rft.date=2013-10-01&rft.volume=99&rft.issue=10&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22313
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Epithelial cells; Data processing; Biopolymers; Mucus; Glycosylation; Polysaccharides; Cancer; Reactive oxygen species; Glycopeptides; Magnetic resonance spectroscopy; mucin; Glycoproteins; Gastritis; Threonine; pH effects; Serine; Lung cancer
DO  - http://dx.doi.org/10.1002/bip.22313
ER  - 



TY  - JOUR
T1  - Plasma cytokine levels and human papillomavirus infection at the cervix in rural Nigerian women.
AN  - 1431623839; 23972725
AB  - We conducted a study to test the hypothesis that systemic dysregulation of Th1/Th2 cytokine levels was associated with detection of carcinogenic or overall human papillomavirus (HPV) at the cervix among 964 women residing in a rural village in Nigeria.
          Levels in plasma were measured for 19 cytokines, including Th1-like cytokines IL-2, IL-12 (p40), TNF-a, IFN-g; Th2-like cytokines IL-4, IL-5, IL-6, IL-10, IL-13; innate/inflammation cytokines IL-1a, IL-1b, IL-8, eotaxin, MCP-1, MIP-1a, and IL-7; and cell development cytokines G-CSF, VEGF, and IL-17. Analysis was restricted to 5 cytokines, TNF-α (Th1), IL-8 (Th2), eotaxin and MCP-1 (innate/inflammation), and G-CSF (cell development), whose levels were detected in 80% or more of the samples measured as well as had a coefficient of variation of <30%.
          Strong correlations were noted between levels of eotaxin and TNF-α (r=0.75), IL-8 and MCP-1 (r=0.60), eotaxin and G-CSF (r=0.44), and G-CSF and IFN-γ (r=0.43). Detection of carcinogenic or non-carcinogenic HPV DNA was unrelated to cytokine levels, except for levels of eotaxin and TNF-α, which were inversely correlated, albeit weakly, with detection of any carcinogenic HPV (P=0.048 and P=0.067, respectively). In analyses stratified by age group, levels of eotaxin were inversely correlated with detection of any HPV DNA (P=0.026) and carcinogenic HPV (P=0.042) in older, but not younger, women. Our results do not support the hypothesis of association between systemic cytokine dysregulation and detection of HPV at the cervix in Nigerian women, but subgroup analyses raise questions about inverse associations between eotaxin and TNF-α in older women.
          Published by Elsevier Ltd.
JF  - Cytokine
AU  - Mbulaiteye, S M
AU  - Kemp, T
AU  - Gage, J C
AU  - Ajenifuja, K O
AU  - Kiruthu, C
AU  - Wentzensen, N A
AU  - Adepiti, C
AU  - Wacholder, S
AU  - Burk, R D
AU  - Schiffman, M
AU  - Pinto, L
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD, USA. Electronic address: mbulaits@mail.nih.gov.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 146
EP  - 151
VL  - 64
IS  - 1
KW  - Cytokines
KW  - 0
KW  - DNA, Viral
KW  - Index Medicus
KW  - Plasmodium falciparum malaria
KW  - Cervical cancer
KW  - Inflammation
KW  - Th2 Cells -- metabolism
KW  - Humans
KW  - Adult
KW  - Malaria -- blood
KW  - Th1 Cells -- metabolism
KW  - Middle Aged
KW  - DNA, Viral -- isolation & purification
KW  - Nigeria -- epidemiology
KW  - Papillomaviridae -- immunology
KW  - Female
KW  - Cytokines -- blood
KW  - Cervix Uteri -- metabolism
KW  - Papillomavirus Infections -- virology
KW  - Cervix Uteri -- virology
KW  - Papillomavirus Infections -- blood
KW  - Papillomavirus Infections -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1431623839?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytokine&rft.atitle=Plasma+cytokine+levels+and+human+papillomavirus+infection+at+the+cervix+in+rural+Nigerian+women.&rft.au=Mbulaiteye%2C+S+M%3BKemp%2C+T%3BGage%2C+J+C%3BAjenifuja%2C+K+O%3BKiruthu%2C+C%3BWentzensen%2C+N+A%3BAdepiti%2C+C%3BWacholder%2C+S%3BBurk%2C+R+D%3BSchiffman%2C+M%3BPinto%2C+L&rft.aulast=Mbulaiteye&rft.aufirst=S&rft.date=2013-10-01&rft.volume=64&rft.issue=1&rft.spage=146&rft.isbn=&rft.btitle=&rft.title=Cytokine&rft.issn=1096-0023&rft_id=info:doi/10.1016%2Fj.cyto.2013.07.028
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-15
N1  - Date created - 2013-09-10
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Int J Cancer. 2012 Jan 15;130(2):245-50 [21796634]
Cytokine. 2011 Dec;56(3):798-803 [22015106]
Int J Cancer. 2002 Jun 10;99(5):737-41 [12115509]
J Med Virol. 2002 Nov;68(3):417-23 [12226831]
Nat Rev Immunol. 2003 Sep;3(9):733-44 [12949497]
Br J Cancer. 2004 Feb 9;90(3):638-45 [14760378]
J Exp Med. 1994 Mar 1;179(3):881-7 [7509365]
N Engl J Med. 1998 Feb 12;338(7):423-8 [9459645]
J Immunol. 1999 Aug 1;163(3):1602-10 [10415065]
Lancet Oncol. 2005 Apr;6(4):204 [15830458]
Br J Cancer. 2005 Oct 31;93(9):1068-76 [16106268]
Int J Cancer. 2007 Aug 1;121(3):621-32 [17405118]
Lancet Oncol. 2008 Jul;9(7):683-92 [18598933]
Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3450-6 [19064561]
Br J Cancer. 2009 Jul 7;101(1):202-8 [19536089]
Parasitology. 2009 Nov;136(13):1707-18 [19450373]
J Natl Cancer Inst. 2010 Nov 3;102(21):1653-62 [20944077]
Cancer Epidemiol Biomarkers Prev. 2011 Sep;20(9):1902-11 [21715603]
J Natl Cancer Inst. 2011 Oct 5;103(19):1444-51 [21908768]
Int J Cancer. 2012 May 1;130(9):2111-7 [21630264]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.cyto.2013.07.028
ER  - 



TY  - JOUR
T1  - Pharmacogenetics of ABC and SLC transporters in metastatic colorectal cancer patients receiving first-line FOLFIRI treatment.
AN  - 1431615013; 24018773
AB  - Membrane transporters are widely recognized as important determinants of drug disposition and response, generating increasing interest on the pharmacological implications of their genetic variations. The aim of this study was to elucidate the predictive/prognostic role of ATP-binding cassette (ABC) and solute carrier (SLC) protein polymorphisms on irinotecan (FOLFIRI regimen) outcome.
          A total of 250 White metastatic colorectal cancer patients homogenously treated with a first-line FOLFIRI regimen were genotyped for a panel of variants in five transporter genes. The primary study endpoints were the response rate (partial or complete response), overall survival, and time to progression. Toxicity was considered a secondary endpoint. Irinotecan pharmacokinetic data of 71 patients were used for polymorphism functional analysis. Two variants of the ABCG2 (-15622C>T, rs7699188) gene were found to be predictive (P T, rs7699188) and ABCB1 (rs2032582) polymorphisms were not found to be associated with pharmacokinetic parameters.
          This study showed that ABC/SLC polymorphisms have a crucial contribution toward the FOLFIRI outcome. This could represent a further step toward personalized therapy.
JF  - Pharmacogenetics and genomics
AU  - De Mattia, Elena
AU  - Toffoli, Giuseppe
AU  - Polesel, Jerry
AU  - D'Andrea, Mario
AU  - Corona, Giuseppe
AU  - Zagonel, Vittorina
AU  - Buonadonna, Angela
AU  - Dreussi, Eva
AU  - Cecchin, Erika
AD  - aExperimental and Clinical Pharmacology Unit bEpidemiology and Biostatistics Unit cMedical Oncology Unit, 'Centro di Riferimento Oncologico' - National Cancer Institute, Aviano dMedical Oncology Unit, 'San Filippo Neri Hospital', Rome eMedical Oncology Unit 1, Istituto Oncologico Veneto - IRCCS, Padova, Italy.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 549
EP  - 557
VL  - 23
IS  - 10
KW  - Organic Anion Transporters
KW  - 0
KW  - SLCO1B1 protein, human
KW  - Solute Carrier Organic Anion Transporter Family Member 1b1
KW  - irinotecan
KW  - 0H43101T0J
KW  - Leucovorin
KW  - Q573I9DVLP
KW  - Fluorouracil
KW  - U3P01618RT
KW  - Camptothecin
KW  - XT3Z54Z28A
KW  - Index Medicus
KW  - Genotype
KW  - Fluorouracil -- therapeutic use
KW  - Genetic Variation
KW  - Polymorphism, Single Nucleotide
KW  - Humans
KW  - Treatment Outcome
KW  - Neoplasm Metastasis
KW  - Linkage Disequilibrium
KW  - Pharmacogenetics
KW  - Leucovorin -- therapeutic use
KW  - Organic Anion Transporters -- genetics
KW  - Colorectal Neoplasms -- pathology
KW  - Camptothecin -- analogs & derivatives
KW  - ATP-Binding Cassette Transporters -- genetics
KW  - Colorectal Neoplasms -- genetics
KW  - Camptothecin -- therapeutic use
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Colorectal Neoplasms -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1431615013?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenetics+and+genomics&rft.atitle=Pharmacogenetics+of+ABC+and+SLC+transporters+in+metastatic+colorectal+cancer+patients+receiving+first-line+FOLFIRI+treatment.&rft.au=De+Mattia%2C+Elena%3BToffoli%2C+Giuseppe%3BPolesel%2C+Jerry%3BD%27Andrea%2C+Mario%3BCorona%2C+Giuseppe%3BZagonel%2C+Vittorina%3BBuonadonna%2C+Angela%3BDreussi%2C+Eva%3BCecchin%2C+Erika&rft.aulast=De+Mattia&rft.aufirst=Elena&rft.date=2013-10-01&rft.volume=23&rft.issue=10&rft.spage=549&rft.isbn=&rft.btitle=&rft.title=Pharmacogenetics+and+genomics&rft.issn=1744-6880&rft_id=info:doi/10.1097%2FFPC.0b013e328364b6cf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-12
N1  - Date created - 2013-09-10
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/FPC.0b013e328364b6cf
ER  - 



TY  - JOUR
T1  - Glutamatergic targets for new alcohol medications.
AN  - 1431614942; 23995381
AB  - An increasingly compelling literature points to a major role for the glutamate system in mediating the effects of alcohol on behavior and the pathophysiology of alcoholism. Preclinical studies indicate that glutamate signaling mediates certain aspects of ethanol's intoxicating and rewarding effects, and undergoes adaptations following chronic alcohol exposure that may contribute to the withdrawal, craving and compulsive drug-seeking that drive alcohol abuse and alcoholism.
          We discuss the potential for targeting the glutamate system as a novel pharmacotherapeutic approach to treating alcohol use disorders, focusing on five major components of the glutamate system: the N-methyl-D-aspartate (NMDA) receptor and specific NMDA subunits, the glycineB site on the NMDA receptors (NMDAR), L-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid ionotropic (AMPA) and kainate (KAR) receptors, metabotropic receptors (mGluR), and glutamate transporters. Chronic alcohol abuse produces a hyperglutamatergic state, characterized by elevated extracellular glutamate and altered glutamate receptors and transporters. Pharmacologically manipulating glutamatergic neurotransmission alters alcohol-related behaviors including intoxication, withdrawal, and alcohol-seeking, in rodents and human subjects. Blocking NMDA and AMPA receptors reduces alcohol consumption in rodents, but side-effects may limit this as a therapeutic approach. Selectively targeting NMDA and AMPA receptor subunits (e.g., GluN2B, GluA3), or the NMDAR glycineB site offers an alternative approach. Blocking mGluR5 potently affects various alcohol-related behaviors in rodents, and mGluR2/3 agonism also suppresses alcohol consumption. Finally, glutamate transporter upregulation may mitigate behavioral and neurotoxic sequelae of excess glutamate caused by alcohol.
          Despite the many challenges that remain, targeting the glutamate system offers genuine promise for developing new treatments for alcoholism.
JF  - Psychopharmacology
AU  - Holmes, Andrew
AU  - Spanagel, Rainer
AU  - Krystal, John H
AD  - Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA, holmesan@mail.nih.gov.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 539
EP  - 554
VL  - 229
IS  - 3
KW  - Protein Subunits
KW  - 0
KW  - Receptors, AMPA
KW  - Receptors, Kainic Acid
KW  - Receptors, N-Methyl-D-Aspartate
KW  - Glutamic Acid
KW  - 3KX376GY7L
KW  - Index Medicus
KW  - Drug-Seeking Behavior -- drug effects
KW  - Animals
KW  - Substance Withdrawal Syndrome -- metabolism
KW  - Substance Withdrawal Syndrome -- prevention & control
KW  - Receptors, Kainic Acid -- metabolism
KW  - Humans
KW  - Substance Withdrawal Syndrome -- psychology
KW  - Receptors, N-Methyl-D-Aspartate -- metabolism
KW  - Receptors, AMPA -- metabolism
KW  - Glutamic Acid -- metabolism
KW  - Alcoholism -- metabolism
KW  - Molecular Targeted Therapy -- methods
KW  - Alcoholism -- psychology
KW  - Alcoholism -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1431614942?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Glutamatergic+targets+for+new+alcohol+medications.&rft.au=Holmes%2C+Andrew%3BSpanagel%2C+Rainer%3BKrystal%2C+John+H&rft.aulast=Holmes&rft.aufirst=Andrew&rft.date=2013-10-01&rft.volume=229&rft.issue=3&rft.spage=539&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=1432-2072&rft_id=info:doi/10.1007%2Fs00213-013-3226-2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-24
N1  - Date created - 2013-09-10
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Alcohol Alcohol. 2007 Jul-Aug;42(4):296-300 [17548369]
JAMA. 2007 Oct 10;298(14):1641-51 [17925516]
Alcohol Clin Exp Res. 2007 Nov;31(11):1900-7 [17877781]
ScientificWorldJournal. 2007;7:9-21 [17982573]
Neuropsychopharmacology. 2008 Jan;33(1):166-80 [17805308]
Biochem Pharmacol. 2008 Jan 1;75(1):218-65 [17706608]
J Neurophysiol. 2007 Dec;98(6):3185-96 [17898152]
Eur J Pharmacol. 1999 Nov 19;384(2-3):139-46 [10611433]
Alcohol Clin Exp Res. 1999 Dec;23(12):1914-20 [10630610]
Alcohol Clin Exp Res. 2000 Feb;24(2):220-5 [10698375]
Eur J Pharmacol. 2000 Apr 14;394(2-3):221-31 [10771287]
Prog Drug Res. 2000;54:152-89 [10857388]
Crit Rev Neurobiol. 2000;14(1):69-89 [11253956]
J Pharmacol Exp Ther. 2001 Oct;299(1):12-20 [11561058]
J Biol Chem. 2001 Nov 30;276(48):44729-35 [11572853]
N Engl J Med. 2001 Dec 13;345(24):1734-9 [11742047]
Med Arh. 2002;56(4):211-2 [12518536]
Alcohol Clin Exp Res. 2003 Mar;27(3):465-70 [12658112]
Psychopharmacology (Berl). 2003 May;167(3):225-34 [12669179]
J Neurosci. 2004 Feb 18;24(7):1594-603 [14973247]
Trends Pharmacol Sci. 2009 Nov;30(11):563-9 [19837463]
Psychopharmacology (Berl). 2010 Jan;207(4):529-34 [19823810]
J Neurosci. 2010 Mar 31;30(13):4590-600 [20357110]
Neuroscience. 2010 May 5;167(2):361-71 [20153402]
Biol Psychiatry. 2010 May 1;67(9):812-22 [19897175]
Biol Psychiatry. 2010 May 1;67(9):823-30 [20132926]
Biol Psychiatry. 2010 May 1;67(9):804-11 [20189165]
J Neurosci. 2010 Apr 14;30(15):5357-67 [20392957]
Eur J Pharmacol. 2010 Aug 10;639(1-3):17-25 [20363219]
Pharmacogenet Genomics. 2010 Sep;20(9):553-64 [20657349]
Biol Psychiatry. 2010 Oct 15;68(8):704-11 [20655511]
J Neurosci. 1996 Mar 15;16(6):2034-43 [8604048]
Eur J Pharmacol. 1996 Jun 3;305(1-3):51-6 [8813531]
J Neurosci. 1997 Apr 15;17(8):2921-7 [9092613]
Alcohol. 1997 Jul-Aug;14(4):345-50 [9209549]
Eur J Pharmacol. 1997 Jul 30;332(1):1-8 [9298919]
Alcohol Clin Exp Res. 1997 Dec;21(9):1638-42 [9438524]
Pharmacol Biochem Behav. 1998 Jan;59(1):135-43 [9443548]
Psychopharmacology (Berl). 1998 Jan;135(1):44-51 [9489933]
Annu Rev Med. 1998;49:173-84 [9509257]
Arch Gen Psychiatry. 1998 Apr;55(4):354-60 [9554431]
Am J Psychiatry. 1998 Jun;155(6):726-32 [9619143]
Amino Acids. 1998;14(1-3):207-16 [9871463]
Alcohol Clin Exp Res. 1999 Jan;23(1):1-6 [10029196]
Alcohol Clin Exp Res. 1999 Feb;23(2):363-70 [10069569]
Alcohol Clin Exp Res. 2001 Oct;25(10):1536-41 [11696675]
JAMA. 1999 Apr 14;281(14):1318-25 [10208148]
Alcohol Alcohol. 1999 Mar-Apr;34(2):175-82 [10344778]
Mol Pharmacol. 1999 Jul;56(1):85-90 [10385687]
Nat Med. 2005 Jan;11(1):35-42 [15608650] Alcohol Clin Exp Res. 2005 Jan;29(1):17-26 [15654287]
Mol Pharmacol. 2005 Feb;67(2):349-55 [15548766]
JAMA. 2005 Apr 6;293(13):1617-25 [15811981]
Synapse. 2005 Jun 15;56(4):222-5 [15803501]
Psychopharmacology (Berl). 2005 Apr;179(1):262-70 [15717208]
Psychopharmacology (Berl). 2004 Feb;172(1):16-24 [14530901]
Neuropsychopharmacology. 2004 May;29(5):921-8 [14735132]
Alcohol Clin Exp Res. 2004 Apr;28(4):558-65 [15100606]
Neuroreport. 2004 Jan 19;15(1):207-10 [15106859]
Alcohol Clin Exp Res. 2004 Jul;28(7):1074-83 [15252294]
Neuroscientist. 2004 Aug;10(4):325-36 [15271260]
Behav Neurosci. 2004 Aug;118(4):822-34 [15301608]
Arch Gen Psychiatry. 2004 Sep;61(9):905-12 [15351769]
J Neurosci. 2004 Sep 8;24(36):7859-68 [15356198]
Am J Psychiatry. 2004 Oct;161(10):1776-82 [15465973]
Nature. 1985 Feb 7-13;313(6002):479-81 [2982106]
JAMA. 1986 Sep 19;256(11):1449-55 [3528541]
Neuropharmacology. 1988 Nov;27(11):1183-5 [2849731]
Science. 1989 Mar 31;243(4899):1721-4 [2467382]
Eur J Pharmacol. 1990 Feb 13;176(3):289-96 [2158451]
Alcohol. 1990 Sep-Oct;7(5):389-95 [1977412]
J Physiol. 1990 Sep;428:313-31 [2172523]
Neuron. 1991 Oct;7(4):605-13 [1681832]
Neuropharmacology. 1991 Nov;30(11):1167-71 [1663594]
J Pharmacol Exp Ther. 1992 Aug;262(2):487-94 [1380078]
J Pharmacol Exp Ther. 1993 Mar;264(3):1241-7 [8450461]
Pharmacol Biochem Behav. 1993 Aug;45(4):983-6 [8415841]
Neurosci Lett. 1994 Aug 29;178(1):99-102 [7816349]
Alcohol Clin Exp Res. 2007 May;31(5):775-82 [17378918]
Psychopharmacology (Berl). 2007 Jul;192(4):571-80 [17347848]
Pharmacol Biochem Behav. 2007 May;87(1):65-72 [17482246]
Mol Pharmacol. 2007 Jul;72(1):95-102 [17440117]
Nat Med. 2007 Sep;13(9):1102-7 [17767166]
Neuropsychopharmacology. 2006 Apr;31(4):778-86 [16123768]
Alcohol Clin Exp Res. 2008 Jan;32(1):36-42 [18028532]
Alcohol Clin Exp Res. 2008 Jan;32(1):67-76 [18070246]
Alcohol Clin Exp Res. 2008 Feb;32(2):209-21 [18162077]
Int J Neuropsychopharmacol. 2008 Mar;11(2):229-41 [17517168]
Addict Biol. 2008 Mar;13(1):70-9 [18269381]
Alcohol Clin Exp Res. 2008 Mar;32(3):489-97 [18215213]
Neuropsychopharmacology. 2008 May;33(6):1379-90 [17625498]
Alcohol. 2008 May;42(3):191-7 [18420113]
Br J Pharmacol. 2008 May;154(2):299-315 [18311194]
Neuropsychopharmacology. 2008 Jun;33(7):1713-23 [17851540]
Arch Gen Psychiatry. 2008 Jul;65(7):826-38 [18606955]
Psychopharmacology (Berl). 1992;109(1-2):92-8 [1365677]
Psychopharmacology (Berl). 1994 Jan;113(3-4):453-6 [7862858]
Brain Res. 1995 Mar 13;674(1):82-90 [7773698]
Alcohol Clin Exp Res. 2006 May;30(5):783-90 [16634846]
JAMA. 2006 May 3;295(17):2003-17 [16670409]
J Psychiatr Res. 2006 Aug;40(5):383-93 [16546214]
Behav Brain Res. 2006 Aug 10;171(2):207-15 [16678921]
Psychopharmacology (Berl). 2006 Sep;187(4):455-66 [16835771]
J Neurosci. 2006 Sep 27;26(39):9967-74 [17005860]
Drug Alcohol Depend. 2006 Nov 8;85(2):142-56 [16697125]
Neuropsychopharmacology. 2006 Nov;31(11):2405-14 [16482087]
Cell Mol Neurobiol. 2006 Jul-Aug;26(4-6):365-84 [16773445]
Psychopharmacology (Berl). 2007 Jan;190(1):21-9 [17096086]
Alcohol Alcohol. 2007 Jan-Feb;42(1):11-8 [17098748]
Synapse. 2007 Mar;61(3):150-6 [17146766]
Am J Psychiatry. 2007 Mar;164(3):519-23 [17329479]
Alcohol Clin Exp Res. 2007 Apr;31(4):604-11 [17374039]
Alcohol. 2009 Mar;43(2):127-35 [19251114]
Eur J Pharmacol. 2009 Apr 1;607(1-3):114-20 [19326478]
Neuropsychopharmacology. 2009 May;34(6):1454-66 [18843265]
Alcohol Clin Exp Res. 2009 May;33(5):772-82 [19298331]
Addiction. 2008 Dec;103(12):2035-44 [18855810]
Psychopharmacology (Berl). 2009 Jul;204(4):587-97 [19225761]
Lancet. 2009 Jun 27;373(9682):2223-33 [19560604]
J Neurosci. 2009 Jul 8;29(27):8655-68 [19587272]
Psychopharmacology (Berl). 2009 Aug;205(3):389-97 [19418040]
Alcohol Clin Exp Res. 2009 Nov;33(11):1924-34 [19673743]
Proc Natl Acad Sci U S A. 2012 Jan 31;109(5):E278-87 [22219357]
Pharmacol Biochem Behav. 2012 May;101(3):329-35 [22296815]
Neuropharmacology. 2012 Jun;62(7):2430-9 [22387532]
Brain Res. 2012 May 25;1456:14-21 [22521042]
Biol Psychiatry. 2012 Jun 1;71(11):1015-21 [21907974]
Alcohol. 2012 Jun;46(4):377-87 [22444953]
Alcohol. 2012 Jun;46(4):389-400 [22445805]
PLoS One. 2012;7(5):e37541 [22666364]
Neuropharmacology. 2012 Aug;63(2):181-9 [22342743]
Addict Biol. 2012 Jul;17(4):783-5 [21507155]
Curr Top Behav Neurosci. 2013;13:583-609 [22389180]
Drug Alcohol Depend. 2012 Sep 1;125(1-2):27-36 [22503310]
Alcohol Clin Exp Res. 2012 Sep;36(9):1623-33 [22432643]
Addict Biol. 2012 Sep;17(5):897-907 [21955180]
J Clin Psychiatry. 2003 May;64(5):612 [12755670]
Lancet. 2003 May 17;361(9370):1677-85 [12767733]
Proc Natl Acad Sci U S A. 2003 May 27;100(11):6813-8 [12732711]
Behav Neurosci. 2003 Jun;117(3):641-9 [12802892]
Pharmacol Ther. 2003 Jul;99(1):79-94 [12804700]
J Clin Psychopharmacol. 2003 Jun;23(3):281-93 [12826990]
J Pharmacol Exp Ther. 2003 Aug;306(2):546-55 [12734392]
Neuropharmacology. 2003 Sep;45(3):325-33 [12871650]
Pharmacol Ther. 2003 Sep;99(3):311-26 [12951163]
J Pharmacol Exp Ther. 2003 Dec;307(3):1020-9 [14534353]
Pharmacopsychiatry. 2004 Jan;37(1):37-40 [14750047]
Alcohol Clin Exp Res. 2008 Jul;32(7):1251-9 [18482157]
Int J Neuropsychopharmacol. 2008 Sep;11(6):775-93 [18377703]
Int J Neuropsychopharmacol. 2008 Sep;11(6):765-74 [18400131]
Neuropharmacology. 2008 Sep;55(4):546-54 [18619984]
Alcohol Clin Exp Res. 2008 Aug;32(8):1479-92 [18565157]
Neuropharmacology. 2008 Oct;55(5):661-8 [18617194]
Alcohol Clin Exp Res. 2008 Oct;32(10):1714-20 [18627359]
Biol Psychiatry. 2008 Nov 1;64(9):810-4 [18550032]
Alcohol Alcohol. 2008 Nov-Dec;43(6):626-9 [18945754]
Ann N Y Acad Sci. 2008 Oct;1139:10-9 [18991843]
Alcohol Clin Exp Res. 2008 Nov;32(11):1992-8 [18782337]
Neuropsychopharmacology. 2009 Jan;34(1):248-9 [19079073]
Neuropsychopharmacology. 2009 Jan;34(2):290-8 [18563060]
Physiol Behav. 2009 Jan 8;96(1):169-73 [18938187]
Alcohol Clin Exp Res. 2008 Dec;32(12):2128-35 [18828800]
Neuroscience. 2009 Jan 23;158(2):465-73 [18977415]
Alcohol Alcohol. 2009 Mar-Apr;44(2):115-27 [18940959]
Arch Gen Psychiatry. 2010 Oct;67(10):1069-77 [20921123]
Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):20093-8 [21041654]
Addict Biol. 2011 Jan;16(1):43-54 [20331561]
Addict Biol. 2011 Jan;16(1):163-5 [20192946]
Neuropsychopharmacology. 2011 Feb;36(3):701-10 [21124304]
Genes Brain Behav. 2011 Feb;10(1):111-26 [20807241]
Behav Genet. 2011 Mar;41(2):273-7 [20931356]
BMC Psychiatry. 2011;11:41 [21401921]
Alcohol Alcohol. 2011 May-Jun;46(3):239-46 [21422004]
Addict Biol. 2011 Jul;16(3):428-39 [21309945]
Psychopharmacology (Berl). 2011 Sep;217(1):3-12 [21424693]
Chronobiol Int. 2011 Oct;28(8):664-72 [21929298]
Eur J Pharmacol. 1999 Mar 5;368(2-3):137-42 [10193649]
Genes Brain Behav. 2011 Oct;10(7):805-16 [21762461]
Eur J Pharmacol. 2011 Nov 16;670(1):154-61 [21946112]
Eur J Pharmacol. 1995 Sep 5;283(1-3):177-83 [7498307]
Pharmacol Biochem Behav. 1995 Nov;52(3):609-14 [8545482]
Nat Neurosci. 2012 Oct;15(10):1359-61 [22941108]
Alcohol Clin Exp Res. 2012 Oct;36(10):1659-68 [22432593]
Alcohol Clin Exp Res. 2012 Oct;36(10):1678-87 [22486492]
J Neurosci. 2012 Oct 24;32(43):15124-32 [23100433]
Neuroscience. 2012 Dec 27;227:327-35 [23059796]
Lancet. 2012 Dec 15;380(9859):2224-60 [23245609]
Addict Biol. 2013 Jan;18(1):54-65 [23126443]
Psychopharmacology (Berl). 2013 Jan;225(1):151-9 [22820868]
Psychopharmacology (Berl). 2013 Jan;225(2):275-81 [22847457]
Neuropharmacology. 2013 Mar;66:290-301 [22659409]
Addiction. 2013 Feb;108(2):275-93 [23075288]
Biol Psychiatry. 2013 Feb 1;73(3):263-70 [22902169]
Alcohol Clin Exp Res. 2013 Feb;37(2):223-33 [22934986]
J Neurosci. 2013 Feb 13;33(7):2794-806 [23407939]
J Neurosci. 2013 Mar 13;33(11):4834-42 [23486954]
Biol Psychiatry. 2013 Aug 15;74(4):257-64 [23206319]
Nat Neurosci. 2013 Aug;16(8):1111-7 [23792945]
Nat Neurosci. 2013 Aug;16(8):1101-10 [23831965]
Drug Alcohol Depend. 2013 Sep 1;132(1-2):122-6 [23434041]
Neuropharmacology. 2005 May;48(6):822-9 [15829254]
Addict Biol. 2005 Sep;10(3):243-9 [16109585]
Psychopharmacology (Berl). 2005 Aug;180(4):583-94 [15834536]
J Pharmacol Exp Ther. 2005 Nov;315(2):590-600 [16014750]
Psychopharmacology (Berl). 2006 Jan;183(4):429-38 [16292590]
Eur J Pharmacol. 2005 Dec 28;528(1-3):110-8 [16324694]
Pharmacol Ther. 2006 Jan;109(1-2):227-37 [16102840]
Biol Psychiatry. 2006 Jan 1;59(1):85-93 [16289397]
Alcohol. 2005 Jun;36(2):83-90 [16396741]
J Neurosci. 2006 Jan 25;26(4):1231-8 [16436610]
J Neurosci. 2006 Feb 1;26(5):1331-3 [16452656]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s00213-013-3226-2
ER  - 



TY  - JOUR
T1  - Whole-body pharmacokinetics of HDAC inhibitor drugs, butyric acid, valproic acid and 4-phenylbutyric acid measured with carbon-11 labeled analogs by PET.
AN  - 1431298719; 23906667
AB  - The fatty acids, n-butyric acid (BA), 4-phenylbutyric acid (PBA) and valproic acid (VPA, 2-propylpentanoic acid) have been used for many years in the treatment of a variety of CNS and peripheral organ diseases including cancer. New information that these drugs alter epigenetic processes through their inhibition of histone deacetylases (HDACs) has renewed interest in their biodistribution and pharmacokinetics and the relationship of these properties to their therapeutic and side effect profiles. In order to determine the pharmacokinetics and biodistribution of these drugs in primates, we synthesized their carbon-11 labeled analogues and performed dynamic positron emission tomography (PET) in six female baboons over 90 min. The carbon-11 labeled carboxylic acids were prepared by using (11)CO2 and the appropriate Grignard reagents. [(11)C]BA was metabolized rapidly (only 20% of the total carbon-11 in plasma was parent compound at 5 min post injection) whereas for VPA and PBA 98% and 85% of the radioactivity were the unmetabolized compound at 30 min after their administration respectively. The brain uptake of all three carboxylic acids was very low (VPA>PBA), which is consistent with the need for very high doses for therapeutic efficacy. Most of the radioactivity was excreted through the kidneys and accumulated in the bladder. However, the organ biodistribution between the drugs differed. [(11)C]BA showed relatively high uptake in spleen and pancreas whereas [(11)C]PBA showed high uptake in liver and heart. Notably, [(11)C]VPA showed exceptionally high heart uptake possibly due to its involvement in lipid metabolism. The unique biodistribution of each of these drugs may be of relevance in understanding their therapeutic and side effect profile including their teratogenic effects. © 2013.
JF  - Nuclear medicine and biology
AU  - Kim, Sung Won
AU  - Hooker, Jacob M
AU  - Otto, Nicola
AU  - Win, Khaing
AU  - Muench, Lisa
AU  - Shea, Colleen
AU  - Carter, Pauline
AU  - King, Payton
AU  - Reid, Alicia E
AU  - Volkow, Nora D
AU  - Fowler, Joanna S
AD  - Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Upton, NY, USA. Electronic address: sunny.kim@nih.gov.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 912
EP  - 918
VL  - 40
IS  - 7
KW  - Blood Proteins
KW  - 0
KW  - Carbon Radioisotopes
KW  - Histone Deacetylase Inhibitors
KW  - Phenylbutyrates
KW  - Butyric Acid
KW  - 107-92-6
KW  - Valproic Acid
KW  - 614OI1Z5WI
KW  - 4-phenylbutyric acid
KW  - 7WY7YBI87E
KW  - Index Medicus
KW  - (11)C]valproic acid
KW  - Positron emission tomography
KW  - [(11)C]butyric acid
KW  - [(11)C]4-phenylbutyric acid
KW  - Pharmacokinetics
KW  - Histone deacetylase (HDAC)
KW  - Papio
KW  - Animals
KW  - Phenylbutyrates -- metabolism
KW  - Phenylbutyrates -- blood
KW  - Brain -- metabolism
KW  - Butyric Acid -- blood
KW  - Valproic Acid -- metabolism
KW  - Tissue Distribution
KW  - Brain -- diagnostic imaging
KW  - Isotope Labeling
KW  - Radiochemistry
KW  - Butyric Acid -- metabolism
KW  - Butyric Acid -- pharmacokinetics
KW  - Valproic Acid -- blood
KW  - Phenylbutyrates -- pharmacokinetics
KW  - Blood Proteins -- metabolism
KW  - Female
KW  - Valproic Acid -- pharmacokinetics
KW  - Positron-Emission Tomography
KW  - Histone Deacetylase Inhibitors -- metabolism
KW  - Histone Deacetylase Inhibitors -- pharmacokinetics
KW  - Histone Deacetylase Inhibitors -- blood
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1431298719?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nuclear+medicine+and+biology&rft.atitle=Whole-body+pharmacokinetics+of+HDAC+inhibitor+drugs%2C+butyric+acid%2C+valproic+acid+and+4-phenylbutyric+acid+measured+with+carbon-11+labeled+analogs+by+PET.&rft.au=Kim%2C+Sung+Won%3BHooker%2C+Jacob+M%3BOtto%2C+Nicola%3BWin%2C+Khaing%3BMuench%2C+Lisa%3BShea%2C+Colleen%3BCarter%2C+Pauline%3BKing%2C+Payton%3BReid%2C+Alicia+E%3BVolkow%2C+Nora+D%3BFowler%2C+Joanna+S&rft.aulast=Kim&rft.aufirst=Sung&rft.date=2013-10-01&rft.volume=40&rft.issue=7&rft.spage=912&rft.isbn=&rft.btitle=&rft.title=Nuclear+medicine+and+biology&rft.issn=1872-9614&rft_id=info:doi/10.1016%2Fj.nucmedbio.2013.06.007
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-01
N1  - Date created - 2013-09-09
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Pediatr Blood Cancer. 2008 Feb;50(2):357-9 [17253639]
Biol Psychiatry. 2007 Jul 1;62(1):55-64 [16945350]
Mol Cancer. 2008;7:24 [18325101]
Mol Ther. 2008 Sep;16(9):1546-55 [18648350]
Anticancer Res. 2008 Jul-Aug;28(4C):2437-42 [18751431]
Amyotroph Lateral Scler. 2009 Apr;10(2):99-106 [18688762]
Nucl Med Biol. 2009 Apr;36(3):323-34 [19324278]
Nature. 2009 May 7;459(7243):55-60 [19424149]
Neuropsychopharmacology. 2009 Jun;34(7):1721-32 [19145227]
Reprod Toxicol. 2009 Jul;28(1):1-10 [19490988]
Cancer Prev Res (Phila). 2009 Jun;2(6):581-9 [19470789]
BMC Cancer. 2010;10:387 [20663136]
Clin Nutr. 2010 Dec;29(6):738-44 [20471725]
J Neurochem. 2011 Feb;116(4):636-45 [21166804]
Behav Brain Res. 2011 Aug 1;221(1):329-32 [21421011]
Mol Cancer Ther. 2011 Aug;10(8):1430-9 [21632462]
J Alzheimers Dis. 2011;26(1):187-97 [21593570]
Behav Brain Res. 2011 Nov 20;225(1):110-6 [21767572]
Cochrane Database Syst Rev. 2011;(10):CD009183 [21975791]
Gut. 2000 Sep;47(3):397-403 [10940278]
Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9808-13 [11504946]
Indian J Pediatr. 2001 Oct;68(10):989-90 [11758141]
J Pediatr Hematol Oncol. 2002 Dec;24(9):737-41 [12468915]
Epilepsy Res. 2003 Feb;53(1-2):19-27 [12576164]
J Biol Chem. 1978 May 25;253(10):3364-6 [649576]
Cancer Res. 1979 Nov;39(11):4720-3 [498098]
Neurology. 1981 Apr;31(4):486-7 [6783980]
Biochem Biophys Res Commun. 1981 Dec 15;103(3):806-12 [6174120]
Br J Clin Pharmacol. 1983 Apr;15(4):503-6 [6405774]
Ann Neurol. 1983 Jul;14(1):38-42 [6412620]
Eur J Cancer Clin Oncol. 1987 Sep;23(9):1283-7 [3678322]
Gastroenterology. 1992 Jul;103(1):51-6 [1612357]
N Engl J Med. 1992 Aug 20;327(8):569-70 [1378939]
Drugs. 1992 Sep;44(3):326-35 [1382932]
Neuropsychopharmacology. 2011 Nov;36(12):2406-21 [21796107]
J Dermatol Sci. 2011 Dec;64(3):163-73 [21924869]
Cochrane Database Syst Rev. 2011;(12):CD006282 [22161400]
J Inherit Metab Dis. 2008 Apr;31(2):205-16 [18392741]
J Pharm Pharmacol. 1992 May;44(5):408-12 [1359055]
N Engl J Med. 1993 Jan 14;328(2):81-6 [7677966]
Gut. 1993 Mar;34(3):386-91 [8386131]
Am J Pediatr Hematol Oncol. 1994 Feb;16(1):67-71 [7508690]
Blood. 1994 Jul 1;84(1):339-43 [7517215]
Blood. 1994 Sep 1;84(5):1690-1 [7520784]
Blood. 1995 Jan 1;85(1):43-9 [7528572]
Gut. 1996 Apr;38(4):568-73 [8707089]
Blood. 1997 Jul 15;90(2):891-3 [9226193]
Int J Oncol. 2004 Dec;25(6):1795-9 [15547719]
J Clin Oncol. 2005 Jun 10;23(17):3906-11 [15851763]
Brain Res. 2005 Aug 2;1052(1):56-62 [16061211]
Lancet. 2005 Aug 13-19;366(9485):549-55 [16099290]
Cancer. 2006 Jan 1;106(1):112-9 [16323176]
J Clin Psychiatry. 2006 Oct;67(10):1501-10 [17107240]
Epilepsia. 2006 Dec;47(12):2027-31 [17201699]
Clin Pharmacokinet. 2007;46(4):307-18 [17375982]
Nature. 2007 May 10;447(7141):178-82 [17468743]
Biochem J. 2008 Jan 15;409(2):581-9 [17868033]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.nucmedbio.2013.06.007
ER  - 



TY  - JOUR
T1  - Alzheimer's disease-associated polymorphisms in human OGG1 alter catalytic activity and sensitize cells to DNA damage.
AN  - 1415603492; 23684897
AB  - Brain tissues from Alzheimer's disease (AD) patients show increased levels of oxidative DNA damage and 7,8-dihydro-8-oxoguanine (8-oxoG) accumulation. In humans, the base excision repair protein 8-oxoguanine-DNA glycosylase (OGG1) is the major enzyme that recognizes and excises the mutagenic DNA base lesion 8-oxoG. Recently, two polymorphisms of OGG1, A53T and A288V, have been identified in brain tissues of AD patients, but little is known about how these polymorphisms may contribute to AD. We characterized the A53T and A288V polymorphic variants and detected a significant reduction in the catalytic activity for both proteins in vitro and in cells. Additionally, the A53T polymorphism has decreased substrate binding, whereas the A288V polymorphism has reduced AP lyase activity. Both variants have decreased binding to known OGG1 binding partners PARP-1 and XRCC1. We found that OGG1(-/-) cells expressing A53T and A288V OGG1 were significantly more sensitive to DNA damage and had significantly decreased survival. Our results provide both biochemical and cellular evidence that A53T and A288V polymorphic proteins have deficiencies in catalytic and protein-binding activities that could be related to the increase in oxidative damage to DNA found in AD brains. 
          Published by Elsevier Inc.
JF  - Free radical biology & medicine
AU  - Jacob, Kimberly D
AU  - Noren Hooten, Nicole
AU  - Tadokoro, Takashi
AU  - Lohani, Althaf
AU  - Barnes, Janice
AU  - Evans, Michele K
AD  - Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224-6825, USA.
Y1  - 2013/10//
PY  - 2013
DA  - October 2013
SP  - 115
EP  - 125
VL  - 63
KW  - 7,8-dihydro-8-oxoguanine
KW  - 0
KW  - DNA-Binding Proteins
KW  - X-ray repair cross complementing protein 1
KW  - Guanine
KW  - 5Z93L87A1R
KW  - PARP1 protein, human
KW  - EC 2.4.2.30
KW  - Poly (ADP-Ribose) Polymerase-1
KW  - Poly(ADP-ribose) Polymerases
KW  - DNA Glycosylases
KW  - EC 3.2.2.-
KW  - oxoguanine glycosylase 1, human
KW  - Index Medicus
KW  - poly(ADP-ribose) polymerase 1
KW  - ROS
KW  - Alzheimer's disease
KW  - PARP-1
KW  - 8-Oxoguanine
KW  - XRCC1
KW  - Oxidative stress
KW  - poly(ADP-ribosyl)ation
KW  - reactive oxygen species
KW  - Free radicals
KW  - 8-Oxoguanine-DNA glycosylase
KW  - base excision repair
KW  - DNA repair
KW  - mouse embryo fibroblast
KW  - DNA damage
KW  - AD
KW  - PAR
KW  - 8-oxoguanine-DNA glycosylase
KW  - 8-oxoG
KW  - MEF
KW  - X-ray cross-complementing protein 1
KW  - Base excision repair
KW  - BER
KW  - OGG1
KW  - DNA Repair -- genetics
KW  - Polymorphism, Genetic
KW  - Humans
KW  - Guanine -- analogs & derivatives
KW  - Substrate Specificity
KW  - Protein Binding
KW  - Poly(ADP-ribose) Polymerases -- metabolism
KW  - Guanine -- metabolism
KW  - DNA-Binding Proteins -- metabolism
KW  - Catalysis
KW  - Alzheimer Disease -- genetics
KW  - DNA Glycosylases -- metabolism
KW  - Oxidative Stress
KW  - DNA Glycosylases -- genetics
KW  - Alzheimer Disease -- metabolism
KW  - DNA Damage -- genetics
KW  - Alzheimer Disease -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1415603492?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alzheimer%27s+disease-associated+polymorphisms+in+human+OGG1+alter+catalytic+activity+and+sensitize+cells+to+DNA+damage.&rft.au=Jacob%2C+Kimberly+D%3BNoren+Hooten%2C+Nicole%3BTadokoro%2C+Takashi%3BLohani%2C+Althaf%3BBarnes%2C+Janice%3BEvans%2C+Michele+K&rft.aulast=Jacob&rft.aufirst=Kimberly&rft.date=2013-10-01&rft.volume=63&rft.issue=&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2013.05.010
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-01
N1  - Date created - 2013-07-29
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nucleic Acids Res. 2007;35(8):2759-66 [17426120]
DNA Repair (Amst). 2007 Mar 1;6(3):317-28 [17126083]
Nucleic Acids Res. 2007;35(16):5545-55 [17704129]
Cell Res. 2008 Jan;18(1):48-63 [18166976]
Curr Protoc Mol Biol. 2001 May;Chapter 16:Unit16.7 [18265134]
Biochem Biophys Res Commun. 2008 Nov 14;376(2):336-40 [18774780]
Curr Alzheimer Res. 2009 Feb;6(1):36-47 [19199873]
FEBS J. 2009 Sep;276(18):5149-62 [19674107]
PLoS Genet. 2010 May;6(5):e1000951 [20485567]
Mutat Res. 2011 Jun 3;711(1-2):100-12 [21167187]
J Biol Chem. 2011 Dec 30;286(52):44679-90 [22057269]
Mech Ageing Dev. 2013 Mar;134(3-4):139-57 [23428415]
Nature. 2000 Feb 24;403(6772):859-66 [10706276]
Nucleic Acids Res. 2001 Jan 15;29(2):430-8 [11139613]
Nucleic Acids Res. 2001 Mar 15;29(6):1285-92 [11238994]
J Neurosci. 2001 May 1;21(9):3017-23 [11312286]
Mutat Res. 2001 Jun 5;486(1):31-40 [11356334]
Science. 2002 Jul 19;297(5580):353-6 [12130773]
Neurobiol Aging. 2002 Sep-Oct;23(5):655-64 [12392766]
Biochemistry. 2003 Feb  18;42(6):1564-72 [12578369]
J Biol Chem. 2003 Nov 7;278(45):44068-74 [12933815]
Nucleic Acids Res. 2004;32(2):570-8 [14752045]
Neurotoxicology. 1986 Spring;7(1):195-206 [3714121]
Biopolymers. 1987 Nov;26(11):1859-77 [3689874]
Nucleic Acids Res. 1989 Aug 11;17(15):6419 [2771659]
Nature. 1991 Feb 21;349(6311):704-6 [1671712]
Ann Neurol. 1992;32 Suppl:S22-7 [1510377]
Ann Neurol. 1993 Oct;34(4):609-16 [8215249]
Science. 1993 Oct 29;262(5134):689-95 [7901908]
Ann Neurol. 1994 Nov;36(5):747-51 [7979220]
Nature. 1995 Jun 29;375(6534):754-60 [7596406]
Science. 1995 Aug 18;269(5226):973-7 [7638622]
Nature. 1995 Aug 31;376(6543):775-8 [7651536]
J Neurochem. 1995 Nov;65(5):2146-56 [7595501]
Ann Neurol. 1997 May;41(5):646-53 [9153527]
Free Radic Biol Med. 1997;23(1):134-47 [9165306]
Mol Chem Neuropathol. 1997 May;31(1):53-64 [9271005]
J Neurochem. 1997 Sep;69(3):1326-9 [9282961]
J Neurochem. 1997 Nov;69(5):2064-74 [9349552]
Fold Des. 1998;3(2):119-26 [9565756]
Biochemistry. 1998 May 26;37(21):7733-40 [9601033]
Mol Carcinog. 2005 Mar;42(3):127-41 [15584022]
Nature. 2005 Mar 31;434(7033):612-8 [15800616]
J Neurochem. 2006 Feb;96(3):825-32 [16405502]
Nucleic Acids Res. 2006;34(5):1620-32 [16549874]
J Neurochem. 2006 Jun;97(6):1634-58 [16805774]
Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982]
Anal Biochem. 2006 Oct 15;357(2):289-98 [16962548]
Free Radic Res. 2006 Dec;40(12):1295-302 [17090419]
Cancer Detect Prev. 2007;31(3):237-43 [17651912]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.freeradbiomed.2013.05.010
ER  - 



TY  - JOUR
T1  - Predicting county-level cancer incidence rates and counts in the USA
AN  - 1458537423; 18769411
AB  - Many countries, including the USA, publish predicted numbers of cancer incidence and death in current and future years for the whole country. These predictions provide important information on the cancer burden for cancer control planners, policymakers and the general public. Based on evidence from several empirical studies, the joinpoint (segmented-line linear regression) model (JPM) has been adopted by the American Cancer Society to estimate the number of new cancer cases in the USA and in individual states since 2007. Recently, cancer incidence in smaller geographic regions such as counties, and local policy makers are increasingly interested with Federal Information Processing Standard code regions. The natural extension is to directly apply the JPM to county-level cancer incidence data. The direct application has several drawbacks and its performance has not been evaluated. To address the concerns, we developed a spatial random-effects JPM for county-level cancer incidence data. The proposed model was used to predict both cancer incidence rates and counts at the county level. The standard JPM and the proposed method were compared through a validation study. The proposed method outperformed the standard JPM for almost all cancer sites, especially for moderate or rare cancer sites and for counties with small population sizes. As an application, we predicted county-level prostate cancer incidence rates and counts for the year 2011 in Connecticut. Published 2013. This article is a US Government work and is in the public domain in the USA.
JF  - Statistics in Medicine
AU  - Yu, B
AD  - Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Bethesda, MA 20892, USA, whybb@yahoo.com
Y1  - 2013/09/30/
PY  - 2013
DA  - 2013 Sep 30
SP  - 3911
EP  - 3925
VL  - 32
IS  - 22
SN  - 0277-6715, 0277-6715
KW  - Risk Abstracts
KW  - Prediction
KW  - Mortality
KW  - Prostate cancer
KW  - USA, Connecticut
KW  - Population number
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458537423?accountid=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=Statistics+in+Medicine&rft.atitle=Predicting+county-level+cancer+incidence+rates+and+counts+in+the+USA&rft.au=Yu%2C+B&rft.aulast=Yu&rft.aufirst=B&rft.date=2013-09-30&rft.volume=32&rft.issue=22&rft.spage=3911&rft.isbn=&rft.btitle=&rft.title=Statistics+in+Medicine&rft.issn=02776715&rft_id=info:doi/10.1002%2Fsim.5833
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2013-12-04
N1  - SubjectsTermNotLitGenreText - Prediction; Mortality; Prostate cancer; Population number; USA, Connecticut
DO  - http://dx.doi.org/10.1002/sim.5833
ER  - 



TY  - JOUR
T1  - Protection Against Malaria by Intravenous Immunization with a Nonreplicating Sporozoite Vaccine
AN  - 1551645833; 20374663
AB  - Malaria Sporozoite VaccineEach year, hundreds of millions of people are infected with Plasmodium falciparum, the mosquito-borne parasite that causes malaria. A preventative vaccine is greatly needed. Seder et al. (p. 1359, published online 8 August; see the Perspective by Good) now report the results from a phase I clinical trial where subjects were immunized intravenously with a whole, attenuated sporozoite vaccine. Three of 9 subjects who received four doses and zero of 6 subjects who received five doses of the vaccine went on to develop malaria after controlled malaria infection. Both antibody titers and cellular immune responses correlated positively with the dose of vaccine received, suggesting that both arms of the adaptive immune response may have participated in the observed protection.
JF  - Science
AU  - Seder, Robert A
AU  - Chang, Lee-Jah
AU  - Enama, Mary E
AU  - Zephir, Kathryn L
AU  - Sarwar, Uzma N
AU  - Gordon, Ingelise J
AU  - Holman, LaSonji A
AU  - James, Eric R
AU  - Billingsley, Peter F
AU  - Gunasekera, Anusha
AU  - Richman, Adam
AU  - Chakravarty, Sumana
AU  - Manoj, Anita
AU  - Velmurugan, Soundarapandian
AU  - Li, MingLin
AU  - Ruben, Adam J
AU  - Li, Tao
AU  - Eappen, Abraham G
AU  - Stafford, Richard E
AU  - Plummer, Sarah H
AU  - Hendel, Cynthia S
AU  - Novik, Laura
AU  - Costner, Pamela JM
AU  - Mendoza, Floreliz H
AU  - Saunders, Jamie G
AU  - Nason, Martha C
AU  - Richardson, Jason H
AU  - Murphy, Jittawadee
AU  - Davidson, Silas A
AU  - Richie, Thomas L
AU  - Sedegah, Martha
AU  - Sutamihardja, Awalludin
AU  - Fahle, Gary A
AU  - Lyke, Kirsten E
AU  - Laurens, Matthew B
AU  - Roederer, Mario
AU  - Tewari, Kavita
AU  - Epstein, Judith E
AU  - Sim, BKim Lee
AU  - Ledgerwood, Julie E
AU  - Graham, Barney S
AU  - Hoffman, Stephen L
AU  - DiGiovanni, Cassandra
AU  - Williams, Pernell
AU  - Luongo, Nicole
AU  - Mitchell, Jillian
AU  - Florez, Maria Burgos
AU  - Larkin, Brenda
AU  - Berkowitz, Nina
AU  - Wilson, Brandon
AU  - et. al.
AD  - Vaccine Research Center (VRC), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20852, USA, rseder@mail.nih.gov
Y1  - 2013/09/20/
PY  - 2013
DA  - 2013 Sep 20
SP  - 1359
EP  - 1365
PB  - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States
VL  - 341
IS  - 6152
SN  - 0036-8075, 0036-8075
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Parasites
KW  - Intravenous administration
KW  - Human diseases
KW  - Disease control
KW  - Sporozoites
KW  - Malaria
KW  - Plasmodium falciparum
KW  - Infection
KW  - Defence mechanisms
KW  - Clinical trials
KW  - Immunization
KW  - Public health
KW  - Antibodies
KW  - Immune response
KW  - Vaccines
KW  - Aquatic insects
KW  - Internet
KW  - K 03350:Immunology
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/1551645833?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science&rft.atitle=Protection+Against+Malaria+by+Intravenous+Immunization+with+a+Nonreplicating+Sporozoite+Vaccine&rft.au=Seder%2C+Robert+A%3BChang%2C+Lee-Jah%3BEnama%2C+Mary+E%3BZephir%2C+Kathryn+L%3BSarwar%2C+Uzma+N%3BGordon%2C+Ingelise+J%3BHolman%2C+LaSonji+A%3BJames%2C+Eric+R%3BBillingsley%2C+Peter+F%3BGunasekera%2C+Anusha%3BRichman%2C+Adam%3BChakravarty%2C+Sumana%3BManoj%2C+Anita%3BVelmurugan%2C+Soundarapandian%3BLi%2C+MingLin%3BRuben%2C+Adam+J%3BLi%2C+Tao%3BEappen%2C+Abraham+G%3BStafford%2C+Richard+E%3BPlummer%2C+Sarah+H%3BHendel%2C+Cynthia+S%3BNovik%2C+Laura%3BCostner%2C+Pamela+JM%3BMendoza%2C+Floreliz+H%3BSaunders%2C+Jamie+G%3BNason%2C+Martha+C%3BRichardson%2C+Jason+H%3BMurphy%2C+Jittawadee%3BDavidson%2C+Silas+A%3BRichie%2C+Thomas+L%3BSedegah%2C+Martha%3BSutamihardja%2C+Awalludin%3BFahle%2C+Gary+A%3BLyke%2C+Kirsten+E%3BLaurens%2C+Matthew+B%3BRoederer%2C+Mario%3BTewari%2C+Kavita%3BEpstein%2C+Judith+E%3BSim%2C+BKim+Lee%3BLedgerwood%2C+Julie+E%3BGraham%2C+Barney+S%3BHoffman%2C+Stephen+L%3BDiGiovanni%2C+Cassandra%3BWilliams%2C+Pernell%3BLuongo%2C+Nicole%3BMitchell%2C+Jillian%3BFlorez%2C+Maria+Burgos%3BLarkin%2C+Brenda%3BBerkowitz%2C+Nina%3BWilson%2C+Brandon%3Bet.+al.&rft.aulast=Seder&rft.aufirst=Robert&rft.date=2013-09-20&rft.volume=341&rft.issue=6152&rft.spage=1359&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1241800
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Antibodies; Human diseases; Disease control; Malaria; Vaccines; Defence mechanisms; Aquatic insects; Public health; Intravenous administration; Sporozoites; Immune response; Infection; Clinical trials; Immunization; Internet; Plasmodium falciparum
DO  - http://dx.doi.org/10.1126/science.1241800
ER  - 



TY  - JOUR
T1  - Risk Factors for Inflammatory Breast Cancer and Other Invasive Breast Cancers
AN  - 1492612310; 18892586
AB  - Background We investigated risk factors for inflammatory breast cancer (IBC), a rare, aggressive, and poorly understood breast cancer that is characterized by diffuse breast skin erythema and edema. Methods We included 617 IBC case subjects in a nested case-control study from the Breast Cancer Surveillance Consortium database (1994-2009). We also included 1151 noninflammatory, locally advanced, invasive breast cancers with chest wall/breast skin involvement (LABC), 7600 noninflammatory invasive case subjects without chest wall/breast skin involvement (BC), and 93 654 control subjects matched to case subjects on age and year at diagnosis and mammography registry. We present estimates of rate ratios (RRs) and 95% confidence intervals (CI) from conditional logistic regression analyses for each case group vs control subjects based on multiply imputed datasets. Results First-degree family history of breast cancer and high mammographic breast density increased risk of IBC, LABC, and BC. High body mass index (BMI) increased IBC risk irrespective of menopausal status and estrogen receptor (ER) expression; rate ratios for BMI 30 and greater vs BMI less than 25 were 3.90 (95% CI = 1.50 to 10.14) in premenopausal women and 3.70 (95% CI = 1.98 to 6.94) in peri/postmenopausal women not currently using hormones. BMI 30 and greater slightly increased risk of ER-positive BC (RR = 1.40; 95% CI = 1.11 to 1.76). Statistically significant reductions in risk of ER-negative IBC with older age at first birth and of ER-positive IBC with higher education were not seen for LABC and BC of the same ER status. Conclusions Different associations with BMI, age at first birth, and education between IBC and/or LABC and BC suggest a distinct etiology for IBC.
JF  - Journal of the National Cancer Institute
AU  - Schairer, Catherine
AU  - Li, Yan
AU  - Frawley, Peter
AU  - Graubard, Barry I
AU  - Wellman, Robert D
AU  - Buist, Diana S M
AU  - Kerlikowske, Karla
AU  - Onega, Tracy L
AU  - Anderson, William F
AU  - Miglioretti, Diana L
AD  - Affiliations of authors: Joint Program for Survey Methodology, University of Maryland, College Park, MD (YL); Group Health Research Institute, Group Health Cooperative, Seattle, WA (PF, RDW, DSMB, DLM); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (CS, BIG, WFA); Departments of Medicine and Epidemiology/Biostatistics University of California-San Francisco, San Francisco, CA (KK); Dartmouth Medical School, Hanover, NH (TLO); Department of Public Health Sciences, University of California Davis School of Medicine, Davis, CA (DLM)., schairec@exchange.nih.gov
Y1  - 2013/09/18/
PY  - 2013
DA  - 2013 Sep 18
SP  - 1373
EP  - 1384
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 18
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Age
KW  - Breast cancer
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492612310?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Risk+Factors+for+Inflammatory+Breast+Cancer+and+Other+Invasive+Breast+Cancers&rft.au=Schairer%2C+Catherine%3BLi%2C+Yan%3BFrawley%2C+Peter%3BGraubard%2C+Barry+I%3BWellman%2C+Robert+D%3BBuist%2C+Diana+S+M%3BKerlikowske%2C+Karla%3BOnega%2C+Tracy+L%3BAnderson%2C+William+F%3BMiglioretti%2C+Diana+L&rft.aulast=Schairer&rft.aufirst=Catherine&rft.date=2013-09-18&rft.volume=105&rft.issue=18&rft.spage=1373&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjt206
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Breast cancer
DO  - http://dx.doi.org/10.1093/jnci/djt206
ER  - 



TY  - JOUR
T1  - Systematic study of mitochondrial toxicity of environmental chemicals using quantitative high throughput screening.
AN  - 1433270917; 23895456
AB  - A goal of the Tox21 program is to transit toxicity testing from traditional in vivo models to in vitro assays that assess how chemicals affect cellular responses and toxicity pathways. A critical contribution of the NIH Chemical Genomics center (NCGC) to the Tox21 program is the implementation of a quantitative high throughput screening (qHTS) approach, using cell- and biochemical-based assays to generate toxicological profiles for thousands of environmental compounds. Here, we evaluated the effect of chemical compounds on mitochondrial membrane potential in HepG2 cells by screening a library of 1,408 compounds provided by the National Toxicology Program (NTP) in a qHTS platform. Compounds were screened over 14 concentrations, and results showed that 91 and 88 compounds disrupted mitochondrial membrane potential after treatment for 1 or 5 h, respectively. Seventy-six compounds active at both time points were clustered by structural similarity, producing 11 clusters and 23 singletons. Thirty-eight compounds covering most of the active chemical space were more extensively evaluated. Thirty-six of the 38 compounds were confirmed to disrupt mitochondrial membrane potential using a fluorescence plate reader, and 35 were confirmed using a high content imaging approach. Among the 38 compounds, 4 and 6 induced LDH release, a measure of cytotoxicity, at 1 or 5 h, respectively. Compounds were further assessed for mechanism of action (MOA) by measuring changes in oxygen consumption rate, which enabled the identification of 20 compounds as uncouplers. This comprehensive approach allows for the evaluation of thousands of environmental chemicals for mitochondrial toxicity and identification of possible MOAs.
JF  - Chemical research in toxicology
AU  - Attene-Ramos, Matias S
AU  - Huang, Ruili
AU  - Sakamuru, Srilatha
AU  - Witt, Kristine L
AU  - Beeson, Gyda C
AU  - Shou, Louie
AU  - Schnellmann, Rick G
AU  - Beeson, Craig C
AU  - Tice, Raymond R
AU  - Austin, Christopher P
AU  - Xia, Menghang
AD  - National Center for Advancing Translational Sciences, National Institutes of Health , Bethesda, Maryland 20892, United States.
Y1  - 2013/09/16/
PY  - 2013
DA  - 2013 Sep 16
SP  - 1323
EP  - 1332
VL  - 26
IS  - 9
KW  - Environmental Pollutants
KW  - 0
KW  - Index Medicus
KW  - Molecular Structure
KW  - Tumor Cells, Cultured
KW  - Hep G2 Cells
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Structure-Activity Relationship
KW  - High-Throughput Screening Assays
KW  - Environmental Pollutants -- toxicity
KW  - Mitochondrial Membranes -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1433270917?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Systematic+study+of+mitochondrial+toxicity+of+environmental+chemicals+using+quantitative+high+throughput+screening.&rft.au=Attene-Ramos%2C+Matias+S%3BHuang%2C+Ruili%3BSakamuru%2C+Srilatha%3BWitt%2C+Kristine+L%3BBeeson%2C+Gyda+C%3BShou%2C+Louie%3BSchnellmann%2C+Rick+G%3BBeeson%2C+Craig+C%3BTice%2C+Raymond+R%3BAustin%2C+Christopher+P%3BXia%2C+Menghang&rft.aulast=Attene-Ramos&rft.aufirst=Matias&rft.date=2013-09-16&rft.volume=26&rft.issue=9&rft.spage=1323&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=1520-5010&rft_id=info:doi/10.1021%2Ftx4001754
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-01-02
N1  - Date created - 2013-09-16
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biol Chem. 1999 Oct;380(10):1157-66 [10595578]
J Bioenerg Biomembr. 2012 Aug;44(4):421-37 [22689143]
J Bioenerg Biomembr. 1999 Dec;31(6):581-90 [10682916]
Annu Rev Pharmacol Toxicol. 2000;40:353-88 [10836141]
J Biomol Screen. 2002 Aug;7(4):383-9 [12230893]
Antioxid Redox Signal. 2002 Oct;4(5):769-81 [12470504]
FEBS Lett. 2003 Jul 10;546(2-3):355-8 [12832068]
Nature. 2003 Sep 11;425(6954):191-6 [12939617]
Proc Natl Acad Sci U S A. 1968 Feb;59(2):484-90 [5238978]
Biochem J. 1968 Apr;107(3):367-75 [4172100]
Eur J Biochem. 1970 Jan;12(1):117-25 [5434277]
Biochem Pharmacol. 1971 Apr;20(4):737-48 [4328324]
J Appl Bacteriol. 1971 Sep;34(3):579-91 [4945521]
J Appl Bacteriol. 1974 Mar;37(1):117-31 [4846735]
Physiol Rev. 1980 Jul;60(3):825-63 [6248908]
FEBS Lett. 1986 Jun 9;201(2):267-70 [3086126]
Chem Biol Interact. 1987;62(2):179-89 [3594640]
Int Rev Cytol. 1992;141:217-32 [1452432]
J Exp Med. 1995 May 1;181(5):1661-72 [7722446]
Exp Cell Res. 1961 Mar;23:228-37 [13762256]
Nature. 1961 Jul 8;191:144-8 [13771349]
J Biol Chem. 1962 Aug;237:2670-7 [13925019]
Adv Enzymol Relat Subj Biochem. 1956;17:65-134 [13313307]
Biochim Biophys Acta. 2006 Jan;1757(1):21-30 [16375850]
Cell Calcium. 2006 Aug;40(2):155-64 [16759697]
Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11473-8 [16864780]
Apoptosis. 2007 May;12(5):913-22 [17453160]
Toxicol In Vitro. 2007 Aug;21(5):902-11 [17346924]
Toxicol Sci. 2007 Jun;97(2):539-47 [17361016]
Drug Discov Today. 2007 Sep;12(17-18):777-85 [17826691]
Environ Health Perspect. 2008 Mar;116(3):284-91 [18335092]
J Pharmacol Exp Ther. 2008 May;325(2):536-43 [18267976]
Trends Pharmacol Sci. 2008 Jul;29(7):361-6 [18501972]
Curr Drug Saf. 2009 Jan;4(1):34-54 [19149524]
Toxicol Sci. 2009 Nov;112(1):153-63 [19502547]
Adv Drug Deliv Rev. 2009 Nov 30;61(14):1234-49 [19733603]
J Neurosci Res. 2010 Mar;88(4):877-86 [19813266]
J Toxicol Environ Health B Crit Rev. 2010 Feb;13(2-4):51-138 [20574894]
Anal Biochem. 2010 Sep 1;404(1):75-81 [20465991]
Curr Drug Targets. 2011 Jun;12(6):774-82 [21275886]
Curr Protoc Toxicol. 2011 Aug;Chapter 2:Unit2.20 [21818751]
Nucleic Acids Res. 2012 Jan;40(Database issue):D400-12 [22140110]
Toxicol In Vitro. 2012 Apr;26(3):511-25 [22261204]
Physiol Genomics. 2012 May 1;44(9):495-503 [22433785]
Eur J Cancer. 1999 Oct;35(10):1517-25 [10673981]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1021/tx4001754
ER  - 



TY  - JOUR
T1  - Occupational Exposure to Hepatitis C Virus: Early T-Cell Responses in the Absence of Seroconversion in a Longitudinal Cohort Study
AN  - 1622605897; 20881954
AB  - Background. T-cell responses have been described in seronegative patients who test negative for hepatitis C virus (HCV) RNA despite frequent HCV exposure. However, the cross-sectional design of those studies did not clarify whether T cells were indeed induced by low-level HCV exposure without seroconversion or whether they resulted from regular acute infection with subsequent antibody loss. Methods. Over a 10-year period, our longitudinal study recruited 72 healthcare workers with documented HCV exposure. We studied viremia and antibody and T-cell responses longitudinally for 6 months. Results. All healthcare workers remained negative for HCV RNA and antibodies. However, 48% developed proliferative T-cell response and 42% developed responses in interferon-gamma enzyme-linked immunosorbent spot assays, with 29 healthy HCV-unexposed controls used to define assay cutoffs. The response prevalence was associated with the transmission risk score. T-cell responses peaked at week 4 and returned to baseline by week 12 after exposure. They predominantly targeted nonstructural HCV proteins, which are not part of the HCV particle and thus must have been synthesized in infected cells. Conclusions. Subclinical transmission of HCV occurs frequently, resulting in infection and synthesis of nonstructural proteins despite undetectable systemic viremia. T-cell responses are more sensitive indicators of this low-level HCV exposure than antibodies.
JF  - Journal of Infectious Diseases
AU  - Heller, Theo
AU  - Werner, Jens Martin
AU  - Rahman, Fareed
AU  - Mizukoshi, Eishiro
AU  - Sobao, Yuji
AU  - Gordon, Ann Marie
AU  - Sheets, Arlene
AU  - Sherker, Averell H
AU  - Kessler, Ellen
AU  - Bean, Kathleen S
AU  - Herrine, Steven K
AU  - Stevens, M'Lou
AU  - Schmitt, James
AU  - Rehermann, Barbara
AD  - Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, rehermann@nih.gov
Y1  - 2013/09/15/
PY  - 2013
DA  - 2013 Sep 15
SP  - 1020
EP  - 1025
PB  - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 208
IS  - 6
SN  - 0022-1899, 0022-1899
KW  - Immunology Abstracts; Virology & AIDS Abstracts; Health & Safety Science Abstracts
KW  - exposure
KW  - needlestick
KW  - antibody
KW  - T cell
KW  - hepatitis
KW  - healthcare worker
KW  - Longitudinal studies
KW  - gamma -Interferon
KW  - RNA viruses
KW  - Particulates
KW  - Infection
KW  - Medical personnel
KW  - Immunosorbents
KW  - Antibodies
KW  - Hepatitis C virus
KW  - Infectious diseases
KW  - RNA
KW  - Nonstructural proteins
KW  - Lymphocytes T
KW  - Proteins
KW  - Seroconversion
KW  - Hepatitis C
KW  - Viremia
KW  - Occupational exposure
KW  - V 22350:Immunology
KW  - H 1000:Occupational Safety and Health
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622605897?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Occupational+Exposure+to+Hepatitis+C+Virus%3A+Early+T-Cell+Responses+in+the+Absence+of+Seroconversion+in+a+Longitudinal+Cohort+Study&rft.au=Heller%2C+Theo%3BWerner%2C+Jens+Martin%3BRahman%2C+Fareed%3BMizukoshi%2C+Eishiro%3BSobao%2C+Yuji%3BGordon%2C+Ann+Marie%3BSheets%2C+Arlene%3BSherker%2C+Averell+H%3BKessler%2C+Ellen%3BBean%2C+Kathleen+S%3BHerrine%2C+Steven+K%3BStevens%2C+M%27Lou%3BSchmitt%2C+James%3BRehermann%2C+Barbara&rft.aulast=Heller&rft.aufirst=Theo&rft.date=2013-09-15&rft.volume=208&rft.issue=6&rft.spage=1020&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjit270
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Last updated - 2016-04-13
N1  - SubjectsTermNotLitGenreText - gamma -Interferon; Antibodies; RNA; Nonstructural proteins; Lymphocytes T; Seroconversion; RNA viruses; Viremia; Infection; Immunosorbents; Medical personnel; Occupational exposure; Longitudinal studies; Infectious diseases; Proteins; Particulates; Hepatitis C; Hepatitis C virus
DO  - http://dx.doi.org/10.1093/infdis/jit270
ER  - 



TY  - JOUR
T1  - Parental Dietary Fat Intake Alters Offspring Microbiome and Immunity
AN  - 1551641134; 20355708
AB  - Mechanisms underlying modern increases in prevalence of human inflammatory diseases remain unclear. The hygiene hypothesis postulates that decreased microbial exposure has, in part, driven this immune dysregulation. However, dietary fatty acids also influence immunity, partially through modulation of responses to microbes. Prior reports have described the direct effects of high-fat diets on the gut microbiome and inflammation, and some have additionally shown metabolic consequences for offspring. Our study sought to expand on these previous observations to identify the effects of parental diet on offspring immunity using mouse models to provide insights into challenging aspects of human health. To test the hypothesis that parental dietary fat consumption during gestation and lactation influences offspring immunity, we compared pups of mice fed either a Western diet (WD) fatty acid profile or a standard low-fat diet. All pups were weaned onto the control diet to specifically test the effects of early developmental fat exposure on immune development. Pups from WD breeders were not obese or diabetic, but still had worse outcomes in models of infection, autoimmunity, and allergic sensitization. They had heightened colonic inflammatory responses, with increased circulating bacterial LPS and muted systemic LPS responsiveness. These deleterious impacts of the WD were associated with alterations of the offspring gut microbiome. These results indicate that parental fat consumption can leave a "lard legacy" impacting offspring immunity and suggest inheritable microbiota may contribute to the modern patterns of human health and disease.
JF  - Journal of Immunology
AU  - Myles, Ian A
AU  - Fontecilla, Natalia M
AU  - Janelsins, Brian M
AU  - Vithayathil, Paul J
AU  - Segre, Julia A
AU  - Datta, Sandip K
AD  - Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and
Y1  - 2013/09/15/
PY  - 2013
DA  - 2013 Sep 15
SP  - 3200
EP  - 3209
PB  - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States
VL  - 191
IS  - 6
SN  - 0022-1767, 0022-1767
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Immunology Abstracts
KW  - Obesity
KW  - Animal models
KW  - Autoimmunity
KW  - Immunity
KW  - Infection
KW  - Lactation
KW  - Inflammation
KW  - Diabetes mellitus
KW  - Digestive tract
KW  - Inflammatory diseases
KW  - High fat diet
KW  - Gestation
KW  - Fatty acids
KW  - Lipopolysaccharides
KW  - Progeny
KW  - Hygiene
KW  - F 06925:Hypersensitivity
KW  - A 01300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551641134?accountid=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+Immunology&rft.atitle=Parental+Dietary+Fat+Intake+Alters+Offspring+Microbiome+and+Immunity&rft.au=Myles%2C+Ian+A%3BFontecilla%2C+Natalia+M%3BJanelsins%2C+Brian+M%3BVithayathil%2C+Paul+J%3BSegre%2C+Julia+A%3BDatta%2C+Sandip+K&rft.aulast=Myles&rft.aufirst=Ian&rft.date=2013-09-15&rft.volume=191&rft.issue=6&rft.spage=3200&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1301057
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Obesity; Animal models; Autoimmunity; Immunity; Infection; Inflammation; Lactation; Diabetes mellitus; Digestive tract; High fat diet; Inflammatory diseases; Gestation; Fatty acids; Lipopolysaccharides; Progeny; Hygiene
DO  - http://dx.doi.org/10.4049/jimmunol.1301057
ER  - 



TY  - JOUR
T1  - Integration of metabolomics and transcriptomics revealed a fatty acid network exerting growth inhibitory effects in human pancreatic cancer.
AN  - 1443402922; 23918603
AB  - To identify metabolic pathways that are perturbed in pancreatic ductal adenocarcinoma (PDAC), we investigated gene-metabolite networks with integration of metabolomics and transcriptomics.
          We conducted global metabolite profiling analysis on two independent cohorts of resected PDAC cases to identify critical metabolites alteration that may contribute to the progression of pancreatic cancer. We then searched for gene surrogates that were significantly correlated with the key metabolites, by integrating metabolite and gene expression profiles. Fifty-five metabolites were consistently altered in tumors as compared with adjacent nontumor tissues in a test cohort (N = 33) and an independent validation cohort (N = 31). Weighted network analysis revealed a unique set of free fatty acids (FFA) that were highly coregulated and decreased in PDAC. Pathway analysis of 157 differentially expressed gene surrogates revealed a significantly altered lipid metabolism network, including key lipolytic enzymes PNLIP, CLPS, PNLIPRP1, and PNLIPRP2. Gene expressions of these lipases were significantly decreased in pancreatic tumors as compared with nontumor tissues, leading to reduced FFAs. More importantly, a lower gene expression of PNLIP in tumors was associated with poorer survival in two independent cohorts. We further showed that two saturated FFAs, palmitate and stearate, significantly induced TRAIL expression, triggered apoptosis, and inhibited proliferation in pancreatic cancer cells.
          Our results suggest that impairment in a lipolytic pathway involving lipases, and a unique set of FFAs, may play an important role in the development and progression of pancreatic cancer and provide potential targets for therapeutic intervention. ©2013 AACR.
JF  - Clinical cancer research : an official journal of the American Association for Cancer Research
AU  - Zhang, Geng
AU  - He, Peijun
AU  - Tan, Hanson
AU  - Budhu, Anuradha
AU  - Gaedcke, Jochen
AU  - Ghadimi, B Michael
AU  - Ried, Thomas
AU  - Yfantis, Harris G
AU  - Lee, Dong H
AU  - Maitra, Anirban
AU  - Hanna, Nader
AU  - Alexander, H Richard
AU  - Hussain, S Perwez
AD  - Authors' Affiliations: Pancreatic Cancer Unit, Laboratory of Human Carcinogenesis, Center for Cancer Research, Genetics Branch, National Cancer Institute, NIH, Bethesda; Pathology and Laboratory Medicine, Baltimore Veterans Affairs Medical Center, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Division of Surgical Oncology, The Department of Surgery and the Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland; and Department of General and Visceral Surgery, University Medicine, Göttingen, Germany.
Y1  - 2013/09/15/
PY  - 2013
DA  - 2013 Sep 15
SP  - 4983
EP  - 4993
VL  - 19
IS  - 18
SN  - 1078-0432, 1078-0432
KW  - Biomarkers, Tumor
KW  - 0
KW  - Fatty Acids
KW  - RNA, Messenger
KW  - Index Medicus
KW  - Real-Time Polymerase Chain Reaction
KW  - Pancreas -- pathology
KW  - Adenocarcinoma -- metabolism
KW  - Apoptosis
KW  - Oligonucleotide Array Sequence Analysis
KW  - Neoplasm Staging
KW  - Humans
KW  - Carcinoma, Pancreatic Ductal -- genetics
KW  - Adenocarcinoma -- genetics
KW  - Reverse Transcriptase Polymerase Chain Reaction
KW  - RNA, Messenger -- genetics
KW  - Cell Proliferation
KW  - Adenocarcinoma -- pathology
KW  - Tumor Cells, Cultured
KW  - Carcinoma, Pancreatic Ductal -- metabolism
KW  - Pancreas -- metabolism
KW  - Cohort Studies
KW  - Gas Chromatography-Mass Spectrometry
KW  - Carcinoma, Pancreatic Ductal -- pathology
KW  - Enzyme-Linked Immunosorbent Assay
KW  - Signal Transduction
KW  - Lipid Metabolism
KW  - Biomarkers, Tumor -- metabolism
KW  - Gene Expression Profiling
KW  - Biomarkers, Tumor -- genetics
KW  - Pancreatic Neoplasms -- pathology
KW  - Pancreatic Neoplasms -- metabolism
KW  - Gene Regulatory Networks
KW  - Pancreatic Neoplasms -- genetics
KW  - Metabolomics
KW  - Fatty Acids -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443402922?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Integration+of+metabolomics+and+transcriptomics+revealed+a+fatty+acid+network+exerting+growth+inhibitory+effects+in+human+pancreatic+cancer.&rft.au=Zhang%2C+Geng%3BHe%2C+Peijun%3BTan%2C+Hanson%3BBudhu%2C+Anuradha%3BGaedcke%2C+Jochen%3BGhadimi%2C+B+Michael%3BRied%2C+Thomas%3BYfantis%2C+Harris+G%3BLee%2C+Dong+H%3BMaitra%2C+Anirban%3BHanna%2C+Nader%3BAlexander%2C+H+Richard%3BHussain%2C+S+Perwez&rft.aulast=Zhang&rft.aufirst=Geng&rft.date=2013-09-15&rft.volume=19&rft.issue=18&rft.spage=4983&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-13-0209
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-09-01
N1  - Date created - 2013-09-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biochim Biophys Acta. 1999 Nov 23;1441(2-3):173-84 [10570245]
Proc Natl Acad Sci U S A. 2006 Aug 22;103(34):12741-6 [16912112]
J Biol Chem. 2001 May 4;276(18):14890-5 [11278654]
Science. 2002 Mar 1;295(5560):1662-4 [11872829]
Diabetes. 2002 Jul;51(7):2241-8 [12086956]
Diabetes. 2003 Jan;52(1):1-8 [12502486]
J Biol Chem. 2003 Aug 22;278(34):31861-70 [12805375]
Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17402-7 [17090670]
Curr Gastroenterol Rep. 2007 Apr;9(2):116-22 [17418056]
J Clin Oncol. 2007 Jul 1;25(19):2840-6 [17502626]
Bioinformatics. 2008 Mar 1;24(5):719-20 [18024473]
Nature. 2008 Mar 27;452(7186):429-35 [18344982]
PLoS Genet. 2008 Mar;4(3):e1000034 [18369453]
Cell. 2008 Sep 5;134(5):703-7 [18775299]
Clin Cancer Res. 2009 Jan 15;15(2):431-40 [19147747]
Future Oncol. 2009 Apr;5(3):313-21 [19374539]
Am J Emerg Med. 2009 Nov;27(9):1167.e5-7 [19931776]
Anal Chem. 2009 Aug 15;81(16):6656-67 [19624122]
Mol Biosyst. 2010 May;6(5):909-21 [20567778]
Oncogene. 2010 Aug 5;29(31):4369-77 [20514019]
Future Oncol. 2010 Sep;6(9):1395-406 [20919825]
Cancer Epidemiol Biomarkers Prev. 2011 Jan;20(1):140-7 [21098649]
Cell. 2011 Mar 4;144(5):646-74 [21376230]
Pancreas. 2011 Apr;40(3):383-9 [21283039]
Nature. 2011 Jun 16;474(7351):380-4 [21614001]
Nat Protoc. 2011 Jul;6(7):1060-83 [21720319]
PLoS One. 2012;7(2):e31507 [22363658]
Genes Dev. 2012 May 1;26(9):877-90 [22549953]
Science. 2012 May 25;336(6084):990-1 [22628644]
Nature. 2012 May 31;485(7400):590-1 [22660317]
Clin Cancer Res. 2012 Aug 15;18(16):4285-90 [22896695]
CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087]
Int Urol Nephrol. 2013 Apr;45(2):477-84 [22907629]
Gastroenterology. 2013 May;144(5):1066-1075.e1 [23376425]
Nat Rev Cancer. 2004 Jul;4(7):551-61 [15229480]
Nature. 2004 Jul 1;430(6995):88-93 [15190252]
Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10205-10 [15199185]
Mol Cancer. 2003 Jan 6;2:4 [12556242]
J Biol Chem. 1997 Feb 7;272(6):3324-9 [9013572]
Cancer Res. 1997 Sep 15;57(18):3979-88 [9307282]
Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2498-502 [9482914]
Annu Rev Biochem. 1963;32:241-68 [14144482]
Curr Opin Mol Ther. 2004 Dec;6(6):584-92 [15663322]
Nature. 2005 Jun 30;435(7046):1262-6 [15988529]
Biochim Biophys Acta. 2006 Jan;1761(1):4-10 [16497549]
Cancer Res. 2000 Nov 15;60(22):6353-8 [11103797]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/1078-0432.CCR-13-0209
ER  - 



TY  - JOUR
T1  - NANOG modulates stemness in human colorectal cancer.
AN  - 1432618724; 23085761
AB  - NANOG is a stem cell transcription factor that is essential for embryonic development, reprogramming normal adult cells and malignant transformation and progression. The nearly identical retrogene NANOGP8 is expressed in multiple cancers, but generally not in normal tissues and its function is not well defined. Our postulate is that NANOGP8 directly modulates the stemness of individual human colorectal carcinoma (CRC) cells. Stemness was measured in vitro as the spherogenicity of single CRC cells in serum-free medium and the size of the side population (SP) and in vivo as tumorigenicity and experimental metastatic potential in NOD/SCID mice. We found that 80% of clinical liver metastases express a NANOG with 75% of the positive metastases containing NANOGP8 transcripts. In all, 3-62% of single cells within six CRC lines form spheroids in serum-free medium in suspension. NANOGP8 is translated into protein. The relative expression of a NANOG gene increased 8- to 122-fold during spheroid formation, more than the increase in OCT4 or SOX2 transcripts with NANOGP8 the more prevalent family member. Short hairpin RNA (shRNA) to NANOG not only inhibits spherogenicity but also reduces expression of OCT4 and SOX2, the size of the SP and tumor growth in vivo. Inhibition of NANOG gene expression is associated with inhibition of proliferation and decreased phosphorylation of G2-related cell-cycle proteins. Overexpression of NANOGP8 rescues single-cell spherogenicity when NANOG gene expression is inhibited and increases the SP in CRC. Thus, NANOGP8 can substitute for NANOG in directly promoting stemness in CRC.
JF  - Oncogene
AU  - Zhang, J
AU  - Espinoza, L A
AU  - Kinders, R J
AU  - Lawrence, S M
AU  - Pfister, T D
AU  - Zhou, M
AU  - Veenstra, T D
AU  - Thorgeirsson, S S
AU  - Jessup, J M
AD  - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/09/12/
PY  - 2013
DA  - 2013 Sep 12
SP  - 4397
EP  - 4405
VL  - 32
IS  - 37
KW  - Homeodomain Proteins
KW  - 0
KW  - NANOG protein, human
KW  - Nanog Homeobox Protein
KW  - Index Medicus
KW  - Animals
KW  - Spheroids, Cellular
KW  - Cell Transformation, Neoplastic -- metabolism
KW  - Humans
KW  - Mice, Inbred NOD
KW  - Disease Models, Animal
KW  - Cell Line, Tumor
KW  - Mice
KW  - Gene Expression Regulation, Neoplastic
KW  - Tumor Cells, Cultured
KW  - Neoplasm Metastasis
KW  - Mice, SCID
KW  - Cell Transformation, Neoplastic -- genetics
KW  - Homeodomain Proteins -- genetics
KW  - Colorectal Neoplasms -- pathology
KW  - Colorectal Neoplasms -- metabolism
KW  - Homeodomain Proteins -- metabolism
KW  - Colorectal Neoplasms -- genetics
KW  - Neoplastic Stem Cells -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1432618724?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=NANOG+modulates+stemness+in+human+colorectal+cancer.&rft.au=Zhang%2C+J%3BEspinoza%2C+L+A%3BKinders%2C+R+J%3BLawrence%2C+S+M%3BPfister%2C+T+D%3BZhou%2C+M%3BVeenstra%2C+T+D%3BThorgeirsson%2C+S+S%3BJessup%2C+J+M&rft.aulast=Zhang&rft.aufirst=J&rft.date=2013-09-12&rft.volume=32&rft.issue=37&rft.spage=4397&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2012.461
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-08
N1  - Date created - 2013-09-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cell. 2005 Sep 23;122(6):947-56 [16153702]
J Exp Med. 1996 Apr 1;183(4):1797-806 [8666936]
FEBS J. 2006 Apr;273(8):1723-30 [16623708]
Cell. 2006 Aug 25;126(4):663-76 [16904174]
Science. 2006 Oct 13;314(5797):294-7 [17038621]
Methods Enzymol. 2006;420:255-64 [17161700]
Am J Surg Pathol. 2007 Jun;31(6):836-45 [17527070]
Cell. 2007 Nov 30;131(5):861-72 [18035408]
Nature. 2007 Dec 20;450(7173):1230-4 [18097409]
Cell. 2008 Mar 21;132(6):1049-61 [18358816]
Cell Stem Cell. 2007 Oct 11;1(4):403-15 [18159219]
Nat Genet. 2008 May;40(5):499-507 [18443585]
Cell. 2008 Jun 13;133(6):1106-17 [18555785]
Cell. 2008 Sep 5;134(5):877-86 [18691744]
Anticancer Res. 2009 Apr;29(4):1233-41 [19414369]
Science. 2009 May 8;324(5928):797-801 [19325077]
Stem Cells. 2009 May;27(5):993-1005 [19415763]
Cancer Res. 2009 Jul 15;69(14):5716-25 [19567677]
Ann Surg Oncol. 2009 Sep;16(9):2638-44 [19554373]
Cell. 2009 Aug 21;138(4):722-37 [19703398]
Immunology. 2009 Oct;128(2):206-17 [19740377]
J Cell Sci. 2009 Oct 1;122(Pt 19):3502-10 [19723802]
Nat Genet. 2009 Nov;41(11):1238-42 [19801978]
Nucleic Acids Res. 2009 Dec;37(22):7560-9 [19815667]
Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):40-5 [20018687]
J Gastrointest Surg. 2010 Aug;14(8):1220-6 [20532662]
Am J Surg Pathol. 2010 Aug;34(8):1193-8 [20631605]
EMBO J. 2010 Aug 4;29(15):2659-74 [20581802]
EMBO J. 2010 Aug 4;29(15):2646-58 [20581804]
PLoS One. 2010;5(8):e12445 [20805998]
Nucleic Acids Res. 2010 Sep;38(16):5384-95 [20427424]
Hum Pathol. 2010 Oct;41(10):1438-47 [20709360]
J Clin Pathol. 2010 Oct;63(10):879-83 [20876318]
Clin Cancer Res. 2010 Nov 15;16(22):5447-57 [20924131]
Curr Pharm Biotechnol. 2011 Feb 1;12(2):160-70 [21044011]
Int J Dev Biol. 2010;54(11-12):1743-54 [21136380]
J Biol Chem. 2011 Apr 1;286(13):11593-603 [21296877]
Cell. 2011 Aug 5;146(3):353-8 [21802130]
Oncogene. 2011 Sep 8;30(36):3833-45 [21499299]
Cell Res. 2012 Jan;22(1):155-67 [22083510]
Biochem Biophys Res Commun. 2012 Feb 10;418(2):199-204 [22079639]
Oncogene. 2012 Mar 15;31(11):1354-65 [21822303]
Nature. 2012 Mar 22;483(7390):470-3 [22327294]
Dig Dis Sci. 2012 Sep;57(9):2340-6 [22562535]
Oncogene. 2012 Nov 22;31(47):4898-911 [22286766]
Cancer Biol Ther. 2010 Feb;9(4):295-302 [20026903]
Development. 2000 Jun;127(11):2367-82 [10804179] Cell. 2003 May 30;113(5):631-42 [12787504]
Cell. 2003 May 30;113(5):643-55 [12787505]
Genomics. 2004 Aug;84(2):229-38 [15233988]
Cancer Res. 1989 Dec 15;49(24 Pt 1):6906-10 [2582433]
Lancet. 1994 Nov 26;344(8935):1470-2 [7526103]
Nature. 1996 Apr 11;380(6574):544-7 [8606777]
Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5953-8 [16585504]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/onc.2012.461
ER  - 



TY  - CPAPER
T1  - Update on Jobs Syndrome: Hyper-Ige and the Role of Stat3
T2  - 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2013)
AN  - 1510106900; 6271575
JF  - 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2013)
AU  - Freeman, Alexandra
Y1  - 2013/09/10/
PY  - 2013
DA  - 2013 Sep 10
KW  - Symptoms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510106900?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2013%29&rft.atitle=Update+on+Jobs+Syndrome%3A+Hyper-Ige+and+the+Role+of+Stat3&rft.au=Freeman%2C+Alexandra&rft.aulast=Freeman&rft.aufirst=Alexandra&rft.date=2013-09-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.abstractsonline.com/plan/start.aspx?mkey={7DD36E88-52C3-4FF1-A5DF-1D00766558B8}
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Infectious Manifestations of Transcription Factor Disorders
T2  - 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2013)
AN  - 1510105758; 6271574
JF  - 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2013)
AU  - Holland, Steven
Y1  - 2013/09/10/
PY  - 2013
DA  - 2013 Sep 10
KW  - Transcription factors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510105758?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2013%29&rft.atitle=Infectious+Manifestations+of+Transcription+Factor+Disorders&rft.au=Holland%2C+Steven&rft.aulast=Holland&rft.aufirst=Steven&rft.date=2013-09-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.abstractsonline.com/plan/start.aspx?mkey={7DD36E88-52C3-4FF1-A5DF-1D00766558B8}
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - JOUR
T1  - Depalmitoylation preferentially downregulates AMPA induced Ca2+ signaling and neurotoxicity in motor neurons.
AN  - 1426512636; 23850769
AB  - Excessive activation of AMPA receptor has been implicated in motor neuron degeneration in amyotrophic lateral sclerosis (ALS). However, it is not clear why motor neurons are preferentially sensitive to AMPA receptor mediated excessive [Ca(2+)]i rise and excitotoxicity. In the present study we examined whether palmitoylation regulates Ca(2+) permeability of AMPA receptor and excitotoxicity in cultured spinal cord neurons. We adapted chronic 2-bromopalmitate (2-BrP) treatment to achieve depalmitoylation and examined its effect on the cytotoxicity in spinal cord neurons exposed to AMPA. The change in AMPA induced signaling and cytotoxicity in motor neurons and other spinal neurons under identical conditions of exposure to AMPA was studied. 2-BrP treatment inhibited AMPA induced rise in [Ca(2+)]i and cytotoxicity in both types of neurons but the degree of inhibition was significantly higher in motor neurons as compared to other spinal neurons. The AMPA induced [Na(+)]i rise was moderately affected in both type of neurons on depalmitoylation. Depalmitoylation reduced the expression levels of AMPA receptor subunits (GluR1 and GluR2) and also PSD-95 but stargazin levels remained unaffected. Our results demonstrate that 2-BrP attenuates AMPA receptor activated Ca(2+) signaling and cytotoxicity preferentially in motor neurons and suggest that AMPA receptor modulation by depalmitoylation could play a significant role in preventing motor neuron degeneration. Copyright © 2013 Elsevier B.V. All rights reserved.
JF  - Brain research
AU  - Krishnamurthy, Karthik
AU  - Mehta, Bhupesh
AU  - Singh, Mahendra
AU  - Tewari, Bhanu P
AU  - Joshi, Preeti G
AU  - Joshi, Nanda B
AD  - Department of Biophysics, National Institute of Mental Health and Neuro Sciences, Bangalore 560029, India.
Y1  - 2013/09/05/
PY  - 2013
DA  - 2013 Sep 05
SP  - 143
EP  - 153
VL  - 1529
KW  - Dlgh4 protein, rat
KW  - 0
KW  - Hypoglycemic Agents
KW  - Intracellular Signaling Peptides and Proteins
KW  - Membrane Proteins
KW  - Microtubule-Associated Proteins
KW  - Palmitates
KW  - Receptors, AMPA
KW  - 2-bromopalmitate
KW  - 18263-25-7
KW  - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
KW  - 77521-29-0
KW  - Sodium
KW  - 9NEZ333N27
KW  - Calcium
KW  - SY7Q814VUP
KW  - Index Medicus
KW  - TARPs
KW  - Eagle′s minimal essential medium
KW  - Motor neuron
KW  - N-2-hydroxyethyl piperazine-n-2-ethanesulphonic acid
KW  - EMEM
KW  - Calcium signaling
KW  - Depalmitoylation
KW  - Transmembrane AMPA receptor regulatory proteins
KW  - HEPES
KW  - HBSS
KW  - Amyotrophic lateral sclerosis
KW  - 2-Bromopalmitate
KW  - AMPA
KW  - α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid
KW  - 2-BrP
KW  - Transmembrane AMPA receptor regulatory protein
KW  - Hanks buffered salt saline
KW  - Excitotoxicity
KW  - AMPA receptor
KW  - Animals
KW  - Microtubule-Associated Proteins -- metabolism
KW  - Membrane Proteins -- metabolism
KW  - Palmitates -- toxicity
KW  - Calcium -- metabolism
KW  - Rats
KW  - Rats, Sprague-Dawley
KW  - Hypoglycemic Agents -- toxicity
KW  - Intracellular Signaling Peptides and Proteins -- metabolism
KW  - Cell Survival -- drug effects
KW  - Cells, Cultured
KW  - Embryo, Mammalian
KW  - Spinal Cord -- cytology
KW  - Sodium -- metabolism
KW  - Motor Neurons -- metabolism
KW  - Calcium Signaling -- drug effects
KW  - Lipoylation -- drug effects
KW  - Calcium Signaling -- physiology
KW  - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid -- pharmacology
KW  - Receptors, AMPA -- metabolism
KW  - Lipoylation -- physiology
KW  - Motor Neurons -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1426512636?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Depalmitoylation+preferentially+downregulates+AMPA+induced+Ca2%2B+signaling+and+neurotoxicity+in+motor+neurons.&rft.au=Krishnamurthy%2C+Karthik%3BMehta%2C+Bhupesh%3BSingh%2C+Mahendra%3BTewari%2C+Bhanu+P%3BJoshi%2C+Preeti+G%3BJoshi%2C+Nanda+B&rft.aulast=Krishnamurthy&rft.aufirst=Karthik&rft.date=2013-09-05&rft.volume=1529&rft.issue=&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=1872-6240&rft_id=info:doi/10.1016%2Fj.brainres.2013.06.039
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-17
N1  - Date created - 2013-08-19
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.brainres.2013.06.039
ER  - 



TY  - JOUR
T1  - The Healthy Eating Index 2005 and Risk for Pancreatic Cancer in the NIH-AARP Study
AN  - 1492605572; 18892582
AB  - Background Dietary pattern analyses characterizing combinations of food intakes offer conceptual and statistical advantages over food- and nutrient-based analyses of disease risk. However, few studies have examined dietary patterns and pancreatic cancer risk and none focused on the 2005 Dietary Guidelines for Americans. We used the Healthy Eating Index 2005 (HEI-2005) to estimate the association between meeting those dietary guidelines and pancreatic cancer risk. Methods We calculated the HEI-2005 score for 537 218 men and women in the National Institutes of Health-American Association of Retired Persons Diet and Health Study using responses to food frequency questionnaires returned in 1995 and 1996. We used Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of pancreatic cancer according to HEI-2005 quintiles and explored effect modification by known risk factors. P sub(interaction) values were calculated using the Wald test. All statistical tests were two-sided. Results We identified 2383 incident, exocrine pancreatic cancer cases (median = 10.5 years follow-up). Comparing participants who met the most dietary guidelines (Q5) with those who met the fewest guidelines (Q1), we observed a reduced risk of pancreatic cancer (HR = 0.85, 95% CI = 0.74 to 0.97). Among men there was an interaction by body mass index (P sub(interaction) = .03), with a hazard ratio of 0.72 (95% CI = 0.59 to 0.88) comparing Q5 vs Q1 in overweight/obese men (body mass index greater than or equal to 25kg/m super(2)) but no association among normal weight men. Conclusions Our findings support the hypothesis that consuming a high-quality diet, as scored by the HEI-2005, may reduce the risk of pancreatic cancer.
JF  - Journal of the National Cancer Institute
AU  - Arem, Hannah
AU  - Reedy, Jill
AU  - Sampson, Josh
AU  - Jiao, Li
AU  - Hollenbeck, Albert R
AU  - Risch, Harvey
AU  - Mayne, Susan T
AU  - Stolzenberg-Solomon, Rachael Z
AD  - Affiliations of authors: Yale School of Public Health, New Haven, CT (HA, HR, STM); Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (HA, JS, RZS-S); Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD (JR); Baylor College of Medicine, Houston, TX (LJ); AARP, Washington, DC (ARH); Yale Cancer Center, New Haven, CT (HR, STM)., Aremhe2@mail.nih.gov
Y1  - 2013/09/04/
PY  - 2013
DA  - 2013 Sep 04
SP  - 1298
EP  - 1305
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 17
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Body mass
KW  - Diets
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492605572?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=The+Healthy+Eating+Index+2005+and+Risk+for+Pancreatic+Cancer+in+the+NIH-AARP+Study&rft.au=Arem%2C+Hannah%3BReedy%2C+Jill%3BSampson%2C+Josh%3BJiao%2C+Li%3BHollenbeck%2C+Albert+R%3BRisch%2C+Harvey%3BMayne%2C+Susan+T%3BStolzenberg-Solomon%2C+Rachael+Z&rft.aulast=Arem&rft.aufirst=Hannah&rft.date=2013-09-04&rft.volume=105&rft.issue=17&rft.spage=1298&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjt185
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Diets
DO  - http://dx.doi.org/10.1093/jnci/djt185
ER  - 



TY  - JOUR
T1  - Tubal ligation in relation to menopausal symptoms and breast cancer risk
AN  - 1443373510; 18562241
AB  - Background: Local inflammation after tubal ligation may affect ovarian function and breast cancer risk. Methods: We analysed tubal ligation, menopausal characteristics, and breast cancer risk in the Sister Study cohort (N=50 884 women). Results: Tubal ligation was associated with hot flashes (hazard ratio (HR) 1.09; 95% confidence interval (CI): 1.06-1.12) but not menopausal age (HR 0.99; 95% CI: 0.96-1.02). Tubal ligation did not have an impact on breast cancer overall (HR 0.95; 95% CI: 0.85-1.06), but had a suggested inverse relation with oestrogen receptor+/progesterone receptor+ invasive tumours (HR 0.84; 95% CI: 0.70-1.01), possibly because of subsequent hysterectomy/bilateral oophorectomy. Conclusion: Tubal ligation does not influence overall breast cancer risk.
JF  - British Journal of Cancer
AU  - Nichols, H B
AU  - Baird, D D
AU  - DeRoo, L A
AU  - Kissling, G E
AU  - Sandler, D P
AD  - Epidemiology Branch, National Institute of Environmental Health Sciences, PO Box 12233, 111 TW Alexander Drive, MD A3-05, Research Triangle Park, NC 27709, USA
Y1  - 2013/09/03/
PY  - 2013
DA  - 2013 Sep 03
SP  - 1291
EP  - 1295
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 109
IS  - 5
SN  - 0007-0920, 0007-0920
KW  - Risk Abstracts
KW  - Health risks
KW  - Age
KW  - Breast cancer
KW  - Tumors
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443373510?accountid=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=Tubal+ligation+in+relation+to+menopausal+symptoms+and+breast+cancer+risk&rft.au=Nichols%2C+H+B%3BBaird%2C+D+D%3BDeRoo%2C+L+A%3BKissling%2C+G+E%3BSandler%2C+D+P&rft.aulast=Nichols&rft.aufirst=H&rft.date=2013-09-03&rft.volume=109&rft.issue=5&rft.spage=1291&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.433
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Health risks; Age; Breast cancer; Tumors
DO  - http://dx.doi.org/10.1038/bjc.2013.433
ER  - 



TY  - JOUR
T1  - The association of coffee intake with liver cancer incidence and chronic liver disease mortality in male smokers
AN  - 1443373143; 18562235
AB  - Background: Coffee intake is associated with reduced risk of liver cancer and chronic liver disease as reported in previous studies, including prospective ones conducted in Asian populations where hepatitis B viruses (HBVs) and hepatitis C viruses (HCVs) are the dominant risk factors. Yet, prospective studies in Western populations with lower HBV and HCV prevalence are sparse. Also, although preparation methods affect coffee constituents, it is unknown whether different methods affect disease associations. Methods: We evaluated the association of coffee intake with incident liver cancer and chronic liver disease mortality in 27 037 Finnish male smokers, aged 50-69, in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, who recorded their coffee consumption and were followed up to 24 years for incident liver cancer or chronic liver disease mortality. Multivariate relative risks (RRs) and 95% confidence intervals (CIs) were estimated by Cox proportional hazard models. Results: Coffee intake was inversely associated with incident liver cancer (RR per cup per day=0.82, 95% CI: 0.73-0.93; P-trend across categories=0.0007) and mortality from chronic liver disease (RR=0.55, 95% CI: 0.48-0.63; P-trend<0.0001). Inverse associations persisted in those without diabetes, HBV- and HCV-negative cases, and in analyses stratified by age, body mass index, alcohol and smoking dose. We observed similar associations for those drinking boiled or filtered coffee. Conclusion: These findings suggest that drinking coffee may have benefits for the liver, irrespective of whether coffee was boiled or filtered.
JF  - British Journal of Cancer
AU  - Lai, G Y
AU  - Weinstein, S J
AU  - Albanes, D
AU  - Taylor, P R
AU  - McGlynn, K A
AU  - Virtamo, J
AU  - Sinha, R
AU  - Freedman, N D
AD  - 1] Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, 9609 Medical Center Drive, Room 2W136 MSC 9712, Bethesda, MD 20892, USA [2] Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room 1E326, MSC 9704, Bethesda, MD 20892, USA
Y1  - 2013/09/03/
PY  - 2013
DA  - 2013 Sep 03
SP  - 1344
EP  - 1351
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 109
IS  - 5
SN  - 0007-0920, 0007-0920
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Coffee
KW  - Health risks
KW  - Mortality
KW  - Alcohol
KW  - Hepatitis B virus
KW  - Hepatitis C virus
KW  - Males
KW  - Viruses
KW  - Liver
KW  - Hepatitis C
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/1443373143?accountid=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=The+association+of+coffee+intake+with+liver+cancer+incidence+and+chronic+liver+disease+mortality+in+male+smokers&rft.au=Lai%2C+G+Y%3BWeinstein%2C+S+J%3BAlbanes%2C+D%3BTaylor%2C+P+R%3BMcGlynn%2C+K+A%3BVirtamo%2C+J%3BSinha%2C+R%3BFreedman%2C+N+D&rft.aulast=Lai&rft.aufirst=G&rft.date=2013-09-03&rft.volume=109&rft.issue=5&rft.spage=1344&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.405
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Coffee; Alcohol; Mortality; Health risks; Males; Viruses; Liver; Hepatitis C; Cancer; Hepatitis C virus; Hepatitis B virus
DO  - http://dx.doi.org/10.1038/bjc.2013.405
ER  - 



TY  - JOUR
T1  - Revisiting Geschwindʼs hypothesis on brain lateralisation: A functional MRI study of digit ratio (2D:4D) and sex interaction effects on spatial working memory
AN  - 1698869118
AB  - The Geschwind-Behan-Galaburda (GBG) hypothesis links cerebral lateralisation with prenatal testosterone exposure. Digit ratio measures in adults have been established as potential markers of foetal sex hormonal milieu. The aim of the study was to evaluate the sex-dependent interaction of digit ratio measures and cerebral lateralization as well as their neurohemodynamic correlates using functional MRI (fMRI). Digit ratio measures—ratio of index finger (2D) length to ring finger (4D) length (2D:4D) and difference between 2D:4D of two hands, i.e., right minus left (D R–L)—were calculated using high resolution digital images in 70 right-handed participants (42 men) based on reliable and valid method. fMRI was acquired during the performance of a spatial working memory task in a subset of 25 individuals (14 men), and analysed using Statistical Parametric Mapping 8 (SPM8) and the Laterality Index toolbox for SPM8. Men had significantly less bilateral 2D:4D than women. There was a significant negative correlation between right 2D:4D and 2-Back task accuracy (2B ACC) in women. A significant sex-by-right 2D:4D interaction was observed in left parahippocampal gyrus activation. Additionally, sex-by-D R–L interaction was observed in left IPL activation. D R–L showed a significant positive correlation with the whole brain Laterality Index (LI), and LI, in turn, demonstrated a significant negative correlation with 2B ACC. Our study observations suggest several novel sex-differential relationships between 2D:4D measures and fMRI activation during spatial working memory task performance. Given the pre-existing background data supporting digit ratio measures as putative indicator of prenatal sex hormonal milieu, our study findings add support to the Geschwind-Behan-Galaburda (GBG) hypothesis.
JF  - Laterality
AU  - Kalmady, Sunil Vasu
AU  - Agarwal, Sri Mahavir
AU  - Shivakumar, Venkataram
AU  - Jose, Dania
AU  - Venkatasubramanian, Ganesan
AU  - Reddy, Y C Janardhan
AD  - Department of Psychiatry & Translational Psychiatry Laboratory, National Institute of Mental Health & Neurosciences, Bangalore, India ; Department of Psychiatry & Translational Psychiatry Laboratory, National Institute of Mental Health & Neurosciences, Bangalore, India
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 625
EP  - 640
CY  - Hove
PB  - Taylor & Francis Ltd.
VL  - 18
IS  - 5
SN  - 1357-650X
KW  - Psychology
KW  - Accuracy
KW  - Mapping
KW  - Task performance
KW  - Testosterone
KW  - Working memory
KW  - Antenatal
KW  - Brain
KW  - Brain laterality
KW  - Fetal exposure
KW  - Functional magnetic resonance imaging
KW  - Hands
KW  - Laterality
KW  - Lateralization
KW  - Magnetic resonance imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698869118?accountid=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=Laterality&rft.atitle=Revisiting+Geschwind%CA%BCs+hypothesis+on+brain+lateralisation%3A+A+functional+MRI+study+of+digit+ratio+%282D%3A4D%29+and+sex+interaction+effects+on+spatial+working+memory&rft.au=Kalmady%2C+Sunil+Vasu%3BAgarwal%2C+Sri+Mahavir%3BShivakumar%2C+Venkataram%3BJose%2C+Dania%3BVenkatasubramanian%2C+Ganesan%3BReddy%2C+Y+C+Janardhan&rft.aulast=Kalmady&rft.aufirst=Sunil&rft.date=2013-09-01&rft.volume=18&rft.issue=5&rft.spage=625&rft.isbn=&rft.btitle=&rft.title=Laterality&rft.issn=1357650X&rft_id=info:doi/10.1080%2F1357650X.2012.744414
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2015-07-23
N1  - Last updated - 2016-08-16
DO  - http://dx.doi.org/10.1080/1357650X.2012.744414
ER  - 



TY  - JOUR
T1  - Prevention of radiation-induced salivary hypofunction by delivering HSFRP2 into submandibular glands
AN  - 1673398709; PQ0001372829
AB  - Dry mouth, xerostomia, is a common side effect of irradiation treatment in patients with head and neck cancers which leads to significant patient morbidity. Secreted frizzled-related protein 2 (SFRP2) is an interesting protein, which can inhibit apoptosis, reduce fibrosis, enhance regeneration/proliferation and promote morphogenesis. SFRP2 is a Wnt inhibitor, and also considered a tumor suppressor gene. Based on these biological functions, we hypothesized that overexpression of SFRP2 may be able to prevent radiation induced salivary gland damage without negatively affecting cancer therapy. To test our hypothesis, we constructed a hybrid adenoretroviral vector encoding human (h)SFRP2 (AdLTR2EF1[functionof]N-hSFRP2) and transduced murine submandibular glands (SMGs) 24 hours before beginning fractionated IR (6 Gy x 5 days). Our results demonstrate that the hSFRP2 gene transfer (108-1010 particles/gland; both SMGs/ mouse) could preserve saliva flow rate while saliva flow rates, from animals transduced with the Ad-control vector were >50% lower than those of a non-IR group after 1,2 and 8 months. Gland and body weights from the SFRP2 gene transfer group were the same as the non-IR group and significantly higher than that of the Adcontrol-treated group. Initial results also demonstrated that SFRP2 gene transfer did not affect growth of the mouse squamous cell carcinoma, SCC VII. Further studies are required to fully understand the mechanisms by which hSFRP2 gene transfer protects murine SMGs from IR damage.
JF  - Molecular Therapy
AU  - Zheng, Changyu
AU  - Cotrim, Ana P
AU  - Goldsmith, Corinne
AU  - Aquilina, Stefanie
AU  - Sowers, Anastasia
AU  - Ambudkar, Indu S
AU  - Mitchel, James B
AU  - Baum, Bruce J
AD  - NIDCR, NIH, Bethesda, MD
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - e40
EP  - e41
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 9
SN  - 1525-0016, 1525-0016
KW  - Biotechnology and Bioengineering Abstracts
KW  - Tumor suppressor genes
KW  - secreted frizzled-related protein 2
KW  - Apoptosis
KW  - Wnt protein
KW  - Fibrosis
KW  - Morphogenesis
KW  - squamous cell carcinoma
KW  - Salivary gland
KW  - Morbidity
KW  - Expression vectors
KW  - Body weight
KW  - Gene transfer
KW  - Hybrids
KW  - Head and neck cancer
KW  - Submandibular gland
KW  - Saliva
KW  - Mouth
KW  - Side effects
KW  - xerostomia
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673398709?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prevention+of+radiation-induced+salivary+hypofunction+by+delivering+HSFRP2+into+submandibular+glands&rft.au=Zheng%2C+Changyu%3BCotrim%2C+Ana+P%3BGoldsmith%2C+Corinne%3BAquilina%2C+Stefanie%3BSowers%2C+Anastasia%3BAmbudkar%2C+Indu+S%3BMitchel%2C+James+B%3BBaum%2C+Bruce+J&rft.aulast=Zheng&rft.aufirst=Changyu&rft.date=2013-09-01&rft.volume=21&rft.issue=9&rft.spage=e40&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-04-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - secreted frizzled-related protein 2; Tumor suppressor genes; Wnt protein; Apoptosis; Fibrosis; Morphogenesis; squamous cell carcinoma; Salivary gland; Morbidity; Expression vectors; Body weight; Gene transfer; Hybrids; Head and neck cancer; Submandibular gland; Saliva; Mouth; Side effects; xerostomia
ER  - 



TY  - JOUR
T1  - HIV Latency: Activating Virus Expression with Combined Genetic and Chemical Tools
AN  - 1673391642; PQ0001372786
AB  - One difficulty in curing HIV/AIDS is the tendency of the virus to enter into latency, where minimal or no viral gene expression occurs. The sequestered virus thus is immune to chemotherapy. One way to subject the virus to therapy again would be to activate viral gene expression. Latency likely involves block both of transcriptional initiation and transcript elongation. We have tested this idea by combination genetic and chemical approaches. We used a cell culture model of latency where lymphocytic Jurkat cells harbor latent provirus [env-/GFP+], We subjected these cells to treatment, singly and in combination, with prototype agents that induce transcriptional initiation, [NFkB activation with prostratin (5 uM)]; agents of chromatin remodeling [hydroxamic acid (SAHA) (5uM)]; and agents that cause promoter demethylation [Aza-deoxycytidine (AzaCdR) (1 uM)], along with deblockers of elongation by transactivation with Tat-1 by way of lentiviral vector transduction (50 ul). The results (see Table 1 ) support the idea that latent virus expression can be activated and it is advantageous to activate both transcriptional initiation and elongation. The opinion expressed in this abstract are those of the authors and do not necessarily represent views of the National Cancer Institute.
JF  - Molecular Therapy
AU  - Arya, Suresh K
AU  - Holczbauer, Agnes
AD  - National Cancer Institute, Center for Cancer Research, Bethesda, MD 20892
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 9
SN  - 1525-0016, 1525-0016
KW  - Genetics Abstracts; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Acquired immune deficiency syndrome
KW  - Chromatin remodeling
KW  - Chemotherapy
KW  - Transcription
KW  - Cell culture
KW  - Hydroxamic acid
KW  - Cell activation
KW  - NF- Kappa B protein
KW  - Transcription initiation
KW  - Gene expression
KW  - Promoters
KW  - Elongation
KW  - Demethylation
KW  - Human immunodeficiency virus
KW  - Transcription elongation
KW  - Transcription activation
KW  - W 30905:Medical Applications
KW  - V 22360:AIDS and HIV
KW  - G 07730:Development & Cell Cycle
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673391642?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=HIV+Latency%3A+Activating+Virus+Expression+with+Combined+Genetic+and+Chemical+Tools&rft.au=Arya%2C+Suresh+K%3BHolczbauer%2C+Agnes&rft.aulast=Arya&rft.aufirst=Suresh&rft.date=2013-09-01&rft.volume=21&rft.issue=9&rft.spage=e12&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-04-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; Chromatin remodeling; Chemotherapy; Transcription; Cell culture; Hydroxamic acid; Transcription initiation; NF- Kappa B protein; Cell activation; Gene expression; Elongation; Promoters; Demethylation; Transcription elongation; Transcription activation; Human immunodeficiency virus
ER  - 



TY  - JOUR
T1  - Preclinical development of an AAV vector for the treatment of X-linked retinitis pigmentosa due to RPGRorf15 mutation
AN  - 1673391389; PQ0001372797
AB  - Mutations in retinitis pigmentosa GTPase regulator (RPGR) account for >70% of X-linked retinitis pigmentosa (RP) and approximately 15% of all RP cases. These mutations cause a progressive blinding disease which typically begins with night blindness in the first decade and results in central vision loss by the forth decade. The disease afflicts approximately 10K people in the United States and 220K people worldwide. To develop a clinical candidate, we evaluated dose-efficacy profiles of AAV vectors expressing mouse and human RPGRorf15 in the RPGR knock-out mouse model. This data demonstrates that an AAV8 human RPGRorf15 vector is able to inhibit rod and cone degeneration in a mouse model of RP. Vectors administered at 6 weeks and 12 months of age both showed efficacy, indicating that this therapy may be relevant to juvenile and adult patients. The AAV8 human RPGRorf15 vector fits our criteria for further clinical development.
JF  - Molecular Therapy
AU  - Wu, Zhijian
AU  - Hiriyanna, Suja
AU  - Qian, Haohua
AU  - Mookherjee, Suddhasil
AU  - Kaneshiro, Kayleigh
AU  - Campos, Maria
AU  - Gao, Chun
AU  - Fariss, Robert
AU  - Swaroop, Anand
AU  - Li, Tiansen
AU  - Colosi, Peter
AD  - National Eye Institute, National Institutes of Health
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 9
SN  - 1525-0016, 1525-0016
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Age
KW  - Data processing
KW  - Cones
KW  - X chromosome
KW  - Animal models
KW  - Adeno-associated virus
KW  - Nyctalopia
KW  - Vision
KW  - Degeneration
KW  - Mutation
KW  - Retinitis pigmentosa
KW  - Guanosinetriphosphatase
KW  - G 07730:Development & Cell Cycle
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673391389?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preclinical+development+of+an+AAV+vector+for+the+treatment+of+X-linked+retinitis+pigmentosa+due+to+RPGRorf15+mutation&rft.au=Wu%2C+Zhijian%3BHiriyanna%2C+Suja%3BQian%2C+Haohua%3BMookherjee%2C+Suddhasil%3BKaneshiro%2C+Kayleigh%3BCampos%2C+Maria%3BGao%2C+Chun%3BFariss%2C+Robert%3BSwaroop%2C+Anand%3BLi%2C+Tiansen%3BColosi%2C+Peter&rft.aulast=Wu&rft.aufirst=Zhijian&rft.date=2013-09-01&rft.volume=21&rft.issue=9&rft.spage=e20&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-04-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Age; Cones; Data processing; Vision; Nyctalopia; X chromosome; Animal models; Degeneration; Mutation; Retinitis pigmentosa; Guanosinetriphosphatase; Adeno-associated virus
ER  - 



TY  - JOUR
T1  - A versatile method for titration of chimeric antigen receptor-expressing retroviral vectors based on translocation of CD3-epsilon
AN  - 1673391285; PQ0001372804
AB  - Chimeric antigen receptors (CARs) are artificial membrane proteins with modular structure, designed to recognize extracellular antigens through a antibody moiety and to transduce a T cell activating signal thereafter. In the present study we explored the effects of multiple CAR designs on the membrane expression of endogenous CD3. As a consequence, membrane expression of TCR alpha chain and CD3 complex is inhibited at post-transcriptional level, but can be rescued upon introduction of an exogenous TCR beta chain. Our results show that presence of a CD3-derived transmembrane region is not necessary for upregulation of endogenous CD3-epsilon chain upon transduction of a CAR. In addition, we show that assessment of CD3-epsilon translocation in CAR-transduced J.RT1-T3.5 cells can be used as a standardized method for titration of CAR-expressing vector preparations, which is not affected by the binding properties of extracellular region of the immune receptor.
JF  - Molecular Therapy
AU  - Abate-Daga, Daniel
AU  - Feldman, Steve A
AU  - Beard, Rachel E
AU  - Rosenberg, Steven A
AU  - Morgan, Richard A
AD  - Surgery Branch. Center for Cancer Research, National Cancer Institute, NIH. 10 Center Dr. Bethesda, MD 20892
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - e24
EP  - e25
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 9
SN  - 1525-0016, 1525-0016
KW  - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts
KW  - T-cell receptor
KW  - Antibodies
KW  - Receptor mechanisms
KW  - Titration
KW  - Lymphocytes T
KW  - CD3 antigen
KW  - Membrane proteins
KW  - Post-transcription
KW  - Translocation
KW  - W 30905:Medical Applications
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673391285?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+versatile+method+for+titration+of+chimeric+antigen+receptor-expressing+retroviral+vectors+based+on+translocation+of+CD3-epsilon&rft.au=Abate-Daga%2C+Daniel%3BFeldman%2C+Steve+A%3BBeard%2C+Rachel+E%3BRosenberg%2C+Steven+A%3BMorgan%2C+Richard+A&rft.aulast=Abate-Daga&rft.aufirst=Daniel&rft.date=2013-09-01&rft.volume=21&rft.issue=9&rft.spage=e24&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-04-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Antibodies; T-cell receptor; Receptor mechanisms; Titration; Lymphocytes T; Membrane proteins; CD3 antigen; Post-transcription; Translocation
ER  - 



TY  - JOUR
T1  - The cancer psychosocial care matrix: a community-derived evaluative tool for designing quality psychosocial cancer care delivery
AN  - 1665158633
AB  - Objective Although the Institute of Medicine provided a vision for effective psychosocial care for cancer survivors, limited guidance exists regarding the essential components of comprehensive care or progressive steps for implementing each component. This paper describes the development of a unique tool for assessing capacity to provide quality psychosocial care to cancer survivors and the results of the first implementation of this tool in community settings. Methods The psychosocial working group of the National Cancer Institute Community Cancer Centers Program (NCCCP) developed the Cancer Psychosocial Care Matrix assessment tool. All NCCCP sites ( n=30, enrolled in 2007 and 2010) completed the matrix indicating their capacity for providing psychosocial care at entry into NCCCP (‘baseline’) after 2years of NCCCP participation (2007 sites only) and within the coming year (‘future aspirations’). Results At baseline, matrix responses reflected few or no systematic processes in place for most components of comprehensive psychosocial care. However, reported capacity to deliver specific components improved at 2years post-NCCCP entry for the 2007 sites and in all NCCCP sitesʼ future aspirations. Conclusions With growing demand on cancer centers to meet new metrics of quality care, the psychosocial matrix can help centers systematically identify and develop steps to address gap areas in their capacity to meet these new standards. The Cancer Psychosocial Care Matrix appears to enable evaluation of psychosocial programs, may promote intentions to improve psychosocial services, and can facilitate communication of ‘best practices’ among cancer centers. Copyright © 2013 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Forsythe, Laura P
AU  - Rowland, Julia H
AU  - Padgett, Lynne
AU  - Blaseg, Karyl
AU  - Siegel, Scott D
AU  - Dingman, Chad M
AU  - Gillis, Theresa A
AD  - Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Rockville, MD, USA., Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Rockville, MD, USA., Patient-Centered Outcomes Research Institute, Washington, DC, USA. ; Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Rockville, MD, USA. ; Billings Clinic Cancer Center, Billings, USA. ; Helen F. Graham Cancer Center, Christiana Care Health System, Newark, USA. ; Gibbs Cancer Center, Spartanburg Regional Healthcare System, Spartanburg, USA. ; Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Rockville, MD, USA.; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Rockville, MD, USA.; Patient-Centered Outcomes Research Institute, Washington, DC, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1953
EP  - 1962
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 9
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Aspirations
KW  - Communities
KW  - Best practice
KW  - Cancer
KW  - Capacity
KW  - Care delivery
KW  - Communication
KW  - Guidance
KW  - Psychosocial factors
KW  - Psychosocial intervention
KW  - Quality of care
KW  - Survivors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665158633?accountid=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=The+cancer+psychosocial+care+matrix%3A+a+community-derived+evaluative+tool+for+designing+quality+psychosocial+cancer+care+delivery&rft.au=Forsythe%2C+Laura+P%3BRowland%2C+Julia+H%3BPadgett%2C+Lynne%3BBlaseg%2C+Karyl%3BSiegel%2C+Scott+D%3BDingman%2C+Chad+M%3BGillis%2C+Theresa+A&rft.aulast=Forsythe&rft.aufirst=Laura&rft.date=2013-09-01&rft.volume=22&rft.issue=9&rft.spage=1953&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3254
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Name - Institute of Medicine; National Cancer Institute
N1  - Date revised - 2015-01-09
N1  - Last updated - 2016-08-16
DO  - http://dx.doi.org/10.1002/pon.3254
ER  - 



TY  - JOUR
T1  - Can mindfulness-based interventions help adolescents with cancer?
AN  - 1665154259
AB  - During the past 30years, there has been an increase in the incidence of cancer in adolescents. While recent studies have illustrated remarkable resilience in youth living with cancer, they can also face daunting acute and chronic adjustment struggles, cognitive and school problems, family and peer relational difficulties, depression, post-traumatic stress symptoms, and other anxiety disorders. Mindfulness-based interventions (MBIs), increasingly shown to be effective in a variety of medical and mental health settings, may be particularly beneficial for adolescents with cancer. This paper reviews evidence from clinical trials of MBIs showing a variety of benefits for adult cancer patients, adolescents with anxiety disorders and chronic pain, and clinically healthy teenagers, which collectively point to likely benefits of MBIs for teen cancer patients. The authors also explore ways that the particular psychological problems often faced by teen cancer patients, including anxiety about the future, may be especially well suited to mindfulness approaches such as learning to observe physical sensations, thoughts, and emotions, as well as cultivating compassion towards themselves and others. The paper concludes with an exploration of unanswered and potential research questions regarding the future use of MBIs with adolescents with cancer, and potentially with teenagers with other chronic diseases. Copyright © 2013 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Jones, Paul
AU  - Blunda, Megan
AU  - Biegel, Gina
AU  - Carlson, Linda E
AU  - Biel, Matthew
AU  - Wiener, Lori
AD  - National Cancer Institute, Center for Cancer Research, Bethesda, MD, 20892, USA. ; National Cancer Institute, Center for Cancer Research, Bethesda, MD, 20892, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 2148
EP  - 2151
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 9
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Adjustment
KW  - Clinical research
KW  - Clinical trials
KW  - Psychological problems
KW  - Psychological trauma
KW  - Resilience
KW  - Sympathy
KW  - Traumatic stress
KW  - Adolescents
KW  - Anxiety disorders
KW  - Anxiety-Depression
KW  - Awareness
KW  - Cancer
KW  - Chronic diseases
KW  - Chronic pain
KW  - Depression
KW  - Emotions
KW  - Interventions
KW  - Learning styles
KW  - Mental health
KW  - Pain
KW  - Posttraumatic stress disorder
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665154259?accountid=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=Can+mindfulness-based+interventions+help+adolescents+with+cancer%3F&rft.au=Jones%2C+Paul%3BBlunda%2C+Megan%3BBiegel%2C+Gina%3BCarlson%2C+Linda+E%3BBiel%2C+Matthew%3BWiener%2C+Lori&rft.aulast=Jones&rft.aufirst=Paul&rft.date=2013-09-01&rft.volume=22&rft.issue=9&rft.spage=2148&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3251
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.3251
ER  - 



TY  - JOUR
T1  - Changes in Tuberculin Skin Test Positivity Over 20 Years in Periurban Shantytowns in Lima, Peru
AN  - 1647022972; 21172221
AB  - A cross-sectional, community-based study was performed in 2012 with 428 residents of periurban shanty-towns in Lima, Peru to study risk factors for and changes in latent tuberculosis infection in age-stratified groups compared with our data from the same region in 1990 (N = 219) and 2005 (N = 103). Tuberculin skin test positivity in these communities was highly prevalent at 52% overall, increased with age (P  or = 25 year old group remained high (71%, P = 0.3), suggesting that prevalent latent tuberculosis infection persists in the adult population despite improving medical care and socioeconomic development in this region.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Martinez, Leonardo
AU  - Arman, Alyssa
AU  - Haveman, Nathan
AU  - Lundgren, Ashley
AU  - Cabrera, Lilia
AU  - Evans, Carlton A
AU  - Pelly, Tom F
AU  - Saito, Mayuko
AU  - Callacondo, David
AU  - Oberhelman, Richard
AU  - Collazo, Gisela
AU  - Carnero, Andres M
AU  - Gilman, Robert H
AD  - Global Community Health and Behavioral Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana; California State University, Fullerton, Fullerton, California; Weill Cornell Medical College, New York, New York; Asociacion Benefica PRISMA, Lima, Peru; Wellcome Trust Centre for Clinical Tropical Medicine, Department of Infectious Diseases and Immunity, Imperial College London Hammersmith Hospital Campus, London, United Kingdom; IFHAD - Innovation For Health And Development, Universidad Peruana Cayetano Heredia LID#218, Lima, Peru; University of California, San Diego, San Diego, California; Molecular and Clinical Hematology Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland; Tulane University, New Orleans, Louisiana; Postgraduate School, Universidad Peruana Cayetano Heredia, Lima, Peru; Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, rgilman@jhsph.edu
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 507
EP  - 515
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
IS  - 3
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Risk Abstracts; Health & Safety Science Abstracts
KW  - Age
KW  - Data processing
KW  - Mycobacterium
KW  - Community involvement
KW  - Socioeconomics
KW  - Development
KW  - Infection
KW  - Skin tests
KW  - Socio-economic aspects
KW  - Risk factors
KW  - Peru
KW  - Tuberculin
KW  - Tuberculosis
KW  - Peru, Lima
KW  - K 03400:Human Diseases
KW  - J 02400:Human Diseases
KW  - R2 23060:Medical and environmental health
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022972?accountid=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=Changes+in+Tuberculin+Skin+Test+Positivity+Over+20+Years+in+Periurban+Shantytowns+in+Lima%2C+Peru&rft.au=Martinez%2C+Leonardo%3BArman%2C+Alyssa%3BHaveman%2C+Nathan%3BLundgren%2C+Ashley%3BCabrera%2C+Lilia%3BEvans%2C+Carlton+A%3BPelly%2C+Tom+F%3BSaito%2C+Mayuko%3BCallacondo%2C+David%3BOberhelman%2C+Richard%3BCollazo%2C+Gisela%3BCarnero%2C+Andres+M%3BGilman%2C+Robert+H&rft.aulast=Martinez&rft.aufirst=Leonardo&rft.date=2013-09-01&rft.volume=89&rft.issue=3&rft.spage=507&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0005
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Socio-economic aspects; Age; Data processing; Risk factors; Tuberculosis; Tuberculin; Development; Infection; Skin tests; Community involvement; Socioeconomics; Mycobacterium; Peru; Peru, Lima
DO  - http://dx.doi.org/10.4269/ajtmh.13-0005
ER  - 



TY  - JOUR
T1  - High Anti-Cryptosporidium parvum IgG Seroprevalence in HIV-Infected Adults in Limpopo, South Africa
AN  - 1647016049; 21172226
AB  - A seroepidemiological study was performed to determine the seroprevalence of Cryptosporidium in human immunodeficiency virus (HIV)-infected adults and local university students in the Limpopo Province, South Africa. Using a custom anti-C. parvum immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA), the seroprevalence of Cryptosporidium was found to be significantly higher (75.3%; 146 of 193) in HIV-infected individuals compared with student volunteers (32.8%; 19 of 58) (P < 0.001). A more recent diagnosis of HIV was associated with anti-C. parvum IgG seropositivity, as was lower weight among HIV-infected women. This is the first seroepidemiologic study of Cryptosporidium in rural South Africa, and it shows high endemicity among the HIV-infected population. In addition to raising the possibility of significant Cryptosporidium-related morbidities, this finding reveals that in Limpopo and perhaps in other low-income, rural populations, interrupting waterborne pathogen transmission will require strategies effective against environmentally hardy parasites such as Cryptosporidium.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Bartelt, Luther A
AU  - Sevilleja, Jesus Emmanuel
AU  - Barrett, Leah J
AU  - Warren, Cirle A
AU  - Guerrant, Richard L
AU  - Bessong, Pascal O
AU  - Dillingham, Rebecca
AU  - Samie, Amidou
AD  - Center for Global Health, Division of Infectious Diseases, University of Virginia, Charlottesville, Virginia; Institute of Molecular Biology and Biotechnology, National Institutes of Health, University of the Philippines, Manila, Philippines; HIV/AIDS & Global Health Research Programme, University of Venda, Thohoyandou, Limpopo, South Africa; Department of Microbiology, University of Venda, Thohoyandou, Limpopo, South Africa, lab2za@virginia.edu
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 531
EP  - 534
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
IS  - 3
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW  - Parasites
KW  - Enzyme-linked immunosorbent assay
KW  - Rural populations
KW  - Pathogens
KW  - Endoparasites
KW  - Environmental factors
KW  - Morbidity
KW  - Disease transmission
KW  - Endemism
KW  - Human immunodeficiency virus
KW  - Cryptosporidium
KW  - Immunoglobulin G
KW  - ELISA
KW  - South Africa
KW  - Seroepidemiology
KW  - Hygiene
KW  - V 22360:AIDS and HIV
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - J 02400:Human Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647016049?accountid=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=High+Anti-Cryptosporidium+parvum+IgG+Seroprevalence+in+HIV-Infected+Adults+in+Limpopo%2C+South+Africa&rft.au=Bartelt%2C+Luther+A%3BSevilleja%2C+Jesus+Emmanuel%3BBarrett%2C+Leah+J%3BWarren%2C+Cirle+A%3BGuerrant%2C+Richard+L%3BBessong%2C+Pascal+O%3BDillingham%2C+Rebecca%3BSamie%2C+Amidou&rft.aulast=Bartelt&rft.aufirst=Luther&rft.date=2013-09-01&rft.volume=89&rft.issue=3&rft.spage=531&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0550
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Parasites; Endemism; ELISA; Pathogens; Hygiene; Endoparasites; Environmental factors; Disease transmission; Enzyme-linked immunosorbent assay; Immunoglobulin G; Rural populations; Seroepidemiology; Morbidity; Human immunodeficiency virus; Cryptosporidium; South Africa
DO  - http://dx.doi.org/10.4269/ajtmh.12-0550
ER  - 



TY  - JOUR
T1  - Short Report: Potential for Autoimmune Pathogenesis of Rift Valley Fever Virus Retinitis
AN  - 1647005052; 21172218
AB  - Rift Valley Fever (RVF) is a significant threat to human health because it can progress to retinitis, encephalitis, and hemorrhagic fever. The timing of onset of Rift Valley Fever virus (RVFV) retinitis suggests an autoimmune origin. To determine whether RVFV retinitis is associated with increased levels of IgG against retinal tissue, we measured and compared levels of IgG against healthy human eye tissue by immunohistochemical analysis. We found that serum samples from RVFV-exposed Kenyans with retinitis (n = 8) were slightly more likely to have antibodies against retinal tissue than control populations, but the correlation was not statistically significant. Further investigation into the possible immune pathogenesis of RVFV retinitis could lead to improved therapies to prevent or treat this severe complication.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Newman-Gerhardt, Shoshana
AU  - Muiruri, Samuel
AU  - Muchiri, Eric
AU  - Peters, Clarence J
AU  - Morrill, John
AU  - Lucas, Alexander H
AU  - King, Charles H
AU  - Kazura, James
AU  - LaBeaud, Angelle Desiree
AD  - Center for Immunobiology and Vaccine Development, Children's Hospital Oakland Research Institute, Oakland, California; Division of Vector-Borne and Neglected Tropical Diseases, Ministry of Health, Nairobi, Kenya; Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas; Center for Global Health and Disease, Case Western Reserve University, Cleveland, Ohio; National Institutes of Health, Building 29B, Room 2c17, 29 Lincoln Way, Bethesda, MD 20892, snhypheng@gmail.com
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 495
EP  - 497
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
IS  - 3
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts; Virology & AIDS Abstracts; Immunology Abstracts
KW  - Retina
KW  - Eye
KW  - Autoimmune diseases
KW  - Retinitis
KW  - Immunoglobulin G
KW  - Statistical analysis
KW  - Rift Valley fever virus
KW  - Hemorrhagic fever
KW  - Rift Valley fever
KW  - Encephalitis
KW  - V 22350:Immunology
KW  - J 02490:Miscellaneous
KW  - F 06910:Microorganisms & Parasites
KW  - N3 11024:Neuroimmunology
KW  - K 03420:Plant Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647005052?accountid=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=Short+Report%3A+Potential+for+Autoimmune+Pathogenesis+of+Rift+Valley+Fever+Virus+Retinitis&rft.au=Newman-Gerhardt%2C+Shoshana%3BMuiruri%2C+Samuel%3BMuchiri%2C+Eric%3BPeters%2C+Clarence+J%3BMorrill%2C+John%3BLucas%2C+Alexander+H%3BKing%2C+Charles+H%3BKazura%2C+James%3BLaBeaud%2C+Angelle+Desiree&rft.aulast=Newman-Gerhardt&rft.aufirst=Shoshana&rft.date=2013-09-01&rft.volume=89&rft.issue=3&rft.spage=495&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0562
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Eye; Retina; Autoimmune diseases; Statistical analysis; Immunoglobulin G; Retinitis; Hemorrhagic fever; Rift Valley fever; Encephalitis; Rift Valley fever virus
DO  - http://dx.doi.org/10.4269/ajtmh.12-0562
ER  - 



TY  - JOUR
T1  - 332Duration as a proxy for cumulative exposure: Should we trust positive results?
AN  - 1551619364; 20364247
AB  - ObjectivesWe considered a problem common to occupational epidemiology, where cumulative exposure is the true dose metric for disease but investigators are only able to measure duration of exposure.Methods and ResultsWe considered the problem from the theoretical perspective and explored our results in simulations of an occupational cohort of medium size. The duration of exposure is related to cumulative exposure by measurement error with some properties of Berkson-type error. This arises because cumulative exposure = duration*intensity and can be re-written as true = observed*error, with error term having distribution of average long-term exposure intensity for a worker. When duration and intensity are independent, the theory predicts that fitting duration instead of cumulative exposure will not inflate probability of type-I error under the null hypothesis. However, when there is an association between cumulative exposure and the outcome, loss of power to detect an association is expected. In practice, data do not always conform to assumptions made in the theoretical study. We confirmed these predictions in a simulation study for a cohort of 1000 workers with rare outcome in unexposed and with varying correlation of intensity and duration. We first analysed the data using logistic regression models including metrics of exposure as continuous variables. We then explored the situation where exposure groups are formed using quartiles of observed exposure metrics among "cases" and odds in the highest quartile are compared to the lowest. Patterns observed in both analyses were consistent with those expected from theory.ConclusionsEpidemiologists should be more confident in interpreting positive results that arise from use of duration of exposure in lieu of true dose metrics when it is cumulative exposure because type-I error remains at nominal values. The interpretation of null associations remains difficult due to loss of power.
JF  - Occupational and Environmental Medicine
AU  - Barone Adesi, F
AU  - Burstyn
AD  - National Cancer Institute, Bethesda, United States of America
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - A113
PB  - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom
VL  - 70
IS  - Suppl 1
SN  - 1351-0711, 1351-0711
KW  - Health & Safety Science Abstracts
KW  - Prediction
KW  - Simulation
KW  - Occupational exposure
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551619364?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=332Duration+as+a+proxy+for+cumulative+exposure%3A+Should+we+trust+positive+results%3F&rft.au=Barone+Adesi%2C+F%3BBurstyn&rft.aulast=Barone+Adesi&rft.aufirst=F&rft.date=2013-09-01&rft.volume=70&rft.issue=Suppl+1&rft.spage=A113&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-101717.332
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Prediction; Simulation; Occupational exposure
DO  - http://dx.doi.org/10.1136/oemed-2013-101717.332
ER  - 



TY  - JOUR
T1  - 389Risk of total and aggressive prostate cancer and pesticide use in the Agricultural Health Study
AN  - 1551617063; 20364299
AB  - ObjectivesPesticides have been associated with prostate cancer risk, but few studies have evaluated specific pesticides and studies have not explored differences by subtype to identify important risk for the more lethal, aggressive, form of prostate cancer. Therefore, we studied the risk of prostate cancer associated with specific pesticides among 1,962 incident cases, including 919 cases of aggressive prostate cancer (distant Stage or poorly differentiated or Gleason greater than or equal to 7 or fatal prostate cancer) diagnosed between 1993 and 2007 from 54,412 men of the Agricultural Health Study (AHS) cohort.MethodsPoisson regression analysis was used to calculate rate ratios (RR) and 95% confidence intervals (95% CI) for lifetime use of 48 pesticides and prostate cancer incidence.ResultsThere was no overall association between any specific pesticide and prostate cancer risk. However, three organophosphate insecticides were significantly associated with aggressive prostate cancer: fonofos (RR for the highest quartile of exposure (Q4) versus nonexposed = 1.63, 95% CI: 1.22-2.17; p-trend <0.001), malathion (RR for Q4 versus nonexposed = 1.43, 95% CI: 1.08-1.88; p-trend = 0.04), and terbufos (RR for Q4 versus nonexposed = 1.29, 95% CI: 1.02-1.64; p-trend = 0.03). The organochlorine insecticide aldrin was also significantly associated with risk of aggressive prostate cancer with a RR for Q4 versus nonexposed = 1.49, 95% CI: 1.03-2.18; p-trend = 0.02.ConclusionsFour insecticides were observed to increase the risk of aggressive prostate cancer in the AHS. Advantages of this analysis over previous analyses include a large number of prostate cancer cases and detailed information on lifetime use of specific pesticides. This is the first time specific pesticides have been studied and implicated as risk factors for aggressive prostate cancer and may suggest that pesticides play a role in prostate cancer progression rather than at the earlier initiation stage of transformation.
JF  - Occupational and Environmental Medicine
AU  - Koutros, S K
AD  - National Cancer Institute, Rockville, United Stated of America
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - A133
PB  - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom
VL  - 70
IS  - Suppl 1
SN  - 1351-0711, 1351-0711
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Prostate cancer
KW  - Insecticides
KW  - Organochlorine compounds
KW  - Organophosphates
KW  - Risk factors
KW  - Pesticides
KW  - Aldrin
KW  - Malathion
KW  - H 1000:Occupational Safety and Health
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551617063?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=389Risk+of+total+and+aggressive+prostate+cancer+and+pesticide+use+in+the+Agricultural+Health+Study&rft.au=Koutros%2C+S+K&rft.aulast=Koutros&rft.aufirst=S&rft.date=2013-09-01&rft.volume=70&rft.issue=Suppl+1&rft.spage=A133&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-101717.389
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Organochlorine compounds; Insecticides; Prostate cancer; Organophosphates; Risk factors; Aldrin; Pesticides; Malathion
DO  - http://dx.doi.org/10.1136/oemed-2013-101717.389
ER  - 



TY  - JOUR
T1  - 289Using hierarchical clustering methods to identify jobs with similar response patterns in a population-based case-control study
AN  - 1551616755; 20364196
AB  - ObjectivesStudies have demonstrated the utility of developing expert-based decision rules based on questionnaire response patterns to assign exposure in population-based studies. However, each expert may identify different response patterns to represent exposure scenarios. To improve the reproducibility of identifying these patterns and increase the efficiency of assigning exposures, we used hierarchical clustering methods to identify groups of jobs (clusters) with similar response patterns.MethodsFor each job module in the New England Bladder Cancer Case-Control Study, we applied Ward's average linkage hierarchical cluster models to the questionnaire responses related to occupational diesel exhaust exposure to identify the most distinct 25 and 50 clusters of jobs per module. We assessed the clusters' homogeneity based on the proportion of jobs assigned the same probability category (<50% vs. greater than or equal to 50% probability of occupational diesel exhaust exposure) from a previous expert-based assessment of each job. A cluster was 'homogeneous' if greater than or equal to 75% of the jobs were assigned the same probability category. Here we present the results for three modules: carpenter (357 jobs, 17% exposed, 52 unique response patterns), office professional (3,328 jobs, 22% exposed, 87 unique response patterns), and truck driver (508 jobs, 74% exposed, 404 unique response patterns).ResultsFor carpenters, 76% and 90% of the groups were homogeneous based on 25 and 50 clusters, respectively. For office professionals, 84% and 78% of the groups were homogeneous based on 25 and 50 clusters, respectively. For truck drivers, 76% and 70% of the groups were homogeneous based on 25 and 50 clusters, respectively. bConclusionsThere was reasonable homogeneity using 25-50 clusters per module (representing 3-15% of the number of jobs per questionnaire), but important heterogeneity remained. A more efficient use of expert judgment may be to assess exposure at the cluster-level and then, within expert-identified heterogeneous clusters, at the job-level.
JF  - Occupational and Environmental Medicine
AU  - Friesen, M C
AU  - Shortreed
AU  - Wheeler
AU  - Stewart
AU  - Burstyn
AU  - Vermeulen
AU  - Pronk
AU  - Colt
AU  - Baris
AU  - Karagas
AU  - Schwenn
AU  - McCoy
AU  - Silverman
AU  - Yu
AD  - National Cancer Institute, North Bethesda, United States of America
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - A98
EP  - A99
PB  - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom
VL  - 70
IS  - Suppl 1
SN  - 1351-0711, 1351-0711
KW  - Health & Safety Science Abstracts
KW  - USA, New England
KW  - Urinary bladder
KW  - Trucks
KW  - Diesel engines
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551616755?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=289Using+hierarchical+clustering+methods+to+identify+jobs+with+similar+response+patterns+in+a+population-based+case-control+study&rft.au=Friesen%2C+M+C%3BShortreed%3BWheeler%3BStewart%3BBurstyn%3BVermeulen%3BPronk%3BColt%3BBaris%3BKaragas%3BSchwenn%3BMcCoy%3BSilverman%3BYu&rft.aulast=Friesen&rft.aufirst=M&rft.date=2013-09-01&rft.volume=70&rft.issue=Suppl+1&rft.spage=A98&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-101717.289
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Urinary bladder; Trucks; Diesel engines; USA, New England
DO  - http://dx.doi.org/10.1136/oemed-2013-101717.289
ER  - 



TY  - JOUR
T1  - 391Association between occupational exposure to wood dust and risk of nasopharyngeal cancer: A case-control study from Thailand
AN  - 1551616275; 20364301
AB  - ObjectivesTo explore possible association between occupational wood dust exposure and risk of nasopharyngeal cancer (NPC), a matched case - control study was conducted in Bangkok and 6 regional cancer treatment centers in Thailand.MethodsThree hundred and twenty-seven diagnosed NPC cases were compared with 327 age and gender matched controls. Data of socio-demographic characteristics and potential risk factors were collected by personal interviews. Wood dust exposures were assessed by 3 industrial hygienists by reading lifetime occupational histories of the participants with unknown for case-control status. Assessments were done for probability, frequency and intensity of exposure to wood dust. Multivariate analyses were performed adjusting for educational level, smoking status and histories of chronic sinusitis. ResultsWe found the association between occupational wood dust exposure and NPC risk (OR 1.66, 95% CI 1.03 - 2.67) especially for those who have definite probability of exposure (OR 1.77, 95% CI 1.04 - 3.00), moderate frequency of exposure (OR 2.8, 95% CI 1.22 - 6.39) and low intensity of exposure (OR 2.29, 95% CI 1.15 - 4.59).ConclusionResults of this study shows that occupational exposure to wood dust are likely to be associated with increasing risk of NPC.
JF  - Occupational and Environmental Medicine
AU  - Sangrajrang, S S
AU  - Ekburanawat
AU  - Ekpanyasakul
AU  - Thetkathek
AU  - Saejew
AU  - Ruangsuwan
AU  - Mannetje, T
AD  - National Cancer Institute, Bangkok, Thailand
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - A134
PB  - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom
VL  - 70
IS  - Suppl 1
SN  - 1351-0711, 1351-0711
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Risk assessment
KW  - Historical account
KW  - Age
KW  - Wood
KW  - Thailand, Chacoengsao Prov., Bangkok
KW  - Dust
KW  - Cancer
KW  - Health risks
KW  - Smoking
KW  - Risk factors
KW  - Gender
KW  - Occupational exposure
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/1551616275?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=391Association+between+occupational+exposure+to+wood+dust+and+risk+of+nasopharyngeal+cancer%3A+A+case-control+study+from+Thailand&rft.au=Sangrajrang%2C+S+S%3BEkburanawat%3BEkpanyasakul%3BThetkathek%3BSaejew%3BRuangsuwan%3BMannetje%2C+T&rft.aulast=Sangrajrang&rft.aufirst=S&rft.date=2013-09-01&rft.volume=70&rft.issue=Suppl+1&rft.spage=A134&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-101717.391
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Risk assessment; Smoking; Historical account; Health risks; Age; Risk factors; Gender; Wood; Occupational exposure; Cancer; Dust; Thailand, Chacoengsao Prov., Bangkok
DO  - http://dx.doi.org/10.1136/oemed-2013-101717.391
ER  - 



TY  - JOUR
T1  - 3942,4-D Use and Cancer Incidence in Pesticide Applicators in the Agricultural Health Study
AN  - 1551614007; 20364304
AB  - Objectives2,4-dichlorophenoxyacetic acid (2,4-D) is one of the most widely used herbicides in the world. It has been associated with increased risk of non-Hodgkin lymphoma (NHL) in multiple epidemiologic studies, with some evidence for association with cancer at other sites. Findings from experimental studies, however, have been largely negative with respect to NHL. Within the Agricultural Health Study (AHS), a prospective cohort of licensed pesticide applicators in the United States, we evaluated use of this herbicide and multiple cancer sites.MethodsWe used Poisson regression to estimate relative risks (RR) and 95% confidence intervals for cancers that occurred from enrollment in the AHS (1993-97) through 2008. Total lifetime days of use of 2,4-D were calculated based on information provided at enrollment and at a follow-up interview conducted 5 years later. In addition, an intensity-weighting algorithm was applied to account for factors that modify exposure.ResultsOverall, 78% of the 52,324 applicators who provided information on 2,4-D use and who were cancer free at enrollment reported using 2,4-D. Among this group, there were 5,168 incident cancers. Compared to non-users, there was no association with cancer risk overall (p-trend = 0.68), NHL overall (p-trend = 0.84), or any sub-type of NHL with intensity-weighted lifetime days. Conversely, in the highest quartiles, there was an elevated risk of gastric cancer (RR = 2.3, 95% CI:1.1-5.2, p-trend = 0.03) and a suggestion of elevated risk of brain cancer (RR = 2.3, 95% CI: 0.9-5.7, p-trend = 0.31).ConclusionsThe results from this prospective study showed no association between use of 2,4-D and NHL, the cancer most often linked to this herbicide. The increased risk of gastric cancer is noteworthy but supporting data are limited. Some previous studies of brain cancer have suggested a role for pesticides, particularly herbicides; to our knowledge there is no other study specifically suggesting an association with 2,4-D.
JF  - Occupational and Environmental Medicine
AU  - Beane Freeman, E
AU  - Koutros
AU  - Alavanja
AU  - Zahm
AU  - Sandler
AU  - Hines
AU  - Thomas
AU  - Hoppin
AU  - Blair
AD  - National Cancer Institute, Rockville, United States of America
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - A135
PB  - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom
VL  - 70
IS  - Suppl 1
SN  - 1351-0711, 1351-0711
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Health risks
KW  - Non-Hodgkin's lymphoma
KW  - USA
KW  - Risk factors
KW  - Pesticides
KW  - Brain
KW  - 2,4-Dichlorophenoxyacetic acid
KW  - Herbicides
KW  - Cancer
KW  - R2 23060:Medical and environmental health
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551614007?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=3942%2C4-D+Use+and+Cancer+Incidence+in+Pesticide+Applicators+in+the+Agricultural+Health+Study&rft.au=Beane+Freeman%2C+E%3BKoutros%3BAlavanja%3BZahm%3BSandler%3BHines%3BThomas%3BHoppin%3BBlair&rft.aulast=Beane+Freeman&rft.aufirst=E&rft.date=2013-09-01&rft.volume=70&rft.issue=Suppl+1&rft.spage=A135&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-101717.394
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Non-Hodgkin's lymphoma; Health risks; Risk factors; Pesticides; Brain; 2,4-Dichlorophenoxyacetic acid; Herbicides; Cancer; USA
DO  - http://dx.doi.org/10.1136/oemed-2013-101717.394
ER  - 



TY  - JOUR
T1  - The Prevalence of Undiagnosed Concussions in Athletes
AN  - 1547862497; 20293283
AB  - Previous studies suggest athletes underreport concussions. We sought to determine whether athletes in our clinics have sustained previous concussions that went undiagnosed. Patients diagnosed with sport-related concussions or concussions with injury mechanisms and forces similar to those observed in sports were included. Of the 486 patients included in the final analysis, 148 (30.5%) patients reported a previously undiagnosed concussion. Nearly one-third of athletes have sustained previously undiagnosed concussions, defined as a blow to the head followed by the signs and symptoms included in the PCSS. Furthermore, these previously undiagnosed concussions are associated with higher PCSS scores and higher loss of consciousness rates when future concussions occur.
JF  - Clinical Journal of Sport Medicine
AU  - Meehan, William P, III
AU  - Mannix, Rebekah C
AU  - O'Brien, Michael J
AU  - Collins, Michael W
AD  - Sports Concussion Clinic, Division of Sports Medicine, Boston Children's Hospital, 319 Longwood Ave, Floor 6, Boston, MA 02115; The Micheli Center for Sports Injury Prevention, Boston, Massachusetts; Brain Injury Center, Boston Children's Hospital, Boston, Massachusetts; Division of Emergency Medicine, Department of Medicine, Boston Children's Hospital, Boston, Massachusetts; National Institutes of Health Grants T32 HD040128 to 06A1, concussion.sportsmed@childrens.harvard.edu
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 339
EP  - 342
PB  - Lippincott Williams & Wilkins, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL  - 23
IS  - 5
SN  - 1050-642X, 1050-642X
KW  - Physical Education Index
KW  - mild traumatic brain injury
KW  - loss of consciousness
KW  - sports injury
KW  - Injuries
KW  - Analysis
KW  - Concussion
KW  - Patients
KW  - Sports medicine
KW  - Sports
KW  - Athletes
KW  - scoring
KW  - PE 090:Sports Medicine & Exercise Sport Science
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547862497?accountid=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=Clinical+Journal+of+Sport+Medicine&rft.atitle=The+Prevalence+of+Undiagnosed+Concussions+in+Athletes&rft.au=Meehan%2C+William+P%2C+III%3BMannix%2C+Rebekah+C%3BO%27Brien%2C+Michael+J%3BCollins%2C+Michael+W&rft.aulast=Meehan&rft.aufirst=William&rft.date=2013-09-01&rft.volume=23&rft.issue=5&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=Clinical+Journal+of+Sport+Medicine&rft.issn=1050642X&rft_id=info:doi/
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2014-07-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Injuries; Analysis; Patients; Concussion; Sports; Sports medicine; scoring; Athletes
ER  - 



TY  - JOUR
T1  - A Prospective Study of Statin Drug Use and Lower Urinary Tract Symptoms in Older Men
AN  - 1492628808; 18890527
AB  - Dyslipidemia and chronic inflammation may play a role in the cause of lower urinary tract symptoms (LUTS) in older men. Use of statin drugs, which are prescribed to lower cholesterol and appear to reduce inflammation, may decrease the incidence or progression of LUTS. The associations of statin drug use with LUTS incidence and progression were prospectively evaluated in the Health Professionals Follow-up Study from 1992 to 2008. Hazard ratios and 95% confidence intervals of incident LUTS (from no or a low International Prostate Symptom Score (IPSS) of 0-7 to a moderate or worse IPSS of greater than or equal to 15; n = 5,790 cases in 24,715 men) and of LUTS progression (from modest IPSS of 8-14 to severe IPSS of greater than or equal to 20; n = 2,238 cases in 8,709 men) were calculated comparing current statin use with nonuse. The hazard ratios of LUTS incidence and progression comparing current use to nonuse were greater than 1. However, when comparisons were restricted to participants who used drugs to treat hypertension (a surrogate for uptake of medical care), statin use was not associated with LUTS incidence (hazard ratio = 1.02, 95% confidence interval: 0.94, 1.12) or progression (hazard ratio = 0.98, 95% confidence interval: 0.85, 1.13). Thus, statin use is unlikely to beneficially influence the development or course of LUTS. The present study highlights a methodological issue (confounding) that must be addressed in observational studies on the use of common drugs for indications other than the primary use.
JF  - American Journal of Epidemiology
AU  - Mondul, Alison M
AU  - Giovannucci, Edward
AU  - Platz, Elizabeth A
AD  - Correspondence to Dr. Alison Mondul, 9609 Medical Center Drive, Room 6E328, Rockville, MD 20850., mondulam@mail.nih.gov
Y1  - 2013/09/01/
PY  - 2013
DA  - 2013 Sep 01
SP  - 797
EP  - 803
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 178
IS  - 5
SN  - 0002-9262, 0002-9262
KW  - Health & Safety Science Abstracts
KW  - Statins
KW  - Urine
KW  - Males
KW  - Uptake
KW  - Cholesterol
KW  - Drug abuse
KW  - Drugs
KW  - Hypertension
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492628808?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=A+Prospective+Study+of+Statin+Drug+Use+and+Lower+Urinary+Tract+Symptoms+in+Older+Men&rft.au=Mondul%2C+Alison+M%3BGiovannucci%2C+Edward%3BPlatz%2C+Elizabeth+A&rft.aulast=Mondul&rft.aufirst=Alison&rft.date=2013-09-01&rft.volume=178&rft.issue=5&rft.spage=797&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwt055
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Statins; Urine; Males; Uptake; Cholesterol; Drug abuse; Drugs; Hypertension
DO  - http://dx.doi.org/10.1093/aje/kwt055
ER  - 



TY  - JOUR
T1  - Improved Bloch-Siegert based B sub(1) mapping by reducing off-resonance shift
AN  - 1492624222; 18894690
AB  - An MRI method based on the Bloch-Siegert (BS) shift phenomenon was recently proposed as a fast and precise way to map a radio frequency (RF) transmit field (B sub(1) super(+) field). For MRI at high field, the mapping sensitivity of this approach was limited by tissue heating associated with a BS irradiation pulse. To mitigate this, we investigated the possibility of lowering the off-resonance frequency of this pulse since theoretical analysis indicated that the sensitivity of Bloch-Siegert based B sub(1) super(+) mapping could be substantially improved when irradiating closer to resonance. Using optimized irradiation pulse shape and gradient crushers to minimize direct excitation effects, in vivo experiments on human brains at 7T confirmed improved sensitivity with this approach. Improved sensitivity translated into an 80% reduction in B sub(1) super(+) estimation errors without increasing tissue heating. Published 2013. This article is a U.S. Government work and is in the public domain in the USA. The B sub(1) super(+) mapping method on the Bloch-Siegert (BS) shift is currently limited by tissue heating associated with the BS irradiation pulse. We investigated the possibility of lowering the off-resonance frequency of this pulse, as the sensitivity of BS-based B sub(1) super(+) mapping can be substantially improve when irradiating closer to resonance. Using optimized irradiation pulse shape and gradient crusher to minimize direct excitation effects, in vivo experiments on human brain at 7T confirmed the improved sensitivity.
JF  - NMR in Biomedicine
AU  - Duan, Qi
AU  - Gelderen, Peter
AU  - Duyn, Jeff
AD  - Advanced MRI Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1070
EP  - 1078
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 26
IS  - 9
SN  - 0952-3480, 0952-3480
KW  - Biotechnology and Bioengineering Abstracts
KW  - Brain
KW  - Radiation
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492624222?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Improved+Bloch-Siegert+based+B+sub%281%29+mapping+by+reducing+off-resonance+shift&rft.au=Duan%2C+Qi%3BGelderen%2C+Peter%3BDuyn%2C+Jeff&rft.aulast=Duan&rft.aufirst=Qi&rft.date=2013-09-01&rft.volume=26&rft.issue=9&rft.spage=1070&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.2920
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Radiation
DO  - http://dx.doi.org/10.1002/nbm.2920
ER  - 



TY  - JOUR
T1  - MRI confirms loss of blood-brain barrier integrity in a mouse model of disseminated candidiasis
AN  - 1492613669; 18894684
AB  - Disseminated candidiasis primarily targets the kidneys and brain in mice and humans. Damage to these critical organs leads to the high mortality associated with such infections, and invasion across the blood-brain barrier can result in fungal meningoencephalitis. Candida albicans can penetrate a brain endothelial cell barrier in vitro through transcellular migration, but this mechanism has not been confirmed in vivo. MRI using the extracellular vascular contrast agent gadolinium diethylenetriaminepentaacetic acid demonstrated that integrity of the blood-brain barrier is lost during C. albicans invasion. Intravital two-photon laser scanning microscopy was used to provide the first real-time demonstration of C. albicans colonizing the living brain, where both yeast and filamentous forms of the pathogen were found. Furthermore, we adapted a previously described method utilizing MRI to monitor inflammatory cell recruitment into infected tissues in mice. Macrophages and other phagocytes were visualized in kidney and brain by the administration of ultrasmall iron oxide particles. In addition to obtaining new insights into the passage of C. albicans across the brain microvasculature, these imaging methods provide useful tools to study further the pathogenesis of C. albicans infections, to define the roles of Candida virulence genes in kidney versus brain infection and to assess new therapeutic measures for drug development. Published 2013. This article is a U.S. Government work and is in the public domain in the USA. MRI of mice infected with Candida albicans using gadolinium-enhanced vascular contrast (A) demonstrates that the integrity of the blood-brain barrier is lost on infection. Dynamic contrast studies for cortical and hippocampal regions (B) show first-pass recovery indicating an intact barrier in uninfected mice and vascular leakage in infected brains. Two-photon microscopy through a surgically thinned skull window (C) shows filamentous and yeast forms of C. albicans (green) colonizing the meninges and brain parenchyma, 3 days following intravenous inoculation.
JF  - NMR in Biomedicine
AU  - Navarathna, Dhammika HMLP
AU  - Munasinghe, Jeeva
AU  - Lizak, Martin J
AU  - Nayak, Debasis
AU  - McGavern, Dorian B
AU  - Roberts, David D
AD  - Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1125
EP  - 1134
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 26
IS  - 9
SN  - 0952-3480, 0952-3480
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Animal models
KW  - Brain
KW  - Candida albicans
KW  - W 30910:Imaging
KW  - N3 11027:Neurology & neuropathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492613669?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MRI+confirms+loss+of+blood-brain+barrier+integrity+in+a+mouse+model+of+disseminated+candidiasis&rft.au=Navarathna%2C+Dhammika+HMLP%3BMunasinghe%2C+Jeeva%3BLizak%2C+Martin+J%3BNayak%2C+Debasis%3BMcGavern%2C+Dorian+B%3BRoberts%2C+David+D&rft.aulast=Navarathna&rft.aufirst=Dhammika&rft.date=2013-09-01&rft.volume=26&rft.issue=9&rft.spage=1125&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.2926
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Brain; Candida albicans
DO  - http://dx.doi.org/10.1002/nbm.2926
ER  - 



TY  - JOUR
T1  - Oral fluid/plasma cannabinoid ratios following controlled oral THC and smoked cannabis administration
AN  - 1464557710; 18716490
AB  - Oral fluid (OF) is a valuable biological alternative for clinical and forensic drug testing. Evaluating OF to plasma (OF/P) cannabinoid ratios provides important pharmacokinetic data on the disposition of drug and factors influencing partition between matrices. Eleven chronic cannabis smokers resided on a closed research unit for 51 days. There were four 5-day sessions of 0, 30, 60, and 120 mg oral Delta (9)-tetrahydrocannabinol (THC)/day followed by a five-puff smoked cannabis challenge on Day 5. Each session was separated by 9 days ad libitum cannabis smoking. OF and plasma specimens were analyzed for THC and metabolites. During ad libitum smoking, OF/P THC ratios were high (median, 6.1; range, 0.2-348.5) within 1 h after last smoking, decreasing to 0.1-20.7 (median, 2.1) by 13.0-17.1 h. OF/P THC ratios also decreased during 5-days oral THC dosing, and after the smoked cannabis challenge, median OF/P THC ratios decreased from 1.4 to 5.5 (0.04-245.6) at 0.25 h to 0.12 to 0.17 (0.04-5.1) at 10.5 h post-smoking. In other studies, longer exposure to more potent cannabis smoke and oromucosal cannabis spray was associated with increased OF/P THC peak ratios. Median OF/P 11-nor-9-carboxy-THC (THCCOOH) ratios were 0.3-2.5 (range, 0.1-14.7) ng/ mu g, much more consistent in various dosing conditions over time. OF/P THC, but not THCCOOH, ratios were significantly influenced by oral cavity contamination after smoking or oromucosal spray of cannabinoid products, followed by time-dependent decreases. Establishing relationships between OF and plasma cannabinoid concentrations is essential for making inferences of impairment or other clinical outcomes from OF concentrations.
JF  - Analytical and Bioanalytical Chemistry
AU  - Lee, Dayong
AU  - Vandrey, Ryan
AU  - Milman, Garry
AU  - Bergamaschi, Mateus
AU  - Mendu Damodara, R
AU  - Murray Jeannie, A
AU  - Barnes Allan, J
AU  - Huestis Marilyn, A
AD  - National Institute on Drug Abuse, N1H, Biomedical Research Center, 251 Bayview Boulevard Suite 200, Baltimore, MD 21224, USA, mhuestis@intra.nida.nih.gov
PY  - 2013
SP  - 7269
EP  - 7279
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 405
IS  - 23
SN  - 1618-2642, 1618-2642
KW  - Aqualine Abstracts; Water Resources Abstracts
KW  - Testing Procedures
KW  - Contamination
KW  - Sprays
KW  - Metabolites
KW  - Administration
KW  - Exposure
KW  - Drugs
KW  - AQ 00001:Water Resources and Supplies
KW  - SW 5010:Network design
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464557710?accountid=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=Oral+fluid%2Fplasma+cannabinoid+ratios+following+controlled+oral+THC+and+smoked+cannabis+administration&rft.au=Lee%2C+Dayong%3BVandrey%2C+Ryan%3BMilman%2C+Garry%3BBergamaschi%2C+Mateus%3BMendu+Damodara%2C+R%3BMurray+Jeannie%2C+A%3BBarnes+Allan%2C+J%3BHuestis+Marilyn%2C+A&rft.aulast=Lee&rft.aufirst=Dayong&rft.date=2013-09-01&rft.volume=405&rft.issue=23&rft.spage=7269&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-013-7159-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-12-01
N1  - Number of references - 37
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Testing Procedures; Contamination; Exposure; Administration; Sprays; Metabolites; Drugs
DO  - http://dx.doi.org/10.1007/s00216-013-7159-8
ER  - 



TY  - JOUR
T1  - NGSPE: A pipeline for end-to-end analysis of DNA sequencing data and comparison between different platforms
AN  - 1464515427; 18816708
AB  - We present NGSPE, a pipeline for variation discovery and genotyping of pair-ended Illumina next generation sequencing (NGS) data (http://ngspeanalysis.sourceforge.net/). This pipeline not only describes a set of sequential analytical steps, such as short reads alignment, genotype calling and functional variation annotation that can be conducted using open-source software tools, but also provides users a set of scripts to install the dependent software and resources and implement the pipeline on their data. A sample summary report including the concordance rate between data generated by this pipeline and different resources as well as the comparison between replication samples of two commercial platforms from Illumina and Complete Genomics is also provided. Furthermore, some of the mutations identified by the pipeline were verified using Sanger sequencing.
JF  - Computers in Biology and Medicine
AU  - Huang, Ke
AU  - Yellapantula, Venkata
AU  - Baier, Leslie
AU  - Dinu, Valentin
AD  - Diabetes Molecular Genetics Section, PECRB, NIDDK, National Institutes of Health, Phoenix, AZ, USA
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1171
EP  - 1176
PB  - Elsevier B.V., P.O. Box 800 Kidlington Oxford OX5 1DX United Kingdom
VL  - 43
IS  - 9
SN  - 0010-4825, 0010-4825
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - Computer applications
KW  - Data processing
KW  - N 14810:Methods
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464515427?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=NGSPE%3A+A+pipeline+for+end-to-end+analysis+of+DNA+sequencing+data+and+comparison+between+different+platforms&rft.au=Huang%2C+Ke%3BYellapantula%2C+Venkata%3BBaier%2C+Leslie%3BDinu%2C+Valentin&rft.aulast=Huang&rft.aufirst=Ke&rft.date=2013-09-01&rft.volume=43&rft.issue=9&rft.spage=1171&rft.isbn=&rft.btitle=&rft.title=Computers+in+Biology+and+Medicine&rft.issn=00104825&rft_id=info:doi/10.1016%2Fj.compbiomed.2013.05.025
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Data processing
DO  - http://dx.doi.org/10.1016/j.compbiomed.2013.05.025
ER  - 



TY  - JOUR
T1  - Synergistic combination of clinical and imaging features predicts abnormal imaging patterns of pulmonary infections
AN  - 1464515394; 18816717
AB  - We designed and tested a novel hybrid statistical model that accepts radiologic image features and clinical variables, and integrates this information in order to automatically predict abnormalities in chest computed-tomography (CT) scans and identify potentially important infectious disease biomarkers. In 200 patients, 160 with various pulmonary infections and 40 healthy controls, we extracted 34 clinical variables from laboratory tests and 25 textural features from CT images. From the CT scans, pleural effusion (PE), linear opacity (or thickening) (LT), tree-in-bud (TIB), pulmonary nodules, ground glass opacity (GGO), and consolidation abnormality patterns were analyzed and predicted through clinical, textural (imaging), or combined attributes. The presence and severity of each abnormality pattern was validated by visual analysis of the CT scans. The proposed biomarker identification system included two important steps: (i) a coarse identification of an abnormal imaging pattern by adaptively selected features (AmRMR), and (ii) a fine selection of the most important features from the previous step, and assigning them as biomarkers, depending on the prediction accuracy. Selected biomarkers were used to classify normal and abnormal patterns by using a boosted decision tree (BDT) classifier. For all abnormal imaging patterns, an average prediction accuracy of 76.15% was obtained. Experimental results demonstrated that our proposed biomarker identification approach is promising and may advance the data processing in clinical pulmonary infection research and diagnostic techniques.
JF  - Computers in Biology and Medicine
AU  - Bagci, Ulas
AU  - Jaster-Miller, Kirsten
AU  - Olivier, Kenneth N
AU  - Yao, Jianhua
AU  - Mollura, Daniel J
AD  - Center for Infectious Disease Imaging, Department of Radiology and Imaging Sciences, National Institutes of Health (NIH), Bethesda, MD 20892, United States
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1241
EP  - 1251
PB  - Elsevier B.V., P.O. Box 800 Kidlington Oxford OX5 1DX United Kingdom
VL  - 43
IS  - 9
SN  - 0010-4825, 0010-4825
KW  - Biotechnology and Bioengineering Abstracts
KW  - Chest
KW  - biomarkers
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464515394?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Synergistic+combination+of+clinical+and+imaging+features+predicts+abnormal+imaging+patterns+of+pulmonary+infections&rft.au=Bagci%2C+Ulas%3BJaster-Miller%2C+Kirsten%3BOlivier%2C+Kenneth+N%3BYao%2C+Jianhua%3BMollura%2C+Daniel+J&rft.aulast=Bagci&rft.aufirst=Ulas&rft.date=2013-09-01&rft.volume=43&rft.issue=9&rft.spage=1241&rft.isbn=&rft.btitle=&rft.title=Computers+in+Biology+and+Medicine&rft.issn=00104825&rft_id=info:doi/10.1016%2Fj.compbiomed.2013.06.008
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - biomarkers
DO  - http://dx.doi.org/10.1016/j.compbiomed.2013.06.008
ER  - 



TY  - JOUR
T1  - Around-the-Clock Oral THC Effects on Sleep in Male Chronic Daily Cannabis Smokers
AN  - 1463067752; 201325884
AB  - Background and Objectives: [delta]9-tetrahydrocannabinol (THC) promotes sleep in animals; clinical use of THC is associated with somnolence. Human laboratory studies of oral THC have not shown consistent effects on sleep. We prospectively evaluated self-reported sleep parameters during controlled oral THC administration to research volunteers. Methods: Thirteen male chronic daily cannabis smokers (mean [plus or minus] SD age 24.6 [plus or minus] 3.7 years, self-reported smoking frequency of 5.5 [plus or minus] 5.9 (range 1-24) joint-equivalents daily at study entry) were administered oral THC doses (20 mg) around-the-clock for 7 days (40-120 mg daily) starting the afternoon after admission. The St. Mary's Hospital Sleep Questionnaire was completed every morning. Plasma THC and 11-OH-THC (active metabolite) concentrations were measured in venous blood samples collected every evening. Changes in sleep characteristics over time and associations between sleep characteristics and plasma cannabinoid concentrations were evaluated with repeated measures mixed linear regression. Results: Higher evening THC and 11-OH-THC concentrations were significantly associated with shorter sleep latency, less difficulty falling asleep, and more daytime sleep the following day. In contrast, the duration of calculated and self-reported nighttime sleep decreased slightly (3.54 and 5.34 minutes per night, respectively) but significantly during the study. Conclusions: These findings suggest that tolerance to the somnolent effects of THC may have occurred, but results should be considered preliminary due to design limitations. Scientific Significance: Somnolence from oral THC may dissipate with chronic, high-dose use. This has implications for patients who may take chronic oral THC for medicinal purposes, including cannabis dependence treatment. Adapted from the source document.
JF  - The American Journal on Addictions
AU  - Gorelick, David A
AU  - Goodwin, Robert S
AU  - Schwilke, Eugene
AU  - Schroeder, Jennifer R
AU  - Schwope, David M
AU  - Kelly, Deanna L
AU  - Ortemann-Renon, Catherine
AU  - Bonnet, Denis
AU  - Huestis, Marilyn A
AD  - Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Room 05A721, Baltimore, MD 21224
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 510
EP  - 514
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 5
SN  - 1055-0496, 1055-0496
KW  - Smoking
KW  - Volunteers
KW  - Men
KW  - Sleep
KW  - Cannabis
KW  - Hospitals
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463067752?accountid=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=Around-the-Clock+Oral+THC+Effects+on+Sleep+in+Male+Chronic+Daily+Cannabis+Smokers&rft.au=Gorelick%2C+David+A%3BGoodwin%2C+Robert+S%3BSchwilke%2C+Eugene%3BSchroeder%2C+Jennifer+R%3BSchwope%2C+David+M%3BKelly%2C+Deanna+L%3BOrtemann-Renon%2C+Catherine%3BBonnet%2C+Denis%3BHuestis%2C+Marilyn+A&rft.aulast=Gorelick&rft.aufirst=David&rft.date=2013-09-01&rft.volume=22&rft.issue=5&rft.spage=510&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fj.1521-0391.2013.12003.x
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Sleep; Cannabis; Smoking; Men; Hospitals; Volunteers
DO  - http://dx.doi.org/10.1111/j.1521-0391.2013.12003.x
ER  - 



TY  - JOUR
T1  - Facilitators and Barriers to Survey Participation by Physicians: A Call to Action for Researchers
AN  - 1449098828; 201323949
AB  - Surveys of health care providers are a well-established tool for obtaining information about the organization and delivery of care as well as about provider knowledge and attitudes. However, declining response rates to provider surveys are a widely acknowledged concern. Although a number of studies have identified specific methods for increasing response rates in health care provider-and particularly physician-surveys, few have addressed the more fundamental question of what motivates or deters providers from survey participation. We briefly review theoretical perspectives concerning why providers choose to participate in surveys, and what is known about facilitators and barriers to participation. We then describe several research designs (i.e., focus groups, key informant interviews, diary and office workflow studies, surveying the surveyors, and follow-back studies of respondents/nonrespondents) for obtaining empirical data on facilitators and barriers to survey participation, particularly by physicians and medical groups. Researchers must begin to build an evidence base for understanding provider decisions concerning survey participation. [Reprinted by permission of Sage Publications Inc., copyright holder.]
JF  - Evaluation & the Health Professions
AU  - Klabunde, Carrie N
AU  - Willis, Gordon B
AU  - Casalino, Lawrence P
AD  - Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 279
EP  - 295
PB  - Sage Publications, Thousand Oaks CA
VL  - 36
IS  - 3
SN  - 0163-2787, 0163-2787
KW  - survey physician response rates qualitative research clinicians
KW  - Attitudes
KW  - Doctors
KW  - Health care
KW  - Response rate
KW  - Diaries
KW  - Facilitators
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449098828?accountid=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=Evaluation+%26+the+Health+Professions&rft.atitle=Facilitators+and+Barriers+to+Survey+Participation+by+Physicians%3A+A+Call+to+Action+for+Researchers&rft.au=Klabunde%2C+Carrie+N%3BWillis%2C+Gordon+B%3BCasalino%2C+Lawrence+P&rft.aulast=Klabunde&rft.aufirst=Carrie&rft.date=2013-09-01&rft.volume=36&rft.issue=3&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Evaluation+%26+the+Health+Professions&rft.issn=01632787&rft_id=info:doi/10.1177%2F0163278713496426
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-11-01
N1  - Last updated - 2016-09-27
N1  - CODEN - EHPRDK
N1  - SubjectsTermNotLitGenreText - Facilitators; Health care; Doctors; Response rate; Attitudes; Diaries
DO  - http://dx.doi.org/10.1177/0163278713496426
ER  - 



TY  - JOUR
T1  - What Does It Take to Satisfy Koch's Postulates Two Centuries Later?: Microbial Genomics and Propionibacteria acnes
AN  - 1448215296; 18672867
AB  - For two centuries, Koch's postulates have set the gold standard for establishing the microbiological etiology of infection and disease. Genomic sequencing now brings finer resolution to both bacterial strain variation and the host genetic state that may predispose to disease. In this issue of the JID, Fitz-Gibbons and colleagues present strain-based resolution of Propionibacterium acnes and its association with the common teenage malady acne vulgaris. Here I examine how Koch's postulates were envisioned and incorporate this finer resolution of both host and microbial states.
JF  - Journal of Investigative Dermatology
AU  - Segre, Julia A
AD  - Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 2141
EP  - 2142
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 133
IS  - 9
SN  - 0022-202X, 0022-202X
KW  - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology
KW  - Etiology
KW  - Propionibacterium acnes
KW  - Acne
KW  - genomics
KW  - Infection
KW  - J 02310:Genetics & Taxonomy
KW  - A 01490:Miscellaneous
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448215296?accountid=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+Investigative+Dermatology&rft.atitle=What+Does+It+Take+to+Satisfy+Koch%27s+Postulates+Two+Centuries+Later%3F%3A+Microbial+Genomics+and+Propionibacteria+acnes&rft.au=Segre%2C+Julia+A&rft.aulast=Segre&rft.aufirst=Julia&rft.date=2013-09-01&rft.volume=133&rft.issue=9&rft.spage=2141&rft.isbn=&rft.btitle=&rft.title=Journal+of+Investigative+Dermatology&rft.issn=0022202X&rft_id=info:doi/10.1038%2Fjid.2013.260
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2014-04-17
N1  - SubjectsTermNotLitGenreText - Etiology; Acne; genomics; Infection; Propionibacterium acnes
DO  - http://dx.doi.org/10.1038/jid.2013.260
ER  - 



TY  - JOUR
T1  - Motivations to quit cannabis use in an adult non-treatment sample: Are they related to relapse?
AN  - 1443372681; 18610161
AB  - Background: The majority of cannabis smokers who quit do so without formal treatment, suggesting that motivations to quit are an important part of cessation process. However, little is known about how motivations relate to successful quitting. Method: A convenience sample of 385 non-treatment-seeking adult cannabis smokers (58% male, age 16-64 years at start of quit attempt) who made a "serious" (self-defined) quit attempt without formal treatment while not in a controlled environment were administered the 176-item Marijuana Quit Questionnaire (MJQQ) to assess their motivations to quit and outcome of the quit attempt Exploratory factor analysis was performed to identify significant motivational factors. Subgroup comparisons used t-tests and ANOVA. Cox proportional hazard regression and the General Linear Model were performed to evaluate the influence of motivational factors, gender, and age on relapse status at time of interview and risk of relapse over time, with time between quit attempt and interview as a covariate. Results: Exploratory factor analysis identified 6 motivational factors with eigenvalues > 1 which accounted for 58.4% of the total variance: self-image and self-control, health concerns, interpersonal relationship concerns, legal concerns, social acceptability concerns, and self-efficacy. Women were more likely than men to be motivated by self-image/self-control, health concerns, and social acceptability concerns. Older individuals were more likely to be motivated by health concerns. At the time of interview, 339 subjects had relapsed. Self-image and self-control, health concerns, interpersonal relationship concerns, and social acceptability concerns were associated with greater likelihood of abstinence at the study interview. Legal concerns and social acceptability concerns were associated with significantly lower hazard ratios (0.88, 0.83) for relapse during the abstinent period. Conclusion: These findings show gender and age differences in motivations to quit cannabis smoking and that adult cannabis smokers have motivations to quite similar to those of adolescent cannabis smokers and of adults who quit alcohol and tobacco use without formal treatment. The findings suggest areas of focus to improve secondary prevention and psychosocial treatment efforts.
JF  - Addictive Behaviors
AU  - Chauchard, E
AU  - Levin, KH
AU  - Copersino, M L
AU  - Heishman, S J
AU  - Gorelick, DA
AD  - National Institute on Drug Abuse, 251 Bayview Blvd., Suite 200, Baltimore, MD 21224, USA, emeline.chauchard@gmail.com
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 2422
EP  - 2427
VL  - 38
IS  - 9
SN  - 0306-4603, 0306-4603
KW  - Toxicology Abstracts; Risk Abstracts
KW  - Risk assessment
KW  - Alcohol
KW  - Inventories
KW  - Age
KW  - Motivation
KW  - Factor analysis
KW  - Adolescence
KW  - Acceptability
KW  - Sexual behavior
KW  - Age differences
KW  - Models
KW  - Smoking
KW  - Prevention
KW  - Gender
KW  - Cannabis
KW  - Tobacco
KW  - alcohols
KW  - Regression analysis
KW  - Adolescents
KW  - X 24380:Social Poisons & Drug Abuse
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443372681?accountid=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=Addictive+Behaviors&rft.atitle=Motivations+to+quit+cannabis+use+in+an+adult+non-treatment+sample%3A+Are+they+related+to+relapse%3F&rft.au=Chauchard%2C+E%3BLevin%2C+KH%3BCopersino%2C+M+L%3BHeishman%2C+S+J%3BGorelick%2C+DA&rft.aulast=Chauchard&rft.aufirst=E&rft.date=2013-09-01&rft.volume=38&rft.issue=9&rft.spage=2422&rft.isbn=&rft.btitle=&rft.title=Addictive+Behaviors&rft.issn=03064603&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Smoking; Inventories; Age; Motivation; Adolescence; Factor analysis; Regression analysis; alcohols; Tobacco; Cannabis; Age differences; Models; Risk assessment; Alcohol; Prevention; Gender; Acceptability; Sexual behavior; Adolescents
ER  - 



TY  - JOUR
T1  - Squamous cell carcinomas in patients with Fanconi anemia and dyskeratosis congenita: A search for human papillomavirus
AN  - 1443370410; 18602666
AB  - Patients with Fanconi anemia (FA) and dyskeratosis congenita (DC) are at high risk of head and neck squamous cell carcinomas (HNSCC) and anogenital squamous cell carcinomas (SCC). In the general population, these sites (particularly oropharyngeal SCC) may be associated with infection with human papillomavirus (HPV). In FA and DC, however, the majority of HNSCC occur in the oral cavity. We investigated the HPV status of HNSCC and vulvar SCC from nine patients with FA and four with DC using a very sensitive PCR assay, and found HPV16 DNA in only a single vulvar tumor from one patient with FA, and in none of the HNSCC. These results suggest that HPV may not be the cause of SCC in patients with FA or DC, and that vaccination may not reduce the incidence of HNSCC in these patients. What's new? The incidence of squamous cell carcinoma (SCC) of the oral cavity and gynecologic tract in patients with Fanconi anemia suggests a link to human papillomavirus (HPV) infection. However, the possibility of an association has not been studied extensively, and studies that have been conducted have produced conflicting results. This analysis of tumors from patients with Fanconi anemia or dyskeratosis congenita yielded no evidence for HPV causality, indicating that HPV vaccination may not reduce the incidence of SCC in these patients. The findings warrant etiological investigation into non-HPV mechanisms of SCC in these populations.
JF  - International Journal of Cancer
AU  - Alter, Blanche P
AU  - Giri, Neelam
AU  - Savage, Sharon A
AU  - Quint, Wim GV
AU  - Koning, Maurits NC
AU  - Schiffman, Mark
AD  - Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1513
EP  - 1515
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 133
IS  - 6
SN  - 0020-7136, 0020-7136
KW  - Virology & AIDS Abstracts; Health & Safety Science Abstracts; Risk Abstracts
KW  - Fanconi syndrome
KW  - Anemia
KW  - Human papillomavirus
KW  - V:22370
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/1443370410?accountid=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=Squamous+cell+carcinomas+in+patients+with+Fanconi+anemia+and+dyskeratosis+congenita%3A+A+search+for+human+papillomavirus&rft.au=Alter%2C+Blanche+P%3BGiri%2C+Neelam%3BSavage%2C+Sharon+A%3BQuint%2C+Wim+GV%3BKoning%2C+Maurits+NC%3BSchiffman%2C+Mark&rft.aulast=Alter&rft.aufirst=Blanche&rft.date=2013-09-01&rft.volume=133&rft.issue=6&rft.spage=1513&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28157
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Fanconi syndrome; Anemia; Human papillomavirus
DO  - http://dx.doi.org/10.1002/ijc.28157
ER  - 



TY  - JOUR
T1  - New Rapid Scheme for Distinguishing the Subspecies of the Mycobacterium abscessus Group and Identifying Mycobacterium massiliense Isolates with Inducible Clarithromycin Resistance
AN  - 1439223058; 18450213
AB  - Mycobacterium abscessus (M. abscessus sensu lato, or the M. abscessus group) comprises three closely related taxa whose taxonomic statuses are under revision, i.e., M. abscessus sensu stricto, Mycobacterium bolletii, and Mycobacterium massiliense. We describe here a simple, robust, and cost-effective PCR-based method for distinguishing among M. abscessus, M. massiliense, and M. bolletii. Based on the M. abscessus ATCC 19977T genome, regions that discriminated between M. abscessus and M. massiliense were identified through array-based comparative genomic hybridization. A typing scheme using PCR primers designed for four of these locations was applied to 46 well-characterized clinical isolates comprising 29 M. abscessus, 15 M. massiliense, and 2 M. bolletii isolates previously identified by multitarget sequencing. Interestingly, 2 isolates unequivocally identified as M. massiliense were shown to have a full-length erm(41) gene instead of the expected gene deletion and showed inducible clarithromycin resistance after 14 days. We propose using this PCR-based typing scheme combined with erm(41) PCR for straightforward identification of M. abscessus, M. massiliense, and M. bolletii and the assessment of inducible clarithromycin resistance. This method can be easily integrated into a routine workflow to provide subspecies-level identification within 24 h after isolation of the M. abscessus group.
JF  - Journal of Clinical Microbiology
AU  - Shallom, Shamira J
AU  - Gardina, Paul J
AU  - Myers, Timothy G
AU  - Sebastian, Yinong
AU  - Conville, Patricia
AU  - Calhoun, Leslie B
AU  - Tettelin, Herve
AU  - Olivier, Kenneth N
AU  - Uzel, Gulbu
AU  - Sampaio, Elizabeth P
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 2943
EP  - 2949
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 51
IS  - 9
SN  - 0095-1137, 0095-1137
KW  - Microbiology Abstracts B: Bacteriology
KW  - Genomes
KW  - Clinical isolates
KW  - Clarithromycin
KW  - Gene deletion
KW  - Typing
KW  - Mycobacterium abscessus
KW  - Mycobacterium
KW  - Polymerase chain reaction
KW  - Primers
KW  - genomics
KW  - J 02310:Genetics & Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439223058?accountid=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=New+Rapid+Scheme+for+Distinguishing+the+Subspecies+of+the+Mycobacterium+abscessus+Group+and+Identifying+Mycobacterium+massiliense+Isolates+with+Inducible+Clarithromycin+Resistance&rft.au=Shallom%2C+Shamira+J%3BGardina%2C+Paul+J%3BMyers%2C+Timothy+G%3BSebastian%2C+Yinong%3BConville%2C+Patricia%3BCalhoun%2C+Leslie+B%3BTettelin%2C+Herve%3BOlivier%2C+Kenneth+N%3BUzel%2C+Gulbu%3BSampaio%2C+Elizabeth+P&rft.aulast=Shallom&rft.aufirst=Shamira&rft.date=2013-09-01&rft.volume=51&rft.issue=9&rft.spage=2943&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.01132-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 30
N1  - Last updated - 2016-07-20
N1  - SubjectsTermNotLitGenreText - Clinical isolates; Genomes; Clarithromycin; Gene deletion; Typing; Polymerase chain reaction; Primers; genomics; Mycobacterium abscessus; Mycobacterium
DO  - http://dx.doi.org/10.1128/JCM.01132-13
ER  - 



TY  - JOUR
T1  - Mortality burden of the 2009-10 influenza pandemic in the United States: improving the timeliness of influenza severity estimates using inpatient mortality records
AN  - 1434032327; 18464550
AB  - Delays in the release of national vital statistics hinder timely assessment of influenza severity, especially during pandemics. Inpatient mortality records could provide timelier estimates of influenza-associated mortality. We compiled weekly age-specific deaths for various causes from US State Inpatient Databases (1990-2010) and national vital statistics (1990-2009). We calculated influenza-attributable excess deaths by season based on Poisson regression models driven by indicators of respiratory virus activity, seasonality, and temporal trends. Extrapolations of excess mortality from inpatient data fell within 11% and 17% of vital statistics estimates for pandemic and seasonal influenza, respectively, with high year-to-year correlation (Spearman's rho = 0.87-0.90, P < 0.001, n = 19). We attribute 14 800 excess respiratory and cardiac deaths (95% CI: 10 000-19 650) to pandemic influenza activity during April 2009-April 2010, 79% of which occurred in people under 65 years. Modeling inpatient mortality records provides useful estimates of influenza severity in advance of national vital statistics release, capturing both the magnitude and the age distribution of pandemic and epidemic deaths. We provide the first age- and cause-specific estimates of the 2009 pandemic mortality burden using traditional 'excess mortality' methods, confirming the unusual burden of this virus in young populations. Our inpatient-based approach could help monitor mortality trends in other infectious diseases.
JF  - Influenza and Other Respiratory Viruses
AU  - Charu, Vivek
AU  - Simonsen, Lone
AU  - Lustig, Roger
AU  - Steiner, Claudia
AU  - Viboud, Cecile
AD  - Fogarty International Center. National Institutes of Health
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 863
EP  - 871
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 7
IS  - 5
SN  - 1750-2640, 1750-2640
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - Age composition
KW  - Mortality
KW  - USA
KW  - V 22320:Replication
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434032327?accountid=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=Influenza+and+Other+Respiratory+Viruses&rft.atitle=Mortality+burden+of+the+2009-10+influenza+pandemic+in+the+United+States%3A+improving+the+timeliness+of+influenza+severity+estimates+using+inpatient+mortality+records&rft.au=Charu%2C+Vivek%3BSimonsen%2C+Lone%3BLustig%2C+Roger%3BSteiner%2C+Claudia%3BViboud%2C+Cecile&rft.aulast=Charu&rft.aufirst=Vivek&rft.date=2013-09-01&rft.volume=7&rft.issue=5&rft.spage=863&rft.isbn=&rft.btitle=&rft.title=Influenza+and+Other+Respiratory+Viruses&rft.issn=17502640&rft_id=info:doi/10.1111%2Firv.12096
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Mortality; USA
DO  - http://dx.doi.org/10.1111/irv.12096
ER  - 



TY  - JOUR
T1  - The great balancing act: regulation and fate of antiviral T-cell interactions
AN  - 1434032005; 18464504
AB  - The fate of T lymphocytes revolves around a continuous stream of interactions between the T-cell receptor (TCR) and peptide-major histocompatibility complex (MHC) molecules. Beginning in the thymus and continuing into the periphery, these interactions, refined by accessory molecules, direct the expansion, differentiation, and function of T-cell subsets. The cellular context of T-cell engagement with antigen-presenting cells, either in lymphoid or non-lymphoid tissues, plays an important role in determining how these cells respond to antigen encounters. CD8+ T cells are essential for clearance of a lymphocytic choriomeningitis virus (LCMV) infection, but the virus can present a number of unique challenges that antiviral T cells must overcome. Peripheral LCMV infection can lead to rapid cytolytic clearance or chronic viral persistence; central nervous system infection can result in T-cell-dependent fatal meningitis or an asymptomatic carrier state amenable to immunotherapeutic clearance. These diverse outcomes all depend on interactions that require TCR engagement of cognate peptide-MHC complexes. In this review, we explore the diversity in antiviral T-cell behaviors resulting from TCR engagement, beginning with an overview of the immunological synapse and progressing to regulators of TCR signaling that shape the delicate balance between immunopathology and viral clearance.
JF  - Immunological Reviews
AU  - Moseman, EAshley
AU  - McGavern, Dorian B
AD  - 1National Institute of Neurological Disorders and Stroke. National Institutes of Health
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 110
EP  - 124
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 255
IS  - 1
SN  - 0105-2896, 0105-2896
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Immunology Abstracts
KW  - Central nervous system
KW  - T-cell receptor
KW  - Thymus
KW  - Major histocompatibility complex
KW  - CD8 antigen
KW  - Streams
KW  - Meningitis
KW  - Lymphocytic choriomeningitis virus
KW  - Differentiation
KW  - Reviews
KW  - Chronic infection
KW  - Lymphocytes T
KW  - Antigen-presenting cells
KW  - Immunological synapses
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22350:Immunology
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434032005?accountid=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=Immunological+Reviews&rft.atitle=The+great+balancing+act%3A+regulation+and+fate+of+antiviral+T-cell+interactions&rft.au=Moseman%2C+EAshley%3BMcGavern%2C+Dorian+B&rft.aulast=Moseman&rft.aufirst=EAshley&rft.date=2013-09-01&rft.volume=255&rft.issue=1&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Immunological+Reviews&rft.issn=01052896&rft_id=info:doi/10.1111%2Fimr.12093
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-09-03
N1  - SubjectsTermNotLitGenreText - Central nervous system; T-cell receptor; Thymus; Major histocompatibility complex; CD8 antigen; Streams; Meningitis; Differentiation; Reviews; Chronic infection; Lymphocytes T; Antigen-presenting cells; Immunological synapses; Lymphocytic choriomeningitis virus
DO  - http://dx.doi.org/10.1111/imr.12093
ER  - 



TY  - JOUR
T1  - Evaluation of partial k-space strategies to speed up time-domain EPR imaging
AN  - 1434030801; 18510686
AB  - Narrow-line spin probes derived from the trityl radical have led to the development of fast in vivo time-domain EPR imaging. Pure phase-encoding imaging modalities based on the single-point imaging scheme have demonstrated the feasibility of three-dimensional oximetric images with functional information in minutes. In this article, we explore techniques to improve the temporal resolution and circumvent the relatively short biological half-lives of trityl probes using partial k-space strategies. There are two main approaches: one involves the use of the Hermitian character of the k-space by which only part of the k-space is measured and the unmeasured part is generated using the Hermitian symmetry. This approach is limited in success by the accuracy of numerical estimate of the phase roll in the k-space that corrupts the Hermiticy. The other approach is to measure only a judicially chosen reduced region of k-space (a centrosymmetric ellipsoid region) that more or less accounts for >70% of the k-space energy. Both of these aspects were explored in Fourier transform-EPR imaging with a doubling of scan speed demonstrated by considering ellipsoid geometry of the k-space. Partial k-space strategies help improve the temporal resolution in studying fast dynamics of functional aspects in vivo with infused spin probes. Magn Reson Med 70:745-753, 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Magnetic Resonance in Medicine
AU  - Subramanian, Sankaran
AU  - Chandramouli, Gadisetti VR
AU  - McMillan, Alan
AU  - Gullapalli, Rao P
AU  - Devasahayam, Nallathamby
AU  - Mitchell, James B
AU  - Matsumoto, Shingo
AU  - Krishna, Murali C
AD  - Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 745
EP  - 753
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 70
IS  - 3
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - E.S.R.
KW  - Energy
KW  - Magnetic resonance imaging
KW  - Probes
KW  - imaging
KW  - Spin probes
KW  - Radicals
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434030801?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluation+of+partial+k-space+strategies+to+speed+up+time-domain+EPR+imaging&rft.au=Subramanian%2C+Sankaran%3BChandramouli%2C+Gadisetti+VR%3BMcMillan%2C+Alan%3BGullapalli%2C+Rao+P%3BDevasahayam%2C+Nallathamby%3BMitchell%2C+James+B%3BMatsumoto%2C+Shingo%3BKrishna%2C+Murali+C&rft.aulast=Subramanian&rft.aufirst=Sankaran&rft.date=2013-09-01&rft.volume=70&rft.issue=3&rft.spage=745&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24508
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - E.S.R.; Energy; Magnetic resonance imaging; Probes; imaging; Spin probes; Radicals
DO  - http://dx.doi.org/10.1002/mrm.24508
ER  - 



TY  - JOUR
T1  - Advances in antiviral vaccine development
AN  - 1434029160; 18464506
AB  - Antiviral vaccines have been the most successful biomedical intervention for preventing epidemic viral disease. Vaccination for smallpox in humans and rinderpest in cattle was the basis for disease eradication, and recent progress in polio eradication is promising. Although early vaccines were developed empirically by passage in live animals or eggs, more recent vaccines have been developed because of the advent of new technologies, particularly cell culture and molecular biology. Recent technological advances in gene delivery and expression, nanoparticles, protein manufacturing, and adjuvants have created the potential for new vaccine platforms that may provide solutions for vaccines against viral pathogens for which no interventions currently exist. In addition, the technological convergence of human monoclonal antibody isolation, structural biology, and high-throughput sequencing is providing new opportunities for atomic-level immunogen design. Selection of human monoclonal antibodies can identify immunodominant antigenic sites associated with neutralization and provide reagents for stabilizing and solving the structure of viral surface proteins. Understanding the structural basis for neutralization can guide selection of vaccine targets. Deep sequencing of the antibody repertoire and defining the ontogeny of the desired antibody responses can reveal the junctional recombination and somatic mutation requirements for B-cell recognition and affinity maturation. Collectively, this information will provide new strategic approaches for selecting vaccine antigens, formulations, and regimens. Moreover, it creates the potential for rational vaccine design and establishing a catalogue of vaccine technology platforms that would be effective against any given family or class of viral pathogens and improve our readiness to address new emerging viral threats.
JF  - Immunological Reviews
AU  - Graham, Barney S
AD  - NIAID NIH. Vaccine Research Center
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 230
EP  - 242
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 255
IS  - 1
SN  - 0105-2896, 0105-2896
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Immunology Abstracts
KW  - Epidemics
KW  - Monoclonal antibodies
KW  - Lymphocytes B
KW  - Rinderpest
KW  - Cell culture
KW  - Adjuvants
KW  - Pathogens
KW  - Eggs
KW  - Smallpox
KW  - Recombination
KW  - Gene transfer
KW  - Convergence
KW  - Ontogeny
KW  - Vaccines
KW  - nanoparticles
KW  - Mutation
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22350:Immunology
KW  - F 06900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434029160?accountid=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=Immunological+Reviews&rft.atitle=Advances+in+antiviral+vaccine+development&rft.au=Graham%2C+Barney+S&rft.aulast=Graham&rft.aufirst=Barney&rft.date=2013-09-01&rft.volume=255&rft.issue=1&rft.spage=230&rft.isbn=&rft.btitle=&rft.title=Immunological+Reviews&rft.issn=01052896&rft_id=info:doi/10.1111%2Fimr.12098
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-09-03
N1  - SubjectsTermNotLitGenreText - Epidemics; Lymphocytes B; Monoclonal antibodies; Rinderpest; Cell culture; Pathogens; Adjuvants; Eggs; Smallpox; Recombination; Convergence; Gene transfer; Ontogeny; Vaccines; Mutation; nanoparticles
DO  - http://dx.doi.org/10.1111/imr.12098
ER  - 



TY  - JOUR
T1  - Accuracy Loss Due to Selection Bias in Cohort Studies with Left Truncation
AN  - 1434027480; 18436396
AB  - Selection is a common problem in paediatric and perinatal epidemiology, and truncation can be thought of as missing person time that can result in selection bias. Left truncation, also known as late or staggered entry, may induce selection bias and/or adversely affect precision. There are two kinds of left truncation: fixed left truncation where the start of follow-up is initiated at a set time, and variable left truncation where follow-up begins at a stochastically varying time-point. Using data from a time-to-pregnancy study, augmented by a simulation study, we demonstrate the effects of fixed and variable truncation on estimates of the hazard ratio. First, fixed or variable non-differential left truncation results in a loss of precision. Fixed or variable differential left truncation results in a bias either towards or away from the null as well as a loss of precision. The extent and direction of this bias is a function of the size and direction of the association between exposure and outcome, and occurs in common scenarios and under a wide range of conditions. As demonstrated in simulation studies, selection bias due to left truncation could have a serious impact on inferences, especially in the case of fixed or variable differential left truncation. When present in epidemiologic studies, proper accounting for left truncation is just as important as proper accounting for right censoring.
JF  - Paediatric and Perinatal Epidemiology
AU  - Schisterman, Enrique F
AU  - Cole, Stephen R
AU  - Ye, Aijun
AU  - Platt, Robert W
AD  - Division of Epidemiology, Statistics, and Prevention Research. Eunice Kennedy Shriver National Institute of Child Health and Human Development
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 491
EP  - 502
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 27
IS  - 5
SN  - 0269-5022, 0269-5022
KW  - Health & Safety Science Abstracts
KW  - Simulation
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434027480?accountid=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=Paediatric+and+Perinatal+Epidemiology&rft.atitle=Accuracy+Loss+Due+to+Selection+Bias+in+Cohort+Studies+with+Left+Truncation&rft.au=Schisterman%2C+Enrique+F%3BCole%2C+Stephen+R%3BYe%2C+Aijun%3BPlatt%2C+Robert+W&rft.aulast=Schisterman&rft.aufirst=Enrique&rft.date=2013-09-01&rft.volume=27&rft.issue=5&rft.spage=491&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+Perinatal+Epidemiology&rft.issn=02695022&rft_id=info:doi/10.1111%2Fppe.12073
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-08-03
N1  - SubjectsTermNotLitGenreText - Simulation
DO  - http://dx.doi.org/10.1111/ppe.12073
ER  - 



TY  - JOUR
T1  - Fetal Intelligent Navigation Echocardiography ( FINE ): a novel method for rapid, simple, and automatic examination of the fetal heart
AN  - 1434023879; 18540812
AB  - Objective To describe a novel method (Fetal Intelligent Navigation Echocardiography ( FINE )) for visualization of standard fetal echocardiography views from volume datasets obtained with spatiotemporal image correlation ( STIC ) and application of 'intelligent navigation' technology. Methods We developed a method to: 1) demonstrate nine cardiac diagnostic planes; and 2) spontaneously navigate the anatomy surrounding each of the nine cardiac diagnostic planes (Virtual Intelligent Sonographer Assistance ( VIS -Assistance registered )). The method consists of marking seven anatomical structures of the fetal heart. The following echocardiography views are then automatically generated: 1) four chamber; 2) five chamber; 3) left ventricular outflow tract; 4) short-axis view of great vessels/right ventricular outflow tract; 5) three vessels and trachea; 6) abdomen/stomach; 7) ductal arch; 8) aortic arch; and 9) superior and inferior vena cava. The FINE method was tested in a separate set of 50 STIC volumes of normal hearts (18.6-37.2weeks of gestation), and visualization rates for fetal echocardiography views using diagnostic planes and/or VIS -Assistance registered were calculated. To examine the feasibility of identifying abnormal cardiac anatomy, we tested the method in four cases with proven congenital heart defects (coarctation of aorta, tetralogy of Fallot, transposition of great vessels and pulmonary atresia with intact ventricular septum). Results In normal cases, the FINE method was able to generate nine fetal echocardiography views using: 1) diagnostic planes in 78-100% of cases; 2) VIS -Assistance registered in 98-100% of cases; and 3) a combination of diagnostic planes and/or VIS -Assistance registered in 98-100% of cases. In all four abnormal cases, the FINE method demonstrated evidence of abnormal fetal cardiac anatomy. Conclusions The FINE method can be used to visualize nine standard fetal echocardiography views in normal hearts by applying 'intelligent navigation' technology to STIC volume datasets. This method can simplify examination of the fetal heart and reduce operator dependency. The observation of abnormal echocardiography views in the diagnostic planes and/or VIS -Assistance registered should raise the index of suspicion for congenital heart disease. Published 2013. This article is a U.S. Government work and is in the public domain in the USA
JF  - Ultrasound in Obstetrics and Gynecology
AU  - Yeo, Lami
AU  - Romero, Roberto
AD  - Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, USA and Detroit, MI, USA.
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 268
EP  - 284
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 42
IS  - 3
SN  - 0960-7692, 0960-7692
KW  - Biotechnology and Bioengineering Abstracts
KW  - Heart
KW  - Gynecology
KW  - Aorta
KW  - Abdomen
KW  - Echocardiography
KW  - Transposition
KW  - Fetuses
KW  - Ventricle
KW  - Lung
KW  - Aortic arch
KW  - Gestation
KW  - Septum
KW  - tetralogy of Fallot
KW  - Obstetrics
KW  - Trachea
KW  - Ultrasound
KW  - Stomach
KW  - Heart diseases
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434023879?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fetal+Intelligent+Navigation+Echocardiography+%28+FINE+%29%3A+a+novel+method+for+rapid%2C+simple%2C+and+automatic+examination+of+the+fetal+heart&rft.au=Yeo%2C+Lami%3BRomero%2C+Roberto&rft.aulast=Yeo&rft.aufirst=Lami&rft.date=2013-09-01&rft.volume=42&rft.issue=3&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=Ultrasound+in+Obstetrics+and+Gynecology&rft.issn=09607692&rft_id=info:doi/10.1002%2Fuog.12563
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Heart; Gynecology; Abdomen; Aorta; Echocardiography; Transposition; Fetuses; Ventricle; Aortic arch; Lung; Gestation; Septum; tetralogy of Fallot; Ultrasound; Trachea; Obstetrics; Stomach; Heart diseases
DO  - http://dx.doi.org/10.1002/uog.12563
ER  - 



TY  - JOUR
T1  - Glucocorticoid receptor dimerization is required for proper recovery of LPS-induced inflammation, sickness behavior and metabolism in mice
AN  - 1434022765; 18441660
AB  - Endogenous glucocorticoids are essential for mobilizing energy resources, restraining inflammatory responses and coordinating behavior to an immune challenge. Impaired glucocorticoid receptor (GR) function has been associated with impaired metabolic processes, enhanced inflammation and exaggerated sickness and depressive-like behaviors. To discern the molecular mechanisms underlying GR regulation of physiologic and behavioral responses to a systemic immune challenge, GR super(dim) mice, in which absent GR dimerization leads to impaired GR-DNA-binding-dependent mechanisms but intact GR protein-protein interactions, were administered low-dose lipopolysaccharide (LPS). GR super(dim)-LPS mice exhibited elevated and prolonged levels of plasma corticosterone (CORT), interleukin (IL)-6 and IL-10 (but not plasma tumor necrosis factor- alpha (TNF alpha )), enhanced early expression of brain TNF alpha , IL-1 beta and IL-6 mRNA levels, and impaired later central TNF alpha mRNA expression. Exaggerated sickness behavior (lethargy, piloerection, ptosis) in the GR super(dim)-LPS mice was associated with increased early brain proinflammatory cytokine expression and late plasma CORT levels, but decreased late brain TNF alpha expression. GR super(dim)-LPS mice also exhibited sustained locomotor impairment in the open field, body weight loss and metabolic alterations measured by indirect calorimetry, as well as impaired thermoregulation. Taken together, these data indicate that GR dimerization-dependent DNA-binding mechanisms differentially regulate systemic and central cytokine expression in a cytokine- and time-specific manner, and are essential for the proper regulation and recovery of multiple physiologic responses to low-dose endotoxin. Moreover, these results support the concept that GR protein-protein interactions are not sufficient for glucocorticoids to exert their full anti-inflammatory effects and suggest that glucocorticoid responses limited to GR monomer-mediated transcriptional effects could predispose individuals to prolonged behavioral and metabolic sequelae of an enhanced inflammatory state.
JF  - Molecular Psychiatry
AU  - Silverman, M N
AU  - Mukhopadhyay, P
AU  - Belyavskaya, E
AU  - Tonelli, L H
AU  - Revenis, B D
AU  - Doran, J H
AU  - Ballard, B E
AU  - Tam, J
AU  - Pacher, P
AU  - Sternberg, E M
AD  - Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 1006
EP  - 1017
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 18
IS  - 9
SN  - 1359-4184, 1359-4184
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - Body weight loss
KW  - Inflammation
KW  - N3 11001:Behavioral and Cognitive Neuroscience
KW  - X 24370:Natural Toxins
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434022765?accountid=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=Molecular+Psychiatry&rft.atitle=Glucocorticoid+receptor+dimerization+is+required+for+proper+recovery+of+LPS-induced+inflammation%2C+sickness+behavior+and+metabolism+in+mice&rft.au=Silverman%2C+M+N%3BMukhopadhyay%2C+P%3BBelyavskaya%2C+E%3BTonelli%2C+L+H%3BRevenis%2C+B+D%3BDoran%2C+J+H%3BBallard%2C+B+E%3BTam%2C+J%3BPacher%2C+P%3BSternberg%2C+E+M&rft.aulast=Silverman&rft.aufirst=M&rft.date=2013-09-01&rft.volume=18&rft.issue=9&rft.spage=1006&rft.isbn=&rft.btitle=&rft.title=Molecular+Psychiatry&rft.issn=13594184&rft_id=info:doi/10.1038%2Fmp.2012.131
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Inflammation
DO  - http://dx.doi.org/10.1038/mp.2012.131
ER  - 



TY  - JOUR
T1  - Evolutionary Dynamics of the Prokaryotic Adaptive Immunity System CRISPR-Cas in an Explicit Ecological Context
AN  - 1434015002; 18450148
AB  - A stochastic, agent-based mathematical model of the coevolution of the archaeal and bacterial adaptive immunity system, CRISPR-Cas, and lytic viruses shows that CRISPR-Cas immunity can stabilize the virus-host coexistence rather than leading to the extinction of the virus. In the model, CRISPR-Cas immunity does not specifically promote viral diversity, presumably because the selection pressure on each single proto-spacer is too weak. However, the overall virus diversity in the presence of CRISPR-Cas grows due to the increase of the host and, accordingly, the virus population size. Above a threshold value of total viral diversity, which is proportional to the viral mutation rate and population size, the CRISPR-Cas system becomes ineffective and is lost due to the associated fitness cost. Our previous modeling study has suggested that the ubiquity of CRISPR-Cas in hyperthermophiles, which contrasts its comparative low prevalence in mesophiles, is due to lower rates of mutation fixation in thermal habitats. The present findings offer a complementary, simpler perspective on this contrast through the larger population sizes of mesophiles compared to hyperthermophiles, because of which CRISPR-Cas can become ineffective in mesophiles. The efficacy of CRISPR-Cas sharply increases with the number of proto-spacers per viral genome, potentially explaining the low information content of the proto-spacer-associated motif (PAM) that is required for spacer acquisition by CRISPR-Cas because a higher specificity would restrict the number of spacers available to CRISPR-Cas, thus hampering immunity. The very existence of the PAM might reflect the tradeoff between the requirement of diverse spacers for efficient immunity and avoidance of autoimmunity.
JF  - Journal of Bacteriology
AU  - Iranzo, Jaime
AU  - Lobkovsky, Alexander E
AU  - Wolf, Yuri I
AU  - Koonin, Eugene V
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 3834
EP  - 3844
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 195
IS  - 17
SN  - 0021-9193, 0021-9193
KW  - Microbiology Abstracts B: Bacteriology
KW  - Genomes
KW  - Fitness
KW  - Mathematical models
KW  - Coevolution
KW  - Extinction
KW  - Autoimmunity
KW  - hyperthermophiles
KW  - Coexistence
KW  - Spacer
KW  - Immunity
KW  - Habitat
KW  - Mutation rates
KW  - Stochasticity
KW  - Evolution
KW  - J 02450:Ecology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434015002?accountid=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=Evolutionary+Dynamics+of+the+Prokaryotic+Adaptive+Immunity+System+CRISPR-Cas+in+an+Explicit+Ecological+Context&rft.au=Iranzo%2C+Jaime%3BLobkovsky%2C+Alexander+E%3BWolf%2C+Yuri+I%3BKoonin%2C+Eugene+V&rft.aulast=Iranzo&rft.aufirst=Jaime&rft.date=2013-09-01&rft.volume=195&rft.issue=17&rft.spage=3834&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.00412-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Number of references - 88
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Fitness; Genomes; Mathematical models; Extinction; Coevolution; hyperthermophiles; Autoimmunity; Spacer; Coexistence; Immunity; Mutation rates; Habitat; Stochasticity; Evolution
DO  - http://dx.doi.org/10.1128/JB.00412-13
ER  - 



TY  - JOUR
T1  - Small-Molecule Inhibitors of Lethal Factor Protease Activity Protect against Anthrax Infection
AN  - 1434014703; 18450047
AB  - Bacillus anthracis, the causative agent of anthrax, manifests its pathogenesis through the action of two secreted toxins. The bipartite lethal and edema toxins, a combination of lethal factor or edema factor with the protein protective antigen, are important virulence factors for this bacterium. We previously developed small-molecule inhibitors of lethal factor proteolytic activity (LFIs) and demonstrated their in vivo efficacy in a rat lethal toxin challenge model. In this work, we show that these LFIs protect against lethality caused by anthrax infection in mice when combined with subprotective doses of either antibiotics or neutralizing monoclonal antibodies that target edema factor. Significantly, these inhibitors provided protection against lethal infection when administered as a monotherapy. As little as two doses (10 mg/kg) administered at 2 h and 8 h after spore infection was sufficient to provide a significant survival benefit in infected mice. Administration of LFIs early in the infection was found to inhibit dissemination of vegetative bacteria to the organs in the first 32 h following infection. In addition, neutralizing antibodies against edema factor also inhibited bacterial dissemination with similar efficacy. Together, our findings confirm the important roles that both anthrax toxins play in establishing anthrax infection and demonstrate the potential for small-molecule therapeutics targeting these proteins.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Moayeri, Mahtab
AU  - Crown, Devorah
AU  - Jiao, Guan-Sheng
AU  - Kim, Seongjin
AU  - Johnson, Alan
AU  - Leysath, Clinton
AU  - Leppla, Stephen H
Y1  - 2013/09//
PY  - 2013
DA  - Sep 2013
SP  - 4139
EP  - 4145
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 9
SN  - 0066-4804, 0066-4804
KW  - Toxicology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Animal models
KW  - Bacillus anthracis
KW  - Infection
KW  - A 01340:Antibiotics & Antimicrobials
KW  - X 24370:Natural Toxins
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434014703?accountid=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=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Small-Molecule+Inhibitors+of+Lethal+Factor+Protease+Activity+Protect+against+Anthrax+Infection&rft.au=Moayeri%2C+Mahtab%3BCrown%2C+Devorah%3BJiao%2C+Guan-Sheng%3BKim%2C+Seongjin%3BJohnson%2C+Alan%3BLeysath%2C+Clinton%3BLeppla%2C+Stephen+H&rft.aulast=Moayeri&rft.aufirst=Mahtab&rft.date=2013-09-01&rft.volume=57&rft.issue=9&rft.spage=4139&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00941-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Number of references - 1
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Infection; Bacillus anthracis
DO  - http://dx.doi.org/10.1128/AAC.00941-13
ER  - 



TY  - JOUR
T1  - Phase II study of satraplatin and prednisone in patients with metastatic castration-resistant prostate cancer: a pharmacogenetic assessment of outcome and toxicity.
AN  - 1429217966; 23684781
AB  - We assessed the effect of excision repair cross-complementing group 1 (ERCC1) and x-ray cross-complementing group 1 (XRCC1) gene polymorphisms on treatment outcomes with satraplatin and prednisone in patients with metastatic castration-resistant prostate cancer previously treated with docetaxel-based therapy.
          Twenty-four patients were enrolled in this single arm study. The primary objective was to determine if the presence of ERCC1 Asn118Asn (N118N, 500C>T, rs11615) and XRCC1 Arg399Gln (R399Q, 1301G>A, rs25487) genetic variants might be associated with an impact on progression-free survival (PFS); secondary objectives included overall response, survival, and toxicity.
          After population stratification by race, white patients carrying heterozygous or variant genotypes at the ERCC1 C>T locus had a >3-fold longer median PFS (5.8 vs. 1.8 months; 2P = .18, adjusted) and 5-fold longer median overall survival (OS) (15.7 vs. 3.2 months; 2P = .010, adjusted) than did patients carrying only wild-type alleles. For the XRCC1 G>A variant, without regard to race, patients carrying the wild-type GG alleles had a longer PFS (9.3 months) than those carrying GA or AA alleles (2.7 months; 2P = .02). Similarly, those carrying GG alleles did not reach median OS, whereas those carrying GA or AA alleles had a median OS of 9.6 months (2P = .12, adjusted). Multivariable analysis by using Cox proportional hazards modeling demonstrated that only XRCC1 was associated with PFS.
          To our knowledge, this is the first prospective study to date in patients with metastatic castration-resistant prostate cancer that describes predictive germline polymorphisms of ERCC1 and XRCC1 for assessing the clinical activity of satraplatin. Published by Elsevier Inc.
JF  - Clinical genitourinary cancer
AU  - Figg, William D
AU  - Chau, Cindy H
AU  - Madan, Ravi A
AU  - Gulley, James L
AU  - Gao, Rui
AU  - Sissung, Tristan M
AU  - Spencer, Shawn
AU  - Beatson, Melony
AU  - Aragon-Ching, Jeanny
AU  - Steinberg, Seth M
AU  - Dahut, William L
AD  - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. figgw@helix.nih.gov.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 229
EP  - 237
VL  - 11
IS  - 3
KW  - DNA-Binding Proteins
KW  - 0
KW  - Organoplatinum Compounds
KW  - Taxoids
KW  - X-ray repair cross complementing protein 1
KW  - docetaxel
KW  - 15H5577CQD
KW  - satraplatin
KW  - 8D7B37T28G
KW  - ERCC1 protein, human
KW  - EC 3.1.-
KW  - Endonucleases
KW  - Prednisone
KW  - VB0R961HZT
KW  - Index Medicus
KW  - Satraplatin
KW  - Prostate cancer
KW  - Genotyping
KW  - XRCC1
KW  - ERCC1
KW  - Polymorphism, Single Nucleotide
KW  - Disease-Free Survival
KW  - Humans
KW  - Aged
KW  - Adenocarcinoma -- genetics
KW  - Antineoplastic Combined Chemotherapy Protocols -- pharmacology
KW  - Taxoids -- therapeutic use
KW  - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW  - Genotype
KW  - Aged, 80 and over
KW  - Neoplasm Metastasis -- drug therapy
KW  - Drug Resistance, Neoplasm -- genetics
KW  - Treatment Outcome
KW  - Middle Aged
KW  - Adenocarcinoma -- drug therapy
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Male
KW  - Prednisone -- pharmacology
KW  - Prednisone -- adverse effects
KW  - Organoplatinum Compounds -- adverse effects
KW  - Organoplatinum Compounds -- pharmacology
KW  - Prednisone -- therapeutic use
KW  - Prostatic Neoplasms, Castration-Resistant -- genetics
KW  - Organoplatinum Compounds -- therapeutic use
KW  - DNA-Binding Proteins -- genetics
KW  - Endonucleases -- genetics
KW  - Prostatic Neoplasms, Castration-Resistant -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1429217966?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+genitourinary+cancer&rft.atitle=Phase+II+study+of+satraplatin+and+prednisone+in+patients+with+metastatic+castration-resistant+prostate+cancer%3A+a+pharmacogenetic+assessment+of+outcome+and+toxicity.&rft.au=Figg%2C+William+D%3BChau%2C+Cindy+H%3BMadan%2C+Ravi+A%3BGulley%2C+James+L%3BGao%2C+Rui%3BSissung%2C+Tristan+M%3BSpencer%2C+Shawn%3BBeatson%2C+Melony%3BAragon-Ching%2C+Jeanny%3BSteinberg%2C+Seth+M%3BDahut%2C+William+L&rft.aulast=Figg&rft.aufirst=William&rft.date=2013-09-01&rft.volume=11&rft.issue=3&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Clinical+genitourinary+cancer&rft.issn=1938-0682&rft_id=info:doi/10.1016%2Fj.clgc.2013.04.007
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-31
N1  - Date created - 2013-08-30
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143]
Med Oncol. 2012 Sep;29(3):1622-8 [21805378]
Carcinogenesis. 2000 May;21(5):965-71 [10783319]
Anticancer Res. 2001 Jul-Aug;21(4B):3075-9 [11712813]
Cancer Res. 2001 Dec 15;61(24):8654-8 [11751380]
Lung Cancer. 2004 Jun;44(3):311-6 [15140544]
J Clin Oncol. 2004 Jul 1;22(13):2594-601 [15173214]
Clin Cancer Res. 2004 Aug 1;10(15):4939-43 [15297394]
N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213]
N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214]
Cancer Res. 1992 Oct 15;52(20):5674-80 [1327513]
Cancer Res. 1993 Jun 1;53(11):2581-6 [8388318]
Br J Cancer. 1993 Aug;68(2):240-50 [8347478] Int J Cancer. 1995 Sep 15;62(6):717-23 [7558420]
Cancer Treat Rev. 1998 Oct;24(5):331-44 [9861196]
Cancer Res. 1999 Jun 1;59(11):2557-61 [10363972]
Invest New Drugs. 2005 Jan;23(1):79-84 [15528984]
Oncology. 2005;68(1):2-9 [15741753]
Clin Cancer Res. 2005 Sep 1;11(17):6100-2 [16144907]
Clin Cancer Res. 2005 Sep 1;11(17):6212-7 [16144923]
Clin Adv Hematol Oncol. 2003 Mar;1(3):162-6 [16224397]
Cancer. 2006 Jun 1;106(11):2421-7 [16649224]
Exp Mol Med. 2006 Jun 30;38(3):320-4 [16819291]
J Clin Oncol. 2006 Aug 10;24(23):3789-98 [16785472]
Br J Cancer. 2006 Sep 4;95(5):561-70 [16880786]
J Clin Oncol. 2006 Sep 10;24(26):4333-9 [16896002]
Gynecol Oncol. 2006 Dec;103(3):1031-7 [16875718]
Cancer Chemother Pharmacol. 2007 Feb;59(3):301-12 [16770583]
Ann Oncol. 2007 Mar;18(3):522-8 [17229776]
Lung Cancer. 2007 May;56(2):281-8 [17222938]
Cancer Chemother Pharmacol. 2007 Sep;60(4):589-600 [17541592]
Eur J Hum Genet. 2007 Oct;15(10):1049-53 [17593927]
J Clin Oncol. 2007 Nov 20;25(33):5172-9 [18024864]
J Clin Oncol. 2008 Jan 10;26(2):242-5 [18182665]
Int J Oncol. 2008 May;32(5):1091-6 [18425336]
Mol Cancer Ther. 2008 May;7(5):1246-50 [18483312]
Int J Gynecol Cancer. 2008 Jul-Aug;18(4):702-10 [17961161]
Carcinogenesis. 2008 Sep;29(9):1758-64 [18332046]
Clin Lung Cancer. 2009 Mar;10(2):118-23 [19362955]
J Clin Oncol. 2009 Jun 10;27(17):2863-73 [19332728]
J Exp Clin Cancer Res. 2009;28:91 [19563645]
J Clin Oncol. 2009 Nov 10;27(32):5431-8 [19805692]
Dalton Trans. 2010 Sep 21;39(35):8113-27 [20593091]
Jpn J Clin Oncol. 2010 Oct;40(10):954-60 [20462983]
Lancet. 2010 Oct 2;376(9747):1147-54 [20888992]
Mutat Res. 2011 Mar 15;708(1-2):21-7 [21315089]
Cancer Sci. 2009 Feb;100(2):278-83 [19068092]
N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468]
Gynecol Oncol. 2011 Jul;122(1):121-6 [21496891]
Arch Med Res. 2011 Jul;42(5):412-20 [21827803]
Pharmacogenomics. 2011 Dec;12(12):1641-52 [22026922]
Lung Cancer. 2012 Jan;75(1):102-9 [21676483]
Mutagenesis. 2012 Jan;27(1):67-76 [22002622]
CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781]
Pharmacogenomics. 2012 Mar;13(4):419-27 [22329723]
Tumour Biol. 2012 Jun;33(3):877-84 [22249976]
Carcinogenesis. 2000 Apr;21(4):551-5 [10753184]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.clgc.2013.04.007
ER  - 



TY  - JOUR
T1  - Functional and pharmacodynamic evaluation of metronomic cyclophosphamide and docetaxel regimen in castration-resistant prostate cancer.
AN  - 1428772941; 23980684
AB  - The aim of our study was to investigate the association of docetaxel and metronomic cyclophosphamide (CYC) in castration-resistant prostate cancer (CRPC).
          CRPC xenografts were established with PC3 cells. Mice were treated with a combination of CYC (50 mg/kg/day) and docetaxel (10-30 mg/kg/week) or with docetaxel alone. Docetaxel plasma levels were analyzed in patients receiving the drug alone or combined with CYC. Metronomic CYC is an effective adjuvant in blocking tumor growth in vivo, with comparable efficacy and less toxic effects compared with docetaxel treatment. CYC acts by downregulating cell proliferation and inducing apoptosis thorough upregulation of p21 and inhibition of angiogenesis. Finally, CYC increases docetaxel plasma levels in patients.
          Metronomic CYC exerts anti-tumoral effects in an in vivo model of prostate cancer and in patients with CRPC, and also increases the bioavailability of docetaxel. These results explain the favorable toxicity and activity profiles observed in patients treated with this regimen.
JF  - Future oncology (London, England)
AU  - Cardillo, Irene
AU  - Spugnini, Enrico P
AU  - Galluzzo, Paola
AU  - Contestabile, Michela
AU  - Dell'Anna, Maria Lucia
AU  - Picardo, Mauro
AU  - Crispi, Stefania
AU  - Calogero, Raffaele A
AU  - Piccolo, Maria Teresa
AU  - Arigoni, Maddalena
AU  - Cantarella, Daniela
AU  - Boccellino, Mariarosaria
AU  - Quagliuolo, Lucio
AU  - Ferretti, Gianluigi
AU  - Carlini, Paolo
AU  - Felici, Alessandra
AU  - Boccardo, Francesco
AU  - Cognetti, Francesco
AU  - Baldi, Alfonso
AD  - SAFU Department, Regina Elena National Cancer Institute, Via E. Chianesi 53, Rome, Italy.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 1375
EP  - 1388
VL  - 9
IS  - 9
KW  - Biomarkers, Tumor
KW  - 0
KW  - RNA, Messenger
KW  - Taxoids
KW  - docetaxel
KW  - 15H5577CQD
KW  - Cyclophosphamide
KW  - 8N3DW7272P
KW  - Index Medicus
KW  - Real-Time Polymerase Chain Reaction
KW  - Cyclophosphamide -- administration & dosage
KW  - Animals
KW  - Oligonucleotide Array Sequence Analysis
KW  - Humans
KW  - Aged
KW  - Mice
KW  - Mice, Nude
KW  - Reverse Transcriptase Polymerase Chain Reaction
KW  - RNA, Messenger -- genetics
KW  - Taxoids -- administration & dosage
KW  - Gene Expression Profiling
KW  - Blotting, Western
KW  - Tumor Cells, Cultured
KW  - Xenograft Model Antitumor Assays
KW  - Flow Cytometry
KW  - Immunoenzyme Techniques
KW  - Male
KW  - Cell Proliferation -- drug effects
KW  - Biomarkers, Tumor -- metabolism
KW  - Biomarkers, Tumor -- genetics
KW  - Prostatic Neoplasms, Castration-Resistant -- pathology
KW  - Prostatic Neoplasms, Castration-Resistant -- metabolism
KW  - Apoptosis -- drug effects
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Prostatic Neoplasms, Castration-Resistant -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1428772941?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Future+oncology+%28London%2C+England%29&rft.atitle=Functional+and+pharmacodynamic+evaluation+of+metronomic+cyclophosphamide+and+docetaxel+regimen+in+castration-resistant+prostate+cancer.&rft.au=Cardillo%2C+Irene%3BSpugnini%2C+Enrico+P%3BGalluzzo%2C+Paola%3BContestabile%2C+Michela%3BDell%27Anna%2C+Maria+Lucia%3BPicardo%2C+Mauro%3BCrispi%2C+Stefania%3BCalogero%2C+Raffaele+A%3BPiccolo%2C+Maria+Teresa%3BArigoni%2C+Maddalena%3BCantarella%2C+Daniela%3BBoccellino%2C+Mariarosaria%3BQuagliuolo%2C+Lucio%3BFerretti%2C+Gianluigi%3BCarlini%2C+Paolo%3BFelici%2C+Alessandra%3BBoccardo%2C+Francesco%3BCognetti%2C+Francesco%3BBaldi%2C+Alfonso&rft.aulast=Cardillo&rft.aufirst=Irene&rft.date=2013-09-01&rft.volume=9&rft.issue=9&rft.spage=1375&rft.isbn=&rft.btitle=&rft.title=Future+oncology+%28London%2C+England%29&rft.issn=1744-8301&rft_id=info:doi/10.2217%2Ffon.13.99
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-11
N1  - Date created - 2013-08-28
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.2217/fon.13.99
ER  - 



TY  - JOUR
T1  - Phase I study of intraprostatic vaccine administration in men with locally recurrent or progressive prostate cancer.
AN  - 1428772658; 23836412
AB  - The primary end point of this study was to determine the safety and feasibility of intraprostatic administration of PSA-TRICOM vaccine [encoding transgenes for prostate-specific antigen (PSA) and 3 costimulatory molecules] in patients with locally recurrent or progressive prostate cancer. This trial was a standard 3 + 3 dose escalation with 6 patients each in cohorts 4 and 5 to gather more immunologic data. Nineteen of 21 patients enrolled had locally recurrent prostate cancer after definitive radiation therapy, and 2 had no local therapy. All cohorts received initial subcutaneous vaccination with recombinant vaccinia (rV)-PSA-TRICOM and intraprostatic booster vaccinations with recombinant fowlpox (rF)-PSA-TRICOM. Cohorts 3-5 also received intraprostatic rF-GM-CSF. Cohort 5 received additional subcutaneous boosters with rF-PSA-TRICOM and rF-GM-CSF. Patients had pre- and post-treatment prostate biopsies, and analyses of peripheral and intraprostatic immune cells were performed. There were no dose-limiting toxicities, and the maximum tolerated dose was not reached. The most common grade 2 adverse events were fever (38%) and subcutaneous injection site reactions (33%); the single grade 3 toxicity was transient fever. Overall, 19 of 21 patients on trial had stable (10) or improved (9) PSA values. There was a marked increase in CD4+ (p = 0.0002) and CD8+ (p = 0.0002) tumor infiltrates in post- versus pre-treatment tumor biopsies. Four of 9 patients evaluated had peripheral immune responses to PSA or NGEP. Intraprostatic administration of PSA-TRICOM is safe and feasible and can generate a significant immunologic response. Improved serum PSA kinetics and intense post-vaccination inflammatory infiltrates were seen in the majority of patients. Clinical trials examining clinical end points are warranted.
JF  - Cancer immunology, immunotherapy : CII
AU  - Gulley, James L
AU  - Heery, Christopher R
AU  - Madan, Ravi A
AU  - Walter, Beatriz A
AU  - Merino, Maria J
AU  - Dahut, William L
AU  - Tsang, Kwong-Yok
AU  - Schlom, Jeffrey
AU  - Pinto, Peter A
AD  - Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Dr., 8B09 MSC 1750, Bethesda, MD 20892, USA. gulleyj@mail.nih.gov
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 1521
EP  - 1531
VL  - 62
IS  - 9
KW  - Cancer Vaccines
KW  - 0
KW  - Kallikreins
KW  - EC 3.4.21.-
KW  - kallikrein-related peptidase 3, human
KW  - Prostate-Specific Antigen
KW  - EC 3.4.21.77
KW  - Index Medicus
KW  - Kallikreins -- immunology
KW  - Injections, Intralesional
KW  - Kallikreins -- genetics
KW  - Lymphocytes, Tumor-Infiltrating -- immunology
KW  - Kallikreins -- blood
KW  - Humans
KW  - Transgenes
KW  - Prostate-Specific Antigen -- immunology
KW  - Prostate-Specific Antigen -- genetics
KW  - Aged
KW  - Neoplasm Recurrence, Local -- immunology
KW  - Prostate-Specific Antigen -- blood
KW  - Cohort Studies
KW  - Middle Aged
KW  - Neoplasm Recurrence, Local -- therapy
KW  - T-Lymphocytes -- immunology
KW  - Male
KW  - Prostatic Neoplasms, Castration-Resistant -- therapy
KW  - Cancer Vaccines -- administration & dosage
KW  - Cancer Vaccines -- adverse effects
KW  - Cancer Vaccines -- genetics
KW  - Prostatic Neoplasms, Castration-Resistant -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1428772658?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+study+of+intraprostatic+vaccine+administration+in+men+with+locally+recurrent+or+progressive+prostate+cancer.&rft.au=Gulley%2C+James+L%3BHeery%2C+Christopher+R%3BMadan%2C+Ravi+A%3BWalter%2C+Beatriz+A%3BMerino%2C+Maria+J%3BDahut%2C+William+L%3BTsang%2C+Kwong-Yok%3BSchlom%2C+Jeffrey%3BPinto%2C+Peter+A&rft.aulast=Gulley&rft.aufirst=James&rft.date=2013-09-01&rft.volume=62&rft.issue=9&rft.spage=1521&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.issn=1432-0851&rft_id=info:doi/10.1007%2Fs00262-013-1448-0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-08
N1  - Date created - 2013-08-28
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s00262-013-1448-0
ER  - 



TY  - JOUR
T1  - Role of the vaccinia virus O3 protein in cell entry can be fulfilled by its Sequence flexible transmembrane domain.
AN  - 1428269399; 23816434
AB  - The vaccinia virus O3 protein, a component of the entry-fusion complex, is encoded by all chordopoxviruses. We constructed truncation mutants and demonstrated that the transmembrane domain, which comprises two-thirds of this 35 amino acid protein, is necessary and sufficient for interaction with the entry-fusion complex and function in cell entry. Nevertheless, neither single amino acid substitutions nor alanine scanning mutagenesis revealed essential amino acids within the transmembrane domain. Moreover, replication-competent mutant viruses were generated by randomization of 10 amino acids of the transmembrane domain. Of eight unique viruses, two contained only two amino acids in common with wild type and the remainder contained one or none within the randomized sequence. Although these mutant viruses formed normal size plaques, the entry-fusion complex did not co-purify with the mutant O3 proteins suggesting a less stable interaction. Thus, despite low specific sequence requirements, the transmembrane domain is sufficient for function in entry. 
          Published by Elsevier Inc.
JF  - Virology
AU  - Satheshkumar, P S
AU  - Chavre, James
AU  - Moss, Bernard
AD  - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 33 North Drive, MSC 3210, Bethesda, MD 20892-3210, USA.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 148
EP  - 157
VL  - 444
IS  - 1-2
KW  - Mutant Proteins
KW  - 0
KW  - Viral Fusion Proteins
KW  - Index Medicus
KW  - Entry–fusion complex
KW  - Poxvirus entry
KW  - Membrane fusion
KW  - Transmembrane protein
KW  - Mutagenesis
KW  - Mutant Proteins -- genetics
KW  - Mutant Proteins -- metabolism
KW  - DNA Mutational Analysis
KW  - Amino Acid Substitution
KW  - Sequence Deletion
KW  - Vaccinia virus -- physiology
KW  - Viral Fusion Proteins -- metabolism
KW  - Virus Internalization
KW  - Viral Fusion Proteins -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1428269399?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Role+of+the+vaccinia+virus+O3+protein+in+cell+entry+can+be+fulfilled+by+its+Sequence+flexible+transmembrane+domain.&rft.au=Satheshkumar%2C+P+S%3BChavre%2C+James%3BMoss%2C+Bernard&rft.aulast=Satheshkumar&rft.aufirst=P&rft.date=2013-09-01&rft.volume=444&rft.issue=1-2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=1096-0341&rft_id=info:doi/10.1016%2Fj.virol.2013.06.003
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-06
N1  - Date created - 2013-08-26
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Protein Eng Des Sel. 2005 Dec;18(12):559-61 [16239261]
J Virol. 2005 Sep;79(17):10988-98 [16103150]
J Virol. 2000 Apr;74(7):3353-65 [10708453]
J Virol. 2004 Mar;78(5):2357-66 [14963132]
J Virol. 1998 Feb;72(2):1577-85 [9445060]
J Virol. 1999 Oct;73(10):8750-61 [10482629]
J Virol. 2005 Apr;79(8):4744-54 [15795260]
J Virol. 2006 Jan;80(1):51-61 [16352530]
Virology. 2006 Jan 5;344(1):48-54 [16364735]
Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18572-7 [16339313]
J Virol. 2006 Sep;80(17):8402-10 [16912291]
J Virol. 2006 Sep;80(18):8899-908 [16940502]
J Virol. 2006 Oct;80(19):9455-64 [16973551]
J Virol. 2006 Oct;80(19):9822-30 [16973586]
J Virol. 2007 Mar;81(5):2149-57 [17166913]
J Virol. 2007 Jun;81(12):6286-93 [17409143]
Science. 2008 Apr 25;320(5875):531-5 [18436786]
J Virol. 2008 Aug;82(16):7988-99 [18550675]
J Virol. 2008 Sep;82(17):8687-94 [18596103]
J Virol. 2008 Oct;82(20):10247-61 [18701587]
Virology. 2009 Mar 15;385(2):383-91 [19162290]
Virology. 2009 Jun 20;389(1-2):132-40 [19428041]
J Virol. 2009 Dec;83(24):12822-32 [19812151]
Proc Natl Acad Sci U S A. 2010 May 18;107(20):9346-51 [20439710]
J Virol. 2010 Sep;84(17):8422-32 [20538855]
Protein Eng Des Sel. 2011 Mar;24(3):311-20 [21149273]
PLoS One. 2011;6(2):e17248 [21347205]
PLoS Pathog. 2011 Dec;7(12):e1002446 [22194690]
J Virol. 2012 Feb;86(3):1696-705 [22114343]
Virology. 2012 Nov 25;433(2):506-12 [22999097]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.virol.2013.06.003
ER  - 



TY  - JOUR
T1  - Identification of 2-piperidone as a biomarker of CYP2E1 activity through metabolomic phenotyping.
AN  - 1427748575; 23811823
AB  - Cytochrome P450 2E1 (CYP2E1) is a key enzyme in the metabolic activation of many low molecular weight toxicants and also an important contributor to oxidative stress. A noninvasive method to monitor CYP2E1 activity in vivo would be of great value for studying the role of CYP2E1 in chemical-induced toxicities and stress-related diseases. In this study, a mass spectrometry-based metabolomic approach was used to identify a metabolite biomarker of CYP2E1 through comparing the urine metabolomes of wild-type (WT), Cyp2e1-null, and CYP2E1-humanized mice. Metabolomic analysis with multivariate models of urine metabolites revealed a clear separation of Cyp2e1-null mice from WT and CYP2E1-humanized mice in the multivariate models of urine metabolomes. Subsequently, 2-piperidone was identified as a urinary metabolite that inversely correlated to the CYP2E1 activity in the three mouse lines. Backcrossing of WT and Cyp2e1-null mice, together with targeted analysis of 2-piperidone in mouse serum, confirmed the genotype dependency of 2-piperidone. The accumulation of 2-piperidone in the Cyp2e1-null mice was mainly caused by the changes in the biosynthesis and degradation of 2-piperidone because compared with the WT mice, the conversion of cadaverine to 2-piperidone was higher, whereas the metabolism of 2-piperidone to 6-hydroxy-2-piperidone was lower in the Cyp2e1-null mice. Overall, untargeted metabolomic analysis identified a correlation between 2-piperidone concentrations in urine and the expression and activity of CYP2E1, thus providing a noninvasive metabolite biomarker that can be potentially used in to monitor CYP2E1 activity.
JF  - Toxicological sciences : an official journal of the Society of Toxicology
AU  - Cheng, Jie
AU  - Chen, Chi
AU  - Kristopher, Krausz W
AU  - Manna, Soumen K
AU  - Scerba, Mike
AU  - Friedman, Fred K
AU  - Luecke, Hans
AU  - Idle, Jeffrey R
AU  - Gonzalez, Frank J
AD  - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 37
EP  - 47
VL  - 135
IS  - 1
KW  - Biomarkers
KW  - 0
KW  - Piperidones
KW  - Cytochrome P-450 CYP2E1
KW  - EC 1.14.13.-
KW  - Cadaverine
KW  - L90BEN6OLL
KW  - 2-piperidone
KW  - WLN0GQQ6EK
KW  - Index Medicus
KW  - biomarker
KW  - cadaverine.
KW  - CYP2E1
KW  - metabolomics
KW  - Phenotype
KW  - Animals
KW  - Mice
KW  - Tandem Mass Spectrometry
KW  - Cadaverine -- metabolism
KW  - Female
KW  - Metabolomics -- methods
KW  - Piperidones -- urine
KW  - Cytochrome P-450 CYP2E1 -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427748575?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+2-piperidone+as+a+biomarker+of+CYP2E1+activity+through+metabolomic+phenotyping.&rft.au=Cheng%2C+Jie%3BChen%2C+Chi%3BKristopher%2C+Krausz+W%3BManna%2C+Soumen+K%3BScerba%2C+Mike%3BFriedman%2C+Fred+K%3BLuecke%2C+Hans%3BIdle%2C+Jeffrey+R%3BGonzalez%2C+Frank+J&rft.aulast=Cheng&rft.aufirst=Jie&rft.date=2013-09-01&rft.volume=135&rft.issue=1&rft.spage=37&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%2Fkft143
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-14
N1  - Date created - 2013-08-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Annu Rev Pharmacol Toxicol. 2004;44:27-42 [14744237]
Toxicol Lett. 2012 Mar 7;209(2):161-5 [22222162]
Br J Clin Pharmacol. 2004 Aug;58(2):190-200 [15255802]
Methods Cell Biol. 1976;13:29-83 [177845]
J Neurochem. 1984 Dec;43(6):1631-4 [6436440]
Eur J Clin Nutr. 1993 Oct;47(10):683-90 [7505741]
J Biol Chem. 1996 May 17;271(20):12063-7 [8662637]
J Nutr. 1997 May;127(5 Suppl):838S-841S [9164249]
Pharmacology. 1998 May;56(5):262-6 [9597694]
Biochem Pharmacol. 1999 Aug 1;58(3):461-3 [10424765]
J Pharmacol Exp Ther. 1999 Oct;291(1):213-9 [10490907]
Mutat Res. 2005 Jan 6;569(1-2):101-10 [15603755]
Drug Metab Dispos. 2005 Mar;33(3):449-57 [15576447]
Curr Drug Metab. 2007 Jun;8(5):493-8 [17584020]
Drug Metab Rev. 2007;39(2-3):581-97 [17786640]
J Biol Chem. 2008 Feb 22;283(8):4543-59 [18093979]
Anal Bioanal Chem. 2009 Jul;394(6):1545-56 [19333587]
Expert Opin Drug Metab Toxicol. 2010 Mar;6(3):307-19 [20073996]
Diabetes. 2010 Aug;59(8):2001-9 [20522591]
Biotechnol J. 2010 Oct;5(10):1050-9 [20931601]
Mol Biol Rep. 2011 Apr;38(4):2409-16 [21076874]
J Food Sci. 2010 Sep;75(7):R139-50 [21535566]
Chemphyschem. 2011 Jul 11;12(10):1822-32 [21618379]
Chem Biol Interact. 2011 Aug 15;193(1):50-6 [21600194]
In Vivo. 2011 Sep-Oct;25(5):803-12 [21753138]
Pharmacol Rev. 2011 Sep;63(3):684-99 [21737533]
Clin Res Hepatol Gastroenterol. 2011 Oct;35(10):630-7 [21664213]
Annu Rev Pharmacol Toxicol. 2012;52:37-56 [21819238]
Molecules. 2011;17(1):61-79 [22269864]
Arch Biochem Biophys. 2000 Dec 15;384(2):383-90 [11368328]
Med Chem. 2012 Mar;8(2):208-21 [22385180]
Mol Med Rep. 2012 Aug;6(2):416-20 [22614694]
J Hepatol. 2012 Oct;57(4):860-6 [22668639]
J Appl Toxicol. 2013 Feb;33(2):100-8 [21915887]
Amino Acids. 2004 Jun;26(3):217-33 [15221502]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/toxsci/kft143
ER  - 



TY  - JOUR
T1  - The avian XPR1 gammaretrovirus receptor is under positive selection and is disabled in bird species in contact with virus-infected wild mice.
AN  - 1427744759; 23843647
AB  - Xenotropic mouse leukemia viruses (X-MLVs) are broadly infectious for mammals except most of the classical strains of laboratory mice. These gammaretroviruses rely on the XPR1 receptor for entry, and the unique resistance of laboratory mice is due to two mutations in different putative XPR1 extracellular loops. Cells from avian species differ in susceptibility to X-MLVs, and 2 replacement mutations in the virus-resistant chicken XPR1 (K496Q and Q579E) distinguish it from the more permissive duck and quail receptors. These substitutions align with the two mutations that disable the laboratory mouse XPR1. Mutagenesis of the chicken and duck genes confirms that residues at both sites are critical for virus entry. Among 32 avian species, the 2 disabling XPR1 mutations are found together only in the chicken, an omnivorous, ground-dwelling fowl that was domesticated in India and/or Southeast Asia, which is also where X-MLV-infected house mice evolved. The receptor-disabling mutations are also present separately in 5 additional fowl and raptor species, all of which are native to areas of Asia populated by the virus-infected subspecies Mus musculus castaneus. Phylogenetic analysis showed that the avian XPR1 gene is under positive selection at sites implicated in receptor function, suggesting a defensive role for XPR1 in the avian lineage. Contact between bird species and virus-infected mice may thus have favored selection of mouse virus-resistant receptor orthologs in the birds, and our data suggest that similar receptor-disabling mutations were fixed in mammalian and avian species exposed to similar virus challenges.
JF  - Journal of virology
AU  - Martin, Carrie
AU  - Buckler-White, Alicia
AU  - Wollenberg, Kurt
AU  - Kozak, Christine A
AD  - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 10094
EP  - 10104
VL  - 87
IS  - 18
KW  - Receptors, G-Protein-Coupled
KW  - 0
KW  - Receptors, Virus
KW  - xenotropic and polytropic retrovirus receptor
KW  - Index Medicus
KW  - Poultry Diseases -- genetics
KW  - Animals
KW  - Chickens
KW  - Ducks
KW  - Disease Resistance
KW  - DNA Mutational Analysis
KW  - Molecular Sequence Data
KW  - Poultry Diseases -- immunology
KW  - Mice
KW  - Sequence Analysis, DNA
KW  - Asia
KW  - Retroviridae Infections -- immunology
KW  - Receptors, G-Protein-Coupled -- metabolism
KW  - Xenotropic murine leukemia virus-related virus -- physiology
KW  - Receptors, G-Protein-Coupled -- genetics
KW  - Receptors, Virus -- metabolism
KW  - Receptors, Virus -- genetics
KW  - Virus Internalization
KW  - Selection, Genetic
KW  - Retroviridae Infections -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427744759?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+avian+XPR1+gammaretrovirus+receptor+is+under+positive+selection+and+is+disabled+in+bird+species+in+contact+with+virus-infected+wild+mice.&rft.au=Martin%2C+Carrie%3BBuckler-White%2C+Alicia%3BWollenberg%2C+Kurt%3BKozak%2C+Christine+A&rft.aulast=Martin&rft.aufirst=Carrie&rft.date=2013-09-01&rft.volume=87&rft.issue=18&rft.spage=10094&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.01327-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-06
N1  - Date created - 2013-08-23
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - JX294442; GENBANK; JX294441; JX294440; JX294446; JX294445; JX294444; JX294443; JX294449; JX294448; JX294447; JX294451; JX294450; JX294453; JX294452; JX294455; JX294436; JX294437; JX294454; JX294457; JX294438; JX294456; JX294439; JX294432; JX294458; JX294433; JX294434; JX294435; JX294430; JX294431
N1  - SuppNotes - Cited By:
J Virol. 2007 Oct;81(19):10550-7 [17634227]
Curr Top Microbiol Immunol. 2007;315:85-111 [17848062]
PLoS Genet. 2008 Feb;4(2):e1000010 [18454198]
Science. 2008 Jun 27;320(5884):1763-8 [18583609]
BMC Evol Biol. 2008;8:174 [18544161]
Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3259-63 [19221034]
Retrovirology. 2009;6:87 [19811656]
Sci China C Life Sci. 2009 Nov;52(11):1030-5 [19937201]
Nature. 2010 Apr 1;464(7289):757-62 [20360741]
PLoS One. 2010;5(5):e10639 [20502703]
PLoS Pathog. 2010;6:e1000974 [20617165]
PLoS Biol. 2010;8(9). pii: e1000475. doi: 10.1371/journal.pbio.1000475 [20838655]
J Virol. 2010 Nov;84(22):11970-80 [20844050]
J Virol. 2010 Dec;84(24):12841-9 [20943975]
Retrovirology. 2010;7:101 [21118532]
J Virol. 2011 Feb;85(3):1205-13 [21084477]
Nat Genet. 2011 Jul;43(7):648-55 [21623374]
MBio. 2012;3(5):e00344-12 [23073767]
Nature. 2013 Jan 3;493(7430):51-5 [23235831]
J Virol. 1987 Jul;61(7):2225-31 [3035222]
J Virol. 1987 Oct;61(10):3082-8 [3041030]
Mol Biol Evol. 1988 Jan;5(1):63-78 [2833677]
Virology. 1989 Nov;173(1):58-67 [2554579]
J Virol. 1992 Jan;66(1):78-84 [1370096]
Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6792-5 [8692897]
Comput Appl Biosci. 1997 Oct;13(5):555-6 [9367129]
Hum Mol Genet. 1998 Mar;7(3):399-406 [9466996]
Genetics. 1972 Oct;72(2):239-52 [4345996]
Science. 1973 Dec 14;182(4117):1151-3 [4356281]
Nature. 1975 Jan 10;253(5487):140-2 [163009]
Int J Cancer. 1975 Feb 15;15(2):211-20 [47844]
Virology. 1975 Sep;67(1):288-91 [170737]
Proc Natl Acad Sci U S A. 1975 Dec;72(12):5150-5 [1061100]
J Natl Cancer Inst. 1976 Feb;56(2):423-6 [176389]
Proc Natl Acad Sci U S A. 1977 Feb;74(2):789-92 [191826]
Int J Cancer. 1978 Oct 15;22(4):495-502 [212379]
J Natl Cancer Inst. 1979 Jan;62(1):63-70 [214610]
Cell. 1979 Jul;17(3):623-34 [225036]
J Exp Med. 1980 Mar 1;151(3):542-52 [6244357]
J Virol. 1981 Sep;39(3):777-91 [6270351]
Nucleic Acids Res. 1982 Jan 22;10(2):459-72 [7063411]
J Virol. 1982 Jul;43(1):1-7 [6286989]
J Virol. 1984 Jul;51(1):77-80 [6328046]
J Virol. 1984 Nov;52(2):695-8 [6092693]
Virology. 1985 Jan 30;140(2):239-48 [2982233]
J Virol. 1987 Apr;61(4):1037-44 [3029398]
Genome. 1998 Feb;41(1):104-10 [9549063]
Am J Hum Genet. 1998 Jun;62(6):1507-15 [9585595]
Proc Natl Acad Sci U S A. 1999 Feb 2;96(3):927-32 [9927670]
J Virol. 1999 Mar;73(3):2442-9 [9971829]
Nat Genet. 1999 Feb;21(2):216-9 [9988277]
Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1385-90 [9990033]
J Virol. 1999 Nov;73(11):9362-8 [10516044]
Nature. 2004 Dec 9;432(7018):695-716 [15592404]
Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2832-7 [15689398]
Mol Phylogenet Evol. 2006 Jan;38(1):12-9 [16275023]
Nature. 2006 Jul 6;442(7098):79-81 [16823453]
Mol Biol Evol. 2006 Oct;23(10):1891-901 [16818476]
Biol Lett. 2006 Dec 22;2(4):543-7 [17148284]
Proc Natl Acad Sci U S A. 2007 Jan 30;104(5):1655-60 [17234809]
Virology. 2007 Dec 20;369(2):229-33 [17870141]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1128/JVI.01327-13
ER  - 



TY  - JOUR
T1  - Determinants of buildup of the toxic dopamine metabolite DOPAL in Parkinson's disease.
AN  - 1427744739; 23786406
AB  - Intra-neuronal metabolism of dopamine (DA) begins with production of 3,4-dihydroxyphenylacetaldehyde (DOPAL),which is toxic. According to the 'catecholaldehyde hypothesis', DOPAL destroys nigrostriatal DA terminals and contributes to the profound putamen DA deficiency that characterizes Parkinson’s disease (PD). We tested the feasibility of using post-mortem patterns of putamen tissue catechols to examine contributions of altered activities of the type 2 vesicular monoamine transporter (VMAT2) and aldehyde dehydrogenase(ALDH) to the increased DOPAL levels found in PD. Theoretically, the DA : DOPA concentration ratio indicates vesicular uptake, and the 3,4-dihydroxyphenylacetic acid: DOPAL ratio indicates ALDH activity. We validated these indices in transgenic mice with very low vesicular uptake VMAT2-Lo) or with knockouts of the genes encoding ALDH1A1 and ALDH2 (ALDH1A1,2 KO), applied these indices in PD putamen, and estimated the percent decreases in vesicular uptake and ALDH activity in PD. VMAT2-Lo mice had markedly decreased DA:DOPA (50 vs. 1377, p < 0.0001),and ALDH1A1,2 KO mice had decreased 3,4-dihydroxyphenylacetic acid:DOPAL (1.0 vs. 11.2, p < 0.0001). In PD putamen, vesicular uptake was estimated to be decreased by 89% and ALDH activity by 70%. Elevated DOPAL levels in PD putamen reflect a combination of decreased vesicular uptake of cytosolic DA and decreased DOPAL detoxification by ALDH. Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
JF  - Journal of neurochemistry
AU  - Goldstein, David S
AU  - Sullivan, Patti
AU  - Holmes, Courtney
AU  - Miller, Gary W
AU  - Alter, Shawn
AU  - Strong, Randy
AU  - Mash, Deborah C
AU  - Kopin, Irwin J
AU  - Sharabi, Yehonatan
AD  - Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1620, USA. goldsteind@ninds.nih.gov
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 591
EP  - 603
VL  - 126
IS  - 5
KW  - Catechols
KW  - 0
KW  - SLC18A2 protein, human
KW  - Vesicular Monoamine Transport Proteins
KW  - 3,4-Dihydroxyphenylacetic Acid
KW  - 102-32-9
KW  - 3,4-dihydroxyphenylacetaldehyde
KW  - 5707-55-1
KW  - Dihydroxyphenylalanine
KW  - 63-84-3
KW  - ALDH1A1 protein, human
KW  - EC 1.2.1.3
KW  - ALDH2 protein, human
KW  - Aldehyde Dehydrogenase
KW  - Aldehyde Dehydrogenase, Mitochondrial
KW  - Dopamine
KW  - VTD58H1Z2X
KW  - Index Medicus
KW  - dopamine
KW  - DOPET
KW  - Parkinson's disease
KW  - monoamine oxidase
KW  - DOPAC
KW  - DOPAL
KW  - Animals
KW  - Vesicular Monoamine Transport Proteins -- physiology
KW  - Vesicular Monoamine Transport Proteins -- metabolism
KW  - Aldehyde Dehydrogenase -- genetics
KW  - Catechols -- metabolism
KW  - Brain Chemistry
KW  - Humans
KW  - Aged
KW  - Mice
KW  - Mice, Knockout
KW  - Aldehyde Dehydrogenase -- physiology
KW  - Putamen -- metabolism
KW  - Mice, Inbred C57BL
KW  - Dihydroxyphenylalanine -- metabolism
KW  - Aldehyde Dehydrogenase -- metabolism
KW  - Female
KW  - Male
KW  - 3,4-Dihydroxyphenylacetic Acid -- metabolism
KW  - Parkinson Disease -- metabolism
KW  - Dopamine -- metabolism
KW  - 3,4-Dihydroxyphenylacetic Acid -- analogs & derivatives
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427744739?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Determinants+of+buildup+of+the+toxic+dopamine+metabolite+DOPAL+in+Parkinson%27s+disease.&rft.au=Goldstein%2C+David+S%3BSullivan%2C+Patti%3BHolmes%2C+Courtney%3BMiller%2C+Gary+W%3BAlter%2C+Shawn%3BStrong%2C+Randy%3BMash%2C+Deborah+C%3BKopin%2C+Irwin+J%3BSharabi%2C+Yehonatan&rft.aulast=Goldstein&rft.aufirst=David&rft.date=2013-09-01&rft.volume=126&rft.issue=5&rft.spage=591&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=1471-4159&rft_id=info:doi/10.1111%2Fjnc.12345
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-28
N1  - Date created - 2013-08-23
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Klin Wochenschr. 1960 Dec 15;38:1236-9 [13726012]
Acta Pharmacol Sin. 2005 Jan;26(1):17-26 [15659109]
Ann N Y Acad Sci. 2005 Aug;1053:356-75 [16179542]
J Cereb Blood Flow Metab. 2006 Sep;26(9):1198-212 [16421508]
J Nucl Med. 2006 Nov;47(11):1769-77 [17079809]
Pharmacol Rev. 2007 Jun;59(2):125-50 [17379813]
J Neurosci. 2007 Jul 25;27(30):8138-48 [17652604]
Chem Res Toxicol. 2007 Oct;20(10):1536-42 [17887726]
Acta Neuropathol. 2008 Feb;115(2):193-203 [17965867]
Arch Neurol. 2008 Aug;65(8):1074-80 [18695057]
Toxicol In Vitro. 2008 Sep;22(6):1461-8 [18579341]
J Neurochem. 2008 Sep;106(5):2205-17 [18643795]
Mol Neurobiol. 2009 Apr;39(2):149-70 [19259829]
J Neurosci. 2009 Jun 24;29(25):8103-13 [19553450]
Chem Res Toxicol. 2009 Jul;22(7):1256-63 [19537779]
Nat Genet. 2009 Dec;41(12):1303-7 [19915576]
J Nucl Med. 2010 Feb;51(2):223-8 [20080893]
Clin Chem. 2010 May;56(5):832-8 [20207766]
J Neural Transm (Vienna). 2010 Dec;117(12):1387-93 [21069393]
PLoS One. 2010;5(12):e15251 [21179455]
Eur J Neurol. 2011 May;18(5):703-10 [21073636]
J Biol Chem. 2011 Jul 29;286(30):26978-86 [21642436]
J Cereb Blood Flow Metab. 2011 Oct;31(10):2065-75 [21522164]
PLoS One. 2012;7(2):e31522 [22384032]
Brain. 2012 Jun;135(Pt 6):1900-13 [22451506]
Neurobiol Dis. 2012 Sep;47(3):367-77 [22659302]
Cell Mol Neurobiol. 2012 Jul;32(5):661-6 [22297542]
Mol Neurodegener. 2012;7:26 [22651796]
J Neurochem. 2012 Dec;123(6):932-43 [22906103]
Proc Natl Acad Sci U S A. 2013 Jan 8;110(2):636-41 [23267077]
J Pharmacol Exp Ther. 2000 May;293(2):336-42 [10773000]
Chem Biol Interact. 2001 Jan 30;130-132(1-3):469-80 [11306068]
Brain Res Mol Brain Res. 2001 Sep 10;93(1):1-7 [11532332]
Naunyn Schmiedebergs Arch Pharmacol. 2002 Jan;365(1):38-49 [11862332]
Mol Pharmacol. 2002 Oct;62(4):795-805 [12237326]
Brain Res. 2003 Nov 7;989(2):205-13 [14556942]
Science. 2003 Oct 31;302(5646):841 [14593171]
Neurobiol Dis. 2003 Dec;14(3):637-47 [14678778]
Neurotoxicology. 2004 Jan;25(1-2):101-15 [14697885]
Pharmacol Rev. 2004 Sep;56(3):331-49 [15317907]
Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2721-5 [1688340]
J Chromatogr B Biomed Appl. 1994 Mar 4;653(2):131-8 [8205240]
Neurodegeneration. 1995 Sep;4(3):271-81 [8581559]
Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2696-701 [8610103]
Circulation. 1996 May 1;93(9):1667-76 [8653872]
Science. 1997 Jun 27;276(5321):2045-7 [9197268]
Neuron. 1997 Dec;19(6):1285-96 [9427251]
J Neurochem. 1998 May;70(5):1973-8 [9572281]
Neurology. 1998 Aug;51(2 Suppl 2):S2-9 [9711973]
Exp Neurol. 1999 Mar;156(1):138-48 [10192785]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/jnc.12345
ER  - 



TY  - JOUR
T1  - A large prospective study of risk factors for adenocarcinomas and malignant carcinoid tumors of the small intestine
AN  - 1427002412; 18329016
AB  - Purpose: Small intestinal cancer is increasing in the U.S.A, yet little is known about its etiology. Our aim was to prospectively evaluate risk factors for this malignancy by the two main histologic subtypes (adenocarcinomas and carcinoids). Methods: Hazard ratios and 95 % confidence intervals (CI) were estimated for all incident small intestinal cancers (n = 237), adenocarcinomas (n = 84), and malignant carcinoids (n = 124), by demographic and lifestyle factors among 498,376 men and women. Results: Age was the only risk factor for adenocarcinomas (HR for greater than or equal to 65 vs. 50-55 years = 3.12, 95 % CI 1.33, 7.31). Age (HR for greater than or equal to 65 vs. 50-55 years = 3.31, 95 % CI 1.51, 7.28), male sex (HR = 1.44, 95 % CI 1.01, 2.05), body mass index (BMI, HR for greater than or equal to 35 vs. 18.5-<25 kg/m super(2) = 1.95, 95 % CI 1.06, 3.58), and current menopausal hormone therapy use (HR = 1.94, 95 % CI 1.07, 3.50) were positively associated with malignant carcinoids. A family history of any cancer or colorectal cancer (HR = 1.42, 95 % CI 0.99, 2.03; 1.61, 0.97, 2.65, respectively), or a personal history of colorectal polyps (HR = 1.51, 95 % CI 0.92, 2.46) produced elevated, but not statistically significant, risks for malignant carcinoids. Race, education, diabetes, smoking, physical activity, and alcohol intake were not associated with either histologic subtype. Conclusions: Risk factors differed according to cancer subtype; only age was associated with adenocarcinomas, whereas age, male sex, BMI, and menopausal hormone therapy use were positively associated with malignant carcinoids.
JF  - Cancer Causes & Control
AU  - Cross, Amanda J
AU  - Hollenbeck, Albert R
AU  - Park, Yikyung
AD  - Division of Cancer Epidemiology and Genetics (DCEG), Department of Health and Human Services (DHHS), National Cancer Institute (NCI), National Institutes of Health (NIH), 6120 Executive Blvd, Rockville, MD, 20852, USA, crossa@mail.nih.gov
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 1737
EP  - 1746
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 24
IS  - 9
SN  - 0957-5243, 0957-5243
KW  - Risk Abstracts
KW  - Genetics
KW  - Alcohol
KW  - Age
KW  - Education
KW  - Risk factors
KW  - Physical activity
KW  - Polyps
KW  - Hormones
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427002412?accountid=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=A+large+prospective+study+of+risk+factors+for+adenocarcinomas+and+malignant+carcinoid+tumors+of+the+small+intestine&rft.au=Cross%2C+Amanda+J%3BHollenbeck%2C+Albert+R%3BPark%2C+Yikyung&rft.aulast=Cross&rft.aufirst=Amanda&rft.date=2013-09-01&rft.volume=24&rft.issue=9&rft.spage=1737&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-013-0251-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 33
N1  - Last updated - 2016-09-01
N1  - SubjectsTermNotLitGenreText - Alcohol; Genetics; Education; Age; Physical activity; Risk factors; Polyps; Hormones; Cancer
DO  - http://dx.doi.org/10.1007/s10552-013-0251-8
ER  - 



TY  - JOUR
T1  - Pyrogallol-associated dermal toxicity and carcinogenicity in F344/N rats and B6C3F1/N mice.
AN  - 1427001970; 23231012
AB  - Pyrogallol (CAS No. 87-66-1), a benzenetriol used historically as a hair dye and currently in a number of industrial applications, was nominated to the National Toxicology Program (NTP) for testing based on the lack of toxicity and carcinogenicity data. Three-month and two-year toxicity studies to determine the toxicity and carcinogenicity of pyrogallol when applied to naïve skin (i.e. dermal administration) were conducted in both sexes of F344/N rats and B6C3F1/N mice. In the three-month studies, adult rodents were administered pyrogallol in 95% ethanol five days per week for 3 months at doses of up to 150 mg/kg body weight (rats) or 600 mg/kg (mice). Based on the subchronic studies, the doses for the two-year studies in rats and mice were 5, 20 and 75 mg/kg of pyrogallol. All mice and most rats survived until the end of the three-month study and body weights were comparable to controls. During the two-year study, survival of dosed rats and male mice was comparable to controls; however survival of 75 mg/kg female mice significantly decreased compared to controls. The incidences of microscopic non-neoplastic lesions at the site of application were significantly higher in all dosed groups of rats and mice and in both the 3-months and two-year studies. In the two-year study, hyperplasia, hyperkeratosis and inflammation tended to be more severe in mice than in rats, and in the mice they tended to be more severe in females than in males. The incidence of squamous cell carcinoma at the site of application (SOA) in 75 mg/kg female mice and SOA squamous cell papillomas in 75 mg/kg male mice were greater than controls. Pyrogallol was carcinogenic in female mice and may have caused tumors in male mice.
JF  - Cutaneous and ocular toxicology
AU  - Mercado-Feliciano, Minerva
AU  - Herbert, Ronald A
AU  - Wyde, Michael E
AU  - Gerken, Diane K
AU  - Hejtmancik, Milton R
AU  - Hooth, Michelle J
AD  - National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 234
EP  - 240
VL  - 32
IS  - 3
KW  - Carcinogens
KW  - 0
KW  - Hair Dyes
KW  - Pyrogallol
KW  - 01Y4A2QXY0
KW  - Index Medicus
KW  - Animals
KW  - Hyperplasia -- pathology
KW  - Administration, Cutaneous
KW  - Fibrosis -- chemically induced
KW  - Mice
KW  - Keratosis -- chemically induced
KW  - Rats
KW  - Rats, Inbred F344
KW  - Fibrosis -- pathology
KW  - Hyperplasia -- chemically induced
KW  - Toxicity Tests, Subchronic
KW  - Toxicity Tests, Chronic
KW  - Female
KW  - Male
KW  - Keratosis -- pathology
KW  - Skin -- drug effects
KW  - Papilloma -- pathology
KW  - Carcinoma, Squamous Cell -- pathology
KW  - Skin Neoplasms -- chemically induced
KW  - Skin -- pathology
KW  - Carcinogens -- toxicity
KW  - Skin Neoplasms -- pathology
KW  - Pyrogallol -- toxicity
KW  - Carcinoma, Squamous Cell -- chemically induced
KW  - Papilloma -- chemically induced
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427001970?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cutaneous+and+ocular+toxicology&rft.atitle=Pyrogallol-associated+dermal+toxicity+and+carcinogenicity+in+F344%2FN+rats+and+B6C3F1%2FN+mice.&rft.au=Mercado-Feliciano%2C+Minerva%3BHerbert%2C+Ronald+A%3BWyde%2C+Michael+E%3BGerken%2C+Diane+K%3BHejtmancik%2C+Milton+R%3BHooth%2C+Michelle+J&rft.aulast=Mercado-Feliciano&rft.aufirst=Minerva&rft.date=2013-09-01&rft.volume=32&rft.issue=3&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=Cutaneous+and+ocular+toxicology&rft.issn=1556-9535&rft_id=info:doi/10.3109%2F15569527.2012.746358
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-18
N1  - Date created - 2013-08-21
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Berl Munch Tierarztl Wochenschr. 2000 Mar;113(3):108-11 [10763554]
Toxicol Appl Pharmacol. 2011 Jul 15;254(2):86-99 [21296097]
Biometrics. 1972 Jun;28(2):519-31 [5037867]
Eur J Biochem. 1974 Sep 16;47(3):469-74 [4215654]
J Toxicol Environ Health. 1976 Jul;1(6):1027-40 [966314]
J Natl Cancer Inst. 1976 Jun;56(6):1237-42 [994224]
Drug Chem Toxicol. 1984;7(6):573-86 [6534733]
Australas J Dermatol. 1985 Dec;26(3):144-5 [3835960]
Contact Dermatitis. 1992 Feb;26(2):101-7 [1386005]
Contact Dermatitis. 1992 Feb;26(2):108-11 [1633700]
Mutat Res. 1992 Oct;269(2):217-24 [1383704]
Contact Dermatitis. 1993 Mar;28(3):180-3 [8462298]
J Anim Sci. 1995 May;73(5):1516-28 [7665384]
Arch Dermatol. 1962 Aug;86:212-6 [14454851]
Eur J Cancer. 2006 Apr;42(6):735-44 [16527478]
Contact Dermatitis. 2007 Feb;56(2):87-93 [17244076]
Food Chem Toxicol. 2007 Apr;45(4):643-8 [17140719]
Dermatitis. 2011 Jan-Feb;22(1):16-26 [21291639]
Biometrics. 1971 Mar;27(1):103-17 [5547548]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.3109/15569527.2012.746358
ER  - 



TY  - JOUR
T1  - Short communication: Interferon/ribavirin treatment for HCV is associated with the development of hypophosphatemia in HIV/hepatitis C virus-coinfected patients.
AN  - 1426750563; 23701022
AB  - One-third of all HIV-infected individuals in the United States are estimated to be coinfected with the hepatitis C virus (HCV). Treatment of chronic hepatitis C in patients coinfected with HIV is a complex problem associated with toxicities and drug interactions between HIV antiretrovirals and interferon and ribavirin. In recent HCV treatment studies, we observed a previously unreported development of hypophosphatemia in HIV/HCV-coinfected patients treated with interferon/ribavirin (IFN/RBV). To further investigate this observation, we retrospectively reviewed 61 HIV/HCV-coinfected patients on antiretrovirals (ARVs) during treatment with IFN/RBV as well as 154 HIV-infected patients treated with ARVs alone. We found that HIV/HCV-coinfected patients on IFN/RBV therapy were more likely to develop frequent (57% vs. 13%, IFN/RBV-treated patients vs. no IFN/RBV; χ(2)=0.001) and higher-grade hypophosphatemia (67.0% Grade 2, 33.3% Grade 3 vs. 94.7% Grade 2, 5.3% Grade 3, IFN/RBV-treated patients vs. no IFN/RBV; χ(2)<0.001) than untreated patients. In addition, we found that the new onset of hypophosphatemia after IFN/RBV treatment initiation was followed by a diminished frequency of this toxicity upon cessation of IFN/RBV, supporting the idea that a drug-drug interaction may increase the risk of this toxicity. To understand the risks of developing this toxicity, we evaluated the association between individual ARV use and hypophosphatemia incidence. Our data suggest that concomitant tenofovir (TDF) use may be a risk factor for the development of hypophosphatemia in HIV/HCV-coinfected patients treated with IFN/RBV. Although the etiology of this abnormality is likely multifactorial, clinicians should be aware of hypophosphatemia as a potential marker of renal toxicity in HIV/HCV-coinfected patients being treated with IFN/RBV regimens.
JF  - AIDS research and human retroviruses
AU  - Funk, Emily K
AU  - Shaffer, Ashton
AU  - Shivakumar, Bhavana
AU  - Sneller, Michael
AU  - Polis, Michael A
AU  - Masur, Henry
AU  - Heytens, Laura
AU  - Nelson, Amy
AU  - Kwan, Richard
AU  - Kottilil, Shyam
AU  - Kohli, Anita
AD  - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 1190
EP  - 1194
VL  - 29
IS  - 9
KW  - Anti-HIV Agents
KW  - 0
KW  - Antiviral Agents
KW  - Organophosphonates
KW  - Ribavirin
KW  - 49717AWG6K
KW  - Interferons
KW  - 9008-11-1
KW  - Tenofovir
KW  - 99YXE507IL
KW  - Adenine
KW  - JAC85A2161
KW  - Index Medicus
KW  - AIDS/HIV
KW  - Organophosphonates -- therapeutic use
KW  - Drug Interactions
KW  - Humans
KW  - Retrospective Studies
KW  - Coinfection -- virology
KW  - Adenine -- therapeutic use
KW  - Drug Therapy, Combination
KW  - Anti-HIV Agents -- therapeutic use
KW  - HIV Infections -- complications
KW  - Risk Factors
KW  - Adult
KW  - HIV Infections -- drug therapy
KW  - Middle Aged
KW  - Adenine -- analogs & derivatives
KW  - Male
KW  - Female
KW  - Hepacivirus -- drug effects
KW  - Kidney Diseases -- chemically induced
KW  - Antiviral Agents -- therapeutic use
KW  - Ribavirin -- therapeutic use
KW  - Hypophosphatemia -- etiology
KW  - Hepatitis C, Chronic -- drug therapy
KW  - Interferons -- adverse effects
KW  - Hepatitis C, Chronic -- complications
KW  - Antiviral Agents -- adverse effects
KW  - Hypophosphatemia -- complications
KW  - Interferons -- therapeutic use
KW  - Ribavirin -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1426750563?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=Short+communication%3A+Interferon%2Fribavirin+treatment+for+HCV+is+associated+with+the+development+of+hypophosphatemia+in+HIV%2Fhepatitis+C+virus-coinfected+patients.&rft.au=Funk%2C+Emily+K%3BShaffer%2C+Ashton%3BShivakumar%2C+Bhavana%3BSneller%2C+Michael%3BPolis%2C+Michael+A%3BMasur%2C+Henry%3BHeytens%2C+Laura%3BNelson%2C+Amy%3BKwan%2C+Richard%3BKottilil%2C+Shyam%3BKohli%2C+Anita&rft.aulast=Funk&rft.aufirst=Emily&rft.date=2013-09-01&rft.volume=29&rft.issue=9&rft.spage=1190&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=1931-8405&rft_id=info:doi/10.1089%2FAID.2013.0035
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-20
N1  - Date created - 2013-08-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Infect Dis. 2002 Mar 15;34(6):831-7 [11833007]
Hepatology. 2001 Aug;34(2):283-7 [11481613]
Clin Infect Dis. 2003 Oct 1;37(7):944-50 [13130407]
Antimicrob Agents Chemother. 2004 May;48(5):1469-87 [15105094]
N Engl J Med. 2004 Jul 29;351(5):438-50 [15282351]
J Acquir Immune Defic Syndr. 2004 Sep 1;37 Suppl 1:S2-S12 [15319664]
J Pharmacol Exp Ther. 1996 Nov;279(2):1009-17 [8930211]
Hepatology. 1999 Oct;30(4):1054-8 [10498659]
JAMA. 2004 Dec 15;292(23):2839-48 [15598915]
J Acquir Immune Defic Syndr. 2005 Mar 1;38(3):301-4 [15735448]
Hepatology. 2005 Apr;41(4):779-89 [15800956]
J Acquir Immune Defic Syndr. 2005 Sep 1;40(1):47-52 [16123681]
AIDS. 2005 Oct;19 Suppl 3:S13-9 [16251809]
J Clin Pharmacol. 2006 May;46(5):559-66 [16638739]
Ann Intern Med. 2006 May 16;144(10):705-14 [16702586]
J Viral Hepat. 2006 Oct;13(10):683-9 [16970600]
AIDS. 2008 Oct 1;22(15):1979-91 [18784461]
N Engl J Med. 2009 Aug 6;361(6):580-93 [19625712]
Adv Chronic Kidney Dis. 2010 Jan;17(1):72-82 [20005491]
JAMA. 2011 Jul 20;306(3):294-301 [21771990]
Curr Opin HIV AIDS. 2011 Nov;6(6):478-82 [22001892]
Gut. 2012 May;61 Suppl 1:i47-58 [22504919]
Hepatology. 2002 May;35(5):1247-55 [11981775]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1089/AID.2013.0035
ER  - 



TY  - JOUR
T1  - Long-lasting attenuation of amygdala-kindled seizures after convection-enhanced delivery of botulinum neurotoxins a and B into the amygdala in rats.
AN  - 1426009011; 23772062
AB  - Botulinum neurotoxins (BoNTs) are well recognized to cause potent, selective, and long-lasting neuroparalytic actions by blocking cholinergic neurotransmission to muscles and glands. There is evidence that BoNT isoforms can also inhibit neurotransmission in the brain. In this study, we examined whether locally delivered BoNT/A and BoNT/B can attenuate kindling measures in amygdala-kindled rats. Male rats were implanted with a combination infusion cannula-stimulating electrode assembly into the right basolateral amygdala. Fully kindled animals received a single infusion of vehicle or BoNT/A or BoNT/B at doses of 1, 3.2, or 10 ng over a 20-minute period by convection-enhanced delivery. Electrographic (EEG) and behavioral kindling measures were determined at selected times during the 3- to 64-day period after the infusion. BoNT/B produced a dose-dependent elevation in after-discharge threshold and duration and a reduction in the seizure stage and duration of behavioral seizures that lasted for up to 50 days after infusion. BoNT/A had similar effects on EEG measures; behavioral seizure measures were also reduced, but the effect did not reach statistical significance. The effects of both toxins on EEG and behavioral measures progressively resolved during the latter half of the observation period. Animals gained weight normally, maintained normal body temperature, and did not show altered behavior. This study demonstrates for the first time that locally delivered BoNTs can produce prolonged inhibition of brain excitability, indicating that they could be useful for the treatment of brain disorders, including epilepsy, that would benefit from long-lasting suppression of neurotransmission within a circumscribed brain region.
JF  - The Journal of pharmacology and experimental therapeutics
AU  - Gasior, Maciej
AU  - Tang, Rebecca
AU  - Rogawski, Michael A
AD  - Epilepsy Research Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 528
EP  - 534
VL  - 346
IS  - 3
KW  - rimabotulinumtoxinB
KW  - 0Y70779M1F
KW  - Botulinum Toxins
KW  - EC 3.4.24.69
KW  - Botulinum Toxins, Type A
KW  - Index Medicus
KW  - Rats
KW  - Convection
KW  - Drug Delivery Systems
KW  - Behavior, Animal -- drug effects
KW  - Animals
KW  - Rats, Sprague-Dawley
KW  - Body Temperature -- drug effects
KW  - Area Under Curve
KW  - Electrodes, Implanted
KW  - Dose-Response Relationship, Drug
KW  - Electroencephalography -- drug effects
KW  - Male
KW  - Botulinum Toxins, Type A -- administration & dosage
KW  - Botulinum Toxins -- administration & dosage
KW  - Kindling, Neurologic -- drug effects
KW  - Botulinum Toxins -- pharmacology
KW  - Amygdala -- physiology
KW  - Seizures -- prevention & control
KW  - Botulinum Toxins, Type A -- pharmacology
KW  - Amygdala -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1426009011?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-lasting+attenuation+of+amygdala-kindled+seizures+after+convection-enhanced+delivery+of+botulinum+neurotoxins+a+and+B+into+the+amygdala+in+rats.&rft.au=Gasior%2C+Maciej%3BTang%2C+Rebecca%3BRogawski%2C+Michael+A&rft.aulast=Gasior&rft.aufirst=Maciej&rft.date=2013-09-01&rft.volume=346&rft.issue=3&rft.spage=528&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.205070
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-04
N1  - Date created - 2013-08-16
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Neurotherapeutics. 2009 Apr;6(2):344-51 [19332329]
J Neurochem. 2009 Apr;109(1):15-24 [19154335]
Proc Natl Acad Sci U S A. 2010 Sep 21;107(38):16554-9 [20823219]
J Biol Chem. 2011 Feb 25;286(8):6375-85 [21138836]
Mov Disord. 2011 Feb 1;26(2):313-9 [21259343]
Brain Res Bull. 1981 Dec;7(6):629-33 [7326579]
Epilepsy Res. 2000 Apr;39(2):103-14 [10759298]
Toxicon. 2001 Jan;39(1):27-41 [10936621]
J Biol Chem. 2003 Jan 10;278(2):1363-71 [12381720]
Toxicon. 2003 Mar;41(4):475-81 [12657317]
Dermatol Surg. 2003 May;29(5):519-22; discussion 522 [12752521]
Annu Rev Pharmacol Toxicol. 2004;44:167-93 [14744243]
Neuron. 2004 Feb 19;41(4):599-610 [14980208]
Brain Res Brain Res Rev. 2004 Mar;44(2-3):141-53 [15003390]
Behav Pharmacol. 2004 May;15(3):233-40 [15187581]
Electroencephalogr Clin Neurophysiol. 1972 Mar;32(3):281-94 [4110397]
Epilepsia. 1976 Jun;17(2):197-206 [947748]
Naunyn Schmiedebergs Arch Pharmacol. 1976;292(2):161-5 [59905]
Naunyn Schmiedebergs Arch Pharmacol. 1981 Jun;316(3):244-51 [6114440]
J Neurochem. 1988 Jun;50(6):1808-16 [2897427]
J Neurochem. 1988 Aug;51(2):522-7 [3392543]
Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2076-80 [8134351]
Neurology. 1997 Jul;49(1):189-94 [9222189]
J Neurosci. 1997 Oct 1;17(19):7190-202 [9295365]
Epilepsy Res. 1997 Dec;29(1):17-24 [9416456]
Neurosci Lett. 1998 Nov 13;256(3):135-8 [9855358]
J Neurosurg. 1999 Feb;90(2):315-20 [9950503]
FEBS Lett. 1999 Jul 30;456(1):137-42 [10452545]
Exp Neurol. 2004 Dec;190(2):544-7 [15530893]
J Neurosci. 2005 Feb 23;25(8):1943-51 [15728834]
Otolaryngol Head Neck Surg. 2005 Dec;133(6):836-8 [16360499]
Neurotox Res. 2006 Apr;9(2-3):197-203 [16785118]
Acta Neurol Taiwan. 2006 Dec;15(4):225-31 [17214084]
Traffic. 2007 Feb;8(2):142-53 [17241445]
J Pharmacol Exp Ther. 2007 Nov;323(2):458-68 [17717191]
J Neurosci. 2008 Apr 2;28(14):3689-96 [18385327]
Mov Disord. 2008 Mar 15;23(4):510-7 [18098274]
Epilepsia. 2009 Apr;50(4):963-6 [19175393]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1124/jpet.113.205070
ER  - 



TY  - JOUR
T1  - Mortality from solid tumors among workers in formaldehyde industries: an update of the NCI cohort.
AN  - 1426006247; 23788167
AB  - Formaldehyde, a widely used chemical, is considered a human carcinogen.
          We extended follow-up of the largest industrial cohort of workers in formaldehyde industries (n = 25,619) by 10 years through 2004. Standardized mortality ratios (SMRs) and rate ratios (RRs) were calculated for deaths from solid tumors using quantitative formaldehyde exposure estimates. During 998,239 person-years, 13,951 deaths occurred. With one additional death, previously observed excesses for nasopharyngeal cancer (n = 10) persisted for peak, average intensity and cumulative exposure; RRs in the highest exposure categories were 7.66 (95% CI: 0.94, 62.34), P-trend = 0.005, 11.54 (95% CI: 1.38, 96.81), P-trend = 0.09, and 2.94 (95% CI: 0.65, 13.28), P-trend = 0.06, respectively. For all cancer, solid tumors and lung cancer, SMRs among exposed workers were elevated, but internal analyses revealed no positive associations with formaldehyde exposure.
          Consistent with previous analyses of this cohort, this update continues to suggest a link between formaldehyde exposure and nasopharyngeal cancer. Copyright © 2013 Wiley Periodicals, Inc.
JF  - American journal of industrial medicine
AU  - Beane Freeman, Laura E
AU  - Blair, Aaron
AU  - Lubin, Jay H
AU  - Stewart, Patricia A
AU  - Hayes, Richard B
AU  - Hoover, Robert N
AU  - Hauptmann, Michael
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. freemala@mail.nih.gov
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 1015
EP  - 1026
VL  - 56
IS  - 9
KW  - Formaldehyde
KW  - 1HG84L3525
KW  - Index Medicus
KW  - formaldehyde
KW  - epidemiology
KW  - cancer
KW  - Aged, 80 and over
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Models, Statistical
KW  - Middle Aged
KW  - Follow-Up Studies
KW  - United States -- epidemiology
KW  - Occupational Exposure -- statistics & numerical data
KW  - Neoplasms -- mortality
KW  - Neoplasms -- chemically induced
KW  - Occupational Exposure -- adverse effects
KW  - Formaldehyde -- adverse effects
KW  - Occupational Diseases -- chemically induced
KW  - Chemical Industry
KW  - Occupational Diseases -- mortality
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1426006247?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Mortality+from+solid+tumors+among+workers+in+formaldehyde+industries%3A+an+update+of+the+NCI+cohort.&rft.au=Beane+Freeman%2C+Laura+E%3BBlair%2C+Aaron%3BLubin%2C+Jay+H%3BStewart%2C+Patricia+A%3BHayes%2C+Richard+B%3BHoover%2C+Robert+N%3BHauptmann%2C+Michael&rft.aulast=Beane+Freeman&rft.aufirst=Laura&rft.date=2013-09-01&rft.volume=56&rft.issue=9&rft.spage=1015&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=1097-0274&rft_id=info:doi/10.1002%2Fajim.22214
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-04-04
N1  - Date created - 2013-08-15
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Comment In:
Am J Ind Med. 2014 Apr;57(4):486-7 [24501017]
Am J Ind Med. 2014 Apr;57(4):488-9 [24478120]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1002/ajim.22214
ER  - 



TY  - JOUR
T1  - Toxicokinetics of α-thujone following intravenous and gavage administration of α-thujone or α- and β-thujone mixture in male and female F344/N rats and B6C3F1 mice.
AN  - 1420169674; 23669748
AB  - Plants containing thujone have widespread use and hence have significant human exposure. α-Thujone caused seizures in rodents following gavage administration. We investigated the toxicokinetics of α-thujone in male and female F344/N rats and B6C3F1 mice following intravenous and gavage administration of α-thujone or a mixture of α- and β-thujone (which will be referred to as α,β-thujone). Absorption of α-thujone following gavage administration was rapid without any dose-, species-, sex- or test article-related effect. Absolute bioavailability of α-thujone following administration of α-thujone or α,β-thujone was generally higher in rats than in mice. In rats, females had higher bioavailability than males following administration of either test article although a sex difference was not observed in mice. Cmax and AUC∞ increased greater than proportional to the dose in female rats following administration of α-thujone and in male and female mice following administration of α,β-thujone suggesting possible saturation of elimination kinetics with increasing dose. Dose-adjusted AUC∞ for male and female rats was 5- to 15-fold and 3- to 24-fold higher than mice counterparts following administration of α-thujone and α,β-thujone, respectively (p-value<0.0001 for all comparisons). Following both intravenous and gavage administration, α-thujone was distributed to the brains of rats and mice with females, in general, having higher brain:plasma ratios than males. These data are in support of the observed toxicity of α-thujone and α,β-thujone where females were more sensitive than males of both species to α-thujone-induced neurotoxicity. In general there was no difference in toxicokinetics between test articles when normalized to α-thujone concentration. 
          Published by Elsevier Inc.
JF  - Toxicology and applied pharmacology
AU  - Waidyanatha, Suramya
AU  - Johnson, Jerry D
AU  - Hong, S Peter
AU  - Robinson, Veronica Godfrey
AU  - Gibbs, Seth
AU  - Graves, Steven W
AU  - Hooth, Michelle J
AU  - Smith, Cynthia S
AD  - Division of National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. waidyanathas@niehs.nih.gov
Y1  - 2013/09/01/
PY  - 2013
DA  - 2013 Sep 01
SP  - 216
EP  - 228
VL  - 271
IS  - 2
KW  - Monoterpenes
KW  - 0
KW  - beta-thujone
KW  - 1125-12-8
KW  - Index Medicus
KW  - Bioavailability
KW  - Gavage
KW  - Thujone
KW  - Toxicokinetics
KW  - Neurotoxicity
KW  - Rodents
KW  - Animals
KW  - Area Under Curve
KW  - Injections, Intravenous
KW  - Chemistry, Pharmaceutical
KW  - Brain Chemistry -- drug effects
KW  - Intubation, Gastrointestinal
KW  - Algorithms
KW  - Mice
KW  - Pharmacokinetics
KW  - Biological Availability
KW  - Rats
KW  - Mice, Inbred Strains
KW  - Rats, Inbred F344
KW  - Half-Life
KW  - Isomerism
KW  - Gas Chromatography-Mass Spectrometry
KW  - Data Interpretation, Statistical
KW  - Male
KW  - Female
KW  - Monoterpenes -- toxicity
KW  - Monoterpenes -- pharmacokinetics
KW  - Monoterpenes -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420169674?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxicokinetics+of+%CE%B1-thujone+following+intravenous+and+gavage+administration+of+%CE%B1-thujone+or+%CE%B1-+and+%CE%B2-thujone+mixture+in+male+and+female+F344%2FN+rats+and+B6C3F1+mice.&rft.au=Waidyanatha%2C+Suramya%3BJohnson%2C+Jerry+D%3BHong%2C+S+Peter%3BRobinson%2C+Veronica+Godfrey%3BGibbs%2C+Seth%3BGraves%2C+Steven+W%3BHooth%2C+Michelle+J%3BSmith%2C+Cynthia+S&rft.aulast=Waidyanatha&rft.aufirst=Suramya&rft.date=2013-09-01&rft.volume=271&rft.issue=2&rft.spage=216&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2013.05.001
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-21
N1  - Date created - 2013-08-12
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.taap.2013.05.001
ER  - 



TY  - JOUR
T1  - Transarterial chemoembolization for the treatment of hepatocellular carcinoma: a single center experience including 221 patients.
AN  - 1420166391; 23932751
AB  - Hepatocelluar carcinoma (HCC) is a major health problem in Egypt as well as in many countries. Transarterial chemoemoblization (TACE) is a treatment modality applicable to locally advanced HCC beyond surgery or ablative therapies and is associated with survival improvements. The aim of this study was to assess the outcomes of TACE in our center over the past four years.
          This is a retrospective cohort study that included 221 patients with locally advanced HCC treated with TACE in a single center between the years 2007 and 2010. The median age was 57 years with male predominance. Liver cirrhosis, viral hepatitis and Bilharziasis were encountered in 64%, 31% and 8% of patients, respectively. Abdominal pain was the most common presenting symptom (67%). Most cases were diagnosed based on radiology (57%) with a TNM stage I or II (73%) and a median AFP value of 150 ng/mL. 221 patients received 440 cycles of TACE with a median of 2 cycles per patient. Cisplatin and doxorubicin (50mg per cycle, each) were the most commonly used drugs. Impaired liver function was the most common toxicity. Liver cell failure occurred in 17% of patients. An objective tumor response was achieved in 44% of cases. The median overall survival (OS) was 16 months (95% CI, 13-19 months) and the median progression free survival (PFS) was 6 months (95% CI, 4.3-7.8 months). Responding patients, Child-Pugh class A and patients receiving standard doses of chemotherapy had a significantly better OS than their counterparts. Only Child-Pugh class A was associated with significantly longer PFS (p < 0.001).
          TACE produces reasonable responses and fair survival rates in locally advanced HCC but with noticeable toxicities. Proper patients' selection and prompt liver support are mandates for improving TACE outcomes. Copyright © 2013. Production and hosting by Elsevier B.V.
JF  - Journal of the Egyptian National Cancer Institute
AU  - Zeeneldin, Ahmed Abdelmabood
AU  - Salem, Salem Eid
AU  - Tabashy, Reda Hassan
AU  - Ibrahim, Asmaa Ahmed
AU  - Alieldin, Nelly Hassan
AD  - Department of Medical Oncology/Hematology, National Cancer Institute, Cairo University, Cairo, Egypt.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 143
EP  - 150
VL  - 25
IS  - 3
SN  - 1110-0362, 1110-0362
KW  - Index Medicus
KW  - Egypt
KW  - Transarterial chemoemoblization
KW  - National Cancer Institute
KW  - Treatment
KW  - Hepatocellular carcinoma
KW  - Hepatitis, Viral, Human -- complications
KW  - Hepacivirus -- isolation & purification
KW  - Humans
KW  - Retrospective Studies
KW  - Aged
KW  - Liver Cirrhosis -- complications
KW  - Hepatitis, Viral, Human -- epidemiology
KW  - Hepatitis, Viral, Human -- mortality
KW  - Aged, 80 and over
KW  - Adult
KW  - Cohort Studies
KW  - Middle Aged
KW  - Liver Cirrhosis -- epidemiology
KW  - Liver Cirrhosis -- mortality
KW  - Male
KW  - Female
KW  - Survival Analysis
KW  - Chemoembolization, Therapeutic -- statistics & numerical data
KW  - Liver Neoplasms -- complications
KW  - Carcinoma, Hepatocellular -- complications
KW  - Liver Neoplasms -- therapy
KW  - Chemoembolization, Therapeutic -- methods
KW  - Liver Neoplasms -- mortality
KW  - Carcinoma, Hepatocellular -- therapy
KW  - Liver Neoplasms -- epidemiology
KW  - Carcinoma, Hepatocellular -- mortality
KW  - Carcinoma, Hepatocellular -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420166391?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Egyptian+National+Cancer+Institute&rft.atitle=Transarterial+chemoembolization+for+the+treatment+of+hepatocellular+carcinoma%3A+a+single+center+experience+including+221+patients.&rft.au=Zeeneldin%2C+Ahmed+Abdelmabood%3BSalem%2C+Salem+Eid%3BTabashy%2C+Reda+Hassan%3BIbrahim%2C+Asmaa+Ahmed%3BAlieldin%2C+Nelly+Hassan&rft.aulast=Zeeneldin&rft.aufirst=Ahmed&rft.date=2013-09-01&rft.volume=25&rft.issue=3&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Egyptian+National+Cancer+Institute&rft.issn=11100362&rft_id=info:doi/10.1016%2Fj.jnci.2013.05.003
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-14
N1  - Date created - 2013-08-12
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.jnci.2013.05.003
ER  - 



TY  - JOUR
T1  - Pediatric uveitis: new and future treatments.
AN  - 1419342297; 23872814
AB  - Pediatric uveitis is relatively uncommon, accounting for only 5-10% of all patients with uveitis. However, owing to high prevalence of complications and devastating outcomes, its lifetime burden can be significant.
          Immunomodulatory therapy has been associated with better outcomes in noninfectious pediatric uveitis. However, effective treatments are limited by medication-related complications, including multiorgan toxicities and systemic side effects. We review the current therapies available to treat pediatric uveitis, discuss novel and future therapies, and provide clinical recommendations utilizing these new agents. The consideration for treatment regimens in noninfectious pediatric uveitis is multifactorial. Understanding past, present, and future technology will aid in treatment of a complex and refractory disease.
JF  - Current opinion in ophthalmology
AU  - Mehta, Preema J
AU  - Alexander, Janet L
AU  - Sen, H Nida
AD  - National Eye Institute/National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 453
EP  - 462
VL  - 24
IS  - 5
KW  - Immunosuppressive Agents
KW  - 0
KW  - Index Medicus
KW  - Infant
KW  - Humans
KW  - Child
KW  - Adolescent
KW  - Child, Preschool
KW  - Biological Therapy
KW  - Uveitis -- therapy
KW  - Uveitis -- etiology
KW  - Immunosuppressive Agents -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419342297?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+ophthalmology&rft.atitle=Pediatric+uveitis%3A+new+and+future+treatments.&rft.au=Mehta%2C+Preema+J%3BAlexander%2C+Janet+L%3BSen%2C+H+Nida&rft.aulast=Mehta&rft.aufirst=Preema&rft.date=2013-09-01&rft.volume=24&rft.issue=5&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+ophthalmology&rft.issn=1531-7021&rft_id=info:doi/10.1097%2FICU.0b013e3283641ede
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-25
N1  - Date created - 2013-08-08
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/ICU.0b013e3283641ede
ER  - 



TY  - JOUR
T1  - Microglia during development and aging.
AN  - 1418646788; 23644076
AB  - Microglia are critical nervous system-specific cells influencing brain development, maintenance of the neural environment, response to injury, and repair. They contribute to neuronal proliferation and differentiation, pruning of dying neurons, synaptic remodeling and clearance of debris and aberrant proteins. Colonization of the brain occurs during gestation with an expansion following birth with localization stimulated by programmed neuronal death, synaptic pruning, and axonal degeneration. Changes in microglia phenotype relate to cellular processes including specific neurotransmitter, pattern recognition, or immune-related receptor activation. Upon activation, microglia cells have the capacity to release a number of substances, e.g., cytokines, chemokines, nitric oxide, and reactive oxygen species, which could be detrimental or beneficial to the surrounding cells. With aging, microglia shift their morphology and may display diminished capacity for normal functions related to migration, clearance, and the ability to shift from a pro-inflammatory to an anti-inflammatory state to regulate injury and repair. This shift in microglia potentially contributes to increased susceptibility and neurodegeneration as a function of age. In the current review, information is provided on the colonization of the brain by microglia, the expression of various pattern recognition receptors to regulate migration and phagocytosis, and the shift in related functions that occur in normal aging. 
          Published by Elsevier Inc.
JF  - Pharmacology & therapeutics
AU  - Harry, G Jean
AD  - National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, MD C1-04, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA. harry@niehs.nih.gov
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 313
EP  - 326
VL  - 139
IS  - 3
KW  - Index Medicus
KW  - purinergic receptors
KW  - MAPK
KW  - fractalkine receptor
KW  - TREM-2
KW  - pattern recognition receptors
KW  - PRR
KW  - K(+)
KW  - CNS
KW  - Alzheimer's disease
KW  - lipopolysaccharide
KW  - tumor necrosis factor
KW  - TLR
KW  - Development
KW  - P2X receptors
KW  - Cl(−)
KW  - transforming growth factor beta
KW  - BBB
KW  - adenosine triphosphate
KW  - PND
KW  - gestational day
KW  - major histocompatibility complex
KW  - IL
KW  - chloride
KW  - Synapse stripping
KW  - Microglia
KW  - phosphoinositide 3-kinase
KW  - AD
KW  - complement 1q
KW  - CX3CR1
KW  - potassium
KW  - complement receptor 3
KW  - fractalkine or neurotactin
KW  - interferon
KW  - Aβ
KW  - postnatal day
KW  - GD
KW  - TNF
KW  - blood brain barrier
KW  - Aging
KW  - PI3K
KW  - CX3CL1
KW  - NO
KW  - IFN
KW  - TGFβ
KW  - CR3
KW  - LPS
KW  - nitric oxide
KW  - central nervous system
KW  - ATP
KW  - interleukin
KW  - mitogen-activated protein kinase
KW  - cluster of differentiation
KW  - P2
KW  - MHC
KW  - C1q
KW  - triggering receptor expressed on myeloid cells-2
KW  - amyloid beta
KW  - toll-like receptors
KW  - CD
KW  - Phagocytosis -- physiology
KW  - Animals
KW  - Cell Differentiation -- physiology
KW  - Nerve Degeneration -- metabolism
KW  - Humans
KW  - Cell Movement -- physiology
KW  - Neurons -- physiology
KW  - Cell Proliferation
KW  - Aging -- physiology
KW  - Brain -- physiology
KW  - Brain -- growth & development
KW  - Microglia -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1418646788?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Microglia+during+development+and+aging.&rft.au=Harry%2C+G+Jean&rft.aulast=Harry&rft.aufirst=G&rft.date=2013-09-01&rft.volume=139&rft.issue=3&rft.spage=313&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=1879-016X&rft_id=info:doi/10.1016%2Fj.pharmthera.2013.04.013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-03-05
N1  - Date created - 2013-08-07
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Neuroreport. 1994 Jun 2;5(10):1224-6 [7919169]
Br J Pharmacol. 1994 Sep;113(1):29-34 [7812623]
Adv Neuroimmunol. 1994;4(3):273-81 [7874395]
Brain Res Brain Res Rev. 1995 Mar;20(3):269-87 [7550361]
J Neurosci. 1995 Nov;15(11):7712-26 [7472522]
J Comp Neurol. 1995 Oct 30;361(4):602-16 [8576417]
Dev Neurosci. 1995;17(5-6):324-34 [8829921]
Glia. 1995 Dec;15(4):447-57 [8926038]
Development. 1996 Sep;122(9):2661-72 [8787741]
Brain Res Brain Res Rev. 1995 Sep;21(2):195-218 [8866675]
Glia. 1996 Dec;18(4):269-81 [8972796]
J Comp Neurol. 1997 Jan 6;377(1):70-84 [8986873]
J Exp Med. 1997 Feb 3;185(3):579-82 [9053458]
Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):4080-5 [9108108]
Proc Natl Acad Sci U S A. 1997 May 13;94(10):5296-301 [9144231]
J Comp Neurol. 1997 Oct 6;386(4):661-80 [9378859]
Glia. 1998 Jan;22(1):72-85 [9436789]
Glia. 1998 Apr;22(4):401-7 [9517572]
Acta Neuropathol. 1998 Mar;95(3):229-34 [9542587]
J Leukoc Biol. 2004 Mar;75(3):388-97 [14612429]
Am J Anat. 1981 Mar;160(3):247-55 [6164286]
Neuroscience. 1985 Jun;15(2):313-26 [3895031]
J Comp Neurol. 1985 Nov 8;241(2):237-49 [4067017]
J Neuroimmunol. 1987 Dec;17(1):71-82 [3316271]
Exp Neurol. 1989 Aug;105(2):115-26 [2753113]
J Anat. 1989 Oct;166:253-64 [2621143]
Brain Res Dev Brain Res. 1990 Aug 1;55(1):95-102 [2208643]
Trends Neurosci. 1990 Sep;13(9):366 [1699325]
Neuroscience. 1990;39(1):151-70 [2089275]
J Clin Pathol. 1991 Feb;44(2):102-6 [1864982]
Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):7438-42 [1651506]
Neuroscience. 1991;45(3):513-27 [1663599]
Acta Anat (Basel). 1991;142(2):118-25 [1781250]
Anat Rec. 1992 Apr;232(4):527-50 [1554104]
Neuroscience. 1992;48(2):405-15 [1603325]
J Biol Chem. 1992 Jul 25;267(21):14987-97 [1321822]
J Biol Chem. 1992 Jul 25;267(21):14998-5004 [1378843]
Glia. 1993 Jan;7(1):60-7 [8423063]
Brain Res Dev Brain Res. 1999 Nov 18;117(2):145-52 [10567732]
J Neurosci. 2000 Jan 1;20(1):251-8 [10627602]
Exp Neurol. 2000 Jan;161(1):285-96 [10683294]
Pathobiology. 1999;67(5-6):222-6 [10725788]
Neuroscience. 2000;96(4):807-15 [10727798]
Genes Cells. 2000 May;5(5):397-406 [10886367]
Semin Immunol. 2000 Jun;12(3):185-8; discussion 257-344 [10910738]
J Neurochem. 2000 Sep;75(3):965-72 [10936177]
Eur J Neurosci. 2000 Aug;12(8):2721-34 [10971615]
Science. 2000 Dec 1;290(5497):1768-71 [11099416]
Brain Behav Immun. 2000 Dec;14(4):288-304 [11120597]
J Immunol. 2001 Jan 1;166(1):249-55 [11123299]
J Neurosci. 2001 Mar 15;21(6):2028-38 [11245686]
FASEB J. 2001 Apr;15(6):1086-8 [11292676]
Acta Neuropathol. 2001 Mar;101(3):249-55 [11307625]
Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8862-7 [11438693]
Glia. 2001 Nov;36(2):191-9 [11596127]
Nat Med. 2001 Dec;7(12):1356-61 [11726978]
Pharmacol Rev. 2001 Dec;53(4):527-52 [11734617]
Science. 2002 Mar 22;295(5563):2282-5 [11910117]
Anat Rec. 2002 May 1;267(1):1-6 [11984786]
Trends Immunol. 2002 Jun;23(6):285-90 [12072366]
Physiol Rev. 2002 Oct;82(4):1013-67 [12270951]
J Physiol Paris. 2002 Apr-Jun;96(3-4):183-92 [12445895]
J Neurochem. 2002 Dec;83(6):1309-20 [12472885]
J Comp Neurol. 2003 Mar 31;458(2):144-57 [12596255]
J Biol Chem. 2003 Apr 11;278(15):13309-17 [12551918]
Eur J Neurosci. 2003 Jun;17(11):2267-76 [12814360]
Cell. 2003 Jun 27;113(7):817-20 [12837239]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8514-9 [12824464]
Brain Res. 2003 Aug 15;981(1-2):174-83 [12885439]
J Neurochem. 2003 Aug;86(4):1051-4 [12887702]
Cereb Cortex. 2003 Sep;13(9):950-61 [12902394]
Nature. 2003 Aug 14;424(6950):778-83 [12917686]
J Immunol. 2003 Sep 15;171(6):3034-46 [12960329]
Glia. 2004 Jan 1;45(1):75-88 [14648548]
Int J Dev Neurosci. 2003 Dec;21(8):445-50 [14659995]
Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15983-8 [14668448]
J Neurosci. 2004 Jan 7;24(1):1-7 [14715932]
Glia. 2004 Jan 15;45(2):208-12 [14730714]
J Immunol. 2004 Mar 1;172(5):2744-7 [14978072]
Neuron. 2004 Feb 19;41(4):535-47 [14980203]
Glia. 1993 Jan;7(1):93-101 [7678582]
Exp Neurol. 1993 Mar;120(1):123-31 [8477825]
J Anat. 1992 Dec;181 ( Pt 3):423-30 [1304580]
J Neurosci. 1993 Oct;13(10):4403-11 [7692013]
Immunity. 2010 May 28;32(5):593-604 [20510870]
Brain Behav Immun. 2010 Aug;24(6):874-80 [20116424]
Brain Behav Immun. 2010 Oct;24(7):1190-201 [20570721]
Cell Stem Cell. 2010 Oct 8;7(4):483-95 [20887954]
ASN Neuro. 2010;2(5):e00047 [20967131]
Am J Pathol. 2010 Nov;177(5):2549-62 [20864679]
Science. 2010 Nov 5;330(6005):841-5 [20966214]
Science. 2010 Nov 5;330(6005):783-8 [21051630]
PLoS Biol. 2010;8(11):e1000527 [21072242]
Am J Physiol Cell Physiol. 2010 Dec;299(6):C1267-76 [20826760]
Neurotox Res. 2011 Feb;19(2):341-52 [20524106]
Mult Scler. 2011 Jan;17(1):2-15 [20813772]
J Neurosci Res. 2011 Mar;89(3):286-98 [21259316]
J Neurochem. 2008 Jul;106(1):271-80 [18384650]
PLoS One. 2011;6(1):e15846 [21264342]
PLoS One. 2011;6(1):e15973 [21283568]
Glia. 2011 Apr;59(4):675-95 [21305616]
Curr Opin Neurobiol. 2011 Feb;21(1):5-10 [20817438]
Aging Cell. 2011 Apr;10(2):263-76 [21108733]
Neurobiol Aging. 2011 May;32(5):763-77 [19464758]
Physiol Rev. 2011 Apr;91(2):461-553 [21527731]
EMBO J. 2011 May 4;30(9):1864-73 [21441897]
Brain Behav Immun. 2011 Jun;25 Suppl 1:S137-45 [21376806]
J Immunol. 2011 Jun 1;186(11):6191-8 [21502377]
Brain Behav Immun. 2011 Jul;25(5):850-62 [20833246]
J Alzheimers Dis. 2011;25(2):279-93 [21403390]
PLoS One. 2011;6(8):e22818 [21850237]
Nat Neurosci. 2011 Sep;14(9):1142-9 [21804537]
Science. 2011 Sep 9;333(6048):1456-8 [21778362]
Neurobiol Aging. 2011 Nov;32(11):2030-44 [20018408]
Glia. 2011 Nov;59(11):1744-53 [21800362]
PLoS One. 2011;6(10):e26317 [22046273]
Nature. 2011 Nov 10;479(7372):232-6 [22048312]
J Neurochem. 2011 Dec;119(5):901-8 [21951310]
Glia. 2012 Feb;60(2):306-21 [22072381]
Adv Exp Med Biol. 2012;723:37-42 [22183313]
J Neuroinflammation. 2011;8:174 [22152337]
Glia. 2012 Apr;60(4):541-58 [22223464]
Glia. 2012 Apr;60(4):630-8 [22271465]
Brain Behav Immun. 2012 Mar;26(3):419-28 [22198120]
Glia. 2012 May;60(5):717-27 [22290798]
Brain Behav Immun. 2012 Jul;26(5):766-77 [22024136]
J Neuroinflammation. 2012;9:90 [22569158]
J Neurosci. 2012 Aug 15;32(33):11285-98 [22895712]
Stroke. 2012 Nov;43(11):3063-70 [22933588]
Br J Pharmacol. 2012 Dec;167(8):1575-82 [22563843]
Neurobiol Aging. 2013 Mar;34(3):943-60 [22819137]
Yale J Biol Med. 2012 Dec;85(4):447-68 [23239947]
Neuropathol Appl Neurobiol. 2013 Feb;39(1):19-34 [23039106]
J Neurosci. 2013 Feb 13;33(7):2761-72 [23407936]
Nat Neurosci. 2013 Mar;16(3):273-80 [23334579]
Trends Immunol. 2013 May;34(5):224-33 [23352728]
ASN Neuro. 2012;4(5). pii: e00094. doi: 10.1042/AN20120044 [22770428]
CNS Neurol Disord Drug Targets. 2011 Feb;10(1):108-18 [21143141]
Brain Res Brain Res Rev. 2004 Mar;44(2-3):154-78 [15003391]
FASEB J. 2004 Apr;18(6):743-5 [14766802]
J Immunol. 2004 Jun 1;172(11):7144-53 [15153538]
J Immunol. 2004 Sep 15;173(6):3916-24 [15356140]
Trends Neurosci. 2004 Oct;27(10):607-13 [15374672]
J Neurocytol. 1974 Oct;3(4):405-29 [4373545]
J Am Geriatr Soc. 1976 Jan;24(1):4-11 [172540]
J Comp Neurol. 1978 Jul 1;180(1):139-63 [649786]
Blood. 1979 Aug;54(2):485-500 [454850]
J Comp Neurol. 1981 Mar 10;196(4):683-94 [7204674]
Histopathology. 2007 Jun;50(7):897-910 [17543080]
Neuroscience. 2007 Jul 29;147(4):867-83 [17459594]
J Neurosci. 2007 Aug 1;27(31):8309-13 [17670977]
Physiol Behav. 2007 Sep 10;92(1-2):15-20 [17574632]
Neurotherapeutics. 2007 Oct;4(4):571-9 [17920538]
Trends Neurosci. 2007 Oct;30(10):527-35 [17904651]
Nat Neurosci. 2007 Nov;10(11):1387-94 [17965659]
J Neuroimmunol. 2007 Oct;190(1-2):28-33 [17854911]
Adv Immunol. 2007;96:1-40 [17981203]
Cell Physiol Biochem. 2007;20(6):947-56 [17982277]
J Neurosci. 2007 Nov 7;27(45):12396-406 [17989304]
Trends Neurosci. 2007 Nov;30(11):596-602 [17950926]
Prog Neurobiol. 2007 Dec;83(5):263-76 [17804147]
J Neuroimmune Pharmacol. 2006 Jun;1(2):127-37 [18040779]
J Neuroimmune Pharmacol. 2007 Dec;2(4):297-312 [18040848]
Nat Neurosci. 2007 Dec;10(12):1538-43 [18026097]
J Neurosci. 2007 Nov 28;27(48):13065-73 [18045900]
Cell. 2007 Dec 14;131(6):1164-78 [18083105]
Brain Behav Immun. 2008 Feb;22(2):234-44 [17905568]
Aging Cell. 2008 Jan;7(1):58-68 [17988243]
Brain Res. 2008 Feb 15;1194:45-55 [18177631]
Exp Mol Med. 2008 Feb 29;40(1):19-26 [18305394]
J Neurosci. 2008 Mar 5;28(10):2320-31 [18322079]
Stroke. 2008 Apr;39(4):1314-20 [18309167]
J Neurosci Res. 2008 May 15;86(7):1511-9 [18183622]
Front Biosci. 2008;13:3423-38 [18508444]
Neuron. 2008 Jun 12;58(5):749-62 [18549786]
Glia. 2008 Aug 1;56(10):1048-60 [18442088]
Neurobiol Dis. 2008 Jul;31(1):33-40 [18486483]
Psychoneuroendocrinology. 2008 Jul;33(6):755-65 [18407425]
J Neurosci. 2008 Aug 6;28(32):8138-43 [18685038]
Exp Gerontol. 2008 Sep;43(9):840-6 [18602982]
Nature. 2008 Aug 28;454(7208):1065-71 [18756247]
Exp Neurol. 2008 Oct;213(2):372-80 [18692046]
J Leukoc Biol. 2008 Oct;84(4):932-9 [18495785]
Glia. 2008 Dec;56(16):1799-808 [18661554]
J Neurosci. 2008 Oct 29;28(44):11263-8 [18971468]
Nat Rev Immunol. 2008 Dec;8(12):958-69 [19029990]
Brain. 2009 Feb;132(Pt 2):288-95 [18567623]
Brain Behav Immun. 2009 Mar;23(3):309-17 [18814846]
J Neurosci. 2009 Mar 18;29(11):3518-28 [19295157]
Neuroimmunomodulation. 2001;9(4):183-92 [11847480]
Glia. 2002 Mar 1;37(3):229-40 [11857681]
Glia. 2002 Mar 15;37(4):314-27 [11870871]
Mol Neurobiol. 2002 Feb;25(1):1-17 [11890454]
Mol Neurobiol. 2009 Jun;39(3):190-208 [19283516]
J Neuroimmunol. 2009 May 29;210(1-2):3-12 [19269040]
Annu Rev Physiol. 2009;71:333-59 [18851707]
Curr Opin Investig Drugs. 2009 Jul;10(7):672-80 [19579173]
Curr Top Microbiol Immunol. 2009;336:137-53 [19688332]
Acta Neuropathol. 2009 Oct;118(4):475-85 [19513731]
J Neurosci. 2009 Sep 23;29(38):11982-92 [19776284]
J Neurosci. 2009 Oct 28;29(43):13435-44 [19864556]
Glia. 2010 Jan 1;58(1):11-28 [19544386]
Brain Behav Immun. 2010 Jan;24(1):31-40 [19559784]
Glia. 2010 Feb;58(3):253-63 [19705460]
J Neurosci Res. 2010 May 1;88(6):1348-54 [20025063]
J Cell Mol Med. 2009 Sep;13(9B):3251-9 [19298529]
Arch Immunol Ther Exp (Warsz). 2010 Apr;58(2):91-6 [20143170]
Biochem Soc Trans. 2010 Apr;38(2):476-81 [20298206]
J Neurotrauma. 2010 Mar;27(3):565-85 [20030560]
Glia. 2010 May;58(7):790-801 [20091784]
CNS Neurol Disord Drug Targets. 2010 Apr;9(2):174-91 [20205642]
Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7975-80 [20375278]
Nature. 2006 Apr 20;440(7087):1054-9 [16547515]
Brain Res. 2006 May 17;1089(1):171-8 [16635480]
J Cereb Blood Flow Metab. 2006 Jul;26(7):974-82 [16395292]
Nat Neurosci. 2006 Jul;9(7):917-24 [16732273]
Annu Rev Immunol. 2009;27:119-45 [19302036]
Eur J Neurosci. 2009 Mar;29(6):1108-18 [19302147]
J Neurosci. 2009 Apr 1;29(13):3974-80 [19339593]
J Neurochem. 2009 May;109 Suppl 1:117-25 [19393017]
Neurobiol Aging. 1998 Jan-Feb;19(1):47-55 [9562503]
Br J Pharmacol. 1998 Apr;123(7):1304-10 [9579723]
FEBS Lett. 1998 Jun 12;429(2):167-72 [9650583]
J Comp Neurol. 1998 Aug 31;398(3):333-46 [9714147]
Prog Neurobiol. 1998 Oct;56(2):173-89 [9760700]
Brain Res. 1998 Dec 14;814(1-2):13-25 [9838024]
J Neurosci. 1999 Mar 1;19(5):1708-16 [10024357]
Neuroscience. 1999;89(4):1379-90 [10362322]
J Neuroimmunol. 1999 Jan 1;93(1-2):139-48 [10378877]
Microsc Res Tech. 1999 Jun 15;45(6):359-82 [10402264]
Immunol Rev. 1999 Jun;169:225-39 [10450520]
J Neurosci Res. 1999 Oct 1;58(1):191-201 [10491582]
J Neuroimmunol. 2005 Feb;159(1-2):12-9 [15652398]
Brain Res Brain Res Rev. 2005 Feb;48(1):16-42 [15708626]
Curr Opin Neurobiol. 2005 Feb;15(1):101-7 [15721751]
J Exp Med. 2005 Feb 21;201(4):647-57 [15728241]
Behav Brain Res. 2005 Apr 15;159(1):145-51 [15795008]
Mol Cell Neurosci. 2005 May;29(1):128-38 [15866053]
J Exp Med. 2005 May 16;201(10):1579-89 [15897275]
Nat Neurosci. 2005 Jun;8(6):752-8 [15895084]
Science. 2005 May 27;308(5726):1314-8 [15831717]
Cereb Cortex. 2005 Jul;15(7):938-49 [15483047]
J Immunol. 2005 Jul 1;175(1):342-9 [15972667]
J Neurosci Res. 2005 Aug 1;81(3):302-13 [15954124]
J Neurosci. 2005 Aug 17;25(33):7548-57 [16107642]
Glia. 2005 Nov 1;52(2):119-26 [15920729]
J Immunol. 2005 Oct 1;175(7):4320-30 [16177072]
Nature. 2005 Dec 15;438(7070):1017-21 [16355225]
Neuron. 2006 Feb 16;49(4):489-502 [16476660]
Cell. 2006 Feb 24;124(4):783-801 [16497588]
BMC Neurol. 2006;6:12 [16512913]
FASEB J. 2006 Apr;20(6):750-2 [16464958]
Neurobiol Aging. 2006 May;27(5):717-22 [15890435]
Neurotoxicology. 2012 Mar;33(2):191-206 [22322212]
Neurobiol Aging. 2012 Jun;33(6):1067-72 [21051106]
Science. 2012 Apr 6;336(6077):86-90 [22442384]
Purinergic Signal. 2012 Jun;8(2):301-10 [22222817]
Immunol Rev. 2006 Oct;213:48-65 [16972896]
Biochem Biophys Res Commun. 2006 Oct 27;349(3):913-9 [16962563]
FASEB J. 2006 Oct;20(12):2081-92 [17012260]
J Comp Neurol. 2006 Dec 1;499(4):565-82 [17029271]
J Neuropathol Exp Neurol. 2006 Nov;65(11):1090-7 [17086106]
Nat Neurosci. 2006 Dec;9(12):1512-9 [17115040]
J Exp Med. 2006 Nov 27;203(12):2627-38 [17116734]
J Neurosci. 2006 Dec 6;26(49):12826-37 [17151286]
Glia. 2007 Feb;55(3):233-8 [17106878]
Pediatr Res. 2007 Jan;61(1):15-20 [17211134]
Glia. 2007 Mar;55(4):360-8 [17136771]
Glia. 2007 Mar;55(4):412-24 [17203473]
J Exp Med. 2007 Jan 22;204(1):171-80 [17190836]
Brain Res Rev. 2007 Feb;53(2):344-54 [17188751]
Glia. 2007 Apr 15;55(6):604-16 [17299767]
Rejuvenation Res. 2007 Mar;10(1):61-74 [17378753]
Glia. 2007 Jun;55(8):810-21 [17357150]
Neuroscience. 2007 Apr 25;146(1):248-54 [17293054]
J Neurosci. 2007 May 2;27(18):4957-68 [17475804]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.pharmthera.2013.04.013
ER  - 



TY  - JOUR
T1  - A new approach to synergize academic and guideline-compliant research: the CLARITY-BPA research program.
AN  - 1416694340; 23747832
AB  - Recently, medical research has seen a strong push toward translational research, or "bench to bedside" collaborations, that strive to enhance the utility of laboratory science for improving medical treatment. The success of that paradigm supports the potential application of the process to other fields, such as risk assessment. Close collaboration among academic, government, and industry scientists may enhance the translation of scientific findings to regulatory decision making. The National Toxicology Program (NTP), National Institute of Environmental Health Sciences (NIEHS), and U.S. Food and Drug Administration (FDA) developed a consortium-based research program to link more effectively academic and guideline-compliant research. An initial proof-of-concept collaboration, the Consortium Linking Academic and Regulatory Insights on BPA Toxicity (CLARITY-BPA), uses bisphenol A (BPA) as a test chemical. The CLARITY-BPA program combines a core perinatal guideline-compliant 2-year chronic toxicity study with mechanistic studies/endpoints conducted by academic investigators. Twelve extramural grantees were selected by NIEHS through an RFA-based initiative to participate in the overall study design and conduct disease-relevant investigations using tissues and animals from the core study. While the study is expected to contribute to our understanding of potential effects of BPA, it also has ramifications beyond this specific focus. Through CLARITY-BPA, NIEHS has established an unprecedented level of collaboration among extramural grantees and regulatory researchers. By drawing upon the strengths of academic and regulatory expertise and research approaches, CLARITY-BPA represents a potential new model for filling knowledge gaps, enhancing quality control, informing chemical risk assessment, and identifying new methods or endpoints for regulatory hazard assessments. Published by Elsevier Inc.
JF  - Reproductive toxicology (Elmsford, N.Y.)
AU  - Schug, Thaddeus T
AU  - Heindel, Jerrold J
AU  - Camacho, Luísa
AU  - Delclos, K Barry
AU  - Howard, Paul
AU  - Johnson, Anne F
AU  - Aungst, Jason
AU  - Keefe, Dennis
AU  - Newbold, Retha
AU  - Walker, Nigel J
AU  - Thomas Zoeller, R
AU  - Bucher, John R
AD  - National Institute of Environmental Health Sciences/National Institutes of Health, Division of Extramural Research, Research Triangle Park, NC 27709, United States. Schugt@niehs.nih.gov
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 35
EP  - 40
VL  - 40
KW  - Benzhydryl Compounds
KW  - 0
KW  - Estrogens, Non-Steroidal
KW  - Phenols
KW  - bisphenol A
KW  - MLT3645I99
KW  - Index Medicus
KW  - Bisphenol A
KW  - NTP
KW  - Consortium-based research
KW  - FDA
KW  - NIEHS
KW  - Low dose
KW  - United States
KW  - Animals
KW  - Cooperative Behavior
KW  - United States Food and Drug Administration
KW  - Guideline Adherence
KW  - Humans
KW  - Risk Assessment -- standards
KW  - National Institute of Environmental Health Sciences (U.S.)
KW  - Benzhydryl Compounds -- toxicity
KW  - Estrogens, Non-Steroidal -- toxicity
KW  - Phenols -- toxicity
KW  - Research Design -- standards
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1416694340?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=A+new+approach+to+synergize+academic+and+guideline-compliant+research%3A+the+CLARITY-BPA+research+program.&rft.au=Schug%2C+Thaddeus+T%3BHeindel%2C+Jerrold+J%3BCamacho%2C+Lu%C3%ADsa%3BDelclos%2C+K+Barry%3BHoward%2C+Paul%3BJohnson%2C+Anne+F%3BAungst%2C+Jason%3BKeefe%2C+Dennis%3BNewbold%2C+Retha%3BWalker%2C+Nigel+J%3BThomas+Zoeller%2C+R%3BBucher%2C+John+R&rft.aulast=Schug&rft.aufirst=Thaddeus&rft.date=2013-09-01&rft.volume=40&rft.issue=&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2013.05.010
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-20
N1  - Date created - 2013-07-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.reprotox.2013.05.010
ER  - 



TY  - JOUR
T1  - Neem leaf glycoprotein is superior than cisplatin and sunitinib malate in restricting melanoma growth by normalization of tumor microenvironment.
AN  - 1399934035; 23747315
AB  - We have observed earlier that therapeutic treatment with neem leaf glycoprotein (NLGP) inhibits murine B16-melanoma growth in vivo and improves survivability of treated mice. Anti-tumor effect of NLGP is directly associated with enhanced CD8(+) T cell activity and downregulation of suppressive cellular functions. Objective of this present study is to know the efficacy of NLGP in comparison to two popular drugs, Cisplatin and Sunitinib malate (Sutent) in relation to the modulation of tumor microenvironment (TME). Analysis of cytokine milieu within TME revealed IL-10, TGFβ, IL-6 rich type 2 characters was significantly switched to type 1 microenvironment with dominance of IFNγ and IL-2 within NLGP-TME, which was not found in other cases; however Cisplatin-TME appeared better in type 2 to type 1 conversion than Sutent-TME as evidenced by RT-PCR, ELISA and immunohistochemical analysis. NLGP-TME educated CD8(+) T cells exhibited greater cytotoxicity to B16 Melanoma cells in vitro and these cells showed comparatively higher expression of cytotoxicity related molecules, perforin and granzyme B than Cisplatin-TME and Sutent-TME educated T cells. Adoptive transfer of NLGP-TME exposed T cells, but not PBS-TME exposed cells in mice, is able to significantly inhibit the growth of melanoma in vivo. Such tumor growth inhibition was in significantly lower extent when therapeutic CD8(+) T cells were exposed to either Cisplatin-TME or Sutent-TME or control-TME. Accumulated evidences strongly suggest that non toxic NLGP normalized TME allows T cells to perform optimally than other TMEs under study to inhibit the melanoma growth. 
          Copyright © 2013 Elsevier B.V. All rights reserved.
JF  - International immunopharmacology
AU  - Barik, Subhasis
AU  - Bhuniya, Avishek
AU  - Banerjee, Saptak
AU  - Das, Arnab
AU  - Sarkar, Madhurima
AU  - Paul, Tanmoy
AU  - Ghosh, Tithi
AU  - Ghosh, Sarbari
AU  - Roy, Soumyabrata
AU  - Pal, Smarajit
AU  - Bose, Anamika
AU  - Baral, Rathindranath
AD  - Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India.
Y1  - 2013/09//
PY  - 2013
DA  - September 2013
SP  - 42
EP  - 49
VL  - 17
IS  - 1
KW  - Antineoplastic Agents
KW  - 0
KW  - Cytokines
KW  - Glycoproteins
KW  - Indoles
KW  - Pyrroles
KW  - Cisplatin
KW  - Q20Q21Q62J
KW  - sunitinib
KW  - V99T50803M
KW  - Index Medicus
KW  - B16 melanoma
KW  - Neem leaf glycoprotein
KW  - Tumor microenvironment
KW  - Sunitinib malate
KW  - Animals
KW  - Cytokines -- genetics
KW  - CD8-Positive T-Lymphocytes
KW  - Gene Expression Regulation, Neoplastic -- physiology
KW  - Mice, Inbred C57BL
KW  - Mice
KW  - Cytokines -- metabolism
KW  - Cell Line, Tumor
KW  - Neoplasms, Experimental -- drug therapy
KW  - Antineoplastic Agents -- therapeutic use
KW  - Female
KW  - Cisplatin -- therapeutic use
KW  - Glycoproteins -- chemistry
KW  - Indoles -- therapeutic use
KW  - Azadirachta -- chemistry
KW  - Pyrroles -- therapeutic use
KW  - Plant Leaves -- chemistry
KW  - Glycoproteins -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399934035?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neem+leaf+glycoprotein+is+superior+than+cisplatin+and+sunitinib+malate+in+restricting+melanoma+growth+by+normalization+of+tumor+microenvironment.&rft.au=Barik%2C+Subhasis%3BBhuniya%2C+Avishek%3BBanerjee%2C+Saptak%3BDas%2C+Arnab%3BSarkar%2C+Madhurima%3BPaul%2C+Tanmoy%3BGhosh%2C+Tithi%3BGhosh%2C+Sarbari%3BRoy%2C+Soumyabrata%3BPal%2C+Smarajit%3BBose%2C+Anamika%3BBaral%2C+Rathindranath&rft.aulast=Barik&rft.aufirst=Subhasis&rft.date=2013-09-01&rft.volume=17&rft.issue=1&rft.spage=42&rft.isbn=&rft.btitle=&rft.title=International+immunopharmacology&rft.issn=1878-1705&rft_id=info:doi/10.1016%2Fj.intimp.2013.05.005
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-03
N1  - Date created - 2013-07-12
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.intimp.2013.05.005
ER  - 



TY  - JOUR
T1  - MicroRNA-106b-25 cluster expression is associated with early disease recurrence and targets caspase-7 and focal adhesion in human prostate cancer.
AN  - 1429215303; 22986525
AB  - The miR-106b-25 microRNA (miRNA) cluster is a candidate oncogene in human prostate cancer. Here, we report that miRNAs encoded by miR-106b-25 are upregulated in both primary tumors and distant metastasis. Moreover, increased tumor miR-106b expression was associated with disease recurrence and the combination of high miR-106b and low CASP7 (caspase-7) expressions in primary tumors was an independent predictor of early disease recurrence (adjusted hazard ratio=4.1; 95% confidence interval: 1.6-12.3). To identify yet unknown oncogenic functions of miR-106b, we overexpressed it in LNCaP human prostate cancer cells to examine miR-106b-induced global expression changes among protein-coding genes. The approach revealed that CASP7 is a direct target of miR-106b, which was confirmed by western blot analysis and a 3'-untranslated region reporter assay. Moreover, selected phenotypes induced by miR-106b knockdown in DU145 human prostate cancer cells did not develop when both miR-106b and CASP7 expression were inhibited. Further analyses showed that CASP7 is downregulated in primary prostate tumors and metastatic lesions across multiple data sets and is by itself associated with disease recurrence and disease-specific survival. Using bioinformatics, we also observed that miR-106b-25 may specifically influence focal adhesion-related pathways. This observation was experimentally examined using miR-106b-25-transduced 22Rv1 human prostate cancer cells. After infection with a miR-106b-25 lentiviral expression construct, 22Rv1 cells showed increased adhesion to basement membrane- and bone matrix-related filaments and enhanced soft agar growth. In summary, miR-106b-25 was found to be associated with prostate cancer progression and disease outcome and may do so by altering apoptosis- and focal adhesion-related pathways.
JF  - Oncogene
AU  - Hudson, R S
AU  - Yi, M
AU  - Esposito, D
AU  - Glynn, S A
AU  - Starks, A M
AU  - Yang, Y
AU  - Schetter, A J
AU  - Watkins, S K
AU  - Hurwitz, A A
AU  - Dorsey, T H
AU  - Stephens, R M
AU  - Croce, C M
AU  - Ambs, S
AD  - Laboratory of Human Carcinogenesis, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892-4258, USA.
Y1  - 2013/08/29/
PY  - 2013
DA  - 2013 Aug 29
SP  - 4139
EP  - 4147
VL  - 32
IS  - 35
KW  - 3' Untranslated Regions
KW  - 0
KW  - MIRN106 microRNA, human
KW  - MIRN32 microRNA, human
KW  - MicroRNAs
KW  - CASP7 protein, human
KW  - EC 3.4.22.-
KW  - Caspase 7
KW  - Index Medicus
KW  - Extracellular Matrix -- metabolism
KW  - Humans
KW  - Neoplasm Metastasis
KW  - Cell Line, Tumor
KW  - Male
KW  - Prostatic Neoplasms -- etiology
KW  - Gene Expression Regulation, Neoplastic
KW  - Prostatic Neoplasms -- pathology
KW  - Neoplasm Recurrence, Local -- etiology
KW  - Prostatic Neoplasms -- genetics
KW  - Focal Adhesions
KW  - Caspase 7 -- genetics
KW  - MicroRNAs -- physiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1429215303?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=MicroRNA-106b-25+cluster+expression+is+associated+with+early+disease+recurrence+and+targets+caspase-7+and+focal+adhesion+in+human+prostate+cancer.&rft.au=Hudson%2C+R+S%3BYi%2C+M%3BEsposito%2C+D%3BGlynn%2C+S+A%3BStarks%2C+A+M%3BYang%2C+Y%3BSchetter%2C+A+J%3BWatkins%2C+S+K%3BHurwitz%2C+A+A%3BDorsey%2C+T+H%3BStephens%2C+R+M%3BCroce%2C+C+M%3BAmbs%2C+S&rft.aulast=Hudson&rft.aufirst=R&rft.date=2013-08-29&rft.volume=32&rft.issue=35&rft.spage=4139&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2012.424
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-04
N1  - Date created - 2013-08-30
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Res. 2011 Oct 1;71(19):6230-9 [21816906]
Eur Urol. 2011 May;59(5):671-81 [21296484]
Oncogene. 2012 Oct 11;31(41):4460-71 [22266859]
Oncogene. 2012 Dec 13;31(50):5162-71 [22286770]
J Med Genet. 2009 Aug;46(8):497-510 [19505876]
Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020]
Nat Cell Biol. 2003 Aug;5(8):733-40 [12844146]
Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43 [7724580]
Cell. 2005 Mar 11;120(5):635-47 [15766527]
Nature. 2005 Jun 9;435(7043):828-33 [15944707]
Oncogene. 2006 Feb 16;25(7):1090-8 [16247466]
Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279]
Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9136-41 [16754881]
Biochem Biophys Res Commun. 2006 Oct 13;349(1):59-68 [16934749]
Nature. 2007 Jun 28;447(7148):1130-4 [17554337]
Nat Genet. 2008 Jan;40(1):43-50 [18066065]
Nature. 2008 Jan 10;451(7175):147-52 [18185580]
Cancer Cell. 2008 Mar;13(3):272-86 [18328430]
Mol Cell Biol. 2008 Apr;28(7):2167-74 [18212054]
Prostate. 2008 Aug 1;68(11):1152-64 [18459106]
Cancer Res. 2008 Aug 1;68(15):6162-70 [18676839]
Nature. 2008 Sep 4;455(7209):64-71 [18668037]
Cancer Res. 2008 Oct 15;68(20):8191-4 [18922889]
Science. 2008 Dec 12;322(5908):1695-9 [19008416]
Gastroenterology. 2009 May;136(5):1689-700 [19422085]
Cancer Sci. 2009 Jul;100(7):1234-42 [19486339]
Cancer Res. 2009 Sep 15;69(18):7165-9 [19738047]
Sci Signal. 2010;3(117):ra29 [20388916]
Mol Cancer Res. 2010 Apr;8(4):529-38 [20353999]
BMC Med Genomics. 2010;3:8 [20233430]
Cancer Cell. 2010 Jul 13;18(1):11-22 [20579941]
PLoS One. 2011;6(1):e16138 [21283765]
Oncogene. 2011 Feb 17;30(7):806-21 [20956944]
Prostate. 2011 May;71(6):567-74 [20878953]
Oncogene. 2012 Feb 23;31(8):978-91 [21765474]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/onc.2012.424
ER  - 



TY  - JOUR
T1  - Mimicking of Estradiol Binding by Flame Retardants and Their Metabolites: A Crystallographic Analysis
AN  - 1677960185; 18741291
AB  - Background: Brominated flame retardants (BFRs), used in many types of consumer goods, are being studied because of concerns about possible health effects related to endocrine disruption, immunotoxicity, reproductive toxicity, and neurotoxicity. Tetrabromobisphenol A (TBBPA), the most widely used BFR, and human metabolites of certain congeners of polybrominated diphenyl ether (e.g., 3-OH-BDE-47) have been suggested to inhibit estrogen sulfotransferase, potentially affecting estrogen metabolism. Objectives: Our primary goal was to understand the structural mechanism for inhibition of the hormone-metabolizing enzyme estrogen sulfotransferase by certain BFRs. We also sought to understand various factors that facilitate the binding of flame retardants in the enzyme binding pocket. Methods: We used X-ray crystallography to obtain atomic detail of the binding modes of TBBPA and 3-OH-BDE-47 to estrogen sulfotransferase for comparison with binding of the endogenous substrate estradiol. Results: The crystal structures reveal how BFRs mimic estradiol binding as well as the various interactions between the compounds and protein residues that facilitate its binding. In addition, the structures provide insights into the ability of the sulfotransferase substrate binding pocket to accommodate a range of halogenated compounds that satisfy minimal structural criteria. Conclusions: Our results show how BFRs or their metabolites can bind to and inhibit a key hormone-metabolizing enzyme, potentially causing endocrine disruption. Citation: Gosavi RA, Knudsen GA, Birnbaum LS, Pedersen LC. 2013. Mimicking of estradiol binding by flame retardants and their metabolites: a crystallographic analysis. Environ Health Perspect 121:1194-1199; http://dx.doi.org/10.1289/ehp.1306902
JF  - Environmental Health Perspectives
AU  - Gosavi, Rajendrakumar A
AU  - Knudsen, Gabriel A
AU  - Birnbaum, Linda S
AU  - Pedersen, Lars C
AD  - Laboratory of Structural Biology, National Institute of Environmental Health Sciences, and
Y1  - 2013/08/19/
PY  - 2013
DA  - 2013 Aug 19
SP  - 1194
EP  - 1199
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 0
SN  - 0091-6765, 0091-6765
KW  - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - Estrogens
KW  - Flame retardants
KW  - Enzymes
KW  - Crystallography
KW  - Metabolites
KW  - Health
KW  - Disruption
KW  - Binding
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677960185?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Mimicking+of+Estradiol+Binding+by+Flame+Retardants+and+Their+Metabolites%3A+A+Crystallographic+Analysis&rft.au=Gosavi%2C+Rajendrakumar+A%3BKnudsen%2C+Gabriel+A%3BBirnbaum%2C+Linda+S%3BPedersen%2C+Lars+C&rft.aulast=Gosavi&rft.aufirst=Rajendrakumar&rft.date=2013-08-19&rft.volume=121&rft.issue=0&rft.spage=1194&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306902
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2015-05-04
DO  - http://dx.doi.org/10.1289/ehp.1306902
ER  - 



TY  - JOUR
T1  - Prospective Study of Ultraviolet Radiation Exposure and Mortality Risk in the United States
AN  - 1434030640; 18453454
AB  - Geographic variations in mortality rate in the United States could be due to several hypothesized factors, one of which is exposure to solar ultraviolet radiation (UVR). Limited evidence from previous prospective studies has been inconclusive. The association between ambient residential UVR exposure and total and cause-specific mortality risks in a regionally diverse cohort (346,615 white, non-Hispanic subjects, 50-71 years of age, in the National Institutes of Health (NIH)-AARP Diet and Health Study) was assessed, with accounting for individual-level confounders. UVR exposure (averaged for 1978-1993 and 1996-2005) from NASA's Total Ozone Mapping Spectrometer was linked to the US Census Bureau 2000 census tract of participants' baseline residence. Multivariate-adjusted Cox proportional-hazards models were used to estimate hazard ratios and 95% confidence intervals. Over 12 years, UVR exposure was associated with total deaths (n = 41,425; hazard ratio for highest vs. lowest quartiles (HR sub(Q4 vs. Q1)) = 1.06, 95% confidence interval (CI): 1.03, 1.09; P sub(trend) < 0.001) and with deaths (all P sub(trend) < 0.05) due to cancer (HR sub(Q4 vs. Q1) = 1.06, 95% CI: 1.02, 1.11), cardiovascular disease (HR sub(Q4 vs. Q1) = 1.06, 95% CI: 1.00, 1.12), respiratory disease (HR sub(Q4 vs. Q1) = 1.37, 95% CI: 1.21, 1.55), and stroke (HR sub(Q4 vs. Q1) = 1.16, 95% CI: 1.01, 1.33) but not with deaths due to injury, diabetes, or infectious disease. These results suggest that UVR exposure might not be beneficial for longevity.
JF  - American Journal of Epidemiology
AU  - Lin, Shih-Wen
AU  - Wheeler, David C
AU  - Park, Yikyung
AU  - Spriggs, Michael
AU  - Hollenbeck, Albert R
AU  - Freedman, D Michal
AU  - Abnet, Christian C
AD  - Correspondence to Dr. Shih-Wen Lin, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, 6E404, MSC9768, Bethesda, MD 20892., lins4@mail.nih.gov
Y1  - 2013/08/15/
PY  - 2013
DA  - 2013 Aug 15
SP  - 521
EP  - 533
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 178
IS  - 4
SN  - 0002-9262, 0002-9262
KW  - Toxicology Abstracts; Risk Abstracts
KW  - epidemiology
KW  - mortality
KW  - prospective
KW  - sunlight
KW  - ultraviolet radiation
KW  - vitamin D
KW  - Age
KW  - Injuries
KW  - Respiratory diseases
KW  - Models
KW  - U.V. radiation
KW  - Infectious diseases
KW  - Ultraviolet radiation
KW  - Mapping
KW  - Geographical variations
KW  - Ozone
KW  - Diets
KW  - Mortality
KW  - Stroke
KW  - Longevity
KW  - Cancer
KW  - Diabetes mellitus
KW  - Health risks
KW  - USA
KW  - Census
KW  - Cardiovascular diseases
KW  - X 24390:Radioactive Materials
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434030640?accountid=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=Prospective+Study+of+Ultraviolet+Radiation+Exposure+and+Mortality+Risk+in+the+United+States&rft.au=Lin%2C+Shih-Wen%3BWheeler%2C+David+C%3BPark%2C+Yikyung%3BSpriggs%2C+Michael%3BHollenbeck%2C+Albert+R%3BFreedman%2C+D+Michal%3BAbnet%2C+Christian+C&rft.aulast=Lin&rft.aufirst=Shih-Wen&rft.date=2013-08-15&rft.volume=178&rft.issue=4&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws589
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Diets; Mortality; Age; Injuries; Stroke; Cancer; Longevity; Models; Diabetes mellitus; U.V. radiation; Infectious diseases; Census; Geographical variations; Cardiovascular diseases; Mapping; Ozone; Health risks; Ultraviolet radiation; Respiratory diseases; USA
DO  - http://dx.doi.org/10.1093/aje/kws589
ER  - 



TY  - JOUR
T1  - Research on the Premotor Symptoms of Parkinson's Disease: Clinical and Etiological Implications
AN  - 1492641092; 18963485
AB  - Background: The etiology and natural history of Parkinson's disease (PD) are not well understood. Some non-motor symptoms such as hyposmia, rapid eye movement sleep behavior disorder, and constipation may develop during the prodromal stage of PD and precede PD diagnosis by years. Objectives: We examined the promise and pitfalls of research on premotor symptoms of PD and developed priorities and strategies to understand their clinical and etiological implications. Methods: This review was based on a workshop, Parkinson's Disease Premotor Symptom Symposium, held 7-8 June 2012 at the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina. Discussion: Research on premotor symptoms of PD may offer an excellent opportunity to characterize high-risk populations and to better understand PD etiology. Such research may lead to evaluation of novel etiological hypotheses such as the possibility that environmental toxicants or viruses may initiate PD pathogenesis in the gastrointestinal tract or olfactory bulb. At present, our understanding of premotor symptoms of PD is in its infancy and faces many obstacles. These symptoms are often not specific to PD and have low positive predictive value for early PD diagnosis. Further, the pathological bases and biological mechanisms of these premotor symptoms and their relevance to PD pathogenesis are poorly understood. Conclusion: This is an emerging research area with important data gaps to be filled. Future research is needed to understand the prevalence of multiple premotor symptoms and their etiological relevance to PD. Animal experiments and mechanistic studies will further understanding of the biology of these premotor symptoms and test novel etiological hypothesis. Citation: Chen H, Burton EA, Ross GW, Huang X, Savica R, Abbott RD, Ascherio A, Caviness JN, Gao X, Gray KA, Hong JS, Kamel F, Jennings D, Kirshner A, Lawler C, Liu R, Miller GW, Nussbaum R, Peddada SD, Comstock Rick A, Ritz B, Siderowf AD, Tanner CM, Troster AI, Zhang J. 2013. Research on the premotor symptoms of Parkinson's Disease: clinical and etiological implications. Environ Health Perspect 121:1245-1252; http://dx.doi.org/10.1289/ehp.1306967
JF  - Environmental Health Perspectives
AU  - Chen, Honglei
AU  - Burton, Edward A
AU  - Ross, GWebster
AU  - Huang, Xuemei
AU  - Savica, Rodolfo
AU  - Abbott, Robert D
AU  - Ascherio, Alberto
AU  - Caviness, John N
AU  - Gao, Xiang
AU  - Gray, Kimberly A
AU  - Hong, Jau-Shyong
AU  - Kamel, Freya
AU  - Jennings, Danna
AU  - Kirshner, Annette
AU  - Lawler, Cindy
AU  - Liu, Rui
AU  - Miller, Gary W
AU  - Nussbaum, Robert
AU  - Peddada, Shyamal D
AU  - Rick, Amy Comstock
AU  - Ritz, Beate
AU  - Siderowf, Andrew D
AU  - Tanner, Caroline M
AU  - Troster, Alexander I
AU  - Zhang, Jing
AD  - National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
Y1  - 2013/08/09/
PY  - 2013
DA  - 2013 Aug 09
SP  - 1245
EP  - 1252
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 2
SN  - 0091-6765, 0091-6765
KW  - Risk Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - USA, North Carolina
KW  - Historical account
KW  - Etiology
KW  - Toxicants
KW  - Parkinson's disease
KW  - Reviews
KW  - Viruses
KW  - Environmental health
KW  - Priorities
KW  - R2 23060:Medical and environmental health
KW  - H 12000:Epidemiology and Public Health
KW  - ENA 07:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492641092?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Research+on+the+Premotor+Symptoms+of+Parkinson%27s+Disease%3A+Clinical+and+Etiological+Implications&rft.au=Chen%2C+Honglei%3BBurton%2C+Edward+A%3BRoss%2C+GWebster%3BHuang%2C+Xuemei%3BSavica%2C+Rodolfo%3BAbbott%2C+Robert+D%3BAscherio%2C+Alberto%3BCaviness%2C+John+N%3BGao%2C+Xiang%3BGray%2C+Kimberly+A%3BHong%2C+Jau-Shyong%3BKamel%2C+Freya%3BJennings%2C+Danna%3BKirshner%2C+Annette%3BLawler%2C+Cindy%3BLiu%2C+Rui%3BMiller%2C+Gary+W%3BNussbaum%2C+Robert%3BPeddada%2C+Shyamal+D%3BRick%2C+Amy+Comstock%3BRitz%2C+Beate%3BSiderowf%2C+Andrew+D%3BTanner%2C+Caroline+M%3BTroster%2C+Alexander+I%3BZhang%2C+Jing&rft.aulast=Chen&rft.aufirst=Honglei&rft.date=2013-08-09&rft.volume=121&rft.issue=2&rft.spage=1245&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306967
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Historical account; Etiology; Toxicants; Reviews; Parkinson's disease; Viruses; Priorities; Environmental health; USA, North Carolina
DO  - http://dx.doi.org/10.1289/ehp.1306967
ER  - 



TY  - JOUR
T1  - Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial
AN  - 1427005142; 18328696
AB  - Background Studies of dietary omega -3 fatty acid intake and prostate cancer risk are inconsistent; however, recent large prospective studies have found increased risk of prostate cancer among men with high blood concentrations of long-chain omega -3 polyunsaturated fatty acids ([LC omega -3PUFA] 20:5 omega 3; 22:5 omega 3; 22:6 omega 3]. This case-cohort study examines associations between plasma phospholipid fatty acids and prostate cancer risk among participants in the Selenium and Vitamin E Cancer Prevention Trial. Methods Case subjects were 834 men diagnosed with prostate cancer, of which 156 had high-grade cancer. The subcohort consisted of 1393 men selected randomly at baseline and from within strata frequency matched to case subjects on age and race. Proportional hazards models estimated hazard ratios (HR) and 95% confidence intervals (CI) for associations between fatty acids and prostate cancer risk overall and by grade. All statistical tests were two-sided. Results Compared with men in the lowest quartiles of LC omega -3PUFA, men in the highest quartile had increased risks for low-grade (HR = 1.44, 95% CI = 1.08 to 1.93), high-grade (HR = 1.71, 95% CI = 1.00 to 2.94), and total prostate cancer (HR = 1.43, 95% CI = 1.09 to 1.88). Associations were similar for individual long-chain omega -3 fatty acids. Higher linoleic acid ( omega -6) was associated with reduced risks of low-grade (HR = 0.75, 95% CI = 0.56 to 0.99) and total prostate cancer (HR = 0.77, 95% CI = 0.59 to 1.01); however, there was no dose response. Conclusions This study confirms previous reports of increased prostate cancer risk among men with high blood concentrations of LC omega -3PUFA. The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis. Recommendations to increase LC omega -3PUFA intake should consider its potential risks.
JF  - Journal of the National Cancer Institute
AU  - Brasky, Theodore M
AU  - Darke, Amy K
AU  - Song, Xiaoling
AU  - Tangen, Catherine M
AU  - Goodman, Phyllis J
AU  - Thompson, Ian M
AU  - Meyskens, Frank L
AU  - Goodman, Gary E
AU  - Minasian, Lori M
AU  - Parnes, Howard L
AU  - Klein, Eric A
AU  - Kristal, Alan R
AD  - Affiliations of authors:Department of Internal Medicine, Division of Cancer Prevention and Control, The Ohio State University College of Medicine, Columbus, OH (TMB); Cancer Prevention Program (TMB, XS, GEG, ARK) and SWOG Statistical Center (AKD, CMT, PJG), Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Urology, University of Texas-San Antonio Health Science Center, San Antonio, TX (IMT); Chao Family Comprehensive Cancer Center, University of California Irvine, Irvine, CA (FLM); Department of Environmental Health (GEG) and Department of Epidemiology (ARK), University of Washington, Seattle, WA; Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD (LMM, HLP); Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH (EAK)., Theodore.Brasky@osumc.edu
Y1  - 2013/08/07/
PY  - 2013
DA  - 2013 Aug 07
SP  - 1132
EP  - 1141
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 15
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Age
KW  - Prostate cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427005142?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Plasma+Phospholipid+Fatty+Acids+and+Prostate+Cancer+Risk+in+the+SELECT+Trial&rft.au=Brasky%2C+Theodore+M%3BDarke%2C+Amy+K%3BSong%2C+Xiaoling%3BTangen%2C+Catherine+M%3BGoodman%2C+Phyllis+J%3BThompson%2C+Ian+M%3BMeyskens%2C+Frank+L%3BGoodman%2C+Gary+E%3BMinasian%2C+Lori+M%3BParnes%2C+Howard+L%3BKlein%2C+Eric+A%3BKristal%2C+Alan+R&rft.aulast=Brasky&rft.aufirst=Theodore&rft.date=2013-08-07&rft.volume=105&rft.issue=15&rft.spage=1132&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjt174
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Prostate cancer
DO  - http://dx.doi.org/10.1093/jnci/djt174
ER  - 



TY  - JOUR
T1  - Cancer Incidence Trends Among Asian American Populations in the United States, 1990-2008
AN  - 1427003487; 18328700
AB  - Background National cancer incidence trends are presented for eight Asian American groups: Asian Indians/Pakistanis, Chinese, Filipinos, Japanese, Kampucheans, Koreans, Laotians, and Vietnamese. Methods Cancer incidence data from 1990 through 2008 were obtained from 13 Surveillance, Epidemiology, End Results (SEER) registries. Incidence rates from 1990 through 2008 and average percentage change were computed using SEER*Stat and Joinpoint software. The annual percentage change (APC) in incidence rates was estimated with 95% confidence intervals (95% CIs) calculated for both the rate and APC estimates. Rates for non-Hispanic whites are presented for comparison. Results Prostate cancer was the most common malignancy among most groups, followed by lung, colorectal, liver, and stomach cancers. Breast cancer was generally the most common cancer in women, followed by colorectal and lung cancers; liver, cervix, thyroid, and stomach cancers also ranked highly. Among men, increasing trends were observed for prostate (Asian Indians and Pakistanis: APC 1990-2003 = 2.2, 95% CI = 0.3 to 4.1; Filipinos: APC 1990-1994 = 19.0, 95% CI = 4.5 to 35.4; Koreans: APC 1990-2008 = 2.9, 95% CI = 1.8 to 4.0), colorectal (Koreans: APC 1990-2008 = 2.2, 95% CI = 0.9 to 3.5), and liver cancers (Filipinos: APC 1990-2008 = 1.6, 95% CI = 0.4 to 2.7; Koreans: APC 1990-2006 = 2.1, 95% CI = 0.4 to 3.7; Vietnamese: APC 1990-2008 = 1.6, 95% CI = 0.3 to 2.8), whereas lung and stomach cancers generally remained stable or decreased. Among women, increases were observed for uterine cancer (Asian Indians: APC 1990-2008 = 3.0, 95% CI = 0.3 to 5.8; Chinese: APC 2004-2008 = 7.0, 95% CI = 1.4 to 12.9; Filipina: APC 1990-2008 = 3.0, 95% CI = 2.4 to 3.7; Japanese: APC 1990-2008 = 1.1, 95% CI = 0.1 to 2.0), colorectal cancer (Koreans: APC 1990-2008 = 2.8, 95% CI = 1.7 to 3.9; Laotians: APC: 1990-2008 = 5.9, 95% CI = 4.0 to 7.7), lung cancer (Filipinas: APC 1990-2008 = 2.1, 95% CI = 1.4 to 2.8; Koreans: APC 1990-2008 = 2.1, 95% CI = 0.6 to 3.6), thyroid cancer (Filipinas: APC 1990-2008 = 2.5, 95% CI = 1.7 to 3.3), and breast cancer in most groups (APC 1990-2008 from 1.2 among Vietnamese and Chinese to 4.7 among Koreans). Decreases were observed for stomach (Chinese and Japanese), colorectal (Chinese), and cervical cancers (Laotians and Vietnamese). Conclusions These data fill a critical knowledge gap concerning the cancer experience of Asian American groups and highlight where increased preventive, screening, and surveillance efforts are needed-in particular, lung cancer among Filipina and Korean women and Asian Indian/Pakistani men, breast cancer among all women, and liver cancer among Vietnamese, Laotian, and Kampuchean women and Filipino, Kampuchean, and Vietnamese men.
JF  - Journal of the National Cancer Institute
AU  - Gomez, Scarlett Lin
AU  - Noone, Anne-Michelle
AU  - Lichtensztajn, Daphne Y
AU  - Scoppa, Steve
AU  - Gibson, James T
AU  - Liu, Lihua
AU  - Morris, Cyllene
AU  - Kwong, Sandy
AU  - Fish, Kari
AU  - Wilkens, Lynne R
AU  - Goodman, Marc T
AU  - Deapen, Dennis
AU  - Miller, Barry A
AD  - Affiliations of authors:Cancer Prevention Institute of California, Fremont, CA (SLG, DYL); Department of Health Research and Policy, School of Medicine, Stanford, CA (SLG); Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD (A-MN, BAM); Information Management Services, Silver Spring, MD (SS, JTG); Los Angeles Cancer Surveillance Program, Keck School of Medicine, Los Angeles, CA (LL, DMD); California Cancer Registry, Sacramento, CA (CM, SK); Cancer Registry of Greater California, Sacramento, CA (KF); University of Hawaii Cancer Center, Honolulu, HI (LRW); Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA (DMD)., scarlett@cpic.org
Y1  - 2013/08/07/
PY  - 2013
DA  - 2013 Aug 07
SP  - 1096
EP  - 1110
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 15
SN  - 0027-8874, 0027-8874
KW  - Health & Safety Science Abstracts
KW  - Breast cancer
KW  - INW, Japan
KW  - Lung cancer
KW  - H 11000:Diseases/Injuries/Trauma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427003487?accountid=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+the+National+Cancer+Institute&rft.atitle=Cancer+Incidence+Trends+Among+Asian+American+Populations+in+the+United+States%2C+1990-2008&rft.au=Gomez%2C+Scarlett+Lin%3BNoone%2C+Anne-Michelle%3BLichtensztajn%2C+Daphne+Y%3BScoppa%2C+Steve%3BGibson%2C+James+T%3BLiu%2C+Lihua%3BMorris%2C+Cyllene%3BKwong%2C+Sandy%3BFish%2C+Kari%3BWilkens%2C+Lynne+R%3BGoodman%2C+Marc+T%3BDeapen%2C+Dennis%3BMiller%2C+Barry+A&rft.aulast=Gomez&rft.aufirst=Scarlett&rft.date=2013-08-07&rft.volume=105&rft.issue=15&rft.spage=1096&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjt157
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Lung cancer; INW, Japan
DO  - http://dx.doi.org/10.1093/jnci/djt157
ER  - 



TY  - JOUR
T1  - Hormonal risk factors and invasive epithelial ovarian cancer risk by parity
AN  - 1427003557; 18326514
AB  - Background: Recent studies have suggested that several ovarian cancer risk factors differ by parity status, but these findings have not been confirmed. We evaluated whether known risk factors of ovarian cancer differ between nulliparous and parous women using data from two large prospective cohorts. Methods: Data from the National Institutes of Health-AARP Diet and Health Study and the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial were combined for this analysis. Cox regression models were used to estimate associations with ovarian cancer risk. Risk heterogeneity by parity status was assessed using likelihood-ratio tests. Results: Among the 125 437 women included in the analysis, there were 16 589 (13%) nulliparous women and 108 848 (87%) parous women. Of the 623 women diagnosed with invasive epithelial ovarian cancer, 102 (16%) were nulliparous and 521 (84%) were parous. While parity reduced ovarian cancer risk, no differences were found for other risk factors by parity. Among ever users of hormone therapy, body mass index suggestively increased the risk of ovarian cancer by 1.5-fold in nulliparous but not parous women (P-heterogeneity=0.08). Conclusion: While nulliparous women have higher ovarian cancer risk than parous women, our findings suggest that the relative effects of most other risk factors do not differ by parity.
JF  - British Journal of Cancer
AU  - Bodelon, C
AU  - Wentzensen, N
AU  - Schonfeld, S J
AU  - Visvanathan, K
AU  - Hartge, P
AU  - Park, Y
AU  - Pfeiffer, R M
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, USA
Y1  - 2013/08/06/
PY  - 2013
DA  - 2013 Aug 06
SP  - 769
EP  - 776
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 109
IS  - 3
SN  - 0007-0920, 0007-0920
KW  - Risk Abstracts
KW  - Parity
KW  - Diets
KW  - Lung
KW  - Risk factors
KW  - Body mass
KW  - Ovarian carcinoma
KW  - Hormones
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427003557?accountid=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=Hormonal+risk+factors+and+invasive+epithelial+ovarian+cancer+risk+by+parity&rft.au=Bodelon%2C+C%3BWentzensen%2C+N%3BSchonfeld%2C+S+J%3BVisvanathan%2C+K%3BHartge%2C+P%3BPark%2C+Y%3BPfeiffer%2C+R+M&rft.aulast=Bodelon&rft.aufirst=C&rft.date=2013-08-06&rft.volume=109&rft.issue=3&rft.spage=769&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.344
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Diets; Parity; Lung; Body mass; Risk factors; Ovarian carcinoma; Hormones; Cancer
DO  - http://dx.doi.org/10.1038/bjc.2013.344
ER  - 



TY  - JOUR
T1  - A prospective investigation of fish, meat and cooking-related carcinogens with endometrial cancer incidence
AN  - 1427003419; 18326505
AB  - Background: There are limited prospective studies of fish and meat intakes with risk of endometrial cancer and findings are inconsistent. Methods: We studied associations between fish and meat intakes and endometrial cancer incidence in the large, prospective National Institutes of Health-AARP Diet and Health Study. Intakes of meat mutagens 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) and benzo(a)pyrene (BaP) were also calculated. We used Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: We observed no associations with endometrial cancer risk comparing the highest to lowest intake quintiles of red (HR=0.91, 95% CI 0.77-1.08), white (0.98, 0.83-1.17), processed meats (1.02, 0.86-1.21) and fish (1.10, 95% CI 0.93-1.29). We also found no associations between meat mutagen intakes and endometrial cancer. Conclusion: Our findings do not support an association between meat or fish intakes or meat mutagens and endometrial cancer.
JF  - British Journal of Cancer
AU  - Arem, H
AU  - Gunter, M J
AU  - Cross, A J
AU  - Hollenbeck, A R
AU  - Sinha, R
AD  - Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Rockville, MD 20852, USA
Y1  - 2013/08/06/
PY  - 2013
DA  - 2013 Aug 06
SP  - 756
EP  - 760
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 109
IS  - 3
SN  - 0007-0920, 0007-0920
KW  - Risk Abstracts
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427003419?accountid=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=A+prospective+investigation+of+fish%2C+meat+and+cooking-related+carcinogens+with+endometrial+cancer+incidence&rft.au=Arem%2C+H%3BGunter%2C+M+J%3BCross%2C+A+J%3BHollenbeck%2C+A+R%3BSinha%2C+R&rft.aulast=Arem&rft.aufirst=H&rft.date=2013-08-06&rft.volume=109&rft.issue=3&rft.spage=756&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.252
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Cancer
DO  - http://dx.doi.org/10.1038/bjc.2013.252
ER  - 



TY  - JOUR
T1  - Vacated niches, competitive release and the community ecology of pathogen eradication
AN  - 1566850678; 20369870
AB  - A recurring theme in the epidemiological literature on disease eradication is that each pathogen occupies an ecological niche, and eradication of one pathogen leaves a vacant niche that favours the emergence of new pathogens to replace it. However, eminent figures have rejected this view unequivocally, stating that there is no basis to fear pathogen replacement and even that pathogen niches do not exist. After exploring the roots of this controversy, I propose resolutions to disputed issues by drawing on broader ecological theory, and advance a new consensus based on robust mechanistic principles. I argue that pathogen eradication (and cessation of vaccination) leads to a 'vacated niche', which could be re-invaded by the original pathogen if introduced. Consequences for other pathogens will vary, with the crucial mechanisms being competitive release, whereby the decline of one species allows its competitors to perform better, and evolutionary adaptation. Hence, eradication can cause a quantitative rise in the incidence of another infection, but whether this leads to emergence as an endemic pathogen depends on additional factors. I focus on the case study of human monkeypox and its rise following smallpox eradication, but also survey how these ideas apply to other pathogens and discuss implications for eradication policy.
JF  - Philosophical Transactions of the Royal Society of London, Series B: Biological Sciences
AU  - Lloyd-Smith, James O
AD  - Fogarty International Center, National Institutes of Health, , Bethesda, MD 20892, USA, jlloydsmith@ucla.edu
Y1  - 2013/08/05/
PY  - 2013
DA  - 2013 Aug 05
SP  - 20120150
PB  - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom
VL  - 368
IS  - 1623
SN  - 0962-8436, 0962-8436
KW  - Ecology Abstracts
KW  - pathogen eradication
KW  - competitive release
KW  - ecological niche
KW  - monkeypox
KW  - zoonosis
KW  - emerging infectious disease
KW  - Smallpox
KW  - Monkeypox
KW  - Adaptations
KW  - Fear
KW  - Niches
KW  - Leaves
KW  - Roots
KW  - Pathogens
KW  - Infection
KW  - Vaccination
KW  - Evolution
KW  - D 04040:Ecosystem and Ecology Studies
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566850678?accountid=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=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=Vacated+niches%2C+competitive+release+and+the+community+ecology+of+pathogen+eradication&rft.au=Lloyd-Smith%2C+James+O&rft.aulast=Lloyd-Smith&rft.aufirst=James&rft.date=2013-08-05&rft.volume=368&rft.issue=1623&rft.spage=20120150&rft.isbn=&rft.btitle=&rft.title=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628436&rft_id=info:doi/10.1098%2Frstb.2012.0150
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2016-07-07
N1  - SubjectsTermNotLitGenreText - Smallpox; Monkeypox; Adaptations; Fear; Niches; Leaves; Roots; Pathogens; Infection; Vaccination; Evolution
DO  - http://dx.doi.org/10.1098/rstb.2012.0150
ER  - 



TY  - JOUR
T1  - Prokaryotic Proteasomes: Nanocompartments of Degradation
AN  - 1768582633; PQ0002686728
AB  - Proteasomes are self-compartmentalized energy-dependent proteolytic machines found in Archaea, Actinobacteria species of bacteria and eukaryotes. Proteasomes consist of two separate protein complexes, the core particle that hydrolyzes peptide bonds and an AAA+ ATPase domain responsible for the binding, unfolding and translocation of protein substrates into the core particle for degradation. Similarly to eukaryotes, proteasomes play a central role in protein degradation and can be essential in Archaea. Core particles associate with and utilize a variety of ATPase complexes to carry out protein degradation in Archaea. In actinobacterial species, such as Mycobacterium tuberculosis, proteasome-mediated degradation is associated with pathogenesis and does not appear to be essential. Interestingly, both actinobacterial species and Archaea use small proteins to covalently modify proteins, prokaryotic ubiquitin-like proteins (Pup) in Actinobacteria and ubiquitin-like small archaeal modifier proteins (SAMP) in Archaea. These modifications may play a role in proteasome targeting similar to the ubiquitin-proteasome system in eukaryotes. Copyright copyright 2013 S. Karger AG, Basel
JF  - Journal of Molecular Microbiology and Biotechnology
AU  - Humbard, Matthew A
AU  - Maupin-Furlow, Julie A
AD  - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Md.
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 321
EP  - 334
PB  - S. Karger AG, P.O. Box Basel CH-4009 Switzerland
VL  - 23
IS  - 4-5
SN  - 1464-1801, 1464-1801
KW  - Biotechnology and Bioengineering Abstracts
KW  - Prokaryotic ubiquitin-like protein
KW  - Pupylation
KW  - Small archaeal modifier proteins
KW  - Sampylation
KW  - Proteolysis
KW  - Protein transport
KW  - Adenosinetriphosphatase
KW  - Archaea
KW  - Core particles
KW  - Actinobacteria
KW  - proteasomes
KW  - Mycobacterium tuberculosis
KW  - Ubiquitin
KW  - W 30940:Products
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768582633?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Molecular+Microbiology+and+Biotechnology&rft.atitle=Prokaryotic+Proteasomes%3A+Nanocompartments+of+Degradation&rft.au=Humbard%2C+Matthew+A%3BMaupin-Furlow%2C+Julie+A&rft.aulast=Humbard&rft.aufirst=Matthew&rft.date=2013-08-01&rft.volume=23&rft.issue=4-5&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Microbiology+and+Biotechnology&rft.issn=14641801&rft_id=info:doi/10.1159%2F000351348
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-02-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Proteolysis; Protein transport; Adenosinetriphosphatase; Core particles; proteasomes; Ubiquitin; Archaea; Actinobacteria; Mycobacterium tuberculosis
DO  - http://dx.doi.org/10.1159/000351348
ER  - 



TY  - JOUR
T1  - Prospero-related homeobox 1 (Prox1) functions as a novel modulator of retinoic acid-related orphan receptors alpha - and gamma -mediated transactivation
AN  - 1701488760; PQ0001757635
AB  - In this study, we identify Prospero-related homeobox 1 (Prox1) as a novel co-repressor of the retinoic acid-related orphan receptors, ROR alpha and ROR gamma . Prox1 interacts directly with ROR gamma and ROR alpha and negatively regulates their transcriptional activity. The AF2 domain of RORs is essential for the interaction, whereas Prox1 interacts with RORs through either its 28 amino acids N-terminal region or its C-terminal prospero-like domain. ROR gamma antagonists stabilize the interaction between ROR gamma and Prox1. The homeodomain and the interaction through the prospero-like domain of Prox1 are critical for its repression of ROR transcriptional activity. Chromatin immunoprecipitation analysis demonstrated that in liver, Prox1 is recruited to the ROR response element sites of the clock genes, brain and muscle Arnt-like protein 1 (Bmal1), neuronal PAS domain protein 2 (Npas2) and cryptochrome 1 (Cry1), as part of the same complex as RORs. Knockdown of Prox1 by siRNAs in human hepatoma Huh-7 cells increased the expression of ROR gamma and several ROR-target genes, along with increased histone acetylation at these ROR response element sites. Chromatin immunoprecipitation sequencing analysis suggests that Prox1 is a potential ROR target gene in liver, which is supported by the regulation of the rhythmic expression of Prox1 by ROR gamma . Our data suggest that Prox1 is part of a feedback loop that negatively regulates the transcriptional control of clock and metabolic networks by RORs.
JF  - Nucleic Acids Research
AU  - Takeda, Yukimasa
AU  - Jetten, Anton M
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 6992
EP  - 7008
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 41
IS  - 14
SN  - 0305-1048, 0305-1048
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids
KW  - Histones
KW  - Chromatin
KW  - Orphan receptors
KW  - metabolic networks
KW  - Immunomodulation
KW  - Antagonists
KW  - Hepatoma
KW  - Neuromodulation
KW  - Feedback
KW  - Cryptochromes
KW  - Data processing
KW  - Amino acids
KW  - BMAL1 protein
KW  - Regulatory sequences
KW  - Muscles
KW  - Brain
KW  - Immunoprecipitation
KW  - Transcription
KW  - Homeobox
KW  - Acetylation
KW  - siRNA
KW  - Liver
KW  - Rhythms
KW  - NPAS2 protein
KW  - Gene silencing
KW  - G 07720:Immunogenetics
KW  - N 14820:DNA Metabolism & Structure
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701488760?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Prospero-related+homeobox+1+%28Prox1%29+functions+as+a+novel+modulator+of+retinoic+acid-related+orphan+receptors+alpha+-+and+gamma+-mediated+transactivation&rft.au=Takeda%2C+Yukimasa%3BJetten%2C+Anton+M&rft.aulast=Takeda&rft.aufirst=Yukimasa&rft.date=2013-08-01&rft.volume=41&rft.issue=14&rft.spage=6992&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/10.1093%2Fnar%2Fgkt447
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-08-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Histones; Chromatin; Orphan receptors; metabolic networks; Immunomodulation; Antagonists; Hepatoma; Neuromodulation; Feedback; Cryptochromes; Amino acids; Data processing; Regulatory sequences; BMAL1 protein; Immunoprecipitation; Brain; Muscles; Transcription; Homeobox; Acetylation; siRNA; Liver; NPAS2 protein; Rhythms; Gene silencing
DO  - http://dx.doi.org/10.1093/nar/gkt447
ER  - 



TY  - JOUR
T1  - Beta-blockers may reduce intrusive thoughts in newly diagnosed cancer patients
AN  - 1665153905
AB  - Objective A cancer diagnosis provokes significant levels of emotional distress, with intrusive thoughts being the most common manifestation among breast cancer survivors. Cancer-related intrusive thoughts can take the form of emotional memories, flashbacks, nightmares, and intrusive images. Emotional arousal after a severe life stressor prolongs adrenergic activation, which in turn may increase risk for post-traumatic symptomatology. However, antihypertensive beta-blockers block adrenergic activation and are known to reduce traumatic memories and related psychological distress. Thus, the current study examined the association between beta-blocker use and the severity of cancer-related intrusive thoughts and related symptoms following a cancer diagnosis. Methods The 174 breast and 36 female colorectal cancer patients who had recently undergone diagnostic screening or biopsy included 39 beta-blocker users and 171 non-users. Prior to any cancer treatment including surgery, participants completed questionnaires that included the Impact of Events Scale and the Center for Epidemiological Studies Depression Scale. Analyses controlled for age, education, cancer stage, cancer type, days since diagnosis, marital status, depression, and comorbidities. Results Although the high rates of cancer-related distress in this sample were similar to those of other studies with recently diagnosed patients, beta-blocker users endorsed 32% fewer cancer-related intrusive thoughts than non-users. Conclusions Recently diagnosed cancer patients using beta-blockers reported less cancer-related psychological distress. These results suggest that beta-blocker use may benefit cancer patientsʼ psychological adjustment following diagnosis, and provide a promising direction for future investigations on the pharmacological benefits of beta-blockers for cancer-related distress. Copyright © 2012 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Lindgren, Monica E
AU  - Fagundes, Christopher P
AU  - Alfano, Catherine M
AU  - Povoski, Stephen P
AU  - Agnese, Doreen M
AU  - Arnold, Mark W
AU  - Farrar, William B
AU  - Yee, Lisa D
AU  - Carson, William E
AU  - Schmidt, Carl R
AU  - Kiecolt-Glaser, Janice K
AD  - Institute for Behavioral Medicine Research, College of Medicine, The Ohio State University, Columbus, OH, USA., Department of Psychology, The Ohio State University, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, College of Medicine, The Ohio State University, Columbus, OH, USA. ; National Cancer Institute, Bethesda, MD, USA. ; Department of Surgery, College of Medicine, The Ohio State University, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, College of Medicine, The Ohio State University, Columbus, OH, USA., Department of Psychology, The Ohio State University, Columbus, OH, USA., National Cancer Institute, Bethesda, MD, USA., Department of Psychiatry, College of Medicine, The Ohio State University, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, College of Medicine, The Ohio State University, Columbus, OH, USA.; Department of Psychology, The Ohio State University, Columbus, OH, USA.
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 1889
EP  - 1894
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 8
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Adjustment
KW  - Nightmares
KW  - Psychological distress
KW  - Screening
KW  - Severity
KW  - Surgery
KW  - Survivors
KW  - Arousal
KW  - Beta-blockers
KW  - Biopsy
KW  - Breast cancer
KW  - Cancer
KW  - Clinical assessment
KW  - Colorectal cancer
KW  - Depression
KW  - Diagnosis
KW  - Emotional distress
KW  - Health education
KW  - Marital status
KW  - Memories
KW  - Newly diagnosed
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665153905?accountid=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=Beta-blockers+may+reduce+intrusive+thoughts+in+newly+diagnosed+cancer+patients&rft.au=Lindgren%2C+Monica+E%3BFagundes%2C+Christopher+P%3BAlfano%2C+Catherine+M%3BPovoski%2C+Stephen+P%3BAgnese%2C+Doreen+M%3BArnold%2C+Mark+W%3BFarrar%2C+William+B%3BYee%2C+Lisa+D%3BCarson%2C+William+E%3BSchmidt%2C+Carl+R%3BKiecolt-Glaser%2C+Janice+K&rft.aulast=Lindgren&rft.aufirst=Monica&rft.date=2013-08-01&rft.volume=22&rft.issue=8&rft.spage=1889&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3233
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.3233
ER  - 



TY  - JOUR
T1  - Borrelia burgdorferi Linear Plasmid 28-3 Confers a Selective Advantage in an Experimental Mouse-Tick Infection Model
AN  - 1664211512; PQ0001204310
AB  - Borrelia burgdorferi, the bacterium that causes Lyme disease, has a unique segmented genome consisting of numerous linear and circular plasmids and a linear chromosome. Many of these genetic elements have been found to encode factors critical for B. burgdorferi to complete the infectious cycle. However, several plasmids remain poorly characterized, and their roles during infection with B. burgdorferi have not been elucidated. To more fully characterize the role of one of the four 28-kb linear plasmids, lp28-3, we generated strains specifically lacking lp28-3 and assayed the contribution of genes carried by lp28-3 to B. burgdorferi infection. We found that lp28-3 does not carry any genes that are strictly required for infection of a mouse or tick and that lp28-3-deficient spirochetes are competent at causing a disseminated infection. Interestingly, spirochetes containing lp28-3 were at a selective advantage compared to lp28-3-deficient spirochetes when coinjected into a mouse, and this advantage was reflected in the population of spirochetes acquired by feeding ticks. Our data demonstrate that genes carried by lp28-3, although not essential, contribute to the fitness of B. burgdorferi during infection.
JF  - Infection and Immunity
AU  - Dulebohn, Daniel P
AU  - Bestor, Aaron
AU  - Rosa, Patricia A
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 2986
EP  - 2996
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 8
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Immunology Abstracts
KW  - Fitness
KW  - Genomes
KW  - Feeding
KW  - Data processing
KW  - Borrelia burgdorferi
KW  - Ixodidae
KW  - Disseminated infection
KW  - Animal models
KW  - Plasmids
KW  - Models
KW  - Spirochetes
KW  - Chromosomes
KW  - Lyme disease
KW  - J 02410:Animal Diseases
KW  - F 06910:Microorganisms & Parasites
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664211512?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Borrelia+burgdorferi+Linear+Plasmid+28-3+Confers+a+Selective+Advantage+in+an+Experimental+Mouse-Tick+Infection+Model&rft.au=Dulebohn%2C+Daniel+P%3BBestor%2C+Aaron%3BRosa%2C+Patricia+A&rft.aulast=Dulebohn&rft.aufirst=Daniel&rft.date=2013-08-01&rft.volume=81&rft.issue=8&rft.spage=2986&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00219-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Number of references - 57
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Genomes; Fitness; Feeding; Spirochetes; Chromosomes; Data processing; Disseminated infection; Animal models; Plasmids; Models; Lyme disease; Borrelia burgdorferi; Ixodidae
DO  - http://dx.doi.org/10.1128/IAI.00219-13
ER  - 



TY  - JOUR
T1  - Differential Virulence and Disease Progression following Mycobacterium tuberculosis Complex Infection of the Common Marmoset (Callithrix jacchus)
AN  - 1664202218; PQ0001204339
AB  - Existing small-animal models of tuberculosis (TB) rarely develop cavitary disease, limiting their value for assessing the biology and dynamics of this highly important feature of human disease. To develop a smaller primate model with pathology similar to that seen in humans, we experimentally infected the common marmoset (Callithrix jacchus) with diverse strains of Mycobacterium tuberculosis of various pathogenic potentials. These included recent isolates of the modern Beijing lineage, the Euro-American X lineage, and M. africanum. All three strains produced fulminant disease in this animal with a spectrum of progression rates and clinical sequelae that could be monitored in real time using 2-deoxy-2-[18F]fluoro-d-glucose (FDG) positron emission tomography (PET)/computed tomography (CT). Lesion pathology at sacrifice revealed the entire spectrum of lesions observed in human TB patients. The three strains produced different rates of progression to disease, various extents of extrapulmonary dissemination, and various degrees of cavitation. The majority of live births in this species are twins, and comparison of results from siblings with different infecting strains allowed us to establish that the infection was highly reproducible and that the differential virulence of strains was not simply host variation. Quantitative assessment of disease burden by FDG-PET/CT provided an accurate reflection of the pathology findings at necropsy. These results suggest that the marmoset offers an attractive small-animal model of human disease that recapitulates both the complex pathology and spectrum of disease observed in humans infected with various M. tuberculosis strain clades.
JF  - Infection and Immunity
AU  - Via, Laura E
AU  - Weiner, Danielle M
AU  - Schimel, Daniel
AU  - Lin, Philana Ling
AU  - Dayao, Emmanuel
AU  - Tankersley, Sarah L
AU  - Cai, Ying
AU  - Coleman, M Teresa
AU  - Tomko, Jaime
AU  - Paripati, Praveen
AD  - National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, USA, cbarry@niaid.nih.gov.
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 2909
EP  - 2919
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 8
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Autopsy
KW  - Complications
KW  - Callithrix jacchus
KW  - Animal models
KW  - Infection
KW  - Virulence
KW  - Twins
KW  - Cavitation
KW  - Computed tomography
KW  - Positron emission tomography
KW  - Tuberculosis
KW  - Siblings
KW  - Mycobacterium tuberculosis
KW  - J 02410:Animal Diseases
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664202218?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Differential+Virulence+and+Disease+Progression+following+Mycobacterium+tuberculosis+Complex+Infection+of+the+Common+Marmoset+%28Callithrix+jacchus%29&rft.au=Via%2C+Laura+E%3BWeiner%2C+Danielle+M%3BSchimel%2C+Daniel%3BLin%2C+Philana+Ling%3BDayao%2C+Emmanuel%3BTankersley%2C+Sarah+L%3BCai%2C+Ying%3BColeman%2C+M+Teresa%3BTomko%2C+Jaime%3BParipati%2C+Praveen&rft.aulast=Via&rft.aufirst=Laura&rft.date=2013-08-01&rft.volume=81&rft.issue=8&rft.spage=2909&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00632-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Number of references - 63
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Virulence; Autopsy; Twins; Cavitation; Complications; Computed tomography; Positron emission tomography; Animal models; Siblings; Tuberculosis; Infection; Callithrix jacchus; Mycobacterium tuberculosis
DO  - http://dx.doi.org/10.1128/IAI.00632-13
ER  - 



TY  - JOUR
T1  - Borrelia hermsii Acquisition Order in Superinfected Ticks Determines Transmission Efficiency
AN  - 1664201332; PQ0001204337
AB  - Multilocus sequence typing of Borrelia hermsii isolates reveals its divergence into two major genomic groups (GG), but no differences in transmission efficiency or host pathogenicity are associated with these genotypes. To compare GGI and GGII in the tick-host infection cycle, we first determined if spirochetes from the two groups could superinfect the tick vector Ornithodoros hermsi. We infected mice with isolates from each group and fed ticks sequentially on these mice. We then fed the infected ticks on naive mice and measured GGI and GGII spirochete densities in vector and host, using quantitative PCR of genotype-specific chromosomal DNA sequences. Sequential feedings resulted in dual tick infections, showing that GGI or GGII primary acquisition did not block superinfection by a secondary agent. On transmission to naive mice at short intervals after acquisition, ticks with primary GGI and secondary GGII spirochete infections caused mixed GGI and GGII infections in mice. However, ticks with primary GGII and secondary GGI spirochete infections caused only GGII infections with all isolate pairs examined. At longer intervals after acquisition, the exclusion of GGI by GGII spirochetes declined and cotransmission predominated. We then examined GGI and GGII spirochetemia in mice following single inoculation and coinoculation by needle and found that GGI spirochete densities were reduced on multiple days when coinoculated with GGII. These findings indicate that dual GGI-GGII spirochete infections can persist in ticks and that transmission to a vertebrate host is dependent on the order of tick acquisition and the interval between acquisition and transmission events.
JF  - Infection and Immunity
AU  - Policastro, Paul F
AU  - Raffel, Sandra J
AU  - Schwan, Tom G
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 2899
EP  - 2908
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 8
SN  - 0019-9567, 0019-9567
KW  - Entomology Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Feeding
KW  - Borrelia hermsii
KW  - Ixodidae
KW  - Nucleotide sequence
KW  - Vectors
KW  - Genotypes
KW  - Superinfection
KW  - Disease transmission
KW  - multilocus sequence typing
KW  - Spirochetes
KW  - Pathogenicity
KW  - Inoculation
KW  - Polymerase chain reaction
KW  - genomics
KW  - Ornithodoros
KW  - Z 05360:Genetics and Evolution
KW  - J 02350:Immunology
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664201332?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Borrelia+hermsii+Acquisition+Order+in+Superinfected+Ticks+Determines+Transmission+Efficiency&rft.au=Policastro%2C+Paul+F%3BRaffel%2C+Sandra+J%3BSchwan%2C+Tom+G&rft.aulast=Policastro&rft.aufirst=Paul&rft.date=2013-08-01&rft.volume=81&rft.issue=8&rft.spage=2899&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00542-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Number of references - 33
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Feeding; Spirochetes; Pathogenicity; Nucleotide sequence; Inoculation; Polymerase chain reaction; Vectors; Genotypes; genomics; Superinfection; multilocus sequence typing; Disease transmission; Borrelia hermsii; Ixodidae; Ornithodoros
DO  - http://dx.doi.org/10.1128/IAI.00542-13
ER  - 



TY  - JOUR
T1  - Recruiting Trainees for a Global Health Research Workforce: The National Institutes of Health Fogarty International Clinical Research Scholars Program Selection Process
AN  - 1647016059; 21172183
AB  - Between 2004 and 2012, the National Institutes of Health Fogarty International Clinical Research Scholars (FICRS) Program provided 1-year mentored research training at low- and middle-income country sites for American and international health science doctoral students. We describe the centralized application process, US applicant characteristics, and predictors of selection/enrollment. FICRS received 1,084 applicants representing many health professions and biomedical disciplines at 132 US academic institutions; 219 students from 72 institutions were accepted and enrolled. Medical/osteopathic students comprised 88.9% of applicants and 85.8% of enrollees. Applicants from institutions with higher applicant numbers were two times as likely to be selected. In 2012, FICRS was decentralized among 20 institutions in five consortia (Global Health Fellows), with autonomous selection processes that emphasize post-doctoral trainees. If academia, government, or charitable foundations offer future opportunities to health professions students for international research, the FICRS experience predicts that they can attract substantial numbers of motivated trainees from diverse backgrounds.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Heimburger, Douglas C
AU  - Warner, Tokesha L
AU  - Carothers, Catherine Lem
AU  - Blevins, Meridith
AU  - Thomas, Yolanda
AU  - Gardner, Pierce
AU  - Primack, Aron
AU  - Vermund, Sten H
AD  - Vanderbilt Institute for Global Health, Departments of Medicine, Biostatistics, and Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee; Fogarty International Clinical Research Scholars and Fellows Support Center at Vanderbilt, Vanderbilt University, Nashville, Tennessee; Stony Brook University School of Medicine, Stony Brook, New York; Fogarty International Center, National Institutes of Health, Bethesda, Maryland; Vanderbilt University Institute for Global Health, 2525 West End Avenue, Suite 750, Nashville, TN 37203, douglas.heimburger@vanderbilt.edu
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 281
EP  - 287
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
IS  - 2
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology
KW  - K 03490:Miscellaneous
KW  - J 02490:Miscellaneous
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647016059?accountid=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=Recruiting+Trainees+for+a+Global+Health+Research+Workforce%3A+The+National+Institutes+of+Health+Fogarty+International+Clinical+Research+Scholars+Program+Selection+Process&rft.au=Heimburger%2C+Douglas+C%3BWarner%2C+Tokesha+L%3BCarothers%2C+Catherine+Lem%3BBlevins%2C+Meridith%3BThomas%2C+Yolanda%3BGardner%2C+Pierce%3BPrimack%2C+Aron%3BVermund%2C+Sten+H&rft.aulast=Heimburger&rft.aufirst=Douglas&rft.date=2013-08-01&rft.volume=89&rft.issue=2&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0677
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
DO  - http://dx.doi.org/10.4269/ajtmh.12-0677
ER  - 



TY  - JOUR
T1  - Prime-Boost Interval Matters: A Randomized Phase 1 Study to Identify the Minimum Interval Necessary to Observe the H5 DNA Influenza Vaccine Priming Effect
AN  - 1635033419; 20881927
AB  - Background. H5 DNA priming was previously shown to improve the antibody response to influenza A(H5N1) monovalent inactivated vaccine (MIV) among individuals for whom there was a 24-week interval between prime and boost receipt. This study defines the shortest prime-boost interval associated with an improved response to MIV. Methods. We administered H5 DNA followed by MIV at intervals of 4, 8, 12, 16, or 24 weeks and compared responses to that of 2 doses of MIV (prime-boost interval, 24 weeks). Results. H5 DNA priming with an MIV boost > or =12 weeks later showed an improved response, with a positive hemagglutination inhibition (HAI) titer in 91% of recipients (geometric mean titer [GMT], 141-206), compared with 55%-70% of recipients with an H5 DNA and MIV prime-boost interval of [< or =]8 weeks (GMT, 51-70) and 44% with an MIV-MIV primeboost interval of 24 weeks (GMT, 27). Conclusion. H5 DNA priming enhances antibody responses after an MIV boost when the prime-boost interval is 12-24 weeks.
JF  - Journal of Infectious Diseases
AU  - Ledgerwood, Julie E
AU  - Zephir, Kathryn
AU  - Hu, Zonghui
AU  - Wei, Chih-Jen
AU  - C, Lee Jah
AU  - Enama, Mary E
AU  - Hendel, Cynthia S
AU  - Sitar, Sandra
AU  - Bailer, Robert T
AU  - Koup, Richard A
AU  - Mascola, John R
AU  - Nabel, Gary J
AU  - Graham, Barney S
AD  - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bldg 10, Rm 5-2436, Bethesda, MD 20892, ledgerwood@mail.nih.gov
Y1  - 2013/08/01/
PY  - 2013
DA  - 2013 Aug 01
SP  - 418
EP  - 422
PB  - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 208
IS  - 3
SN  - 0022-1899, 0022-1899
KW  - Virology & AIDS Abstracts; Health & Safety Science Abstracts; Biochemistry Abstracts 2: Nucleic Acids
KW  - Avian influenza
KW  - DNA vaccine
KW  - H5N1
KW  - boost interval
KW  - hemagglutination inhibition
KW  - Influenza
KW  - Infectious diseases
KW  - DNA vaccines
KW  - Hemagglutination inhibition
KW  - DNA
KW  - Vaccines
KW  - Antibody response
KW  - V 22340:Antiviral Agents
KW  - N 14810:Methods
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635033419?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Prime-Boost+Interval+Matters%3A+A+Randomized+Phase+1+Study+to+Identify+the+Minimum+Interval+Necessary+to+Observe+the+H5+DNA+Influenza+Vaccine+Priming+Effect&rft.au=Ledgerwood%2C+Julie+E%3BZephir%2C+Kathryn%3BHu%2C+Zonghui%3BWei%2C+Chih-Jen%3BC%2C+Lee+Jah%3BEnama%2C+Mary+E%3BHendel%2C+Cynthia+S%3BSitar%2C+Sandra%3BBailer%2C+Robert+T%3BKoup%2C+Richard+A%3BMascola%2C+John+R%3BNabel%2C+Gary+J%3BGraham%2C+Barney+S&rft.aulast=Ledgerwood&rft.aufirst=Julie&rft.date=2013-08-01&rft.volume=208&rft.issue=3&rft.spage=418&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjit180
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-12-01
N1  - Last updated - 2016-04-13
N1  - SubjectsTermNotLitGenreText - Influenza; DNA vaccines; Hemagglutination inhibition; DNA; Antibody response; Vaccines; Infectious diseases
DO  - http://dx.doi.org/10.1093/infdis/jit180
ER  - 



TY  - JOUR
T1  - Use of OMIC technologies to study arsenic exposure in human populations
AN  - 1566842991; 20026861
AB  - Exposure to arsenic (As) in drinking water is a major health concern. More than 100 million individuals are exposed to levels over the current World Health Organization standard of 10 mu g/L worldwide. Arsenic is one of the few agents established as a human carcinogen prior to understanding its mechanism of carcinogenicity. OMIC technologies have enabled researchers to utilize agnostic approaches to explore new, unknown mechanisms through which As causes disease in exposed human populations. In this article, we present recent studies in which OMIC technologies have been used to explore differences in human biological samples to identify markers of exposure, disease susceptibility, and effect in As-exposed and/or diseased tissues. Environ. Mol. Mutagen. 54:589-595, 2013. copyright 2013 Wiley Periodicals, Inc.
JF  - Environmental and Molecular Mutagenesis
AU  - Moore, Lee E
AU  - Karami, Sara
AU  - Steinmaus, Craig
AU  - Cantor, Kenneth P
AD  - Division of Cancer Epidemiology and Genetics (DCEG), US National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland.
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 589
EP  - 595
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 54
IS  - 7
SN  - 0893-6692, 0893-6692
KW  - Toxicology Abstracts; Health & Safety Science Abstracts
KW  - Mutagens
KW  - Arsenic
KW  - Human populations
KW  - Carcinogens
KW  - Mutagenesis
KW  - Carcinogenicity
KW  - Drinking water
KW  - Technology
KW  - H 3000:Environment and Ecology
KW  - X 24360:Metals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566842991?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Use+of+OMIC+technologies+to+study+arsenic+exposure+in+human+populations&rft.au=Moore%2C+Lee+E%3BKarami%2C+Sara%3BSteinmaus%2C+Craig%3BCantor%2C+Kenneth+P&rft.aulast=Moore&rft.aufirst=Lee&rft.date=2013-08-01&rft.volume=54&rft.issue=7&rft.spage=589&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/10.1002%2Fem.21792
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Mutagens; Arsenic; Carcinogenicity; Carcinogens; Drinking water; Mutagenesis; Human populations; Technology
DO  - http://dx.doi.org/10.1002/em.21792
ER  - 



TY  - JOUR
T1  - Francisella tularensis SchuS4 and SchuS4 Lipids Inhibit IL-12p40 in Primary Human Dendritic Cells by Inhibition of IRF1 and IRF8
AN  - 1551630286; 20355555
AB  - Induction of innate immunity is essential for host survival of infection. Evasion and inhibition of innate immunity constitute a strategy used by pathogens, such as the highly virulent bacterium Francisella tularensis, to ensure their replication and transmission. The mechanism and bacterial components responsible for this suppression of innate immunity by F. tularensis are not defined. In this article, we demonstrate that lipids enriched from virulent F. tularensis strain SchuS4, but not attenuated live vaccine strain, inhibit inflammatory responses in vitro and in vivo. Suppression of inflammatory responses is associated with I Kappa B alpha -independent inhibition of NF- Kappa Bp65 activation and selective inhibition of activation of IFN regulatory factors. Interference with NF- Kappa Bp65 and IFN regulatory factors is also observed following infection with viable SchuS4. Together these data provide novel insight into how highly virulent bacteria selectively modulate the host to interfere with innate immune responses required for survival of infection.
JF  - Journal of Immunology
AU  - Ireland, Robin
AU  - Wang, Rong
AU  - Alinger, Joshua B
AU  - Small, Pamela
AU  - Bosio, Catharine M
AD  - Immunity to Pulmonary Pathogens Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; and
Y1  - 2013/08/01/
PY  - 2013
DA  - 2013 Aug 01
SP  - 1276
EP  - 1286
PB  - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States
VL  - 191
IS  - 3
SN  - 0022-1767, 0022-1767
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Data processing
KW  - Replication
KW  - Lipids
KW  - Survival
KW  - Francisella tularensis
KW  - Pathogens
KW  - Immunity
KW  - Infection
KW  - Inflammation
KW  - Dendritic cells
KW  - Interleukin 12
KW  - Interferon
KW  - Interferon regulatory factor 1
KW  - Immune response
KW  - Vaccines
KW  - F 06905:Vaccines
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551630286?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=Francisella+tularensis+SchuS4+and+SchuS4+Lipids+Inhibit+IL-12p40+in+Primary+Human+Dendritic+Cells+by+Inhibition+of+IRF1+and+IRF8&rft.au=Ireland%2C+Robin%3BWang%2C+Rong%3BAlinger%2C+Joshua+B%3BSmall%2C+Pamela%3BBosio%2C+Catharine+M&rft.aulast=Ireland&rft.aufirst=Robin&rft.date=2013-08-01&rft.volume=191&rft.issue=3&rft.spage=1276&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1300867
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-10-02
N1  - SubjectsTermNotLitGenreText - Data processing; Replication; Lipids; Survival; Immunity; Pathogens; Infection; Inflammation; Interferon; Interleukin 12; Dendritic cells; Interferon regulatory factor 1; Vaccines; Immune response; Francisella tularensis
DO  - http://dx.doi.org/10.4049/jimmunol.1300867
ER  - 



TY  - JOUR
T1  - Earth science input for evaluating spatially-distributed mesothelioma risk factors associated with environmental exposures to erionite and other elongate mineral particles
AN  - 1510396433; 2014-021210
JF  - International Conference on Medical Geology
AU  - Plumlee, Geoffrey S
AU  - Meeker, Gregory P
AU  - Van Gosen, Bradley S
AU  - San Juan, Carma A
AU  - Blitz, Thomas
AU  - Ellefsen, Karl J
AU  - Morman, Suzette A
AU  - Buck, Brenda J
AU  - Merkler, Doug
AU  - Miller, Aubrey
AU  - Finkelman, Robert B
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 71
PB  - [varies], [varies]
VL  - 5
KW  - silicates
KW  - erionite
KW  - medical geology
KW  - pollutants
KW  - pollution
KW  - diseases
KW  - air pollution
KW  - toxicity
KW  - zeolite group
KW  - mesothelioma
KW  - risk assessment
KW  - framework silicates
KW  - public health
KW  - 22:Environmental geology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510396433?accountid=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=International+Conference+on+Medical+Geology&rft.atitle=Earth+science+input+for+evaluating+spatially-distributed+mesothelioma+risk+factors+associated+with+environmental+exposures+to+erionite+and+other+elongate+mineral+particles&rft.au=Plumlee%2C+Geoffrey+S%3BMeeker%2C+Gregory+P%3BVan+Gosen%2C+Bradley+S%3BSan+Juan%2C+Carma+A%3BBlitz%2C+Thomas%3BEllefsen%2C+Karl+J%3BMorman%2C+Suzette+A%3BBuck%2C+Brenda+J%3BMerkler%2C+Doug%3BMiller%2C+Aubrey%3BFinkelman%2C+Robert+B&rft.aulast=Plumlee&rft.aufirst=Geoffrey&rft.date=2013-08-01&rft.volume=5&rft.issue=&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=International+Conference+on+Medical+Geology&rft.issn=&rft_id=info:doi/
LA  - English
DB  - GeoRef
N1  - Conference title - The 5th international conference on Medical geology and the 2nd symposium on Advances in geospatial technologies for health
N1  - Copyright - GeoRef, Copyright 2014, American Geosciences Institute.
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-03-27
N1  - CODEN - #07748
N1  - SubjectsTermNotLitGenreText - air pollution; diseases; erionite; framework silicates; medical geology; mesothelioma; pollutants; pollution; public health; risk assessment; silicates; toxicity; zeolite group
ER  - 



TY  - JOUR
T1  - Adequacy of human health data sources for evaluating spatially-distributed mesothelioma risk factors
AN  - 1510396160; 2014-021211
JF  - International Conference on Medical Geology
AU  - Weissman, David
AU  - Miller, Aubrey
AU  - Lockey, James E
AU  - Wood, John
AU  - Baumann, Francine
AU  - Ryan, Patrick H
AU  - Plumlee, Geoffrey S
AU  - San Juan, Carma A
AU  - Weis, Christopher P
AU  - Bennett, April L
AU  - Finkelman, Robert B
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 71
EP  - 72
PB  - [varies], [varies]
VL  - 5
KW  - United States
KW  - silicates
KW  - erionite
KW  - medical geology
KW  - pollutants
KW  - pollution
KW  - information management
KW  - diseases
KW  - data management
KW  - air pollution
KW  - toxicity
KW  - zeolite group
KW  - mesothelioma
KW  - framework silicates
KW  - public health
KW  - 22:Environmental geology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510396160?accountid=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=International+Conference+on+Medical+Geology&rft.atitle=Adequacy+of+human+health+data+sources+for+evaluating+spatially-distributed+mesothelioma+risk+factors&rft.au=Weissman%2C+David%3BMiller%2C+Aubrey%3BLockey%2C+James+E%3BWood%2C+John%3BBaumann%2C+Francine%3BRyan%2C+Patrick+H%3BPlumlee%2C+Geoffrey+S%3BSan+Juan%2C+Carma+A%3BWeis%2C+Christopher+P%3BBennett%2C+April+L%3BFinkelman%2C+Robert+B&rft.aulast=Weissman&rft.aufirst=David&rft.date=2013-08-01&rft.volume=5&rft.issue=&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=International+Conference+on+Medical+Geology&rft.issn=&rft_id=info:doi/
LA  - English
DB  - GeoRef
N1  - Conference title - The 5th international conference on Medical geology and the 2nd symposium on Advances in geospatial technologies for health
N1  - Copyright - GeoRef, Copyright 2014, American Geosciences Institute.
N1  - Date revised - 2014-01-01
N1  - Document feature - 1 table
N1  - Last updated - 2014-03-27
N1  - CODEN - #07748
N1  - SubjectsTermNotLitGenreText - air pollution; data management; diseases; erionite; framework silicates; information management; medical geology; mesothelioma; pollutants; pollution; public health; silicates; toxicity; United States; zeolite group
ER  - 



TY  - JOUR
T1  - International Adaptation: Psychosocial and Parenting Experiences of Caregivers Who Travel to the United States to Obtain Acute Medical Care for Their Seriously Ill Child
AN  - 1494299391; 201400729
AB  - Despite the increasing trend of travel for medical purposes, little is known about the experience of parents and other caregivers who come to the United States specifically to obtain medical treatment for their seriously ill child. In this exploratory, descriptive qualitative study, we used a semi-structured narrative guide to conduct in-depth interviews with 22 Spanish- or English-speaking caregivers about the challenges encountered and adaptation required when entering a new medical and cultural environment. Caregivers identified the language barrier and transnational parenting as challenges while reporting hospital staff and their own families as major sources of support. Using the results of the study as a guide, clinical and program implications are provided and recommendations for social work practice discussed. Adapted from the source document.
JF  - Social Work in Health Care
AU  - Margolis, Rachel
AU  - Ludi, Erica
AU  - Pao, Maryland
AU  - Wiener, Lori
AD  - Clinical Center, Social Work Department, National Institutes of Health, Bethesda, Maryland, USA Rachel.margolis@nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 669
EP  - 683
PB  - Taylor & Francis, Philadelphia PA
VL  - 52
IS  - 7
SN  - 0098-1389, 0098-1389
KW  - Methodology (Data Collection)
KW  - Caregivers
KW  - Terminal Illness
KW  - United States of America
KW  - Medicine
KW  - Childrearing Practices
KW  - Children
KW  - Child Care Services
KW  - Hospitals
KW  - article
KW  - 6140: illness & health care
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1494299391?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Work+in+Health+Care&rft.atitle=International+Adaptation%3A+Psychosocial+and+Parenting+Experiences+of+Caregivers+Who+Travel+to+the+United+States+to+Obtain+Acute+Medical+Care+for+Their+Seriously+Ill+Child&rft.au=Margolis%2C+Rachel%3BLudi%2C+Erica%3BPao%2C+Maryland%3BWiener%2C+Lori&rft.aulast=Margolis&rft.aufirst=Rachel&rft.date=2013-08-01&rft.volume=52&rft.issue=7&rft.spage=669&rft.isbn=&rft.btitle=&rft.title=Social+Work+in+Health+Care&rft.issn=00981389&rft_id=info:doi/10.1080%2F00981389.2013.798391
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2014-02-01
N1  - Last updated - 2016-09-28
N1  - CODEN - SWHCDO
N1  - SubjectsTermNotLitGenreText - Caregivers; Medicine; Childrearing Practices; United States of America; Children; Terminal Illness; Child Care Services; Hospitals; Methodology (Data Collection)
DO  - http://dx.doi.org/10.1080/00981389.2013.798391
ER  - 



TY  - JOUR
T1  - Work-related fatal injury among young persons in Australia, July 2000-June 2007
AN  - 1492606765; 18931785
AB  - Every year, young people are killed as a result of their work and the work of others in Australia. The loss of a young life is disproportionately high in potential years of life lost and lost productivity. The purpose of this study was to provide a detailed description of the industry and mechanism-specific fatal incidents involving young workers aged 15-24-years in Australia, and compare them with all workers. We retrospectively reviewed coronial records extracted from the National Coronial Information System (NCIS) for all work-related deaths in Australia from July 2000 to June 2007. A total of 232 young persons were fatally injured as a result of work-related activity in the seven year study period. Working for income, commuter and bystander deaths accounted for 148, 67 and 17 deaths respectively. The death rate for young workers was 1.24 per 100,000 employed person-years. This compared to an all age death rate of 2.22 per 100,000 employed person-years. The Agriculture, Forestry and Fishing sector had the highest industry-specific fatality rate for young workers. This was followed by the Transport, Postal and Warehousing industry, and Mining. In each sector, young worker's fatality rates were higher than the overall rate. The use of publicly available data did not allow for stratification by age group. However, these results update what is currently known about young worker deaths, using a low-cost, publicly available data source. In the absence of a rigorous surveillance and reporting system documenting young worker injury and fatality, these findings serve a quasi-surveillance role.
JF  - Safety Science
AU  - Ehsani, J P
AU  - McNeilly, B
AU  - Ibrahim, JE
AU  - Ozanne-Smith, J
AD  - University of Michigan School of Public Health, Ann Arbor, MI, United States, johnathon.ehsani@nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 57
SN  - 0925-7535, 0925-7535
KW  - Health & Safety Science Abstracts
KW  - Agriculture
KW  - Mortality
KW  - Age
KW  - Injuries
KW  - Stratification
KW  - Income
KW  - Fishing
KW  - Reviews
KW  - Australia
KW  - Mining
KW  - Information systems
KW  - Forestry
KW  - H 1000:Occupational Safety and Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492606765?accountid=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=Safety+Science&rft.atitle=Work-related+fatal+injury+among+young+persons+in+Australia%2C+July+2000-June+2007&rft.au=Ehsani%2C+J+P%3BMcNeilly%2C+B%3BIbrahim%2C+JE%3BOzanne-Smith%2C+J&rft.aulast=Ehsani&rft.aufirst=J&rft.date=2013-08-01&rft.volume=57&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Safety+Science&rft.issn=09257535&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Agriculture; Fishing; Mortality; Age; Injuries; Reviews; Mining; Stratification; Income; Forestry; Information systems; Australia
ER  - 



TY  - JOUR
T1  - Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells.
AN  - 1443381294; 23775793
AB  - The effects of diverse stresses on promoter selectivity and transcription regulation by the tumor suppressor p53 are poorly understood. We have taken a comprehensive approach to characterizing the human p53 network that includes p53 levels, binding, expression and chromatin changes under diverse stresses. Human osteosarcoma U2OS cells treated with anti-cancer drugs Doxorubicin (DXR) or Nutlin-3 (Nutlin) led to strikingly different p53 gene binding patterns based on chromatin immunoprecipitation with high-throughput sequencing experiments. Although two contiguous RRRCWWGYYY decamers is the consensus binding motif, p53 can bind a single decamer and function in vivo. Although the number of sites bound by p53 was six times greater for Nutlin than DXR, expression changes induced by Nutlin were much less dramatic compared with DXR. Unexpectedly, the solvent dimethylsulphoxide (DMSO) alone induced p53 binding to many sites common to DXR; however, this binding had no effect on target gene expression. Together, these data imply a two-stage mechanism for p53 transactivation where p53 binding only constitutes the first stage. Furthermore, both p53 binding and transactivation were associated with increased active histone modification histone H3 lysine 4 trimethylation. We discovered 149 putative new p53 target genes including several that are relevant to tumor suppression, revealing potential new targets for cancer therapy and expanding our understanding of the p53 regulatory network.
JF  - Nucleic acids research
AU  - Menendez, Daniel
AU  - Nguyen, Thuy-Ai
AU  - Freudenberg, Johannes M
AU  - Mathew, Viju J
AU  - Anderson, Carl W
AU  - Jothi, Raja
AU  - Resnick, Michael A
AD  - Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Research Triangle Park, NC 27709, USA, Systems Biology Group, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Research Triangle Park, NC 27709, USA, William G. Enloe High School, Raleigh, NC 27610, USA and Department of Biology, Brookhaven National Laboratory, Upton, NY 11973, USA.
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 7286
EP  - 7301
VL  - 41
IS  - 15
KW  - Antineoplastic Agents
KW  - 0
KW  - DNA, Neoplasm
KW  - Histones
KW  - Imidazoles
KW  - Piperazines
KW  - Tumor Suppressor Protein p53
KW  - nutlin 3
KW  - 53IA0V845C
KW  - Doxorubicin
KW  - 80168379AG
KW  - Dimethyl Sulfoxide
KW  - YOW8V9698H
KW  - Index Medicus
KW  - Dimethyl Sulfoxide -- pharmacology
KW  - Imidazoles -- pharmacology
KW  - Humans
KW  - Osteosarcoma -- pathology
KW  - Gene Regulatory Networks
KW  - HCT116 Cells
KW  - Piperazines -- pharmacology
KW  - Protein Binding
KW  - Binding Sites
KW  - Nucleotide Motifs
KW  - Doxorubicin -- pharmacology
KW  - Genes, p53
KW  - Histones -- metabolism
KW  - Osteosarcoma -- genetics
KW  - Consensus Sequence
KW  - Methylation
KW  - Antineoplastic Agents -- pharmacology
KW  - Histones -- genetics
KW  - Gene Expression Regulation, Neoplastic
KW  - Promoter Regions, Genetic
KW  - DNA, Neoplasm -- genetics
KW  - Tumor Suppressor Protein p53 -- genetics
KW  - Tumor Suppressor Protein p53 -- metabolism
KW  - DNA, Neoplasm -- metabolism
KW  - Transcriptional Activation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443381294?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diverse+stresses+dramatically+alter+genome-wide+p53+binding+and+transactivation+landscape+in+human+cancer+cells.&rft.au=Menendez%2C+Daniel%3BNguyen%2C+Thuy-Ai%3BFreudenberg%2C+Johannes+M%3BMathew%2C+Viju+J%3BAnderson%2C+Carl+W%3BJothi%2C+Raja%3BResnick%2C+Michael+A&rft.aulast=Menendez&rft.aufirst=Daniel&rft.date=2013-08-01&rft.volume=41&rft.issue=15&rft.spage=7286&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgkt504
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-28
N1  - Date created - 2013-08-28
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Am J Hum Genet. 2005 May;76(5):794-803 [15756637]
Cancer Res. 2008 Dec 1;68(23):9671-7 [19047144]
Nucleic Acids Res. 2000 Jan 1;28(1):316-9 [10592259]
Genes Dev. 2000 Apr 15;14(8):981-93 [10783169]
Int J Cancer. 2001 Oct 15;94(2):218-21 [11668501]
Nat Genet. 2002 Mar;30(3):315-20 [11919562]
Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238]
J Biol Chem. 2003 Sep 26;278(39):37536-44 [12860987]
Mol Cell. 2003 Oct;12(4):1015-27 [14580351]
Oncogene. 2004 Aug 26;23(39):6541-7 [15221010]
Hum Mol Genet. 2004 Oct 15;13(20):2473-82 [15317751]
Proc Natl Acad Sci U S A. 1990 Jul;87(14):5435-9 [2142531]
J Neurooncol. 2009 Feb;91(3):265-70 [18974932]
Nat Protoc. 2009;4(1):44-57 [19131956]
Cancer Res. 2009 May 1;69(9):3788-94 [19366810]
J Mol Biol. 2005 May 6;348(3):589-96 [15826656]
Nucleic Acids Res. 2005;33(20):e175 [16284200]
Cancer Res. 2005 Nov 15;65(22):10255-64 [16288013]
Cell. 2006 Jan 13;124(1):207-19 [16413492]
Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1406-11 [16432214]
Cell Death Differ. 2006 Jun;13(6):951-61 [16575405]
Mol Cell. 2006 Jun 23;22(6):741-53 [16793544]
Mol Cell Biol. 2006 Oct;26(19):7030-45 [16980608]
BMC Genomics. 2006;7:260 [17042939]
Trends Mol Med. 2007 Jan;13(1):23-31 [17126603]
Genomics. 2007 Feb;89(2):178-88 [17085012]
Cancer Res. 2007 Oct 1;67(19):9006-12 [17909001]
Mod Pathol. 2008 Feb;21(2):85-95 [18084254]
Nucleic Acids Res. 2008 Mar;36(5):1589-98 [18234719]
Nat Rev Mol Cell Biol. 2008 May;9(5):402-12 [18431400]
Nucleic Acids Res. 2008 Jun;36(11):3639-54 [18474530]
Oncogene. 2008 Jul 3;27(29):4013-23 [18278067]
PLoS Genet. 2008 Jun;4(6):e1000104 [18714371]
Nucleic Acids Res. 2008 Sep;36(16):5221-31 [18684996]
BMC Genomics. 2008;9:486 [18922183]
PLoS Genet. 2009 May;5(5):e1000462 [19424414]
Genome Biol. 2009;10(3):R25 [19261174]
Lancet. 2009 Jun 6;373(9679):1974-86 [19476995]
J Biol Chem. 2009 Jul 17;284(29):19280-9 [19433585]
Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14373-8 [19597154]
BMC Bioinformatics. 2009;10:234 [19640299]
Nat Rev Cancer. 2009 Oct;9(10):724-37 [19776742]
Cancer Res. 2009 Nov 1;69(21):8463-71 [19843844]
Hum Pathol. 2010 Jan;41(1):48-58 [19733895]
Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):69-74 [20018659]
Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1500-5 [20080630]
Nat Struct Mol Biol. 2010 Apr;17(4):423-9 [20364130]
Cell Cycle. 2010 Mar 1;9(5):870-9 [20160511]
Nucleic Acids Res. 2011 Jan;39(Database issue):D945-50 [20952405]
PLoS One. 2011;6(3):e17574 [21394211]
PLoS Genet. 2011 Mar;7(3):e1001360 [21483755]
Breast Cancer Res Treat. 2011 Sep;129(2):617-22 [21607584]
Mol Carcinog. 2011 Nov;50(11):846-56 [21438024]
Cell Cycle. 2011 Dec 15;10(24):4237-49 [22127205]
Mol Cell. 2012 Apr 13;46(1):30-42 [22387025]
Mol Cell Biol. 2012 Jun;32(11):2160-7 [22473991]
Nature. 2012 May 10;485(7397):237-41 [22495306]
Cell. 2012 Jun 8;149(6):1269-83 [22682249]
J Biochem. 2012 Jul;152(1):99-110 [22577164]
Cell Death Differ. 2012 Dec;19(12):1992-2002 [22790872]
Mol Cell Biol. 1992 Jun;12(6):2866-71 [1588974]
Nat Genet. 1992 Apr;1(1):45-9 [1301998]
Proc Int Conf Intell Syst Mol Biol. 1994;2:28-36 [7584402]
Bioinformatics. 1998;14(1):48-54 [9520501]
Nature. 2004 Dec 9;432(7018):775-9 [15592418]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/nar/gkt504
ER  - 



TY  - JOUR
T1  - Signaling via the IL-20 receptor inhibits cutaneous production of IL-1 beta and IL-17A to promote infection with methicillin-resistant Staphylococcus aureus
AN  - 1443374837; 18646147
AB  - Staphylococcus aureus causes most infections of human skin and soft tissue and is a major infectious cause of mortality. Host defense mechanisms against S. aureus are incompletely understood. Interleukin 19 (IL-19), IL-20 and IL-24 signal through type I and type II IL-20 receptors and are associated with inflammatory skin diseases such as psoriasis and atopic dermatitis. We found here that those cytokines promoted cutaneous infection with S. aureus in mice by downregulating IL-1 beta - and IL-17A-dependent pathways. We noted similar effects of those cytokines in human keratinocytes after exposure to S. aureus, and antibody blockade of the IL-20 receptor improved outcomes in infected mice. Our findings identify an immunosuppressive role for IL-19, IL-20 and IL-24 during infection that could be therapeutically targeted to alter susceptibility to infection.
JF  - Nature Immunology
AU  - Myles, Ian A
AU  - Fontecilla, Natalia M
AU  - Valdez, Patricia A
AU  - Vithayathil, Paul J
AU  - Naik, Shruti
AU  - Belkaid, Yasmine
AU  - Ouyang, Wenjun
AU  - Datta, Sandip K
AD  - Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 804
EP  - 811
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 14
IS  - 8
SN  - 1529-2908, 1529-2908
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Antibodies
KW  - Staphylococcus aureus
KW  - Infection
KW  - F:06925
KW  - J:02350
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443374837?accountid=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=Nature+Immunology&rft.atitle=Signaling+via+the+IL-20+receptor+inhibits+cutaneous+production+of+IL-1+beta+and+IL-17A+to+promote+infection+with+methicillin-resistant+Staphylococcus+aureus&rft.au=Myles%2C+Ian+A%3BFontecilla%2C+Natalia+M%3BValdez%2C+Patricia+A%3BVithayathil%2C+Paul+J%3BNaik%2C+Shruti%3BBelkaid%2C+Yasmine%3BOuyang%2C+Wenjun%3BDatta%2C+Sandip+K&rft.aulast=Myles&rft.aufirst=Ian&rft.date=2013-08-01&rft.volume=14&rft.issue=8&rft.spage=804&rft.isbn=&rft.btitle=&rft.title=Nature+Immunology&rft.issn=15292908&rft_id=info:doi/10.1038%2Fni.2637
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Infection; Staphylococcus aureus
DO  - http://dx.doi.org/10.1038/ni.2637
ER  - 



TY  - JOUR
T1  - A sequence of events in the uterus prior to implantation in the mouse
AN  - 1443368789; 18686430
AB  - I reviewed a series of events in the mouse uterus before implantation on Day 4 of pregnancy (the sperm positive day is counted as Day 1). Major events are spacing of embryos along the uterine horns, shedding of the zona pellucida, and closure of the uterine lumen. How subtle they may be, there appear to exist interactions between intrauterine blastocysts and the uterus which is regulated by ovarian steroids. Spacing of embryos along the uterine horn is not random, but they are rather evenly distributed along the entire horn. The mechanism of even distribution of embryos needs clarification, although studies indicate that adrenergic nerve activity, prostaglandins, and other molecules appear to be involved. Shedding of the zona pellucida involves trypsin-like proteinase lysis of the zona. Through the opening created by zona lysis, blastocyst gets out of the zona by repeating expansion-collapse movements. Closure of rat uterine lumen is reported to be the result of absorption of uterine fluid through uterine glands. This needs to be confirmed in other species of rodents. Since these events influence blastocyst implantation, we need more detailed information on their regulatory mechanisms in order to improve the rate of healthy implantation of transferred embryo.
JF  - Journal of Assisted Reproduction and Genetics
AU  - Yoshinaga, Koji
AD  - Fertility and Infertility Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, DHHS, Bldg. 6100, Rm. 8B01, NIH, Bethesda, MD, 20892-7510, USA, ky6a@nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 1017
EP  - 1022
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 30
IS  - 8
SN  - 1058-0468, 1058-0468
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - Uterus
KW  - Prostaglandins
KW  - Adrenergic nerves
KW  - Steroid hormones
KW  - Sperm
KW  - Pregnancy
KW  - Horns
KW  - blastocysts
KW  - Zona pellucida
KW  - Reviews
KW  - Glands
KW  - Proteinase
KW  - Embryos
KW  - G 07730:Development & Cell Cycle
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443368789?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Assisted+Reproduction+and+Genetics&rft.atitle=A+sequence+of+events+in+the+uterus+prior+to+implantation+in+the+mouse&rft.au=Yoshinaga%2C+Koji&rft.aulast=Yoshinaga&rft.aufirst=Koji&rft.date=2013-08-01&rft.volume=30&rft.issue=8&rft.spage=1017&rft.isbn=&rft.btitle=&rft.title=Journal+of+Assisted+Reproduction+and+Genetics&rft.issn=10580468&rft_id=info:doi/10.1007%2Fs10815-013-0093-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 45
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Uterus; Prostaglandins; Adrenergic nerves; Sperm; Steroid hormones; Pregnancy; Horns; blastocysts; Zona pellucida; Glands; Reviews; Embryos; Proteinase
DO  - http://dx.doi.org/10.1007/s10815-013-0093-z
ER  - 



TY  - JOUR
T1  - Standardized Generation and Differentiation of Neural Precursor Cells from Human Pluripotent Stem Cells
AN  - 1439238515; 18475546
AB  - Precise, robust and scalable directed differentiation of pluripotent stem cells is an important goal with respect to disease modeling or future therapies. Using the AggreWell(TM)400 system we have standardized the differentiation of human embryonic and induced pluripotent stem cells to a neuronal fate using defined conditions. This allows reproducibility in replicate experiments and facilitates the direct comparison of cell lines. Since the starting point for EB formation is a single cell suspension, this protocol is suitable for standard and novel methods of pluripotent stem cell culture. Moreover, an intermediate population of neural precursor cells, which are routinely >95% NCAM super(pos) and Tra-1-60 super(neg) by FACS analysis, may be expanded and frozen prior to differentiation allowing a convenient starting point for downstream experiments.
JF  - Stem Cell Reviews
AU  - Kozhich, O A
AU  - Hamilton, R S
AU  - Mallon, B S
AD  - Laboratory of Molecular Biology, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA, mallonb@mail.nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 531
EP  - 536
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 9
IS  - 4
SN  - 1550-8943, 1550-8943
KW  - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts
KW  - Flow cytometry
KW  - Cell suspensions
KW  - Differentiation
KW  - Stem cells
KW  - Cell culture
KW  - Embryos
KW  - Neural stem cells
KW  - W 30945:Fermentation & Cell Culture
KW  - N3 11145:Methodology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439238515?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Cell+Reviews&rft.atitle=Standardized+Generation+and+Differentiation+of+Neural+Precursor+Cells+from+Human+Pluripotent+Stem+Cells&rft.au=Kozhich%2C+O+A%3BHamilton%2C+R+S%3BMallon%2C+B+S&rft.aulast=Kozhich&rft.aufirst=O&rft.date=2013-08-01&rft.volume=9&rft.issue=4&rft.spage=531&rft.isbn=&rft.btitle=&rft.title=Stem+Cell+Reviews&rft.issn=15508943&rft_id=info:doi/10.1007%2Fs12015-012-9357-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 32
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Cell suspensions; Flow cytometry; Differentiation; Stem cells; Embryos; Cell culture; Neural stem cells
DO  - http://dx.doi.org/10.1007/s12015-012-9357-8
ER  - 



TY  - JOUR
T1  - Epigenetic Regulation of SOX9 by the NF-[kappa]B Signaling Pathway in Pancreatic Cancer Stem Cells
AN  - 1434033005; 18510833
AB  - Pancreatic cancer is the fourth leading cause of cancer-related mortality in the world. Pancreatic cancer can be localized, locally advanced, or metastatic. The median 1- and 5-year survival rates are 25% and 6%, respectively. Epigenetic modifications such as DNA methylation play a significant role during both normal human development and cancer progression. To investigate epigenetic regulation of genes in the tumor-initiating population of pancreatic cancer cells, which are also termed cancer stem cells (CSCs), we conducted epigenetic arrays in PANC1 and HPAC pancreatic cancer cell lines and compared the global DNA methylation status of CpG promoters in invasive cells, demonstrated to be CSCs, to their noninvasive counterparts, or non-CSCs. Our results suggested that the NF-[kappa]B pathway is one of the most activated pathways in pancreatic CSCs. In agreement with this, we determined that upon treatment with NF-[kappa]B pathway inhibitors, the stem cell-like properties of cells are significantly disrupted. Moreover, SOX9, demethylated in CSCs, is shown to play a crucial role in the invasion process. Additionally, we found a potential NF-[kappa]B binding site located in the SOX9 promoter and determined that the NF-[kappa]B subunit p65 positively regulates SOX9 expression by binding to its promoter directly. This interaction can be efficiently blocked by NF-[kappa]B inhibitors. Thus, our work establishes a link between the classic NF-[kappa]B signaling transduction pathway and the invasiveness of pancreatic CSCs, which may result in the identification of novel signals and molecules that function at an epigenetic level, and could potentially be targeted for pharmaceutical investigations and clinical trials. STEM Cells 2013; 31:1454-1466
JF  - Stem Cells
AU  - Sun, Lei
AU  - Mathews, Lesley A
AU  - Cabarcas, Stephanie M
AU  - Zhang, Xiaohu
AU  - Yang, Acong
AU  - Zhang, Ying
AU  - Young, Matthew R
AU  - Klarmann, Kimberly D
AU  - Keller, Jonathan R
AU  - Farrar, William L
AD  - Division of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, USA., lei.sun@nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 1454
EP  - 1466
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 8
SN  - 1066-5099, 1066-5099
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - Mortality
KW  - Invasiveness
KW  - Pancreatic cancer
KW  - Transcription
KW  - CpG islands
KW  - Sox9 protein
KW  - Clinical trials
KW  - NF- Kappa B protein
KW  - Metastases
KW  - Promoters
KW  - Tumor cell lines
KW  - Stem cells
KW  - epigenetics
KW  - Gene regulation
KW  - DNA methylation
KW  - Pharmaceuticals
KW  - Signal transduction
KW  - N 14820:DNA Metabolism & Structure
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434033005?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epigenetic+Regulation+of+SOX9+by+the+NF-%5Bkappa%5DB+Signaling+Pathway+in+Pancreatic+Cancer+Stem+Cells&rft.au=Sun%2C+Lei%3BMathews%2C+Lesley+A%3BCabarcas%2C+Stephanie+M%3BZhang%2C+Xiaohu%3BYang%2C+Acong%3BZhang%2C+Ying%3BYoung%2C+Matthew+R%3BKlarmann%2C+Kimberly+D%3BKeller%2C+Jonathan+R%3BFarrar%2C+William+L&rft.aulast=Sun&rft.aufirst=Lei&rft.date=2013-08-01&rft.volume=31&rft.issue=8&rft.spage=1454&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1394
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Mortality; Invasiveness; Pancreatic cancer; Transcription; CpG islands; Sox9 protein; Clinical trials; NF- Kappa B protein; Metastases; Promoters; Stem cells; Tumor cell lines; epigenetics; Gene regulation; DNA methylation; Pharmaceuticals; Signal transduction
DO  - http://dx.doi.org/10.1002/stem.1394
ER  - 



TY  - JOUR
T1  - Polycomb Determines Responses to Smad2/3 Signaling in Embryonic Stem Cell Differentiation and in Reprogramming
AN  - 1434030996; 18510832
AB  - Integration of extrinsic signals, epigenetic regulators, and intrinsic transcription factors establishes pluripotent stem cell identity. Interplay between these components also underlies the capacity of stem cells to undergo differentiation, and of differentiated cells to re-establish the pluripotent state in direct reprogramming. Polycomb repressive complexes are epigenetic regulators that play key roles in stem cell identity and in differentiated cell fates. Smad2 and Smad3 (Smad2/3), the intracellular mediators of the Nodal/Activin/transforming growth factor (TGF) [beta] cell-cell signaling pathway also are implicated in stem cell pluripotency and in differentiation. Here, we show that Polycomb imposes responses to Smad2/3-mediated signaling to selectively regulate expression of the master pluripotency factor Oct4 during initiation of differentiation, but not in the self-renewing pluripotent ground state. During reprogramming back to the ground state, we find that the enhancement of reprogramming efficiency stemming from blocking Nodal/Activin/TGF[beta] signaling also depends on Polycomb. These context-dependent responses to Smad2/3 imposed by Polycomb action provide a mechanism for selective gene regulation that can reconcile the apparently conflicting roles of this signaling pathway in pluripotency, differentiation, and reprogramming. STEM Cells 2013; 31:1488-1497
JF  - Stem Cells
AU  - Dahle, Oeyvind
AU  - Kuehn, Michael R
AD  - Bldg. 560/Rm. 12-90, NCI, Frederick, Maryland 21702, USA., mkuehn@mail.nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 1488
EP  - 1497
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 8
SN  - 1066-5099, 1066-5099
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Transforming growth factor
KW  - polycomb group proteins
KW  - Smad2 protein
KW  - Activin
KW  - Differentiation
KW  - Integration
KW  - Stem cells
KW  - Embryo cells
KW  - epigenetics
KW  - Gene regulation
KW  - Transcription factors
KW  - Smad3 protein
KW  - Cell fate
KW  - Oct-4 protein
KW  - Signal transduction
KW  - W 30910:Imaging
KW  - G 07730:Development & Cell Cycle
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434030996?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Polycomb+Determines+Responses+to+Smad2%2F3+Signaling+in+Embryonic+Stem+Cell+Differentiation+and+in+Reprogramming&rft.au=Dahle%2C+Oeyvind%3BKuehn%2C+Michael+R&rft.aulast=Dahle&rft.aufirst=Oeyvind&rft.date=2013-08-01&rft.volume=31&rft.issue=8&rft.spage=1488&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1417
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Transforming growth factor; polycomb group proteins; Smad2 protein; Activin; Integration; Differentiation; Stem cells; Embryo cells; epigenetics; Transcription factors; Gene regulation; Smad3 protein; Cell fate; Oct-4 protein; Signal transduction
DO  - http://dx.doi.org/10.1002/stem.1417
ER  - 



TY  - JOUR
T1  - Bermuda Triangle for the liver: Alcohol, obesity, and viral hepatitis
AN  - 1430853337; 18282808
AB  - Despite major progress in understanding and managing liver disease in the past 30 years, it is now among the top 10 most common causes of death globally. Several risk factors, such as genetics, diabetes, obesity, excessive alcohol consumption, viral infection, gender, immune dysfunction, and medications, acting individually or in concert, are known to precipitate liver damage. Viral hepatitis, excessive alcohol consumption, and obesity are the major factors causing liver injury. Estimated numbers of hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected subjects worldwide are staggering (370 and 175 million, respectively), and of the 40 million known human immunodeficiency virus positive subjects, 4 and 5 million are coinfected with HBV and HCV, respectively. Alcohol and HCV are the leading causes of end-stage liver disease worldwide and the most common indication for liver transplantation in the United States and Europe. In addition, the global obesity epidemic that affects up to 40 million Americans, and 396 million worldwide, is accompanied by an alarming incidence of end-stage liver disease, a condition exacerbated by alcohol. This article focuses on the interactions between alcohol, viral hepatitis, and obesity (euphemistically described here as the Bermuda Triangle of liver disease), and discusses common mechanisms and synergy.
JF  - Journal of Gastroenterology and Hepatology
AU  - Zakhari, Samir
AD  - Division of Metabolism and Health Effects. NIAAA, NIH
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 18
EP  - 25
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 28
SN  - 0815-9319, 0815-9319
KW  - Risk Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - Injuries
KW  - Europe
KW  - Infection
KW  - Liver transplantation
KW  - Genetics
KW  - Risk factors
KW  - Hepatitis B
KW  - Hepatitis C
KW  - Ethanol
KW  - Mortality
KW  - Alcohol
KW  - Obesity
KW  - ANW, Atlantic, Bermuda Triangle
KW  - Liver diseases
KW  - Epidemics
KW  - Hepatitis B virus
KW  - Hepatitis
KW  - Diabetes mellitus
KW  - USA
KW  - Hepatitis C virus
KW  - Human immunodeficiency virus
KW  - Gender
KW  - Liver
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - V 22360:AIDS and HIV
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430853337?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Gastroenterology+and+Hepatology&rft.atitle=Bermuda+Triangle+for+the+liver%3A+Alcohol%2C+obesity%2C+and+viral+hepatitis&rft.au=Zakhari%2C+Samir&rft.aulast=Zakhari&rft.aufirst=Samir&rft.date=2013-08-01&rft.volume=28&rft.issue=&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Journal+of+Gastroenterology+and+Hepatology&rft.issn=08159319&rft_id=info:doi/10.1111%2Fjgh.12207
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Diabetes mellitus; Obesity; Epidemics; Liver diseases; Injuries; Risk factors; Infection; Liver transplantation; Ethanol; Alcohol; Mortality; Hepatitis; Genetics; Gender; Liver; Hepatitis B; Hepatitis C; Hepatitis C virus; Hepatitis B virus; Human immunodeficiency virus; USA; ANW, Atlantic, Bermuda Triangle; Europe
DO  - http://dx.doi.org/10.1111/jgh.12207
ER  - 



TY  - JOUR
T1  - The Role of Religious and Existential Well-being in Families with Lynch Syndrome: Prevention, Family Communication, and Psychosocial Adjustment
AN  - 1430188773; 201318927
AB  - This study explored the role of religious (RWB) and existential well-being (EWB) on psychosocial factors, support network characteristics, and screening practices in families with Lynch syndrome, also referred to as hereditary nonpolyposis colon cancer (HNPCC). Participants were individuals with Lynch syndrome associated cancers and their first-degree relatives at risk of inheriting an identified deleterious mutation. Analyses considered both family RWB and EWB norms and individual deviations from that norm. Analyses controlled for age, gender, cancer diagnosis, number of respondents, and network size. Higher family RWB was associated with increased depressive symptoms (p<.05) and avoidant cognitions (p<.05). Higher family EWB was related to decreased depression symptoms (p<.001). Higher family EWB was associated with fecal occult blood testing (p<.01), and family communication about genetic counselling and testing (p<.01). Analyses pointed to individual effects of EWB above and beyond family-level effects. Individuals with lower EWB than their family had lower perceived risk for colorectal cancer (p<.05), communicated disease risk information to less family members (p<.05), and were less likely to undergo recent colonoscopies (p<.05). Participants with lower EWB than their family also had higher cancer worry (p<.01) and increased depressive symptoms (p<.001). Findings indicate the importance of assessing individuals within the context of their family network and being aware of family characteristics which may impact individual adjustment to disease risk. Interventions considering family-level factors may provide efficient pathways to improving psychosocial factors, screening practices, communication about disease risk and genetic testing, and cancer prevention. Adapted from the source document.
JF  - Journal of Genetic Counseling
AU  - Morris, Bronwyn A
AU  - Hadley, Donald W
AU  - Koehly, Laura M
AD  - Social and Behavioral Research Branch, National Human Genome Research Institute, Bethesda, MD, USA b.morris@griffith.edu.au
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 482
EP  - 491
PB  - Springer Science+Business Media, New York NY
VL  - 22
IS  - 4
SN  - 1059-7700, 1059-7700
KW  - Religious aspects
KW  - Prevention
KW  - Depression
KW  - Relatives
KW  - Psychosocial factors
KW  - Cancer
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430188773?accountid=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=The+Role+of+Religious+and+Existential+Well-being+in+Families+with+Lynch+Syndrome%3A+Prevention%2C+Family+Communication%2C+and+Psychosocial+Adjustment&rft.au=Morris%2C+Bronwyn+A%3BHadley%2C+Donald+W%3BKoehly%2C+Laura+M&rft.aulast=Morris&rft.aufirst=Bronwyn&rft.date=2013-08-01&rft.volume=22&rft.issue=4&rft.spage=482&rft.isbn=&rft.btitle=&rft.title=Journal+of+Genetic+Counseling&rft.issn=10597700&rft_id=info:doi/10.1007%2Fs10897-013-9571-9
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JGCOET
N1  - SubjectsTermNotLitGenreText - Cancer; Depression; Psychosocial factors; Relatives; Religious aspects; Prevention
DO  - http://dx.doi.org/10.1007/s10897-013-9571-9
ER  - 



TY  - JOUR
T1  - Use of Emergency Departments among Working Age Adults with Disabilities: A Problem of Access and Service Needs
AN  - 1430188226; 201319305
AB  - To examine the relationship between emergency department (ED) use and access to medical care and prescription medications among working age Americans with disabilities. Pooled data from the 2006-2008 Medical Expenditure Panel Survey (MEPS), a U.S. health survey representative of community-dwelling civilians. We compared the health and service utilization of two groups of people with disabilities to a contrast group without disability. We modeled ED visits on the basis of disability status, measures of health and health conditions, access to care, and sociodemographics. These variables were aggregated from the household component, the medical condition, and event files to provide average annual estimates for the period spanning 2006-2008. People with disabilities accounted for almost 40 percent of the annual visits made to U.S. EDs each year. Three key factors affect their ED use: access to regular medical care (including prescription medications), disability status, and the complexity of individuals' health profiles. Given the volume of health conditions among people with disabilities, the ED will always play a role in their care. However, some ED visits could potentially be avoided if ongoing care were optimized. Adapted from the source document.
JF  - Health Services Research
AU  - Rasch, Elizabeth K
AU  - Gulley, Stephen P
AU  - Chan, Leighton
AD  - Epidemiology and Biostatistics Section Mark O. Hatfield Clinical Research Center Rehabilitation Medicine Department. National Institutes of Health
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 1334
EP  - 1358
PB  - Blackwell Publishers, Oxford UK
VL  - 48
IS  - 4
SN  - 0017-9124, 0017-9124
KW  - Prescriptions
KW  - American people
KW  - Health care
KW  - Disabled people
KW  - Accident and emergency departments
KW  - Health
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430188226?accountid=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=Use+of+Emergency+Departments+among+Working+Age+Adults+with+Disabilities%3A+A+Problem+of+Access+and+Service+Needs&rft.au=Rasch%2C+Elizabeth+K%3BGulley%2C+Stephen+P%3BChan%2C+Leighton&rft.aulast=Rasch&rft.aufirst=Elizabeth&rft.date=2013-08-01&rft.volume=48&rft.issue=4&rft.spage=1334&rft.isbn=&rft.btitle=&rft.title=Health+Services+Research&rft.issn=00179124&rft_id=info:doi/10.1111%2F1475-6773.12025
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - HESEA5
N1  - SubjectsTermNotLitGenreText - Accident and emergency departments; Disabled people; Health; Prescriptions; Health care; American people
DO  - http://dx.doi.org/10.1111/1475-6773.12025
ER  - 



TY  - JOUR
T1  - Gait characteristics of multiple sclerosis patients in the absence of clinical disability
AN  - 1430187927; 201319011
AB  - Purpose: Motor deficits in lower extremities and gait abnormalities are a major feature of the multiple sclerosis (MS) patients. Patients with minimal clinical disability have subtle gait changes. The aim of this study was to analyze the gait characteristics of MS patients in the absence of clinical disability. Method: A case-control study was carried out with 12 MS patients and 12 matched healthy controls. The subjects underwent a clinical neurological evaluation to determine their disability level (EDSS = 1.5). Then, the subjects were referred for completion self-report questionnaires (gait, perceived balance confidence, physical activity and fatigue), gait clinical trials, and 3D kinematic analysis. Results: MS patients showed more impairment of perceived fatigue, perceived of walking impact and perceived balance confidence, despite having no disability. Gait characteristics showed no differences when they were determined by clinical observation. The 3D kinematic analysis of gait showed slight but significant changes in ankle movement. Conclusion: MS patients with no clinical disability have discrete changes in gait that can be evidenced by perceived impact on walking and kinematic evaluation, mainly of ankle movement. Moreover, there is a decrease in perceived balance confidence and an increase in perceived fatigue, which are correlated despite having different origins. Implications for Rehabilitation . Multiple sclerosis patients showed changes in gait pattern even with no clinical disability. . The reduction of plantar flexion movement at toe off may be the first compensatory strategy on early phases of disease. . Fatigue, higher walking impact, and less balance confidence are early symptoms of Multiple Sclerosis. Adapted from the source document.
JF  - Disability and Rehabilitation
AU  - Nogueira, Leandro Alberto Calazans
AU  - Teixeira, Luciano
AU  - Sabino, Pollyane
AU  - Filho, Helcio Alvarenga
AU  - Alvarenga, Regina Maria Papais
AU  - Thuler, Luiz Claudio
AD  - Neurology Postgraduate Program, Federal University of Rio de Janeiro State, Rio de Janeiro, Brazil and National Cancer Institute (INCA), Rio de Janeiro, Brazil
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 1472
EP  - 1478
PB  - Informa Healthcare, New York NY
VL  - 35
IS  - 17
SN  - 0963-8288, 0963-8288
KW  - Gait, kinematics, mobility, multiple sclerosis
KW  - Kinematics
KW  - Fatigue
KW  - Multiple sclerosis
KW  - Walking
KW  - Disability
KW  - Gait
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430187927?accountid=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=Disability+and+Rehabilitation&rft.atitle=Gait+characteristics+of+multiple+sclerosis+patients+in+the+absence+of+clinical+disability&rft.au=Nogueira%2C+Leandro+Alberto+Calazans%3BTeixeira%2C+Luciano%3BSabino%2C+Pollyane%3BFilho%2C+Helcio+Alvarenga%3BAlvarenga%2C+Regina+Maria+Papais%3BThuler%2C+Luiz+Claudio&rft.aulast=Nogueira&rft.aufirst=Leandro+Alberto&rft.date=2013-08-01&rft.volume=35&rft.issue=17&rft.spage=1472&rft.isbn=&rft.btitle=&rft.title=Disability+and+Rehabilitation&rft.issn=09638288&rft_id=info:doi/10.3109%2F09638288.2012.738760
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - DREHET
N1  - SubjectsTermNotLitGenreText - Gait; Multiple sclerosis; Disability; Fatigue; Kinematics; Walking
DO  - http://dx.doi.org/10.3109/09638288.2012.738760
ER  - 



TY  - JOUR
T1  - Exploration of factors associated with social worker attitudes toward suicide
AN  - 1429626826; 201307861
AB  - Background: Social workers are expected to play important roles in suicide intervention. Caregiving behaviours of medical personnel to suicidal individuals have been reported to be influenced by their own attitudes toward suicide. In this context, only a limited number of studies have examined social workers' attitudes toward suicide. Aim: The purpose of this study was to explore associations between personal or occupational factors of social workers and their attitudes toward suicide. Methods: A self-administered questionnaire was mailed to 2,999 study participants registered with the Tokyo chapter of the Japanese Association of Certified Social Workers. We adopted the Attitudes Toward Suicide Scale (ATTS) to measure attitudes toward suicide. MANCOVA was used to test for the effects of demographic, personal and occupational factors on ATTS sub-scale scores. Results: Participants with a history of suicidal thoughts had stronger attitudes regarding the right to suicide than those with no history; these attitudes were not affected by a history of participating in suicide-prevention training. Conclusions: Our findings suggest that suicide education should incorporate programmes directed at altering permissive attitudes toward suicide. [Reprinted by permission of Sage Publications Ltd., copyright holder.]
JF  - International Journal of Social Psychiatry
AU  - Kodaka, Manami
AU  - Inagaki, Masatoshi
AU  - Postuvan, Vita
AU  - Yamada, Mitsuhiko
AD  - Centre for Suicide Prevention, National Institute of Mental Health, National Centre of Neurology and Psychiatry, Tokyo, Japan
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 452
EP  - 459
PB  - Sage Publications, London UK
VL  - 59
IS  - 5
SN  - 0020-7640, 0020-7640
KW  - Attitudes toward suicide social worker suicide-prevention training
KW  - Caregivers
KW  - Attitudes
KW  - Tokyo, Japan
KW  - Educational Programs
KW  - Training
KW  - Social Attitudes
KW  - Social Workers
KW  - Intervention
KW  - Suicide
KW  - article
KW  - 6150: professional issues in social work
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1429626826?accountid=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=International+Journal+of+Social+Psychiatry&rft.atitle=Exploration+of+factors+associated+with+social+worker+attitudes+toward+suicide&rft.au=Kodaka%2C+Manami%3BInagaki%2C+Masatoshi%3BPostuvan%2C+Vita%3BYamada%2C+Mitsuhiko&rft.aulast=Kodaka&rft.aufirst=Manami&rft.date=2013-08-01&rft.volume=59&rft.issue=5&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764012440674
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-28
N1  - CODEN - IJSPAG
N1  - SubjectsTermNotLitGenreText - Suicide; Attitudes; Social Workers; Social Attitudes; Intervention; Tokyo, Japan; Educational Programs; Caregivers; Training
DO  - http://dx.doi.org/10.1177/0020764012440674
ER  - 



TY  - JOUR
T1  - Rapid Wuchereria bancrofti-Specific Antigen Wb123-Based IgG4 Immunoassays as Tools for Surveillance following Mass Drug Administration Programs on Lymphatic Filariasis
AN  - 1427013302; 18417957
AB  - The Global Programme to Eliminate Lymphatic Filariasis has an urgent need for rapid assays to detect ongoing transmission of lymphatic filariasis (LF) following multiple rounds of mass drug administration (MDA). Current WHO guidelines support using the antigen card immunochromatographic test (ICT), which detects active filarial infection but does not detect early exposure to LF. Recent studies found that antibody-based assays better serve this function. In the present study, two tests, a rapid IgG4 enzyme-linked immunosorbent assay (ELISA) and a lateral-flow strip immunoassay, were developed based on the highly sensitive and specific Wuchereria bancrofti antigen Wb123. A comparison of W. bancrofti-infected and -uninfected patients (with or without other helminth infections) demonstrated that both tests had high sensitivities and specificities (93 and 97% [ELISA] and 92 and 96% [strips], respectively). When the W. bancrofti-uninfected group was separated into those with other filarial/helminth infections (i.e., onchocerciasis, loiasis, and strongyloidiasis) and those who were parasite uninfected, the specificities of the assays varied between 91 and 100%. In addition, the geometric mean response by ELISA of W. bancrofti-infected patients was significantly higher than the response of those without W. bancrofti infection (P < 0.0001). Furthermore, the Wb123 ELISA and the lateral-flow strips had high positive and negative predictive values, giving valuable information on the size of survey population needed to be reasonably certain whether or not transmission is ongoing. These highly sensitive and specific IgG4 tests to the W. bancrofti Wb123 protein give every indication that they will serve as useful tools for post-MDA monitoring.
JF  - Clinical and Vaccine Immunology
AU  - Steel, Cathy
AU  - Golden, Allison
AU  - Kubofcik, Joseph
AU  - LaRue, Nicole
AU  - los Santos, Tala de
AU  - Domingo, Gonzalo J
AU  - Nutman, Thomas B
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 1155
EP  - 1161
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 20
IS  - 8
SN  - 1556-6811, 1556-6811
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts
KW  - Prediction
KW  - Environmental monitoring
KW  - Parasites
KW  - Enzyme-linked immunosorbent assay
KW  - onchocerciasis
KW  - Specificity
KW  - Filariasis
KW  - Infection
KW  - Wuchereria
KW  - strongyloidiasis
KW  - Wuchereria bancrofti
KW  - Antigens
KW  - Immunoglobulin G
KW  - ELISA
KW  - Vaccines
KW  - Immunoassays
KW  - Drugs
KW  - F 06905:Vaccines
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427013302?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+and+Vaccine+Immunology&rft.atitle=Rapid+Wuchereria+bancrofti-Specific+Antigen+Wb123-Based+IgG4+Immunoassays+as+Tools+for+Surveillance+following+Mass+Drug+Administration+Programs+on+Lymphatic+Filariasis&rft.au=Steel%2C+Cathy%3BGolden%2C+Allison%3BKubofcik%2C+Joseph%3BLaRue%2C+Nicole%3Blos+Santos%2C+Tala+de%3BDomingo%2C+Gonzalo+J%3BNutman%2C+Thomas+B&rft.aulast=Steel&rft.aufirst=Cathy&rft.date=2013-08-01&rft.volume=20&rft.issue=8&rft.spage=1155&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=15566811&rft_id=info:doi/10.1128%2FCVI.00252-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 17
N1  - Last updated - 2016-04-29
N1  - SubjectsTermNotLitGenreText - Environmental monitoring; Prediction; Parasites; Antigens; Specificity; ELISA; Vaccines; Drugs; Immunoassays; strongyloidiasis; Enzyme-linked immunosorbent assay; onchocerciasis; Immunoglobulin G; Filariasis; Infection; Wuchereria; Wuchereria bancrofti
DO  - http://dx.doi.org/10.1128/CVI.00252-13
ER  - 



TY  - JOUR
T1  - Risk Factors for Specific Histopathological Types of Postmenopausal Breast Cancer in the NIH-AARP Diet and Health Study
AN  - 1427003989; 18315459
AB  - Risk factor associations for rare breast cancer variants are often imprecise, obscuring differences between tumor types. To clarify differences, we examined risk factors for 5 histological types of breast cancer in the National Institutes of Health-AARP Diet and Health Study. Risk factor information was self-reported. We followed 192,076 postmenopausal women aged 50-71 years from 1995-1996 through 2006. During that time period, 5,334 ductal, 836 lobular, 639 mixed ductal-lobular, 216 mucinous, and 132 tubular breast cancers were diagnosed. Hazard ratios and 95% confidence intervals were estimated using Cox proportional hazards regression. Heterogeneity was evaluated using case-only logistic regression. The strongest differences were for menopausal hormone therapy (P sub(heterogeneity) < 0.01) and age at first birth (P sub(heterogeneity) < 0.01). Risk of tubular cancer in relation to current menopausal hormone therapy (for current use vs. never use, hazard ratio (HR) = 4.39, 95% confidence interval (CI): 2.77, 6.96) was several times stronger than risk of other histological types (range of HRs, 1.39-1.75). Older age at first birth was unassociated with risk of mucinous (for greater than or equal to 30 years vs. 20-24 years, HR = 0.62, 95% CI: 0.27, 1.42) or tubular (HR = 1.08, 95% CI: 0.51, 2.29) tumors, in contrast to clear positive associations with lobular (HR = 1.82, 95% CI: 1.39, 2.37) and mixed ductal-lobular (HR = 1.87, 95% CI: 1.39, 2.51) tumors. Differing associations for hormonal factors and mucinous and tubular cancers suggest etiologies distinct from those of common breast cancers.
JF  - American Journal of Epidemiology
AU  - Nyante, Sarah J
AU  - Dallal, Cher M
AU  - Gierach, Gretchen L
AU  - Park, Yikyung
AU  - Hollenbeck, Albert R
AU  - Brinton, Louise A
AD  - Correspondence to Dr. Sarah J. Nyante, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room 7-E236, MSC 9774, Bethesda, MD 20892-9774., sarah.nyante@nih.gov
Y1  - 2013/08/01/
PY  - 2013
DA  - 2013 Aug 01
SP  - 359
EP  - 371
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 178
IS  - 3
SN  - 0002-9262, 0002-9262
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Diets
KW  - Health risks
KW  - Age
KW  - Etiology
KW  - Post-menopause
KW  - Risk factors
KW  - Breast cancer
KW  - Histopathology
KW  - Tumors
KW  - Hormones
KW  - Cancer
KW  - H 11000:Diseases/Injuries/Trauma
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427003989?accountid=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=Risk+Factors+for+Specific+Histopathological+Types+of+Postmenopausal+Breast+Cancer+in+the+NIH-AARP+Diet+and+Health+Study&rft.au=Nyante%2C+Sarah+J%3BDallal%2C+Cher+M%3BGierach%2C+Gretchen+L%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BBrinton%2C+Louise+A&rft.aulast=Nyante&rft.aufirst=Sarah&rft.date=2013-08-01&rft.volume=178&rft.issue=3&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws471
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Diets; Health risks; Etiology; Age; Post-menopause; Risk factors; Histopathology; Breast cancer; Tumors; Hormones; Cancer
DO  - http://dx.doi.org/10.1093/aje/kws471
ER  - 



TY  - JOUR
T1  - Assessing Non-Cancer-Related Health Status of US Cancer Patients: Other-Cause Survival and Comorbidity Prevalence
AN  - 1427002761; 18315462
AB  - With advances in prevention, screening, and treatment, cancer patients are living longer; hence, non-cancer-related health status will likely play a larger role in determining their life expectancy. In this study, we present a novel method for characterizing non-cancer--related health status of cancer patients using population-based cancer registry data. We assessed non-cancer-related health status in the context of survival from other causes of death and prevalence of comorbidities. Data from the Surveillance, Epidemiology, and End Results program (2000-2006) were used to analyze cancer patients' survival probabilities by cause of death. Other-cause survival was estimated using a left-truncated survival method with the hazard of death due to other causes characterized as a function of age. Surveillance, Epidemiology, and End Results data linked to Medicare claims (1992-2005) were used to quantify comorbidity prevalence. Relative to the US population, survival from a non-cancer-related death was higher for patients diagnosed with early stage breast and prostate cancer but lower for lung cancer patients at all stages. Lung cancer patients had worse comorbidity status than did other cancer patients. The present study represents the first attempt to evaluate the non-cancer-related health status of US cancer patients by cancer site (breast, prostate, colorectal, and lung) and stage. The findings provide insight into non-cancer-related health issues among cancer patients and their risk of dying from other causes.
JF  - American Journal of Epidemiology
AU  - Cho, Hyunsoon
AU  - Mariotto, Angela B
AU  - Mann, Bhupinder S
AU  - Klabunde, Carrie N
AU  - Feuer, Eric J
AD  - Correspondence to Dr. Hyunsoon Cho, Data Modeling Branch, Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Room 4E568, Bethesda, MD 20892, choh3@mail.nih.gov
Y1  - 2013/08/01/
PY  - 2013
DA  - 2013 Aug 01
SP  - 339
EP  - 349
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 178
IS  - 3
SN  - 0002-9262, 0002-9262
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Mortality
KW  - Health risks
KW  - USA
KW  - Prevention
KW  - Age
KW  - Prostate cancer
KW  - Life span
KW  - Survival
KW  - Cancer
KW  - Morbidity
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/1427002761?accountid=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=Assessing+Non-Cancer-Related+Health+Status+of+US+Cancer+Patients%3A+Other-Cause+Survival+and+Comorbidity+Prevalence&rft.au=Cho%2C+Hyunsoon%3BMariotto%2C+Angela+B%3BMann%2C+Bhupinder+S%3BKlabunde%2C+Carrie+N%3BFeuer%2C+Eric+J&rft.aulast=Cho&rft.aufirst=Hyunsoon&rft.date=2013-08-01&rft.volume=178&rft.issue=3&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws580
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Health risks; Mortality; Age; Prevention; Prostate cancer; Life span; Survival; Morbidity; Cancer; Lung cancer; USA
DO  - http://dx.doi.org/10.1093/aje/kws580
ER  - 



TY  - JOUR
T1  - Alcoholic liver disease and pancreatitis: Global health problems being addressed by the US National Institute on Alcohol Abuse and Alcoholism
AN  - 1419370947; 18282823
AB  - The review article summarizes the mission of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) with focus on the NIAAA's current and future research version for alcoholic liver disease and alcoholic pancreatitis.
JF  - Journal of Gastroenterology and Hepatology
AU  - Warren, Kenneth R
AU  - Murray, Margaret M
AD  - National Institute on Alcohol Abuse and Alcoholism. National Institutes of Health
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 4
EP  - 6
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 28
SN  - 0815-9319, 0815-9319
KW  - Health & Safety Science Abstracts
KW  - Alcohol
KW  - USA
KW  - Health problems
KW  - Reviews
KW  - Alcoholism
KW  - Liver
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419370947?accountid=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+Gastroenterology+and+Hepatology&rft.atitle=Alcoholic+liver+disease+and+pancreatitis%3A+Global+health+problems+being+addressed+by+the+US+National+Institute+on+Alcohol+Abuse+and+Alcoholism&rft.au=Warren%2C+Kenneth+R%3BMurray%2C+Margaret+M&rft.aulast=Warren&rft.aufirst=Kenneth&rft.date=2013-08-01&rft.volume=28&rft.issue=&rft.spage=4&rft.isbn=&rft.btitle=&rft.title=Journal+of+Gastroenterology+and+Hepatology&rft.issn=08159319&rft_id=info:doi/10.1111%2Fjgh.12246
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Alcohol; Health problems; Reviews; Alcoholism; Liver; USA
DO  - http://dx.doi.org/10.1111/jgh.12246
ER  - 



TY  - JOUR
T1  - Efficacy and Safety of Metronidazole for Pulmonary Multidrug-Resistant Tuberculosis
AN  - 1419361923; 18272390
AB  - Pulmonary lesions from active tuberculosis patients are thought to contain persistent, nonreplicating bacilli that arise from hypoxic stress. Metronidazole, approved for anaerobic infections, has antituberculosis activity against anoxic bacilli in vitro and in some animal models and may target persistent, nonreplicating bacilli. In this double-blind, placebo-controlled trial, pulmonary multidrug-resistant tuberculosis subjects were randomly assigned to receive metronidazole (500 mg thrice daily) or placebo for 8 weeks in addition to an individualized background regimen. Outcomes were measured radiologically (change on high-resolution computed tomography [HRCT]), microbiologically (time to sputum smear and culture conversion), and clinically (status 6 months after stopping therapy). Enrollment was stopped early due to excessive peripheral neuropathies in the metronidazole arm. Among 35 randomized subjects, 31 (15 metronidazole, 16 placebo) were included in the modified intent-to-treat analysis. There were no significant differences by arm in improvement of HRCT lesions from baseline to 2 or 6 months. More subjects in the metronidazole arm converted their sputum smear (P = 0.04) and liquid culture (P = 0.04) to negative at 1 month, but these differences were lost by 2 months. Overall, 81% showed clinical success 6 months after stopping therapy, with no differences by arm. However, 8/16 (50%) of subjects in the metronidazole group and 2/17 (12%) of those in the placebo group developed peripheral neuropathy. Subjects who received metronidazole were 4.3-fold (95% confidence interval [CI], 1.1 to 17.1) more likely to develop peripheral neuropathies than subjects who received placebo. Metronidazole may have increased early sputum smear and culture conversion but was too neurotoxic to use over the longer term. Newer nitroimidazoles with both aerobic and anaerobic activity, now in clinical trials, may increase the sterilizing potency of future treatment regimens.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Carroll, Matthew W
AU  - Jeon, Doosoo
AU  - Mountz, James M
AU  - Lee, Jong Doo
AU  - Jeong, Yeon Joo
AU  - Zia, Nadeem
AU  - Lee, Myungsun
AU  - Lee, Jongseok
AU  - Via, Laura E
AU  - Lee, Soyoung
Y1  - 2013/08//
PY  - 2013
DA  - Aug 2013
SP  - 3903
EP  - 3909
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 8
SN  - 0066-4804, 0066-4804
KW  - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Bacilli
KW  - Metronidazole
KW  - Mycobacterium
KW  - Drug resistance
KW  - Animal models
KW  - Stress
KW  - Infection
KW  - Clinical trials
KW  - Lung
KW  - Peripheral neuropathy
KW  - Liquid culture
KW  - Hypoxia
KW  - Neurotoxicity
KW  - Computed tomography
KW  - nitroimidazoles
KW  - Tuberculosis
KW  - Sputum
KW  - J 02410:Animal Diseases
KW  - A 01340:Antibiotics & Antimicrobials
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419361923?accountid=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=Efficacy+and+Safety+of+Metronidazole+for+Pulmonary+Multidrug-Resistant+Tuberculosis&rft.au=Carroll%2C+Matthew+W%3BJeon%2C+Doosoo%3BMountz%2C+James+M%3BLee%2C+Jong+Doo%3BJeong%2C+Yeon+Joo%3BZia%2C+Nadeem%3BLee%2C+Myungsun%3BLee%2C+Jongseok%3BVia%2C+Laura+E%3BLee%2C+Soyoung&rft.aulast=Carroll&rft.aufirst=Matthew&rft.date=2013-08-01&rft.volume=57&rft.issue=8&rft.spage=3903&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00753-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 33
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Metronidazole; Bacilli; Drug resistance; Animal models; Stress; Infection; Clinical trials; Lung; Hypoxia; Liquid culture; Peripheral neuropathy; Computed tomography; Neurotoxicity; nitroimidazoles; Tuberculosis; Sputum; Mycobacterium
DO  - http://dx.doi.org/10.1128/AAC.00753-13
ER  - 



TY  - JOUR
T1  - Diet-induced obesity increases tumor growth and promotes anaplastic change in thyroid cancer in a mouse model.
AN  - 1411627737; 23748362
AB  - Recent epidemiological studies provide strong evidence suggesting obesity is a risk factor in several cancers, including thyroid cancer. However, the molecular mechanisms by which obesity increases the risk of thyroid cancer are poorly understood. In this study, we evaluated the effect of diet-induced obesity on thyroid carcinogenesis in a mouse model that spontaneously develops thyroid cancer (Thrb(PV/PV)Pten(+/-) mice). These mice harbor a mutated thyroid hormone receptor-β (denoted as PV) and haplodeficiency of the Pten gene. A high-fat diet (HFD) efficiently induced the obese phenotype in Thrb(PV/PV)Pten(+/-) mice after 15 weeks. Thyroid tumor growth was markedly greater and survival was significantly lower in Thrb(PV/PV)Pten(+/-) mice fed an HFD than in controls fed a low-fat diet (LFD). The HFD increased thyroid tumor cell proliferation by increasing the protein levels of cyclin D1 and phosphorylated retinoblastoma protein to propel cell cycle progression. Histopathological analysis showed that the frequency of anaplasia of thyroid cancer was significantly greater (2.6-fold) in the HFD group than the LFD group. The HFD treatment led to an increase in parametrial/epididymal fat pad and elevated serum leptin levels in Thrb(PV/PV)Pten(+/-) mice. Further molecular analyses indicated that the HFD induced more aggressive pathological changes that were mediated by increased activation of the Janus kinase 2-signaling transducer and activator of transcription 3 (STAT3) signaling pathway and induction of STAT3 target gene expression. Our findings demonstrate that diet-induced obesity exacerbates thyroid cancer progression in Thrb(PV/PV)Pten(+/-) mice and suggest that the STAT3 signaling pathway could be tested as a potential target for the treatment of thyroid cancer.
JF  - Endocrinology
AU  - Kim, Won Gu
AU  - Park, Jeong Won
AU  - Willingham, Mark C
AU  - Cheng, Sheue-yann
AD  - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-4264, USA.
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 2936
EP  - 2947
VL  - 154
IS  - 8
KW  - Bcl2l1 protein, mouse
KW  - 0
KW  - Leptin
KW  - Myc protein, mouse
KW  - Proto-Oncogene Proteins c-myc
KW  - Retinoblastoma Protein
KW  - STAT3 Transcription Factor
KW  - Thyroid Hormone Receptors beta
KW  - bcl-X Protein
KW  - Cyclin D1
KW  - 136601-57-5
KW  - Jak2 protein, mouse
KW  - EC 2.7.10.2
KW  - Janus Kinase 2
KW  - PTEN Phosphohydrolase
KW  - EC 3.1.3.67
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - bcl-X Protein -- genetics
KW  - Animals
KW  - Proto-Oncogene Proteins c-myc -- genetics
KW  - Cyclin D1 -- genetics
KW  - Mice
KW  - Proto-Oncogene Proteins c-myc -- metabolism
KW  - Reverse Transcriptase Polymerase Chain Reaction
KW  - Cell Proliferation
KW  - bcl-X Protein -- metabolism
KW  - PTEN Phosphohydrolase -- genetics
KW  - Leptin -- blood
KW  - Cyclin D1 -- metabolism
KW  - Phosphorylation
KW  - Heterozygote
KW  - Retinoblastoma Protein -- metabolism
KW  - Thyroid Hormone Receptors beta -- genetics
KW  - STAT3 Transcription Factor -- metabolism
KW  - Janus Kinase 2 -- metabolism
KW  - Cell Cycle
KW  - Mutation
KW  - Signal Transduction
KW  - Female
KW  - Male
KW  - Obesity -- etiology
KW  - Diet, High-Fat -- adverse effects
KW  - Thyroid Neoplasms -- genetics
KW  - Thyroid Gland -- pathology
KW  - Disease Models, Animal
KW  - Thyroid Neoplasms -- pathology
KW  - Obesity -- physiopathology
KW  - Thyroid Gland -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1411627737?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diet-induced+obesity+increases+tumor+growth+and+promotes+anaplastic+change+in+thyroid+cancer+in+a+mouse+model.&rft.au=Kim%2C+Won+Gu%3BPark%2C+Jeong+Won%3BWillingham%2C+Mark+C%3BCheng%2C+Sheue-yann&rft.aulast=Kim&rft.aufirst=Won&rft.date=2013-08-01&rft.volume=154&rft.issue=8&rft.spage=2936&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/10.1210%2Fen.2013-1128
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-29
N1  - Date created - 2013-07-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Thyroid. 2002 Nov;12(11):963-9 [12490073]
J Clin Invest. 2001 Oct;108(8):1113-21 [11602618]
Arch Otolaryngol Head Neck Surg. 1988 Jan;114(1):40-4 [3334817]
Cancer. 1990 Jul 15;66(2):321-30 [1695118]
J Clin Invest. 1991 Dec;88(6):2123-30 [1661299]
J Biol Chem. 1995 Nov 10;270(45):26746-9 [7592907]
Nat Med. 1995 Nov;1(11):1155-61 [7584987]
Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836]
Cancer Res. 2005 Jun 15;65(12):5054-62 [15958548]
Endocrinology. 2005 Oct;146(10):4456-63 [16002527]
Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1780-5 [16446424]
J Clin Invest. 2006 Nov;116(11):2972-84 [17039256]
Carcinogenesis. 2007 May;28(5):932-9 [17127711] Gastroenterology. 2007 May;132(6):2087-102 [17498505]
Lancet. 2008 Feb 16;371(9612):569-78 [18280327]
Mol Cell Biol. 2008 Jul;28(14):4598-608 [18474620]
Expert Opin Investig Drugs. 2009 Jan;18(1):45-56 [19053881]
Cancer Prev Res (Phila). 2009 Jan;2(1):60-9 [19139019]
Oncogene. 2009 Jan 29;28(4):509-17 [18997818]
Cancer Causes Control. 2009 Jul;20(5):525-31 [19016336]
Nat Rev Cancer. 2009 Nov;9(11):798-809 [19851315]
Am J Epidemiol. 2010 Jan 15;171(2):242-52 [19951937]
Endocrinology. 2010 Apr;151(4):1929-39 [20133453]
Surgery. 2010 Jun;147(6):847-53 [20045163]
Mol Carcinog. 2010 Jul;49(7):700-9 [20564347]
Carcinogenesis. 2010 Jul;31(7):1284-91 [20299527]
Front Biosci (Landmark Ed). 2011;16:1634-50 [21196253]
Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520]
Oncol Rep. 2011 Nov;26(5):1265-71 [21750869]
Thyroid. 2011 Sep;21(9):957-63 [21767143]
Nat Rev Cancer. 2011 Dec;11(12):886-95 [22113164]
Clin Cancer Res. 2012 Mar 1;18(5):1281-90 [22271876]
Proc Natl Acad Sci U S A. 2012 Jun 12;109(24):9623-8 [22623533]
Clin Endocrinol (Oxf). 2012 Sep;77(3):459-64 [22458627]
Clin Endocrinol (Oxf). 2013 Jan;78(1):134-40 [22812676]
Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13209-14 [11069286]
J Biomed Sci. 2004 Jul-Aug;11(4):517-27 [15153787]
Cell. 2010 Jan 22;140(2):197-208 [20141834]
Endocr Rev. 2001 Apr;22(2):153-83 [11294822]
Comment In:
Endocrinology. 2013 Aug;154(8):2567-9 [23873767]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1210/en.2013-1128
ER  - 



TY  - JOUR
T1  - Outcomes of allogeneic hematopoietic cell transplantation in patients with dyskeratosis congenita.
AN  - 1411626419; 23751955
AB  - We describe outcomes after allogeneic transplantation in 34 patients with dyskeratosis congenita who underwent transplantation between 1981 and 2009. The median age at transplantation was 13 years (range, 2 to 35). Approximately 50% of transplantations were from related donors. Bone marrow was the predominant source of stem cells (24 of 34). The day-28 probability of neutrophil recovery was 73% and the day-100 platelet recovery was 72%. The day-100 probability of grade II to IV acute GVHD and the 3-year probability of chronic graft-versus-host disease were 24% and 37%, respectively. The 10-year probability of survival was 30%; 14 patients were alive at last follow-up. Ten deaths occurred within 4 months from transplantation because of graft failure (n = 6) or other transplantation-related complications; 9 of these patients had undergone transplantation from mismatched related or from unrelated donors. Another 10 deaths occurred after 4 months; 6 of them occurred more than 5 years after transplantation, and 4 of these were attributed to pulmonary failure. Transplantation regimen intensity and transplantations from mismatched related or unrelated donors were associated with early mortality. Transplantation of grafts from HLA-matched siblings with cyclophosphamide-containing nonradiation regimens was associated with early low toxicity. Late mortality was attributed mainly to pulmonary complications and likely related to the underlying disease. 
          Copyright © 2013 American Society for Blood and Marrow Transplantation. All rights reserved.
JF  - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
AU  - Gadalla, Shahinaz M
AU  - Sales-Bonfim, Carmem
AU  - Carreras, Jeanette
AU  - Alter, Blanche P
AU  - Antin, Joseph H
AU  - Ayas, Mouhab
AU  - Bodhi, Prasad
AU  - Davis, Jeffrey
AU  - Davies, Stella M
AU  - Deconinck, Eric
AU  - Deeg, H Joachim
AU  - Duerst, Reggie E
AU  - Fasth, Anders
AU  - Ghavamzadeh, Ardeshir
AU  - Giri, Neelam
AU  - Goldman, Frederick D
AU  - Kolb, E Anders
AU  - Krance, Robert
AU  - Kurtzberg, Joanne
AU  - Leung, Wing H
AU  - Srivastava, Alok
AU  - Or, Reuven
AU  - Richman, Carol M
AU  - Rosenberg, Philip S
AU  - Toledo Codina, Jose Sanchez de
AU  - Shenoy, Shalini
AU  - Socié, Gerard
AU  - Tolar, Jakub
AU  - Williams, Kirsten M
AU  - Eapen, Mary
AU  - Savage, Sharon A
AD  - Clinical Genetic Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA.
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 1238
EP  - 1243
VL  - 19
IS  - 8
KW  - Index Medicus
KW  - Long-term survival
KW  - Pulmonary toxicity
KW  - Dyskeratosis congenita
KW  - Allogeneic transplantation
KW  - Young Adult
KW  - Humans
KW  - Adult
KW  - Treatment Outcome
KW  - Retrospective Studies
KW  - Child
KW  - Transplantation, Homologous
KW  - Adolescent
KW  - Male
KW  - Female
KW  - Survival Analysis
KW  - Child, Preschool
KW  - Dyskeratosis Congenita -- surgery
KW  - Dyskeratosis Congenita -- therapy
KW  - Hematopoietic Stem Cell Transplantation -- methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1411626419?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Outcomes+of+allogeneic+hematopoietic+cell+transplantation+in+patients+with+dyskeratosis+congenita.&rft.au=Gadalla%2C+Shahinaz+M%3BSales-Bonfim%2C+Carmem%3BCarreras%2C+Jeanette%3BAlter%2C+Blanche+P%3BAntin%2C+Joseph+H%3BAyas%2C+Mouhab%3BBodhi%2C+Prasad%3BDavis%2C+Jeffrey%3BDavies%2C+Stella+M%3BDeconinck%2C+Eric%3BDeeg%2C+H+Joachim%3BDuerst%2C+Reggie+E%3BFasth%2C+Anders%3BGhavamzadeh%2C+Ardeshir%3BGiri%2C+Neelam%3BGoldman%2C+Frederick+D%3BKolb%2C+E+Anders%3BKrance%2C+Robert%3BKurtzberg%2C+Joanne%3BLeung%2C+Wing+H%3BSrivastava%2C+Alok%3BOr%2C+Reuven%3BRichman%2C+Carol+M%3BRosenberg%2C+Philip+S%3BToledo+Codina%2C+Jose+Sanchez+de%3BShenoy%2C+Shalini%3BSoci%C3%A9%2C+Gerard%3BTolar%2C+Jakub%3BWilliams%2C+Kirsten+M%3BEapen%2C+Mary%3BSavage%2C+Sharon+A&rft.aulast=Gadalla&rft.aufirst=Shahinaz&rft.date=2013-08-01&rft.volume=19&rft.issue=8&rft.spage=1238&rft.isbn=&rft.btitle=&rft.title=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.issn=1523-6536&rft_id=info:doi/10.1016%2Fj.bbmt.2013.05.021
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-09
N1  - Date created - 2013-07-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Br J Haematol. 2010 Apr;149(1):14-21 [20136826]
Blood. 2009 Jun 25;113(26):6549-57 [19282459]
Genet Med. 2010 Dec;12(12):753-64 [21189492]
Bone Marrow Transplant. 2011 Jan;46(1):98-104 [20383216]
Pediatr Transplant. 2011 Mar;15(2):161-6 [21176016]
Haematologica. 2013 Mar;98(3):334-8 [22899577]
Hum Genet. 2013 Apr;132(4):473-80 [23329068]
Hematol Oncol Clin North Am. 1999 Oct;13(5):1091-112, viii-ix [10553263]
Pediatr Transplant. 1999 Nov;3(4):315-21 [10562977]
Bone Marrow Transplant. 2013 Sep;48(9):1168-72 [23542225]
Biol Blood Marrow Transplant. 2002;8(11):597-600 [12463478]
Lancet. 2003 Nov 15;362(9396):1628-30 [14630445]
Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076]
Int J Hematol. 2006 Apr;83(3):275-6 [16720563]
Stat Med. 1999 Mar 30;18(6):695-706 [10204198]
Br J Haematol. 1998 Oct;103(1):243-8 [9792316]
Nat Med. 2007 Jun;13(6):742-7 [17486088]
Pediatr Transplant. 2007 Sep;11(6):584-94 [17663679]
Blood. 2007 Sep 1;110(5):1439-47 [17468339]
Mech Ageing Dev. 2008 Jan-Feb;129(1-2):35-47 [18160098]
Blood. 2009 Jan 29;113(5):1175-83 [18971419]
Acta Haematol. 2010;124(4):200-3 [21042011]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.bbmt.2013.05.021
ER  - 



TY  - JOUR
T1  - Hepatocellular carcinomas in B6C3F1 mice treated with Ginkgo biloba extract for two years differ from spontaneous liver tumors in cancer gene mutations and genomic pathways.
AN  - 1406177180; 23262642
AB  - Ginkgo biloba leaf extract (GBE) has been used for centuries in traditional Chinese medicine and today is used as an herbal supplement touted for improving neural function and for its antioxidant and anticancer effects. Herbal supplements have the potential for consumption over extended periods of time, with a general lack of sufficient data on long-term carcinogenicity risk. Exposure of B6C3F1 mice to GBE in the 2-year National Toxicology Program carcinogenicity bioassay resulted in a dose-dependent increase in hepatocellular tumors, including hepatocellular carcinoma (HCC). We show that the mechanism of hepatocarcinogenesis in GBE exposed animals is complex, involving alterations in H-ras and Ctnnb1 mutation spectra, WNT pathway dysregulation, and significantly altered gene expression associated with oncogenesis, HCC development, and chronic xenobiotic and oxidative stress compared to spontaneous HCC. This study provides a molecular context for the genetic changes associated with hepatocarcinogenesis in GBE exposed mice and illustrates the marked differences between these tumors and those arising spontaneously in the B6C3F1 mouse. The molecular changes observed in HCC from GBE-treated animals may be of relevance to those seen in human HCC and other types of cancer, and provide important data on potential mechanisms of GBE hepatocarcinogenesis.
JF  - Toxicologic pathology
AU  - Hoenerhoff, Mark J
AU  - Pandiri, Arun R
AU  - Snyder, Stephanie A
AU  - Hong, Hue-Hua L
AU  - Ton, Thai-Vu
AU  - Peddada, Shyamal
AU  - Shockley, Keith
AU  - Witt, Kristine
AU  - Chan, Po
AU  - Rider, Cynthia
AU  - Kooistra, Linda
AU  - Nyska, Abraham
AU  - Sills, Robert C
AD  - Cellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences and National Toxicology Program, Research Triangle Park, NC 27519, USA. hoenerhm@niehs.nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 826
EP  - 841
VL  - 41
IS  - 6
KW  - Drugs, Chinese Herbal
KW  - 0
KW  - beta Catenin
KW  - Index Medicus
KW  - carcinogenesis
KW  - toxicogenomics
KW  - liver
KW  - microarray
KW  - molecular pathology
KW  - Administration, Oral
KW  - Animals
KW  - Liver -- pathology
KW  - Reproducibility of Results
KW  - Dose-Response Relationship, Drug
KW  - Mice
KW  - Gene Expression Regulation, Neoplastic -- drug effects
KW  - Liver -- chemistry
KW  - Mutagenicity Tests
KW  - Liver -- drug effects
KW  - beta Catenin -- metabolism
KW  - Signal Transduction -- drug effects
KW  - Oxidative Stress -- drug effects
KW  - Carcinogenicity Tests
KW  - Cluster Analysis
KW  - Immunohistochemistry
KW  - Female
KW  - Male
KW  - Liver Neoplasms, Experimental -- genetics
KW  - Liver Neoplasms, Experimental -- pathology
KW  - Liver Neoplasms, Experimental -- metabolism
KW  - Drugs, Chinese Herbal -- toxicity
KW  - Liver Neoplasms, Experimental -- chemically induced
KW  - Ginkgo biloba -- chemistry
KW  - Drugs, Chinese Herbal -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1406177180?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hepatocellular+carcinomas+in+B6C3F1+mice+treated+with+Ginkgo+biloba+extract+for+two+years+differ+from+spontaneous+liver+tumors+in+cancer+gene+mutations+and+genomic+pathways.&rft.au=Hoenerhoff%2C+Mark+J%3BPandiri%2C+Arun+R%3BSnyder%2C+Stephanie+A%3BHong%2C+Hue-Hua+L%3BTon%2C+Thai-Vu%3BPeddada%2C+Shyamal%3BShockley%2C+Keith%3BWitt%2C+Kristine%3BChan%2C+Po%3BRider%2C+Cynthia%3BKooistra%2C+Linda%3BNyska%2C+Abraham%3BSills%2C+Robert+C&rft.aulast=Hoenerhoff&rft.aufirst=Mark&rft.date=2013-08-01&rft.volume=41&rft.issue=6&rft.spage=826&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623312467520
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-05-08
N1  - Date created - 2013-07-18
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1177/0192623312467520
ER  - 



TY  - JOUR
T1  - Alternative matrices for cocaine, heroin, and methadone in utero drug exposure detection.
AN  - 1400624689; 23851907
AB  - Drug determination in biological matrices from the mother and the newborn is an objective measure of maternal and fetal drug exposure. The aim of this study was to compare maternal hair, meconium, umbilical cord, and placenta for detecting in utero drug exposure to cocaine, opiates, methadone, and amphetamines.
          Maternal hair, meconium, umbilical cord, and placenta were collected from 175 mother-newborn dyads. Maternal hair (segmented in trimesters) and meconium specimens were analyzed for cocaine, opiates, methadone, and amphetamines. If either maternal hair or meconium tested positive, umbilical cord and placenta were analyzed. Analyses were performed by liquid chromatography tandem mass spectrometry. In hair, 24 participants tested positive; 21 for cocaine [cocaine 20-50,605, benzoylecgonine (BE) 17-46,668 pg/mg], 7 for methadone (76-26,845 pg/mg), 2 for opiates (morphine 298-2398 pg/mg, codeine 65-914 pg/mg, 6-acetylmorphine 1635-15,657 pg/mg), and 1 for amphetamines (amphetamine 1990 pg/mg, 3,4-methylenedioxyamphetamine 30 pg/mg, 3,4-methylenedioxymethamphetamine 294 pg/mg). In meconium, 6 were positive; 5 for methadone [methadone 88-3752, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) 642-25,179 ng/g], 3 for cocaine (cocaine 7, BE 79, hydroxybenzoylecgonine 5-135, ecgonine-methyl ester 2-56 ng/g), and 2 for opiates (morphine 152-1025, morphine-3-glucuronide 22-23, codeine 4-34 ng/g). Placenta and umbilical cord were positive in 5 and 6 cases, respectively; 5 for methadone in placenta (methadone 7-543, EDDP 10-51 ng/g) and cord (methadone 3-183, EDDP 2-109 ng/g); 1 for cocaine in placenta (cocaine 7, BE 2 ng/g) and cord (BE 6 ng/g); and 1 for opiates in placenta (morphine 6, morphine-3-glucuronide 48 ng/g), and 2 in cord (morphine 2, morphine-3-glucuronide 15-38, morphine-6-glucuronide 5 ng/g). Meconium, placenta, and umbilical cord only tested positive if hair concentrations were greater than Society of Hair Testing cutoffs.
          Maternal hair is the most sensitive specimen to detect drug consumption during pregnancy. Placenta and umbilical cord could be alternatives to meconium for detecting high in utero drug exposure.
JF  - Therapeutic drug monitoring
AU  - Concheiro, Marta
AU  - González-Colmenero, Eva
AU  - Lendoiro, Elena
AU  - Concheiro-Guisán, Ana
AU  - de Castro, Ana
AU  - Cruz-Landeira, Angelines
AU  - López-Rivadulla, Manuel
AD  - Sección de Toxicología, Instituto de Ciencias Forenses, Universidad de Santiago de Compostela, Santiago de Compostela, Spain. marta.concheiro-guisan@nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 502
EP  - 509
VL  - 35
IS  - 4
KW  - Heroin
KW  - 70D95007SX
KW  - Cocaine
KW  - I5Y540LHVR
KW  - Methadone
KW  - UC6VBE7V1Z
KW  - Index Medicus
KW  - Drug Monitoring -- methods
KW  - Uterus -- chemistry
KW  - Placenta -- chemistry
KW  - Maternal-Fetal Exchange
KW  - Chromatography, Liquid -- methods
KW  - Meconium -- chemistry
KW  - Humans
KW  - Hair -- chemistry
KW  - Tandem Mass Spectrometry -- methods
KW  - Female
KW  - Umbilical Cord -- chemistry
KW  - Pregnancy
KW  - Heroin -- analysis
KW  - Cocaine -- analysis
KW  - Methadone -- chemistry
KW  - Cocaine -- chemistry
KW  - Heroin -- chemistry
KW  - Substance Abuse Detection -- methods
KW  - Methadone -- analysis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1400624689?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Therapeutic+drug+monitoring&rft.atitle=Alternative+matrices+for+cocaine%2C+heroin%2C+and+methadone+in+utero+drug+exposure+detection.&rft.au=Concheiro%2C+Marta%3BGonz%C3%A1lez-Colmenero%2C+Eva%3BLendoiro%2C+Elena%3BConcheiro-Guis%C3%A1n%2C+Ana%3Bde+Castro%2C+Ana%3BCruz-Landeira%2C+Angelines%3BL%C3%B3pez-Rivadulla%2C+Manuel&rft.aulast=Concheiro&rft.aufirst=Marta&rft.date=2013-08-01&rft.volume=35&rft.issue=4&rft.spage=502&rft.isbn=&rft.btitle=&rft.title=Therapeutic+drug+monitoring&rft.issn=1536-3694&rft_id=info:doi/10.1097%2FFTD.0b013e31828a6148
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-20
N1  - Date created - 2013-07-16
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1097/FTD.0b013e31828a6148
ER  - 



TY  - JOUR
T1  - PPIP5K1 modulates ligand competition between diphosphoinositol polyphosphates and PtdIns(3,4,5)P3 for polyphosphoinositide-binding domains.
AN  - 1400398206; 23682967
AB  - We describe new signalling consequences for PPIP5K1 (diphosphoinositol pentakisphosphate kinase type 1)-mediated phosphorylation of InsP6 and 5-InsP7 to 1-InsP7 and InsP8. In NIH 3T3 cells, either hyperosmotic stress or receptor activation by PDGF (platelet-derived growth factor) promoted translocation of PPIP5K1 from the cytoplasm to the plasma membrane. The PBD1 (polyphosphoinositide-binding domain) in PPIP5K1 recapitulated that translocation. Mutagenesis of PBD1 to reduce affinity for PtdIns(3,4,5)P3 prevented translocation. Using surface plasmon resonance, we found that PBD1 association with vesicular PtdIns(3,4,5)P3 was inhibited by InsP6 and diphosphoinositol polyphosphates. However, the inhibition by PPIP5K1 substrates (IC50: 5-InsP7=5 μM and InsP6=7 μM) was substantially more potent than that of the PPIP5K1 products (IC50: InsP8=32 μM and 1-InsP7=43 μM). This rank order of ligand competition with PtdIns(3,4,5)P3 was also exhibited by the PH (pleckstrin homology) domains of Akt (also known as protein kinase B), GRP1 (general receptor for phosphoinositides 1) and SIN1 (stress-activated protein kinase-interaction protein 1). We propose that, in vivo, PH domain binding of InsP6 and 5-InsP7 suppresses inappropriate signalling ('noise') from stochastic increases in PtdIns(3,4,5)P3. That restraint may be relieved by localized depletion of InsP6 and 5-InsP7 at the plasma membrane following PPIP5K1 recruitment. We tested this hypothesis in insulin-stimulated L6 myoblasts, using mTOR (mechanistic/mammalian target of rapamycin)-mediated phosphorylation of Akt on Ser473 as a readout for SIN1-mediated translocation of mTORC (mTOR complex) 2 to the plasma membrane [Zoncu, Efeyan and Sabatini (2011) Nat. Rev. Mol. Cell Biol. 12, 21-35]. Knockdown of PPIP5K1 expression was associated with a 40% reduction in Ser473 phosphorylation. A common feature of PtdIns(3,4,5)P3-based signalling cascades may be their regulation by PPIP5K1.
JF  - The Biochemical journal
AU  - Gokhale, Nikhil A
AU  - Zaremba, Angelika
AU  - Janoshazi, Agnes K
AU  - Weaver, Jeremy D
AU  - Shears, Stephen B
AD  - Inositol Signaling Section, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences NIEHS, National Institutes of Health NIH, Department of Health and Human Services DHHS, Research Triangle Park, NC 27709, USA.
Y1  - 2013/08/01/
PY  - 2013
DA  - 2013 Aug 01
SP  - 413
EP  - 426
VL  - 453
IS  - 3
KW  - Phosphatidylinositol Phosphates
KW  - 0
KW  - Platelet-Derived Growth Factor
KW  - phosphatidylinositol 3,4,5-triphosphate
KW  - Phosphotransferases (Phosphate Group Acceptor)
KW  - EC 2.7.4.-
KW  - PPIP5K1 protein, human
KW  - EC 2.7.4.21
KW  - Index Medicus
KW  - Real-Time Polymerase Chain Reaction
KW  - Cell Proliferation -- drug effects
KW  - Immunoblotting
KW  - Animals
KW  - Cell Membrane -- drug effects
KW  - Humans
KW  - Surface Plasmon Resonance
KW  - Platelet-Derived Growth Factor -- pharmacology
KW  - Mice
KW  - Cell Membrane -- metabolism
KW  - NIH 3T3 Cells
KW  - Cell Line
KW  - Phosphatidylinositol Phosphates -- metabolism
KW  - Phosphotransferases (Phosphate Group Acceptor) -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1400398206?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=PPIP5K1+modulates+ligand+competition+between+diphosphoinositol+polyphosphates+and+PtdIns%283%2C4%2C5%29P3+for+polyphosphoinositide-binding+domains.&rft.au=Gokhale%2C+Nikhil+A%3BZaremba%2C+Angelika%3BJanoshazi%2C+Agnes+K%3BWeaver%2C+Jeremy+D%3BShears%2C+Stephen+B&rft.aulast=Gokhale&rft.aufirst=Nikhil&rft.date=2013-08-01&rft.volume=453&rft.issue=3&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=1470-8728&rft_id=info:doi/10.1042%2FBJ20121528
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-23
N1  - Date created - 2013-07-15
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Acta Crystallogr Sect F Struct Biol Cryst Commun. 2012 Apr 1;68(Pt 4):386-92 [22505404]
Dev Cell. 2012 Jun 12;22(6):1286-98 [22609160]
Biochem J. 2013 Feb 15;450(1):115-25 [23186306]
Biosci Rep. 2013;33(2):e00022 [23240582]
J Biol Chem. 1999 Dec 10;274(50):35963-8 [10585485]
Cell Signal. 2001 Mar;13(3):151-8 [11282453]
J Biol Chem. 2001 Oct 19;276(42):39179-85 [11502751]
Comp Biochem Physiol A Mol Integr Physiol. 2001 Oct;130(3):421-8 [11913455]
Sci STKE. 2002 Mar 26;2002(125):pl3 [11917154]
Biol Chem. 2002 Mar-Apr;383(3-4):577-83 [12033446]
J Biol Chem. 2003 Aug 22;278(34):32344-51 [12783890]
Cell. 2003 Sep 5;114(5):559-72 [13678580]
J Biomech. 2003 Oct;36(10):1409-24 [14499290]
Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10673-8 [15247420]
EMBO J. 2004 Oct 1;23(19):3711-20 [15359279]
J Biol Chem. 2004 Oct 15;279(42):43378-81 [15316027]
J Biol Chem. 1993 Mar 25;268(9):6161-7 [8384201]
Mol Biol Cell. 1994 Jan;5(1):17-27 [8186462]
Science. 1997 Mar 28;275(5308):1927-30 [9072969]
Biochem J. 1997 Oct 15;327 ( Pt 2):553-60 [9359429]
J Biol Chem. 1997 Oct 24;272(43):27401-10 [9341192]
EMBO J. 1998 Dec 15;17(24):7294-303 [9857186]
Biochem J. 1999 Feb 1;337 ( Pt 3):575-83 [9895304]
Science. 2004 Dec 17;306(5704):2101-5 [15604408]
Science. 2005 Sep 2;309(5740):1534-9 [16141067]
Biochem Biophys Res Commun. 2005 Oct 14;336(1):157-62 [16139247]
J Cell Sci. 2005 Oct 15;118(Pt 20):4879-88 [16219693]
J Biol Chem. 2005 Dec 30;280(52):42831-40 [16230353]
Cell Mol Life Sci. 2006 Mar;63(5):552-64 [16429326]
Methods. 2006 Jun;39(2):122-33 [16829131]
Cell. 2006 Oct 6;127(1):125-37 [16962653]
J Cell Sci. 2006 Dec 15;119(Pt 24):5160-8 [17158918]
Pflugers Arch. 2007 May;454(2):173-85 [17206446]
Nature. 2007 Apr 5;446(7136):640-5 [17410169]
Science. 2007 Apr 6;316(5821):106-9 [17412958]
Science. 2007 Apr 6;316(5821):109-12 [17412959]
Proc Natl Acad Sci U S A. 2007 Aug 28;104(35):13978-83 [17709751]
Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15305-10 [17873058]
Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15653-8 [17895383]
Physiol Rev. 2007 Oct;87(4):1441-74 [17928589]
J Biol Chem. 2007 Oct 19;282(42):30754-62 [17690096]
J Biol Chem. 2007 Oct 19;282(42):30763-75 [17702752]
J Biol Chem. 2007 Nov 2;282(44):32093-105 [17823121]
Biochem J. 2007 Dec 15;408(3):335-45 [17705785]
Nat Chem Biol. 2008 Jan;4(1):25-32 [18059263]
PLoS Comput Biol. 2008 Jan;4(1):e8 [18179281]
Chem Biol. 2008 Mar;15(3):274-86 [18355727]
Mol Cell. 2008 May 9;30(3):381-92 [18471983]
J Biol Chem. 2009 Jan 16;284(3):1863-72 [18981179]
J Cell Physiol. 2009 Jul;220(1):8-15 [19326391]
Mol Pharmacol. 2009 Aug;76(2):236-52 [19439500]
J Biol Chem. 2009 Nov 27;284(48):33614-22 [19797057]
Proc Natl Acad Sci U S A. 2009 Dec 15;106(50):21161-6 [19934039]
Cell Mol Life Sci. 2009 Dec;66(24):3851-71 [19714294]
J Biol Chem. 2010 Apr 23;285(17):12620-8 [20177066]
Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):20126-31 [21041639]
Cell. 2010 Dec 10;143(6):897-910 [21145457]
Nat Rev Mol Cell Biol. 2011 Jan;12(1):21-35 [21157483]
Biochem J. 2011 Mar 15;434(3):415-26 [21222653]
Adv Enzyme Regul. 2011;51(1):13-25 [21035493]
Nat Immunol. 2011 Aug;12(8):752-60 [21685907]
Sci Signal. 2011 Aug 30;4(188):re1 [21878680]
J Vis Exp. 2011;(55):e3027 [21912370]
Nat Chem Biol. 2012 Jan;8(1):111-6 [22119861]
J Mol Cell Cardiol. 2012 Feb;52(2):401-9 [21704043]
Comment In:
Biochem J. 2013 Aug 1;453(3):e3-4 [23849059]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1042/BJ20121528
ER  - 



TY  - JOUR
T1  - The fate of β-hexabromocyclododecane in female C57BL/6 mice.
AN  - 1399926523; 23733921
AB  - 1,2,5,6,9,10-Hexabromocyclododecane (HBCD) is a high production volume cycloaliphatic used as an additive flame retardant primarily in polystyrene foam building materials. HBCD mixtures contain three major stereoisomers, alpha (α), beta (β), and gamma (γ), at a typical ratio of 1.2:0.6:8.2. The toxicokinetic properties of the α and γ isomers differ. For instance, α-HBCD has greater bioavailability and potential for accumulation in mice than γ-HBCD. The present study reports comparative kinetics data for β-HBCD needed to support toxicological evaluations of HBCD mixtures. Results indicated that a single oral dose of 3mg/kg of [(14)C]-labeled β-HBCD was absorbed rapidly (≥ 85% total dose) in the female C57BL/6 mouse. The C max for β-HBCD-derived radioactivity in tissues, except adipose, was observed 3h following gavage. Approximately 90% of the administered dose was excreted in urine and feces within 24h, primarily as β-HBCD-derived metabolites. A portion of the dose (circa 9%) was excreted in feces as γ-HBCD. Oral administration of 30 or 100mg/kg of β-HBCD resulted initially in slower rates of [(14)C] elimination; however, cumulative excretion data were similar across the dosing range 4 days postdosing. Residual concentrations of [(14)C] in tissues were highest in adipose and liver. β-HBCD-derived radioactivity accumulated in most tissues following four consecutive daily oral doses of 3mg/kg. The extent of metabolism and excretion of β-HBCD in female C57BL/6 mice was similar to that for γ-HBCD. The potential for accumulation of β-HBCD-derived material in most tissues appeared to be less than for α-HBCD.
JF  - Toxicological sciences : an official journal of the Society of Toxicology
AU  - Sanders, J Michael
AU  - Knudsen, Gabriel A
AU  - Birnbaum, Linda S
AD  - Toxicology and Toxicokinetics Group, Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Research Triangle Park, North Carolina 27709, USA. sander10@mail.nih.gov
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 251
EP  - 257
VL  - 134
IS  - 2
KW  - Flame Retardants
KW  - 0
KW  - Hydrocarbons, Brominated
KW  - hexabromocyclododecane
KW  - 5I9835JO3M
KW  - Index Medicus
KW  - mouse
KW  - persistent organic pollutant.
KW  - brominated flame retardant
KW  - risk assessment
KW  - toxicokinetics
KW  - disposition
KW  - Animals
KW  - Half-Life
KW  - Mice, Inbred C57BL
KW  - Mice
KW  - Female
KW  - Chromatography, High Pressure Liquid
KW  - Biological Availability
KW  - Hydrocarbons, Brominated -- pharmacokinetics
KW  - Flame Retardants -- pharmacokinetics
KW  - Hydrocarbons, Brominated -- toxicity
KW  - Flame Retardants -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399926523?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+fate+of+%CE%B2-hexabromocyclododecane+in+female+C57BL%2F6+mice.&rft.au=Sanders%2C+J+Michael%3BKnudsen%2C+Gabriel+A%3BBirnbaum%2C+Linda+S&rft.aulast=Sanders&rft.aufirst=J&rft.date=2013-08-01&rft.volume=134&rft.issue=2&rft.spage=251&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%2Fkft121
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-03
N1  - Date created - 2013-07-11
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Toxicol Sci. 2006 Jul;92(1):157-73 [16601080]
Environ Sci Technol. 2012 Dec 18;46(24):13494-503 [23171393]
Toxicol Sci. 2006 Dec;94(2):281-92 [16984958]
Chemosphere. 2008 Feb;70(11):1935-44 [18037156]
Chemosphere. 2008 Mar;71(4):656-62 [18093636]
J Chromatogr A. 2008 May 9;1190(1-2):74-9 [18378256]
Reprod Toxicol. 2008 Apr;25(3):335-51 [18262388]
Toxicol In Vitro. 2008 Sep;22(6):1520-7 [18644697]
Environ Sci Technol. 2008 Sep 15;42(18):6910-6 [18853808]
Chemosphere. 2008 Nov;73(8):1201-10 [18768199]
Toxicol Lett. 2009 Feb 25;185(1):51-62 [19118610]
Xenobiotica. 2000 Mar;30(3):263-72 [10752641]
Environ Sci Technol. 2005 Apr 1;39(7):2095-100 [15871242]
Chemosphere. 2005 Sep;61(1):65-73 [16157171]
Toxicology. 2006 Feb 1;218(2-3):229-36 [16325980]
Environ Sci Technol. 2009 Aug 1;43(15):6058-63 [19731718]
Chemosphere. 2010 Jun;80(2):165-9 [20378152]
Sci Total Environ. 2010 Jul 1;408(15):2885-918 [19815253]
Toxicol Sci. 2010 Oct;117(2):282-93 [20562218]
Environ Int. 2011 Feb;37(2):443-8 [21167604]
Cerebellum. 2011 Mar;10(1):22-31 [20967578]
Chemosphere. 2011 Mar;82(11):1662-8 [21111444]
Chemosphere. 2011 Mar;83(2):193-9 [21269658]
Folia Biol (Praha). 2011;57(1):35-9 [21457653]
Toxicol Sci. 2011 Jun;121(2):234-44 [21441408]
Sci Total Environ. 2011 Sep 1;409(19):4048-53 [21708397]
Environ Sci Technol. 2011 Oct 15;45(20):8613-23 [21913722]
Environ Res. 2011 Nov;111(8):1116-23 [21917248]
Mol Med Rep. 2012 Mar;5(3):761-6 [22179484]
PLoS One. 2012;7(4):e33059 [22485137]
Chemosphere. 2012 Oct;89(4):398-403 [22748388]
Environ Int. 2012 Oct 15;47:56-65 [22766500]
Environ Health Perspect. 2012 Sep;120(9):1260-4 [22647707]
Environ Sci Technol. 2006 Jun 15;40(12):3679-88 [16830527]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/toxsci/kft121
ER  - 



TY  - JOUR
T1  - Occupational trichloroethylene exposure and risk of lymphatic and haematopoietic cancers: a meta-analysis.
AN  - 1399925690; 23723297
AB  - The carcinogenic potential of trichloroethylene (TCE) continues to generate much controversy, even after the US Environmental Protection Agency raised its classification to 'carcinogenic to humans'. We conducted a meta-analysis of published cohort and case-control studies exploring occupational TCE exposure in relation to five different lymphatic and haematopoietic cancers: non-Hodgkin's lymphoma (NHL, N=24), Hodgkin's lymphoma (HL, N=13), multiple myeloma (MM, N=11), leukaemia (N=12) and chronic/small lymphocytic leukaemia (CLL/SLL, N=7).  Studies published between 1950 and 2011 were identified through a PubMed Medline search. All studies included in analyses were classified as those that assessed either occupational TCE exposure specifically ('TCE-exposure' studies) or a broader classification of all chlorinated solvents ('chlorinated solvent-exposure' studies).  A significantly raised summary estimate for NHL was seen for all cohort and case-control 'TCE-exposure' studies combined (N=19; relative risk (RR)=1.32, 95% CI 1.14 to 1.54; I(2)=25.20; p-heterogeneity=0.12) and for cohort 'TCE-exposure' studies (N=10; RR=1.52, 95% CI 1.29 to 1.79; I(2)=7.09; p-heterogeneity=0.63). A non-significant but raised summary estimate was seen for NHL case-control 'TCE-exposure' studies. No significant association with NHL risk was detected overall for any 'chlorinated solvent-exposure' studies. Summary estimates for occupational TCE exposure were not associated with risk of HL, MM, leukaemia or CLL/SLL.  Our updated meta-analysis of NHL, which incorporates new analytical results from three cohort and four case-control studies, supports an association between occupational TCE exposure and NHL.
JF  - Occupational and environmental medicine
AU  - Karami, Sara
AU  - Bassig, Bryan
AU  - Stewart, Patricia A
AU  - Lee, Kyoung-Mu
AU  - Rothman, Nathaniel
AU  - Moore, Lee E
AU  - Lan, Qing
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 20852, USA.
Y1  - 2013/08//
PY  - 2013
DA  - August 2013
SP  - 591
EP  - 599
VL  - 70
IS  - 8
KW  - Carcinogens
KW  - 0
KW  - Solvents
KW  - Trichloroethylene
KW  - 290YE8AR51
KW  - Index Medicus
KW  - Multiple Myeloma -- etiology
KW  - Humans
KW  - Leukemia -- etiology
KW  - Hodgkin Disease -- etiology
KW  - Solvents -- toxicity
KW  - Occupational Diseases -- etiology
KW  - Lymphoma, Non-Hodgkin -- etiology
KW  - Occupational Exposure -- adverse effects
KW  - Trichloroethylene -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399925690?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Occupational+trichloroethylene+exposure+and+risk+of+lymphatic+and+haematopoietic+cancers%3A+a+meta-analysis.&rft.au=Karami%2C+Sara%3BBassig%2C+Bryan%3BStewart%2C+Patricia+A%3BLee%2C+Kyoung-Mu%3BRothman%2C+Nathaniel%3BMoore%2C+Lee+E%3BLan%2C+Qing&rft.aulast=Karami&rft.aufirst=Sara&rft.date=2013-08-01&rft.volume=70&rft.issue=8&rft.spage=591&rft.isbn=&rft.btitle=&rft.title=Occupational+and+environmental+medicine&rft.issn=1470-7926&rft_id=info:doi/10.1136%2Foemed-2012-101212
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-09
N1  - Date created - 2013-07-11
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1136/oemed-2012-101212
ER  - 



TY  - JOUR
T1  - HIV immune activation drives increased Eomes expression in memory CD8 T cells in association with transcriptional downregulation of CD127
AN  - 1765969906; PQ0002559302
AB  - Background: During HIV infection distinct mechanisms drive immune activation of the CD4 and CD8 T cells leading to CD4 T-cell depletion and expansion of the CD8 T-cell pool. This immune activation is polyclonal and extends beyond HIV-specific T cells. One consequence of this immune activation is a profound decrease in IL-7R alpha (CD127) expression on memory CD8 T cells. The mechanisms leading to this are unknown and because of the potential impact of reduced IL-7 signaling in memory T cells specific to HIV and other pathogens, in the present study we examined the molecular mechanisms implicated in this downregulation of CD127. Methods: Membrane bound (mlL7RA) and soluble (slL7RA) mRNA expression was determined by qRT-PCR. CD127, Eomesodermin (Eomes) and T-bet expression in healthy controls and HIV-infected patients were studied by flow cytometry. Results: CD127 downregulation occurs at the transcriptional level for both mlL7RA and slL7RA alternative spliced forms in the CD127 super(low) memory CD8 T cells. CD127 super(low) memory CD8 T cells exhibited increased Eomes expression and an 'effector-like' gene profile. These changes were associated with higher HIV-RNA levels. Following combination antiretroviral therapy (cART), there was an increase in CD127 expression over an extended period of time (>5 months) which was associated with decreased Eomes expression. Conclusion: CD127 is downregulated at a transcriptional level in memory CD8 T cells in association with upregulation of Eomes expression.
JF  - AIDS
AU  - Hasley, Rebecca B
AU  - Hong, Changwan
AU  - Li, Wenqing
AU  - Friesen, Travis
AU  - Nakamura, Yoriko
AU  - Kim, Grace Y
AU  - Park, Jung-Hyun
AU  - Hixon, Julie A
AU  - Durum, Scott
AU  - Hu, Zonghui
AU  - Sneller, Michael C
AU  - Oguariri, Raphael
AU  - Imamichi, Tomozumi
AU  - Lane, H Clifford
AU  - Catalfamo, Marta
AD  - CMRS/Laboratory of Immunoregulation, NIAID, catalfam@mail.nih.gov
Y1  - 2013/07/31/
PY  - 2013
DA  - 2013 Jul 31
SP  - 1867
EP  - 1877
PB  - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL  - 27
IS  - 12
SN  - 0269-9370, 0269-9370
KW  - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW  - CD127
KW  - Eomes
KW  - HIV
KW  - T-bet
KW  - T-box transcription factors
KW  - Molecular modelling
KW  - Interleukin 7
KW  - Acquired immune deficiency syndrome
KW  - Membranes
KW  - antiretroviral therapy
KW  - Memory cells
KW  - Immunological memory
KW  - Transcription
KW  - Pathogens
KW  - CD8 antigen
KW  - Infection
KW  - Antiretroviral agents
KW  - Flow cytometry
KW  - Gene expression
KW  - CD4 antigen
KW  - Human immunodeficiency virus
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/1765969906?accountid=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=HIV+immune+activation+drives+increased+Eomes+expression+in+memory+CD8+T+cells+in+association+with+transcriptional+downregulation+of+CD127&rft.au=Hasley%2C+Rebecca+B%3BHong%2C+Changwan%3BLi%2C+Wenqing%3BFriesen%2C+Travis%3BNakamura%2C+Yoriko%3BKim%2C+Grace+Y%3BPark%2C+Jung-Hyun%3BHixon%2C+Julie+A%3BDurum%2C+Scott%3BHu%2C+Zonghui%3BSneller%2C+Michael+C%3BOguariri%2C+Raphael%3BImamichi%2C+Tomozumi%3BLane%2C+H+Clifford%3BCatalfamo%2C+Marta&rft.aulast=Hasley&rft.aufirst=Rebecca&rft.date=2013-07-31&rft.volume=27&rft.issue=12&rft.spage=1867&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0b013e3283618487
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-02-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Interleukin 7; Molecular modelling; antiretroviral therapy; Immunological memory; Memory cells; Transcription; CD8 antigen; Pathogens; Infection; Gene expression; Flow cytometry; CD4 antigen; Lymphocytes T; Acquired immune deficiency syndrome; Membranes; Human immunodeficiency virus; Antiretroviral agents
DO  - http://dx.doi.org/10.1097/QAD.0b013e3283618487
ER  - 



TY  - JOUR
T1  - c-Src regulates cell cycle proteins expression through protein kinase B/glycogen synthase kinase 3 beta and extracellular signal-regulated kinases 1/2 pathways in MCF-7 cells
AN  - 1660407302; 20378426
AB  - We have demonstrated that c-Src suppression inhibited the epithelial to mesenchymal transition in human breast cancer cells. Here, we investigated the role of c-Src on the cell cycle progression using siRNAs and small molecule inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2). Western blot analysis demonstrated the down-regulation of cyclin D1 and cyclin E and up-regulation of p27 Kip1 after c-Src suppression by PP2. Incubation of cells in the presence of PP2 significantly blocked the phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2), protein kinase B (AKT), and glycogen synthase kinase 3 beta (GSK3 beta ). Specific pharmacological inhibitors of MEK1/2/ERK1/2 and phosphatidylinositide 3-kinase/AKT pathways were used to demonstrate the relationship between the signal cascade and cell cycle proteins expression. The expression of cyclin D1 and cyclin E were decreased after inhibition of ERK1/2 or AKT activity, whereas the p27 Kip1 expression was increased. In addition, knockdown of c-Src by siRNAs reduced cell proliferation and phosphorylation of ERK1/2, AKT, and GSK3 beta . After c-Src depletion by siRNAs, we observed significant down-regulation of cyclin D1 and cyclin E, and up-regulation of p27 Kip1. These results suggest that c-Src suppression by PP2 or siRNAs may regulate the progression of cell cycle through AKT/GSK3 beta and ERK1/2 pathways.
JF  - Acta Biochimica et Biophysica Sinica
AU  - Liu, Xiang
AU  - Du, Liying
AU  - Feng, Renqing
AD  - Present address: Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20892, USA, rqfeng@pku.edu.cn
Y1  - 2013/07/23/
PY  - 2013
DA  - 2013 Jul 23
SP  - 586
EP  - 592
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 45
IS  - 7
SN  - 1672-9145, 1672-9145
KW  - Biotechnology and Bioengineering Abstracts
KW  - breast cancer
KW  - cell cycle proteins
KW  - c-Src suppression
KW  - PP2
KW  - siRNAs
KW  - Western blotting
KW  - phosphatidylinositides
KW  - Cell cycle
KW  - Glycogen synthase kinase 3
KW  - Extracellular signal-regulated kinase
KW  - Phosphorylation
KW  - siRNA
KW  - Cyclin-dependent kinase inhibitor p27
KW  - AKT protein
KW  - Src protein
KW  - Breast cancer
KW  - Mesenchyme
KW  - Cell proliferation
KW  - Cyclin E
KW  - cyclin D1
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660407302?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+Biochimica+et+Biophysica+Sinica&rft.atitle=c-Src+regulates+cell+cycle+proteins+expression+through+protein+kinase+B%2Fglycogen+synthase+kinase+3+beta+and+extracellular+signal-regulated+kinases+1%2F2+pathways+in+MCF-7+cells&rft.au=Liu%2C+Xiang%3BDu%2C+Liying%3BFeng%2C+Renqing&rft.aulast=Liu&rft.aufirst=Xiang&rft.date=2013-07-23&rft.volume=45&rft.issue=7&rft.spage=586&rft.isbn=&rft.btitle=&rft.title=Acta+Biochimica+et+Biophysica+Sinica&rft.issn=16729145&rft_id=info:doi/10.1093%2Fabbs%2Fgmt042
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-03-04
N1  - SubjectsTermNotLitGenreText - Western blotting; phosphatidylinositides; Cell cycle; Glycogen synthase kinase 3; Extracellular signal-regulated kinase; siRNA; Phosphorylation; Cyclin-dependent kinase inhibitor p27; Src protein; AKT protein; Breast cancer; Cell proliferation; Mesenchyme; Cyclin E; cyclin D1
DO  - http://dx.doi.org/10.1093/abbs/gmt042
ER  - 



TY  - JOUR
T1  - Benign Breast Disease, Mammographic Breast Density, and the Risk of Breast Cancer
AN  - 1419363078; 18270262
AB  - Background Benign breast disease and high breast density are prevalent, strong risk factors for breast cancer. Women with both risk factors may be at very high risk. Methods We included 42818 women participating in the Breast Cancer Surveillance Consortium who had no prior diagnosis of breast cancer and had undergone at least one benign breast biopsy and mammogram; 1359 women developed incident breast cancer in 6.1 years of follow-up (78.1% invasive, 21.9% ductal carcinoma in situ). We calculated hazard ratios (HRs) using Cox regression analysis. The referent group was women with nonproliferative changes and average density. All P values are two-sided. Results Benign breast disease and breast density were independently associated with breast cancer. The combination of atypical hyperplasia and very high density was uncommon (0.6% of biopsies) but was associated with the highest risk for breast cancer (HR = 5.34; 95% confidence interval [CI] = 3.52 to 8.09, P < .001). Proliferative disease without atypia (25.6% of biopsies) was associated with elevated risk that varied little across levels of density: average (HR = 1.37; 95% CI = 1.11 to 1.69, P = .003), high (HR = 2.02; 95% CI = 1.68 to 2.44, P < .001), or very high (HR = 2.05; 95% CI = 1.54 to 2.72, P < .001). Low breast density (4.5% of biopsies) was associated with low risk (HRs <1) for all benign pathology diagnoses. Conclusions Women with high breast density and proliferative benign breast disease are at very high risk for future breast cancer. Women with low breast density are at low risk, regardless of their benign pathologic diagnosis.
JF  - Journal of the National Cancer Institute
AU  - Tice, Jeffrey A
AU  - O'Meara, Ellen S
AU  - Weaver, Donald L
AU  - Vachon, Celine
AU  - Ballard-Barbash, Rachel
AU  - Kerlikowske, Karla
AD  - Affiliations of authors: Division of General Internal Medicine, Department of Medicine (JAT), San Francisco, CA and General Internal Medicine Section, Department of Veteran Affairs, Department of Medicine, and Department of Epidemiology and Biostatistics (KK), University of California, San Francisco, San Francisco, CA; Group Health Research Institute (ESO); Seattle, WA. Department of Pathology, University of Vermont College of Medicine and Vermont Cancer Center (DLW); Burlington, VT. Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute (RB-B); Bethesda, MD., jtice@medicine.ucsf.edu
Y1  - 2013/07/17/
PY  - 2013
DA  - 2013 Jul 17
SP  - 1043
EP  - 1049
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 14
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Pathology
KW  - Risk factors
KW  - Breast cancer
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419363078?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Benign+Breast+Disease%2C+Mammographic+Breast+Density%2C+and+the+Risk+of+Breast+Cancer&rft.au=Tice%2C+Jeffrey+A%3BO%27Meara%2C+Ellen+S%3BWeaver%2C+Donald+L%3BVachon%2C+Celine%3BBallard-Barbash%2C+Rachel%3BKerlikowske%2C+Karla&rft.aulast=Tice&rft.aufirst=Jeffrey&rft.date=2013-07-17&rft.volume=105&rft.issue=14&rft.spage=1043&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjt124
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Pathology; Risk factors; Breast cancer; Cancer
DO  - http://dx.doi.org/10.1093/jnci/djt124
ER  - 



TY  - JOUR
T1  - A novel manganese complex, Mn-(II) N-(2-hydroxy acetophenone) glycinate overcomes multidrug-resistance in cancer.
AN  - 1400624346; 23665413
AB  - Multidrug resistance (MDR) remains a significant problem for effective cancer chemotherapy. In spite of considerable advances in drug discovery, most of the cancer cases still stay incurable because of resistance to chemotherapy. We synthesized a novel, Mn (II) complex (chelate), viz., manganese N-(2-hydroxy acetophenone) glycinate (MnNG) that exhibits considerable efficacy to overcome drug resistant cancer. The antiproliferative activity of MnNG was studied on doxorubicin resistant and sensitive human T lymphoblastic leukemia cells (CEM/ADR 5000 and CCRF/CEM). MnNG induced apoptosis significantly in CEM/ADR 5000 cells probably through generation of reactive oxygen species. Moreover, intraperitoneal (i.p.) application of MnNG at non-toxic doses caused significant increase in the life-span of Swiss albino mice bearing sensitive and doxorubicin resistant subline of Ehrlich ascites carcinoma cells. 
          Copyright © 2013 Elsevier B.V. All rights reserved.
JF  - European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
AU  - Ghosh, Ruma Dey
AU  - Banerjee, Kaushik
AU  - Das, Satyajit
AU  - Ganguly, Avishek
AU  - Chakraborty, Paramita
AU  - Sarkar, Avijit
AU  - Chatterjee, Mitali
AU  - Choudhuri, Soumitra K
AD  - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India.
Y1  - 2013/07/16/
PY  - 2013
DA  - 2013 Jul 16
SP  - 737
EP  - 747
VL  - 49
IS  - 4
KW  - Antineoplastic Agents
KW  - 0
KW  - Organometallic Compounds
KW  - Manganese
KW  - 42Z2K6ZL8P
KW  - Doxorubicin
KW  - 80168379AG
KW  - Glycine
KW  - TE7660XO1C
KW  - Index Medicus
KW  - reverse transcription-polymerase chain reaction
KW  - MDR
KW  - PHAG
KW  - Apoptosis
KW  - ROS
KW  - propidium iodide
KW  - alkaline phosphatase
KW  - RT-PCR
KW  - glutathione
KW  - fluoroscein isothiocyanate conjugate
KW  - 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide
KW  - EAC
KW  - IC(50)
KW  - Leukemic cells
KW  - dose for 50% death of animals
KW  - SGOT
KW  - DTNB
KW  - H(2)-DCFDA
KW  - LD(50)
KW  - Ehrlich ascites carcinoma
KW  - potassium N-(2-hydroxy acetophenone) glycinate
KW  - FITC
KW  - dose for 50% growth inhibition of cell
KW  - manganese N-(2-hydroxy acetophenone) glycinate
KW  - reactive oxygen species
KW  - P-glycoprotein
KW  - 5,5′- Dithio bis(2-nitrobenzoic acid)
KW  - GSH
KW  - ALP
KW  - P-gp
KW  - serum glutamine pyruvate transaminase
KW  - multidrug resistance
KW  - MnNG
KW  - MTT
KW  - PI
KW  - Manganese complex
KW  - serum glutamate ortho-transferase
KW  - Multidrug resistance
KW  - 2′,7′-dihydrodichlorofluorescin diacetate
KW  - SGPT
KW  - Bone Marrow Cells -- drug effects
KW  - Animals
KW  - Spleen -- cytology
KW  - Humans
KW  - Cell Line, Tumor
KW  - Mice
KW  - Drug Resistance, Multiple
KW  - Cell Survival -- drug effects
KW  - Cells, Cultured
KW  - Apoptosis -- drug effects
KW  - Antineoplastic Agents -- pharmacology
KW  - Female
KW  - Neoplasms -- drug therapy
KW  - Manganese -- pharmacology
KW  - Organometallic Compounds -- pharmacology
KW  - Glycine -- pharmacology
KW  - Manganese -- chemistry
KW  - Glycine -- analogs & derivatives
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1400624346?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmaceutical+sciences+%3A+official+journal+of+the+European+Federation+for+Pharmaceutical+Sciences&rft.atitle=A+novel+manganese+complex%2C+Mn-%28II%29+N-%282-hydroxy+acetophenone%29+glycinate+overcomes+multidrug-resistance+in+cancer.&rft.au=Ghosh%2C+Ruma+Dey%3BBanerjee%2C+Kaushik%3BDas%2C+Satyajit%3BGanguly%2C+Avishek%3BChakraborty%2C+Paramita%3BSarkar%2C+Avijit%3BChatterjee%2C+Mitali%3BChoudhuri%2C+Soumitra+K&rft.aulast=Ghosh&rft.aufirst=Ruma&rft.date=2013-07-16&rft.volume=49&rft.issue=4&rft.spage=737&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmaceutical+sciences+%3A+official+journal+of+the+European+Federation+for+Pharmaceutical+Sciences&rft.issn=1879-0720&rft_id=info:doi/10.1016%2Fj.ejps.2013.05.002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-11
N1  - Date created - 2013-07-16
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.ejps.2013.05.002
ER  - 



TY  - JOUR
T1  - DrugMap Central: an on-line query and visualization tool to facilitate drug repositioning studies
AN  - 1412563842; 18258541
AB  - Summary: Systematic studies of drug repositioning require the integration of multi-level drug data, including basic chemical information (such as SMILES), drug targets, target-related signaling pathways, clinical trial information and Food and Drug Administration (FDA)-approval information, to predict new potential indications of existing drugs. Currently available databases, however, lack query support for multi-level drug information and thus are not designed to support drug repositioning studies. DrugMap Central (DMC), an online tool, is developed to help fill the gap. DMC enables the users to integrate, query, visualize, interrogate, and download multi-level data of known drugs or compounds quickly for drug repositioning studies all within one system.
JF  - Bioinformatics
AU  - Fu, Changhe
AU  - Jin, Guangxu
AU  - Gao, Junfeng
AU  - Zhu, Rui
AU  - Ballesteros-villagrana, Efren
AU  - Wong, Stephen T C
AD  - super(1)Department of Systems Medicine and Bioengineering, The Methodist Hospital Research Institute, Weill Cornell Medical College and super(2)NCI Center for Modeling Cancer Development, The Methodist Hospital Research Institute, Houston, TX 77030
Y1  - 2013/07/15/
PY  - 2013
DA  - 2013 Jul 15
SP  - 1834
EP  - 1836
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 14
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Integration
KW  - Databases
KW  - Data processing
KW  - Bioinformatics
KW  - Clinical trials
KW  - Internet
KW  - Signal transduction
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412563842?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DrugMap+Central%3A+an+on-line+query+and+visualization+tool+to+facilitate+drug+repositioning+studies&rft.au=Fu%2C+Changhe%3BJin%2C+Guangxu%3BGao%2C+Junfeng%3BZhu%2C+Rui%3BBallesteros-villagrana%2C+Efren%3BWong%2C+Stephen+T+C&rft.aulast=Fu&rft.aufirst=Changhe&rft.date=2013-07-15&rft.volume=29&rft.issue=14&rft.spage=1834&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt279
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Databases; Integration; Data processing; Bioinformatics; Clinical trials; Internet; Signal transduction
DO  - http://dx.doi.org/10.1093/bioinformatics/btt279
ER  - 



TY  - JOUR
T1  - Perinatal exposure of patas monkeys to antiretroviral nucleoside reverse-transcriptase inhibitors induces genotoxicity persistent for up to 3 years of age.
AN  - 1370124168; 23559463
AB  - Erythrocebus patas (patas) monkeys were used to model antiretroviral (ARV) drug in human immunodeficiency virus type 1-infected pregnant women.
          Pregnant patas dams were given human-equivalent doses of ARVs daily during 50% of gestation. Mesenchymal cells, cultured from bone marrow of patas offspring obtained at birth and at 1 and 3 years of age, were examined for genotoxicity, including centrosomal amplification, micronuclei, and micronuclei containing whole chromosomes. Compared with controls, statistically significant increases (P < .05) in centrosomal amplification, micronuclei, and micronuclei containing whole chromosomes were found in mesenchymal cells from most groups of offspring at the 3 time points.
          Transplacental nucleoside reverse-transcriptase inhibitor exposures induced fetal genotoxicity that was persistent for 3 years.
JF  - The Journal of infectious diseases
AU  - Olivero, Ofelia A
AU  - Torres, Lorangelly Rivera
AU  - Gorjifard, Sayeh
AU  - Momot, Dariya
AU  - Marrogi, Eryney
AU  - Divi, Rao L
AU  - Liu, Yongmin
AU  - Woodward, Ruth A
AU  - Sowers, Marsha J
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 (NIH), Bethesda, MD 20892-4255, USA.
Y1  - 2013/07/15/
PY  - 2013
DA  - 2013 Jul 15
SP  - 244
EP  - 248
VL  - 208
IS  - 2
KW  - Anti-HIV Agents
KW  - 0
KW  - Nucleosides
KW  - Reverse Transcriptase Inhibitors
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - centrosomal amplification
KW  - nevirapine
KW  - abacavir
KW  - Erythrocebus patas
KW  - mesenchymal fibroblasts
KW  - lamivudine
KW  - aneuploidy
KW  - zidovudine
KW  - micronuclei
KW  - Nucleosides -- genetics
KW  - Animals, Newborn
KW  - Animals
KW  - Mesenchymal Stromal Cells -- virology
KW  - Humans
KW  - Pregnancy Complications, Infectious -- virology
KW  - Female
KW  - Pregnancy
KW  - Reverse Transcriptase Inhibitors -- adverse effects
KW  - Mesoderm -- drug effects
KW  - Erythrocebus patas -- virology
KW  - Anti-HIV Agents -- adverse effects
KW  - Mesoderm -- cytology
KW  - HIV-1
KW  - Prenatal Exposure Delayed Effects
KW  - Erythrocebus patas -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1370124168?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Perinatal+exposure+of+patas+monkeys+to+antiretroviral+nucleoside+reverse-transcriptase+inhibitors+induces+genotoxicity+persistent+for+up+to+3+years+of+age.&rft.au=Olivero%2C+Ofelia+A%3BTorres%2C+Lorangelly+Rivera%3BGorjifard%2C+Sayeh%3BMomot%2C+Dariya%3BMarrogi%2C+Eryney%3BDivi%2C+Rao+L%3BLiu%2C+Yongmin%3BWoodward%2C+Ruth+A%3BSowers%2C+Marsha+J%3BPoirier%2C+Miriam+C&rft.aulast=Olivero&rft.aufirst=Ofelia&rft.date=2013-07-15&rft.volume=208&rft.issue=2&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjit146
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-13
N1  - Date created - 2013-06-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Lancet. 2000 Jun 24;355(9222):2237-44 [10881908]
J Infect Dis. 2013 Jul 15;208(2):235-43 [23559464]
Toxicol Appl Pharmacol. 2004 Sep 1;199(2):151-61 [15313587]
J Natl Cancer Inst. 1997 Nov 5;89(21):1602-8 [9362158]
Cardiovasc Toxicol. 2005;5(3):333-46 [16244378]
Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18974-9 [16365316]
Environ Mol Mutagen. 2007 Apr-May;48(3-4):283-98 [17358026]
Environ Mol Mutagen. 2007 Apr-May;48(3-4):330-43 [17358027]
Environ Mol Mutagen. 2007 Apr-May;48(3-4):270-82 [17358030]
Environ Mol Mutagen. 2007 Apr-May;48(3-4):322-9 [17358032]
Toxicol Appl Pharmacol. 2008 Jan 15;226(2):206-11 [17949768]
AIDS. 2008 Oct 18;22(16):2165-77 [18832880]
Mutat Res. 2009 Jun 1;665(1-2):67-74 [19427513]
Toxicol Sci. 2010 Nov;118(1):191-201 [20702595]
J Acquir Immune Defic Syndr. 2002 Apr 1;29(4):323-9 [11917235]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/infdis/jit146
ER  - 



TY  - JOUR
T1  - The STIM1 CTID domain determines access of SARAF to SOAR to regulate Orai1 channel function.
AN  - 1399265846; 23816623
AB  - Ca(2+) influx by store-operated Ca(2+) channels (SOCs) mediates all Ca(2+)-dependent cell functions, but excess Ca(2+) influx is highly toxic. The molecular components of SOC are the pore-forming Orai1 channel and the endoplasmic reticulum Ca(2+) sensor STIM1. Slow Ca(2+)-dependent inactivation (SCDI) of Orai1 guards against cell damage, but its molecular mechanism is unknown. Here, we used homology modeling to identify a conserved STIM1(448-530) C-terminal inhibitory domain (CTID), whose deletion resulted in spontaneous clustering of STIM1 and full activation of Orai1 in the absence of store depletion. CTID regulated SCDI by determining access to and interaction of the STIM1 inhibitor SARAF with STIM1 Orai1 activation region (SOAR), the STIM1 domain that activates Orai1. CTID had two lobes, STIM1(448-490) and STIM1(490-530), with distinct roles in mediating access of SARAF to SOAR. The STIM1(448-490) lobe restricted, whereas the STIM1(490-530) lobe directed, SARAF to SOAR. The two lobes cooperated to determine the features of SCDI. These findings highlight the central role of STIM1 in SCDI and provide a molecular mechanism for SCDI of Orai1.
JF  - The Journal of cell biology
AU  - Jha, Archana
AU  - Ahuja, Malini
AU  - Maléth, József
AU  - Moreno, Claudia M
AU  - Yuan, Joseph P
AU  - Kim, Min Seuk
AU  - Muallem, Shmuel
AD  - Epithelial Signaling and Transport Section, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/07/08/
PY  - 2013
DA  - 2013 Jul 08
SP  - 71
EP  - 79
VL  - 202
IS  - 1
KW  - Calcium Channels
KW  - 0
KW  - Membrane Proteins
KW  - Neoplasm Proteins
KW  - ORAI1 Protein
KW  - ORAI1 protein, human
KW  - STIM1 protein, human
KW  - Stromal Interaction Molecule 1
KW  - TMEM66 protein, human
KW  - Calcium
KW  - SY7Q814VUP
KW  - Index Medicus
KW  - Models, Molecular
KW  - HEK293 Cells
KW  - Humans
KW  - Cell Membrane -- genetics
KW  - Amino Acid Sequence
KW  - Protein Binding
KW  - Structure-Activity Relationship
KW  - Structural Homology, Protein
KW  - Calcium -- metabolism
KW  - Conserved Sequence
KW  - Protein Interaction Mapping
KW  - Cell Membrane -- metabolism
KW  - Protein Structure, Tertiary
KW  - Sequence Deletion
KW  - Protein Conformation
KW  - Calcium Channels -- metabolism
KW  - Membrane Proteins -- metabolism
KW  - Neoplasm Proteins -- genetics
KW  - Calcium Channels -- genetics
KW  - Membrane Proteins -- genetics
KW  - Neoplasm Proteins -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399265846?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cell+biology&rft.atitle=The+STIM1+CTID+domain+determines+access+of+SARAF+to+SOAR+to+regulate+Orai1+channel+function.&rft.au=Jha%2C+Archana%3BAhuja%2C+Malini%3BMal%C3%A9th%2C+J%C3%B3zsef%3BMoreno%2C+Claudia+M%3BYuan%2C+Joseph+P%3BKim%2C+Min+Seuk%3BMuallem%2C+Shmuel&rft.aulast=Jha&rft.aufirst=Archana&rft.date=2013-07-08&rft.volume=202&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+cell+biology&rft.issn=1540-8140&rft_id=info:doi/10.1083%2Fjcb.201301148
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-09
N1  - Date created - 2013-07-09
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Cell Biol. 2005 May 9;169(3):435-45 [15866891]
Physiol Rev. 2005 Apr;85(2):757-810 [15788710]
Nature. 2006 May 11;441(7090):179-85 [16582901]
Science. 2006 May 26;312(5777):1220-3 [16645049]
Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9357-62 [16751269]
Nat Cell Biol. 2006 Sep;8(9):1003-10 [16906149]
Cell. 2008 Oct 3;135(1):110-22 [18854159]
J Biol Chem. 2009 Jan 9;284(2):728-32 [19019825]
Nat Cell Biol. 2009 Mar;11(3):337-43 [19182790]
Cell. 2009 Mar 6;136(5):876-90 [19249086]
Biochem Biophys Res Commun. 2009 Jul 17;385(1):49-54 [19433061]
Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14687-92 [19706554]
J Biol Chem. 2009 Sep 11;284(37):24933-8 [19622747]
Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15495-500 [19706428]
Circ Res. 2009 Nov 6;105(10):1023-30 [19797170]
FEBS Lett. 2010 May 17;584(10):2022-7 [19944100]
Sci Signal. 2010;3(148):ra82 [21081754]
Bioinformatics. 2011 Feb 1;27(3):343-50 [21134891]
EMBO J. 2011 May 4;30(9):1678-89 [21427704]
Front Biosci (Landmark Ed). 2012;17:1304-22 [22201805]
Front Biosci (Landmark Ed). 2012;17:1613-26 [22201824]
Proc Natl Acad Sci U S A. 2012 Apr 10;109(15):5657-62 [22451904]
Cell. 2012 Apr 13;149(2):425-38 [22464749]
Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W526-31 [15215442]
J Physiol. 1993 Jun;465:359-86 [8229840]
J Biol Chem. 1995 Jun 16;270(24):14445-51 [7540169]
J Biol Chem. 1998 Jun 12;273(24):14925-32 [9614097]
Curr Biol. 2005 Jul 12;15(13):1235-41 [16005298]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1083/jcb.201301148
ER  - 



TY  - JOUR
T1  - Self-assembling influenza nanoparticle vaccines elicit broadly neutralizing H1N1 antibodies
AN  - 1660429943; PQ0001088010
AB  - Influenza viruses pose a significant threat to the public and are a burden on global health systems. Each year, influenza vaccines must be rapidly produced to match circulating viruses, a process constrained by dated technology and vulnerable to unexpected strains emerging from humans and animal reservoirs. Here we use knowledge of protein structure to design self-assembling nanoparticles that elicit broader and more potent immunity than traditional influenza vaccines. The viral haemagglutinin was genetically fused to ferritin, a protein that naturally forms nanoparticles composed of 24 identical polypeptides. Haemagglutinin was inserted at the interface of adjacent subunits so that it spontaneously assembled and generated eight trimeric viral spikes on its surface. Immunization with this influenza nanoparticle vaccine elicited haemagglutination inhibition antibody titres more than tenfold higher than those from the licensed inactivated vaccine. Furthermore, it elicited neutralizing antibodies to two highly conserved vulnerable haemagglutinin structures that are targets of universal vaccines: the stem and the receptor binding site on the head. Antibodies elicited by a 1999 haemagglutinin-nanoparticle vaccine neutralized H1N1 viruses from 1934 to 2007 and protected ferrets from an unmatched 2007 H1N1 virus challenge. This structure-based, self-assembling synthetic nanoparticle vaccine improves the potency and breadth of influenza virus immunity, and it provides a foundation for building broader vaccine protection against emerging influenza viruses and other pathogens.
JF  - Nature
AU  - Kanekiyo, Masaru
AU  - Wei, Chih-Jen
AU  - Yassine, Hadi M
AU  - McTamney, Patrick M
AU  - Boyington, Jeffrey C
AU  - Whittle, James RR
AU  - Rao, Srinivas S
AU  - Kong, Wing-Pui
AU  - Wang, Lingshu
AU  - Nabel, Gary J
AD  - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
PY  - 2013
SP  - 102
EP  - 106
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 499
IS  - 7456
SN  - 0028-0836, 0028-0836
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - Head
KW  - Hemagglutinins
KW  - Viruses
KW  - Immunity
KW  - Pathogens
KW  - Immunization
KW  - Public health
KW  - Influenza
KW  - Protein structure
KW  - Antibodies
KW  - Influenza virus
KW  - Mustela
KW  - Proteins
KW  - Ferritin
KW  - Vulnerability
KW  - Vaccines
KW  - Reservoirs
KW  - nanoparticles
KW  - Technology
KW  - V 22320:Replication
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660429943?accountid=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=Nature&rft.atitle=Self-assembling+influenza+nanoparticle+vaccines+elicit+broadly+neutralizing+H1N1+antibodies&rft.au=Kanekiyo%2C+Masaru%3BWei%2C+Chih-Jen%3BYassine%2C+Hadi+M%3BMcTamney%2C+Patrick+M%3BBoyington%2C+Jeffrey+C%3BWhittle%2C+James+RR%3BRao%2C+Srinivas+S%3BKong%2C+Wing-Pui%3BWang%2C+Lingshu%3BNabel%2C+Gary+J&rft.aulast=Kanekiyo&rft.aufirst=Masaru&rft.date=2013-07-04&rft.volume=499&rft.issue=7456&rft.spage=102&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/10.1038%2Fnature12202
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-12-23
N1  - SubjectsTermNotLitGenreText - Protein structure; Influenza; Antibodies; Head; Hemagglutinins; Ferritin; Pathogens; Immunity; Vaccines; nanoparticles; Immunization; Viruses; Proteins; Vulnerability; Reservoirs; Technology; Public health; Influenza virus; Mustela
DO  - http://dx.doi.org/10.1038/nature12202
ER  - 



TY  - JOUR
T1  - MuB is an AAA+ ATPase that forms helical filaments to control target selection for DNA transposition.
AN  - 1393789378; 23776210
AB  - MuB is an ATP-dependent nonspecific DNA-binding protein that regulates the activity of the MuA transposase and captures target DNA for transposition. Mechanistic understanding of MuB function has previously been hindered by MuB's poor solubility. Here we combine bioinformatic, mutagenic, biochemical, and electron microscopic analyses to unmask the structure and function of MuB. We demonstrate that MuB is an ATPase associated with diverse cellular activities (AAA+ ATPase) and forms ATP-dependent filaments with or without DNA. We also identify critical residues for MuB's ATPase, DNA binding, protein polymerization, and MuA interaction activities. Using single-particle electron microscopy, we show that MuB assembles into a helical filament, which binds the DNA in the axial channel. The helical parameters of the MuB filament do not match those of the coated DNA. Despite this protein-DNA symmetry mismatch, MuB does not deform the DNA duplex. These findings, together with the influence of MuB filament size on strand-transfer efficiency, lead to a model in which MuB-imposed symmetry transiently deforms the DNA at the boundary of the MuB filament and results in a bent DNA favored by MuA for transposition.
JF  - Proceedings of the National Academy of Sciences of the United States of America
AU  - Mizuno, Naoko
AU  - Dramićanin, Marija
AU  - Mizuuchi, Michiyo
AU  - Adam, Julia
AU  - Wang, Yi
AU  - Han, Yong-Woon
AU  - Yang, Wei
AU  - Steven, Alasdair C
AU  - Mizuuchi, Kiyoshi
AU  - Ramón-Maiques, Santiago
AD  - Laboratory of Structural Biology, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/07/02/
PY  - 2013
DA  - 2013 Jul 02
SP  - E2441
EP  - E2450
VL  - 110
IS  - 27
KW  - DNA, Viral
KW  - 0
KW  - DNA-Binding Proteins
KW  - MuB protein, Enterobacteria phage Mu
KW  - Viral Proteins
KW  - Adenosine Triphosphate
KW  - 8L70Q75FXE
KW  - Transposases
KW  - EC 2.7.7.-
KW  - Adenosine Triphosphatases
KW  - EC 3.6.1.-
KW  - Index Medicus
KW  - Phage Mu
KW  - nucleoprotein filament
KW  - Mutagenesis, Site-Directed
KW  - Microscopy, Electron, Transmission
KW  - Imaging, Three-Dimensional
KW  - Transposases -- metabolism
KW  - Transposases -- genetics
KW  - Models, Molecular
KW  - Adenosine Triphosphate -- metabolism
KW  - Protein Multimerization -- genetics
KW  - Molecular Sequence Data
KW  - Amino Acid Sequence
KW  - Binding Sites -- genetics
KW  - Sequence Homology, Amino Acid
KW  - DNA, Viral -- metabolism
KW  - Viral Proteins -- genetics
KW  - DNA-Binding Proteins -- chemistry
KW  - Viral Proteins -- chemistry
KW  - DNA-Binding Proteins -- genetics
KW  - Adenosine Triphosphatases -- metabolism
KW  - Viral Proteins -- metabolism
KW  - Bacteriophage mu -- enzymology
KW  - Adenosine Triphosphatases -- chemistry
KW  - Bacteriophage mu -- genetics
KW  - Adenosine Triphosphatases -- genetics
KW  - DNA-Binding Proteins -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1393789378?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MuB+is+an+AAA%2B+ATPase+that+forms+helical+filaments+to+control+target+selection+for+DNA+transposition.&rft.au=Mizuno%2C+Naoko%3BDrami%C4%87anin%2C+Marija%3BMizuuchi%2C+Michiyo%3BAdam%2C+Julia%3BWang%2C+Yi%3BHan%2C+Yong-Woon%3BYang%2C+Wei%3BSteven%2C+Alasdair+C%3BMizuuchi%2C+Kiyoshi%3BRam%C3%B3n-Maiques%2C+Santiago&rft.aulast=Mizuno&rft.aufirst=Naoko&rft.date=2013-07-02&rft.volume=110&rft.issue=27&rft.spage=E2441&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.1309499110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-26
N1  - Date created - 2013-07-03
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Mol Cell. 2002 Dec;10(6):1367-78 [12504012]
Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11317-21 [12177413]
J Struct Biol. 2004 Apr-May;146(1-2):180-8 [15037249]
J Biol Chem. 2004 Apr 16;279(16):16736-43 [14871890]
Nature. 2004 Jun 17;429(6993):724-30 [15201901]
J Struct Biol. 2004 Nov;148(2):194-204 [15477099]
Anal Biochem. 1976 May 7;72:248-54 [942051]
J Bacteriol. 1977 Jan;129(1):407-14 [318647]
J Biol Chem. 1977 May 10;252(9):2891-9 [16006]
Proc Natl Acad Sci U S A. 1983 Nov;80(22):6765-9 [6316324]
Mol Gen Genet. 1984;194(1-2):149-58 [6328211]
EMBO J. 1982;1(8):945-51 [6329717]
Nucleic Acids Res. 1984 Nov 26;12(22):8627-38 [6095204]
J Biol Chem. 1985 Mar 10;260(5):2662-9 [2982832]
Proc Natl Acad Sci U S A. 1985 Nov;82(22):7570-4 [2999771]
Proc Natl Acad Sci U S A. 1987 Feb;84(3):699-703 [2949325]
J Bacteriol. 1987 Sep;169(9):4388-90 [3040693]
Cell. 1988 Apr 22;53(2):257-66 [2965985]
J Biol Chem. 1988 Aug 5;263(22):10851-7 [3292529]
J Biol Chem. 1991 Feb 15;266(5):3118-24 [1847140]
J Biol Chem. 1991 Apr 5;266(10):6159-67 [1826105]
Cell. 1991 Jun 14;65(6):1003-13 [1646076]
Annu Rev Biochem. 1992;61:1011-51 [1323232]
Cell. 1993 Aug 27;74(4):723-33 [8395353]
Annu Rev Biochem. 1997;66:437-74 [9242914]
EMBO J. 1998 Sep 15;17(18):5509-18 [9736628]
Mol Microbiol. 1999 May;32(3):595-606 [10320581]
Science. 2005 Mar 25;307(5717):1972-5 [15790859]
Nucleic Acids Res. 2005 Jul 1;33(Web Server issue):W244-8 [15980461]
J Mol Biol. 2006 Mar 24;357(2):481-92 [16430918]
Annu Rev Biophys Biomol Struct. 2006;35:93-114 [16689629]
J Struct Biol. 2006 Oct;156(1):2-11 [16828312]
J Struct Biol. 2007 Jan;157(1):83-94 [16919474]
J Struct Biol. 2007 Jan;157(1):3-18 [17011211]
Nature. 2008 May 22;453(7194):489-4 [18497818]
Nat Protoc. 2008;3(6):977-90 [18536645]
Nat Protoc. 2008;3(12):1941-74 [19180078]
Nat Protoc. 2009;4(3):363-71 [19247286]
Proc Natl Acad Sci U S A. 2010 Mar 9;107(10):4590-5 [20176965]
Structure. 2010 May 12;18(5):553-62 [20462489]
Mol Cell. 2010 Jul 9;39(1):48-58 [20603074]
Mol Microbiol. 2010 Oct;78(1):78-91 [20659294]
Nature. 2011 Oct 13;478(7368):209-13 [21964332]
Biochim Biophys Acta. 2012 Jan;1823(1):2-14 [21839118]
Nature. 2012 Nov 15;491(7424):413-7 [23135398]
J Struct Biol. 1999 Dec 1;128(1):82-97 [10600563]
EMBO J. 2000 Nov 1;19(21):5625-34 [11060014]
EMBO J. 2002 Mar 15;21(6):1477-86 [11889053]
Biochemistry. 2002 Mar 26;41(12):3916-24 [11900534]
Mol Cell. 2002 May;9(5):1079-89 [12049743]
J Biol Chem. 2003 Aug 15;278(33):31210-7 [12791691]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1073/pnas.1309499110
ER  - 



TY  - JOUR
T1  - Collapse of the Tumor Stroma is Triggered by IL-12 Induction of Fas
AN  - 1668246344; PQ0001244803
AB  - Engineering CD8 super(+) T cells to deliver interleukin 12 (IL-12) to the tumor site can lead to striking improvements in the ability of adoptively transferred T cells to induce the regression of established murine cancers. We have recently shown that IL-12 triggers an acute inflammatory environment that reverses dysfunctional antigen presentation by myeloid-derived cells within tumors and leads to an increase in the infiltration of adoptively transferred antigen-specific CD8 super(+) T cells. Here, we find that local delivery of IL-12 increased the expression of Fas within tumor-infiltrating macrophages, dendritic cells, and myeloid-derived suppressor cells (MDSC), and that these changes were abrogated in mice deficient in IL-12-receptor signaling. Importantly, upregulation of Fas in host mice played a critical role in the proliferation and antitumor activity of adoptively transferred IL-12-modified CD8 super(+) T cells. We also observed higher percentages of myeloid-derived cell populations within tumors in Fas-deficient mice, indicating that tumor stromal destruction was dependent on the Fas death receptor. Taken together, these results describe the likely requirement for costimulatory reverse signaling through Fasl on T cells that successfully infiltrate tumors, a mechanism triggered by the induction of Fas expression on myeloid-derived cells by IL-12 and the subsequent collapse of the tumor stroma.
JF  - Molecular Therapy
AU  - Kerkar, Sid P
AU  - Leonardi, Anthony J
AU  - van Panhuys, Nicolas
AU  - Zhang, Ling
AU  - Yu, Zhiya
AU  - Crompton, Joseph G
AU  - Pan, Jenny H
AU  - Palmer, Douglas C
AU  - Morgan, Richard A
AU  - Rosenberg, Steven A
AU  - Restifo, Nicholas P
AD  - National Cancer Institute, National Institutes of Health, Room 3-5762, 10 Center Drive, Bethesda, Maryland 208 92-1502, USA, kerkars@mail.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1369
EP  - 1377
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 7
SN  - 1525-0016, 1525-0016
KW  - Biotechnology and Bioengineering Abstracts
KW  - Macrophages
KW  - Stroma
KW  - FasL protein
KW  - CD8 antigen
KW  - Antigen presentation
KW  - Cancer
KW  - Inflammation
KW  - Metastases
KW  - Dendritic cells
KW  - Interleukin 12
KW  - Fas antigen
KW  - Lymphocytes T
KW  - CD95 antigen
KW  - Suppressor cells
KW  - Cell proliferation
KW  - death receptors
KW  - Antitumor activity
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668246344?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Collapse+of+the+Tumor+Stroma+is+Triggered+by+IL-12+Induction+of+Fas&rft.au=Kerkar%2C+Sid+P%3BLeonardi%2C+Anthony+J%3Bvan+Panhuys%2C+Nicolas%3BZhang%2C+Ling%3BYu%2C+Zhiya%3BCrompton%2C+Joseph+G%3BPan%2C+Jenny+H%3BPalmer%2C+Douglas+C%3BMorgan%2C+Richard+A%3BRosenberg%2C+Steven+A%3BRestifo%2C+Nicholas+P&rft.aulast=Kerkar&rft.aufirst=Sid&rft.date=2013-07-01&rft.volume=21&rft.issue=7&rft.spage=1369&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2013.77
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Stroma; Macrophages; FasL protein; CD8 antigen; Antigen presentation; Cancer; Inflammation; Metastases; Interleukin 12; Dendritic cells; Fas antigen; Lymphocytes T; CD95 antigen; Suppressor cells; Cell proliferation; death receptors; Antitumor activity
DO  - http://dx.doi.org/10.1038/mt.2013.77
ER  - 



TY  - JOUR
T1  - Borrelia burgdorferi bba66 Gene Inactivation Results in Attenuated Mouse Infection by Tick Transmission
AN  - 1664207581; PQ0001204276
AB  - The impact of the Borrelia burgdorferi surface-localized immunogenic lipoprotein BBA66 on vector and host infection was evaluated by inactivating the encoding gene, bba66, and characterizing the mutant phenotype throughout the natural mouse-tick-mouse cycle. The BBA66-deficient mutant isolate, Bb Delta A66, remained infectious in mice by needle inoculation of cultured organisms, but differences in spirochete burden and pathology in the tibiotarsal joint were observed relative to the parental wild-type (WT) strain. Ixodes scapularis larvae successfully acquired Bb Delta A66 following feeding on infected mice, and the organisms persisted in these ticks through the molt to nymphs. A series of tick transmission experiments (n = 7) demonstrated that the ability of Bb Delta A66-infected nymphs to infect laboratory mice was significantly impaired compared to that of mice fed upon by WT-infected ticks. trans-complementation of Bb Delta A66 with an intact copy of bba66 restored the WT infectious phenotype in mice via tick transmission. These results suggest a role for BBA66 in facilitating B. burgdorferi dissemination and transmission from the tick vector to the mammalian host as part of the disease process for Lyme borreliosis.
JF  - Infection and Immunity
AU  - Patton, Toni G
AU  - Brandt, Kevin S
AU  - Nolder, Christi
AU  - Clifton, Dawn R
AU  - Carroll, James A
AU  - Gilmore, Robert D
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 2488
EP  - 2498
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 7
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Immunology Abstracts
KW  - Feeding
KW  - Borrelia burgdorferi
KW  - Ixodidae
KW  - Larvae
KW  - Vectors
KW  - Ixodes scapularis
KW  - Infection
KW  - Molting
KW  - Disease transmission
KW  - Joints
KW  - Spirochetes
KW  - Immunogenicity
KW  - Borreliosis
KW  - Lipoproteins
KW  - Inoculation
KW  - J 02350:Immunology
KW  - F 06910:Microorganisms & Parasites
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664207581?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Borrelia+burgdorferi+bba66+Gene+Inactivation+Results+in+Attenuated+Mouse+Infection+by+Tick+Transmission&rft.au=Patton%2C+Toni+G%3BBrandt%2C+Kevin+S%3BNolder%2C+Christi%3BClifton%2C+Dawn+R%3BCarroll%2C+James+A%3BGilmore%2C+Robert+D&rft.aulast=Patton&rft.aufirst=Toni&rft.date=2013-07-01&rft.volume=81&rft.issue=7&rft.spage=2488&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00140-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Number of references - 54
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Spirochetes; Feeding; Immunogenicity; Lipoproteins; Borreliosis; Larvae; Inoculation; Vectors; Molting; Infection; Joints; Disease transmission; Borrelia burgdorferi; Ixodidae; Ixodes scapularis
DO  - http://dx.doi.org/10.1128/IAI.00140-13
ER  - 



TY  - JOUR
T1  - Regulation of Aedes aegypti Population Dynamics in Field Systems: Quantifying Direct and Delayed Density Dependence
AN  - 1647000663; 21172140
AB  - Transgenic strains of Aedes aegypti have been engineered to help control transmission of dengue virus. Although resources have been invested in developing the strains, we lack data on the ecology of mosquitoes that could impact the success of this approach. Although studies of intra-specific competition have been conducted using Ae. aegypti larvae, none of these studies examine mixed age cohorts at densities that occur in the field, with natural nutrient levels. Experiments were conducted in Mexico to determine the impact of direct and delayed density dependence on Ae. aegypti populations. Natural water, food, and larval densities were used to estimate the impacts of density dependence on larval survival, development, and adult body size. Direct and delayed density-dependent factors had a significant impact on larval survival, larval development, and adult body size. These results indicate that control methods attempting to reduce mosquito populations may be counteracted by density-dependent population regulation.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Walsh, Rachael K
AU  - Aguilar, Cristobal L
AU  - Facchinelli, Luca
AU  - Valerio, Laura
AU  - Ramsey, Janine M
AU  - Scott, Thomas W
AU  - Lloyd, Alun L
AU  - Gould, Fred
AD  - Centro Regional de Investigacio en Salud Publica/CISEI3, Instituto Nacional de Salud Publica, Tapachula, Chiapas, Mexico; Pasteur Institute-Cenci Bolognetti Foundation, University of Rome, Rome, Italy; Fogarty International Center, National Institutes of Health, Bethesda, Maryland; Department of Entomology, North Carolina State University, Raleigh, NC 27695; Department of Entomology, University of California-Davis, Davis, California, rachael_katz@ncsu.edu
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 68
EP  - 77
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 89
IS  - 1
SN  - 0002-9637, 0002-9637
KW  - Entomology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Sustainability Science Abstracts
KW  - Dengue virus
KW  - Aedes aegypti
KW  - Age
KW  - Density dependence
KW  - Food
KW  - Survival
KW  - Nutrients
KW  - Development
KW  - Population dynamics
KW  - Larval development
KW  - Public health
KW  - Ecology
KW  - Dengue
KW  - Body size
KW  - Competition
KW  - Aquatic insects
KW  - Data processing
KW  - Population regulation
KW  - Larvae
KW  - Pest control
KW  - Strains
KW  - Mexico
KW  - Hygiene
KW  - Resource development
KW  - J 02410:Animal Diseases
KW  - M3 1010:Issues in Sustainable Development
KW  - Z 05350:Medical, Veterinary, and Agricultural Entomology
KW  - Q1 08423:Behaviour
KW  - Q5 08502:Methods and instruments
KW  - K 03450:Ecology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647000663?accountid=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=Regulation+of+Aedes+aegypti+Population+Dynamics+in+Field+Systems%3A+Quantifying+Direct+and+Delayed+Density+Dependence&rft.au=Walsh%2C+Rachael+K%3BAguilar%2C+Cristobal+L%3BFacchinelli%2C+Luca%3BValerio%2C+Laura%3BRamsey%2C+Janine+M%3BScott%2C+Thomas+W%3BLloyd%2C+Alun+L%3BGould%2C+Fred&rft.aulast=Walsh&rft.aufirst=Rachael&rft.date=2013-07-01&rft.volume=89&rft.issue=1&rft.spage=68&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0378
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Density dependence; Pest control; Resource development; Hygiene; Strains; Larval development; Aquatic insects; Public health; Age; Data processing; Food; Population regulation; Body size; Survival; Nutrients; Development; Population dynamics; Competition; Ecology; Dengue; Larvae; Dengue virus; Aedes aegypti; Mexico
DO  - http://dx.doi.org/10.4269/ajtmh.12-0378
ER  - 



TY  - JOUR
T1  - Biomarker surrogates do not accurately predict sputum eosinophil and neutrophil percentages in asthmatic subjects
AN  - 1644782345; 23706399
AB  - Background  
Sputum eosinophil percentages are a strong predictor of airway inflammation and exacerbations and aid asthma management, whereas sputum neutrophil percentages indicate a different severe asthma phenotype that is potentially less responsive to TH2-targeted therapy. Variables, such as blood eosinophil counts, total IgE levels, fraction of exhaled nitric oxide (Feno) levels, or FEV1percent predicted, might predict airway eosinophil percentages, whereas age, FEV1percent predicted, or blood neutrophil counts might predict sputum neutrophil percentages. Availability and ease of measurement are useful characteristics, but accuracy in predicting airway eosinophil and neutrophil percentages either individually or combined is not established.  
Objectives  
We sought to determine whether blood eosinophil counts, Fenolevels, and IgE levels accurately predict sputum eosinophil percentages and whether age, FEV1percent predicted, and blood neutrophil counts accurately predict sputum neutrophil percentages.  
Methods  
Subjects in the Wake Forest Severe Asthma Research Program (n = 328) were characterized by blood and sputum cell counts, health care use, lung function, Fenolevels, and IgE levels. Multiple analytic techniques were used.  
Results  
Despite significant association with sputum eosinophil percentages, blood eosinophil counts, Fenolevels, and total IgE levels did not accurately predict sputum eosinophil percentages, and combinations of these variables did not improve prediction. Age, FEV1percent predicted, and blood neutrophil counts were similarly unsatisfactory for the prediction of sputum neutrophil percentages. Factor analysis and stepwise selection found Fenolevels, IgE levels, and FEV1percent predicted, but not blood eosinophil counts, correctly predicted 69% of sputum eosinophil percentages of less than 2% or 2% and greater. Likewise, age, asthma duration, and blood neutrophil counts correctly predicted 64% of sputum neutrophil percentages of less than 40% or 40% and greater. A model to predict both sputum eosinophil and neutrophil percentages accurately assigned only 41% of samples.  
Conclusion  
Despite statistically significant associations, Fenolevels, IgE levels, blood eosinophil and neutrophil counts, FEV1percent predicted, and age are poor surrogates, both separately and combined, for accurately predicting sputum eosinophil and neutrophil percentages.
JF  - Journal of Allergy and Clinical Immunology
AU  - Hastie, Annette T
AU  - Moore, Wendy C
AU  - Li, Huashi
AU  - Rector, Brian M
AU  - Ortega, Victor E
AU  - Pascual, Rodolfo M
AU  - Peters, Stephen P
AU  - Meyers, Deborah A
AU  - Bleecker, Eugene R
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 72
EP  - 80
CY  - St. Louis
PB  - Elsevier Science Ltd.
VL  - 132
IS  - 1
SN  - 00916749
KW  - Abstracting And Indexing Services
KW  - Biological Markers
KW  - Immunoglobulin E
KW  - Asthma
KW  - Accuracy
KW  - Skin
KW  - Age
KW  - Outdoor air quality
KW  - Nitric oxide
KW  - Studies
KW  - Biomarkers
KW  - Variables
KW  - Hospitalization
KW  - Intensive care
KW  - ROC Curve
KW  - Immunoglobulin E -- blood
KW  - Humans
KW  - Adult
KW  - Middle Aged
KW  - Forced Expiratory Volume
KW  - Male
KW  - Leukocyte Count
KW  - Female
KW  - Asthma -- physiopathology
KW  - Sputum -- cytology
KW  - Eosinophils -- physiology
KW  - Neutrophils -- physiology
KW  - Asthma -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1644782345?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthcompleteshell&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Allergy+and+Clinical+Immunology&rft.atitle=Biomarker+surrogates+do+not+accurately+predict+sputum+eosinophil+and+neutrophil+percentages+in+asthmatic+subjects&rft.au=Hastie%2C+Annette+T%3BMoore%2C+Wendy+C%3BLi%2C+Huashi%3BRector%2C+Brian+M%3BOrtega%2C+Victor+E%3BPascual%2C+Rodolfo+M%3BPeters%2C+Stephen+P%3BMeyers%2C+Deborah+A%3BBleecker%2C+Eugene+R&rft.aulast=Hastie&rft.aufirst=Annette&rft.date=2013-07-01&rft.volume=132&rft.issue=1&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=Journal+of+Allergy+and+Clinical+Immunology&rft.issn=00916749&rft_id=info:doi/10.1016%2Fj.jaci.2013.03.044
LA  - English
DB  - ProQuest Central
N1  - Copyright - Copyright Elsevier Limited Jul 2013
N1  - Last updated - 2015-01-16
DO  - http://dx.doi.org/10.1016/j.jaci.2013.03.044
ER  - 



TY  - JOUR
T1  - HIV Treatments Have Malaria Gametocyte Killing and Transmission Blocking Activity
AN  - 1635013566; 20900233
AB  - Background. Millions of individuals being treated for human immunodeficiency virus (HIV) live in malaria-endemic areas, but the effects of these treatments on malaria transmission are unknown. While drugs like HIV protease inhibitors (PIs) and trimethoprim-sulfamethoxazole (TMP-SMX) have known activity against parasites during liver or asexual blood stages, their effects on transmission stages require further study. Methods. The HIV PIs lopinavir and saquinavir, the nonnucleoside reverse-transcriptase inhibitor nevirapine, and the antibiotic TMP-SMX were assessed for activity against Plasmodium falciparum transmission stages. The alamarBlue assay was used to determine the effects of drugs on gametocyte viability, and exflagellation was assessed to determine the effects of drugs on gametocyte maturation. The effects of drug on transmission were assessed by calculating the mosquito oocyst count as a marker for infectivity, using standard membrane feeding assays. Results. Lopinavir and saquinavir have gametocytocidal and transmission blocking activities at or approaching clinically relevant treatment levels, while nevirapine does not. TMP-SMX is not gametocytocidal, but at prophylactic levels it blocks transmission. Conclusions. Specific HIV treatments have gametocyte killing and transmission-blocking effects. Clinical studies are warranted to evaluate these findings and their potential impact on eradication efforts.
JF  - Journal of Infectious Diseases
AU  - Hobbs, Charlotte V
AU  - Tanaka, Takeshi Q
AU  - Muratova, Olga
AU  - Van Vliet, Jillian
AU  - Borkowsky, William
AU  - Williamson, Kim C
AU  - Duffy, Patrick E
AD  - Laboratory of Malaria Immunology and Vaccinology, NIH, NIAID, 12735 Twinbrook Pkwy, Rockville, MD 20852, charlotte.hobbs@nih.gov
Y1  - 2013/07/01/
PY  - 2013
DA  - 2013 Jul 01
SP  - 139
EP  - 148
PB  - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 208
IS  - 1
SN  - 0022-1899, 0022-1899
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - HIV
KW  - malaria
KW  - antiretrovirals
KW  - TMP-SMX
KW  - gametocytes
KW  - transmission
KW  - Exflagellation
KW  - Parasites
KW  - Human diseases
KW  - Saquinavir
KW  - Disease control
KW  - Malaria
KW  - Antibiotics
KW  - Public health
KW  - Lopinavir
KW  - Infectious diseases
KW  - Inhibitors
KW  - Drugs
KW  - Feeding
KW  - Oocysts
KW  - Gametocytes
KW  - Proteinase inhibitors
KW  - trimethoprim-sulfamethoxazole
KW  - Plasmodium falciparum
KW  - Blood
KW  - Nevirapine
KW  - Infectivity
KW  - Human immunodeficiency virus
KW  - Liver
KW  - V 22360:AIDS and HIV
KW  - K 03400:Human Diseases
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/1635013566?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=HIV+Treatments+Have+Malaria+Gametocyte+Killing+and+Transmission+Blocking+Activity&rft.au=Hobbs%2C+Charlotte+V%3BTanaka%2C+Takeshi+Q%3BMuratova%2C+Olga%3BVan+Vliet%2C+Jillian%3BBorkowsky%2C+William%3BWilliamson%2C+Kim+C%3BDuffy%2C+Patrick+E&rft.aulast=Hobbs&rft.aufirst=Charlotte&rft.date=2013-07-01&rft.volume=208&rft.issue=1&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjit132
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-12-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Infectious diseases; Disease control; Inhibitors; Antibiotics; Malaria; Drugs; Public health; Exflagellation; Feeding; Gametocytes; Oocysts; Saquinavir; Proteinase inhibitors; trimethoprim-sulfamethoxazole; Blood; Infectivity; Nevirapine; Lopinavir; Liver; Human immunodeficiency virus; Plasmodium falciparum
DO  - http://dx.doi.org/10.1093/infdis/jit132
ER  - 



TY  - JOUR
T1  - Oxidative DNA damage after acute exposure to arsenite and monomethylarsonous acid in biomethylation-deficient human cells
AN  - 1560128692; 20247139
AB  - The carcinogen inorganic arsenic (iAs) undergoes biomethylation (BMT) in some cells. The methylated metabolite, monomethylarsonous (MMA super(3+)), may cause oxidative DNA damage (ODD). With chronic iAs exposure, BMT-competent cells show ODD while BMT-deficient do not. To further define these events, we studied ODD produced by acute iAs or MMA super(3+) in the BMT-deficient human prostate cell line, RWPE-1. ODD, measured by the immuno-spin trapping method, was assessed after exposure to iAs or MMA super(3+) alone, with the arsenic BMT inhibitor selenite or after glutathione (GSH) depletion. The expression of oxidative stress-related genes (HO-1, SOD-1, SOD-2, Nrf2 and Keap-1) was also assessed. Exposure to iAs at 24 h (0-20 mu M), stimulated ODD only at levels above the LC sub(50) of a 48 h exposure (17 mu M). If iAs induced ODD, it also activated oxidative stress-related genes. Selenium did not alter iAs-induced ODD. MMA super(3+) at 24 h (0-0.5 mu M) caused ODD at levels below the LC sub(50) of a 48 h exposure (1.5 mu M), which were greatly increased by GSH depletion but not selenite. MMA super(3+) induced ODD at levels not activating oxidant stress response genes. Overall, iAs induced ODD in BMT-deficient cells only at toxic levels. MMA super(3+) caused ODD at non-toxic levels, independently of cellular BMT capacity and in a fashion not requiring further BMT.
JF  - Toxicology Mechanisms and Methods
AU  - Orihuela, Ruben
AU  - Kojima, Chikara
AU  - Tokar, Erik J
AU  - Person, Rachel J
AU  - Xu, Yuanyuan
AU  - Qu, Wei
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, NC, USA, waalkes@niehs.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 389
EP  - 395
PB  - Informa Healthcare
VL  - 23
IS  - 6
SN  - 1537-6516, 1537-6516
KW  - Biochemistry Abstracts 2: Nucleic Acids; Health & Safety Science Abstracts; Environment Abstracts; Toxicology Abstracts
KW  - Arsenic
KW  - immuno-spin trapping
KW  - reactive oxygen species
KW  - Glutathione
KW  - Arsenite
KW  - Stress
KW  - selenite
KW  - Metabolites
KW  - Carcinogens
KW  - Trapping
KW  - DNA damage
KW  - Selenium
KW  - DNA
KW  - Prostate
KW  - Oxidants
KW  - N 14820:DNA Metabolism & Structure
KW  - H 14000:Toxicology
KW  - X 24360:Metals
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560128692?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+Mechanisms+and+Methods&rft.atitle=Oxidative+DNA+damage+after+acute+exposure+to+arsenite+and+monomethylarsonous+acid+in+biomethylation-deficient+human+cells&rft.au=Orihuela%2C+Ruben%3BKojima%2C+Chikara%3BTokar%2C+Erik+J%3BPerson%2C+Rachel+J%3BXu%2C+Yuanyuan%3BQu%2C+Wei%3BWaalkes%2C+Michael+P&rft.aulast=Orihuela&rft.aufirst=Ruben&rft.date=2013-07-01&rft.volume=23&rft.issue=6&rft.spage=389&rft.isbn=&rft.btitle=&rft.title=Toxicology+Mechanisms+and+Methods&rft.issn=15376516&rft_id=info:doi/10.3109%2F15376516.2012.762570
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Selenium; DNA damage; Arsenic; Glutathione; Arsenite; Stress; Metabolites; selenite; Carcinogens; Prostate; Trapping; Oxidants; DNA
DO  - http://dx.doi.org/10.3109/15376516.2012.762570
ER  - 



TY  - JOUR
T1  - P3.006Prevalence of HIV and Syphilis Among Voluntary Blood Donors at a Regional Blood Centre in Sri Lanka For Three Year Period
AN  - 1551640239; 20376324
AB  - BackgroundThis study was conducted to estimate the prevalence of HIV and Syphilis among voluntary blood donors at a regional blood centre in western province of Sri Lanka, contributing to 7% of total blood collection in the country.All units collected by the blood centre were screened for HIV1 & 2, HBV, HCV, syphilis and Malaria. 4th generation Enzyme immunoassay (EIA) for HIV p24 antigen and HIV-1 and 2 antibodies (Genscreen-ULTRA HIV Ag-Ab) was the screening test for HIV and confirmation was done by standard immunoblotting (western blot) technique.Venereal Disease Reference Laboratory (VDRL) test was used for screening of syphilis confirmed by Treponema pallidum hemagglutination (TPHA) test.MethodThis is a descriptive analysis of retrospective donor records from January 2010 to December 2012.Results66087 allogenic donation (Community, apheresis, in-house) records were analysed. 77.5% of donors were male and 37.3% of donors were within 26-35year age group. 91% of donations were collected from community based donation campaigns.Overall prevalence of HIV was 0.00004% (3 cases) and incidence was 0.0001%, 0.000% and 0.00004 in 2010, 2011 and 2012 respectively. Overall prevalence of syphilis was 0.0005% (37 cases) and was 0.0007%, 0.0007% and 0.0006% in 2010, 2011 and 2012 respectively. There were no HIV positive female blood donors and HIV prevalence among male donors was 0.00005%. Prevalence of syphilis in female donors was 0.0002% and 0.0006% in male donors. The highest Syphilis prevalence of 0.0007% was in 26-35 year age group. All HIV cases were in 36-45 year age group.ConclusionIn 2011, HIV prevalence was < 0.1 in adult general population of Sri Lanka and reported cases of syphilis was 799. This study shows a low prevalence among blood donors due to the existing strategies of the National blood service which could further improved by strengthening of donor selection and testing strategies.
JF  - Sexually Transmitted Infections
AU  - Morawakage, L
AD  - Regional Blood Centre, National Cancer Institute of Sri Lanka, Maharagama, Sri Lanka
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - A149
PB  - British Medical Association, BMA House Square London WC1H 9JP United Kingdom
VL  - 89
IS  - Suppl 1
SN  - 1472-3263, 1472-3263
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology
KW  - Blood donors
KW  - HIV
KW  - Syphilis
KW  - Age
KW  - Human diseases
KW  - Malaria
KW  - VDRL test
KW  - Hemagglutination
KW  - Public health
KW  - Population genetics
KW  - Antigens
KW  - Human immunodeficiency virus 1
KW  - Treponema pallidum
KW  - Screening
KW  - Immunoblotting
KW  - Western blotting
KW  - p24 protein
KW  - Apheresis
KW  - Hepatitis B virus
KW  - ISW, Sri Lanka
KW  - Papua New Guinea, Western Prov.
KW  - Enzyme immunoassay
KW  - Blood
KW  - Antibodies
KW  - Hepatitis C virus
KW  - Human immunodeficiency virus
KW  - Globus pallidus
KW  - Age groups
KW  - Immunoassays
KW  - Q1 08482:Ecosystems and energetics
KW  - J 02400:Human Diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551640239?accountid=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=Sexually+Transmitted+Infections&rft.atitle=P3.006Prevalence+of+HIV+and+Syphilis+Among+Voluntary+Blood+Donors+at+a+Regional+Blood+Centre+in+Sri+Lanka+For+Three+Year+Period&rft.au=Morawakage%2C+L&rft.aulast=Morawakage&rft.aufirst=L&rft.date=2013-07-01&rft.volume=89&rft.issue=Suppl+1&rft.spage=A149&rft.isbn=&rft.btitle=&rft.title=Sexually+Transmitted+Infections&rft.issn=14723263&rft_id=info:doi/10.1136%2Fsextrans-2013-051184.0466
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Screening; Population genetics; Blood; Human diseases; Antibodies; Antigens; Age groups; Immunoassays; Public health; Blood donors; p24 protein; Western blotting; Immunoblotting; Age; Apheresis; VDRL test; Malaria; Hemagglutination; Enzyme immunoassay; Globus pallidus; Syphilis; Hepatitis C virus; Hepatitis B virus; Human immunodeficiency virus; Treponema pallidum; Human immunodeficiency virus 1; ISW, Sri Lanka; Papua New Guinea, Western Prov.
DO  - http://dx.doi.org/10.1136/sextrans-2013-051184.0466
ER  - 



TY  - JOUR
T1  - S02.1The Public Health Need For Diagnostics and the Differing Pathways to Approval and Use Around the World
AN  - 1551635160; 20375829
AB  - The global impact of STIs is difficult to understand due to the lack of systematic, coordinated, and standardised surveillance of disease prevalence and incidence. A barrier to these efforts is the lack of easy to use, rapid, diagnostic tests in all regions of the world. Regulatory evaluation and approval of diagnostics varies by country. Common to most approval processes is the need for the diagnostic test to be evaluated for the performance characteristics in an appropriate clinical setting. Parameters that need to be understood are the sensitivity and specificity of the test, as well as practical considerations such as stability and ease of use. The degree of clinical validation and the various ways to design the studies are some of the areas that are approached differently by the various regulatory authorities. Understanding of the various regulatory pathways is important to understanding the scientific considerations necessary to map out a product development plan as diagnostic developers embark on product development in this arena.
JF  - Sexually Transmitted Infections
AU  - Deal, C
AD  - National Institute of Allergy and Infectious Diseases, Bethesda, MD, United States
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - A6
PB  - British Medical Association, BMA House Square London WC1H 9JP United Kingdom
VL  - 89
IS  - Suppl 1
SN  - 1472-3263, 1472-3263
KW  - Health & Safety Science Abstracts
KW  - Sensitivity
KW  - Infectious diseases
KW  - Sexually transmitted diseases
KW  - Public health
KW  - H 11000:Diseases/Injuries/Trauma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551635160?accountid=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=Sexually+Transmitted+Infections&rft.atitle=S02.1The+Public+Health+Need+For+Diagnostics+and+the+Differing+Pathways+to+Approval+and+Use+Around+the+World&rft.au=Deal%2C+C&rft.aulast=Deal&rft.aufirst=C&rft.date=2013-07-01&rft.volume=89&rft.issue=Suppl+1&rft.spage=A6&rft.isbn=&rft.btitle=&rft.title=Sexually+Transmitted+Infections&rft.issn=14723263&rft_id=info:doi/10.1136%2Fsextrans-2013-051184.0016
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-08-21
N1  - SubjectsTermNotLitGenreText - Sensitivity; Infectious diseases; Sexually transmitted diseases; Public health
DO  - http://dx.doi.org/10.1136/sextrans-2013-051184.0016
ER  - 



TY  - JOUR
T1  - KL01Ending the HIV/AIDS Pandemic: From Scientific Advances to Public Health Implementation
AN  - 1551631105; 20375821
AB  - Extraordinary advances in basic and clinical HIV/AIDS research over three decades have led to the development of effective interventions, particularly for treating and preventing HIV infection. These interventions have clearly been shown to be efficacious in clinical trials and effective when properly implemented "on the ground." For example, combination antiretroviral therapy (ART) dramatically improves the health and longevity of HIV-infected people. Adult male circumcision is highly effective in protecting heterosexual men from acquiring HIV infection. Preventing mother-to-child transmission of HIV infection with antiretroviral drugs has been highly successful. Antiretroviral drugs also play a critical role in preventing the sexual transmission of HIV; thus, treatment of HIV-infected people decreases dramatically the likelihood that they will transmit the virus to others. In addition, pre-exposure prophylaxis with antiretroviral drugs delivered orally or at the genital mucosa reduces the risk of acquiring HIV infection. Significant scientific challenges remain in HIV research, notably in developing a cure and a vaccine for HIV infection; however, the scientifically proven interventions currently available offer unprecedented opportunities to make major gains in the fight against HIV/AIDS. In many settings, the implementation of these interventions in a cohort or well-defined population has already resulted in impressive results, strongly indicating that global implementation scale-up could have the effect of dramatically changing the trajectory of the HIV/AIDS pandemic and ultimately leading to the end of the AIDS pandemic. We are on scientifically solid ground that this goal is achievable with a major global commitment.
JF  - Sexually Transmitted Infections
AU  - Fauci, A S
AD  - National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD, United States
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - A1
PB  - British Medical Association, BMA House Square London WC1H 9JP United Kingdom
VL  - 89
IS  - Suppl 1
SN  - 1472-3263, 1472-3263
KW  - Risk Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - HIV
KW  - prevention
KW  - therapy
KW  - Acquired immune deficiency syndrome
KW  - Mucosa
KW  - Intervention
KW  - Risk reduction
KW  - Infection
KW  - Clinical trials
KW  - Public health
KW  - Disease transmission
KW  - pandemics
KW  - Infectious diseases
KW  - Antiviral agents
KW  - Drugs
KW  - Sexually transmitted diseases
KW  - antiretroviral therapy
KW  - Antiretroviral agents
KW  - Longevity
KW  - Human immunodeficiency virus
KW  - Prophylaxis
KW  - Vaccines
KW  - V 22360:AIDS and HIV
KW  - R2 23060:Medical and environmental health
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551631105?accountid=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=Sexually+Transmitted+Infections&rft.atitle=KL01Ending+the+HIV%2FAIDS+Pandemic%3A+From+Scientific+Advances+to+Public+Health+Implementation&rft.au=Fauci%2C+A+S&rft.aulast=Fauci&rft.aufirst=A&rft.date=2013-07-01&rft.volume=89&rft.issue=Suppl+1&rft.spage=A1&rft.isbn=&rft.btitle=&rft.title=Sexually+Transmitted+Infections&rft.issn=14723263&rft_id=info:doi/10.1136%2Fsextrans-2013-051184.0001
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-10-02
N1  - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; antiretroviral therapy; Mucosa; Infection; Clinical trials; Longevity; Disease transmission; Public health; pandemics; Antiviral agents; Prophylaxis; Vaccines; Drugs; Intervention; Risk reduction; Antiretroviral agents; Infectious diseases; Human immunodeficiency virus; Sexually transmitted diseases
DO  - http://dx.doi.org/10.1136/sextrans-2013-051184.0001
ER  - 



TY  - JOUR
T1  - Occupational exposure to trichloroethylene and serum concentrations of IL-6, IL-10, and TNF-alpha
AN  - 1540234696; 20026856
AB  - To evaluate the immunotoxicity of trichloroethylene (TCE), we conducted a cross-sectional molecular epidemiology study in China of workers exposed to TCE. We measured serum levels of IL-6, IL-10, and TNF- alpha , which play a critical role in regulating various components of the immune system, in 71 exposed workers and 78 unexposed control workers. Repeated personal exposure measurements were taken in workers before blood collection using 3 M organic vapor monitoring badges. Compared to unexposed workers, the serum concentration of IL-10 in workers exposed to TCE was decreased by 70% (P=0.001) after adjusting for potential confounders. Further, the magnitude of decline in IL-10 was >60% and statistically significant in workers exposed to <12 ppm as well as in workers with exposures greater than or equal to 12 ppm of TCE, compared to unexposed workers. No significant differences in levels of IL-6 or TNF- alpha were observed among workers exposed to TCE compared to unexposed controls. Given that IL-10 plays an important role in immunologic processes, including mediating the Th1/Th2 balance, our findings provide additional evidence that TCE is immunotoxic in humans. Environ. Mol. Mutagen. 54:450-454, 2013. copyright 2013 Wiley Periodicals, Inc.
JF  - Environmental and Molecular Mutagenesis
AU  - Bassig, Bryan A
AU  - Zhang, Luoping
AU  - Tang, Xiaojiang
AU  - Vermeulen, Roel
AU  - Shen, Min
AU  - Smith, Martyn T
AU  - Qiu, Chuangyi
AU  - Ge, Yichen
AU  - Ji, Zhiying
AU  - Reiss, Boris
AU  - Hosgood, HDean
AU  - Liu, Songwang
AU  - Bagni, Rachel
AU  - Guo, Weihong
AU  - Purdue, Mark
AU  - Hu, Wei
AU  - Yue, Fei
AU  - Li, Laiyu
AU  - Huang, Hanlin
AU  - Rothman, Nathaniel
AU  - Lan, Qing
AD  - Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, National Cancer Institute, NIH, DHHS, Bethesda, Maryland.
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 450
EP  - 454
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 54
IS  - 6
SN  - 0893-6692, 0893-6692
KW  - Toxicology Abstracts; Health & Safety Science Abstracts
KW  - Interleukin 6
KW  - Mutagens
KW  - Immune system
KW  - Helper cells
KW  - Statistical analysis
KW  - Interleukin 10
KW  - Mutagenesis
KW  - Workers
KW  - Vapors
KW  - Lymphocytes T
KW  - Trichloroethylene
KW  - Occupational exposure
KW  - Solvents
KW  - Serum levels
KW  - Blood
KW  - Immunotoxicity
KW  - Epidemiology
KW  - China, People's Rep.
KW  - Tumor necrosis factor- alpha
KW  - H 1000:Occupational Safety and Health
KW  - X 24350:Industrial Chemicals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540234696?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Occupational+exposure+to+trichloroethylene+and+serum+concentrations+of+IL-6%2C+IL-10%2C+and+TNF-alpha&rft.au=Bassig%2C+Bryan+A%3BZhang%2C+Luoping%3BTang%2C+Xiaojiang%3BVermeulen%2C+Roel%3BShen%2C+Min%3BSmith%2C+Martyn+T%3BQiu%2C+Chuangyi%3BGe%2C+Yichen%3BJi%2C+Zhiying%3BReiss%2C+Boris%3BHosgood%2C+HDean%3BLiu%2C+Songwang%3BBagni%2C+Rachel%3BGuo%2C+Weihong%3BPurdue%2C+Mark%3BHu%2C+Wei%3BYue%2C+Fei%3BLi%2C+Laiyu%3BHuang%2C+Hanlin%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Bassig&rft.aufirst=Bryan&rft.date=2013-07-01&rft.volume=54&rft.issue=6&rft.spage=450&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/10.1002%2Fem.21789
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-06-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Interleukin 6; Mutagens; Helper cells; Immune system; Statistical analysis; Interleukin 10; Mutagenesis; Serum levels; Workers; Blood; Vapors; Immunotoxicity; Epidemiology; Lymphocytes T; Tumor necrosis factor- alpha; Trichloroethylene; Occupational exposure; Solvents; China, People's Rep.
DO  - http://dx.doi.org/10.1002/em.21789
ER  - 



TY  - JOUR
T1  - Parental educational attainment and sense of control in mid- and late-adulthood
AN  - 1536009317; 4569060
AB  - Sense of control is greater among children who grow up in households of higher socioeconomic status. It is unclear if this childhood advantage persists throughout life or if schooling and adulthood experiences override any early childhood advantage. Using data from 2 nationally representative samples of primarily middle-aged (National Survey of Midlife Development in the United States, or MIDUS), and older adults (Health and Retirement Study, or HRS), I tested if personal mastery and perceived constraints in adulthood were associated with the educational attainment of the participant's father or mother, adjusting for participant's education level, income, and other demographic characteristics. In both samples, personal mastery was not associated with either parent's education level, but perceived constraints had a graded inverse association with mother's education level. These results indicate that childhood experiences continue to be associated with perceived constraints, even in later life, and may not be completely overridden by adult experiences. [Copyright American Psychological Association] Reprinted by permission of the American Psychological Association
JF  - Developmental psychology
AU  - Ward, Michael M
AD  - National Institutes of Health
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1407
EP  - 1412
VL  - 49
IS  - 7
SN  - 0012-1649, 0012-1649
KW  - Sociology
KW  - Education
KW  - Socioeconomic status
KW  - Childhood
KW  - Adulthood
KW  - Households
KW  - U.S.A.
KW  - Parents
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536009317?accountid=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=Developmental+psychology&rft.atitle=Parental+educational+attainment+and+sense+of+control+in+mid-+and+late-adulthood&rft.au=Ward%2C+Michael+M&rft.aulast=Ward&rft.aufirst=Michael&rft.date=2013-07-01&rft.volume=49&rft.issue=7&rft.spage=1407&rft.isbn=&rft.btitle=&rft.title=Developmental+psychology&rft.issn=00121649&rft_id=info:doi/10.1037%2Fa0029557
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2014-06-16
N1  - Last updated - 2014-06-17
N1  - SubjectsTermNotLitGenreText - 11988 4011 3974 9390 11932 2328 11935 5837 2360 2688 2449 10404 11936; 602 652 5676 646 6091; 9184; 6040 5676; 4049; 2211 652 5676 646 6091 2212; 433 293 14
DO  - http://dx.doi.org/10.1037/a0029557
ER  - 



TY  - JOUR
T1  - Working Together: Research- and Science-Based Regulation of BPA
AN  - 1492606949; 18970812
AB  - Both the National Institute of Environmental Health Sciences (NIEHS) and the U.S. Food and Drug Administration (FDA) work to promote and protect public health. The NIEHS achieves this mission by conducting research, including toxicological studies, on agents of public health concern through its intramural laboratories, the National Toxicology Program (NTP), grants and contracts to research labs across the country, and interagency agreements. The FDA, in turn, reviews and uses information from these and other studies and, where needed, performs studies of its own to develop standards to ensure that the products it regulates meet its requirements, maximizing product benefits while protecting the public from unacceptable risks.
JF  - Environmental Health Perspectives
AU  - Birnbaum, Linda S
AU  - Aungst, Jason
AU  - Schug, Thaddeus T
AU  - Goodman, Jesse L
AD  - Director, NIEHS and NTP, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, birnbaumls@niehs.nih.gov
Y1  - 2013/07/01/
PY  - 2013
DA  - 2013 Jul 01
SP  - a206
EP  - a207
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 7
SN  - 0091-6765, 0091-6765
KW  - Risk Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - Risk assessment
KW  - Contracts
KW  - Environmental regulations
KW  - Grants
KW  - Environmental health
KW  - Public health
KW  - Bisphenol A
KW  - Health risks
KW  - USA
KW  - Reviews
KW  - FDA
KW  - Drugs
KW  - Toxicology
KW  - R2 23060:Medical and environmental health
KW  - H 12000:Epidemiology and Public Health
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492606949?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Working+Together%3A+Research-+and+Science-Based+Regulation+of+BPA&rft.au=Birnbaum%2C+Linda+S%3BAungst%2C+Jason%3BSchug%2C+Thaddeus+T%3BGoodman%2C+Jesse+L&rft.aulast=Birnbaum&rft.aufirst=Linda&rft.date=2013-07-01&rft.volume=121&rft.issue=7&rft.spage=a206&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306963
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Bisphenol A; Risk assessment; Health risks; Contracts; Reviews; Environmental regulations; Grants; FDA; Environmental health; Drugs; Toxicology; Public health; USA
DO  - http://dx.doi.org/10.1289/ehp.1306963
ER  - 



TY  - JOUR
T1  - Protein backbone and sidechain torsion angles predicted from NMR chemical shifts using artificial neural networks
AN  - 1468373494; 18657680
AB  - A new program, TALOS-N, is introduced for predicting protein backbone torsion angles from NMR chemical shifts. The program relies far more extensively on the use of trained artificial neural networks than its predecessor, TALOS+. Validation on an independent set of proteins indicates that backbone torsion angles can be predicted for a larger, greater than or equal to 90 % fraction of the residues, with an error rate smaller than ca 3.5 %, using an acceptance criterion that is nearly two-fold tighter than that used previously, and a root mean square difference between predicted and crystallographically observed (, psi ) torsion angles of ca 12 super(o). TALOS-N also reports sidechain chi super(1) rotameric states for about 50 % of the residues, and a consistency with reference structures of 89 %. The program includes a neural network trained to identify secondary structure from residue sequence and chemical shifts.
JF  - Journal of Biomolecular NMR
AU  - Shen, Yang
AU  - Bax, Ad
AD  - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 5, Room 126 NIH, Bethesda, MD, 20892-0520, USA, bax@nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 227
EP  - 241
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 56
IS  - 3
SN  - 0925-2738, 0925-2738
KW  - Biotechnology and Bioengineering Abstracts
KW  - Protein structure
KW  - Neural networks
KW  - Secondary structure
KW  - N.M.R.
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468373494?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+NMR&rft.atitle=Protein+backbone+and+sidechain+torsion+angles+predicted+from+NMR+chemical+shifts+using+artificial+neural+networks&rft.au=Shen%2C+Yang%3BBax%2C+Ad&rft.aulast=Shen&rft.aufirst=Yang&rft.date=2013-07-01&rft.volume=56&rft.issue=3&rft.spage=227&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+NMR&rft.issn=09252738&rft_id=info:doi/10.1007%2Fs10858-013-9741-y
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Number of references - 54
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Protein structure; Neural networks; Secondary structure; N.M.R.
DO  - http://dx.doi.org/10.1007/s10858-013-9741-y
ER  - 



TY  - JOUR
T1  - The Roles of Support Seeking and Race/Ethnicity in Posttraumatic Growth Among Breast Cancer Survivors
AN  - 1463026169; 201309309
AB  - Posttraumatic growth (PTG) after cancer can minimize the emotional impact of disease and treatment; however, the facilitators of PTG, including support seeking, are unclear. The authors examined the role of support seeking on PTG among 604 breast cancer survivors ages 40 to 64 from the Health Eating, Activity, and Lifestyle (HEAL) Study. Multivariable linear regression was used to examine predictors of support seeking (participation in support groups and confiding in health care providers) as well as the relationship between support seeking and PTG. Support program participation was moderate (61.1%) compared to the high rates of confiding in health professionals (88.6%), and African Americans were less likely to report participating than non-Hispanic Whites (odds ratio = .14, confidence intervals [0.08, 0.23]). The mean (SD) PTG score was 48.8 (27.4) (range 0-105). Support program participation (Beta = 10.4) and confiding in health care providers (Beta = 12.9) were associated (p < .001) with higher PTG. In analyses stratified by race/ethnicity, PTG was significantly higher in non-Hispanic Whites and African American support program participants (p < .01), but not significantly higher in Hispanics/Latinas. Confiding in a health care provider was only associated with PTG for non-Hispanic Whites (p = .02). Support program experiences and patient-provider encounters should be examined to determine which attributes facilitate PTG in diverse populations. Adapted from the source document.
JF  - Journal of Psychosocial Oncology
AU  - Kent, Erin E
AU  - Alfano, Catherine M
AU  - Smith, Ashley Wilder
AU  - Bernstein, Leslie
AU  - McTiernan, Anne
AU  - Baumgartner, Kathy B
AU  - Ballard-Barbash, Rachel
AD  - Division of Cancer Control and Population Sciences and Center for Cancer Training, National Cancer Institute, National Institutes of Health
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 393
EP  - 412
PB  - Taylor & Francis, Philadelphia PA
VL  - 31
IS  - 4
SN  - 0734-7332, 0734-7332
KW  - Health Professions
KW  - Black White Differences
KW  - Ethnicity
KW  - Participation
KW  - Self Help Groups
KW  - Race
KW  - Breast Cancer
KW  - Social Development
KW  - Cancer
KW  - article
KW  - 6121: therapeutic interventions
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463026169?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Psychosocial+Oncology&rft.atitle=The+Roles+of+Support+Seeking+and+Race%2FEthnicity+in+Posttraumatic+Growth+Among+Breast+Cancer+Survivors&rft.au=Kent%2C+Erin+E%3BAlfano%2C+Catherine+M%3BSmith%2C+Ashley+Wilder%3BBernstein%2C+Leslie%3BMcTiernan%2C+Anne%3BBaumgartner%2C+Kathy+B%3BBallard-Barbash%2C+Rachel&rft.aulast=Kent&rft.aufirst=Erin&rft.date=2013-07-01&rft.volume=31&rft.issue=4&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychosocial+Oncology&rft.issn=07347332&rft_id=info:doi/10.1080%2F07347332.2013.798759
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-09-28
N1  - CODEN - JPONED
N1  - SubjectsTermNotLitGenreText - Health Professions; Black White Differences; Participation; Ethnicity; Breast Cancer; Social Development; Cancer; Race; Self Help Groups
DO  - http://dx.doi.org/10.1080/07347332.2013.798759
ER  - 



TY  - JOUR
T1  - Socio-Environmental Factors Associated With Lone Parenting Chronically Ill Children
AN  - 1449096421; 201325328
AB  - This article reports findings from 2 studies assessing the relation between parental perception of "lone" parenting and socioeconomic factors, including low income, perception of child health, and parental emotional distress among parents of chronically ill children. In both studies, parents who considered themselves a lone parent when caring for their ill child had significantly lower incomes and greater distress (i.e., were more likely to score at or above clinical or "case" cutoffs on the Brief Symptom Inventory) than those who considered themselves to be married or partnered. Longitudinal research is needed to determine the impact of lone parenting and low income on parental and child health outcomes over time. Adapted from the source document.
JF  - Children's Health Care
AU  - Wiener, Lori
AU  - Pao, Maryland
AU  - Battles, Haven
AU  - Zadeh, Sima
AU  - Patenaude, Andrea Farkas
AU  - Madan-Swain, Avi
AU  - Friebert, Sarah
AU  - Elkin, David
AU  - Kupst, Mary Jo
AD  - Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD wienerl@mail.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 264
EP  - 280
PB  - Taylor & Francis, Philadelphia PA
VL  - 42
IS  - 3
SN  - 0273-9615, 0273-9615
KW  - Socioeconomic factors
KW  - Parenting
KW  - Sick children
KW  - Children
KW  - Parents
KW  - Low income people
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449096421?accountid=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=Children%27s+Health+Care&rft.atitle=Socio-Environmental+Factors+Associated+With+Lone+Parenting+Chronically+Ill+Children&rft.au=Wiener%2C+Lori%3BPao%2C+Maryland%3BBattles%2C+Haven%3BZadeh%2C+Sima%3BPatenaude%2C+Andrea+Farkas%3BMadan-Swain%2C+Avi%3BFriebert%2C+Sarah%3BElkin%2C+David%3BKupst%2C+Mary+Jo&rft.aulast=Wiener&rft.aufirst=Lori&rft.date=2013-07-01&rft.volume=42&rft.issue=3&rft.spage=264&rft.isbn=&rft.btitle=&rft.title=Children%27s+Health+Care&rft.issn=02739615&rft_id=info:doi/10.1080%2F02739615.2013.816612
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-11-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Parents; Parenting; Children; Sick children; Socioeconomic factors; Low income people
DO  - http://dx.doi.org/10.1080/02739615.2013.816612
ER  - 



TY  - JOUR
T1  - Reproductive factors and menopausal hormone therapy and bladder cancer risk in the NIH-AARP Diet and Health Study
AN  - 1443369651; 18602650
AB  - The incidence of bladder cancer among women is at least one-third to one-fourth that observed among men in many countries. Even after accounting for known risk factors, the reason for this gender disparity remains unexplained. We conducted a comprehensive evaluation of reproductive factors and exogenous hormone use with a primary focus on menopausal hormone therapy use and risk of bladder cancer in women in the NIH-AARP Diet and Health Study. Reproductive and hormonal factors were ascertained on the baseline questionnaire in 1995-1996 among 201,492 females who were followed until December 31, 2006. During follow-up, 651 cases of bladder cancer were diagnosed. A subset of women provided detailed information on use of MHT in a second questionnaire in 1996-1997. In this analysis, 127,361 females were followed through June 30, 2002 and 198 incident bladder cancer cases were identified. Cox proportional hazard models, adjusted for smoking status, cigarettes per day and body mass index using age as the time metric, were used to obtain hazard ratios (HRs). A reduced risk was observed among parous women (HR=0.76; 95% CI 0.62-0.93) and women who reported late age at menarche ( greater than or equal to 15 years) (HR=0.57; 95% CI 0.39-0.84). Women who reported ever using estrogen and progestin therapy had a decreased risk (HR=0.53; 95% CI: 0.34-0.83) compared with women who did not report MHT use. No association was observed for estrogen only users (HR=0.82; 95% CI: 0.58-1.15). Our results suggest a putative role for sex hormones in the etiology of bladder cancer among women. What's new? Women have 1/3 to 1/4 the risk of developing bladder cancer compared to men. Even after accounting for known risk factors, the reason for this gender disparity remains unexplained. Daugherty and colleagues speculate that menopausal hormone therapy (MHT) may reduce the risk for bladder cancer and investigate the potential influence of MHT formulation. They find that women who reported having ever used estrogen and progestin therapy have a 40-50% reduction in risk of bladder cancer as compared to women who never used MHT. Interestingly, no significant association overall with bladder cancer risk was observed in women who used estrogen alone, suggesting MHT formulation type is an important consideration when evaluating risk for bladder cancer in women.
JF  - International Journal of Cancer
AU  - Daugherty, Sarah E
AU  - Lacey, James V
AU  - Pfeiffer, Ruth M
AU  - Park, Yikyung
AU  - Hoover, Robert N
AU  - Silverman, Debra T
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD.
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 462
EP  - 472
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 133
IS  - 2
SN  - 0020-7136, 0020-7136
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Diets
KW  - Etiology
KW  - Age
KW  - Estrogens
KW  - Cigarettes
KW  - Urinary bladder
KW  - Body mass
KW  - Risk reduction
KW  - Hormones
KW  - Cancer
KW  - Health risks
KW  - Risk factors
KW  - Gender
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/1443369651?accountid=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=Reproductive+factors+and+menopausal+hormone+therapy+and+bladder+cancer+risk+in+the+NIH-AARP+Diet+and+Health+Study&rft.au=Daugherty%2C+Sarah+E%3BLacey%2C+James+V%3BPfeiffer%2C+Ruth+M%3BPark%2C+Yikyung%3BHoover%2C+Robert+N%3BSilverman%2C+Debra+T&rft.aulast=Daugherty&rft.aufirst=Sarah&rft.date=2013-07-01&rft.volume=133&rft.issue=2&rft.spage=462&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28022
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-12-04
N1  - SubjectsTermNotLitGenreText - Diets; Estrogens; Age; Etiology; Cigarettes; Urinary bladder; Body mass; Risk reduction; Hormones; Cancer; Health risks; Risk factors; Gender
DO  - http://dx.doi.org/10.1002/ijc.28022
ER  - 



TY  - JOUR
T1  - Enhancing children against unhealthy behaviors-an ethical and policy assessment of using a nicotine vaccine
AN  - 1435358370; 4483376
AB  - Health behaviors such as tobacco use contribute significantly to poor health. It is widely recognized that efforts to prevent poor health outcomes should begin in early childhood. Biomedical enhancements, such as a nicotine vaccine, are now emerging and have potential to be used for primary prevention of common diseases. In anticipation of such enhancements, it is important that we begin to consider the ethical and policy appropriateness of their use with children. The main ethical concerns raised by enhancing children relate to their impact on children's well-being and autonomy. These concerns are significant, however they do not appear to apply in the case of the nicotine vaccine; indeed the vaccine could even further these goals for children. Nevertheless, concerns about broadly applying this enhancement may be more challenging. The vaccine may be less cost-effective than alternative public efforts to prevent tobacco use, utilizing it could distract from addressing the foundational causes of smoking and it might not be publically acceptable. Empirical research about these concerns is needed to ascertain their likelihood and impact as well as how they could be minimized. This research could help determine whether behavior-related enhancements hold promise for improving children's health.
JF  - Public health ethics
AU  - Lev, Ori
AU  - Wilfond, Benjamin S
AU  - McBride, Colleen M
AD  - Sapir Academic College ; University of Washington ; National Institutes of Health
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 197
EP  - 206
VL  - 6
IS  - 2
SN  - 1754-9973, 1754-9973
KW  - Sociology
KW  - Cost-effectiveness
KW  - Early childhood
KW  - Health care
KW  - Children
KW  - Child health
KW  - Immunization
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1435358370?accountid=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=Public+health+ethics&rft.atitle=Enhancing+children+against+unhealthy+behaviors-an+ethical+and+policy+assessment+of+using+a+nicotine+vaccine&rft.au=Lev%2C+Ori%3BWilfond%2C+Benjamin+S%3BMcBride%2C+Colleen+M&rft.aulast=Lev&rft.aufirst=Ori&rft.date=2013-07-01&rft.volume=6&rft.issue=2&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Public+health+ethics&rft.issn=17549973&rft_id=info:doi/10.1093%2Fphe%2Fpht006
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-09-23
N1  - Last updated - 2013-09-24
N1  - SubjectsTermNotLitGenreText - 2212; 6237 5775 13521; 3827 2211 652 5676 646 6091 2212; 2933 2920 971 2934 3883; 5775 13521; 2199 5772
DO  - http://dx.doi.org/10.1093/phe/pht006
ER  - 



TY  - JOUR
T1  - Concise Review: Erythroid Versus Myeloid Lineage Commitment: Regulating the Master Regulators
AN  - 1434028653; 18501564
AB  - Developmental processes, like blood formation, are orchestrated by transcriptional networks. Those transcriptional networks are highly responsive to various environmental stimuli and affect common precursors resulting in increased production of cells of the erythroid lineage or myeloid lineage (granulocytes, neutrophils, and macrophages). A significant body of knowledge has accumulated describing transcription factors that drive differentiation of these two major cellular pathways, in particular the antagonistic master regulators such as GATA-1 and PU.1. However, little is known about factors that work upstream of master regulators to enhance differentiation toward one lineage. These functions become especially important under various stress conditions like sudden loss of red blood cells or pathogen infection. This review describes recent studies that begin to provide evidence for such factors. An increased understanding of factors regulating cellular commitment will advance our understanding of the etiology of diseases like anemia, cancer, and possibly other blood related disorders. STEM Cells2013; 31:1237-1244
JF  - Stem Cells
AU  - Wolff, Linda
AU  - Humeniuk, Rita
AD  - 37 Convent Drive, Bethesda, Maryland 20892, USA., wolffl@mail.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1237
EP  - 1244
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 7
SN  - 1066-5099, 1066-5099
KW  - Biotechnology and Bioengineering Abstracts
KW  - Macrophages
KW  - Etiology
KW  - Erythrocytes
KW  - Leukocytes (neutrophilic)
KW  - Anemia
KW  - Stress
KW  - Pathogens
KW  - Infection
KW  - Cancer
KW  - Leukocytes (granulocytic)
KW  - Differentiation
KW  - Stem cells
KW  - Reviews
KW  - Transcription factors
KW  - PU.1 protein
KW  - Environmental effects
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434028653?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Concise+Review%3A+Erythroid+Versus+Myeloid+Lineage+Commitment%3A+Regulating+the+Master+Regulators&rft.au=Wolff%2C+Linda%3BHumeniuk%2C+Rita&rft.aulast=Wolff&rft.aufirst=Linda&rft.date=2013-07-01&rft.volume=31&rft.issue=7&rft.spage=1237&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1379
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Macrophages; Etiology; Erythrocytes; Anemia; Leukocytes (neutrophilic); Stress; Pathogens; Infection; Cancer; Differentiation; Leukocytes (granulocytic); Stem cells; Transcription factors; Reviews; Environmental effects; PU.1 protein
DO  - http://dx.doi.org/10.1002/stem.1379
ER  - 



TY  - JOUR
T1  - Structure of the NLRP1 caspase recruitment domain suggests potential mechanisms for its association with procaspase-1
AN  - 1434014979; 18498876
AB  - The NLRP1 inflammasome responds to microbial challenges such as Bacillus anthracis infection and is implicated in autoimmune disease such as vitiligo. Human NLRP1 contains both an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD), with the latter being essential for its association with the downstream effector procaspase-1. Here we report a 2.0 Aa crystal structure of the human NLRP1 CARD as a fusion with the maltose-binding protein. The structure reveals the six-helix bundle fold of the NLRP1 CARD, typical of the death domain superfamily. The charge surface of the NLRP1 CARD structure and a procaspase-1 CARD model suggests potential mechanisms for their association through electrostatic attraction. Proteins 2013; 81:1266-1270. [copy 2013 Wiley Periodicals, Inc.
JF  - Proteins: Structure, Function and Bioinformatics
AU  - Jin, Tengchuan
AU  - Curry, James
AU  - Smith, Patrick
AU  - Jiang, Jiansheng
AU  - Xiao, TSam
AD  - Structural Immunobiology Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, 20892-0430.
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1266
EP  - 1270
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States
VL  - 81
IS  - 7
SN  - 0887-3585, 0887-3585
KW  - Biotechnology and Bioengineering Abstracts
KW  - Recruitment
KW  - Autoimmune diseases
KW  - Bacillus anthracis
KW  - Infection
KW  - Vitiligo
KW  - Models
KW  - Pyrin protein
KW  - Protein structure
KW  - Crystal structure
KW  - Caspase-1
KW  - Caspase
KW  - Bioinformatics
KW  - maltose-binding protein
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434014979?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Structure+of+the+NLRP1+caspase+recruitment+domain+suggests+potential+mechanisms+for+its+association+with+procaspase-1&rft.au=Jin%2C+Tengchuan%3BCurry%2C+James%3BSmith%2C+Patrick%3BJiang%2C+Jiansheng%3BXiao%2C+TSam&rft.aulast=Jin&rft.aufirst=Tengchuan&rft.date=2013-07-01&rft.volume=81&rft.issue=7&rft.spage=1266&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24287
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Protein structure; Pyrin protein; Autoimmune diseases; Recruitment; Crystal structure; Caspase; Caspase-1; Bioinformatics; Infection; maltose-binding protein; Vitiligo; Models; Bacillus anthracis
DO  - http://dx.doi.org/10.1002/prot.24287
ER  - 



TY  - JOUR
T1  - Lipoprotein succession in Borrelia burgdorferi: similar but distinct roles for OspC and VlsE at different stages of mammalian infection
AN  - 1430851182; 18281750
AB  - Borrelia burgdorferi alternates between ticks and mammals, requiring variable gene expression and protein production to adapt to these diverse niches. These adaptations include shifting among the major outer surface lipoproteins OspA, OspC, and VlsE at different stages of the infectious cycle. We hypothesize that these proteins carry out a basic but essential function, and that OspC and VlsE fulfil this requirement during early and persistent stages of mammalian infection respectively. Previous work by other investigators suggested that several B. burgdorferi lipoproteins, including OspA and VlsE, could substitute for OspC at the initial stage of mouse infection, when OspC is transiently but absolutely required. In this study, we assessed whether vlsE and ospA could restore infectivity to an ospC mutant, and found that neither gene product effectively compensated for the absence of OspC during early infection. In contrast, we determined that OspC production was required by B. burgdorferi throughout SCID mouse infection if the vlsE gene were absent. Together, these results indicate that OspC can substitute for VlsE when antigenic variation is unnecessary, but that these two abundant lipoproteins are optimized for their related but specific roles during early and persistent mammalian infection by B. burgdorferi.
JF  - Molecular Microbiology
AU  - Tilly, Kit
AU  - Bestor, Aaron
AU  - Rosa, Patricia A
AD  - Laboratory of Zoonotic Pathogens NIAID NIH. Rocky Mountain Laboratories
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 216
EP  - 227
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 89
IS  - 2
SN  - 0950-382X, 0950-382X
KW  - Microbiology Abstracts B: Bacteriology
KW  - vlsE gene
KW  - Adaptations
KW  - Borrelia burgdorferi
KW  - Ixodidae
KW  - Niches
KW  - Infection
KW  - Succession
KW  - OspA protein
KW  - Gene expression
KW  - Infectivity
KW  - Lipoproteins
KW  - Severe combined immunodeficiency
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430851182?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Lipoprotein+succession+in+Borrelia+burgdorferi%3A+similar+but+distinct+roles+for+OspC+and+VlsE+at+different+stages+of+mammalian+infection&rft.au=Tilly%2C+Kit%3BBestor%2C+Aaron%3BRosa%2C+Patricia+A&rft.aulast=Tilly&rft.aufirst=Kit&rft.date=2013-07-01&rft.volume=89&rft.issue=2&rft.spage=216&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fmmi.12271
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-04-29
N1  - SubjectsTermNotLitGenreText - vlsE gene; Gene expression; Infectivity; Adaptations; Niches; Lipoproteins; Severe combined immunodeficiency; Succession; Infection; OspA protein; Borrelia burgdorferi; Ixodidae
DO  - http://dx.doi.org/10.1111/mmi.12271
ER  - 



TY  - JOUR
T1  - New paradigms for treatment-resistant depression
AN  - 1427002809; 18305821
AB  - Clinical depression is a serious mental disorder characterized by low mood, anhedonia, loss of interest in daily activities, and other symptoms, and is associated with severe consequences including suicide and increased risk of cardiovascular events. Depression affects nearly 15% of the population. The standard of care for the last 50 years has focused on monoamine neurotransmitters, including such treatments as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). However, these treatments have significant limitations: they can take weeks before showing mood-altering effects, and only one to two out of ten patients shows clinical effects beyond those associated with placebo. A major paradigm shift in research into the treatment of depression is underway, based on promising results with the glutamatergic NMDA receptor antagonist ketamine. Further research has demonstrated the significance of glutamatergic pathways in depression and the association of this system with the stress pathway and magnesium homeostasis. Treatment with NMDA receptor antagonists and magnesium have shown the ability to sprout new synaptic connections and reverse stress-induced neural changes, opening up promising new territory for the development of drugs to meet the unmet need in patients with clinical depression.
JF  - Annals of the New York Academy of Sciences
AU  - Zarate, Carlos
AU  - Duman, Ronald S
AU  - Liu, Guosong
AU  - Sartori, Simone
AU  - Quiroz, Jorge
AU  - Murck, Harald
AD  - Experimental Therapeutics & Pathophysiology Branch, Division of Intramural Research Program, National Institute of Mental Health. National Institutes of Health, and Department of Health and Human Services
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 21
EP  - 31
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 1292
IS  - 1
SN  - 0077-8923, 0077-8923
KW  - Risk Abstracts
KW  - Mental disorders
KW  - Depression
KW  - Stress
KW  - Suicide
KW  - Territory
KW  - Magnesium
KW  - Drugs
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427002809?accountid=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=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=New+paradigms+for+treatment-resistant+depression&rft.au=Zarate%2C+Carlos%3BDuman%2C+Ronald+S%3BLiu%2C+Guosong%3BSartori%2C+Simone%3BQuiroz%2C+Jorge%3BMurck%2C+Harald&rft.aulast=Zarate&rft.aufirst=Carlos&rft.date=2013-07-01&rft.volume=1292&rft.issue=1&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fnyas.12223
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Mental disorders; Depression; Suicide; Stress; Territory; Magnesium; Drugs
DO  - http://dx.doi.org/10.1111/nyas.12223
ER  - 



TY  - JOUR
T1  - Lay meanings of mental health in urban Indian college youth: insights for mental health promotion
AN  - 1419690849; 4469724
JF  - Journal of community and applied social psychology
AU  - Elias, Jereesh K
AU  - Mehrotra, Seema
AU  - Tripathi, Ravikesh
AD  - National Institute of Mental Health and Neurosciences, Bangalore
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 286
EP  - 299
VL  - 23
IS  - 4
SN  - 1052-9284, 1052-9284
KW  - Sociology
KW  - Indians
KW  - Well-being
KW  - Mental health
KW  - Students
KW  - Life satisfaction
KW  - Youth
KW  - India
KW  - Health promotion
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419690849?accountid=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+community+and+applied+social+psychology&rft.atitle=Lay+meanings+of+mental+health+in+urban+Indian+college+youth%3A+insights+for+mental+health+promotion&rft.au=Elias%2C+Jereesh+K%3BMehrotra%2C+Seema%3BTripathi%2C+Ravikesh&rft.aulast=Elias&rft.aufirst=Jereesh&rft.date=2013-07-01&rft.volume=23&rft.issue=4&rft.spage=286&rft.isbn=&rft.btitle=&rft.title=Journal+of+community+and+applied+social+psychology&rft.issn=10529284&rft_id=info:doi/10.1002%2Fcasp.2119
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-08-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 7947 5772 7954; 5790 5772; 13530 13521; 7400 11272; 6301 1335 4424; 12334 4049; 13779 652 5676 646 6091; 175 387 30
DO  - http://dx.doi.org/10.1002/casp.2119
ER  - 



TY  - JOUR
T1  - Genomic insights into the fate of colistin resistance and Acinetobacter baumannii during patient treatment
AN  - 1419368809; 18285786
AB  - Bacterial whole-genome sequencing (WGS) of human pathogens has provided unprecedented insights into the evolution of antibiotic resistance. Most studies have focused on identification of resistance mutations, leaving one to speculate on the fate of these mutants once the antibiotic selective pressure is removed. We performed WGS on longitudinal isolates of Acinetobacter baumannii from patients undergoing colistin treatment, and upon subsequent drug withdrawal. In each of the four patients, colistin resistance evolved via mutations at the pmr locus. Upon colistin withdrawal, an ancestral susceptible strain outcompeted resistant isolates in three of the four cases. In the final case, resistance was also lost, but by a compensatory inactivating mutation in the transcriptional regulator of the pmr locus. Notably, this inactivating mutation reduced the probability of reacquiring colistin resistance when subsequently challenged in vitro. On face value, these results supported an in vivo fitness cost preventing the evolution of stable colistin resistance. However, more careful analysis of WGS data identified genomic evidence for stable colistin resistance undetected by clinical microbiological assays. Transcriptional studies validated this genomic hypothesis, showing increased pmr expression of the initial isolate. Moreover, altering the environmental growth conditions of the clinical assay recapitulated the classification as colistin resistant. Additional targeted sequencing revealed that this isolate evolved undetected in a patient undergoing colistin treatment, and was then transmitted to other hospitalized patients, further demonstrating its stability in the absence of colistin. This study provides a unique window into mutational pathways taken in response to antibiotic pressure in vivo, and demonstrates the potential for genome sequence data to predict resistance phenotypes.
JF  - Genome Research
AU  - Snitkin, E S
AU  - Zelazny, A M
AU  - Gupta, J
AU  - Palmore, T N
AU  - Murray, PR
AU  - Segre, JA
AD  - Epithelial Biology Section, GMBB, NHGRI, Bethesda, Maryland 20892, USA, jsegre@nhgri.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 1155
EP  - 1162
VL  - 23
IS  - 7
SN  - 1088-9051, 1088-9051
KW  - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology; Genetics Abstracts
KW  - Genomes
KW  - Fitness
KW  - Data processing
KW  - Growth conditions
KW  - Nucleotide sequence
KW  - Transcription
KW  - Antibiotics
KW  - Pathogens
KW  - Colistin
KW  - Acinetobacter baumannii
KW  - Classification
KW  - genomics
KW  - Mutation
KW  - Antibiotic resistance
KW  - Evolution
KW  - J 02410:Animal Diseases
KW  - N 14830:RNA
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419368809?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+Research&rft.atitle=Genomic+insights+into+the+fate+of+colistin+resistance+and+Acinetobacter+baumannii+during+patient+treatment&rft.au=Snitkin%2C+E+S%3BZelazny%2C+A+M%3BGupta%2C+J%3BPalmore%2C+T+N%3BMurray%2C+PR%3BSegre%2C+JA&rft.aulast=Snitkin&rft.aufirst=E&rft.date=2013-07-01&rft.volume=23&rft.issue=7&rft.spage=1155&rft.isbn=&rft.btitle=&rft.title=Genome+Research&rft.issn=10889051&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Fitness; Genomes; Data processing; Growth conditions; Nucleotide sequence; Transcription; Antibiotics; Pathogens; Colistin; Classification; genomics; Mutation; Evolution; Antibiotic resistance; Acinetobacter baumannii
ER  - 



TY  - JOUR
T1  - I know not to, but I can't help it: weight gain and changes in impulsivity-related personality traits
AN  - 1418134682; 4465937
AB  - Reciprocal relations between weight and psychological factors suggest that there are deep connections between mind and body. Personality traits are linked to weight gain; weight gain may likewise be associated with personality change. Using data from two diverse longitudinal samples (N = 1,919) collected at two time points an average of 10 years apart, we showed that significant weight gain is associated with increases in both impulsiveness and deliberation: In both samples, middle-aged adults who gained 10% or more of their baseline body weight by follow-up increased in their tendency to give in to temptation, yet were more thoughtful about the consequences of their actions. The present research moves beyond life events to implicate health status in adult personality development. The findings also suggest that interventions focusing on the emotional component of impulse control may be more effective because even people who become more thoughtful about the consequences of their actions may have limited success at inhibiting their behavior. Reprinted by permission of Sage Publications
JF  - Psychological science
AU  - Sutin, Angelina R
AU  - Costa, Paul T
AU  - Chan, Wayne
AU  - Milaneschi, Yuri
AU  - Eaton, William W
AU  - Zonderman, Alan B
AU  - Ferrucci, Luigi
AU  - Terracciano, Antonio
AD  - Florida State University ; National Institute on Aging ; Free University of Amsterdam ; Johns Hopkins University
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1323
EP  - 1328
VL  - 24
IS  - 7
SN  - 0956-7976, 0956-7976
KW  - Sociology
KW  - Social action
KW  - Personality traits
KW  - Personality
KW  - Personality development
KW  - Health
KW  - Adults
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1418134682?accountid=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=Psychological+science&rft.atitle=I+know+not+to%2C+but+I+can%27t+help+it%3A+weight+gain+and+changes+in+impulsivity-related+personality+traits&rft.au=Sutin%2C+Angelina+R%3BCosta%2C+Paul+T%3BChan%2C+Wayne%3BMilaneschi%2C+Yuri%3BEaton%2C+William+W%3BZonderman%2C+Alan+B%3BFerrucci%2C+Luigi%3BTerracciano%2C+Antonio&rft.aulast=Sutin&rft.aufirst=Angelina&rft.date=2013-07-01&rft.volume=24&rft.issue=7&rft.spage=1323&rft.isbn=&rft.btitle=&rft.title=Psychological+science&rft.issn=09567976&rft_id=info:doi/10.1177%2F0956797612469212
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-07-29
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 5772; 9416 2153; 9421 9416 2153; 9429 9416 2153; 11766; 603
DO  - http://dx.doi.org/10.1177/0956797612469212
ER  - 



TY  - JOUR
T1  - Acculturation of personality: a three-culture study of Japanese, Japanese Americans, and European Americans
AN  - 1418122979; 4449641
AB  - The present study tests the hypothesis that involvement with a new culture instigates changes in personality of immigrants that result in (a) better fit with the norms of the culture of destination and (b) reduced fit with the norms of the culture of origin. Participants were 40 Japanese first-generation immigrants to the United States, 57 Japanese monoculturals, and 60 U.S. monoculturals. All participants completed the Jackson Personality Inventory as a measure of the Big Five; immigrants completed the Japanese American Acculturation Scale. Immigrants' fits with the cultures of destination and origin were calculated by correlating Japanese American mothers' patterns of ratings on the Big Five with the average patterns of ratings of European Americans and Japanese on the same personality dimensions. Japanese Americans became more 'American' and less 'Japanese' in their personality as they reported higher participation in the U.S. culture. The results support the view that personality can be subject to cultural influence.
JF  - Journal of cross-cultural psychology
AU  - Güngör, Derya
AU  - Bornstein, Marc H
AU  - Leersnyder, Jozefien De
AU  - Cote, Linda
AU  - Ceulemans, Eva
AU  - Mesquita, Batja
AD  - Catholic University Leuven ; National Institutes of Health, U.S.A. ; University of Leuven, Belgium
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 701
EP  - 718
VL  - 44
IS  - 5
SN  - 0022-0221, 0022-0221
KW  - Sociology
KW  - Acculturation
KW  - Social participation
KW  - Cultural influence
KW  - Immigrants
KW  - Personality
KW  - U.S.A.
KW  - Migration
KW  - Cultural history
KW  - Japan
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1418122979?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cross-cultural+psychology&rft.atitle=Acculturation+of+personality%3A+a+three-culture+study+of+Japanese%2C+Japanese+Americans%2C+and+European+Americans&rft.au=G%C3%BCng%C3%B6r%2C+Derya%3BBornstein%2C+Marc+H%3BLeersnyder%2C+Jozefien+De%3BCote%2C+Linda%3BCeulemans%2C+Eva%3BMesquita%2C+Batja&rft.aulast=G%C3%BCng%C3%B6r&rft.aufirst=Derya&rft.date=2013-07-01&rft.volume=44&rft.issue=5&rft.spage=701&rft.isbn=&rft.btitle=&rft.title=Journal+of+cross-cultural+psychology&rft.issn=00220221&rft_id=info:doi/10.1177%2F0022022112470749
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-17
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 9416 2153; 539 3105 3198; 11880 11878 9003; 3151 3178 3121 3198 3549 2688 2449 10404; 6232 8037; 3144 3192 12867 5889; 8040; 433 293 14; 191 300 30
DO  - http://dx.doi.org/10.1177/0022022112470749
ER  - 



TY  - JOUR
T1  - Genetic variants in DNA repair pathway genes and risk of esophageal squamous cell carcinoma and gastric adenocarcinoma in a Chinese population
AN  - 1412561317; 18242962
AB  - The DNA repair pathways help to maintain genomic integrity and therefore genetic variation in the pathways could affect the propensity to develop cancer. Selected germline single nucleotide polymorphisms (SNPs) in the pathways have been associated with esophageal cancer and gastric cancer (GC) but few studies have comprehensively examined the pathway genes. We aimed to investigate associations between DNA repair pathway genes and risk of esophageal squamous cell carcinoma (ESCC) and GC, using data from a genome-wide association study in a Han Chinese population where ESCC and GC are the predominant cancers. In sum, 1942 ESCC cases, 1758 GC cases and 2111 controls from the Shanxi Upper Gastrointestinal Cancer Genetics Project (discovery set) and the Linxian Nutrition Intervention Trials (replication set) were genotyped for 1675 SNPs in 170 DNA repair-related genes. Logistic regression models were applied to evaluate SNP-level associations. Gene- and pathway-level associations were determined using the resampling-based adaptive rank-truncated product approach. The DNA repair pathways overall were significantly associated with risk of ESCC (P = 6.37 x 10 super(-) super(4)), but not with GC (P = 0.20). The most significant gene in ESCC was CHEK2 (P = 2.00 x 10 super(-) super(6)) and in GC was CLK2 (P = 3.02 x 10 super(-) super(4)). We observed several other genes significantly associated with either ESCC (SMUG1, TDG, TP53, GTF2H3, FEN1, POLQ, HEL308, RAD54B, MPG, FANCE and BRCA1) or GC risk (MRE11A, RAD54L and POLE) (P < 0.05). We provide evidence for an association between specific genes in the DNA repair pathways and the risk of ESCC and GC. Further studies are warranted to validate these associations and to investigate underlying mechanisms.
JF  - Carcinogenesis
AU  - Li, Wen-Qing
AU  - Hu, Nan
AU  - Hyland, Paula L
AU  - Gao, Ying
AU  - Wang, Zhao-Ming
AU  - Yu, Kai
AU  - Su, Hua
AU  - Wang, Chao-Yu
AU  - Wang, Le-Min
AU  - Chanock, Stephen J
AU  - Burdett, Laurie
AU  - Ding, Ti
AU  - Qiao, You-Lin
AU  - Fan, Jin-Hu
AU  - Wang, Yuan
AU  - Xu, Yi
AU  - Shi, Jian-Xin
AU  - Gu, Fangyi
AU  - Wheeler, William
AU  - Xiong, Xiao-Qin
AU  - Giffen, Carol
AU  - Tucker, Margaret A
AU  - Dawsey, Sanford M
AU  - Freedman, Neal D
AU  - Abnet, Christian C
AU  - Goldstein, Alisa M
AU  - Taylor, Philip R
AD  - super(1)Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institute of Health, Bethesda, MD 20852, USA,, liw9@mail.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1536
EP  - 1542
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 34
IS  - 7
SN  - 0143-3334, 0143-3334
KW  - Oncogenes & Growth Factors Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Risk Abstracts
KW  - Adenocarcinoma
KW  - Guanylate cyclase
KW  - Cancer
KW  - N:14820
KW  - G:07730
KW  - R2 23060:Medical and environmental health
KW  - B:26640
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412561317?accountid=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=Carcinogenesis&rft.atitle=Genetic+variants+in+DNA+repair+pathway+genes+and+risk+of+esophageal+squamous+cell+carcinoma+and+gastric+adenocarcinoma+in+a+Chinese+population&rft.au=Li%2C+Wen-Qing%3BHu%2C+Nan%3BHyland%2C+Paula+L%3BGao%2C+Ying%3BWang%2C+Zhao-Ming%3BYu%2C+Kai%3BSu%2C+Hua%3BWang%2C+Chao-Yu%3BWang%2C+Le-Min%3BChanock%2C+Stephen+J%3BBurdett%2C+Laurie%3BDing%2C+Ti%3BQiao%2C+You-Lin%3BFan%2C+Jin-Hu%3BWang%2C+Yuan%3BXu%2C+Yi%3BShi%2C+Jian-Xin%3BGu%2C+Fangyi%3BWheeler%2C+William%3BXiong%2C+Xiao-Qin%3BGiffen%2C+Carol%3BTucker%2C+Margaret+A%3BDawsey%2C+Sanford+M%3BFreedman%2C+Neal+D%3BAbnet%2C+Christian+C%3BGoldstein%2C+Alisa+M%3BTaylor%2C+Philip+R&rft.aulast=Li&rft.aufirst=Wen-Qing&rft.date=2013-07-01&rft.volume=34&rft.issue=7&rft.spage=1536&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt094
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Guanylate cyclase; Cancer
DO  - http://dx.doi.org/10.1093/carcin/bgt094
ER  - 



TY  - JOUR
T1  - Phylogenetic analysis of multiprobe fluorescence in situ hybridization data from tumor cell populations
AN  - 1412561087; 18242927
AB  - Motivation: Development and progression of solid tumors can be attributed to a process of mutations, which typically includes changes in the number of copies of genes or genomic regions. Although comparisons of cells within single tumors show extensive heterogeneity, recurring features of their evolutionary process may be discerned by comparing multiple regions or cells of a tumor. A useful source of data for studying likely progression of individual tumors is fluorescence in situ hybridization (FISH), which allows one to count copy numbers of several genes in hundreds of single cells. Novel algorithms for interpreting such data phylogenetically are needed, however, to reconstruct likely evolutionary trajectories from states of single cells and facilitate analysis of tumor evolution.Results: In this article, we develop phylogenetic methods to infer likely models of tumor progression using FISH copy number data and apply them to a study of FISH data from two cancer types. Statistical analyses of topological characteristics of the tree-based model provide insights into likely tumor progression pathways consistent with the prior literature. Furthermore, tree statistics from the resulting phylogenies can be used as features for prediction methods. This results in improved accuracy, relative to unstructured gene copy number data, at predicting tumor state and future metastasis.
JF  - Bioinformatics
AU  - Chowdhury, Salim Akhter
AU  - Shackney, Stanley E
AU  - Heselmeyer-Haddad, Kerstin
AU  - Ried, Thomas
AU  - Schaeffer, Alejandro A
AU  - Schwartz, Russell
AD  - super(1)Joint Carnegie Mellon/University of Pittsburgh Ph.D. Program in Computational Biology, super(2)Lane Center for Computational Biology, Carnegie Mellon University, Pittsburgh, PA 15213, USA, super(3)Intelligent Oncotherapeutics, Pittsburgh, PA 15243, USA, super(4)Genetics Branch, Center for Cancer Research, NCI, NIH, super(5)Computational Biology Branch, NCBI, NIH, Bethesda, MD, USA and super(6)Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213, USA
Y1  - 2013/07/01/
PY  - 2013
DA  - 2013 Jul 01
SP  - i189
EP  - i198
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 13
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Phylogeny
KW  - Data processing
KW  - Solid tumors
KW  - Algorithms
KW  - Statistical analysis
KW  - Tumors
KW  - Tumor cells
KW  - copy number
KW  - Computer programs
KW  - software
KW  - Breast cancer
KW  - genomics
KW  - Bioinformatics
KW  - Cervix
KW  - Mutation
KW  - Internet
KW  - Fluorescence in situ hybridization
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412561087?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phylogenetic+analysis+of+multiprobe+fluorescence+in+situ+hybridization+data+from+tumor+cell+populations&rft.au=Chowdhury%2C+Salim+Akhter%3BShackney%2C+Stanley+E%3BHeselmeyer-Haddad%2C+Kerstin%3BRied%2C+Thomas%3BSchaeffer%2C+Alejandro+A%3BSchwartz%2C+Russell&rft.aulast=Chowdhury&rft.aufirst=Salim&rft.date=2013-07-01&rft.volume=29&rft.issue=13&rft.spage=i189&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt205
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Phylogeny; Data processing; Solid tumors; Statistical analysis; Algorithms; Tumors; Tumor cells; copy number; Computer programs; software; Breast cancer; Bioinformatics; genomics; Cervix; Mutation; Internet; Fluorescence in situ hybridization
DO  - http://dx.doi.org/10.1093/bioinformatics/btt205
ER  - 



TY  - JOUR
T1  - Genome-wide identification and predictive modeling of tissue-specific alternative polyadenylation
AN  - 1412559912; 18242951
AB  - Motivation: Pre-mRNA cleavage and polyadenylation are essential steps for 3'-end maturation and subsequent stability and degradation of mRNAs. This process is highly controlled by cis-regulatory elements surrounding the cleavage/polyadenylation sites (polyA sites), which are frequently constrained by sequence content and position. More than 50% of human transcripts have multiple functional polyA sites, and the specific use of alternative polyA sites (APA) results in isoforms with variable 3'-untranslated regions, thus potentially affecting gene regulation. Elucidating the regulatory mechanisms underlying differential polyA preferences in multiple cell types has been hindered both by the lack of suitable data on the precise location of cleavage sites, as well as of appropriate tests for determining APAs with significant differences across multiple libraries.Results: We applied a tailored paired-end RNA-seq protocol to specifically probe the position of polyA sites in three human adult tissue types. We specified a linear-effects regression model to identify tissue-specific biases indicating regulated APA; the significance of differences between tissue types was assessed by an appropriately designed permutation test. This combination allowed to identify highly specific subsets of APA events in the individual tissue types. Predictive models successfully classified constitutive polyA sites from a biologically relevant background (auROC = 99.6%), as well as tissue-specific regulated sets from each other. We found that the main cis-regulatory elements described for polyadenylation are a strong, and highly informative, hallmark for constitutive sites only. Tissue-specific regulated sites were found to contain other regulatory motifs, with the canonical polyadenylation signal being nearly absent at brain-specific polyA sites. Together, our results contribute to the understanding of the diversity of post-transcriptional gene regulation.Availability: Raw data are deposited on SRA, accession numbers: brain SRX208132, kidney SRX208087 and liver SRX208134. Processed datasets as well as model code are published on our website: http://www.genome.duke.edu/labs/ohler/research/UTR/Contact:[/ bold] uwe.ohler sub(u)ke.edu
JF  - Bioinformatics
AU  - Hafez, Dina
AU  - Ni, Ting
AU  - Mukherjee, Sayan
AU  - Zhu, Jun
AU  - Ohler, Uwe
AD  - super(1)Department of Computer Science, Duke University, Durham, NC, 27708, USA, super(2)Berlin Institute for Medical Systems Biology, Max Delbrueck Center, 13125 Berlin, Germany, super(3)Genetics and Development Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA, super(4)State Key Laboratory of Genetics Engineering & MOE Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, 200433, China, super(5)Institute for Genome Sciences & Policy, Duke University Medical Center, Durham, NC 27708, USA and super(6)Department of Statistical Science, Duke University, Durham, NC 27708, USA
Y1  - 2013/07/01/
PY  - 2013
DA  - 2013 Jul 01
SP  - i108
EP  - i116
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 13
SN  - 1367-4803, 1367-4803
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - Place preferences
KW  - Data processing
KW  - 3' Untranslated regions
KW  - DNA probes
KW  - Brain
KW  - Polyadenylation
KW  - Gene regulation
KW  - Kidney
KW  - Liver
KW  - Regression analysis
KW  - Bioinformatics
KW  - Post-transcription
KW  - N 14810:Methods
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412559912?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genome-wide+identification+and+predictive+modeling+of+tissue-specific+alternative+polyadenylation&rft.au=Hafez%2C+Dina%3BNi%2C+Ting%3BMukherjee%2C+Sayan%3BZhu%2C+Jun%3BOhler%2C+Uwe&rft.aulast=Hafez&rft.aufirst=Dina&rft.date=2013-07-01&rft.volume=29&rft.issue=13&rft.spage=i108&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt233
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Place preferences; Data processing; 3' Untranslated regions; DNA probes; Gene regulation; Regression analysis; Liver; Kidney; Brain; Polyadenylation; Bioinformatics; Post-transcription
DO  - http://dx.doi.org/10.1093/bioinformatics/btt233
ER  - 



TY  - JOUR
T1  - The Association between a Medical History of Depression and Gestational Diabetes in a Large Multi-ethnic Cohort in the United States
AN  - 1412504084; 18199726
AB  - Both major depression and gestational diabetes mellitus (GDM) are prevalent among women of reproductive age. Our objective was to determine whether a medical history of depression is related to subsequent development of GDM. The Consortium on Safe Labor was a US retrospective cohort study of 228 562 births between 2002 and 2008. Exclusion criteria for the present analysis included multiple gestation pregnancies (n = 5059), pre-existing diabetes (n = 12 771), deliveries <24 weeks (n = 395), site GDM prevalence (<1%) (n = 20 721) and missing data on pre-pregnancy body mass index (BMI) (n = 61 321). Using generalised estimating equations, we estimated the association between a history of depression and a pregnancy complicated by GDM. The final analytic population included 121 260 women contributing 128 295 pregnancies, of which 5606 were affected by GDM. A history of depression was significantly associated with an increased risk of developing GDM (multivariate odds ratio [aOR] = 1.42 [95% confidence interval (CI) 1.26, 1.60]). Adjusting for pre-pregnancy BMI and weight gain during pregnancy attenuated the association, although it remained statistically significant (aOR = 1.17 [95% CI 1.03, 1.33]). A history of depression was significantly associated with an increased GDM risk among a large multi-ethnic US cohort of women. If the association is confirmed, depression presents a potentially modifiable risk factor of GDM and provides additional clues to the underlying pathophysiology of GDM.
JF  - Paediatric and Perinatal Epidemiology
AU  - Bowers, Katherine
AU  - Laughon, SKatherine
AU  - Kim, Sungduk
AU  - Mumford, Sunni L
AU  - Brite, Jennifer
AU  - Kiely, Michele
AU  - Zhang, Cuilin
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development. National Institutes of Health
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 323
EP  - 328
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 27
IS  - 4
SN  - 0269-5022, 0269-5022
KW  - Risk Abstracts
KW  - Diabetes mellitus
KW  - Historical account
KW  - Obesity
KW  - USA
KW  - Age
KW  - Depression
KW  - Body weight
KW  - Risk factors
KW  - Body mass
KW  - Pregnancy
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412504084?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Paediatric+and+Perinatal+Epidemiology&rft.atitle=The+Association+between+a+Medical+History+of+Depression+and+Gestational+Diabetes+in+a+Large+Multi-ethnic+Cohort+in+the+United+States&rft.au=Bowers%2C+Katherine%3BLaughon%2C+SKatherine%3BKim%2C+Sungduk%3BMumford%2C+Sunni+L%3BBrite%2C+Jennifer%3BKiely%2C+Michele%3BZhang%2C+Cuilin&rft.aulast=Bowers&rft.aufirst=Katherine&rft.date=2013-07-01&rft.volume=27&rft.issue=4&rft.spage=323&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+Perinatal+Epidemiology&rft.issn=02695022&rft_id=info:doi/10.1111%2Fppe.12057
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2013-07-26
N1  - SubjectsTermNotLitGenreText - Diabetes mellitus; Obesity; Historical account; Age; Depression; Body weight; Body mass; Risk factors; Pregnancy; USA
DO  - http://dx.doi.org/10.1111/ppe.12057
ER  - 



TY  - JOUR
T1  - Identification of Small-Molecule Agonists of Human Relaxin Family Receptor 1 (RXFP1) by Using a Homogenous Cell-Based cAMP Assay
AN  - 1399920520; 18222588
AB  - The relaxin hormone is involved in a variety of biological functions, including female reproduction and parturition, as well as regulation of cardiovascular, renal, pulmonary, and hepatic functions. It regulates extracellular matrix remodeling, cell invasiveness, proliferation, differentiation, and overall tissue homeostasis. The G protein-coupled receptor (GPCR) relaxin family receptor 1 (RXFP1) is a cognate relaxin receptor that mainly signals through cyclic AMP second messenger. Although agonists of the receptor could have a wide range of pharmacologic utility, until now there have been no reported small-molecule agonists for relaxin receptors. Here, we report the development of a quantitative high-throughput platform for an RXFP1 agonist screen based on homogenous cell-based HTRF cyclic AMP (cAMP) assay technology. Two small molecules of similar structure were independently identified from a screen of more than 365 677 compounds. Neither compound showed activity in a counterscreen with HEK293T cells transfected with an unrelated GPCR vasopressin 1b receptor. These small-molecule agonists also demonstrated selectivity against the RXFP2 receptor, providing a basis for future medicinal chemistry optimization of selective relaxin receptor agonists.
JF  - Journal of Biomolecular Screening
AU  - Chen, Catherine Z
AU  - Southall, Noel
AU  - Xiao, Jingbo
AU  - Marugan, Juan J
AU  - Ferrer, Marc
AU  - Hu, Xin
AU  - Jones, Raisa E
AU  - Feng, Shu
AU  - Agoulnik, Irina U
AU  - Zheng, Wei
AU  - Agoulnik, Alexander I
AD  - National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD, USA
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 670
EP  - 677
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 18
IS  - 6
SN  - 1087-0571, 1087-0571
KW  - Biotechnology and Bioengineering Abstracts
KW  - Invasiveness
KW  - relaxin
KW  - Cyclic AMP
KW  - Parturition
KW  - Homeostasis
KW  - Hormones
KW  - Differentiation
KW  - Second messengers
KW  - Vasopressin
KW  - G protein-coupled receptors
KW  - Lung
KW  - Extracellular matrix
KW  - Liver
KW  - Kidney
KW  - Reproduction
KW  - W 30935:Food Biotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399920520?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+Small-Molecule+Agonists+of+Human+Relaxin+Family+Receptor+1+%28RXFP1%29+by+Using+a+Homogenous+Cell-Based+cAMP+Assay&rft.au=Chen%2C+Catherine+Z%3BSouthall%2C+Noel%3BXiao%2C+Jingbo%3BMarugan%2C+Juan+J%3BFerrer%2C+Marc%3BHu%2C+Xin%3BJones%2C+Raisa+E%3BFeng%2C+Shu%3BAgoulnik%2C+Irina+U%3BZheng%2C+Wei%3BAgoulnik%2C+Alexander+I&rft.aulast=Chen&rft.aufirst=Catherine&rft.date=2013-07-01&rft.volume=18&rft.issue=6&rft.spage=670&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057112469406
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 19
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Invasiveness; relaxin; Cyclic AMP; Parturition; Homeostasis; Hormones; Differentiation; Second messengers; G protein-coupled receptors; Vasopressin; Lung; Extracellular matrix; Kidney; Liver; Reproduction
DO  - http://dx.doi.org/10.1177/1087057112469406
ER  - 



TY  - JOUR
T1  - Lack of Serum Antibodies against Borrelia burgdorferi in Children with Autism
AN  - 1399920433; 18225666
AB  - It has been proposed that Borrelia burgdorferi infection is present in similar to 25% of children with autism spectrum disorders. In this study, antibodies against Borrelia burgdorferi were assessed in autistic (n = 104), developmentally delayed (n = 24), and healthy control (n = 55) children. No seropositivity against Borrelia burgdorferi was detected in the children with and without autism. There was no evidence of an association between Lyme disease and autism.
JF  - Clinical and Vaccine Immunology
AU  - Burbelo, Peter D
AU  - Swedo, Susan E
AU  - Thurm, Audrey
AU  - Bayat, Ahmad
AU  - Levin, Andrew E
AU  - Marques, Adriana
AU  - Iadarola, Michael J
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1092
EP  - 1093
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 20
IS  - 7
SN  - 1556-679X, 1556-679X
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Antibodies
KW  - Borrelia burgdorferi
KW  - Children
KW  - Infection
KW  - Autism
KW  - Lyme disease
KW  - F 06905:Vaccines
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399920433?accountid=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=Lack+of+Serum+Antibodies+against+Borrelia+burgdorferi+in+Children+with+Autism&rft.au=Burbelo%2C+Peter+D%3BSwedo%2C+Susan+E%3BThurm%2C+Audrey%3BBayat%2C+Ahmad%3BLevin%2C+Andrew+E%3BMarques%2C+Adriana%3BIadarola%2C+Michael+J&rft.aulast=Burbelo&rft.aufirst=Peter&rft.date=2013-07-01&rft.volume=20&rft.issue=7&rft.spage=1092&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=1556679X&rft_id=info:doi/10.1128%2FCVI.00643-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 12
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Antibodies; Infection; Children; Autism; Lyme disease; Borrelia burgdorferi
DO  - http://dx.doi.org/10.1128/CVI.00643-12
ER  - 



TY  - JOUR
T1  - Toxicology and Carcinogenesis Study of Senna in C3B6.129F1-Trp53tm1Brd N12 Haploinsufficient Mice
AN  - 1399918713; 18215260
AB  - Senna is a pod or leaf of Senna alexandrina P. Mill and is used as a stimulant laxative. In the large intestine, bacterial enzymes reduce sennosides to rhein-9-anthrone, the active form for the laxative effect. To determine the potential toxic effects of senna, a 5-week dose range finding study in the C57BL/6N mouse and a 40-week toxicology and carcinogenesis study in the C3B6.129F1-Trp53tm1Brd N12 haploinsufficient (p53+/-) mouse were conducted. In the 5-week study, C57BL/6N mice were exposed to up to 10,000 ppm senna in feed. Increased incidences of epithelial hyperplasia of the cecum and colon were observed in males and females exposed to 5,000 or 10,000 ppm senna. These intestinal lesions were not considered to be of sufficient severity to cause mortality and, thus, in the p53+/- mouse 40-week study, the high dose of 10,000 ppm was selected. Significant increases in the incidences of epithelial hyperplasia of the colon and cecum were observed at 10,000 ppm in p53+/- males and females, and the incidence of hyperplasia of the colon was significantly increased at 3,000 ppm in females. In conclusion, the large intestine was the major target of senna-induced toxicity in both wild-type and the p53+/- mouse model. There was no neoplastic change when senna was administered to p53+/- mouse.
JF  - Toxicologic Pathology
AU  - Surh, Inok
AU  - Brix, Amy
AU  - French, John E
AU  - Collins, Bradley J
AU  - Sanders, JMichael
AU  - Vallant, Molly
AU  - Dunnick, June K
AD  - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, dunnickj@niehs.nih.gov
PY  - 2013
SP  - 770
EP  - 778
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 41
IS  - 5
SN  - 0192-6233, 0192-6233
KW  - Toxicology Abstracts
KW  - senna
KW  - Trp53
KW  - carcinogenesis
KW  - toxicity
KW  - laxative
KW  - large intestine.
KW  - Mortality
KW  - Animal models
KW  - Leaves
KW  - Enzymes
KW  - Large intestine
KW  - Stimulants
KW  - Toxicity
KW  - Hyperplasia
KW  - Laxatives
KW  - Colon
KW  - Carcinogenesis
KW  - Cecum
KW  - X 24300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399918713?accountid=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=Toxicology+and+Carcinogenesis+Study+of+Senna+in+C3B6.129F1-Trp53tm1Brd+N12+Haploinsufficient+Mice&rft.au=Surh%2C+Inok%3BBrix%2C+Amy%3BFrench%2C+John+E%3BCollins%2C+Bradley+J%3BSanders%2C+JMichael%3BVallant%2C+Molly%3BDunnick%2C+June+K&rft.aulast=Surh&rft.aufirst=Inok&rft.date=2013-07-01&rft.volume=41&rft.issue=5&rft.spage=770&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623312464304
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 68
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Mortality; Laxatives; Hyperplasia; Colon; Carcinogenesis; Leaves; Animal models; Enzymes; Cecum; Stimulants; Large intestine; Toxicity
DO  - http://dx.doi.org/10.1177/0192623312464304
ER  - 



TY  - JOUR
T1  - Automatic Segmentation and Measurement of Pleural Effusions on CT
AN  - 1399918472; 18226031
AB  - Pleural effusion is an important biomarker for the diagnosis of many diseases. We develop an automated method to evaluate pleural effusion on CT scans, the measurement of which is prohibitively time consuming when performed manually. The method is based on parietal and visceral pleura extraction, active contour models, region growing, Bezier surface fitting, and deformable surface modeling. Twelve CT scans with three manual segmentations were used to validate the automatic segmentation method. The method was then applied on 91 additional scans for visual assessment. The segmentation method yielded a correlation coefficient of 0.97 and a Dice coefficient of 0.72 plus or minus 0.13 when compared to a professional manual segmentation. The visual assessment estimated 83% cases with negligible or small segmentation errors, 14% with medium errors, and 3% with large errors.
JF  - IEEE Transactions on Biomedical Engineering
AU  - Yao, Jianhua
AU  - Bliton, John
AU  - Summers, Ronald M
AD  - National Institutes of Health , Bethesda, USA
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 1834
EP  - 1840
PB  - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States
VL  - 60
IS  - 7
SN  - 0018-9294, 0018-9294
KW  - Biotechnology and Bioengineering Abstracts
KW  - Pleura
KW  - Energy
KW  - Computed tomography
KW  - Segmentation
KW  - Automation
KW  - Pleural effusion
KW  - biomarkers
KW  - Models
KW  - W 30905:Medical Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399918472?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=IEEE+Transactions+on+Biomedical+Engineering&rft.atitle=Automatic+Segmentation+and+Measurement+of+Pleural+Effusions+on+CT&rft.au=Yao%2C+Jianhua%3BBliton%2C+John%3BSummers%2C+Ronald+M&rft.aulast=Yao&rft.aufirst=Jianhua&rft.date=2013-07-01&rft.volume=60&rft.issue=7&rft.spage=1834&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Biomedical+Engineering&rft.issn=00189294&rft_id=info:doi/10.1109%2FTBME.2013.2243446
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Pleura; Energy; Computed tomography; Segmentation; Automation; Pleural effusion; biomarkers; Models
DO  - http://dx.doi.org/10.1109/TBME.2013.2243446
ER  - 



TY  - JOUR
T1  - Molecular Identification of Bacterial DNA in the Chorioretinal Scars of Chronic Granulomatous Disease
AN  - 1399915130; 18190309
AB  - Purpose: Chronic granulomatous disease (CGD) is an inherited disorder characterized by defects in phagocyte-derived nicotinamide adenine dinucleotide phosphate oxidase. It is typically diagnosed in childhood and leads to severe, recurrent bacterial or fungal infections. Chorioretinal lesions are the most common ocular manifestation. We sought to determine whether there are infectious agents in CGD-associated chorioretinopathy. Methods: Medical records and ocular histopathology from CGD cases from January 1983 to January 2012 at the National Institutes of Health were retrospectively reviewed. Chorioretinal cells from normal and lesional tissues of the same eye were microdissected. Primers for Staphylococcus epidermidis, Staphylococcus aureus, Pseudomonas aeruginosa, Burkholderia sp., and a panbacterial 16S ribosomal DNA were used for polymerase chain reaction. Results: Seventeen CGD patients had ocular tissues (16 autopsied cases and 1 chorioretinal biopsy) examined. Of these 17, 8 demonstrated CGD-associated chorioretinal lesions in at least one eye on histopathology. Of these 8, 7 showed amplification of 16S ribosomal DNA within the lesion; of these 7, two also amplified S. epidermidis and one P. aeruginosa. One had no bacterial DNA amplified. Importantly, no microbial DNA was amplified from the normal, non-lesional ocular tissues of these 8 cases. Furthermore, only 1 of the 9 eyes without chorioretinopathy had amplified Burkholderia DNA, that patient had a history of Burkholderia infection. Conclusions: We detected bacterial DNA in 7 of 8 (88 %) cases with CGD-associated chorioretinopathy and only in 1 normal ocular tissue of 17 CGD cases. Bacterial infection may play a role in the pathogenesis of CGD-associated chorioretinal lesions.
JF  - Journal of Clinical Immunology
AU  - Wang, Yujuan
AU  - Marciano, Beatriz E
AU  - Shen, Defen
AU  - Bishop, Rachel J
AU  - Park, Stanley
AU  - Holland, Steven M
AU  - Chan, Chi-Chao
AD  - Immunopathology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, 10 Center Dr., 10/10N103, NIH/NEI, Bethesda, MD, 20892-1857, USA, chanc@nei.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 917
EP  - 924
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 33
IS  - 5
SN  - 0271-9142, 0271-9142
KW  - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Hereditary diseases
KW  - Eye
KW  - medical records
KW  - Biopsy
KW  - Burkholderia
KW  - Children
KW  - Polymerase chain reaction
KW  - Primers
KW  - Recurrent infection
KW  - NAD(P)H oxidase
KW  - Pseudomonas aeruginosa
KW  - Staphylococcus aureus
KW  - Chronic granulomatous disease
KW  - Staphylococcus epidermidis
KW  - J 02400:Human Diseases
KW  - F 06910:Microorganisms & Parasites
KW  - N 14810:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399915130?accountid=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=Molecular+Identification+of+Bacterial+DNA+in+the+Chorioretinal+Scars+of+Chronic+Granulomatous+Disease&rft.au=Wang%2C+Yujuan%3BMarciano%2C+Beatriz+E%3BShen%2C+Defen%3BBishop%2C+Rachel+J%3BPark%2C+Stanley%3BHolland%2C+Steven+M%3BChan%2C+Chi-Chao&rft.aulast=Wang&rft.aufirst=Yujuan&rft.date=2013-07-01&rft.volume=33&rft.issue=5&rft.spage=917&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Immunology&rft.issn=02719142&rft_id=info:doi/10.1007%2Fs10875-013-9899-9
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 35
N1  - Last updated - 2013-07-15
N1  - SubjectsTermNotLitGenreText - Hereditary diseases; Eye; medical records; Polymerase chain reaction; NAD(P)H oxidase; Recurrent infection; Primers; Biopsy; Children; Chronic granulomatous disease; Staphylococcus aureus; Pseudomonas aeruginosa; Burkholderia; Staphylococcus epidermidis
DO  - http://dx.doi.org/10.1007/s10875-013-9899-9
ER  - 



TY  - JOUR
T1  - Modeling pathogenesis of primary liver cancer in lineage-specific mouse cell types.
AN  - 1372702469; 23523670
AB  - Human primary liver cancer is classified into biologically distinct subgroups based on cellular origin. Liver cancer stem cells (CSCs) have been recently described. We investigated the ability of distinct lineages of hepatic cells to become liver CSCs and the phenotypic and genetic heterogeneity of primary liver cancer.
          We transduced mouse primary hepatic progenitor cells, lineage-committed hepatoblasts, and differentiated adult hepatocytes with transgenes encoding oncogenic H-Ras and SV40LT. The CSC properties of transduced cells and their ability to form tumors were tested by standard in vitro and in vivo assays and transcriptome profiling. Irrespective of origin, all transduced cells acquired markers of CSC/progenitor cells, side populations, and self-renewal capacity in vitro. They also formed a broad spectrum of liver tumors, ranging from cholangiocarcinoma to hepatocellular carcinoma, which resembled human liver tumors, based on genomic and histologic analyses. The tumor cells coexpressed hepatocyte (hepatocyte nuclear factor 4α), progenitor/biliary (keratin 19, epithelial cell adhesion molecule, A6), and mesenchymal (vimentin) markers and showed dysregulation of genes that control the epithelial-mesenchymal transition. Gene expression analyses could distinguish tumors of different cellular origin, indicating the contribution of lineage stage-dependent genetic changes to malignant transformation. Activation of c-Myc and its target genes was required to reprogram adult hepatocytes into CSCs and for tumors to develop. Stable knockdown of c-Myc in transformed adult hepatocytes reduced their CSC properties in vitro and suppressed growth of tumors in immunodeficient mice.
          Any cell type in the mouse hepatic lineage can undergo oncogenic reprogramming into a CSC by activating different cell type-specific pathways. Identification of common and cell of origin-specific phenotypic and genetic changes could provide new therapeutic targets for liver cancer. Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.
JF  - Gastroenterology
AU  - Holczbauer, Agnes
AU  - Factor, Valentina M
AU  - Andersen, Jesper B
AU  - Marquardt, Jens U
AU  - Kleiner, David E
AU  - Raggi, Chiara
AU  - Kitade, Mitsuteru
AU  - Seo, Daekwan
AU  - Akita, Hirofumi
AU  - Durkin, Marian E
AU  - Thorgeirsson, Snorri S
AD  - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 221
EP  - 231
VL  - 145
IS  - 1
KW  - Antigens, Polyomavirus Transforming
KW  - 0
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Animals
KW  - Genes, ras -- physiology
KW  - Mice, Inbred C57BL
KW  - Antigens, Polyomavirus Transforming -- physiology
KW  - Cell Differentiation
KW  - Mice
KW  - Hepatocytes -- pathology
KW  - Genes, myc -- physiology
KW  - Epithelial-Mesenchymal Transition
KW  - Liver Neoplasms -- pathology
KW  - Cell Lineage
KW  - Liver Neoplasms -- etiology
KW  - Neoplastic Stem Cells -- cytology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1372702469?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modeling+pathogenesis+of+primary+liver+cancer+in+lineage-specific+mouse+cell+types.&rft.au=Holczbauer%2C+Agnes%3BFactor%2C+Valentina+M%3BAndersen%2C+Jesper+B%3BMarquardt%2C+Jens+U%3BKleiner%2C+David+E%3BRaggi%2C+Chiara%3BKitade%2C+Mitsuteru%3BSeo%2C+Daekwan%3BAkita%2C+Hirofumi%3BDurkin%2C+Marian+E%3BThorgeirsson%2C+Snorri+S&rft.aulast=Holczbauer&rft.aufirst=Agnes&rft.date=2013-07-01&rft.volume=145&rft.issue=1&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2013.03.013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-11
N1  - Date created - 2013-06-28
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517]
Proc Natl Acad Sci U S A. 2005 May 10;102(19):6942-7 [15860580]
Oncogene. 2006 Jun 26;25(27):3818-22 [16799623]
Hepatology. 2006 Jul;44(1):240-51 [16799977]
Cold Spring Harb Symp Quant Biol. 2005;70:251-61 [16869761]
Semin Cancer Biol. 2006 Aug;16(4):313-7 [16935001]
Cancer Res. 2007 Apr 1;67(7):3450-60 [17409456]
Gastroenterology. 2007 Jun;132(7):2542-56 [17570225]
Cancer Cell. 2007 Aug;12(2):160-70 [17692807]
Cell Stem Cell. 2008 Apr 10;2(4):333-44 [18397753]
Nat Genet. 2008 May;40(5):499-507 [18443585]
Cell. 2008 May 16;133(4):704-15 [18485877]
Nat Rev Cancer. 2009 Apr;9(4):265-73 [19262571]
Cancer Res. 2009 Apr 1;69(7):2775-82 [19276364]
Development. 2009 Jun;136(11):1951-60 [19429791]
Gastroenterology. 2006 Apr;130(4):1117-28 [16618406]
Nat Neurosci. 2010 Jan;13(1):133-40 [20023653]
Nature. 2010 Jan 21;463(7279):364-8 [20010808]
Cancer Res. 2010 Apr 15;70(8):3034-41 [20395200]
Gut. 2010 May;59(5):645-54 [20427399]
J Gastroenterol Hepatol. 2010 Sep;25(9):1485-92 [20796144]
Nature. 2010 Sep 16;467(7313):285-90 [20644535]
Cell. 2010 Oct 15;143(2):313-24 [20946988]
Nature. 2011 Jan 20;469(7330):314-22 [21248838]
Semin Liver Dis. 2011 May;31(2):173-87 [21538283]
Nat Cell Biol. 2011 May;13(5):541-9 [21499256]
Proc Natl Acad Sci U S A. 2011 May 10;108(19):7950-5 [21498687]
Cancer Cell. 2011 Jun 14;19(6):754-64 [21665149]
Cancer Cell. 2011 Jul 12;20(1):39-52 [21741595]
Nat Cell Biol. 2011 Sep;13(9):1051-61 [21857669]
Hepatology. 2011 Sep 2;54(3):1031-42 [21618577]
Cancer Cell. 2012 Mar 20;21(3):283-96 [22439924]
Hepatology. 2012 Apr;55(4):1215-26 [22095660]
Stem Cells. 2012 May;30(5):997-1007 [22378611]
Hepatology. 2012 Jun;55(6):1776-86 [22234953]
Hepatology. 2012 Jun;55(6):1876-88 [22271564]
J Clin Invest. 2012 Aug;122(8):2911-5 [22797301]
Cancer Res. 2012 Nov 1;72(21):5635-45 [22964580]
Genes Dev. 2000 Feb 15;14(4):464-74 [10691738]
Semin Cancer Biol. 2000 Jun;10(3):161-71 [10936066]
Am J Pathol. 2001 Apr;158(4):1313-23 [11290549]
Semin Liver Dis. 2004 Feb;24(1):65-75 [15085487]
Nature. 2004 Oct 28;431(7012):1112-7 [15475948]
Mol Cell Biol. 1985 Apr;5(4):780-6 [2581126]
Am J Pathol. 1994 Aug;145(2):409-22 [8053498]
Biochem Biophys Res Commun. 1996 May 6;222(1):64-70 [8630075]
Mol Endocrinol. 2005 Jan;19(1):76-89 [15388794]
Comment In:
Gastroenterology. 2013 Jul;145(1):53-5 [23726876]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1053/j.gastro.2013.03.013
ER  - 



TY  - JOUR
T1  - When environmental chemicals act like uncontrolled medicine.
AN  - 1372078410; 23660158
AB  - In the same way as medicines are delivered to produce effects in the endocrine system, environmental chemicals can be similarly delivered to produce unwanted endocrine effects, resulting in a staggering increase in several diseases. These effects on endocrine and other physiological systems can have significant population-level impacts and thus require public health approaches to disease control. 
          Published by Elsevier Ltd.
JF  - Trends in endocrinology and metabolism: TEM
AU  - Birnbaum, Linda S
AD  - National Institute of Environmental Health Sciences and National Toxicology Program, Research Triangle Park, NC 27709, USA. birnbaumls@niehs.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 321
EP  - 323
VL  - 24
IS  - 7
KW  - Endocrine Disruptors
KW  - 0
KW  - Environmental Pollutants
KW  - Index Medicus
KW  - Environmental Pollution -- prevention & control
KW  - Animals
KW  - Health Transition
KW  - Humans
KW  - United States -- epidemiology
KW  - Environmental Illness -- epidemiology
KW  - Endocrine Disruptors -- toxicity
KW  - Environmental Illness -- prevention & control
KW  - Environmental Pollutants -- toxicity
KW  - Environmental Illness -- chemically induced
KW  - Ecotoxicology -- trends
KW  - Ecotoxicology -- methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1372078410?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+endocrinology+and+metabolism%3A+TEM&rft.atitle=When+environmental+chemicals+act+like+uncontrolled+medicine.&rft.au=Birnbaum%2C+Linda+S&rft.aulast=Birnbaum&rft.aufirst=Linda&rft.date=2013-07-01&rft.volume=24&rft.issue=7&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Trends+in+endocrinology+and+metabolism%3A+TEM&rft.issn=1879-3061&rft_id=info:doi/10.1016%2Fj.tem.2012.12.005
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-27
N1  - Date created - 2013-06-26
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.tem.2012.12.005
ER  - 



TY  - JOUR
T1  - Nutrient supplementation with n3 polyunsaturated fatty acids, lutein, and zeaxanthin decrease A2E accumulation and VEGF expression in the retinas of Ccl2/Cx3cr1-deficient mice on Crb1rd8 background.
AN  - 1370637527; 23677863
AB  - The Age-Related Eye Diseases Study 2 (AREDS2) clinical trial is assessing the effects of higher dietary xanthophyll (lutein and zeaxanthin) and long-chain n3 polyunsaturated fatty acid (LCPUFA) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) intake on progression to advanced age-related macular degeneration (AMD). This study's purpose was to examine the retinal effects of the AREDS2 formulation on Chemokine (C-C motif) ligand 2 (Ccl2(-/-))/CX3C chemokine receptor 1 (Cx3cr1(-/-)) mice on Crumbs homolog 1 retinal degeneration phenotype 8 (Crb1(rd8)) background (DKO), which develop focal retinal lesions with certain features similar to AMD. DKO and C57BL/6N rd8 background mice (WT) were bred and randomized into 4 groups. Two groups, WT mice on AREDS2 diet (A-WT) and DKO mice on AREDS2 diet (A-DKO), were supplemented daily with 1.76 μmol of lutein, 35.1 μmol of zeaxanthin, 215 μmol EPA, and 107 μmol of DHA, and 2 control groups, WT mice on control diet (C-WT) and DKO mice on control diet (C-DKO), were fed an isocaloric diet. All mice had monthly fundus photos and were killed after 3 mo for biochemical and histologic analyses. After 3 mo, 81% of A-DKO mice had lesion regression compared with 25% of C-DKO mice (P < 0.05). Toxic retinal 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetra-enyl]-1-(2-hydroxyethyl)-4-[4-methyl-6(2,6,6-trimethyl-1-cyclohexen-1-yl) 1E,3E,5E,7E-hexatrienyl]-pyridinium (A2E) concentrations were significantly lower in A-DKO compared with C-DKO mice. The outer nuclear layer thickness in A-DKO mice was significantly greater than that in C-DKO mice. Retinal expression of inducible nitric oxide synthase (iNos) tumor necrosis factor-α (Tnf-α), Cyclooxygenase-2 (Cox-2), interleukin1beta (IL-1β), and vascular endothelial growth factor (Vegf) was significantly lower in A-DKO compared with C-DKO mice. Xanthophylls and LCPUFAs have antiinflammatory, neuroprotective, and antiangiogenic properties. Our data provide potential mechanisms by which the AREDS2 formula has a protective effect on retinal lesions in DKO mice.
JF  - The Journal of nutrition
AU  - Ramkumar, Hema L
AU  - Tuo, Jingsheng
AU  - Shen, De F
AU  - Zhang, Jun
AU  - Cao, Xiaoguang
AU  - Chew, Emily Y
AU  - Chan, Chi-Chao
AD  - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 1129
EP  - 1135
VL  - 143
IS  - 7
KW  - A2-E (N-retinylidene-N-retinylethanolamine)
KW  - 0
KW  - Angiogenesis Inhibitors
KW  - Anti-Inflammatory Agents
KW  - Ccl2 protein, mouse
KW  - Chemokine CCL2
KW  - Cx3cr1 protein, mouse
KW  - Interleukin-1beta
KW  - Pyridinium Compounds
KW  - Receptors, Chemokine
KW  - Retinoids
KW  - Tumor Necrosis Factor-alpha
KW  - Vascular Endothelial Growth Factor A
KW  - Xanthophylls
KW  - Zeaxanthins
KW  - vascular endothelial growth factor A, mouse
KW  - Docosahexaenoic Acids
KW  - 25167-62-8
KW  - Eicosapentaenoic Acid
KW  - AAN7QOV9EA
KW  - Nitric Oxide Synthase Type II
KW  - EC 1.14.13.39
KW  - Nos2 protein, mouse
KW  - Ptgs2 protein, mouse
KW  - EC 1.14.99.-
KW  - Cyclooxygenase 2
KW  - EC 1.14.99.1
KW  - Lutein
KW  - X72A60C9MT
KW  - Index Medicus
KW  - Animals
KW  - Interleukin-1beta -- genetics
KW  - Tumor Necrosis Factor-alpha -- genetics
KW  - Retinoids -- pharmacokinetics
KW  - Mice, Knockout
KW  - Phenotype
KW  - Microscopy, Electron, Transmission
KW  - Macular Degeneration -- pathology
KW  - Macular Degeneration -- drug therapy
KW  - Cyclooxygenase 2 -- metabolism
KW  - Retinal Degeneration -- drug therapy
KW  - Retinal Degeneration -- pathology
KW  - Retina -- metabolism
KW  - Chemokine CCL2 -- genetics
KW  - Cyclooxygenase 2 -- genetics
KW  - Retina -- drug effects
KW  - Receptors, Chemokine -- metabolism
KW  - Anti-Inflammatory Agents -- administration & dosage
KW  - Mice
KW  - Receptors, Chemokine -- genetics
KW  - Chemokine CCL2 -- metabolism
KW  - Angiogenesis Inhibitors -- administration & dosage
KW  - Pyridinium Compounds -- pharmacokinetics
KW  - Gene Expression Profiling
KW  - Macular Degeneration -- genetics
KW  - Interleukin-1beta -- metabolism
KW  - Mice, Inbred C57BL
KW  - Nitric Oxide Synthase Type II -- metabolism
KW  - Nitric Oxide Synthase Type II -- genetics
KW  - Tumor Necrosis Factor-alpha -- metabolism
KW  - Retinal Degeneration -- genetics
KW  - Xanthophylls -- administration & dosage
KW  - Lutein -- administration & dosage
KW  - Eicosapentaenoic Acid -- administration & dosage
KW  - Dietary Supplements
KW  - Docosahexaenoic Acids -- administration & dosage
KW  - Vascular Endothelial Growth Factor A -- genetics
KW  - Vascular Endothelial Growth Factor A -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1370637527?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+nutrition&rft.atitle=Nutrient+supplementation+with+n3+polyunsaturated+fatty+acids%2C+lutein%2C+and+zeaxanthin+decrease+A2E+accumulation+and+VEGF+expression+in+the+retinas+of+Ccl2%2FCx3cr1-deficient+mice+on+Crb1rd8+background.&rft.au=Ramkumar%2C+Hema+L%3BTuo%2C+Jingsheng%3BShen%2C+De+F%3BZhang%2C+Jun%3BCao%2C+Xiaoguang%3BChew%2C+Emily+Y%3BChan%2C+Chi-Chao&rft.aulast=Ramkumar&rft.aufirst=Hema&rft.date=2013-07-01&rft.volume=143&rft.issue=7&rft.spage=1129&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutrition&rft.issn=1541-6100&rft_id=info:doi/10.3945%2Fjn.112.169649
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-26
N1  - Date created - 2013-06-21
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Curr Pharm Des. 2012;18(1):51-6 [22211688]
Invest Ophthalmol Vis Sci. 2011 Aug;52(9):6898-910 [21757580]
Invest Ophthalmol Vis Sci. 2012;53(6):2921-7 [22447858]
PLoS One. 2012;7(5):e36949 [22615852]
J Neuroinflammation. 2012;9:59 [22452753]
Ophthalmology. 2012 Nov;119(11):2282-9 [22840421]
Invest Ophthalmol Vis Sci. 2012 Nov;53(12):7718-26 [23099493]
Synapse. 2013 Aug;67(8):515-31 [23592324]
J Ocul Pharmacol Ther. 2001 Apr;17(2):189-98 [11324986]
Arch Ophthalmol. 2001 Oct;119(10):1417-36 [11594942]
Br J Ophthalmol. 2003 Apr;87(4):481-7 [12642315]
J Nutr. 2003 Apr;133(4):992-8 [12672909]
Prog Retin Eye Res. 2010 May;29(3):169-90 [20206286]
Optometry. 2004 Apr;75(4):216-30 [15117055]
Nature. 1993 Feb 25;361(6414):724-6 [8441466]
J Nutr. 1993 Nov;123(11):1939-51 [8229312]
Adv Pharmacol. 1995;34:323-42 [8562443]
J Biol Chem. 1996 Aug 23;271(34):20507-15 [8702792]
Invest Ophthalmol Vis Sci. 1996 Oct;37(11):2243-57 [8843911]
J Clin Invest. 1997 Jun 1;99(11):2625-34 [9169492]
J Clin Invest. 1997 Dec 15;100(12):3131-9 [9399960]
Biochemistry. 1999 Jan 5;38(1):185-90 [9890897]
J Biol Chem. 1957 May;226(1):497-509 [13428781]
Prog Retin Eye Res. 2005 Jan;24(1):87-138 [15555528]
Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4164-9 [15749821]
Arch Ophthalmol. 2006 Aug;124(8):1151-62 [16908818]
Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3827-36 [17652758]
Arch Ophthalmol. 2007 Sep;125(9):1225-32 [17846363]
Ophthalmology. 2008 Feb;115(2):324-333.e2 [17716735]
Exp Eye Res. 2008 Apr;86(4):675-83 [18308304]
Ophthalmic Res. 2008;40(3-4):124-8 [18421225]
Prog Retin Eye Res. 2008 Jul;27(4):372-90 [18621565]
Invest Ophthalmol Vis Sci. 2008 Sep;49(9):3864-9 [18450596]
Arch Ophthalmol. 2008 Sep;126(9):1274-9 [18779490]
Arch Ophthalmol. 2009 Jan;127(1):110-2 [19139352]
Prog Retin Eye Res. 2009 Jan;28(1):1-18 [19026761]
Arch Ophthalmol. 2009 May;127(5):656-65 [19433717]
J Cell Physiol. 2009 Aug;220(2):469-75 [19418485]
Am J Pathol. 2009 Aug;175(2):799-807 [19608872]
Br J Ophthalmol. 2009 Sep;93(9):1241-6 [19508997]
Exp Eye Res. 2010 Jan;90(1):155-67 [19836390]
Semin Ophthalmol. 2011 May;26(3):131-6 [21609225]
Invest Ophthalmol Vis Sci. 2011 May;52(6):2897-904 [21245403]
Am J Pathol. 2011 May;178(5):2416-23 [21514452]
Invest Ophthalmol Vis Sci. 2011 Mar;52(3):1384-91 [21402953]
Invest Ophthalmol Vis Sci. 2010 Sep;51(9):4738-45 [20393113]
Adv Exp Med Biol. 2010;703:63-74 [20711707]
Proc Natl Acad Sci U S A. 2010 Apr 20;107(16):7275-80 [20368460]
Braz J Med Biol Res. 2003 Apr;36(4):433-46 [12700820]
Neurobiol Aging. 2012 Feb;33(2):433.e1-10 [21397984]
PLoS One. 2012;7(4):e35551 [22545116]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.3945/jn.112.169649
ER  - 



TY  - JOUR
T1  - Antiherpetic medication use and the risk of gastroschisis: findings from the National Birth Defects Prevention Study, 1997-2007.
AN  - 1369716895; 23772935
AB  - Previous studies examining the teratogenic effects of antiherpetic medications have found no associations for birth defects overall but have not examined the risk of specific birth defects.
          The National Birth Defects Prevention Study ascertains population-based cases with birth defects and live-born controls without birth defects in 10 states across the United States for the purpose of identifying potential teratogenic risk factors. Mothers of cases and controls are interviewed within 2 years of their estimated date of delivery about demographic, medical and behavioural factors before and during pregnancy. This analysis examined the possible association between use of antiherpetic medications (acyclovir, valacyclovir or famciclovir) during early pregnancy and gastroschisis, a birth defect of the abdominal wall. The mothers of 1.1% (n = 10) of 941 gastroschisis cases and 0.3% (n = 27) of 8339 controls reported antiherpetic medication use during the month before conception through the third month of pregnancy. The adjusted odds ratios for such use in relation to gastroschisis were 4.7 [95% confidence interval 1.7, 13.3] and 4.7 [95% CI 1.2, 19.0] among women with and without self-reported genital herpes, respectively, when compared with women without antiherpetic use or herpes. Among women reporting no antiherpetic medication use, the odds ratio for self-reported genital herpes in relation to gastroschisis was 3.0 [95% CI 1.6, 5.7]. Our study raises the possibility of an increased risk of gastroschisis because of either antiherpetic medication use during early pregnancy or the underlying genital herpes infection for which it was indicated.
          © 2013 John Wiley & Sons Ltd.
JF  - Paediatric and perinatal epidemiology
AU  - Ahrens, Katherine A
AU  - Anderka, Marlene T
AU  - Feldkamp, Marcia L
AU  - Canfield, Mark A
AU  - Mitchell, Allen A
AU  - Werler, Martha M
AU  - National Birth Defects Prevention Study
AD  - Slone Epidemiology Center, Boston University, USA. katherine.ahrens@nih.gov ; National Birth Defects Prevention Study
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 340
EP  - 345
VL  - 27
IS  - 4
KW  - Antiviral Agents
KW  - 0
KW  - 2-Aminopurine
KW  - 452-06-2
KW  - Valine
KW  - HG18B9YRS7
KW  - valacyclovir
KW  - MZ1IW7Q79D
KW  - famciclovir
KW  - QIC03ANI02
KW  - Acyclovir
KW  - X4HES1O11F
KW  - Index Medicus
KW  - Young Adult
KW  - Regression Analysis
KW  - Humans
KW  - Infant, Newborn
KW  - Valine -- adverse effects
KW  - Acyclovir -- adverse effects
KW  - Pregnancy
KW  - 2-Aminopurine -- adverse effects
KW  - Adult
KW  - Case-Control Studies
KW  - Valine -- analogs & derivatives
KW  - Middle Aged
KW  - 2-Aminopurine -- analogs & derivatives
KW  - Adolescent
KW  - United States -- epidemiology
KW  - Acyclovir -- analogs & derivatives
KW  - Female
KW  - Maternal Exposure -- adverse effects
KW  - Herpes Simplex -- drug therapy
KW  - Gastroschisis -- epidemiology
KW  - Gastroschisis -- chemically induced
KW  - Antiviral Agents -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369716895?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Paediatric+and+perinatal+epidemiology&rft.atitle=Antiherpetic+medication+use+and+the+risk+of+gastroschisis%3A+findings+from+the+National+Birth+Defects+Prevention+Study%2C+1997-2007.&rft.au=Ahrens%2C+Katherine+A%3BAnderka%2C+Marlene+T%3BFeldkamp%2C+Marcia+L%3BCanfield%2C+Mark+A%3BMitchell%2C+Allen+A%3BWerler%2C+Martha+M%3BNational+Birth+Defects+Prevention+Study&rft.aulast=Ahrens&rft.aufirst=Katherine&rft.date=2013-07-01&rft.volume=27&rft.issue=4&rft.spage=340&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+perinatal+epidemiology&rft.issn=1365-3016&rft_id=info:doi/10.1111%2Fppe.12064
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-04
N1  - Date created - 2013-06-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Birth Defects Res A Clin Mol Teratol. 2003 Mar;67(3):193-201 [12797461]
Public Health Rep. 2001;116 Suppl 1:32-40 [11889273]
Birth Defects Res A Clin Mol Teratol. 2004 Apr;70(4):201-7 [15108247]
Am J Surg. 1986 May;151(5):546-9 [2939736]
Teratology. 1987 Apr;35(2):203-10 [2955538]
Arch Toxicol. 1988;61(6):468-79 [3190444]
Br J Obstet Gynaecol. 1998 Aug;105(8):882-9 [9746382]
Birth Defects Res A Clin Mol Teratol. 2006 Nov;76(11):747-56 [17051527]
Am J Med Genet C Semin Med Genet. 2008 Aug 15;148C(3):162-79 [18655097]
Am J Med Genet C Semin Med Genet. 2008 Aug 15;148C(3):199-212 [18655102]
Am J Med Genet C Semin Med Genet. 2008 Aug 15;148C(3):155-61 [18655105]
Handb Exp Pharmacol. 2009;(189):53-84 [19048197]
Birth Defects Res A Clin Mol Teratol. 2010 Feb;88(2):71-5 [19937602]
JAMA. 2010 Aug 25;304(8):859-66 [20736469]
Birth Defects Res A Clin Mol Teratol. 2010 Dec;88(12):1008-16 [20878909]
Am J Obstet Gynecol. 2011 Jul;205(1):51.e1-8 [21514558]
Scand J Infect Dis. 2003;35(4):255-9 [12839155]
Am J Obstet Gynecol. 2000 Jan;182(1 Pt 1):159-63 [10649172]
Comment In:
Paediatr Perinat Epidemiol. 2013 Nov;27(6):610 [24134529]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/ppe.12064
ER  - 



TY  - JOUR
T1  - Pharmacogenetics of drugs used in the treatment of ocular inflammatory diseases.
AN  - 1369233816; 23521173
AB  - Ocular inflammatory diseases comprise uveitis, scleritis, and inflammation of adjacent structures of the eye. Therapy may be challenging and often involves corticosteroids and immunomodulatory agents.
          This review describes the genes involved in noninfectious ocular inflammatory diseases and focuses on pharmacogenetic studies regarding different classes of anti-inflammatory drugs used in the management of uveitis, including corticosteroids, antimetabolites, calcineurin inhibitors, alkylating agents, and biological agents. Pharmacogenetics holds the promise of a personalized medicine with potential to customize treatment that can achieve the best clinical response and avoid toxicity. Several polymorphisms in various genes involved in the metabolism of drugs commonly utilized in the treatment of ocular inflammatory diseases have been described. Most promising is the polymorphism in thiopurinemethyltransferase gene for which a genotype analysis can reveal slow metabolizers of azathioprine and help avoid serious drug toxicity. Although pharmacogenetic studies with specific focus on ocular inflammatory diseases are lacking, knowledge from studies in rheumatologic diseases and transplant medicine can provide a platform for future research. Prospective clinical studies are needed to determine the clinical significance of such polymorphisms and their true effect on drug metabolism and side effects.
JF  - Expert opinion on drug metabolism & toxicology
AU  - Lima, Breno R
AU  - Nussenblatt, Robert B
AU  - Sen, H Nida
AD  - National Eye Institute, National Institutes of Health, Laboratory of Immunology, Bethesda, MD 20892, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 875
EP  - 882
VL  - 9
IS  - 7
KW  - Adrenal Cortex Hormones
KW  - 0
KW  - Alkylating Agents
KW  - Anti-Inflammatory Agents
KW  - Antimetabolites
KW  - Methyltransferases
KW  - EC 2.1.1.-
KW  - thiopurine methyltransferase
KW  - EC 2.1.1.67
KW  - Azathioprine
KW  - MRK240IY2L
KW  - Index Medicus
KW  - Methyltransferases -- genetics
KW  - Azathioprine -- adverse effects
KW  - Polymorphism, Genetic
KW  - Methyltransferases -- antagonists & inhibitors
KW  - Humans
KW  - Adrenal Cortex Hormones -- adverse effects
KW  - Adrenal Cortex Hormones -- administration & dosage
KW  - Antimetabolites -- adverse effects
KW  - Azathioprine -- administration & dosage
KW  - Scleritis -- genetics
KW  - Treatment Outcome
KW  - Antimetabolites -- administration & dosage
KW  - Methyltransferases -- metabolism
KW  - Scleritis -- drug therapy
KW  - Alkylating Agents -- adverse effects
KW  - Alkylating Agents -- administration & dosage
KW  - Uveitis -- genetics
KW  - Anti-Inflammatory Agents -- adverse effects
KW  - Inflammation -- drug therapy
KW  - Anti-Inflammatory Agents -- administration & dosage
KW  - Uveitis -- drug therapy
KW  - Pharmacogenetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369233816?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+metabolism+%26+toxicology&rft.atitle=Pharmacogenetics+of+drugs+used+in+the+treatment+of+ocular+inflammatory+diseases.&rft.au=Lima%2C+Breno+R%3BNussenblatt%2C+Robert+B%3BSen%2C+H+Nida&rft.aulast=Lima&rft.aufirst=Breno&rft.date=2013-07-01&rft.volume=9&rft.issue=7&rft.spage=875&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+metabolism+%26+toxicology&rft.issn=1744-7607&rft_id=info:doi/10.1517%2F17425255.2013.783818
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-04
N1  - Date created - 2013-06-17
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1517/17425255.2013.783818
ER  - 



TY  - JOUR
T1  - Integrated therapeutic approaches in the treatment of locally advanced non-small cell lung cancer.
AN  - 1369232523; 23272968
AB  - Treatment of locally advanced non-small cell lung cancer (NSCLC) remains a significant challenge for oncologists, despite progress made in recent years in early diagnosis and therapy. This review focuses on integrated therapeutic approaches of patients with locally advanced NSCLC, summarizing the available evidence for patients with potentially resectable disease (stage IIIA-0/3) and with unresectable disease (stage IIIA-4/IIIB) and discussing several key questions related to the use of integrated approaches in NSCLC. Based on current evidence, neoadjuvant platinum-based combination chemotherapy is a treatment option in patients with potentially resectable stage IIIA-0/3: a 2-drug combination of platinum combined with a third-generation drug seems preferable, and at least 3 cycles of chemotherapy should be administered. There are no definitive evidences of clear superiority of surgery compared to radiotherapy for patients obtaining a response with neoadjuvant treatment: however, surgery is associated with a better local control, and subgroup analyses of randomized trials suggest improved outcome in patients in whom a complete resection could be obtained with a lobectomy, avoiding the increased surgical mortality associated with pneumonectomy. Standard treatment for patients with locally advanced, unresectable NSCLC is currently represented by combination of chemotherapy and radiotherapy. Concomitant approach has been proven superior to the sequential administration, although it is associated with higher risk of toxicity. All patients should be evaluated by a multidisciplinary team, skilled in multimodality treatment and should be counselled about risks and potential benefits of the different therapeutic approaches.
JF  - Anti-cancer agents in medicinal chemistry
AU  - Di Maio, Massimo
AU  - Costanzo, Raffaele
AU  - Giordano, Pasqualina
AU  - Piccirillo, Maria Carmela
AU  - Sandomenico, Claudia
AU  - Montanino, Agnese
AU  - Carillio, Guido
AU  - Muto, Paolo
AU  - Jones, David R
AU  - Daniele, Gennaro
AU  - Perrone, Francesco
AU  - Rocco, Gaetano
AU  - Morabito, Alessandro
AD  - Medical Oncology, Thoraco- Pulmonary Department, National Cancer Institute, Via Mariano Semmola, Naples, Italy.
Y1  - 2013/07/01/
PY  - 2013
DA  - 2013 Jul 01
SP  - 844
EP  - 851
VL  - 13
IS  - 6
KW  - Index Medicus
KW  - Humans
KW  - Combined Modality Therapy -- methods
KW  - Lung Neoplasms -- therapy
KW  - Lung -- pathology
KW  - Carcinoma, Non-Small-Cell Lung -- therapy
KW  - Lung Neoplasms -- pathology
KW  - Carcinoma, Non-Small-Cell Lung -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369232523?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Integrated+therapeutic+approaches+in+the+treatment+of+locally+advanced+non-small+cell+lung+cancer.&rft.au=Di+Maio%2C+Massimo%3BCostanzo%2C+Raffaele%3BGiordano%2C+Pasqualina%3BPiccirillo%2C+Maria+Carmela%3BSandomenico%2C+Claudia%3BMontanino%2C+Agnese%3BCarillio%2C+Guido%3BMuto%2C+Paolo%3BJones%2C+David+R%3BDaniele%2C+Gennaro%3BPerrone%2C+Francesco%3BRocco%2C+Gaetano%3BMorabito%2C+Alessandro&rft.aulast=Di+Maio&rft.aufirst=Massimo&rft.date=2013-07-01&rft.volume=13&rft.issue=6&rft.spage=844&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 - 2014-01-08
N1  - Date created - 2013-06-17
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
ER  - 



TY  - JOUR
T1  - Individualized therapy for metastatic colorectal cancer.
AN  - 1367880911; 23527888
AB  - Systemic therapeutic efficacy is central to determining the outcome of patients with metastatic colorectal cancer (CRC). In these patients, there is a critical need for predictive biomarkers to optimize efficacy whilst minimizing toxicity. The integration of a new generation of molecularly targeted drugs into the treatment of CRC, coupled with the development of sophisticated technologies for individual tumours as well as patient molecular profiling, underlines the potential for personalized medicine. In this review, we focus on the latest progress made within the genomic and proteomic fields, concerning predictive biomarkers for individualized therapy in metastatic CRC.
          © 2013 The Association for the Publication of the Journal of Internal Medicine.
JF  - Journal of internal medicine
AU  - Silvestri, A
AU  - Pin, E
AU  - Huijbers, A
AU  - Pellicani, R
AU  - Parasido, E M
AU  - Pierobon, M
AU  - Petricoin, E
AU  - Liotta, L
AU  - Belluco, C
AD  - Division of Experimental Oncology 2, CRO-IRCCS, National Cancer Institute, Aviano, Italy.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 1
EP  - 24
VL  - 274
IS  - 1
KW  - Antineoplastic Agents
KW  - 0
KW  - Biomarkers, Tumor
KW  - Chromogenic Compounds
KW  - KRAS protein, human
KW  - Proto-Oncogene Proteins
KW  - Phosphatidylinositol 3-Kinases
KW  - EC 2.7.1.-
KW  - PIK3CA protein, human
KW  - EC 2.7.1.137
KW  - EGFR protein, human
KW  - EC 2.7.10.1
KW  - Receptor, Epidermal Growth Factor
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  - Proto-Oncogene Proteins p21(ras)
KW  - EC 3.6.5.2
KW  - ras Proteins
KW  - Index Medicus
KW  - ras Proteins -- genetics
KW  - Phosphatidylinositol 3-Kinases -- genetics
KW  - Animals
KW  - Polymorphism, Single Nucleotide
KW  - DNA Mutational Analysis
KW  - Humans
KW  - Prognosis
KW  - In Situ Hybridization, Fluorescence
KW  - Predictive Value of Tests
KW  - Interdisciplinary Communication
KW  - PTEN Phosphohydrolase -- genetics
KW  - Proto-Oncogene Proteins B-raf -- genetics
KW  - Gene Expression Regulation, Neoplastic
KW  - Polymerase Chain Reaction
KW  - Gene Expression Profiling
KW  - Loss of Heterozygosity
KW  - Receptor, Epidermal Growth Factor -- genetics
KW  - Polymorphism, Restriction Fragment Length
KW  - In Situ Hybridization -- methods
KW  - Genomics
KW  - Proteomics -- methods
KW  - Biomarkers, Tumor -- genetics
KW  - Proto-Oncogene Proteins -- drug effects
KW  - Proteomics -- trends
KW  - Colorectal Neoplasms -- pathology
KW  - Precision Medicine -- methods
KW  - Proto-Oncogene Proteins -- metabolism
KW  - Precision Medicine -- trends
KW  - Molecular Targeted Therapy -- methods
KW  - Colorectal Neoplasms -- genetics
KW  - Proto-Oncogene Proteins -- genetics
KW  - Colorectal Neoplasms -- drug therapy
KW  - Antineoplastic Agents -- pharmacology
KW  - Molecular Targeted Therapy -- trends
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367880911?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Individualized+therapy+for+metastatic+colorectal+cancer.&rft.au=Silvestri%2C+A%3BPin%2C+E%3BHuijbers%2C+A%3BPellicani%2C+R%3BParasido%2C+E+M%3BPierobon%2C+M%3BPetricoin%2C+E%3BLiotta%2C+L%3BBelluco%2C+C&rft.aulast=Silvestri&rft.aufirst=A&rft.date=2013-07-01&rft.volume=274&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+internal+medicine&rft.issn=1365-2796&rft_id=info:doi/10.1111%2Fjoim.12070
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-09
N1  - Date created - 2013-06-13
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1111/joim.12070
ER  - 



TY  - JOUR
T1  - The tellurium redox immunomodulating compound AS101 inhibits IL-1β-activated inflammation in the human retinal pigment epithelium.
AN  - 1367877300; 23624272
AB  - AS101 is a non-toxic organotellurium-IV compound with demonstrated immunomodulating activity in vitro and in vivo. Inflammatory responses are attributed to the pathophysiology of numerous ocular diseases. In this study, we wished to elucidate whether AS101 could mitigate pro-inflammatory activity in human retinal pigment epithelial (RPE) cells, which are heavily involved in ocular immune responses, induced by pro-inflammatory IL-β activity.
          Primary and transformed RPE cells treated with varying concentrations of AS101 were used in this study. Real-time PCR and ELISA assays were used to detect cytokine/chemokine mRNA expression and protein production. Western blot was used to detect changes in the NFκB pathway. Cell viability and proliferation were detected using a Vi-Cell XR cell counter. To measure the cytoprotective capacity of AS101, cell numbers were compared between cells treated with IL-1β or lipopolysaccharide (LPS) and cells treated with IL-1β or LPS in the presence of AS101. AS101 inhibited IL-1β-induced mRNA expression and protein production of IL-6 and IL-8 in RPE cells. The viability of RPE cells treated with IL-1β and LPS was unaffected. AS101 slightly inhibited RPE cell growth in the presence of higher levels of IL-1β. Also, AS101 downregulated the IL-1β activity by inhibiting the phosphorylation of p65, an NFκB subunit.
          The results demonstrate that AS101 reduces IL-1β-induced inflammatory responses in the RPE. In previous studies, AS101 exhibited therapeutic effects in various disease models and was a safe profile in clinical trials. These results suggest that AS101 may have potent anti-inflammatory potential in the eye and confer the downregulation of RPE inflammatory responses in a pathological environment.
JF  - The British journal of ophthalmology
AU  - Ling, Diamond
AU  - Liu, Baoying
AU  - Jawad, Shayma
AU  - Thompson, Ian A
AU  - Nagineni, Chandrasekharam N
AU  - Dailey, Jennifer
AU  - Chien, Jason
AU  - Sredni, Benjamin
AU  - Nussenblatt, Robert B
AD  - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 934
EP  - 938
VL  - 97
IS  - 7
KW  - Adjuvants, Immunologic
KW  - 0
KW  - Angiogenesis Inhibitors
KW  - Cytokines
KW  - Ethylenes
KW  - Interleukin-1beta
KW  - NF-kappa B
KW  - RNA, Messenger
KW  - ammonium trichloro(dioxoethylene-O,O'-)tellurate
KW  - Index Medicus
KW  - Immunology
KW  - Inflammation
KW  - Real-Time Polymerase Chain Reaction
KW  - Cytokines -- genetics
KW  - Cell Count
KW  - Dose-Response Relationship, Drug
KW  - Electrophoresis, Polyacrylamide Gel
KW  - Humans
KW  - Tissue Donors
KW  - Oxidation-Reduction
KW  - Blotting, Western
KW  - Inflammation -- prevention & control
KW  - RNA, Messenger -- metabolism
KW  - Cells, Cultured
KW  - Adult
KW  - Enzyme-Linked Immunosorbent Assay
KW  - Inflammation -- metabolism
KW  - Cell Line, Transformed
KW  - NF-kappa B -- metabolism
KW  - Angiogenesis Inhibitors -- pharmacology
KW  - Retinal Pigment Epithelium -- metabolism
KW  - Interleukin-1beta -- antagonists & inhibitors
KW  - Retinal Pigment Epithelium -- drug effects
KW  - Interleukin-1beta -- pharmacology
KW  - Adjuvants, Immunologic -- pharmacology
KW  - Ethylenes -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367877300?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+British+journal+of+ophthalmology&rft.atitle=The+tellurium+redox+immunomodulating+compound+AS101+inhibits+IL-1%CE%B2-activated+inflammation+in+the+human+retinal+pigment+epithelium.&rft.au=Ling%2C+Diamond%3BLiu%2C+Baoying%3BJawad%2C+Shayma%3BThompson%2C+Ian+A%3BNagineni%2C+Chandrasekharam+N%3BDailey%2C+Jennifer%3BChien%2C+Jason%3BSredni%2C+Benjamin%3BNussenblatt%2C+Robert+B&rft.aulast=Ling&rft.aufirst=Diamond&rft.date=2013-07-01&rft.volume=97&rft.issue=7&rft.spage=934&rft.isbn=&rft.btitle=&rft.title=The+British+journal+of+ophthalmology&rft.issn=1468-2079&rft_id=info:doi/10.1136%2Fbjophthalmol-2012-301962
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-23
N1  - Date created - 2013-06-13
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1136/bjophthalmol-2012-301962
ER  - 



TY  - JOUR
T1  - Randomized phase III trial of gemcitabine and cisplatin vs. gemcitabine alone in patients with advanced non-small cell lung cancer and a performance status of 2: the CAPPA-2 study.
AN  - 1366579947; 23643177
AB  - Platinum-based chemotherapy is the standard treatment for patients with advanced non-small cell lung cancer (NSCLC), but the evidence of its efficacy among ECOG performance status (PS)2 patients is weak because these patients are usually excluded from clinical trials; concern exists about tolerability and feasibility of standard chemotherapy in these patients. No prospective randomized trial has tested the addition of cisplatin to single-agent chemotherapy in patients with advanced NSCLC and PS2. CAPPA-2 was a multicenter, randomized phase 3 study for first-line treatment of PS2 patients with advanced NSCLC. Patients, aged 18-70, were eligible if they had stage IV or IIIB with malignant pleural effusion or metastatic supraclavicular nodes (TNM VI edition) and adequate organ function. Patients in standard arm received gemcitabine 1200 mg/m(2) days 1 and 8. Patients in experimental arm received cisplatin 60 mg/m(2) day 1 plus gemcitabine 1000 mg/m(2) days 1 and 8. All treatments were repeated every 3 weeks, up to 4 cycles, unless disease progression or unacceptable toxicity. Primary endpoint was overall survival (OS). To have 80% power of detecting hazard ratio (HR) 0.71, corresponding to an increase in median OS from 4.8 to 6.8 months, 285 deaths were required. The study was stopped in June 2012 after the enrolment of 57 patients, due to the slow accrual and the report of positive results from a similar study. Median OS was 3.0 months with single-agent gemcitabine and 5.9 months with cisplatin plus gemcitabine (HR 0.52, 95% CI 0.28-0.98, p = 0.039). Combination chemotherapy produced longer PFS (median 1.7 vs. 3.3 months, HR 0.49, 95% CI 0.27-0.89, p = 0.017) and higher response rate (4% vs. 18%, p = 0.19), without substantial increase in toxicity. The addition of cisplatin to single-agent gemcitabine improves survival as first-line treatment of PS2 patients with advanced NSCLC.
          Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
JF  - Lung cancer (Amsterdam, Netherlands)
AU  - Morabito, Alessandro
AU  - Gebbia, Vittorio
AU  - Di Maio, Massimo
AU  - Cinieri, Saverio
AU  - Viganò, Maria Grazia
AU  - Bianco, Roberto
AU  - Barbera, Santi
AU  - Cavanna, Luigi
AU  - De Marinis, Filippo
AU  - Montesarchio, Vincenzo
AU  - Costanzo, Raffaele
AU  - Sandomenico, Claudia
AU  - Montanino, Agnese
AU  - Mancuso, Gianfranco
AU  - Russo, Paolo
AU  - Nacci, Angelo
AU  - Giordano, Pasqualina
AU  - Daniele, Gennaro
AU  - Piccirillo, Maria Carmela
AU  - Rocco, Gaetano
AU  - Gridelli, Cesare
AU  - Gallo, Ciro
AU  - Perrone, Francesco
AD  - National Cancer Institute, G. Pascale, Foundation, via M. Semmola, 80131 Napoli, Italy.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 77
EP  - 83
VL  - 81
IS  - 1
KW  - Deoxycytidine
KW  - 0W860991D6
KW  - gemcitabine
KW  - B76N6SBZ8R
KW  - Cisplatin
KW  - Q20Q21Q62J
KW  - Index Medicus
KW  - Young Adult
KW  - Cisplatin -- therapeutic use
KW  - Humans
KW  - Adult
KW  - Treatment Outcome
KW  - Aged
KW  - Middle Aged
KW  - Adolescent
KW  - Male
KW  - Female
KW  - Cisplatin -- administration & dosage
KW  - Deoxycytidine -- adverse effects
KW  - Carcinoma, Non-Small-Cell Lung -- mortality
KW  - Deoxycytidine -- analogs & derivatives
KW  - Lung Neoplasms -- drug therapy
KW  - Deoxycytidine -- therapeutic use
KW  - Deoxycytidine -- administration & dosage
KW  - Lung Neoplasms -- mortality
KW  - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Carcinoma, Non-Small-Cell Lung -- drug therapy
KW  - Lung Neoplasms -- pathology
KW  - Carcinoma, Non-Small-Cell Lung -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1366579947?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Randomized+phase+III+trial+of+gemcitabine+and+cisplatin+vs.+gemcitabine+alone+in+patients+with+advanced+non-small+cell+lung+cancer+and+a+performance+status+of+2%3A+the+CAPPA-2+study.&rft.au=Morabito%2C+Alessandro%3BGebbia%2C+Vittorio%3BDi+Maio%2C+Massimo%3BCinieri%2C+Saverio%3BVigan%C3%B2%2C+Maria+Grazia%3BBianco%2C+Roberto%3BBarbera%2C+Santi%3BCavanna%2C+Luigi%3BDe+Marinis%2C+Filippo%3BMontesarchio%2C+Vincenzo%3BCostanzo%2C+Raffaele%3BSandomenico%2C+Claudia%3BMontanino%2C+Agnese%3BMancuso%2C+Gianfranco%3BRusso%2C+Paolo%3BNacci%2C+Angelo%3BGiordano%2C+Pasqualina%3BDaniele%2C+Gennaro%3BPiccirillo%2C+Maria+Carmela%3BRocco%2C+Gaetano%3BGridelli%2C+Cesare%3BGallo%2C+Ciro%3BPerrone%2C+Francesco&rft.aulast=Morabito&rft.aufirst=Alessandro&rft.date=2013-07-01&rft.volume=81&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.issn=1872-8332&rft_id=info:doi/10.1016%2Fj.lungcan.2013.04.008
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-21
N1  - Date created - 2013-06-10
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.lungcan.2013.04.008
ER  - 



TY  - JOUR
T1  - Analyses of the combination of 6-MP and dasatinib in cell culture.
AN  - 1355480759; 23652925
AB  - A major tenet of cancer therapeutics is that combinations of anticancer agents with different mechanisms of action and different toxicities may be effective treatment regimens. Evaluation of additivity/synergy in cell culture may be used to identify drug combination opportunities and to assess risk of additive/synergistic toxicity. The combination of 6-mercaptopurine and dasatinib was assessed for additivity/synergy using the combination index (CI) method and a response surface method in six human tumor cell lines including MCF-7 and MDA-MB‑468 breast cancer, NCI-H23 and NCI-H460 non‑small cell lung cancer, and A498 and 786-O renal cell cancer, based on two experimental end‑points: ATP content and colony formation. Clonal colony formation by human bone marrow CFU-GM was used to assess risk of enhanced toxicity. The concentration ranges tested for each drug were selected to encompass the clinical Cmax concentrations. The combination regimens were found to be additive to sub‑additive by both methods of data analysis, but synergy was not detected. The non-small cell lung cancer cell lines were the most responsive among the tumor lines tested and the renal cell carcinoma lines were the least responsive. The bone marrows CFU-GM were more sensitive to the combination regimens than were the tumor cell lines. Based upon these data, it appears that the possibility of enhanced efficacy from combining 6-mercaptopurine (6-MP) and dasatinib would be associated with increased risk of severe bone marrow toxicity, so the combination is unlikely to provide a therapeutic advantage for treating solid tumor patients where adequate bone marrow function must be preserved.
JF  - International journal of oncology
AU  - Kaur, Gurmeet
AU  - Behrsing, Holger
AU  - Parchment, Ralph E
AU  - Millin, Myrtle Davis
AU  - Teicher, Beverly A
AD  - Molecular Pharmacology Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. kaurgu@mail.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 13
EP  - 22
VL  - 43
IS  - 1
KW  - Pyrimidines
KW  - 0
KW  - Thiazoles
KW  - 6-Mercaptopurine
KW  - E7WED276I5
KW  - Dasatinib
KW  - RBZ1571X5H
KW  - Index Medicus
KW  - MCF-7 Cells -- drug effects
KW  - Humans
KW  - In Vitro Techniques
KW  - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW  - Drug Synergism
KW  - Tumor Stem Cell Assay
KW  - Neoplasms -- drug therapy
KW  - Thiazoles -- administration & dosage
KW  - Pyrimidines -- toxicity
KW  - 6-Mercaptopurine -- toxicity
KW  - Thiazoles -- toxicity
KW  - 6-Mercaptopurine -- administration & dosage
KW  - Pyrimidines -- administration & dosage
KW  - Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1355480759?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+oncology&rft.atitle=Analyses+of+the+combination+of+6-MP+and+dasatinib+in+cell+culture.&rft.au=Kaur%2C+Gurmeet%3BBehrsing%2C+Holger%3BParchment%2C+Ralph+E%3BMillin%2C+Myrtle+Davis%3BTeicher%2C+Beverly+A&rft.aulast=Kaur&rft.aufirst=Gurmeet&rft.date=2013-07-01&rft.volume=43&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=International+journal+of+oncology&rft.issn=1791-2423&rft_id=info:doi/10.3892%2Fijo.2013.1930
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-07
N1  - Date created - 2013-05-24
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Mol Cancer Ther. 2003 Sep;2(9):929-32 [14555712]
Toxicol Sci. 2003 Oct;75(2):355-67 [12883091]
Clin Cancer Res. 2004 Oct 1;10(19):6722-31 [15475463]
Cancer Res. 1969 Dec;29(12):2292-9 [4905235]
J Natl Cancer Inst. 1973 Nov;51(5):1409-16 [4357757]
J Natl Cancer Inst. 1973 Nov;51(5):1417-23 [4357758]
Cancer Res. 1976 Oct;36(10):3779-83 [821607]
Cancer Res. 1997 Dec 1;57(23):5217-20 [9393737]
Pharm Res. 1998 Jul;15(7):1069-76 [9688062]
Blood. 1998 Nov 15;92(10):3569-77 [9808549]
Ann N Y Acad Sci. 1954 Dec 6;60(2):195-9 [14350523]
J Biol Chem. 1960 Feb;235:429-32 [14441085]
Cancer Res. 1965 May;25:539-43 [14297492]
Clin Cancer Res. 2004 Dec 1;10(23):7994-8004 [15585635]
Cancer Res. 2006 Apr 1;66(7):3351-4, discussion 3354 [16585151]
Br J Clin Pharmacol. 2006 Jul;62(1):15-26 [16842375]
Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952]
Clin Cancer Res. 2007 Jan 15;13(2 Pt 2):764s-769s [17255307]
Nat Biotechnol. 2007 Sep;25(9):1035-44 [17721511]
Nat Rev Cancer. 2008 Jan;8(1):24-36 [18097462]
Oncogene. 2008 Jul 17;27(31):4380-4 [18362889]
Mol Cancer Ther. 2008 Oct;7(10):3212-22 [18852125]
Mol Cell Proteomics. 2009 Dec;8(12):2796-808 [19651622]
Front Biosci (Elite Ed). 2010;2:241-9 [20036874]
Cancer Res. 2010 Jan 15;70(2):440-6 [20068163]
Nat Cell Biol. 2010 Dec;12(12):1166-76 [21076410]
J Clin Oncol. 2011 Mar 1;29(7):839-44 [21263099]
Bioorg Med Chem Lett. 2011 May 15;21(10):3152-8 [21450467]
Clin Cancer Res. 2012 Oct 1;18(19):5489-98 [22837181]
In Vitro. 1976 Sep;12(9):623-7 [1010528]
J Natl Cancer Inst. 1977 Feb;58(2):209-14 [833871]
In Vitro. 1978 Sep;14(9):779-86 [721102]
In Vitro. 1978 Nov;14(11):911-5 [730202]
Int J Radiat Oncol Biol Phys. 1979 Jan;5(1):85-91 [422420]
Cancer Res. 1980 Oct;40(10):3502-7 [6108156]
Biochem J. 1981 Mar 1;193(3):799-803 [6895465]
Cancer Res. 1983 Jun;43(6):2831-5 [6850594]
Cancer Res. 1985 Mar;45(3):1187-97 [2578876]
Science. 1989 Apr 7;244(4900):41-7 [2649979]
Science. 1989 Oct 27;246(4929):491-4 [2554494]
Nature. 1989 Dec 7;342(6250):705-8 [2531845]
Antiviral Res. 1990 Oct-Nov;14(4-5):181-205 [2088205]
Oncogene. 1992 Jan;7(1):171-80 [1311061]
Cancer Res. 1992 Aug 15;52(16):4558-60; author reply 4561-5 [1643648]
J Natl Cancer Inst. 1996 Jun 5;88(11):699-700 [8637018]
Cancer Chemother Pharmacol. 1997;39(5):467-72 [9054963]
Biochem J. 1997 Jun 15;324 ( Pt 3):761-75 [9210399]
Annu Rev Pharmacol Toxicol. 2003;43:199-231 [12195027]
Stat Med. 2003 Jul 15;22(13):2091-100 [12820275]
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7977-82 [12799470]
J Pharmacol Exp Ther. 2004 Sep;310(3):981-6 [15175417]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.3892/ijo.2013.1930
ER  - 



TY  - JOUR
T1  - Epigenetics and the adaptive immune response.
AN  - 1353484925; 22789989
AB  - Cells of the adaptive immune response undergo dynamic epigenetic changes as they develop and respond to immune challenge. Plasticity is a necessary prerequisite for the chromosomal dynamics of lineage specification, development, and the immune effector function of the mature cell types. The alterations in DNA methylation and histone modification that characterize activation may be integral to the generation of immunologic memory, thereby providing an advantage on secondary exposure to pathogens. While the immune system benefits from the dynamic nature of the epigenome, such benefit comes at a cost - increased likelihood of disease-causing mutation. Published by Elsevier Ltd.
JF  - Molecular aspects of medicine
AU  - Kondilis-Mangum, Hrisavgi D
AU  - Wade, Paul A
AD  - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
PY  - 2013
SP  - 813
EP  - 825
VL  - 34
IS  - 4
KW  - Histones
KW  - 0
KW  - DNA-Cytosine Methylases
KW  - EC 2.1.1.-
KW  - Index Medicus
KW  - Animals
KW  - V(D)J Recombination
KW  - DNA Methylation
KW  - Humans
KW  - Histones -- metabolism
KW  - Protein Processing, Post-Translational
KW  - DNA-Cytosine Methylases -- physiology
KW  - Immunologic Memory
KW  - T-Lymphocytes -- physiology
KW  - B-Lymphocytes -- physiology
KW  - Epigenesis, Genetic -- immunology
KW  - Adaptive Immunity -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1353484925?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epigenetics+and+the+adaptive+immune+response.&rft.au=Kondilis-Mangum%2C+Hrisavgi+D%3BWade%2C+Paul+A&rft.aulast=Kondilis-Mangum&rft.aufirst=Hrisavgi&rft.date=2013-07-01&rft.volume=34&rft.issue=4&rft.spage=813&rft.isbn=&rft.btitle=&rft.title=Molecular+aspects+of+medicine&rft.issn=1872-9452&rft_id=info:doi/10.1016%2Fj.mam.2012.06.008
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-09
N1  - Date created - 2013-05-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Cell. 2010 Nov 16;18(5):436-47 [21075309]
Semin Immunol. 2010 Dec;22(6):346-52 [20833065]
Nat Immunol. 2011 Jan;12(1):62-9 [21113164]
Mol Cell. 2002 Dec;10(6):1479-87 [12504021]
J Immunol. 2003 Sep 1;171(5):2510-6 [12928400]
Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11577-82 [14500909]
Nat Immunol. 2004 Mar;5(3):299-308 [14985713]
Genes Dev. 2004 Feb 15;18(4):411-22 [15004008]
J Immunol. 2004 Oct 1;173(7):4402-6 [15383570]
Proc Natl Acad Sci U S A. 1983 Sep;80(18):5559-63 [6577443]
J Mol Biol. 1988 Oct 20;203(4):971-83 [3210246]
Science. 1990 Jun 22;248(4962):1517-23 [2360047]
Cell. 1992 Jun 12;69(6):915-26 [1606615]
Cell. 1994 Jan 28;76(2):357-69 [8293469]
Cell. 1994 Oct 7;79(1):143-56 [7923373]
Immunity. 1997 Oct;7(4):505-15 [9354471]
Immunity. 2009 Jan 16;30(1):155-67 [19144320]
Immunology. 2009 Mar;126(3):299-305 [19178593]
Immunity. 2009 Apr 17;30(4):508-20 [19345119]
Curr Opin Immunol. 2009 Apr;21(2):133-9 [19362456]
Curr Opin Immunol. 2009 Apr;21(2):153-60 [19375293]
Cell. 2009 Jun 26;137(7):1194-211 [19563753]
J Exp Med. 2010 Dec 20;207(13):2809-16 [21115692]
Chembiochem. 2011 Jan 24;12(2):206-22 [21243710]
Immunity. 2011 Feb 25;34(2):175-87 [21349430]
Immunol Res. 2011 Apr;49(1-3):192-201 [21128009]
Nature. 2011 Mar 10;471(7337):189-95 [21390126]
Nat Genet. 2011 Apr;43(4):309-15 [21399634]
Nat Immunol. 2004 Mar;5(3):309-16 [14985714]
Adv Immunol. 2011;109:159-96 [21569915]
Cancer Cell. 2011 Jul 12;20(1):25-38 [21723201]
Nature. 2011 Aug 25;476(7361):467-71 [21832993]
Mol Biol Cell. 2011 Sep;22(17):3094-102 [21737684]
Cell. 2011 Sep 16;146(6):866-72 [21925312]
Blood. 2011 Sep 29;118(13):3559-69 [21828137]
Mol Cell. 2011 Oct 7;44(1):17-28 [21924933]
Annu Rev Genet. 2011;45:167-202 [21854230]
Genes Dev. 2011 Dec 1;25(23):2436-52 [22156206]
J Immunol. 2011 Dec 15;187(12):6374-81 [22079986]
N Engl J Med. 2012 Jan 5;366(1):95-6 [22216861]
Curr Opin Immunol. 2012 Apr;24(2):139-45 [22387323]
Trends Immunol. 2012 Apr;33(4):153-9 [22440186]
Curr Opin Genet Dev. 2012 Apr;22(2):148-55 [22440480]
Curr Opin Hematol. 2012 Jul;19(4):292-8 [22517589]
J Immunol. 2012 Jun 15;188(12):5811-7 [22675215]
Mol Cell Biol. 2012 Jul;32(13):2503-14 [22547680]
Cell Cycle. 2012 Mar 1;11(5):833-4 [22333594]
J Exp Med. 1999 Nov 15;190(10):1439-50 [10562319]
Science. 2000 Jan 21;287(5452):495-8 [10642553]
J Exp Med. 2000 Sep 4;192(5):625-36 [10974029]
Immunity. 2001 Jan;14(1):1-11 [11163225]
Curr Opin Genet Dev. 2001 Apr;11(2):124-9 [11250133]
J Exp Med. 1998 Jul 6;188(1):103-17 [9653088]
Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9488-93 [9689107]
Immunity. 1998 Aug;9(2):229-37 [9729043]
Immunity. 1998 Dec;9(6):765-75 [9881967]
Immunity. 1999 Mar;10(3):313-22 [10204487]
Immunity. 1999 Jul;11(1):1-10 [10435574]
J Immunol. 2004 Dec 15;173(12):7377-84 [15585862]
Nat Immunol. 2005 Jan;6(1):31-41 [15580273]
Nat Immunol. 2005 Feb;6(2):189-97 [15640803]
Annu Rev Immunol. 2005;23:601-49 [15771582]
Nat Immunol. 2005 May;6(5):481-9 [15806105]
J Exp Med. 2005 Aug 15;202(4):467-72 [16087716]
Science. 2006 Jan 20;311(5759):395-8 [16424344]
Immunol Rev. 2006 Feb;209:129-41 [16448539]
Curr Top Microbiol Immunol. 2005;290:49-85 [16480039]
Curr Opin Genet Dev. 2006 Apr;16(2):104-11 [16504499]
Annu Rev Immunol. 2006;24:607-56 [16551261]
J Immunol. 2006 Apr 15;176(8):4562-72 [16585546]
Immunity. 2006 Apr;24(4):369-79 [16618596]
Immunity. 2006 Apr;24(4):381-91 [16618597]
Adv Immunol. 2006;91:45-109 [16938538]
Science. 2007 Feb 23;315(5815):1141-3 [17322062]
Nat Immunol. 2007 Apr;8(4):378-87 [17334367]
Nat Immunol. 2007 Aug;8(8):809-16 [17589511]
Immunity. 2007 Oct;27(4):561-71 [17936034]
Nature. 2007 Dec 13;450(7172):1106-10 [18033247]
Structure. 2008 Mar;16(3):341-50 [18334209]
Cell. 2008 Apr 18;133(2):250-64 [18423197]
Cell. 2008 Apr 18;133(2):265-79 [18423198]
Nat Immunol. 2008 Aug;9(8):927-36 [18568028]
Nature. 2008 Aug 7;454(7205):766-70 [18600261]
Immunity. 2001 Nov;15(5):763-74 [11728338]
J Immunol. 2002 Mar 1;168(5):2316-24 [11859121]
Nat Immunol. 2002 Jul;3(7):643-51 [12055628]
J Immunol. 2002 Jul 15;169(2):647-50 [12097365]
J Biol Chem. 2002 Nov 1;277(44):42399-408 [12205084]
Nat Immunol. 2003 Jan;4(1):78-86 [12447360]
Cell. 2009 Aug 7;138(3):435-48 [19665968]
Adv Exp Med Biol. 2009;650:93-102 [19731804]
Adv Exp Med Biol. 2009;650:148-56 [19731808]
Nat Genet. 2009 Nov;41(11):1207-15 [19801979]
Nature. 2009 Nov 19;462(7271):315-22 [19829295]
Mol Cell. 2010 Jan 29;37(2):282-93 [20122409]
Curr Opin Immunol. 2010 Apr;22(2):177-84 [20207529]
Cell. 2010 Apr 30;141(3):419-31 [20398922]
J Immunol. 2010 Jun 15;184(12):6970-7 [20483751]
Cancer Sci. 2010 Jul;101(7):1722-30 [20398054]
Wiley Interdiscip Rev Syst Biol Med. 2010 Nov-Dec;2(6):640-53 [20890962]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.mam.2012.06.008
ER  - 



TY  - JOUR
T1  - A New Rapid Methodological Strategy to Assess BRCA Mutational Status
AN  - 1352296107; 18006316
AB  - Hereditary cancers account for approximately 10 % of breast and ovarian cancers. Mutations of the BRCA1 and BRCA2 genes, encoding two proteins involved in DNA repair, underlie most cases of such hereditary cancers. Women with BRCA mutations develop breast cancer in 50-80 % of cases and ovarian cancer in 10-40 % of cases. Assessing BRCA mutational status is needed to direct the clinical management of women with predisposition to these hereditary cancers. However, BRCA screening constitutes a bottleneck in terms of costs and time to deliver results. We developed a PCR-based assay using 73 primer pairs covering the entire coding regions of BRCA1 and BRCA2. PCR primers, containing at the 5' end the universal M13 primer sequences, were pre-spotted in 96-well plates. Following PCR, direct sequencing was performed using M13 primers, allowing to standardize the conditions. PCR amplification and sequencing were successful for each amplicon. We tested and validated the assay on 10 known gDNAs from patients with Hereditary breast and ovarian cancer (HBOC). Our strategy is a promising time and cost-effective method to detect BRCA mutations in the clinical setting, which is essential to formulate a personalized therapy for patients with HBOC.
JF  - Molecular Biotechnology
AU  - Vuttariello, Emilia
AU  - Borra, Marco
AU  - Calise, Celeste
AU  - Mauriello, Elvira
AU  - Greggi, Stefano
AU  - Vecchione, Aldo
AU  - Biffali, Elio
AU  - Chiappetta, Gennaro
AD  - Functional Genomic Unit, National Cancer Institute, Fondazione "G.Pascale", Via Mariano Semmola, 80131, Naples, Italy, chiappettagennaro@gmail.com
Y1  - 2013/07//
PY  - 2013
DA  - Jul 2013
SP  - 954
EP  - 960
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 54
IS  - 3
SN  - 1073-6085, 1073-6085
KW  - Biotechnology and Bioengineering Abstracts
KW  - Ovarian cancer
KW  - Breast cancer
KW  - Polymerase chain reaction
KW  - BRCA1 protein
KW  - Primers
KW  - BRCA2 protein
KW  - DNA repair
KW  - Mutation
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352296107?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Biotechnology&rft.atitle=A+New+Rapid+Methodological+Strategy+to+Assess+BRCA+Mutational+Status&rft.au=Vuttariello%2C+Emilia%3BBorra%2C+Marco%3BCalise%2C+Celeste%3BMauriello%2C+Elvira%3BGreggi%2C+Stefano%3BVecchione%2C+Aldo%3BBiffali%2C+Elio%3BChiappetta%2C+Gennaro&rft.aulast=Vuttariello&rft.aufirst=Emilia&rft.date=2013-07-01&rft.volume=54&rft.issue=3&rft.spage=954&rft.isbn=&rft.btitle=&rft.title=Molecular+Biotechnology&rft.issn=10736085&rft_id=info:doi/10.1007%2Fs12033-012-9646-0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Number of references - 22
N1  - Last updated - 2013-05-31
N1  - SubjectsTermNotLitGenreText - Ovarian cancer; BRCA1 protein; Polymerase chain reaction; Breast cancer; Primers; BRCA2 protein; DNA repair; Mutation
DO  - http://dx.doi.org/10.1007/s12033-012-9646-0
ER  - 



TY  - JOUR
T1  - Sulfite-mediated oxidation of myeloperoxidase to a free radical: immuno-spin trapping detection in human neutrophils.
AN  - 1350893768; 23376232
AB  - Previous studies focused on catalyzed oxidation of (bi)sulfite, leading to the formation of the reactive sulfur trioxide ((•)SO3(-)), peroxymonosulfate ((-)O3SOO(•)), and sulfate (SO4(•-)) anion radicals, which can damage target proteins and oxidize them to protein radicals. It is known that these very reactive sulfur- and oxygen-centered radicals can be formed by oxidation of (bi)sulfite by peroxidases. Myeloperoxidase (MPO), an abundant heme protein secreted from activated neutrophils that play a central role in host defense mechanisms, allergic reactions, and asthma, is a likely candidate for initiating the respiratory damage caused by sulfur dioxide. The objective of this study was to examine the oxidative damage caused by (bi)sulfite-derived free radicals in human neutrophils through formation of protein radicals. We used immuno-spin trapping and confocal microscopy to study the protein oxidations driven by sulfite-derived radicals. We found that the presence of sulfite can cause MPO-catalyzed oxidation of MPO to a protein radical in phorbol 12-myristate 13-acetate-activated human neutrophils. We trapped the MPO-derived radicals in situ using the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide and detected them immunologically as nitrone adducts in cells. Our present study demonstrates that myeloperoxidase initiates (bi)sulfite oxidation leading to MPO radical damage, possibly leading to (bi)sulfite-exacerbated allergic reactions.
          Published by Elsevier Inc.
JF  - Free radical biology & medicine
AU  - Ranguelova, Kalina
AU  - Rice, Annette B
AU  - Lardinois, Olivier M
AU  - Triquigneaux, Mathilde
AU  - Steinckwich, Natacha
AU  - Deterding, Leesa J
AU  - Garantziotis, Stavros
AU  - Mason, Ronald P
AD  - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 98
EP  - 106
VL  - 60
KW  - Free Radicals
KW  - 0
KW  - Peroxides
KW  - Phorbol Esters
KW  - Proteins
KW  - Sulfates
KW  - Sulfites
KW  - Sulfur Oxides
KW  - peroxymonosulfate
KW  - 22047-43-4
KW  - phorbol-12,13-diacetate
KW  - 24928-15-2
KW  - Peroxidase
KW  - EC 1.11.1.7
KW  - sulfur trioxide
KW  - HH2O7V4LYD
KW  - hydrogen sulfite
KW  - OJ9787WBLU
KW  - Index Medicus
KW  - Neutrophil Activation -- drug effects
KW  - Peroxides -- metabolism
KW  - Oxidation-Reduction -- drug effects
KW  - Sulfur Oxides -- metabolism
KW  - Humans
KW  - Peroxides -- toxicity
KW  - Sulfates -- chemistry
KW  - Sulfur Oxides -- chemistry
KW  - Proteins -- metabolism
KW  - Sulfates -- metabolism
KW  - Phorbol Esters -- pharmacology
KW  - Spin Trapping
KW  - Peroxides -- chemistry
KW  - Sulfates -- toxicity
KW  - Sulfur Oxides -- toxicity
KW  - Neutrophils -- metabolism
KW  - Neutrophils -- drug effects
KW  - Free Radicals -- toxicity
KW  - Hypersensitivity -- pathology
KW  - Sulfites -- toxicity
KW  - Peroxidase -- metabolism
KW  - Hypersensitivity -- etiology
KW  - Sulfites -- metabolism
KW  - Peroxidase -- drug effects
KW  - Free Radicals -- metabolism
KW  - Hypersensitivity -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1350893768?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sulfite-mediated+oxidation+of+myeloperoxidase+to+a+free+radical%3A+immuno-spin+trapping+detection+in+human+neutrophils.&rft.au=Ranguelova%2C+Kalina%3BRice%2C+Annette+B%3BLardinois%2C+Olivier+M%3BTriquigneaux%2C+Mathilde%3BSteinckwich%2C+Natacha%3BDeterding%2C+Leesa+J%3BGarantziotis%2C+Stavros%3BMason%2C+Ronald+P&rft.aulast=Ranguelova&rft.aufirst=Kalina&rft.date=2013-07-01&rft.volume=60&rft.issue=&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2013.01.022
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-01
N1  - Date created - 2013-05-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biochemistry. 1976 Jul 13;15(14):3059-63 [8081]
Environ Health Perspect. 1974 Aug;8:97-121 [4470921]
Clin Allergy. 1977 Sep;7(5):407-15 [412611]
Proc Natl Acad Sci U S A. 1980 Jun;77(6):3715-9 [6997882]
Food Cosmet Toxicol. 1981 Oct;19(5):667-82 [6171492]
J Biol Chem. 1982 May 10;257(9):5050-5 [6279657]
Mol Pharmacol. 1982 Nov;22(3):732-7 [6296662]
J Allergy Clin Immunol. 1984 Oct;74(4 Pt 1):469-72 [6491092]
J Leukoc Biol. 1985 Apr;37(4):431-47 [3855949]
Adv Food Res. 1986;30:1-76 [3526827]
Biochim Biophys Acta. 1986 Nov 4;853(1):65-89 [3021215]
CRC Crit Rev Toxicol. 1987;17(3):185-214 [3556020]
Arch Biochem Biophys. 1988 Dec;267(2):681-9 [2850769]
Chem Biol Interact. 2008 Aug 11;174(3):147-54 [18579106]
Biochemistry. 2008 Oct 28;47(43):11377-85 [18831539]
Free Radic Biol Med. 2010 Aug 1;49(3):317-22 [20406682]
J Biol Chem. 2010 Jul 30;285(31):24195-205 [20501663]
Free Radic Biol Med. 2012 Apr 15;52(8):1264-71 [22326772]
Eur J Biochem. 2000 Oct;267(19):5858-64 [10998045]
Ann Allergy. 1989 May;62(5):402-5 [2719349]
J Clin Invest. 1989 Jun;83(6):1785-93 [2656760]
J Biol Chem. 1990 Aug 15;265(23):13721-9 [2166041]
Am J Respir Cell Mol Biol. 1990 Nov;3(5):507-11 [2223105]
Free Radic Biol Med. 1990;9(3):235-43 [2272532]
Eur Respir J. 1990 Oct;3(9):987-8 [1963153]
Chest. 1991 Nov;100(5):1319-22 [1657539]
Eur Respir J. 1994 Sep;7(9):1585-92 [7995385]
J Leukoc Biol. 1994 Dec;56(6):672-86 [7996043]
Clin Chem. 1995 Jun;41(6 Pt 1):897-903 [7768009]
J Am Coll Nutr. 1995 Jun;14(3):229-32 [8586770]
Biochemistry. 1998 Dec 22;37(51):17923-30 [9922160]
Can J Physiol Pharmacol. 2005 Jan;83(1):69-75 [15759052]
J Leukoc Biol. 2005 May;77(5):598-625 [15689384]
Free Radic Biol Med. 2006 Aug 1;41(3):422-30 [16843823]
Am J Physiol Lung Cell Mol Physiol. 2007 Nov;293(5):L1293-9 [17720872]
Eur J Biochem. 2001 Oct;268(19):5142-8 [11589706]
Free Radic Biol Med. 2002 Aug 1;33(3):364-9 [12126758]
Cytometry B Clin Cytom. 2003 Jan;51(1):21-9 [12500294]
Nutrition. 2003 Jan;19(1):54-61 [12507640]
Biochem Biophys Res Commun. 2003 Feb 7;301(2):551-7 [12565898]
Free Radic Biol Med. 2003 Apr 1;34(7):830-9 [12654471]
Scand J Clin Lab Invest Suppl. 1968;97:77-89 [4179068]
J Biol Chem. 1971 Jan 25;246(2):359-66 [5542006]
Arch Environ Health. 1971 Mar;22(3):389-95 [4100716]
Am Ind Hyg Assoc J. 1974 May;35(5):288-91 [4831035]
N Engl J Med. 1977 Nov 10;297(19):1022-8 [302914]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.022
ER  - 



TY  - JOUR
T1  - Hypericin-mediated photooxidative damage of α-crystallin in human lens epithelial cells.
AN  - 1350891695; 23453985
AB  - St. John's wort (Hypericum perforatum), a perennial herb native to Europe, is widely used for and seems to be effective in treatment of mild to moderate depression. Hypericin, a singlet oxygen-generating photosensitizer that absorbs in both the visible and the UVA range, is considered to be one of the bioactive ingredients of St. John's wort, and commercial preparations are frequently calibrated to contain a standard concentration. Hypericin can accumulate in ocular tissues, including lenses, and can bind in vitro to α-crystallin, a major lens protein. α-crystallin is required for lens transparency and also acts as a chaperone to ensure its own integrity and the integrity of all lens proteins. Because there is no crystallin turnover, damage to α-crystallin is cumulative over the lifetime of the lens and can lead to cataracts, the principal cause of blindness worldwide. In this work we study hypericin photosensitization of α-crystallin and detect extensive polymerization of bovine α-crystallin exposed in vitro to hypericin and UVA. We use fluorescence confocal microscopy to visualize binding between hypericin and α-crystallin in a human lens epithelial (HLE) cell line. Further, we show that UVA irradiation of hypericin-treated HLE cells results in a dramatic decrease in α-crystallin detection concurrent with a dramatic accumulation of the tryptophan oxidation product N-formylkynurenine (NFK). Examination of actin in HLE cells indicates that this cytoskeleton protein accumulates NFK resulting from hypericin-mediated photosensitization. This work also shows that filtration of wavelengths <400nm provides incomplete protection against α-crystallin modification and NFK accumulation, suggesting that even by wearing UV-blocking sunglasses, routine users of St. John's wort cannot adequately shield their lenses from hypericin-mediated photosensitized damage.
          Published by Elsevier Inc.
JF  - Free radical biology & medicine
AU  - Ehrenshaft, Marilyn
AU  - Roberts, Joan E
AU  - Mason, Ronald P
AD  - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ehrensh1@niehs.nih.gov
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 347
EP  - 354
VL  - 60
KW  - Photosensitizing Agents
KW  - 0
KW  - alpha-Crystallins
KW  - N'-formylkynurenine
KW  - 1022-31-7
KW  - Kynurenine
KW  - 343-65-7
KW  - Perylene
KW  - 5QD5427UN7
KW  - hypericin
KW  - 7V2F1075HD
KW  - Index Medicus
KW  - Animals
KW  - Ultraviolet Rays
KW  - Cattle
KW  - Cell Line -- radiation effects
KW  - Photosensitizing Agents -- administration & dosage
KW  - Humans
KW  - Cell Line -- drug effects
KW  - Oxidative Stress
KW  - Kynurenine -- metabolism
KW  - Kynurenine -- analogs & derivatives
KW  - Perylene -- analogs & derivatives
KW  - Cataract -- metabolism
KW  - alpha-Crystallins -- chemistry
KW  - Epithelial Cells -- cytology
KW  - Epithelial Cells -- drug effects
KW  - alpha-Crystallins -- metabolism
KW  - Perylene -- administration & dosage
KW  - Cataract -- etiology
KW  - Cataract -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1350891695?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hypericin-mediated+photooxidative+damage+of+%CE%B1-crystallin+in+human+lens+epithelial+cells.&rft.au=Ehrenshaft%2C+Marilyn%3BRoberts%2C+Joan+E%3BMason%2C+Ronald+P&rft.aulast=Ehrenshaft&rft.aufirst=Marilyn&rft.date=2013-07-01&rft.volume=60&rft.issue=&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2013.02.023
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-01
N1  - Date created - 2013-05-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Exp Eye Res. 2003 Feb;76(2):145-53 [12565801]
Int Clin Psychopharmacol. 2001 Sep;16(5):239-52 [11552767]
Photochem Photobiol. 2003 Jul;78(1):88-92 [12929754]
Br J Pharmacol. 2004 May;142(2):231-55 [15155533]
Photochem Photobiol. 1994 Jan;59(1):40-7 [8127939]
Invest Ophthalmol Vis Sci. 1994 Jun;35(7):3094-102 [8206728]
Photochem Photobiol. 1998 Aug;68(2):135-40 [9723207]
Skin Pharmacol Appl Skin Physiol. 1999 Sep-Oct;12(5):299-304 [10461100]
Photochem Photobiol. 2004 Nov-Dec;80(3):583-6 [15623347]
Biochim Biophys Acta. 2005 Jan 17;1703(2):93-109 [15680218]
Photochem Photobiol. 2005 May-Jun;81(3):524-8 [15643927]
Prog Retin Eye Res. 2007 Jan;26(1):78-98 [17166758]
Semin Cell Dev Biol. 2006 Dec;17(6):698-711 [17145190]
Photochem Photobiol. 2007 May-Jun;83(3):706-13 [17576381]
Mol Vis. 2008;14:249-54 [18334941]
Curr Drug Metab. 2008 Dec;9(10):1027-37 [19075619]
J Am Soc Mass Spectrom. 2010 Jul;21(7):1114-7 [20219394]
Photochem Photobiol. 2010 Jul-Aug;86(4):752-6 [20408979]
J Biol Chem. 2010 Dec 24;285(52):41187-93 [20959464]
Philos Trans R Soc Lond B Biol Sci. 2011 Apr 27;366(1568):1250-64 [21402584]
Curr Opin Ophthalmol. 2011 Jan;22(1):4-9 [21107260]
Photochem Photobiol. 2011 Nov-Dec;87(6):1321-9 [21770952]
Eur Neuropsychopharmacol. 2011 Dec;21(12):841-60 [21601431]
Curr Med Chem. 2012;19(6):793-8 [22214453]
Expert Opin Drug Metab Toxicol. 2012 Jun;8(6):691-708 [22606944]
Med Princ Pract. 2012;21(5):404-28 [22236736]
Biochem J. 2012 Nov 15;448(1):83-91 [22888904]
Photochem Photobiol. 2004 Nov-Dec;80(3):444-9 [15623328]
Free Radic Biol Med. 2009 May 1;46(9):1260-6 [19353782]
Photochem Photobiol. 2009 Jul-Aug;85(4):921-6 [19175752]
Curr Eye Res. 2009 Oct;34(10):863-6 [19895314]
Mol Pharm. 2009 Nov-Dec;6(6):1775-89 [19739671]
Int J Mol Sci. 2010;11(2):562-94 [20386655]
Photochem Photobiol. 2000 Aug;72(2):200-3 [10946573]
Curr Eye Res. 2000 Aug;21(2):597-601 [11148595]
Biochem Biophys Res Commun. 2003 Jun 6;305(3):761-70 [12763058]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.freeradbiomed.2013.02.023
ER  - 



TY  - JOUR
T1  - Robust protein nitration contributes to acetaminophen-induced mitochondrial dysfunction and acute liver injury.
AN  - 1350891115; 23454065
AB  - Acetaminophen (APAP), a widely used analgesic/antipyretic agent, can cause liver injury through increased nitrative stress, leading to protein nitration. However, the identities of nitrated proteins and their roles in hepatotoxicity are poorly understood. Thus, we aimed at studying the mechanism of APAP-induced hepatotoxicity by systematic identification and characterization of nitrated proteins in the absence or presence of an antioxidant, N-acetylcysteine (NAC). The levels of nitrated proteins markedly increased at 2h in mice exposed to a single APAP dose (350mg/kg ip), which caused severe liver necrosis at 24h. Protein nitration and liver necrosis were minimal in mice exposed to nontoxic 3-hydroxyacetanilide or animals co-treated with APAP and NAC. Mass-spectral analysis of the affinity-purified nitrated proteins identified numerous mitochondrial and cytosolic proteins, including mitochondrial aldehyde dehydrogenase, Mn-superoxide dismutase, glutathione peroxidase, ATP synthase, and 3-ketoacyl-CoA thiolase, involved in antioxidant defense, energy supply, or fatty acid metabolism. Immunoprecipitation followed by immunoblot with anti-3-nitrotyrosine antibody confirmed that the aforementioned proteins were nitrated in APAP-exposed mice but not in NAC-cotreated mice. Consistently, NAC cotreatment significantly restored the suppressed activity of these enzymes. Thus, we demonstrate a new mechanism by which many nitrated proteins with concomitantly suppressed activity promotes APAP-induced mitochondrial dysfunction and hepatotoxicity.
          Published by Elsevier Inc.
JF  - Free radical biology & medicine
AU  - Abdelmegeed, Mohamed A
AU  - Jang, Sehwan
AU  - Banerjee, Atrayee
AU  - Hardwick, James P
AU  - Song, Byoung-Joon
AD  - Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 211
EP  - 222
VL  - 60
KW  - Acetanilides
KW  - 0
KW  - Antioxidants
KW  - Nitrates
KW  - Proteins
KW  - Acetaminophen
KW  - 362O9ITL9D
KW  - 3-hydroxyacetanilide
KW  - 621-42-1
KW  - Superoxide Dismutase
KW  - EC 1.15.1.1
KW  - Acetylcysteine
KW  - WYQ7N0BPYC
KW  - Index Medicus
KW  - Animals
KW  - Acetanilides -- administration & dosage
KW  - Oxidative Stress
KW  - Superoxide Dismutase -- metabolism
KW  - Mice
KW  - Proteins -- metabolism
KW  - Acetaminophen -- administration & dosage
KW  - Chemical and Drug Induced Liver Injury -- pathology
KW  - Acetylcysteine -- administration & dosage
KW  - Nitrates -- metabolism
KW  - Mitochondria, Liver -- pathology
KW  - Acetylcysteine -- metabolism
KW  - Mitochondria, Liver -- drug effects
KW  - Chemical and Drug Induced Liver Injury -- metabolism
KW  - Acetaminophen -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1350891115?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Robust+protein+nitration+contributes+to+acetaminophen-induced+mitochondrial+dysfunction+and+acute+liver+injury.&rft.au=Abdelmegeed%2C+Mohamed+A%3BJang%2C+Sehwan%3BBanerjee%2C+Atrayee%3BHardwick%2C+James+P%3BSong%2C+Byoung-Joon&rft.aulast=Abdelmegeed&rft.aufirst=Mohamed&rft.date=2013-07-01&rft.volume=60&rft.issue=&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2013.02.018
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-01
N1  - Date created - 2013-05-13
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Ann Intern Med. 1986 Mar;104(3):399-404 [3511825]
J Am Coll Nutr. 1986;5(2):137-51 [3722629]
J Biol Chem. 1989 Feb 25;264(6):3568-72 [2914964]
Am J Pathol. 1991 Feb;138(2):359-71 [1992763]
JAMA. 1994 Dec 21;272(23):1845-50 [7990219]
Fundam Appl Toxicol. 1995 Feb;24(2):260-74 [7737437]
FEBS Lett. 1996 Apr 29;385(1-2):63-6 [8641468]
Toxicol Lett. 1997 Jan 15;90(1):77-82 [9020405]
Drug Metab Rev. 1997 Feb-May;29(1-2):39-57 [9187510]
Drug Metab Rev. 1997 Feb-May;29(1-2):59-77 [9187511]
N Engl J Med. 1997 Oct 16;337(16):1112-7 [9329933]
Chem Res Toxicol. 1998 Jun;11(6):604-7 [9625727]
J Biol Chem. 1998 Jul 10;273(28):17940-53 [9651401]
Toxicol Appl Pharmacol. 1998 Nov;153(1):109-18 [9875305]
Hepatology. 1999 Jul;30(1):186-95 [10385655]
Med Clin North Am. 2005 Nov;89(6):1145-59 [16227058]
Dig Liver Dis. 2006 Jan;38(1):33-8 [16054882]
Gastroenterology. 2006 Jul;131(1):165-78 [16831600]
J Biol Chem. 2006 Jul 28;281(30):21256-65 [16709574]
Hepatology. 2006 Nov;44(5):1218-30 [17058263]
Gut. 2007 Jul;56(7):982-90 [17185352]
J Biol Chem. 2008 Feb 22;283(8):4543-59 [18093979]
Toxicol Lett. 2008 Apr 1;177(3):188-97 [18313239]
Free Radic Biol Med. 2008 Sep 1;45(5):611-8 [18573333]
Proteomics. 2008 Sep;8(18):3906-18 [18780394]
Gastroenterology. 2008 Oct;135(4):1344-57 [18778711]
Antioxid Redox Signal. 2009 Jul;11(7):1559-67 [19290778]
Hepatology. 2010 Jan;51(1):246-54 [19821517]
Curr Pharm Biotechnol. 2010 Aug;11(5):434-43 [20420575]
Chem Res Toxicol. 2010 Jul 19;23(7):1286-92 [20578685]
Toxicol Lett. 2011 Apr 10;202(1):23-9 [21262334]
J Nutr. 2011 Apr 1;141(4):603-10 [21346097]
J Pharmacol Exp Ther. 2011 Apr;337(1):110-6 [21205919]
Mol Cell Proteomics. 2011 Apr;10(4):M110.002964 [21156839]
J Proteomics. 2011 Nov 18;74(12):2691-702 [21609791]
J Pharmacol Exp Ther. 2012 Jan;340(1):134-42 [22001257]
Cell Physiol Biochem. 2012;29(1-2):41-50 [22415073]
Liver Transpl. 2012 Apr;18(4):405-12 [22213443]
Eur Rev Med Pharmacol Sci. 2012 Apr;16(4):512-8 [22696879]
Gastroenterology. 2012 Sep;143(3):e1-7 [22796239]
J Hepatol. 2012 Oct;57(4):860-6 [22668639]
Curr Med Chem. 2012;19(33):5601-6 [22856659]
Hepatology. 2011 Sep 2;54(3):969-78 [21626531]
Methods Mol Biol. 2008;477:15-29 [19082935]
Biochemistry. 2009 Apr 21;48(15):3417-24 [19265433]
Chem Res Toxicol. 2009 Apr;22(4):699-707 [19256530]
Free Radic Biol Med. 2009 Sep 15;47(6):767-78 [19539749]
Biochem Pharmacol. 2010 Jan 1;79(1):57-66 [19660437]
Toxicol Sci. 2000 Feb;53(2):467-73 [10696795]
Arch Biochem Biophys. 2000 Aug 15;380(2):360-6 [10933892]
Antioxid Redox Signal. 2001 Apr;3(2):261-71 [11396480]
Toxicol Sci. 2001 Aug;62(2):212-20 [11452133]
Mol Pharmacol. 2001 Oct;60(4):847-56 [11562448]
Toxicol Sci. 2002 Jan;65(1):135-50 [11752693]
J Biol Chem. 2002 Jan 25;277(4):2779-84 [11705998]
Toxicol Sci. 2002 Feb;65(2):166-76 [11812920]
Hepatology. 2002 Feb;35(2):289-98 [11826401]
Toxicology. 2002 Jun 14;175(1-3):83-90 [12049838]
J Pharmacol Exp Ther. 2002 Nov;303(2):468-75 [12388625]
Mol Pharmacol. 2003 Feb;63(2):401-8 [12527812]
Hepatology. 2003 Jul;38(1):141-7 [12829996]
J Biol Chem. 2003 Sep 12;278(37):35844-9 [12851409]
Toxicol Sci. 2003 Oct;75(2):458-67 [12883092]
Gastroenterology. 2003 Dec;125(6):1818-33 [14724834]
Gastroenterology. 2003 Dec;125(6):1834-44 [14724835]
Annu Rev Pharmacol Toxicol. 2004;44:27-42 [14744237]
J Am Soc Nephrol. 2004 Feb;15(2):380-9 [14747384]
Arch Intern Med. 2004 Jul 26;164(14):1519-24 [15277282]
JAMA. 1980 Jul 18;244(3):251-3 [7382090]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.freeradbiomed.2013.02.018
ER  - 



TY  - JOUR
T1  - Thyroid hormone receptors and cancer.
AN  - 1349701807; 22507269
AB  - Thyroid hormone receptors (TRs) are ligand-dependent transcription factors that mediate the actions of the thyroid hormone (T3) in development, growth, and differentiation. The THRA and THRB genes encode several TR isoforms that express in a tissue- and development-dependent manner. In the past decades, a significant advance has been made in the understanding of TR actions in maintaining normal cellular functions. However, the roles of TRs in human cancer are less well understood. The reduced expression of TRs because of hypermethylation, or deletion of TR genes found in human cancers suggests that TRs could function as tumor suppressors. A close association of somatic mutations of TRs with human cancers further supports the notion that the loss of normal functions of TR could lead to uncontrolled growth and loss of cell differentiation. In line with the findings from association studies in human cancers, mice deficient in total functional TRs (Thra1(-/-)Thrb(-/-) mice) or with a targeted homozygous mutation of the Thrb gene (denoted PV; Thrb(PV/PV) mice) spontaneously develop metastatic thyroid carcinoma. This review will examine the evidence learned from these genetically engineered mice that provided strong evidence to support the critical role of TRs in human cancer.
          Loss of normal functions of TR by deletion or by mutations could contribute to cancer development, progression and metastasis. Novel mechanistic insights are revealed in how aberrant TR activities lead to carcinogenesis. Mouse models of thyroid cancer provide opportunities to identify molecular targets as potential treatment modalities. This article is part of a Special Issue entitled Thyroid hormone signalling.
          Published by Elsevier B.V.
JF  - Biochimica et biophysica acta
AU  - Kim, Won Gu
AU  - Cheng, Sheue-yann
AD  - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Y1  - 2013/07//
PY  - 2013
DA  - July 2013
SP  - 3928
EP  - 3936
VL  - 1830
IS  - 7
SN  - 0006-3002, 0006-3002
KW  - Receptors, Thyroid Hormone
KW  - 0
KW  - Thyroid Hormones
KW  - Index Medicus
KW  - Animals
KW  - Thyroid Hormones -- genetics
KW  - Humans
KW  - Molecular Sequence Data
KW  - Amino Acid Sequence
KW  - Thyroid Hormones -- metabolism
KW  - Signal Transduction
KW  - Receptors, Thyroid Hormone -- metabolism
KW  - Receptors, Thyroid Hormone -- genetics
KW  - Neoplasms -- genetics
KW  - Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349701807?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thyroid+hormone+receptors+and+cancer.&rft.au=Kim%2C+Won+Gu%3BCheng%2C+Sheue-yann&rft.aulast=Kim&rft.aufirst=Won&rft.date=2013-07-01&rft.volume=1830&rft.issue=7&rft.spage=3928&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagen.2012.04.002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-30
N1  - Date created - 2013-05-08
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Oncogene. 2006 May 4;25(19):2736-47 [16314832]
J Biol Chem. 2006 Jul 28;281(30):20666-72 [16717100]
Curr Opin Cell Biol. 2006 Oct;18(5):516-23 [16919435]
Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14104-9 [16966610]
J Clin Invest. 2006 Nov;116(11):2972-84 [17039256]
Curr Opin Genet Dev. 2007 Feb;17(1):45-51 [17208432]
J Mol Endocrinol. 2007 Feb;38(1-2):221-33 [17293442]
Carcinogenesis. 2007 May;28(5):932-9 [17127711]
Mol Cell Biol. 2007 Sep;27(17):6116-26 [17606624]
Exp Cell Res. 2007 Sep 10;313(15):3175-88 [17651734]
Carcinogenesis. 2007 Dec;28(12):2451-8 [17660507]
J Clin Endocrinol Metab. 2007 Dec;92(12):4766-70 [17911173]
Mol Cell Biol. 2008 Jul;28(14):4598-608 [18474620]
Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19544-9 [19052228]
Nature. 2008 Dec 18;456(7224):997-1000 [19037247]
Oncogene. 2009 Jan 29;28(4):509-17 [18997818]
IUBMB Life. 2009 May;61(5):528-36 [19391168]
Mol Cell Endocrinol. 2009 Sep 24;308(1-2):63-9 [19549593]
Cancer Genet Cytogenet. 2010 Jan 15;196(2):140-5 [20082849]
Mol Cell Biol. 1993 Oct;13(10):5970-80 [8105369]
J Biol Chem. 1994 Jan 14;269(2):903-9 [7904604]
Melanoma Res. 1993 Dec;3(6):457-61 [7909244]
Cancer Res. 1994 Jun 1;54(11):3021-4 [7910519]
EMBO J. 1994 Sep 15;13(18):4241-50 [7925269]
Nature. 1995 Dec 14;378(6558):690-7 [7501015]
Nat Genet. 1996 Jul;13(3):354-7 [8673137]
Ann Surg Oncol. 1996 Jan;3(1):100-5 [8770310]
Mol Endocrinol. 1997 Apr;11(4):433-41 [9092795]
Oncology. 1997 May-Jun;54(3):214-9 [9143402]
EMBO J. 1998 Jan 15;17(2):455-61 [9430637]
Endocrinology. 2010 Apr;151(4):1929-39 [20133453]
Thyroid. 2002 Nov;12(11):963-9 [12490073]
Cancer Lett. 2003 Mar 31;192(2):121-32 [12668276]
Endocr J. 2003 Feb;50(1):77-83 [12733712]
Carcinogenesis. 2003 Sep;24(9):1467-79 [12869418]
Clin Otolaryngol Allied Sci. 2003 Oct;28(5):386-95 [12969338]
Cancer Res. 2003 Sep 1;63(17):5274-80 [14500358]
Endocrinology. 2003 Nov;144(11):4991-8 [12960092]
Endocrinology. 2004 Oct;145(10):4430-8 [15231697]
J Korean Med Sci. 2004 Oct;19(5):710-5 [15483349]
Oncogene. 2004 Oct 18;23(48):7928-46 [15489911]
Proc Natl Acad Sci U S A. 1984 Jul;81(14):4495-9 [6589608]
Nature. 1986 Dec 18-31;324(6098):635-40 [2879242]
Nature. 1986 Dec 18-31;324(6098):641-6 [2879243]
Oncogene. 1988 Mar;2(3):283-7 [3281095]
Am J Hum Genet. 1989 Feb;44(2):282-7 [2536219]
J Natl Cancer Inst. 1989 Dec 6;81(23):1815-20 [2573734]
J Clin Invest. 1991 Dec;88(6):2123-30 [1661299]
Cancer Res. 1992 May 1;52(9):2624-7 [1568230]
Eur J Endocrinol. 1998 Jan;138(1):104-12 [9461325]
Anticancer Res. 1998 Jan-Feb;18(1A):33-40 [9568052]
Cancer Res. 1999 Apr 15;59(8):1811-5 [10213482]
Mol Carcinog. 1999 Sep;26(1):53-61 [10487522]
Int J Mol Med. 1999 Oct;4(4):351-8 [10493974]
Mol Cancer Res. 2004 Nov;2(11):595-605 [15561776]
Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836]
Mol Endocrinol. 2005 Jan;19(1):102-12 [15388791]
Oncogene. 2010 Apr 1;29(13):1909-19 [20062085]
Endocr Rev. 2010 Apr;31(2):139-70 [20051527]
Ann Surg Oncol. 2010 Aug;17(8):2222-8 [20155399]
Pathol Oncol Res. 2010 Dec;16(4):497-507 [20405349]
Mol Endocrinol. 2011 Feb;25(2):212-24 [21239618]
J Clin Endocrinol Metab. 2011 Mar;96(3):E546-53 [21159845]
Steroids. 2011 Aug;76(9):885-91 [21473875]
Oncogene. 2011 Jul 28;30(30):3381-90 [21399657]
Endocrinology. 2011 Nov;152(11):4455-65 [21952241]
Biochem J. 2012 Jan 1;441(1):23-37 [22168437]
Clin Cancer Res. 2012 Mar 1;18(5):1281-90 [22271876]
Thyroid. 2000 Jan;10(1):41-52 [10691312]
Cancer Lett. 2000 Jul 31;155(2):145-52 [10822129]
Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):8985-90 [10908671]
Science. 2000 Aug 25;289(5483):1357-60 [10958784]
Nature. 2000 Sep 28;407(6803):538-41 [11029009]
J Biol Chem. 2000 Nov 24;275(47):36502-5 [11013229]
Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13209-14 [11069286]
Mol Endocrinol. 2001 Mar;15(3):398-410 [11222741]
Thyroid. 2001 Mar;11(3):281-91 [11327621]
Mol Cell. 2001 May;7(5):927-36 [11389840]
Brain Pathol. 2001 Jul;11(3):328-41 [11414475]
Cancer Res. 2001 Aug 15;61(16):6105-11 [11507060]
J Clin Endocrinol Metab. 2001 Oct;86(10):5025-32 [11600580]
J Clin Endocrinol Metab. 2001 Nov;86(11):5572-6 [11701737]
Carcinogenesis. 2002 Jan;23(1):25-33 [11756220]
J Clin Endocrinol Metab. 2002 Mar;87(3):1120-8 [11889175]
Cancer Res. 2002 Apr 1;62(7):1939-43 [11929806]
Oncogene. 2002 Jun 20;21(27):4307-16 [12082618]
Curr Biol. 2002 Jul 23;12(14):R499-R501 [12176352]
Nat Rev Mol Cell Biol. 2005 Jan;6(1):56-68 [15688067]
Oncogene. 2005 Jul 14;24(30):4861-6 [15897900]
Cancer Genet Cytogenet. 2005 Sep;161(2):104-9 [16102579]
Endocrinology. 2005 Oct;146(10):4456-63 [16002527]
J Cell Physiol. 2006 Feb;206(2):309-21 [16021636]
Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1780-5 [16446424]
Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5197-201 [16549781]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.bbagen.2012.04.002
ER  - 



TY  - JOUR
T1  - Phthalate Exposure and Allergy in the U.S. Population: Results from NHANES 2005-2006
AN  - 1458535694; 18741280
AB  - Background: Environmental exposures to phthalates, particularly high-molecular-weight (HMW) phthalates, are suspected to contribute to allergy. Objective: We assessed whether phthalate metabolites are associated with allergic symptoms and sensitization in a large nationally representative sample. Methods: We used data on urinary phthalate metabolites and allergic symptoms (hay fever, rhinitis, allergy, wheeze, asthma) and sensitization from participants greater than or equal to 6 years of age in the National Health and Nutrition Examination Survey (NHANES) 2005-2006. Allergen sensitization was defined as a positive response to at least one of 19 specific IgE antigens ( greater than or equal to 0.35 kU/L). Odds ratios (ORs) per one log10 unit change in phthalate concentration were estimated using logistic regression adjusting for age, race, body mass index, gender, creatinine, and cotinine. Separate analyses were conducted for children (6-17 years of age) and adults. Results: The HMW phthalate metabolite monobenzyl phthalate (MBzP) was the only metabolite positively associated with current allergic symptoms in adults (wheeze, asthma, hay fever, and rhinitis). Mono-(3-carboxypropyl) phthalate and the sum of diethylhexyl phthalate metabolites (both representing HMW phthalate exposures) were positively associated with allergic sensitization in adults. Conversely, in children, HMW phthalate metabolites were inversely associated with asthma and hay fever. Of the low-molecular-weight phthalate metabolites, monoethyl phthalate was inversely associated with allergic sensitization in adults (OR = 0.79; 95% CI: 0.70, 0.90). Conclusion: In this cross-sectional analysis of a nationally representative sample, HMW phthalate metabolites, particularly MBzP, were positively associated with allergic symptoms and sensitization in adults, but there was no strong evidence for associations between phthalates and allergy in children 6-17 years of age. Citation: Hoppin JA, Jaramillo R, London SJ, Bertelsen RJ, Salo PM, Sandler DP, Zeldin DC. 2013. Phthalate exposure and allergy in the U.S. population: results from NHANES 2005-2006. Environ Health Perspect 121:1129-1134; http://dx.doi.org/10.1289/ehp.1206211 [Online 25 June 2013].
JF  - Environmental Health Perspectives
AU  - Hoppin, Jane A
AU  - Jaramillo, Renee
AU  - London, Stephanie J
AU  - Bertelsen, Randi J
AU  - Salo, Paeivi M
AU  - Sandler, Dale P
AU  - Zeldin, Darryl C
AD  - Epidemiology Branch, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Department of Heath and Human Services (DHHS), Research Triangle Park, North Carolina, USA
Y1  - 2013/06/25/
PY  - 2013
DA  - 2013 Jun 25
SP  - 1129
EP  - 1134
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 0
SN  - 0091-6765, 0091-6765
KW  - Toxicology Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - Age
KW  - Body mass
KW  - British Isles, England, Greater London, London
KW  - Rhinitis
KW  - Metabolites
KW  - Respiratory diseases
KW  - Allergies
KW  - Nutrition
KW  - Hypersensitivity
KW  - Phthalates
KW  - Allergens
KW  - Races
KW  - Data processing
KW  - Asthma
KW  - Children
KW  - Phthalic acid
KW  - USA
KW  - Creatinine
KW  - Cotinine
KW  - Urine
KW  - Immunoglobulin E
KW  - Gender
KW  - Body mass index
KW  - Hay fever
KW  - Internet
KW  - H 12000:Epidemiology and Public Health
KW  - X 24350:Industrial Chemicals
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458535694?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Phthalate+Exposure+and+Allergy+in+the+U.S.+Population%3A+Results+from+NHANES+2005-2006&rft.au=Hoppin%2C+Jane+A%3BJaramillo%2C+Renee%3BLondon%2C+Stephanie+J%3BBertelsen%2C+Randi+J%3BSalo%2C+Paeivi+M%3BSandler%2C+Dale+P%3BZeldin%2C+Darryl+C&rft.aulast=Hoppin&rft.aufirst=Jane&rft.date=2013-06-25&rft.volume=121&rft.issue=0&rft.spage=1129&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1206211
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Age; Data processing; Asthma; Metabolites; Rhinitis; Children; Nutrition; Phthalic acid; Hypersensitivity; Cotinine; Creatinine; Immunoglobulin E; Allergens; Body mass index; Hay fever; Races; Internet; Body mass; Respiratory diseases; Allergies; Phthalates; Urine; Gender; USA; British Isles, England, Greater London, London
DO  - http://dx.doi.org/10.1289/ehp.1206211
ER  - 



TY  - JOUR
T1  - Alzheimer's disease: which type of amyloid-preventing drug agents to employ?
AN  - 1355477741; 23450150
AB  - The current paradigm in the amyloid hypothesis brands small β-amyloid (Aβ) oligomers as the toxic species in Alzheimer's disease (AD). These oligomers are fibril-like; contain β-sheet structure, and present exposed hydrophobic surface. Oligomers with this motif are capable of penetrating the cell membrane, gathering to form toxic ion channels. Current agents suppressing precursor Aβ cleavage have only met partial success; and to date, those targeting the peptides and their assemblies in the aqueous environment of the extracellular space largely fail in clinical trials. One possible reason is failure to reach membrane-embedded targets of disease-'infected' cells. Here we provide an overview, point to the need to account for the lipid environment when aiming to prevent the formation of toxic channels, and propose a combination therapy to target the species spectrum.
JF  - Physical chemistry chemical physics : PCCP
AU  - Jang, Hyunbum
AU  - Connelly, Laura
AU  - Arce, Fernando Teran
AU  - Ramachandran, Srinivasan
AU  - Lal, Ratnesh
AU  - Kagan, Bruce L
AU  - Nussinov, Ruth
AD  - Center for Cancer Research, Nanobiology Program, Basic Science Program, SAIC-Frederick, Inc., National Cancer Institute, Frederick, Maryland 21702, USA.
Y1  - 2013/06/21/
PY  - 2013
DA  - 2013 Jun 21
SP  - 8868
EP  - 8877
VL  - 15
IS  - 23
KW  - Amyloid
KW  - 0
KW  - Index Medicus
KW  - Animals
KW  - Models, Molecular
KW  - Humans
KW  - Drug Discovery
KW  - Alzheimer Disease -- drug therapy
KW  - Amyloid -- chemistry
KW  - Alzheimer Disease -- metabolism
KW  - Amyloid -- metabolism
KW  - Amyloid -- antagonists & inhibitors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1355477741?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Physical+chemistry+chemical+physics+%3A+PCCP&rft.atitle=Alzheimer%27s+disease%3A+which+type+of+amyloid-preventing+drug+agents+to+employ%3F&rft.au=Jang%2C+Hyunbum%3BConnelly%2C+Laura%3BArce%2C+Fernando+Teran%3BRamachandran%2C+Srinivasan%3BLal%2C+Ratnesh%3BKagan%2C+Bruce+L%3BNussinov%2C+Ruth&rft.aulast=Jang&rft.aufirst=Hyunbum&rft.date=2013-06-21&rft.volume=15&rft.issue=23&rft.spage=8868&rft.isbn=&rft.btitle=&rft.title=Physical+chemistry+chemical+physics+%3A+PCCP&rft.issn=1463-9084&rft_id=info:doi/10.1039%2Fc3cp00017f
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-09
N1  - Date created - 2013-05-23
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Neurosci Lett. 1995 Nov 17;200(2):105-8 [8614555]
Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1710-5 [8643694]
J Biol Chem. 1996 Dec 27;271(52):33623-31 [8969231]
J Biol Chem. 1997 Jan 3;272(1):44-7 [8995224]
J Biol Chem. 2004 Nov 5;279(45):46363-6 [15385542]
J Am Chem Soc. 2009 Nov 25;131(46):16663-5 [19877631]
Biophys J. 2009 Dec 2;97(11):3029-37 [19948133]
J Biol Chem. 2010 Feb 26;285(9):6071-9 [20018889]
Drug Metab Dispos. 2010 Apr;38(4):554-65 [20075192]
Adv Exp Med Biol. 2010;677:150-67 [20687488]
Chem Rev. 2010 Aug 11;110(8):4820-38 [20402519]
Neurobiol Dis. 2011 Jan;41(1):62-70 [20816785]
J Alzheimers Dis. 2010;22(2):443-57 [20847430]
J Mol Biol. 2010 Dec 17;404(5):917-34 [20970427]
J Alzheimers Dis. 2010;22(3):839-48 [20858948]
Neurobiol Aging. 2011 Feb;32(2):235-48 [19324459]
Proc Natl Acad Sci U S A. 2010 Dec 21;107(51):21990-5 [21131570]
PLoS One. 2011;6(1):e16248 [21267410]
Nat Chem. 2009 Jul;1(4):326-31 [20703363]
J Am Chem Soc. 2011 Mar 16;133(10):3390-400 [21341665]
Biochem Biophys Res Commun. 2011 Jul 29;411(2):312-6 [21726530]
Nat Rev Drug Discov. 2011 Sep;10(9):698-712 [21852788]
Nat Struct Mol Biol. 2007 Dec;14(12):1157-64 [18059284]
J Am Chem Soc. 2011 Oct 12;133(40):16013-22 [21882806]
Chem Soc Rev. 2012 Jan 21;41(2):608-21 [21818468]
J Neurochem. 2012 Jan;120 Suppl 1:71-83 [22122681]
Biochemistry. 2012 Jan 24;51(3):776-85 [22242635]
J Phys Chem B. 2012 Feb 9;116(5):1728-35 [22217000]
Biochemistry. 2006 Jan 17;45(2):498-512 [16401079]
FEBS J. 2006 Feb;273(3):658-68 [16420488]
J Biol Chem. 2006 Jan 27;281(4):2151-61 [16301322]
Chembiochem. 2006 Feb;7(2):257-67 [16444756]
Biochemistry. 2010 Apr 13;49(14):3031-9 [20201586]
Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6538-43 [20308552]
Proc Natl Acad Sci U S A. 2010 May 25;107(21):9490-5 [20448202]
J Phys Chem B. 2010 Jul 29;114(29):9445-51 [20608696]
Mol Pharm. 2012 Apr 2;9(4):708-17 [22081976]
Biochemistry. 2012 Apr 10;51(14):3031-8 [22413858]
Lancet Neurol. 2012 Jul;11(7):597-604 [22677258]
J Biol Chem. 2012 Jul 13;287(29):24765-73 [22547072]
J Mol Biol. 2012 Aug 10;421(2-3):172-84 [22119878]
Biochem J. 2012 Sep 1;446(2):165-77 [22891628]
Biophys J. 2012 Aug 22;103(4):702-10 [22947931]
Biochemistry. 2012 Oct 2;51(39):7676-84 [22970795]
PLoS One. 2012;7(10):e47261 [23077580]
Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20455-60 [23184970]
FEBS Lett. 2004 Nov 5;577(1-2):117-20 [15527771]
Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10427-32 [16020533]
Proc Natl Acad Sci U S A. 2005 Nov 29;102(48):17342-7 [16293696]
Nature. 2006 Mar 16;440(7082):352-7 [16541076]
Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16248-53 [17060612]
J Gen Physiol. 2006 Dec;128(6):637-47 [17101816]
J Gen Physiol. 2006 Dec;128(6):631-3 [17130516]
Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18119-24 [17108084]
J Neurosci. 2007 Jan 24;27(4):796-807 [17251419]
J Biol Chem. 2007 Apr 13;282(15):11590-601 [17308309]
J Neurochem. 2007 Jun;101(5):1172-84 [17286590]
Biophys J. 2007 Sep 15;93(6):1938-49 [17526580]
Trends Biochem Sci. 2008 Feb;33(2):91-100 [18182298]
Proc Natl Acad Sci U S A. 2008 Apr 22;105(16):6033-8 [18408164]
Lancet. 2008 Jul 19;372(9634):216-23 [18640458]
Neurobiol Aging. 2008 Sep;29(9):1334-47 [17403556]
J Biol Chem. 2008 Oct 31;283(44):29613-4 [18650429]
J Biol Chem. 2008 Oct 31;283(44):29615-9 [18650430]
Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3348-53 [19204293]
Neurotox Res. 2009 Jul;16(1):1-13 [19526294]
Ann Neurol. 2009 Jul;66(1):48-54 [19360898]
J Am Chem Soc. 2009 Oct 21;131(41):14938-45 [19824733]
J Neurosci Res. 2000 May 15;60(4):490-4 [10797551]
Nat Cell Biol. 2000 Jul;2(7):E115-9 [10878819]
FEBS Lett. 2000 Oct  13;483(1):6-10 [11033346]
Amyloid. 2001 Jun;8(2):94-100 [11409039]
FASEB J. 2001 Nov;15(13):2433-44 [11689468]
Nature. 2002 Apr 4;416(6880):507-11 [11932737]
Nature. 2002 Apr 4;416(6880):535-9 [11932745]
Amyloid. 2002 Mar;9(1):13-23 [12000193]
Biochem Biophys Res Commun. 2002 May  31;294(1):5-10 [12054732]
Nature. 2002 Jul 18;418(6895):291 [12124613]
Bioorg Med Chem. 2002 Nov;10(11):3565-9 [12213471]
Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14126-31 [12391326]
J Biol Chem. 2002 Nov 8;277(45):42881-90 [12167652]
Eur J Biochem. 2002 Nov;269(22):5642-8 [12423364]
Neurology. 2003 Jul 8;61(1):46-54 [12847155]
J Biol Chem. 2003 Nov 14;278(46):46179-87 [12944403]
J Mol Biol. 2004 Jan 16;335(3):833-42 [14687578]
Nat Rev Neurosci. 2004 Sep;5(9):677-85 [15322526]
Nature. 1987 Feb 19-25;325(6106):733-6 [2881207]
Trends Pharmacol Sci. 1991 Oct;12(10):383-8 [1763432]
J Neurosci. 1992 Feb;12(2):376-89 [1346802]
Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):567-71 [8380642]
J Neurosci. 1993 Apr;13(4):1676-87 [8463843]
Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7951-5 [8367446]
Ann N Y Acad Sci. 1993 Sep 24;695:165-8 [8239277]
Proc Natl Acad Sci U S A. 1993 Nov 15;90(22):10573-7 [7504270]
J Biol Chem. 1994 Apr 15;269(15):10987-90 [8157623]
Biochem Biophys Res Commun. 1994 Jul 29;202(2):1142-8 [7519420]
Mol Cell Biochem. 1994 Nov 23;140(2):119-25 [7898484]
Exp Neurol. 1995 Jun;133(2):225-30 [7544290]
N Engl J Med. 1995 Nov 9;333(19):1242-7 [7566000]
J Biol Chem. 1996 Jan 26;271(4):1988-92 [8567648]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1039/c3cp00017f
ER  - 



TY  - JOUR
T1  - Development of a Pfs25-EPA malaria transmission blocking vaccine as a chemically conjugated nanoparticle
AN  - 1443369407; 18663147
AB  - Successful efforts to control infectious diseases have often required the use of effective vaccines. The current global strategy for control of malaria, including elimination and eradication will also benefit from the development of an effective vaccine that interrupts malaria transmission. To this end, a vaccine that disrupts malaria transmission within the mosquito host has been investigated for several decades targeting a 25 kDa ookinete specific surface protein, identified as Pfs25. Phase 1 human trial results using a recombinant Pfs25H/Montanide ISA51 formulation demonstrated that human Pfs25 specific antibodies block parasite infectivity to mosquitoes; however, the extent of blocking was likely insufficient for an effective transmission blocking vaccine. To overcome the poor immunogenicity, processes to produce and characterize recombinant Pfs25H conjugated to a detoxified form of Pseudomonas aeruginosa exoprotein A (EPA) have been developed and used to manufacture a cGMP pilot lot for use in human clinical trials. The Pfs25-EPA conjugate appears as a nanoparticle with an average molar mass in solution of approximately 600 kDa by static light scattering with an average diameter 20 nm (range 10-40 nm) by dynamic light scattering. The molar ratio of Pfs25H to EPA is about 3 to 1 by amino acid analysis, respectively. Outbred mice immunized with the Pfs25-EPA conjugated nanoparticle formulated on Alhydrogel registered had a 75-110 fold increase in Pfs25H specific antibodies when compared to an unconjugated Pfs25H/Alhydrogel registered formulation. A phase 1 human trial using the Pfs25-EPA/Alhydrogel registered formulation is ongoing in the United States.
JF  - Vaccine
AU  - Shimp, RL Jr
AU  - Rowe, C
AU  - Reiter, K
AU  - Chen, B
AU  - Nguyen, V
AU  - Aebig, J
AU  - Rausch, K M
AU  - Kumar, K
AU  - Wu, Y
AU  - Jin, A J
AU  - Jones, D S
AU  - Narum, D L
AD  - Laboratory of Malaria Immunology and Vaccinology, Twinbrook 1, Room 1115, NIAID, NIH, Rockville, MD 20852, USA, dnarum@niaid.nih.gov
Y1  - 2013/06/19/
PY  - 2013
DA  - 2013 Jun 19
SP  - 2954
EP  - 2962
VL  - 31
IS  - 28
SN  - 0264-410X, 0264-410X
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts
KW  - Parasites
KW  - Human diseases
KW  - Light scattering
KW  - Disease control
KW  - Malaria
KW  - Clinical trials
KW  - Public health
KW  - Infectious diseases
KW  - Pseudomonas aeruginosa
KW  - Aquatic insects
KW  - Amino acids
KW  - Zygotes
KW  - Pest control
KW  - Cyclic GMP
KW  - Recombinants
KW  - USA
KW  - Infectivity
KW  - Antibodies
KW  - Immunogenicity
KW  - Vaccines
KW  - nanoparticles
KW  - K 03410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443369407?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Development+of+a+Pfs25-EPA+malaria+transmission+blocking+vaccine+as+a+chemically+conjugated+nanoparticle&rft.au=Shimp%2C+RL+Jr%3BRowe%2C+C%3BReiter%2C+K%3BChen%2C+B%3BNguyen%2C+V%3BAebig%2C+J%3BRausch%2C+K+M%3BKumar%2C+K%3BWu%2C+Y%3BJin%2C+A+J%3BJones%2C+D+S%3BNarum%2C+D+L&rft.aulast=Shimp&rft.aufirst=RL&rft.date=2013-06-19&rft.volume=31&rft.issue=28&rft.spage=2954&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Recombinants; Antibodies; Human diseases; Disease control; Pest control; Malaria; Vaccines; Aquatic insects; Public health; Parasites; Amino acids; Zygotes; Light scattering; Clinical trials; Cyclic GMP; Infectivity; Infectious diseases; Immunogenicity; nanoparticles; Pseudomonas aeruginosa; USA
ER  - 



TY  - JOUR
T1  - Reproductive Factors and Kidney Cancer Risk in 2 US Cohort Studies, 1993-2010
AN  - 1412506843; 18174299
AB  - Clinical and experimental findings suggest that female hormonal and reproductive factors could influence kidney cancer development. To evaluate this association, we conducted analyses in 2 large prospective cohorts (the National Institutes of Health-AARP Diet and Health Study (NIH-AARP), 1995-2006, and the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO), 1993-2010). Cohort-specific and aggregated hazard ratios and 95% confidence intervals relating reproductive factors and kidney cancer risk were computed by Cox regression. The analysis included 792 incident kidney cancer cases among 283,952 postmenopausal women. Women who had undergone a hysterectomy were at a significantly elevated kidney cancer risk in both NIH-AARP (hazard ratio = 1.28, 95% confidence interval: 1.09, 1.50) and PLCO (hazard ratio = 1.41, 95% confidence interval: 1.06, 1.88). Similar results were observed for both cohorts after analyses were restricted to women who had undergone a hysterectomy with or without an oophorectomy. For the NIH-AARP cohort, an inverse association was observed with increasing age at menarche (P for trend = 0.02) and increasing years of oral contraceptive use (P for trend = 0.02). No clear evidence of an association with parity or other reproductive factors was found. Our results suggest that hysterectomy is associated with increased risk of kidney cancer. The observed associations with age at menarche and oral contraceptive use warrant further investigation.
JF  - American Journal of Epidemiology
AU  - Karami, Sara
AU  - Daugherty, Sarah E
AU  - Schonfeld, Sara J
AU  - Park, Yikyung
AU  - Hollenbeck, Albert R
AU  - Grubb, Robert L
AU  - Hofmann, Jonathan N
AU  - Chow, Wong-Ho
AU  - Purdue, Mark P
AD  - Correspondence to Dr. Sara Karami, National Cancer Institute, Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, 6120 Executive Blvd, EPS 8121, Rockville, MD 20852, karamis@mail.nih.gov
Y1  - 2013/06/15/
PY  - 2013
DA  - 2013 Jun 15
SP  - 1368
EP  - 1377
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 12
SN  - 0002-9262, 0002-9262
KW  - Risk Abstracts
KW  - Diets
KW  - Parity
KW  - USA
KW  - Age
KW  - Post-menopause
KW  - Lung
KW  - Kidney
KW  - Ovarian carcinoma
KW  - Cancer
KW  - Contraceptives
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412506843?accountid=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=Reproductive+Factors+and+Kidney+Cancer+Risk+in+2+US+Cohort+Studies%2C+1993-2010&rft.au=Karami%2C+Sara%3BDaugherty%2C+Sarah+E%3BSchonfeld%2C+Sara+J%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BGrubb%2C+Robert+L%3BHofmann%2C+Jonathan+N%3BChow%2C+Wong-Ho%3BPurdue%2C+Mark+P&rft.aulast=Karami&rft.aufirst=Sara&rft.date=2013-06-15&rft.volume=177&rft.issue=12&rft.spage=1368&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws406
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Parity; Diets; Age; Lung; Post-menopause; Kidney; Ovarian carcinoma; Contraceptives; Cancer; USA
DO  - http://dx.doi.org/10.1093/aje/kws406
ER  - 



TY  - JOUR
T1  - Promoter-proximal CCCTC-factor binding is associated with an increase in the transcriptional pausing index
AN  - 1399917156; 18174343
AB  - Motivation: It has been known for more than 2 decades that after RNA polymerase II (RNAPII) initiates transcription, it can enter into a paused or stalled state immediately downstream of the transcription start site before productive elongation. Recent advances in high-throughput genomic technologies facilitated the discovery that RNAPII pausing at promoters is a widespread physiologically regulated phenomenon. The molecular underpinnings of pausing are incompletely understood. The CCCTC-factor (CTCF) is a ubiquitous nuclear factor that has diverse regulatory functions, including a recently discovered role in promoting RNAPII pausing at splice sites.Results: In this study, we analyzed CTCF binding sites and nascent transcriptomic data from three different cell types, and found that promoter-proximal CTCF binding is significantly associated with RNAPII pausing.
JF  - Bioinformatics
AU  - Paredes, Sur Herrera
AU  - Melgar, Michael F
AU  - Sethupathy, Praveen
AD  - super(1)Curriculum in Bioinformatics and Computational Biology, super(2)Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA, super(3)Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA, super(4)Department of Genetics and super(5)Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Y1  - 2013/06/15/
PY  - 2013
DA  - 2013 Jun 15
SP  - 1485
EP  - 1487
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 12
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Promoters
KW  - Elongation
KW  - DNA-directed RNA polymerase
KW  - Data processing
KW  - Transcription
KW  - Bioinformatics
KW  - genomics
KW  - Internet
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399917156?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Promoter-proximal+CCCTC-factor+binding+is+associated+with+an+increase+in+the+transcriptional+pausing+index&rft.au=Paredes%2C+Sur+Herrera%3BMelgar%2C+Michael+F%3BSethupathy%2C+Praveen&rft.aulast=Paredes&rft.aufirst=Sur&rft.date=2013-06-15&rft.volume=29&rft.issue=12&rft.spage=1485&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbts596
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Elongation; Promoters; DNA-directed RNA polymerase; Data processing; Transcription; genomics; Bioinformatics; Internet
DO  - http://dx.doi.org/10.1093/bioinformatics/bts596
ER  - 



TY  - JOUR
T1  - microRNA and inflammatory gene expression as prognostic marker for overall survival in esophageal squamous cell carcinoma.
AN  - 1326731749; 23175214
AB  - MicroRNAs (miRNAs) and inflammatory genes have a role in the initiation and development of esophageal squamous cell carcinoma (ESCC). In our study, we examined the potential of using miRNA and inflammatory gene expression patterns as prognostic classifiers for ESCC. Five miRNAs and 25 inflammatory-related genes were measured by quantitative reverse transcriptase PCR in tumor tissues and adjacent noncancerous tissues from 178 Chinese patients with ESCC. The expression levels of miR-21 (p = 0.027), miR-181b (p = 0.002) and miR-146b (p = 0.021) in tumor tissue and miR-21 (p = 0.003) in noncancerous tissue were associated with overall survival of patients. These data were combined to generate a miRNA risk score that was significantly associated with worse prognosis (p = 0.0001), suggesting that these miRNAs may be useful prognostic classifiers for ESCC. To construct an inflammatory gene prognostic classifier, we divided the population into training (n = 124) and test cohorts (n = 54). The expression levels of CRY61, CTGF and IL-18 in tumor tissue and VEGF in adjacent noncancerous tissue were modestly associated with prognosis in the training cohort |Z-score| > 1.5 and were subsequently used to construct a Cox regression-based inflammatory risk score (IRS). IRS was significantly associated with survival in both the training cohort (p = 0.002) and the test cohort (p = 0.005). Furthermore, Cox regression models combining both miRNA risk score and IRS performed significantly better than models with either alone (p < 0.001 likelihood ratio test). Therefore, miRNA and inflammatory gene expression patterns, alone or in combination, have potential as prognostic classifiers for ESCC and may help to guide therapeutic decisions.
          Copyright © 2012 UICC.
JF  - International journal of cancer
AU  - Zhao, Yiqiang
AU  - Schetter, Aaron J
AU  - Yang, Geoffrey B
AU  - Nguyen, Giang
AU  - Mathé, Ewy A
AU  - Li, Peng
AU  - Cai, Hong
AU  - Yu, Lei
AU  - Liu, Fangfang
AU  - Hang, Dong
AU  - Yang, Haijun
AU  - Wang, Xin Wei
AU  - Ke, Yang
AU  - Harris, Curtis C
AD  - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/06/15/
PY  - 2013
DA  - 2013 Jun 15
SP  - 2901
EP  - 2909
VL  - 132
IS  - 12
KW  - MicroRNAs
KW  - 0
KW  - Index Medicus
KW  - Gene Expression Profiling
KW  - Neoplasm Staging
KW  - Aged, 80 and over
KW  - Humans
KW  - Adult
KW  - Prognosis
KW  - Aged
KW  - Middle Aged
KW  - Male
KW  - Female
KW  - Gene Expression Regulation, Neoplastic
KW  - MicroRNAs -- genetics
KW  - Carcinoma, Squamous Cell -- pathology
KW  - Carcinoma, Squamous Cell -- mortality
KW  - Esophageal Neoplasms -- genetics
KW  - Carcinoma, Squamous Cell -- genetics
KW  - Inflammation -- genetics
KW  - Esophageal Neoplasms -- pathology
KW  - Esophageal Neoplasms -- mortality
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1326731749?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=microRNA+and+inflammatory+gene+expression+as+prognostic+marker+for+overall+survival+in+esophageal+squamous+cell+carcinoma.&rft.au=Zhao%2C+Yiqiang%3BSchetter%2C+Aaron+J%3BYang%2C+Geoffrey+B%3BNguyen%2C+Giang%3BMath%C3%A9%2C+Ewy+A%3BLi%2C+Peng%3BCai%2C+Hong%3BYu%2C+Lei%3BLiu%2C+Fangfang%3BHang%2C+Dong%3BYang%2C+Haijun%3BWang%2C+Xin+Wei%3BKe%2C+Yang%3BHarris%2C+Curtis+C&rft.aulast=Zhao&rft.aufirst=Yiqiang&rft.date=2013-06-15&rft.volume=132&rft.issue=12&rft.spage=2901&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27954
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-12
N1  - Date created - 2013-04-11
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ijc.27954
ER  - 



TY  - JOUR
T1  - Opinion on adventitious agents testing for vaccines: Why do we worry so much about adventitious agents in vaccines?
AN  - 1443370057; 18663123
AB  - The manner in which viral vaccines are produced in a biological system makes them vulnerable to micro-bial contamination. Considerable effort is expended to avoid such contamination and to detect it if it occurred. Is this effort warranted, efficient, scientifically sound, and rational? When asked for my opinion on these matters, I agreed to discuss the basis and historical context for why we do what we do and proffer opinion on what we might do instead or in addition, as we look forward to the inclusion of new strategies and methods in our arsenal. Being an advocate of the 3 R's policy, I invite a re-examination of the traditional in vivo methods in particular. I also advocate for a risk-based approach consistent with "Quality by Design" as a more scientific and rational means of addressing these issues. In the end, vaccinologists need to reassure the public that the vaccines they or their children receive are safe and pure and that all reasonable measures are taken to safeguard them.
JF  - Vaccine
AU  - Sheets, R L
AD  - CAPT USPHS, USNIH/N1AID/DA1DS, Bethesda, MD 20892, United States, rsheets@niaid.nih.gov
Y1  - 2013/06/10/
PY  - 2013
DA  - 2013 Jun 10
SP  - 2791
EP  - 2795
VL  - 31
IS  - 26
SN  - 0264-410X, 0264-410X
KW  - Health & Safety Science Abstracts; Immunology Abstracts
KW  - Children
KW  - Vaccines
KW  - F:06905
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443370057?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Opinion+on+adventitious+agents+testing+for+vaccines%3A+Why+do+we+worry+so+much+about+adventitious+agents+in+vaccines%3F&rft.au=Sheets%2C+R+L&rft.aulast=Sheets&rft.aufirst=R&rft.date=2013-06-10&rft.volume=31&rft.issue=26&rft.spage=2791&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Vaccines
ER  - 



TY  - JOUR
T1  - Randomized selection design trial evaluating CD8+-enriched versus unselected tumor-infiltrating lymphocytes for adoptive cell therapy for patients with melanoma.
AN  - 1366578103; 23650429
AB  - Adoptive cell therapy (ACT) with autologous tumor-infiltrating lymphocytes (TILs) and high-dose interleukin-2 (IL-2) administered to lymphodepleted patients with melanoma can cause durable tumor regressions. The optimal TIL product for ACT is unknown.
          Patients with metastatic melanoma were prospectively assigned to receive unselected young TILs versus CD8(+)-enriched TILs. All patients received lymphodepleting chemotherapy and high-dose IL-2 therapy and were assessed for response, toxicity, survival, and immunologic end points. Thirty-four patients received unselected young TILs with a median of 8.0% CD4(+) lymphocytes, and 35 patients received CD8(+)-enriched TILs with a median of 0.3% CD4(+) lymphocytes. One month after TIL infusion, patients who received CD8(+)-enriched TILs had significantly fewer CD4(+) peripheral blood lymphocytes (P = .01). Twelve patients responded to therapy with unselected young TILs (according to Response Evaluation Criteria in Solid Tumors [RECIST]), and seven patients responded to CD8(+)-enriched TILs (35% v 20%; not significant). Retrospective studies showed a significant association between response to treatment and interferon gamma secretion by the infused TILs in response to autologous tumor (P = .04), and in the subgroup of patients who received TILs from subcutaneous tumors, eight of 15 patients receiving unselected young TILs responded but none of eight patients receiving CD8(+)-enriched TILs responded. A randomized selection design trial was feasible for improving individualized TIL therapy. Since the evidence indicates that CD8(+)-enriched TILs are not more potent therapeutically and they are more laborious to prepare, future studies should focus on unselected young TILs.
JF  - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU  - Dudley, Mark E
AU  - Gross, Colin A
AU  - Somerville, Robert P T
AU  - Hong, Young
AU  - Schaub, Nicholas P
AU  - Rosati, Shannon F
AU  - White, Donald E
AU  - Nathan, Debbie
AU  - Restifo, Nicholas P
AU  - Steinberg, Seth M
AU  - Wunderlich, John R
AU  - Kammula, Udai S
AU  - Sherry, Richard M
AU  - Yang, James C
AU  - Phan, Giao Q
AU  - Hughes, Marybeth S
AU  - Laurencot, Carolyn M
AU  - Rosenberg, Steven A
AD  - Surgery Branch, National Cancer Institute, National Institutes of Health, CRC 3W-5752, 10 Center Dr, Bethesda, MD 20892, USA. mark_dudley@nih.gov
Y1  - 2013/06/10/
PY  - 2013
DA  - 2013 Jun 10
SP  - 2152
EP  - 2159
VL  - 31
IS  - 17
KW  - Interleukin-2
KW  - 0
KW  - Interferon-gamma
KW  - 82115-62-6
KW  - Index Medicus
KW  - Young Adult
KW  - Interleukin-2 -- administration & dosage
KW  - Prospective Studies
KW  - Tumor Cells, Cultured
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - Interferon-gamma -- immunology
KW  - Child
KW  - Adolescent
KW  - Male
KW  - Female
KW  - CD8-Positive T-Lymphocytes -- pathology
KW  - CD8-Positive T-Lymphocytes -- drug effects
KW  - Lymphocytes, Tumor-Infiltrating -- immunology
KW  - Lymphocytes, Tumor-Infiltrating -- drug effects
KW  - CD8-Positive T-Lymphocytes -- immunology
KW  - Lymphocytes, Tumor-Infiltrating -- pathology
KW  - Immunotherapy, Adoptive -- adverse effects
KW  - Melanoma -- therapy
KW  - Immunotherapy, Adoptive -- methods
KW  - Melanoma -- immunology
KW  - CD8-Positive T-Lymphocytes -- transplantation
KW  - Lymphocytes, Tumor-Infiltrating -- transplantation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1366578103?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Randomized+selection+design+trial+evaluating+CD8%2B-enriched+versus+unselected+tumor-infiltrating+lymphocytes+for+adoptive+cell+therapy+for+patients+with+melanoma.&rft.au=Dudley%2C+Mark+E%3BGross%2C+Colin+A%3BSomerville%2C+Robert+P+T%3BHong%2C+Young%3BSchaub%2C+Nicholas+P%3BRosati%2C+Shannon+F%3BWhite%2C+Donald+E%3BNathan%2C+Debbie%3BRestifo%2C+Nicholas+P%3BSteinberg%2C+Seth+M%3BWunderlich%2C+John+R%3BKammula%2C+Udai+S%3BSherry%2C+Richard+M%3BYang%2C+James+C%3BPhan%2C+Giao+Q%3BHughes%2C+Marybeth+S%3BLaurencot%2C+Carolyn+M%3BRosenberg%2C+Steven+A&rft.aulast=Dudley&rft.aufirst=Mark&rft.date=2013-06-10&rft.volume=31&rft.issue=17&rft.spage=2152&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.2012.46.6441
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-10
N1  - Date created - 2013-06-10
N1  - Date revised - 2017-01-14
N1  - Genetic sequence - NCT00513604; ClinicalTrials.gov
N1  - SuppNotes - Cited By:
J Immunother. 2003 Jul-Aug;26(4):332-42 [12843795]
J Immunol Methods. 1990 Apr 17;128(2):189-201 [1691237]
J Natl Cancer Inst. 1994 Aug 3;86(15):1159-66 [8028037]
J Immunol. 1995 Apr 15;154(8):3961-8 [7706734]
J Immunol. 2005 Mar 1;174(5):2661-70 [15728473]
J Clin Oncol. 2005 Apr 1;23(10):2346-57 [15800326]
N Engl J Med. 2008 Jun 19;358(25):2698-703 [18565862]
J Immunother. 2008 Oct;31(8):742-51 [18779745]
J Clin Oncol. 2008 Nov 10;26(32):5233-9 [18809613]
J Immunother. 2009 Oct;32(8):870-4 [19752747]
J Immunother. 2010 Apr;33(3):305-15 [20445351]
J Immunother. 2010 Jun;33(5):547-56 [20463593]
J Immunother. 2010 Oct;33(8):840-7 [20842052]
Clin Cancer Res. 2010 Dec 15;16(24):6122-31 [20668005]
J Immunother. 2011 Mar;34(2):212-20 [21304398]
Clin Cancer Res. 2011 Jul 1;17(13):4550-7 [21498393]
Nat Rev Clin Oncol. 2011 Oct;8(10):577-85 [21808266]
Clin Cancer Res. 2012 Jan 15;18(2):336-41 [22142824]
J Immunother. 2012 Apr;35(3):283-92 [22421946]
Cancer Immunol Immunother. 2012 May;61(5):725-32 [22202906]
J Immunother. 2012 Jun;35(5):400-8 [22576345]
Blood. 2012 Jun 14;119(24):5688-96 [22555974]
J Transl Med. 2012;10:69 [22475724]
J Immunother. 2012 Oct;35(8):615-20 [22996367]
Cancer Gene Ther. 2012 Dec;19(12):818-21 [23059871]
Clin Cancer Res. 2012 Dec 15;18(24):6758-70 [23032743]
Immunity. 2004 Jan;20(1):107-18 [14738769]
Comment In:
Nat Rev Clin Oncol. 2013 Jul;10(7):368 [23689751]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1200/JCO.2012.46.6441
ER  - 



TY  - JOUR
T1  - Ovarian cancer incidence trends in relation to changing patterns of menopausal hormone therapy use in the United States.
AN  - 1366577902; 23650423
AB  - After a report from the Women's Health Initiative (WHI) in 2002, a precipitous decline in menopausal hormonal therapy (MHT) use in the United States was linked to a decline in breast cancer incidence rates. Given that MHT use is also associated with increased ovarian cancer risk, we tested whether ovarian cancer incidence rates changed after 2002.
          Using the North American Association of Central Cancer Registries database (1995 to 2008; N = 171,142 incident ovarian cancers), we applied standard analytic approaches and age-period-cohort (APC) models to estimate ovarian cancer incidence rate changes before (1995 to 2002) and after (2003 to 2008) the WHI report. Among women age ≥ 50 years, age-standardized ovarian cancer incidence declined by 0.8% per year (95% CI, -1.8% to -0.5% per year) before the WHI announcement; after the WHI report, the rate declined by 2.4% per year (95% CI, -2.5% to -2.2% per year). APC models confirmed an accelerated decline in ovarian cancer incidence after the WHI report, adjusted for age and birth cohort effects. This sudden change was notable among women most likely to have used MHT (ie, women age 50 to 69 years, white women, and residents of regions with highest MHT prescription frequency). The largest changes were found for the endometrioid histologic subtype.
          After a marked reduction in MHT use around 2002, ovarian cancer incidence rates demonstrated an accelerated decline, with the largest changes for endometrioid carcinomas. This strong temporal association, although not proving a causal role of hormones in ovarian carcinogenesis, suggests that future analytic research supporting cancer control efforts should clarify the role of hormonal exposures on the development and behavior of subtypes of ovarian cancer.
JF  - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU  - Yang, Hannah P
AU  - Anderson, William F
AU  - Rosenberg, Philip S
AU  - Trabert, Britton
AU  - Gierach, Gretchen L
AU  - Wentzensen, Nicolas
AU  - Cronin, Kathleen A
AU  - Sherman, Mark E
AD  - National Cancer Institute, Bethesda, MD, MD 20852, USA. yanghan@mail.nih.gov
Y1  - 2013/06/10/
PY  - 2013
DA  - 2013 Jun 10
SP  - 2146
EP  - 2151
VL  - 31
IS  - 17
KW  - Index Medicus
KW  - Menopause -- drug effects
KW  - Humans
KW  - Incidence
KW  - Middle Aged
KW  - United States -- epidemiology
KW  - Female
KW  - Hormone Replacement Therapy -- utilization
KW  - Estrogen Replacement Therapy -- utilization
KW  - Estrogen Replacement Therapy -- methods
KW  - Hormone Replacement Therapy -- methods
KW  - Ovarian Neoplasms -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1366577902?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ovarian+cancer+incidence+trends+in+relation+to+changing+patterns+of+menopausal+hormone+therapy+use+in+the+United+States.&rft.au=Yang%2C+Hannah+P%3BAnderson%2C+William+F%3BRosenberg%2C+Philip+S%3BTrabert%2C+Britton%3BGierach%2C+Gretchen+L%3BWentzensen%2C+Nicolas%3BCronin%2C+Kathleen+A%3BSherman%2C+Mark+E&rft.aulast=Yang&rft.aufirst=Hannah&rft.date=2013-06-10&rft.volume=31&rft.issue=17&rft.spage=2146&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.2012.45.5758
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-10
N1  - Date created - 2013-06-10
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Obstet Gynecol. 2004 Nov;104(5 Pt 1):1042-50 [15516400]
J Gen Intern Med. 2005 Nov;20(11):1026-31 [16307628]
JAMA. 2004 Jan 7;291(1):47-53 [14709575]
Ann Intern Med. 2004 Feb 3;140(3):184-8 [14757616]
N Engl J Med. 1976 Jun 3;294(23):1259-62 [1264151]
Biometrics. 1983 Jun;39(2):311-24 [6626659]
Int J Epidemiol. 1992 Apr;21(2):222-8 [1428473]
J Natl Cancer Inst. 1995 Sep 20;87(18):1359-64 [7658496]
Am J Epidemiol. 1996 Jan 1;143(1):85-91 [8533751]
Adv Anat Pathol. 2006 Sep;13(5):205-27 [16998315]
N Engl J Med. 2007 Apr 19;356(16):1670-4 [17442911]
Adv Anat Pathol. 2007 May;14(3):149-77 [17452813]
Breast Cancer Res. 2007;9(4):108 [17666116]
Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):594-604 [18349277]
Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):132-9 [19124490]
Cancer. 2009 Feb 1;115(3):531-9 [19127543]
JAMA. 2009 Jul 15;302(3):298-305 [19602689]
Breast Cancer Res Treat. 2009 Sep;117(1):223-4 [18979196]
JAMA. 2010 May 5;303(17):1723-8 [20442388]
Cancer Prev Res (Phila). 2010 Jun;3(6):696-706 [20404000]
Obstet Gynecol. 2010 Nov;116(5):1088-95 [20966693]
Int J Cancer. 2010 Dec 15;127(12):2928-35 [21351271]
J Natl Cancer Inst. 2011 May 4;103(9):714-36 [21454908]
Cancer Epidemiol Biomarkers Prev. 2011 Jul;20(7):1263-8 [21610223]
Cancer Causes Control. 2011 Aug;22(8):1075-84 [21637986]
J Clin Oncol. 2012 Aug 1;30(22):2739-44 [22734032]
Nat Rev Cancer. 2012 Dec;12(12):835-48 [23151603]
J Natl Cancer Inst. 2002 Oct 16;94(20):1537-45 [12381706]
Stat Med. 2000 Feb 15;19(3):335-51 [10649300]
Epidemiology. 2000 Mar;11(2):102-5 [11021604]
JAMA. 2002 Jul 17;288(3):321-33 [12117397]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1200/JCO.2012.45.5758
ER  - 



TY  - JOUR
T1  - Hemoglobin redox reactions and red blood cell aging.
AN  - 1347254746; 23025272
AB  - The physiological mechanism(s) for recognition and removal of red blood cells (RBCs) from circulation after 120 days of its lifespan is not fully understood. Many of the processes thought to be associated with the removal of RBCs involve oxidative stress. We have focused on hemoglobin (Hb) redox reactions, which is the major source of RBC oxidative stress.
          The importance of Hb redox reactions have been shown to originate in large parts from the continuous slow autoxidation of Hb producing superoxide and its dramatic increase under hypoxic conditions. In addition, oxidative stress has been shown to be associated with redox reactions that originate from Hb reactions with nitrite and nitric oxide (NO) and the resultant formation of highly toxic peroxynitrite when NO reacts with superoxide released during Hb autoxidation. The interaction of Hb, particularly under hypoxic conditions with band 3 of the RBC membrane is critical for the generating the RBC membrane changes that trigger the removal of cells from circulation. These changes include exposure of antigenic sites, increased calcium leakage into the RBC, and the resultant leakage of potassium out of the RBC causing cell shrinkage and impaired deformability.
          The need to understand the oxidative damage to specific membrane proteins that result from redox reactions occurring when Hb is bound to the membrane. Proteomic studies that can pinpoint the specific proteins damaged under different conditions will help elucidate the cellular aging processes that result in cells being removed from circulation.
JF  - Antioxidants & redox signaling
AU  - Rifkind, Joseph M
AU  - Nagababu, Enika
AD  - Molecular Dynamics Section, National Institute on Aging, Baltimore, MD 21224, USA. rifkindj@mail.nih.gov
Y1  - 2013/06/10/
PY  - 2013
DA  - 2013 Jun 10
SP  - 2274
EP  - 2283
VL  - 18
IS  - 17
KW  - Antioxidants
KW  - 0
KW  - Hemoglobins
KW  - Reactive Nitrogen Species
KW  - Reactive Oxygen Species
KW  - Index Medicus
KW  - Oxidation-Reduction
KW  - Reactive Oxygen Species -- metabolism
KW  - Animals
KW  - Antioxidants -- metabolism
KW  - Humans
KW  - Oxidative Stress
KW  - Reactive Nitrogen Species -- metabolism
KW  - Protein Binding
KW  - Erythrocyte Membrane -- metabolism
KW  - Hemoglobins -- metabolism
KW  - Cell Aging -- physiology
KW  - Erythrocytes -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347254746?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hemoglobin+redox+reactions+and+red+blood+cell+aging.&rft.au=Rifkind%2C+Joseph+M%3BNagababu%2C+Enika&rft.aulast=Rifkind&rft.aufirst=Joseph&rft.date=2013-06-10&rft.volume=18&rft.issue=17&rft.spage=2274&rft.isbn=&rft.btitle=&rft.title=Antioxidants+%26+redox+signaling&rft.issn=1557-7716&rft_id=info:doi/10.1089%2Fars.2012.4867
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-30
N1  - Date created - 2013-04-29
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Biol Chem. 2003 Nov 21;278(47):46349-56 [12952953]
Nat Med. 2003 Dec;9(12):1498-505 [14595407]
Antioxid Redox Signal. 2004 Jun;6(3):657-66 [15130293]
Annu Rev Nutr. 2004;24:105-31 [15189115]
Biochem J. 1978 Sep 15;174(3):819-25 [728088]
J Biol Chem. 1981 Dec 10;256(23):12393-8 [7298665]
Biochem J. 1981 Nov 15;200(2):185-91 [6122443]
Experientia. 1982 May 15;38(5):575 [6124450]
Mech Ageing Dev. 1982 Nov;20(3):223-32 [7162219]
Mech Ageing Dev. 1983 Jul-Aug;22(3-4):295-308 [6632999]
Biochem J. 1984 Mar 1;218(2):531-7 [6712629]
Science. 1985 Feb 1;227(4686):531-3 [2578228]
Mech Ageing Dev. 1985 Oct 14;32(1):57-62 [3012219]
Clin Chim Acta. 1986 Aug 30;159(1):73-6 [3757268]
Biochem Int. 1986 Sep;13(3):467-77 [3790141]
IUBMB Life. 2006 Oct;58(10):572-80 [17050374]
Physiol Rev. 2007 Jan;87(1):315-424 [17237348]
Free Radic Res. 2007 Mar;41(3):316-23 [17364960]
Free Radic Biol Med. 2007 Apr 15;42(8):1146-54 [17382196]
Biorheology. 2007;44(3):179-90 [17851166]
Blood. 2008 Jan 15;111(2):932-8 [17942752]
Cell Physiol Biochem. 2008;21(1-3):183-92 [18209485]
Clin Chim Acta. 2008 Apr;390(1-2):1-11 [18243141]
Curr Opin Hematol. 2008 May;15(3):191-5 [18391783]
J Biol Chem. 2008 Apr 11;283(15):9615-22 [18203719]
Br J Haematol. 2008 May;141(4):549-56 [18419623]
Blood. 2008 May 15;111(10):5205-14 [18270324]
Blood Cells Mol Dis. 2008 Jul-Aug;41(1):60-6 [18262448]
Biochim Biophys Acta. 2008 Jul-Aug;1778(7-8):1591-600 [18439418]
Antioxid Redox Signal. 2008 Sep;10(9):1621-30 [18479207]
IUBMB Life. 2008 Oct;60(10):661-8 [18720418]
Blood. 2008 Nov 15;112(10):3939-48 [18988878]
Nitric Oxide. 2008 Dec;19(4):333-7 [18793740]
Free Radic Res. 2008 Sep;42(9):824-9 [19051108]
Cell Mol Biol Lett. 2009;14(1):23-34 [18839073]
Arch Biochem Biophys. 2009 Apr 15;484(2):146-54 [19061854]
J Biol Chem. 2009 May 8;284(19):12710-8 [19270306]
Mech Ageing Dev. 1987 Jun;39(1):29-44 [3613687]
Biochim Biophys Acta. 1987 Nov 13;904(2):239-50 [3663671]
Biochem Pharmacol. 1987 Nov 15;36(22):3801-7 [3689422]
Mech Ageing Dev. 1988 Jan;42(1):37-47 [3347096]
J Biol Chem. 1988 Sep 25;263(27):13766-73 [2971044]
Biochim Biophys Acta. 1989 Feb 13;979(1):121-6 [2537104]
Am J Hematol. 1990 Apr;33(4):249-54 [2316508]
Exp Gerontol. 1990;25(3-4):279-86 [2226662]
Proc Soc Exp Biol Med. 1991 Jan;196(1):76-82 [1670593]
Biochim Biophys Acta. 1990 Dec 6;1036(3):183-7 [2175215]
Gerontology. 1991;37(1-3):33-67 [2055498]
Free Radic Res Commun. 1991;12-13 Pt 2:645-52 [1648015]
Blood. 1992 Mar 1;79(5):1351-8 [1536958]
Am J Hematol. 1993 Jan;42(1):46-52 [8416296]
Experientia. 1993 Feb 15;49(2):100-9 [8440348]
Cell Mol Biol (Noisy-le-grand). 1993 Mar;39(2):131-53 [8513271]
J Biol Chem. 1994 Feb 11;269(6):4207-14 [8307983]
Methods Enzymol. 1994;231:490-6 [8041270]
Proc Natl Acad Sci U S A. 1994 Aug 16;91(17):8137-41 [8058769]
J Biol Chem. 1994 Oct 7;269(40):24845-53 [7929164]
Adv Exp Med Biol. 1994;361:345-51 [7597958]
Mech Ageing Dev. 1995 Jan 31;78(1):15-26 [7603087]
Biochemistry. 1996 May 21;35(20):6393-8 [8639585]
Mech Ageing Dev. 1996 Mar 29;86(3):145-50 [8733109]
Gerontology. 1998;44(2):111-20 [9523223]
Biochem Biophys Res Commun. 1998 Jun 29;247(3):592-6 [9647738]
Gen Pharmacol. 1998 Sep;31(3):343-7 [9703199]
Blood. 1999 Jan 1;93(1):376-84 [9864184]
Biochim Biophys Acta. 1999 May 5;1411(2-3):290-309 [10320664]
Blood. 1999 Jun 1;93(11):4006-10 [10339510]
Antioxid Redox Signal. 2004 Dec;6(6):967-78 [15548894]
Cell Physiol Biochem. 2005;15(1-4):1-18 [15665511]
Clin Sci (Lond). 2005 Sep;109(3):217-26 [16104842]
Methods Enzymol. 2005;396:229-45 [16291236]
Blood. 2006 Apr 1;107(7):2943-51 [16368881]
Circulation. 2006 Apr 4;113(13):1708-14 [16585403]
Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1193-203 [16910767]
Nat Chem Biol. 2006 Sep;2(9):486-93 [16906150]
FASEB J. 2009 Sep;23(9):3159-70 [19417084]
Am J Physiol Heart Circ Physiol. 2009 Oct;297(4):H1494-503 [19700624]
Life Sci. 2010 Jan 16;86(3-4):133-8 [19958781]
Blood. 2010 Mar 11;115(10):2021-7 [20038785]
J Biol Chem. 2010 Jun 25;285(26):19976-85 [20392689]
Blood Transfus. 2010 Jun;8 Suppl 3:s39-47 [20606748]
Transfus Clin Biol. 2010 Sep;17(3):151-64 [20655788]
Nitric Oxide. 2011 Mar 15;24(2):102-9 [21236353]
Blood. 2011 Jun 2;117(22):5998-6006 [21474668]
J Am Chem Soc. 2011 Aug 24;133(33):13010-22 [21755997]
Blood. 2011 Sep 29;118(13):3694-7 [21832281]
Adv Exp Med Biol. 2012;737:183-9 [22259100]
Curr Opin Hematol. 2000 Mar;7(2):113-6 [10698298]
Biochem Biophys Res Commun. 2000 Jul 14;273(3):839-45 [10891334]
Clin Chem Lab Med. 2000 Mar;38(3):245-9 [10905762]
Biochemistry. 2000 Oct 10;39(40):12503-11 [11015232]
Biochem Biophys Res Commun. 2001 Aug 10;286(1):28-32 [11485303]
Biochemistry. 2001 Dec 18;40(50):15300-9 [11735412]
FEBS Lett. 2002 Feb 27;513(2-3):184-8 [11904147]
Free Radic Biol Med. 2002 Apr 1;32(7):568-76 [11909691]
Biochemistry. 2002 Jun 11;41(23):7407-15 [12044174]
Biochemistry. 2002 Jul 9;41(27):8630-7 [12093280]
Biochem J. 2002 Nov 15;368(Pt 1):137-44 [12175337]
Blood. 2003 Jan 15;101(2):747-51 [12393566]
Biochim Biophys Acta. 2003 Mar 17;1620(1-3):211-7 [12595091]
Clin Hemorheol Microcirc. 2003;28(1):29-40 [12632010]
Cell Death Differ. 2003 Feb;10(2):249-56 [12700653]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1089/ars.2012.4867
ER  - 



TY  - JOUR
T1  - Topographic diversity of fungal and bacterial communities in human skin
AN  - 1560108037; 20501481
AB  - Traditional culture-based methods have incompletely defined the microbial landscape of common recalcitrant human fungal skin diseases, including athlete's foot and toenail infections. Skin protects humans from invasion by pathogenic microorganisms and provides a home for diverse commensal microbiota. Bacterial genomic sequence data have generated novel hypotheses about species and community structures underlying human disorders. However, microbial diversity is not limited to bacteria; microorganisms such as fungi also have major roles in microbial community stability, human health and disease. Genomic methodologies to identify fungal species and communities have been limited compared with those that are available for bacteria. Fungal evolution can be reconstructed with phylogenetic markers, including ribosomal RNA gene regions and other highly conserved genes. Here we sequenced and analysed fungal communities of 14skin sites in 10healthy adults. Eleven core-body and arm sites were dominated by fungi of the genus Malassezia, with only species-level classifications revealing fungal-community composition differences between sites. By contrast, three foot sites-plantar heel, toenail and toe web-showed high fungal diversity. Concurrent analysis of bacterial and fungal communities demonstrated that physiologic attributes and topography of skin differentially shape these two microbial communities. These results provide a framework for future investigation of the contribution of interactions between pathogenic and commensal fungal and bacterial communities to the maintainenace of human health and to disease pathogenesis.
JF  - Nature
AU  - Findley, Keisha
AU  - Oh, Julia
AU  - Yang, Joy
AU  - Conlan, Sean
AU  - Deming, Clayton
AU  - Meyer, Jennifer A
AU  - Schoenfeld, Deborah
AU  - Nomicos, Effie
AU  - Park, Morgan
AU  - Becker, Jesse
AU  - Benjamin, Betty
AU  - Blakesley, Robert
AU  - Bouffard, Gerry
AU  - Brooks, Shelise
AU  - Coleman, Holly
AU  - Dekhtyar, Mila
AU  - Gregory, Michael
AU  - Guan, Xiaobin
AU  - Gupta, Jyoti
AU  - Han, Joel
AU  - Hargrove, April
AU  - Ho, Shi-ling
AU  - Johnson, Taccara
AU  - Legaspi, Richelle
AU  - Lovett, Sean
AU  - Maduro, Quino
AU  - Masiello, Cathy
AU  - Maskeri, Baishali
AU  - McDowell, Jenny
AU  - Montemayor, Casandra
AU  - Mullikin, James
AU  - Riebow, Nancy
AU  - Schandler, Karen
AU  - Schmidt, Brian
AU  - Sison, Christina
AU  - Stantripop, Mal
AU  - Thomas, James
AU  - Thomas, Pam
AU  - Vemulapalli, Meg
AU  - Young, Alice
AU  - Kong, Heidi H
AU  - Segre, Julia A
AD  - Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
PY  - 2013
SP  - 367
EP  - 370
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 498
IS  - 7454
SN  - 0028-0836, 0028-0836
KW  - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Toenail
KW  - Phylogeny
KW  - Bacteria
KW  - Data processing
KW  - Tinea pedis
KW  - Fungi
KW  - Landscape
KW  - Commensals
KW  - Infection
KW  - rRNA
KW  - Classification
KW  - Skin diseases
KW  - Community structure
KW  - Malassezia
KW  - Foot
KW  - Microorganisms
KW  - Evolutionary genetics
KW  - genomics
KW  - Evolution
KW  - Topography
KW  - Toe
KW  - J 02400:Human Diseases
KW  - K 03450:Ecology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560108037?accountid=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=Nature&rft.atitle=Topographic+diversity+of+fungal+and+bacterial+communities+in+human+skin&rft.au=Findley%2C+Keisha%3BOh%2C+Julia%3BYang%2C+Joy%3BConlan%2C+Sean%3BDeming%2C+Clayton%3BMeyer%2C+Jennifer+A%3BSchoenfeld%2C+Deborah%3BNomicos%2C+Effie%3BPark%2C+Morgan%3BBecker%2C+Jesse%3BBenjamin%2C+Betty%3BBlakesley%2C+Robert%3BBouffard%2C+Gerry%3BBrooks%2C+Shelise%3BColeman%2C+Holly%3BDekhtyar%2C+Mila%3BGregory%2C+Michael%3BGuan%2C+Xiaobin%3BGupta%2C+Jyoti%3BHan%2C+Joel%3BHargrove%2C+April%3BHo%2C+Shi-ling%3BJohnson%2C+Taccara%3BLegaspi%2C+Richelle%3BLovett%2C+Sean%3BMaduro%2C+Quino%3BMasiello%2C+Cathy%3BMaskeri%2C+Baishali%3BMcDowell%2C+Jenny%3BMontemayor%2C+Casandra%3BMullikin%2C+James%3BRiebow%2C+Nancy%3BSchandler%2C+Karen%3BSchmidt%2C+Brian%3BSison%2C+Christina%3BStantripop%2C+Mal%3BThomas%2C+James%3BThomas%2C+Pam%3BVemulapalli%2C+Meg%3BYoung%2C+Alice%3BKong%2C+Heidi+H%3BSegre%2C+Julia+A&rft.aulast=Findley&rft.aufirst=Keisha&rft.date=2013-06-09&rft.volume=498&rft.issue=7454&rft.spage=367&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/10.1038%2Fnature12171
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2015-12-23
N1  - SubjectsTermNotLitGenreText - Phylogeny; Toenail; Data processing; Tinea pedis; Fungi; Landscape; Commensals; Infection; rRNA; Skin diseases; Classification; Community structure; Microorganisms; Foot; genomics; Evolutionary genetics; Evolution; Toe; Topography; Bacteria; Malassezia
DO  - http://dx.doi.org/10.1038/nature12171
ER  - 



TY  - JOUR
T1  - Prenatal Exposure to Persistent Organochlorines and Childhood Obesity in the U.S. Collaborative Perinatal Project
AN  - 1660067103; 18597924
AB  - Background: In some previous studies, prenatal exposure to persistent organochlorines such as 1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p-DDE), polychlorinated biphenyls (PCBs), and hexachlorobenzene (HCB) has been associated with higher body mass index (BMI) in children. Objective: Our goal was to evaluate the association of maternal serum levels of beta -hexachlorocyclohexane ( beta -HCH), p,p-DDE, dichlorodiphenyltrichloroethane (p,p-DDT), dieldrin, heptachlor epoxide, HCB, trans-nonachlor, oxychlordane, and PCBs with offspring obesity during childhood. Methods: The analysis was based on a subsample of 1,915 children followed until 7 years of age as part of the U.S. Collaborative Perinatal Project (CPP). The CPP enrolled pregnant women in 1959-1965; exposure levels were measured in third-trimester maternal serum that was collected before these organochlorines were banned in the United States. Childhood overweight and obesity were defined using age- and sex-specific cut points for BMI as recommended by the International Obesity Task Force. Results: Adjusted results did not show clear evidence for an association between organochlorine exposure and obesity; however, a suggestive finding emerged for dieldrin. Compared with those in the lowest quintile (dieldrin, < 0.57 mu g/L), odds of obesity were 3.6 (95% CI: 1.3, 10.5) for the fourth and 2.3 (95% CI: 0.8, 7.1) for the highest quintile. Overweight and BMI were unrelated to organochlorine exposure. Conclusions: In this population with relatively high levels of exposure to organochlorines, no clear associations with obesity or BMI emerged. Citation: Cupul-Uicab LA, Klebanoff MA, Brock JW, Longnecker MP. 2013. Prenatal exposure to persistent organochlorines and childhood obesity in the U.S. Collaborative Perinatal Project. Environ Health Perspect 121:1103-1109; http://dx.doi.org/10.1289/ehp.1205901
JF  - Environmental Health Perspectives
AU  - Cupul-Uicab, Lea A
AU  - Klebanoff, Mark A
AU  - Brock, John W
AU  - Longnecker, Matthew P
AD  - Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
PY  - 2013
SP  - 1103
EP  - 1109
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 9
SN  - 0091-6765, 0091-6765
KW  - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - Obesity
KW  - Dieldrin
KW  - Body size (biology)
KW  - Tasks
KW  - Health
KW  - Children
KW  - Adjustment
KW  - Serums
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660067103?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Prenatal+Exposure+to+Persistent+Organochlorines+and+Childhood+Obesity+in+the+U.S.+Collaborative+Perinatal+Project&rft.au=Cupul-Uicab%2C+Lea+A%3BKlebanoff%2C+Mark+A%3BBrock%2C+John+W%3BLongnecker%2C+Matthew+P&rft.aulast=Cupul-Uicab&rft.aufirst=Lea&rft.date=2013-06-05&rft.volume=121&rft.issue=9&rft.spage=1103&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205901
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2016-01-06
DO  - http://dx.doi.org/10.1289/ehp.1205901
ER  - 



TY  - JOUR
T1  - Household Air Pollution in Low- and Middle-Income Countries: Health Risks and Research Priorities
AN  - 1412506943; 18174516
AB  - William Martin and colleagues report on their stakeholder meetings that reviewed the health risks of household air pollution and cookstoves, and identified research priorities in seven key areas. Please see later in the article for the Editors' Summary
JF  - PLOS Medicine
AU  - Martin, William J
AU  - Glass, Roger I
AU  - Araj, Houmam
AU  - Balbus, John
AU  - Collins, Francis S
AU  - Curtis, Sian
AU  - Diette, Gregory B
AU  - Elwood, William N
AU  - Falk, Henry
AU  - Hibberd, Patricia L
AU  - Keown, Susan EJ
AU  - Mehta, Sumi
AU  - Patrick, Erin
AU  - Rosenbaum, Julia
AU  - Sapkota, Amir
AU  - Tolunay, HEser
AU  - Bruce, Nigel G
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America
Y1  - 2013/06/04/
PY  - 2013
DA  - 2013 Jun 04
PB  - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States
VL  - 10
IS  - 6
SN  - 1549-1277, 1549-1277
KW  - Pollution Abstracts; Risk Abstracts; Health & Safety Science Abstracts
KW  - Health risks
KW  - Pollution effects
KW  - P 0000:AIR POLLUTION
KW  - R2 23060:Medical and environmental health
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412506943?accountid=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=PLOS+Medicine&rft.atitle=Household+Air+Pollution+in+Low-+and+Middle-Income+Countries%3A+Health+Risks+and+Research+Priorities&rft.au=Martin%2C+William+J%3BGlass%2C+Roger+I%3BAraj%2C+Houmam%3BBalbus%2C+John%3BCollins%2C+Francis+S%3BCurtis%2C+Sian%3BDiette%2C+Gregory+B%3BElwood%2C+William+N%3BFalk%2C+Henry%3BHibberd%2C+Patricia+L%3BKeown%2C+Susan+EJ%3BMehta%2C+Sumi%3BPatrick%2C+Erin%3BRosenbaum%2C+Julia%3BSapkota%2C+Amir%3BTolunay%2C+HEser%3BBruce%2C+Nigel+G&rft.aulast=Martin&rft.aufirst=William&rft.date=2013-06-04&rft.volume=10&rft.issue=6&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLOS+Medicine&rft.issn=15491277&rft_id=info:doi/10.1371%2Fjournal.pmed.1001455
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Pollution effects
DO  - http://dx.doi.org/10.1371/journal.pmed.1001455
ER  - 



TY  - JOUR
T1  - Immune targeting of fibroblast activation protein triggers recognition of multipotent bone marrow stromal cells and cachexia.
AN  - 1365053534; 23712432
AB  - Fibroblast activation protein (FAP) is a candidate universal target antigen because it has been reported to be selectively expressed in nearly all solid tumors by a subset of immunosuppressive tumor stromal fibroblasts. We verified that 18/18 human tumors of various histologies contained pronounced stromal elements staining strongly for FAP, and hypothesized that targeting tumor stroma with FAP-reactive T cells would inhibit tumor growth in cancer-bearing hosts. T cells genetically engineered with FAP-reactive chimeric antigen receptors (CARs) specifically degranulated and produced effector cytokines upon stimulation with FAP or FAP-expressing cell lines. However, adoptive transfer of FAP-reactive T cells into mice bearing a variety of subcutaneous tumors mediated limited antitumor effects and induced significant cachexia and lethal bone toxicities in two mouse strains. We found that FAP was robustly expressed on PDGFR-α(+), Sca-1(+) multipotent bone marrow stromal cells (BMSCs) in mice, as well as on well-characterized, clinical-grade multipotent human BMSCs. Accordingly, both mouse and human multipotent BMSCs were recognized by FAP-reactive T cells. The lethal bone toxicity and cachexia observed after cell-based immunotherapy targeting FAP cautions against its use as a universal target. Moreover, the expression of FAP by multipotent BMSCs may point toward the cellular origins of tumor stromal fibroblasts.
JF  - The Journal of experimental medicine
AU  - Tran, Eric
AU  - Chinnasamy, Dhanalakshmi
AU  - Yu, Zhiya
AU  - Morgan, Richard A
AU  - Lee, Chyi-Chia Richard
AU  - Restifo, Nicholas P
AU  - Rosenberg, Steven A
AD  - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. eric.tran@nih.gov
Y1  - 2013/06/03/
PY  - 2013
DA  - 2013 Jun 03
SP  - 1125
EP  - 1135
VL  - 210
IS  - 6
KW  - Antigens, Ly
KW  - 0
KW  - Antigens, Neoplasm
KW  - Membrane Proteins
KW  - Receptors, Antigen
KW  - Receptor, Platelet-Derived Growth Factor alpha
KW  - EC 2.7.10.1
KW  - Serine Endopeptidases
KW  - EC 3.4.21.-
KW  - fibroblast activation protein alpha
KW  - Gelatinases
KW  - EC 3.4.24.-
KW  - Index Medicus
KW  - Animals
KW  - Antigens, Ly -- immunology
KW  - Humans
KW  - Cell Line, Tumor
KW  - Mice
KW  - Mice, Inbred BALB C
KW  - Melanoma, Experimental -- immunology
KW  - Receptor, Platelet-Derived Growth Factor alpha -- immunology
KW  - Receptors, Antigen -- immunology
KW  - Antigens, Neoplasm -- immunology
KW  - T-Lymphocytes -- immunology
KW  - Female
KW  - Male
KW  - Fibroblasts -- immunology
KW  - Gelatinases -- immunology
KW  - Membrane Proteins -- immunology
KW  - Cachexia -- pathology
KW  - Cachexia -- immunology
KW  - Serine Endopeptidases -- immunology
KW  - Mesenchymal Stromal Cells -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1365053534?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=Immune+targeting+of+fibroblast+activation+protein+triggers+recognition+of+multipotent+bone+marrow+stromal+cells+and+cachexia.&rft.au=Tran%2C+Eric%3BChinnasamy%2C+Dhanalakshmi%3BYu%2C+Zhiya%3BMorgan%2C+Richard+A%3BLee%2C+Chyi-Chia+Richard%3BRestifo%2C+Nicholas+P%3BRosenberg%2C+Steven+A&rft.aulast=Tran&rft.aufirst=Eric&rft.date=2013-06-03&rft.volume=210&rft.issue=6&rft.spage=1125&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=1540-9538&rft_id=info:doi/10.1084%2Fjem.20130110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-12
N1  - Date created - 2013-06-04
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Onkologie. 2003 Feb;26(1):44-8 [12624517]
Nat Rev Mol Cell Biol. 2011 Feb;12(2):126-31 [21253000]
Proc Natl Acad Sci U S A. 1988 May;85(9):3110-4 [2896356]
Proc Natl Acad Sci U S A. 1990 Sep;87(18):7235-9 [2402505]
J Clin Oncol. 1994 Jun;12(6):1193-203 [8201382]
Cancer Res. 2005 Dec 1;65(23):11156-63 [16322266]
J Cell Sci. 2006 Jun 1;119(Pt 11):2204-13 [16684817]
J Clin Invest. 2006 Jul;116(7):1955-62 [16794736]
Cancer Biol Ther. 2007 Nov;6(11):1691-9 [18032930]
J Exp Med. 2009 Oct 26;206(11):2483-96 [19841085]
Nat Rev Clin Oncol. 2011 Aug;8(8):456-66 [21448151]
Nature. 2012 Jan 26;481(7382):457-62 [22281595]
J Transl Med. 2012;10:23 [22309358]
Sci Transl Med. 2012 Mar 28;4(127):127ps8 [22461638]
Int Rev Cell Mol Biol. 2012;297:83-116 [22608558]
Cell Adh Migr. 2012 May-Jun;6(3):231-5 [22568983]
Clin Cancer Res. 2012 Aug 15;18(16):4266-76 [22896693]
Cancer Res. 2008 Jun 1;68(11):4331-9 [18519693]
Clin Cancer Res. 2008 Jul 15;14(14):4584-92 [18628473]
Br J Haematol. 2008 Sep;142(5):827-30 [18510677]
Curr Opin Immunol. 2009 Apr;21(2):215-23 [19327974]
Clin Oncol (R Coll Radiol). 2009 Aug;21(6):464-72 [19501491]
BMC Cancer. 2009;9:263 [19643020]
J Clin Invest. 2009 Dec;119(12):3613-25 [19920354]
PLoS One. 2009;4(11):e7965 [19956757]
Hum Gene Ther. 2009 Nov;20(11):1229-39 [19702437]
Nature. 2010 Aug 12;466(7308):829-34 [20703299]
Cancer Sci. 2010 Nov;101(11):2325-32 [20804499]
Science. 2010 Nov 5;330(6005):827-30 [21051638]
Clin Cancer Res. 2003 May;9(5):1639-47 [12738716]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1084/jem.20130110
ER  - 



TY  - JOUR
T1  - Childhood Trauma Exposure and Alcohol Dependence Severity in Adulthood: Mediation by Emotional Abuse Severity and Neuroticism
AN  - 1842510073; 18095528
AB  - Childhood trauma has been linked with a number of negative outcomes later in life, including alcohol dependence (AD). Previous studies have suggested a mediating role for neuroticism in the relationship between childhood trauma and psychopathology. In this study, we investigate the prevalence of multiple types of childhood trauma in treatment-seeking alcohol-dependent patients, and the associations between childhood trauma and AD severity using multiple mediation analysis. The prevalence of 5 types of childhood trauma-emotional abuse, sexual abuse, physical abuse, emotional neglect, and physical neglect-was assessed in treatment-seeking alcohol-dependent patients (n = 280) and healthy controls (n = 137) using the Childhood Trauma Questionnaire. Multiple mediation analyses were used to model associations between childhood trauma measures and alcohol-related outcomes, primarily the severity of AD in the alcohol-dependent sample. Childhood trauma was significantly more prevalent and more severe in the alcohol-dependent subjects. In addition, childhood trauma was found to influence AD severity, an effect that was mediated by neuroticism. When individual trauma types were examined, emotional abuse was found to be the primary predictor of AD severity, both directly and through the mediating effects of the impulsivity subfacet of neuroticism. Physical abuse also had a moderate direct effect on AD severity. Mediation analysis did not reveal any association between childhood trauma and Alcohol Use Disorders Identification Test score in the nondependent control sample. Childhood trauma is highly prevalent in treatment-seeking alcoholics and may play a significant role in the development and severity of AD through an internalizing pathway involving negative affect. Our findings suggest that alcoholics with a history of childhood emotional abuse may be particularly vulnerable to severe dependence.
JF  - Alcoholism: Clinical and Experimental Research
AU  - Schwandt, Melanie L
AU  - Heilig, Markus
AU  - Hommer, Daniel W
AU  - George, David T
AU  - Ramchandani, Vijay A
AD  - Laboratory of Clinical and Translational Studies. National Institute on Alcohol Abuse and Alcoholism
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 984
EP  - 992
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 37
IS  - 6
SN  - 0145-6008, 0145-6008
KW  - Toxicology Abstracts
KW  - Inventories
KW  - Emotions
KW  - Neurosis
KW  - Drug abuse
KW  - Children
KW  - Alcoholics
KW  - Abuse
KW  - Trauma
KW  - Drug dependence
KW  - impulsive behavior
KW  - Alcoholism
KW  - Psychopathology
KW  - Ethanol
KW  - X 24380:Social Poisons & Drug Abuse
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842510073?accountid=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=Childhood+Trauma+Exposure+and+Alcohol+Dependence+Severity+in+Adulthood%3A+Mediation+by+Emotional+Abuse+Severity+and+Neuroticism&rft.au=Schwandt%2C+Melanie+L%3BHeilig%2C+Markus%3BHommer%2C+Daniel+W%3BGeorge%2C+David+T%3BRamchandani%2C+Vijay+A&rft.aulast=Schwandt&rft.aufirst=Melanie&rft.date=2013-06-01&rft.volume=37&rft.issue=6&rft.spage=984&rft.isbn=&rft.btitle=&rft.title=Alcoholism%3A+Clinical+and+Experimental+Research&rft.issn=01456008&rft_id=info:doi/10.1111%2Facer.12053
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Emotions; Inventories; Neurosis; Children; Drug abuse; Abuse; Alcoholics; Trauma; Drug dependence; impulsive behavior; Alcoholism; Psychopathology; Ethanol
DO  - http://dx.doi.org/10.1111/acer.12053
ER  - 



TY  - JOUR
T1  - Loss of sulfiredoxin renders mice resistant to azoxymethane/dextran sulfate sodium-induced colon carcinogenesis
AN  - 1660408572; 18150485
AB  - Sulfiredoxin (Srx) is the enzyme that reduces the hyperoxidized inactive form of peroxiredoxins. To study the function of Srx in carcinogenesis in vivo, we tested whether loss of Srx protects mice from cancer development. Srx null mice were generated and colon carcinogenesis was induced by an azoxymethane (AOM) and dextran sulfate sodium (DSS) protocol. Compared with either wild-type (Wt) or heterozygotes, Srx super(-/-) mice had significantly reduced rates in both tumor multiplicity and volume. Mechanistic studies reveal that loss of Srx did not alter tumor cell proliferation; however, increased apoptosis and decreased inflammatory cell infiltration were obvious in tumors from Srx null mice compared with those from Wt control. In addition to the AOM/DSS model, examination of Srx expression in human reveals a tissue-specific expression pattern. Srx expression was also demonstrated in tumors from colorectal cancer patients and the levels of expression were associated with patients' clinic stages. These data provide the first in vivo evidence that loss of Srx renders mice resistant to AOM/DSS-induced colon carcinogenesis, suggesting that Srx has a critical oncogenic role in cancer development, and Srx may be used as a marker for human colon cancer pathogenicity.
JF  - Carcinogenesis
AU  - Wei, Qiou
AU  - Jiang, Hong
AU  - Baker, Alyson
AU  - Dodge, Lisa K
AU  - Gerard, Matthieu
AU  - Young, Matthew R
AU  - Toledano, Michel B
AU  - Colburn, Nancy H
AD  - super(1)Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD 21702, USA,, qiou.wei@uky.edu
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1403
EP  - 1410
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 34
IS  - 6
SN  - 0143-3334, 0143-3334
KW  - Toxicology Abstracts
KW  - Data processing
KW  - Apoptosis
KW  - Animal models
KW  - Enzymes
KW  - Peroxiredoxin
KW  - Tumors
KW  - Colon cancer
KW  - Tumor cells
KW  - Inflammation
KW  - Metastases
KW  - Sodium
KW  - Dextran sulfate
KW  - Pathogenicity
KW  - Azoxymethane
KW  - Heterozygotes
KW  - Carcinogenesis
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660408572?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Loss+of+sulfiredoxin+renders+mice+resistant+to+azoxymethane%2Fdextran+sulfate+sodium-induced+colon+carcinogenesis&rft.au=Wei%2C+Qiou%3BJiang%2C+Hong%3BBaker%2C+Alyson%3BDodge%2C+Lisa+K%3BGerard%2C+Matthieu%3BYoung%2C+Matthew+R%3BToledano%2C+Michel+B%3BColburn%2C+Nancy+H&rft.aulast=Wei&rft.aufirst=Qiou&rft.date=2013-06-01&rft.volume=34&rft.issue=6&rft.spage=1403&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt059
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-03-04
N1  - SubjectsTermNotLitGenreText - Apoptosis; Data processing; Animal models; Peroxiredoxin; Enzymes; Colon cancer; Tumors; Tumor cells; Inflammation; Sodium; Metastases; Pathogenicity; Dextran sulfate; Azoxymethane; Carcinogenesis; Heterozygotes
DO  - http://dx.doi.org/10.1093/carcin/bgt059
ER  - 



TY  - JOUR
T1  - A Novel, Multi-Parallel, Real-Time Polymerase Chain Reaction Approach for Eight Gastrointestinal Parasites Provides Improved Diagnostic Capabilities to Resource-Limited At-Risk Populations
AN  - 1647006303; 21172102
AB  - Diagnosis of gastrointestinal parasites has traditionally relied on stool microscopy, which has low diagnostic sensitivity and specificity. We have developed a novel, rapid, high-throughput quantitative multi-parallel real-time polymerase chain reaction (qPCR) platform. Species-specific primers/probes were used for eight common gastrointestinal parasite pathogens: Ascaris lumbricoides, Necator americanus, Ancylostoma duodenale, Giardia lamblia, Cryptosporidium spp., Entamoeba histolytica, Trichuris trichiura, and Strongyloides stercoralis. Stool samples from 400 13-month-old children in rural Ecuador were analyzed and the qPCR was compared with a standard direct wet mount slide for stool microscopy, as were 125 8-14-year-old children before and after anthelmintic treatment. The qPCR showed higher detection rates for all parasites compared with direct microscopy, Ascaris (7.0% versus 5.5%) and for Giardia (31.5% versus 5.8%). Using an enhanced DNA extraction method, we were able to detect T. trichiura DNA. These assays will be useful to refine treatment options for affected populations, ultimately leading to better health outcomes.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Mejia, Rojelio
AU  - Vicuna, Yosselin
AU  - Broncano, Nely
AU  - Sandoval, Carlos
AU  - Vaca, Maritza
AU  - Chico, Martha
AU  - Cooper, Philip J
AU  - Nutman, Thomas B
AD  - Helminth Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland; Fundacion Ecuatoriana para la Investigacion en Salud, Quito, Ecuador; Colegio de Ciencias de la Salud, Universidad San Francisco de Quito, Quito, Ecuador; Molecular and Biochemical Parasitology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom, tnutman@niaid.nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 1041
EP  - 1047
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 88
IS  - 6
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Risk Abstracts
KW  - Sensitivity
KW  - Parasites
KW  - Necator americanus
KW  - Ecuador
KW  - Entamoeba histolytica
KW  - Giardia lamblia
KW  - Probes
KW  - Pathogens
KW  - Children
KW  - Trichuris trichiura
KW  - Ascaris
KW  - Strongyloides stercoralis
KW  - Cryptosporidium
KW  - Microscopy
KW  - DNA
KW  - Polymerase chain reaction
KW  - Primers
KW  - Feces
KW  - Rural areas
KW  - K 03400:Human Diseases
KW  - J 02400:Human Diseases
KW  - R2 23010:General: Models, forecasting
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647006303?accountid=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=A+Novel%2C+Multi-Parallel%2C+Real-Time+Polymerase+Chain+Reaction+Approach+for+Eight+Gastrointestinal+Parasites+Provides+Improved+Diagnostic+Capabilities+to+Resource-Limited+At-Risk+Populations&rft.au=Mejia%2C+Rojelio%3BVicuna%2C+Yosselin%3BBroncano%2C+Nely%3BSandoval%2C+Carlos%3BVaca%2C+Maritza%3BChico%2C+Martha%3BCooper%2C+Philip+J%3BNutman%2C+Thomas+B&rft.aulast=Mejia&rft.aufirst=Rojelio&rft.date=2013-06-01&rft.volume=88&rft.issue=6&rft.spage=1041&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0726
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Parasites; Microscopy; Probes; Polymerase chain reaction; Primers; Pathogens; Children; Feces; Sensitivity; DNA; Rural areas; Ascaris; Necator americanus; Strongyloides stercoralis; Entamoeba histolytica; Cryptosporidium; Giardia lamblia; Trichuris trichiura; Ecuador
DO  - http://dx.doi.org/10.4269/ajtmh.12-0726
ER  - 



TY  - JOUR
T1  - Case Report: Halicephalobus gingivalis: A Rare Cause of Fatal Meningoencephalomyelitis in Humans
AN  - 1647001964; 21172104
AB  - The genus Halicephalobus consists of eight species of free-living nematodes. Only one species (H. gingivalis) has been reported to infect vertebrates. Human infection is extremely rare, and only four cases have been reported in the literature. These nematodes seem to exhibit neurotropism, but their life cycle, mode of infection, and risk factors are poorly understood. Neurohelminthiases are not commonly recognized in the United States and when they do occur, pose great diagnostic challenges because of lack of appropriate non-invasive screening and/or confirmatory tests. We report a challenging case of meningoencephalomyelitis caused by a Halicephalobus sp., in which the patient had a rapidly deteriorating clinical course. The case did not raise any clinical suspicion of neurohelminthiases, although increased eosinophils were present in the cerebrospinal fluid. This case presents an opportunity to highlight the importance of considering parasitic infection in meningoencephalitis or meningoencephalomyelitis presenting atypically.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Papadi, Bhavesh
AU  - Boudreaux, Carole
AU  - Tucker, J Allan
AU  - Mathison, Blaine
AU  - Bishop, Henry
AU  - Eberhard, Mark E
AD  - National Cancer Institute, National Institutes of Health, 10 Center Drive, Room 2A19, Bethesda, MD 20892; University of South Alabama Medical Center, Mobile, Alabama; Center for Global Health, Division of Parasitic Diseases and Malaria, Centers for Disease Control and Prevention, Atlanta, Georgia, bhavesh2papadi@yahoo.com
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 1062
EP  - 1064
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 88
IS  - 6
SN  - 0002-9637, 0002-9637
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Risk Abstracts
KW  - Meningoencephalitis
KW  - Life cycle
KW  - Leukocytes (eosinophilic)
KW  - Infection
KW  - Health risks
KW  - USA
KW  - Cerebrospinal fluid
KW  - Case reports
KW  - Risk factors
KW  - Nematoda
KW  - Nematodes
KW  - J 02400:Human Diseases
KW  - R2 23060:Medical and environmental health
KW  - K 03320:Cell Biology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647001964?accountid=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=Case+Report%3A+Halicephalobus+gingivalis%3A+A+Rare+Cause+of+Fatal+Meningoencephalomyelitis+in+Humans&rft.au=Papadi%2C+Bhavesh%3BBoudreaux%2C+Carole%3BTucker%2C+J+Allan%3BMathison%2C+Blaine%3BBishop%2C+Henry%3BEberhard%2C+Mark+E&rft.aulast=Papadi&rft.aufirst=Bhavesh&rft.date=2013-06-01&rft.volume=88&rft.issue=6&rft.spage=1062&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0730
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Cerebrospinal fluid; Case reports; Risk factors; Meningoencephalitis; Life cycle; Leukocytes (eosinophilic); Infection; Health risks; Nematodes; Nematoda; USA
DO  - http://dx.doi.org/10.4269/ajtmh.12-0730
ER  - 



TY  - JOUR
T1  - Patterns and trends in cancer mortality in Colombia 1984-2008
AN  - 1464515351; 18816388
AB  - Background Cancer has become increasingly acknowledged as a public health issue in Colombia. Rates of the most common malignancies have been generally increasing. We update an evaluation of mortality trends in the major cancers in Colombia one decade ago, discussing the trends in the context of cancer control. Methods We calculated the annual age-standardized mortality rates for the major cancer sites by sex between 1984 and 2008; we also present the estimated annual percentage change (EAPC) for the entire period and for the last decade. Results There was an average of 32,000 cancer deaths annually in Colombia in the period studied. Overall cancer mortality rates decreased slightly in both men and women. The four most common sites of cancer death among men were stomach (17.6%), prostate (15.0%), lung (14.8%) and colorectum (6.5%). In women, the most common cancer sites were breast (12.3%), cervix (12.1%), stomach (11.5%) and lung (9.2%). Colorectal and CNS cancers exhibited the greatest increases (EAPC of 2.0% and 3.4% respectively) while the largest declines were seen for cancers of the larynx, stomach and oesophagus (EAPC between -3% and -4%). In the last decade, the greatest declines were seen in cervical cancer mortality rates (EAPC=-3.2). Conclusions The slight decrease in mortality trends from all cancers combined is partially driven by the strong declines in mortality of stomach and cervical cancer. It may be still too early to properly evaluate trends in mortality due to other cancers and the relative impact of changing access to health care in Colombia.
JF  - Cancer Epidemiology
AU  - Pineros, Marion
AU  - Gamboa, Oscar
AU  - Hernandez-Suarez, Gustavo
AU  - Pardo, Constanza
AU  - Bray, Freddie
AD  - National Cancer Institute, Bogota, Colombia
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 233
EP  - 239
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 37
IS  - 3
SN  - 1877-7821, 1877-7821
KW  - Health & Safety Science Abstracts
KW  - Health care
KW  - Mortality
KW  - Colombia
KW  - H 11000:Diseases/Injuries/Trauma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464515351?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology&rft.atitle=Patterns+and+trends+in+cancer+mortality+in+Colombia+1984-2008&rft.au=Pineros%2C+Marion%3BGamboa%2C+Oscar%3BHernandez-Suarez%2C+Gustavo%3BPardo%2C+Constanza%3BBray%2C+Freddie&rft.aulast=Pineros&rft.aufirst=Marion&rft.date=2013-06-01&rft.volume=37&rft.issue=3&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2013.02.003
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Mortality; Colombia
DO  - http://dx.doi.org/10.1016/j.canep.2013.02.003
ER  - 



TY  - JOUR
T1  - Variation in PAH-related DNA adduct levels among non-smokers: The role of multiple genetic polymorphisms and nucleotide excision repair phenotype
AN  - 1448222751; 18602371
AB  - Polycyclic aromatic hydrocarbons (PAHs) likely play a role in many cancers even in never-smokers. We tried to find a model to explain the relationship between variation in PAH-related DNA adduct levels among people with similar exposures, multiple genetic polymorphisms in genes related to metabolic and repair pathways, and nucleotide excision repair (NER) capacity. In 111 randomly selected female never-smokers from the Golestan Cohort Study in Iran, we evaluated 21 SNPs in 14 genes related to xenobiotic metabolism and 12 SNPs in eight DNA repair genes. NER capacity was evaluated by a modified comet assay, and aromatic DNA adduct levels were measured in blood by32P-postlabeling. Multivariable regression models were compared by Akaike's information criterion (AIC). Aromatic DNA adduct levels ranged between 1.7 and 18.6 per 10 super(8) nucleotides (mean: 5.8 plus or minus 3.1). DNA adduct level was significantly lower in homozygotes for NAT2 slow alleles and ERCC5 non-risk-allele genotype, and was higher in the MPO homozygote risk-allele genotype. The sum of risk alleles in these genes significantly correlated with the log-adduct level (r = 0.4, p < 0.001). Compared with the environmental model, adding Phase I SNPs and NER capacity provided the best fit, and could explain 17% more of the variation in adduct levels. NER capacity was affected by polymorphisms in the MTHFR and ERCC1 genes. Female non-smokers in this population had PAH-related DNA adduct levels three to four times higher than smokers and occupationally-exposed groups in previous studies, with large inter-individual variation which could best be explained by a combination of Phase I genes and NER capacity. What's new? Polycyclic aromatic hydrocarbons (PAHs) likely play a role in esophageal squamous cell carcinoma (ESCC) through the formation of DNA adducts. Variation in adduct formation among people with similar exposures is however not well understood. Here the authors show that female non-smokers in a population at high risk of ESCC had exceptionally high DNA adducts, with large inter-individual variations best explained by a combination of PAH phase I metabolizing genes and nucleotide excision repair (NER) capacity. This study shows the importance of studying a large set of combined polymorphisms and NER phenotyping together, and sheds light on PAH-related carcinogenesis in non-smokers.
JF  - International Journal of Cancer
AU  - Etemadi, Arash
AU  - Islami, Farhad
AU  - Phillips, David H
AU  - Godschalk, Roger
AU  - Golozar, Asieh
AU  - Kamangar, Farin
AU  - Malekshah, Akbar Fazel-Tabar
AU  - Pourshams, Akram
AU  - Elahi, Seerat
AU  - Ghojaghi, Farhad
AU  - Strickland, Paul T
AU  - Taylor, Philip R
AU  - Boffetta, Paolo
AU  - Abnet, Christian C
AU  - Dawsey, Sanford M
AU  - Malekzadeh, Reza
AU  - van Schooten, Frederik J
AD  - Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran., arash.etemadi@nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 2738
EP  - 2747
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 12
SN  - 0020-7136, 0020-7136
KW  - Genetics Abstracts; Toxicology Abstracts; Biochemistry Abstracts 2: Nucleic Acids
KW  - Aromatics
KW  - DNA adducts
KW  - N 14820:DNA Metabolism & Structure
KW  - G 07710:Chemical Mutagenesis & Radiation
KW  - X 24350:Industrial Chemicals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448222751?accountid=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=International+Journal+of+Cancer&rft.atitle=Variation+in+PAH-related+DNA+adduct+levels+among+non-smokers%3A+The+role+of+multiple+genetic+polymorphisms+and+nucleotide+excision+repair+phenotype&rft.au=Etemadi%2C+Arash%3BIslami%2C+Farhad%3BPhillips%2C+David+H%3BGodschalk%2C+Roger%3BGolozar%2C+Asieh%3BKamangar%2C+Farin%3BMalekshah%2C+Akbar+Fazel-Tabar%3BPourshams%2C+Akram%3BElahi%2C+Seerat%3BGhojaghi%2C+Farhad%3BStrickland%2C+Paul+T%3BTaylor%2C+Philip+R%3BBoffetta%2C+Paolo%3BAbnet%2C+Christian+C%3BDawsey%2C+Sanford+M%3BMalekzadeh%2C+Reza%3Bvan+Schooten%2C+Frederik+J&rft.aulast=Etemadi&rft.aufirst=Arash&rft.date=2013-06-01&rft.volume=132&rft.issue=12&rft.spage=2738&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27953
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - DNA adducts
DO  - http://dx.doi.org/10.1002/ijc.27953
ER  - 



TY  - JOUR
T1  - Targeting of the Small GTPase Rab6A' by the Legionella pneumophila Effector LidA
AN  - 1443376411; 18642828
AB  - When the bacterium Legionella pneumophila, the causative agent of Legionnaires' disease, is phagocytosed by alveolar macrophages, it delivers a large number of effector proteins through its Dot/Icm type IV secretion system into the host cell cytosol. Among those proteins is LidA, an effector that interacts with several host GTPases of the Rab family, including Rab6A', a regulator of retrograde vesicle trafficking within eukaryotic cells. The effect of LidA on Rab6A' function and the role of Rab6A' for L. pneumophila growth within host cells has been unclear. Here, we show that LidA preferentially binds Rab6A' in the active GTP-bound conformation. Rab6 binding occurred through the central region of LidA and followed a stoichiometry for LidA and Rab6A' of 1:2. LidA maintained Rab6A' in the active conformation by efficiently blocking the hydrolysis of GTP by Rab6A', even in the presence of cellular GTPase-activating proteins, suggesting that the function of Rab6A' must be important for efficient intracellular replication of L. pneumophila. Accordingly, we found that production of constitutively inactive Rab6A'(T27N) but not constitutively active Rab6A'(Q72L) significantly reduced the ability of L. pneumophila to initiate intracellular replication in human macrophages. Thus, the presence of an active pool of Rab6 within host cells early during infection is required to support efficient intracellular growth of L. pneumophila.
JF  - Infection and Immunity
AU  - Chen, Yang
AU  - Machner, Matthias P
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 2226
EP  - 2235
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 6
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Macrophages
KW  - GTPase-activating protein
KW  - Legionella pneumophila
KW  - Replication
KW  - GTP
KW  - Infection
KW  - Hydrolysis
KW  - Alveoli
KW  - Cytosol
KW  - Vesicles
KW  - Guanosinetriphosphatase
KW  - Conformation
KW  - J 02350:Immunology
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443376411?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Targeting+of+the+Small+GTPase+Rab6A%27+by+the+Legionella+pneumophila+Effector+LidA&rft.au=Chen%2C+Yang%3BMachner%2C+Matthias+P&rft.aulast=Chen&rft.aufirst=Yang&rft.date=2013-06-01&rft.volume=81&rft.issue=6&rft.spage=2226&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00157-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 41
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - GTPase-activating protein; Macrophages; Replication; Cytosol; GTP; Vesicles; Infection; Hydrolysis; Alveoli; Conformation; Guanosinetriphosphatase; Legionella pneumophila
DO  - http://dx.doi.org/10.1128/IAI.00157-13
ER  - 



TY  - JOUR
T1  - Anti-Pfs25 Human Plasma Reduces Transmission of Plasmodium falciparum Isolates That Have Diverse Genetic Backgrounds
AN  - 1443375441; 18642818
AB  - Pfs25 is a leading candidate for a malaria transmission-blocking vaccine whose potential has been demonstrated in a phase 1 trial with recombinant Pfs25 formulated with Montanide ISA51. Because of limited sequence polymorphism, the anti-Pfs25 antibodies induced by this vaccine are likely to have transmission-blocking or -reducing activity against most, if not all, field isolates. To test this hypothesis, we evaluated transmission-blocking activities by membrane feeding assay of anti-Pfs25 plasma from the Pfs25/ISA51 phase 1 trial against Plasmodium falciparum parasites from patients in two different geographical regions of the world, Thailand and Burkina Faso. In parallel, parasite isolates from these patients were sequenced for the Pfs25 gene and genotyped for seven microsatellites. The results indicate that despite different genetic backgrounds among parasite isolates, the Pfs25 sequences are highly conserved, with a single nonsynonymous nucleotide polymorphism detected in 1 of 41 patients in Thailand and Burkina Faso. The anti-Pfs25 immune plasma had significantly higher transmission-reducing activity against parasite isolates from the two geographical regions than the nonimmune controls (P < 0.0001).
JF  - Infection and Immunity
AU  - Da, Dari F
AU  - Dixit, Saurabh
AU  - Sattabonkot, Jetsumon
AU  - Mu, Jianbing
AU  - Abate, Luc
AU  - Ramineni, Bhanumati
AU  - Ouedraogo, Jean Bosco
AU  - MacDonald, Nicholas J
AU  - Fay, Michael P
AU  - Su, Xin-zhuan
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1984
EP  - 1989
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 6
SN  - 0019-9567, 0019-9567
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; Genetics Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts
KW  - Feeding
KW  - Parasites
KW  - Human diseases
KW  - Burkina Faso
KW  - Thailand
KW  - Gene polymorphism
KW  - Microsatellites
KW  - Disease control
KW  - Genetic diversity
KW  - Malaria
KW  - Plasmodium falciparum
KW  - Clinical trials
KW  - Nucleotides
KW  - Public health
KW  - Recombinants
KW  - Antibodies
KW  - Vaccines
KW  - G 07720:Immunogenetics
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443375441?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Anti-Pfs25+Human+Plasma+Reduces+Transmission+of+Plasmodium+falciparum+Isolates+That+Have+Diverse+Genetic+Backgrounds&rft.au=Da%2C+Dari+F%3BDixit%2C+Saurabh%3BSattabonkot%2C+Jetsumon%3BMu%2C+Jianbing%3BAbate%2C+Luc%3BRamineni%2C+Bhanumati%3BOuedraogo%2C+Jean+Bosco%3BMacDonald%2C+Nicholas+J%3BFay%2C+Michael+P%3BSu%2C+Xin-zhuan&rft.aulast=Da&rft.aufirst=Dari&rft.date=2013-06-01&rft.volume=81&rft.issue=6&rft.spage=1984&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00016-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 23
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Recombinants; Parasites; Antibodies; Human diseases; Disease control; Malaria; Vaccines; Nucleotides; Public health; Feeding; Gene polymorphism; Microsatellites; Genetic diversity; Clinical trials; Plasmodium falciparum; Burkina Faso; Thailand
DO  - http://dx.doi.org/10.1128/IAI.00016-13
ER  - 



TY  - JOUR
T1  - An investigation of risk factors for renal cell carcinoma by histologic subtype in two case-control studies
AN  - 1443372526; 18602343
AB  - To investigate whether renal cell carcinoma (RCC) histologic subtypes possess different etiologies, we conducted analyses of established RCC risk factors by subtype (clear cell, papillary and chromophobe) in two case-control studies conducted in the United States (1,217 cases, 1,235 controls) and Europe (1,097 cases, 1,476 controls). Histology was ascertained for 706 U.S. cases (58% of total) and 917 European cases (84%) through a central slide review conducted by a single pathologist. For the remaining cases, histology was abstracted from the original diagnostic pathology report. Case-only analyses were performed to compute odds ratios (ORs) and 95% confidence intervals (CI) summarizing subtype differences by age, sex and race. Case-control analyses were performed to compute subtype-specific ORs for other risk factors using polytomous regression. In case-only analyses, papillary cases (N = 237) were older (OR = 1.2, 95% CI = 1.1-1.4 per 10-year increase), less likely to be female (OR = 0.5, 95% CI = 0.4-0.8) and more likely to be black (OR = 2.6, 95% CI = 1.8-3.9) as compared to clear cell cases (N = 1,524). In case-control analyses, BMI was associated with clear cell (OR = 1.2, 95% CI = 1.1-1.3 per 5 kg/m super(2) increase) and chromophobe RCC (N = 80; OR = 1.2, 95% CI = 1.1-1.4), but not papillary RCC (OR = 1.1, 95% CI = 1.0-1.2; test versus clear cell, p = 0.006). No subtype differences were observed for associations with smoking, hypertension or family history of kidney cancer. Our findings support the existence of distinct age, sex and racial distributions for RCC subtypes, and suggest that the obesity-RCC association differs by histology. What's new? Renal cell carcinoma (RCC) is the most common form of kidney cancer, which is the deadliest of all urologic malignancies. The present investigation aimed to better understand whether associations between RCC and established risk factors differed by RCC histologic subtype. Looking across two case-control studies, the authors found that increasing body mass index was associated with clear cell and chromophobe RCC, but not papillary RCC. They also observed distinct age, sex, and racial distributions by subtype. The findings offer new insight into the relationship between obesity and RCC, and underscore the importance of subtype-specific analyses when investigating RCC etiology.
JF  - International Journal of Cancer
AU  - Purdue, Mark P
AU  - Moore, Lee E
AU  - Merino, Maria J
AU  - Boffetta, Paolo
AU  - Colt, Joanne S
AU  - Schwartz, Kendra L
AU  - Bencko, Vladimir
AU  - Davis, Faith G
AU  - Graubard, Barry I
AU  - Janout, Vladimir
AU  - Ruterbusch, Julie J
AU  - Beebe-Dimmer, Jennifer
AU  - Cote, Michele L
AU  - Shuch, Brian
AU  - Mates, Dana
AU  - Hofmann, Jonathan N
AU  - Foretova, Lenka
AU  - Rothman, Nathaniel
AU  - Szeszenia-Dabrowska, Neonilia
AU  - Matveev, Vsevolod
AU  - Wacholder, Sholom
AU  - Zaridze, David
AU  - Linehan, WMarston
AU  - Brennan, Paul
AU  - Chow, Wong-Ho
AD  - Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA., purduem@mail.nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 2640
EP  - 2647
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 11
SN  - 0020-7136, 0020-7136
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Renal
KW  - Health risks
KW  - Genetics
KW  - USA
KW  - Age
KW  - Etiology
KW  - Histology
KW  - Risk factors
KW  - Kidney
KW  - Europe
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/1443372526?accountid=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=An+investigation+of+risk+factors+for+renal+cell+carcinoma+by+histologic+subtype+in+two+case-control+studies&rft.au=Purdue%2C+Mark+P%3BMoore%2C+Lee+E%3BMerino%2C+Maria+J%3BBoffetta%2C+Paolo%3BColt%2C+Joanne+S%3BSchwartz%2C+Kendra+L%3BBencko%2C+Vladimir%3BDavis%2C+Faith+G%3BGraubard%2C+Barry+I%3BJanout%2C+Vladimir%3BRuterbusch%2C+Julie+J%3BBeebe-Dimmer%2C+Jennifer%3BCote%2C+Michele+L%3BShuch%2C+Brian%3BMates%2C+Dana%3BHofmann%2C+Jonathan+N%3BForetova%2C+Lenka%3BRothman%2C+Nathaniel%3BSzeszenia-Dabrowska%2C+Neonilia%3BMatveev%2C+Vsevolod%3BWacholder%2C+Sholom%3BZaridze%2C+David%3BLinehan%2C+WMarston%3BBrennan%2C+Paul%3BChow%2C+Wong-Ho&rft.aulast=Purdue&rft.aufirst=Mark&rft.date=2013-06-01&rft.volume=132&rft.issue=11&rft.spage=2640&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27934
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Renal; Genetics; Health risks; Etiology; Age; Histology; Risk factors; Kidney; Cancer; USA; Europe
DO  - http://dx.doi.org/10.1002/ijc.27934
ER  - 



TY  - JOUR
T1  - Perceived human rights violation in persons with mental illness: role of education
AN  - 1437958842; 4486829
AB  - Background: People with mental illness are vulnerable to human rights violations and people with illiteracy and mental illness are at a double disadvantage. Objective: To determine the role of education in ascertaining human rights needs of people with mental illness. Methodology: This was a descriptive study carried out among randomly selected (N = 100) recovered psychiatric patients with mental illness in the past based on the Clinical Global Impression - Improvement scale at a tertiary care centre. Data were collected through face-to-face interview using structured needs assessment questionnaire comprising two sections related to family and community domains. Data were analysed and interpreted using descriptive and inferential statistics. Findings: Our findings revealed that human rights needs in the physical needs dimension - i.e. access to electricity ([chi] 2 = 5.523, p < .019) and safe drinking water facilities ([chi] 2 = 9.665, p < .022) - were rated higher in illiterates than in literates. The human rights needs in emotional dimension - i.e. feeling separated from their families because of their illness ([chi] 2 = 13.118, p < .004), afraid of family members ([chi] 2 = 13.388, p < .004) and called filthy nicknames ([chi] 2 = 17.759, p < .000) - were rated higher in literates than in illiterates. The human rights needs in the religious needs dimension - i.e. allowed to go to temple, church, mosque etc. ([chi] 2 = 12.000, p < .007) - and in the social needs dimension - i.e. friendliness with family members -were rated higher in illiterates than in literates ([chi] 2 = 9.661, p < .022). Conclusion: Empowering people with mental illness by providing adequate opportunity to pursue education will play an important role in fulfilling the obligation of the United Nations Convention on the Rights of Persons with Disabilities. [Reprinted by permission of Sage Publications Ltd., copyright holder.] Reprinted by permission of Sage Publications Ltd.
JF  - International journal of social psychiatry
AU  - Vijayalakshmi, Poreddi
AU  - Reddemma, Konduru
AU  - Math, Suresh Bada
AD  - National Institute of Mental Health and Neurosciences, Bangalore
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 351
EP  - 364
VL  - 59
IS  - 4
SN  - 0020-7640, 0020-7640
KW  - Sociology
KW  - Rights
KW  - Human rights violations
KW  - Level of education
KW  - Disability
KW  - Social psychiatry
KW  - Water supply
KW  - UN Conventions
KW  - Human rights
KW  - Mental illness
KW  - Basic needs
KW  - Family
KW  - United Nations
KW  - Illiteracy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1437958842?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+social+psychiatry&rft.atitle=Perceived+human+rights+violation+in+persons+with+mental+illness%3A+role+of+education&rft.au=Vijayalakshmi%2C+Poreddi%3BReddemma%2C+Konduru%3BMath%2C+Suresh+Bada&rft.aulast=Vijayalakshmi&rft.aufirst=Poreddi&rft.date=2013-06-01&rft.volume=59&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=International+journal+of+social+psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764012437322
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-09-30
N1  - Last updated - 2013-10-01
N1  - SubjectsTermNotLitGenreText - 7951 6220 7954; 6103 11032 9705; 4748; 1496; 13113 6772 9030; 11032 9705; 13486 12401; 6109 6103 11032 9705; 7353 4049; 6217; 13050 13113 6772 9030 6705 6674; 3584 1678; 11898 10391
DO  - http://dx.doi.org/10.1177/0020764012437322
ER  - 



TY  - JOUR
T1  - Developing Rods Transplanted into the Degenerating Retina of Crx-Knockout Mice Exhibit Neural Activity Similar to Native Photoreceptors
AN  - 1434028796; 18501535
AB  - Replacement of dysfunctional or dying photoreceptors offers a promising approach for retinal neurodegenerative diseases, including age-related macular degeneration and retinitis pigmentosa. Several studies have demonstrated the integration and differentiation of developing rod photoreceptors when transplanted in wild-type or degenerating retina; however, the physiology and function of the donor cells are not adequately defined. Here, we describe the physiological properties of developing rod photoreceptors that are tagged with green fluorescent protein (GFP) driven by the promoter of rod differentiation factor, Nrl. GFP-tagged developing rods show Ca super(2 +) responses and rectifier outward currents that are smaller than those observed in fully developed photoreceptors, suggesting their immature developmental state. These immature rods also exhibit hyperpolarization-activated current (I sub(h)) induced by the activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. When transplanted into the subretinal space of wild-type or retinal degeneration mice, GFP-tagged developing rods can integrate into the photoreceptor outer nuclear layer in wild-type mouse retina and exhibit Ca super(2 +) responses and membrane current comparable to native rod photoreceptors. A proportion of grafted rods develop rhodopsin-positive outer segment-like structures within 2 weeks after transplantation into the retina of Crx-knockout mice and produce rectifier outward current and I sub(h) upon membrane depolarization and hyperpolarization. GFP-positive rods derived from induced pluripotent stem (iPS) cells also display similar membrane current I sub(h) as native developing rod photoreceptors, express rod-specific phototransduction genes, and HCN-1 channels. We conclude that Nrl-promoter-driven GFP-tagged donor photoreceptors exhibit physiological characteristics of rods and that iPS cell-derived rods in vitro may provide a renewable source for cell-replacement therapy. STEM Cells 2013; 31:1149-1159
JF  - Stem Cells
AU  - Homma, Kohei
AU  - Okamoto, Satoshi
AU  - Mandai, Michiko
AU  - Gotoh, Norimoto
AU  - Rajasimha, Harsha K
AU  - Chang, Yi-Sheng
AU  - Chen, Shan
AU  - Li, Wei
AU  - Cogliati, Tiziana
AU  - Swaroop, Anand
AU  - Takahashi, Masayo
AD  - Neurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA., kohei.homma@nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1149
EP  - 1159
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 6
SN  - 1066-5099, 1066-5099
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Donors
KW  - Transplantation
KW  - retinal degeneration
KW  - Retina
KW  - Macular degeneration
KW  - Phototransduction
KW  - Green fluorescent protein
KW  - Membrane currents
KW  - Photoreceptors
KW  - Integration
KW  - Neurodegenerative diseases
KW  - Promoters
KW  - Differentiation
KW  - Stem cells
KW  - ion channels (cyclic nucleotide-gated)
KW  - Rods
KW  - Hyperpolarization
KW  - Depolarization
KW  - Membrane potential
KW  - W 30910:Imaging
KW  - N3 11027:Neurology & neuropathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434028796?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Developing+Rods+Transplanted+into+the+Degenerating+Retina+of+Crx-Knockout+Mice+Exhibit+Neural+Activity+Similar+to+Native+Photoreceptors&rft.au=Homma%2C+Kohei%3BOkamoto%2C+Satoshi%3BMandai%2C+Michiko%3BGotoh%2C+Norimoto%3BRajasimha%2C+Harsha+K%3BChang%2C+Yi-Sheng%3BChen%2C+Shan%3BLi%2C+Wei%3BCogliati%2C+Tiziana%3BSwaroop%2C+Anand%3BTakahashi%2C+Masayo&rft.aulast=Homma&rft.aufirst=Kohei&rft.date=2013-06-01&rft.volume=31&rft.issue=6&rft.spage=1149&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1372
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Donors; Transplantation; Phototransduction; Macular degeneration; Retina; retinal degeneration; Green fluorescent protein; Membrane currents; Photoreceptors; Differentiation; Promoters; Neurodegenerative diseases; Integration; Stem cells; ion channels (cyclic nucleotide-gated); Hyperpolarization; Rods; Membrane potential; Depolarization
DO  - http://dx.doi.org/10.1002/stem.1372
ER  - 



TY  - JOUR
T1  - Gadgetron: An open source framework for medical image reconstruction
AN  - 1434018442; 18496121
AB  - This work presents a new open source framework for medical image reconstruction called the "Gadgetron." The framework implements a flexible system for creating streaming data processing pipelines where data pass through a series of modules or "Gadgets" from raw data to reconstructed images. The data processing pipeline is configured dynamically at run-time based on an extensible markup language configuration description. The framework promotes reuse and sharing of reconstruction modules and new Gadgets can be added to the Gadgetron framework through a plugin-like architecture without recompiling the basic framework infrastructure. Gadgets are typically implemented in C/C++, but the framework includes wrapper Gadgets that allow the user to implement new modules in the Python scripting language for rapid prototyping. In addition to the streaming framework infrastructure, the Gadgetron comes with a set of dedicated toolboxes in shared libraries for medical image reconstruction. This includes generic toolboxes for data-parallel (e.g., GPU-based) execution of compute-intensive components. The basic framework architecture is independent of medical imaging modality, but this article focuses on its application to Cartesian and non-Cartesian parallel magnetic resonance imaging. Magn Reson Med, 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Magnetic Resonance in Medicine
AU  - Hansen, Michael Schacht
AU  - Soerensen, Thomas Sangild
AD  - Department of Computer Science, Aarhus University, Aarhus, Denmark., michael.hansen@nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1768
EP  - 1776
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 6
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - Streaming
KW  - Data processing
KW  - Magnetic resonance imaging
KW  - Image processing
KW  - Language
KW  - N.M.R.
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434018442?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gadgetron%3A+An+open+source+framework+for+medical+image+reconstruction&rft.au=Hansen%2C+Michael+Schacht%3BSoerensen%2C+Thomas+Sangild&rft.aulast=Hansen&rft.aufirst=Michael&rft.date=2013-06-01&rft.volume=69&rft.issue=6&rft.spage=1768&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24389
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Streaming; Data processing; Magnetic resonance imaging; Image processing; N.M.R.; Language
DO  - http://dx.doi.org/10.1002/mrm.24389
ER  - 



TY  - JOUR
T1  - Cumulative incidence of cancer after solid organ transplantation
AN  - 1434016428; 18486716
AB  - BACKGROUND Solid organ transplantation recipients have elevated cancer incidence. Estimates of absolute cancer risk after transplantation can inform prevention and screening. METHODS The Transplant Cancer Match Study links the US transplantation registry with 14 state/regional cancer registries. The authors used nonparametric competing risk methods to estimate the cumulative incidence of cancer after transplantation for 2 periods (1987-1999 and 2000-2008). For recipients from 2000 to 2008, the 5-year cumulative incidence, stratified by organ, sex, and age at transplantation, was estimated for 6 preventable or screen-detectable cancers. For comparison, the 5-year cumulative incidence was calculated for the same cancers in the general population at representative ages using Surveillance, Epidemiology, and End Results data. RESULTS Among 164,156 recipients, 8520 incident cancers were identified. The absolute cancer risk was slightly higher for recipients during the period from 2000 to 2008 than during the period from 1987 to 1999 (5-year cumulative incidence: 4.4% vs 4.2%; P=.006); this difference arose from the decreasing risk of competing events (5-year cumulative incidence of death, graft failure, or retransplantation: 26.6% vs 31.9%; P50 years; range, 0.36%-2.22%). For recipients aged >50 years, the 5-year cumulative incidence was higher for colorectal cancer (range, 0.33%-1.94%) than for the general population at the recommended screening age (aged 50 years: range, 0.25%-0.33%). For recipients aged >50 years, the 5-year cumulative incidence was high for lung cancer among thoracic organ recipients (range, 1.16%-3.87%) and for kidney cancer among kidney recipients (range, 0.53%-0.84%). The 5-year cumulative incidence for prostate cancer and breast cancer was similar or lower in transplantation recipients than at the recommended ages of screening in the general population. CONCLUSIONS Subgroups of transplantation recipients have a high absolute risk of some cancers and may benefit from targeted prevention or screening. Cancer 2013; 119:2300-2308. [copy 2013 American Cancer Society. The cumulative incidence of 6 preventable or screen-detectable cancers after transplantation is estimated using population-based data on 164,156 US transplantation recipients. High-risk subgroups are identified that may benefit from targeted screening or prevention, including thoracic organ recipients at the extremes of age for non-Hodgkin lymphoma, older thoracic organ recipients for lung cancer, and kidney recipients aged >35 years for kidney cancer.
JF  - Cancer
AU  - Hall, Erin C
AU  - Pfeiffer, Ruth M
AU  - Segev, Dorry L
AU  - Engels, Eric A
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland.
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 2300
EP  - 2308
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 12
SN  - 0008-543X, 0008-543X
KW  - Risk Abstracts
KW  - Health risks
KW  - Age
KW  - Prevention
KW  - Transplantation
KW  - Kidney
KW  - Breast cancer
KW  - Organs
KW  - Cancer
KW  - Lung cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434016428?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Cumulative+incidence+of+cancer+after+solid+organ+transplantation&rft.au=Hall%2C+Erin+C%3BPfeiffer%2C+Ruth+M%3BSegev%2C+Dorry+L%3BEngels%2C+Eric+A&rft.aulast=Hall&rft.aufirst=Erin&rft.date=2013-06-01&rft.volume=119&rft.issue=12&rft.spage=2300&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.28043
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Health risks; Prevention; Age; Transplantation; Kidney; Breast cancer; Organs; Cancer; Lung cancer
DO  - http://dx.doi.org/10.1002/cncr.28043
ER  - 



TY  - JOUR
T1  - What Does It Mean to Be Pragmatic? Pragmatic Methods, Measures, and Models to Facilitate Research Translation
AN  - 1430187031; 201317864
AB  - Background. One of the reasons for the slow and uncertain translation of research into practice is likely due to the emphasis in science on explanatory models and efficacy designs rather than more pragmatic approaches. Methods. Following a brief definition of what constitutes a pragmatic approach, I provide examples of pragmatic methods, measures, and models and how they have been applied. Results. Descriptions are provided of pragmatic trials and related designs, practical measures including patient-reported items for the electronic health record, and the Evidence Integration Triangle and RE-AIM practical models, each of which can help increase the relevance of research to policy makers, practitioners, and patients/consumers. Conclusions. By focusing on the perspective of stakeholders and the context for application of scientific findings, pragmatic approaches can accelerate the integration of research, policy, and practice. Progress has been made, especially in pragmatic trials but even more opportunities remain. [Reprinted by permission of Sage Publications Inc., copyright, the Society for Public Health Education.]
JF  - Health Education & Behavior
AU  - Glasgow, Russell E
AD  - National Cancer Institute, Rockville, MD, USA
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 257
EP  - 265
PB  - Sage Publications, Thousand Oaks CA
VL  - 40
IS  - 3
SN  - 1090-1981, 1090-1981
KW  - evaluation implementation measurement pragmatic trial research design theory
KW  - Stakeholders
KW  - Translation
KW  - Policy makers
KW  - Computerized medical records
KW  - Medical research
KW  - Pragmatics
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430187031?accountid=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+Education+%26+Behavior&rft.atitle=What+Does+It+Mean+to+Be+Pragmatic%3F+Pragmatic+Methods%2C+Measures%2C+and+Models+to+Facilitate+Research+Translation&rft.au=Glasgow%2C+Russell+E&rft.aulast=Glasgow&rft.aufirst=Russell&rft.date=2013-06-01&rft.volume=40&rft.issue=3&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Health+Education+%26+Behavior&rft.issn=10901981&rft_id=info:doi/10.1177%2F1090198113486805
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - HEDBFS
N1  - SubjectsTermNotLitGenreText - Pragmatics; Translation; Computerized medical records; Stakeholders; Policy makers; Medical research
DO  - http://dx.doi.org/10.1177/1090198113486805
ER  - 



TY  - JOUR
T1  - Integrating translational neuroscience to improve drug abuse treatment for adolescents.
AN  - 1430186812; 201317098
AB  - Adolescence is an exciting and challenging period of maturation, rapid brain development, and developmental changes in neurobiological, neurocognitive, and neurobehavioral processes. Although behavioral therapies available for adolescent substance abuse have increased, effectiveness research in this area lags considerably behind that of clinical research on treatment for drug-abusing adults. Behavioral treatment approaches show significant promise for treating drug-abusing adolescents, but many have not incorporated innovations in neuroscience on brain development, cognitive processes, and neuroimaging. Linking developmental neuroscience with behavioral treatments can create novel drug abuse interventions and increase the effectiveness of existing interventions for substance-abusing adolescents. Contemporary research on brain development, cognition, and neuroscience is ripe for translation to inform developmentally sensitive drug abuse treatments for adolescents. Neuroscientists and interventionists are challenged to build mutual collaborations for integration of neuroscience and drug abuse treatment for adolescents. [Copyright The American Psychological Association.]
JF  - Psychology of Addictive Behaviors
AU  - Boyce, Cheryl Anne
AU  - Lynne-Landsman, Sarah D
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 547
EP  - 551
PB  - American Psychological Association, Washington DC
VL  - 27
IS  - 2
SN  - 0893-164X, 0893-164X
KW  - adolescence
KW  - drug abuse
KW  - neuroscience
KW  - treatment
KW  - Interventions
KW  - Behaviour therapy
KW  - Brain
KW  - Neurosciences
KW  - Drug abuse
KW  - Adolescents
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430186812?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychology+of+Addictive+Behaviors&rft.atitle=Integrating+translational+neuroscience+to+improve+drug+abuse+treatment+for+adolescents.&rft.au=Boyce%2C+Cheryl+Anne%3BLynne-Landsman%2C+Sarah+D&rft.aulast=Boyce&rft.aufirst=Cheryl&rft.date=2013-06-01&rft.volume=27&rft.issue=2&rft.spage=547&rft.isbn=&rft.btitle=&rft.title=Psychology+of+Addictive+Behaviors&rft.issn=0893164X&rft_id=info:doi/10.1037%2Fa0032434
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - PABEEI
N1  - SubjectsTermNotLitGenreText - Adolescents; Neurosciences; Drug abuse; Brain; Behaviour therapy; Interventions
DO  - http://dx.doi.org/10.1037/a0032434
ER  - 



TY  - JOUR
T1  - Outsourcing Ethical Obligations: Should the Revised Common Rule Address the Responsibilities of Investigators and Sponsors
AN  - 1429653296; 2011-483124
AB  - The Common Rule creates a division of moral labor in research. It implies that investigators and sponsors can outsource their ethical obligations to IRBs and participants, thereby fostering a culture of compliance, rather than one of responsibility. The proposed revisions to the Common Rule are likely to exacerbate this problem. To harness the expressive power of the law, I propose the Common Rule be revised to include the ethical responsibilities of investigators and sponsors. Adapted from the source document.
JF  - The Journal of Law, Medicine & Ethics
AU  - Shah, Seema K
AD  - Faculty member in the Clinical Center Department of Bioethics and has a joint appointment at the Division of AIDS at the National Institutes of Health
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 397
EP  - 410
PB  - Wiley-Blackwell, UK
VL  - 41
IS  - 2
SN  - 1073-1105, 1073-1105
KW  - Law and ethics - Ethics
KW  - Culture and religion - Culture and civilization
KW  - Law and ethics - Law and jurisprudence
KW  - Labor conditions and policy - Work and labor
KW  - Business and service sector - Business organization and administration
KW  - Manufacturing and heavy industry - Industrial management, production, and productivity
KW  - Health conditions and policy - Health and health policy
KW  - Culture
KW  - Responsibility
KW  - Ethics
KW  - Outsourcing
KW  - Health policy
KW  - Law
KW  - Labor
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1429653296?accountid=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=The+Journal+of+Law%2C+Medicine+%26+Ethics&rft.atitle=Outsourcing+Ethical+Obligations%3A+Should+the+Revised+Common+Rule+Address+the+Responsibilities+of+Investigators+and+Sponsors&rft.au=Shah%2C+Seema+K&rft.aulast=Shah&rft.aufirst=Seema&rft.date=2013-06-01&rft.volume=41&rft.issue=2&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Law%2C+Medicine+%26+Ethics&rft.issn=10731105&rft_id=info:doi/10.1111%2Fjlme.12051
LA  - English
DB  - PAIS Index
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Responsibility; Culture; Law; Labor; Outsourcing; Health policy; Ethics
DO  - http://dx.doi.org/10.1111/jlme.12051
ER  - 



TY  - JOUR
T1  - Nanoparticles and the blood coagulation system. Part II: safety concerns
AN  - 1419369856; 18274447
AB  - Nanoparticle interactions with the blood coagulation system can be beneficial or adverse depending on the intended use of a nanomaterial. Nanoparticles can be engineered to be procoagulant or to carry coagulation-initiating factors to treat certain disorders. Likewise, they can be designed to be anticoagulant or to carry anticoagulant drugs to intervene in other pathological conditions in which coagulation is a concern. An overview of the coagulation system was given and a discussion of a desirable interface between this system and engineered nanomaterials was assessed in part I, which was published in the May 2013 issue of Nanomedicine. Unwanted pro- and anti-coagulant properties of nanoparticles represent significant concerns in the field of nanomedicine, and often hamper the development and transition into the clinic of many promising engineered nanocarriers. This part will focus on the undesirable effects of engineered nanomaterials on the blood coagulation system. We will discuss the relationship between the physicochemical properties of nanoparticles (e.g., size, charge and hydrophobicity) that determine their negative effects on the blood coagulation system in order to understand how manipulation of these properties can help to overcome unwanted side effects.
JF  - Nanomedicine
AU  - Ilinskaya, Anna N
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, marina@mail.nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 969
EP  - 981
PB  - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL  - 8
IS  - 6
SN  - 1743-5889, 1743-5889
KW  - Biotechnology and Bioengineering Abstracts
KW  - Blood coagulation
KW  - Anticoagulants
KW  - Reviews
KW  - Physicochemical properties
KW  - Hydrophobicity
KW  - nanoparticles
KW  - Drugs
KW  - Side effects
KW  - nanotechnology
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419369856?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nanoparticles+and+the+blood+coagulation+system.+Part+II%3A+safety+concerns&rft.au=Ilinskaya%2C+Anna+N%3BDobrovolskaia%2C+Marina+A&rft.aulast=Ilinskaya&rft.aufirst=Anna&rft.date=2013-06-01&rft.volume=8&rft.issue=6&rft.spage=969&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/10.2217%2Fnnm.13.49
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 103
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Blood coagulation; Anticoagulants; Reviews; Physicochemical properties; Hydrophobicity; Drugs; nanoparticles; Side effects; nanotechnology
DO  - http://dx.doi.org/10.2217/nnm.13.49
ER  - 



TY  - JOUR
T1  - B Cell Response and Hemagglutinin Stalk-Reactive Antibody Production in Different Age Cohorts following 2009 H1N1 Influenza Virus Vaccination
AN  - 1419369453; 18280345
AB  - The 2009 pandemic H1N1 (pH1N1) influenza virus carried a swine-origin hemagglutinin (HA) that was closely related to the HAs of pre-1947 H1N1 viruses but highly divergent from the HAs of recently circulating H1N1 strains. Consequently, prior exposure to pH1N1-like viruses was mostly limited to individuals over the age of about 60 years. We related age and associated differences in immune history to the B cell response to an inactivated monovalent pH1N1 vaccine given intramuscularly to subjects in three age cohorts: 18 to 32 years, 60 to 69 years, and greater than or equal to 70 years. The day 0 pH1N1-specific hemagglutination inhibition (HAI) and microneutralization (MN) titers were generally higher in the older cohorts, consistent with greater prevaccination exposure to pH1N1-like viruses. Most subjects in each cohort responded well to vaccination, with early formation of circulating virus-specific antibody (Ab)-secreting cells and greater than or equal to 4-fold increases in HAI and MN titers. However, the response was strongest in the 18- to 32-year cohort. Circulating levels of HA stalk-reactive Abs were increased after vaccination, especially in the 18- to 32-year cohort, raising the possibility of elevated levels of cross-reactive neutralizing Abs. In the young cohort, an increase in MN activity against the seasonal influenza virus A/Brisbane/59/07 after vaccination was generally associated with an increase in the anti-Brisbane/59/07 HAI titer, suggesting an effect mediated primarily by HA head-reactive rather than stalk-reactive Abs. Our findings support recent proposals that immunization with a relatively novel HA favors the induction of Abs against conserved epitopes. They also emphasize the need to clarify how the level of circulating stalk-reactive Abs relates to resistance to influenza.
JF  - Clinical and Vaccine Immunology
AU  - Sangster, Mark Y
AU  - Baer, Jane
AU  - Santiago, Felix W
AU  - Fitzgerald, Theresa
AU  - Ilyushina, Natalia A
AU  - Sundararajan, Aarthi
AU  - Henn, Alicia D
AU  - Krammer, Florian
AU  - Yang, Hongmei
AU  - Luke, Catherine J
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 867
EP  - 876
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 20
IS  - 6
SN  - 1556-679X, 1556-679X
KW  - Virology & AIDS Abstracts; Health & Safety Science Abstracts; Immunology Abstracts
KW  - Historical account
KW  - Age
KW  - Lymphocytes B
KW  - Immunology
KW  - Hemagglutinins
KW  - Hemagglutination inhibition
KW  - Viruses
KW  - Vaccination
KW  - Immunization
KW  - Influenza
KW  - Antibodies
KW  - pandemics
KW  - Influenza virus
KW  - Sulfur dioxide
KW  - Influenza A virus
KW  - Vaccines
KW  - Seasonal variations
KW  - Manganese
KW  - Epitopes
KW  - Australia, Queensland, Brisbane
KW  - V 22350:Immunology
KW  - F 06905:Vaccines
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419369453?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+and+Vaccine+Immunology&rft.atitle=B+Cell+Response+and+Hemagglutinin+Stalk-Reactive+Antibody+Production+in+Different+Age+Cohorts+following+2009+H1N1+Influenza+Virus+Vaccination&rft.au=Sangster%2C+Mark+Y%3BBaer%2C+Jane%3BSantiago%2C+Felix+W%3BFitzgerald%2C+Theresa%3BIlyushina%2C+Natalia+A%3BSundararajan%2C+Aarthi%3BHenn%2C+Alicia+D%3BKrammer%2C+Florian%3BYang%2C+Hongmei%3BLuke%2C+Catherine+J&rft.aulast=Sangster&rft.aufirst=Mark&rft.date=2013-06-01&rft.volume=20&rft.issue=6&rft.spage=867&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=1556679X&rft_id=info:doi/10.1128%2FCVI.00735-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 43
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Influenza; pandemics; Antibodies; Age; Lymphocytes B; Hemagglutination inhibition; Hemagglutinins; Vaccines; Manganese; Vaccination; Epitopes; Historical account; Sulfur dioxide; Immunology; Viruses; Seasonal variations; Immunization; Influenza virus; Influenza A virus; Australia, Queensland, Brisbane
DO  - http://dx.doi.org/10.1128/CVI.00735-12
ER  - 



TY  - JOUR
T1  - PathVisio-Faceted Search: an exploration tool for multi-dimensional navigation of large pathways
AN  - 1372059895; 18150476
AB  - Purpose: The PathVisio-Faceted Search plugin helps users explore and understand complex pathways by overlaying experimental data and data from webservices, such as Ensembl BioMart, onto diagrams drawn using formalized notations in PathVisio. The plugin then provides a filtering mechanism, known as a faceted search, to find and highlight diagram nodes (e.g. genes and proteins) of interest based on imported data. The tool additionally provides a flexible scripting mechanism to handle complex queries.
JF  - Bioinformatics
AU  - Fried, Jake Y
AU  - van Iersel, Martijn P
AU  - Aladjem, Mirit I
AU  - Kohn, Kurt W
AU  - Luna, Augustin
AD  - super(1)Computer Engineering, University of Maryland, College Park, MD 20740, USA, super(2)General Bioinformatics Ltd, Berkshire, Reading RG4 7RT, UK, super(3)Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA and super(4)Bioinformatics Program, Boston University, Boston, MA 02215, USA
Y1  - 2013/06/01/
PY  - 2013
DA  - 2013 Jun 01
SP  - 1465
EP  - 1466
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 11
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - Bioinformatics
KW  - Nodes
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1372059895?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=PathVisio-Faceted+Search%3A+an+exploration+tool+for+multi-dimensional+navigation+of+large+pathways&rft.au=Fried%2C+Jake+Y%3Bvan+Iersel%2C+Martijn+P%3BAladjem%2C+Mirit+I%3BKohn%2C+Kurt+W%3BLuna%2C+Augustin&rft.aulast=Fried&rft.aufirst=Jake&rft.date=2013-06-01&rft.volume=29&rft.issue=11&rft.spage=1465&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt146
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Data processing; Bioinformatics; Nodes
DO  - http://dx.doi.org/10.1093/bioinformatics/btt146
ER  - 



TY  - JOUR
T1  - Plasma Cell Neoplasms in US Solid Organ Transplant Recipients
AN  - 1372059512; 18143302
AB  - Transplant recipients have elevated risk for plasma cell neoplasms (PCNs, comprising multiple myeloma and plasmacytoma), but little is known about risk factors in the transplant setting. Through linkage of the US solid organ transplant registry with 15 state/regional cancer registries, we identified 140 PCNs in 202 600 recipients (1987-2009). PCN risk was 1.8-fold increased relative to the general population (standardized incidence ratio [SIR] 1.80, 95%CI 1.51-2.12). Among cases, 102 were multiple myeloma (SIR 1.41) and 38 were plasmacytoma (SIR 7.06). PCN incidence increased with age, but due to the rarity of PCNs in younger people in the general population, SIRs were highest in younger transplant recipients (p = 0.03). PCN risk was especially high in recipients who were Epstein-Barr virus (EBV) seronegative at transplantation (SIR 3.93). EBV status was known for 18 tumors, of which 7 (39%) were EBV positive. Following liver transplantation, PCN risk was higher in recipients with cholestatic liver disease (SIR 2.78); five of these cases had primary biliary cirrhosis (PBC). A role for primary EBV infection after transplantation is supported by the increased PCN risk in young EBV seronegative recipients and the presence of EBV in tumors. PBC may be another risk factor, perhaps by causing chronic immune activation. In this large US population-based study, the authors demonstrate that transplant recipients have an elevated risk for plasma cell neoplasms and document several risk factors for this type of malignancy, including Epstein Barr virus infection, recipient age, and the presence of primary biliary cirrhosis.
JF  - American Journal of Transplantation
AU  - Engels, E A
AU  - Clarke, CA
AU  - Pfeiffer, R M
AU  - Lynch, C F
AU  - Weisenburger, D D
AU  - Gibson, T M
AU  - Landgren, O
AU  - Morton, L M
AD  - Division of Cancer Epidemiology and Genetics. National Cancer Institute
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1523
EP  - 1532
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 13
IS  - 6
SN  - 1600-6135, 1600-6135
KW  - Immunology Abstracts; Risk Abstracts
KW  - Age
KW  - Infection
KW  - Liver transplantation
KW  - Epstein-Barr virus
KW  - Malignancy
KW  - Multiple myeloma
KW  - Risk factors
KW  - Transplantation
KW  - Liver diseases
KW  - primary biliary cirrhosis
KW  - Population studies
KW  - Tumors
KW  - Organs
KW  - Cancer
KW  - USA
KW  - Plasmacytoma
KW  - Immune response
KW  - Plasma cells
KW  - R2 23060:Medical and environmental health
KW  - F 06920:Transplantation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1372059512?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Transplantation&rft.atitle=Plasma+Cell+Neoplasms+in+US+Solid+Organ+Transplant+Recipients&rft.au=Engels%2C+E+A%3BClarke%2C+CA%3BPfeiffer%2C+R+M%3BLynch%2C+C+F%3BWeisenburger%2C+D+D%3BGibson%2C+T+M%3BLandgren%2C+O%3BMorton%2C+L+M&rft.aulast=Engels&rft.aufirst=E&rft.date=2013-06-01&rft.volume=13&rft.issue=6&rft.spage=1523&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Transplantation&rft.issn=16006135&rft_id=info:doi/10.1111%2Fajt.12234
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2014-05-29
N1  - SubjectsTermNotLitGenreText - Age; Liver diseases; primary biliary cirrhosis; Population studies; Tumors; Cancer; Liver transplantation; Malignancy; Multiple myeloma; Plasmacytoma; Risk factors; Immune response; Plasma cells; Transplantation; Infection; Organs; Epstein-Barr virus; USA
DO  - http://dx.doi.org/10.1111/ajt.12234
ER  - 



TY  - JOUR
T1  - Spatial-temporal disease mapping of illicit drug abuse or dependence in the presence of misaligned ZIP codes
AN  - 1372057601; 18152492
AB  - Geo-referenced data often are collected in small, administrative units such as census enumeration districts or postal code areas. Such areas vary in geographic area and population size and may change over time. In research into drug-related health issues within the United States, U.S. Postal Service ZIP codes represent a commonly used unit for data collection, storage, and spatial analysis because of their widespread availability in health databases through patient contact and billing information. However, the ZIP code was developed for the specific purpose of delivering mail and may be changed at any time, and its design and development does not take into consideration problems that may arise in data collection, analysis, and presentation in health studies. In this paper, we propose a spatial hierarchical modeling approach to quantify trends within ZIP-code based counts when some fraction of ZIP codes change over the study period, that is, when the data are spatially misaligned across time. We propose a data vector approach and adjust the spatial auto-correlation structure within our Bayesian hierarchical model to provide inference for our misaligned data. We motivate and illustrate our approach to explore spatio-temporal patterns of amphetamine abuse and/or dependence in Tracy, California over the years 1995-2005. Uncertainty associated with misaligned data is modeled, quantified, and visualized. The approach offers a framework for further investigation into other risk factors in order to more fully understand the dynamics of illicit drug abuse or dependence across time and space in imperfectly measured data.
JF  - GeoJournal
AU  - Zhu, Li
AU  - Waller, Lance A
AU  - Ma, Juan
AD  - Surveillance Research Program, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA, li.zhu@nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 463
EP  - 474
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 78
IS  - 3
SN  - 0343-2521, 0343-2521
KW  - Risk Abstracts; Environment Abstracts; Sustainability Science Abstracts
KW  - Storage
KW  - Data collection
KW  - Risk factors
KW  - Spatial analysis
KW  - Census
KW  - USA, California
KW  - Mapping
KW  - Drug abuse
KW  - Population number
KW  - ENA 13:Population Planning & Control
KW  - M3 1010:Issues in Sustainable Development
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1372057601?accountid=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=GeoJournal&rft.atitle=Spatial-temporal+disease+mapping+of+illicit+drug+abuse+or+dependence+in+the+presence+of+misaligned+ZIP+codes&rft.au=Zhu%2C+Li%3BWaller%2C+Lance+A%3BMa%2C+Juan&rft.aulast=Zhu&rft.aufirst=Li&rft.date=2013-06-01&rft.volume=78&rft.issue=3&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=GeoJournal&rft.issn=03432521&rft_id=info:doi/10.1007%2Fs10708-011-9429-3
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Number of references - 22
N1  - Last updated - 2014-05-02
N1  - SubjectsTermNotLitGenreText - Storage; Data collection; Risk factors; Spatial analysis; Census; Mapping; Drug abuse; Population number; USA, California
DO  - http://dx.doi.org/10.1007/s10708-011-9429-3
ER  - 



TY  - JOUR
T1  - Soluble receptor for advanced glycation end products and risk of liver cancer.
AN  - 1367879345; 23325627
AB  - Binding of advanced glycation end products (AGEs) to their receptor (RAGE) increases oxidative stress and inflammation and may be involved in liver injury and subsequent carcinogenesis. Soluble RAGE (sRAGE) may neutralize the effects mediated by the AGE/RAGE complex. Epidemiologic studies examining sRAGE or AGEs in association with liver cancer are lacking. We examined the associations between prediagnostic serum concentrations of sRAGE or Nϵ-(carboxymethyl)-lysine (CML)-AGE and hepatocellular carcinoma in a case-cohort study within a cohort of 29,133 Finnish male smokers who completed questionnaires and provided a fasting blood sample between 1985 and 1988. During follow-up beginning 5 years after enrollment through April 2006, 145 liver cancers occurred. Serum concentrations of sRAGE, CML-AGE, glucose, and insulin were measured in case subjects and 485 randomly sampled cohort participants. Chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) were available in most cases and in a subset of the study population. Weighted Cox proportional hazards regression was used to calculate relative risks (RR) and 95% confidence intervals (CI) adjusted for age, years of smoking, and body mass index. sRAGE and CML-AGE concentrations were inversely associated with liver cancer. Further adjustment for glucose and insulin or exclusion of case subjects with chronic HBV or HCV did not change the associations.
          Our results support the hypothesis that sRAGE is inversely associated with liver cancer. The findings need confirmation, particularly in populations that include women and nonsmokers. (HEPATOLOGY 2013 ). Copyright © 2013 American Association for the Study of Liver Diseases.
JF  - Hepatology (Baltimore, Md.)
AU  - Moy, Kristin A
AU  - Jiao, Li
AU  - Freedman, Neal D
AU  - Weinstein, Stephanie J
AU  - Sinha, Rashmi
AU  - Virtamo, Jarmo
AU  - Albanes, Demetrius
AU  - Stolzenberg-Solomon, Rachael Z
AD  - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. moyka@mail.nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 2338
EP  - 2345
VL  - 57
IS  - 6
KW  - Advanced Glycosylation End Product-Specific Receptor
KW  - 0
KW  - Glycosylation End Products, Advanced
KW  - Receptors, Immunologic
KW  - N(6)-carboxymethyllysine
KW  - 5746-04-3
KW  - Lysine
KW  - K3Z4F929H6
KW  - Index Medicus
KW  - Randomized Controlled Trials as Topic
KW  - Risk Factors
KW  - Humans
KW  - Aged
KW  - Middle Aged
KW  - Finland -- epidemiology
KW  - Male
KW  - Glycosylation End Products, Advanced -- metabolism
KW  - Carcinoma, Hepatocellular -- blood
KW  - Lysine -- analogs & derivatives
KW  - Liver Neoplasms -- epidemiology
KW  - Receptors, Immunologic -- blood
KW  - Lysine -- metabolism
KW  - Liver Neoplasms -- blood
KW  - Carcinoma, Hepatocellular -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367879345?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Soluble+receptor+for+advanced+glycation+end+products+and+risk+of+liver+cancer.&rft.au=Moy%2C+Kristin+A%3BJiao%2C+Li%3BFreedman%2C+Neal+D%3BWeinstein%2C+Stephanie+J%3BSinha%2C+Rashmi%3BVirtamo%2C+Jarmo%3BAlbanes%2C+Demetrius%3BStolzenberg-Solomon%2C+Rachael+Z&rft.aulast=Moy&rft.aufirst=Kristin&rft.date=2013-06-01&rft.volume=57&rft.issue=6&rft.spage=2338&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.26264
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-16
N1  - Date created - 2013-06-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Hepatology. 2004 Feb;39(2):422-32 [14767995]
Diabetologia. 2004 Aug;47(8):1376-9 [15258735]
Gastroenterology. 2004 Nov;127(5 Suppl 1):S5-S16 [15508102]
Ann Epidemiol. 1994 Jan;4(1):1-10 [8205268]
Am J Epidemiol. 1999 Mar 15;149(6):531-40 [10084242]
J Exp Med. 2005 Feb 7;201(3):473-84 [15699076]
Clin Biochem. 2006 Jan;39(1):39-45 [16321365]
J Gastroenterol Hepatol. 2006 Apr;21(4):682-8 [16677153]
Clin Gastroenterol Hepatol. 2006 Dec;4(12):1514-21 [17162243]
J Clin Pathol. 2007 Apr;60(4):415-8 [16775125]
Gastroenterology. 2007 Jun;132(7):2557-76 [17570226]
J Gastroenterol Hepatol. 2007 Jul;22(7):1112-9 [17559366]
Naunyn Schmiedebergs Arch Pharmacol. 2007 Aug;375(6):401-6 [17571253]
Cancer Invest. 2007 Dec;25(8):720-5 [18058469]
Ann Surg Oncol. 2008 Mar;15(3):923-33 [18080716]
Curr Pharm Des. 2008;14(10):940-5 [18473843]
Curr Pharm Des. 2008;14(10):969-72 [18473847]
FASEB J. 2008 Oct;22(10):3716-27 [18603587]
J Transl Med. 2009;7:17 [19292913]
Clin Biochem. 2009 Jun;42(9):802-7 [19217891]
J Natl Cancer Inst. 2009 Jul 15;101(14):1001-11 [19561318]
Diabetologia. 2009 Nov;52(11):2251-63 [19636529]
Neoplasma. 2010;57(1):55-61 [19895173]
J Am Diet Assoc. 2010 Jun;110(6):911-16.e12 [20497781]
Clin Biochem. 2010 Jul;43(10-11):882-6 [20398646]
J Gerontol A Biol Sci Med Sci. 2010 Sep;65(9):963-75 [20478906]
J Nutr. 2011 Sep;141(9):1726-30 [21775524]
Eur J Clin Nutr. 2012 Jan;66(1):3-9 [21792213]
CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781]
J Viral Hepat. 1999 Jan;6(1):35-47 [10847128]
Diabetologia. 2001 Feb;44(2):129-46 [11270668]
J Hepatol. 2002 Jan;36(1):66-71 [11804666]
Am J Epidemiol. 2002 May 1;155(9):783-92 [11978580]
Acta Oncol. 2002;41(4):381-8 [12234031]
Biochem J. 2003 Mar 15;370(Pt 3):1097-109 [12495433]
Cancer Epidemiol Biomarkers Prev. 2012 Apr;21(4):619-28 [22301828]
Viral Immunol. 2010 Dec;23(6):633-8 [21142449]
Antioxid Redox Signal. 2011 Mar 15;14(6):1167-72 [20969485]
J Visc Surg. 2011 Feb;148(1):3-11 [21306970]
Cancer Res. 2011 May 15;71(10):3582-9 [21540233]
Liver Transpl. 2011 Jun;17(6):633-40 [21438128]
Clin Liver Dis. 2011 May;15(2):223-43, vii-x [21689610]
Cancer Epidemiol Biomarkers Prev. 2011 Jul;20(7):1430-8 [21527578]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/hep.26264
ER  - 



TY  - JOUR
T1  - Selective induction of apoptosis in various cancer cells irrespective of drug sensitivity through a copper chelate, copper N-(2 hydroxy acetophenone) glycinate: crucial involvement of glutathione.
AN  - 1367878366; 23733180
AB  - Drug induced toxicity and drug resistance are the major impediments to successful application of cancer chemotherapy. Therefore, selective targeting of the key biochemical events of the malignant cells may have a great therapeutic potential in specifically kill the cancer cells. We have evaluated in vitro the cytotoxic efficacy of a previously reported copper complex viz. copper N-(2-hydroxy acetophenone) glycinate (CuNG) on different drug sensitive and resistant cancer cell lines by MTT, annexin V positivity and caspase 3 activation assays. We have also investigated the underlying signalling events in CuNG mediated apoptosis of cancer cells by Western blotting technique. We have found that CuNG preferentially induces apoptosis to malignant cells irrespective of drug sensitivity and spares the normal cells. Our studies disclose that CuNG causes cellular redox imbalance in cancer cells through depletion of intracellular GSH level. CuNG mediated depletion of intracellular GSH level induces mitochondrial superoxide generation, which detaches cyto C from mitochondrial membrane through lipid peroxidation. The detached cyto C then release into the extra mitochondrial milieu in Bax mediated pathway where CuNG facilitates the binding of Bax through dissociation of hexokinase II from mitochondrial membrane. The present study opens the possibility of developing effective chemotherapeutic drugs by synthesizing numerous chemical compounds capable of targeting cellular redox environment and thus specifically kills cancer cells of broad spectrum.
JF  - Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine
AU  - Chatterjee, Shilpak
AU  - Chakraborty, Paramita
AU  - Banerjee, Kaushik
AU  - Sinha, Abhinaba
AU  - Adhikary, Arghya
AU  - Das, Tanya
AU  - Choudhuri, Soumitra Kumar
AD  - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, S.P. Mukherjee Road, Kolkata 700026, India.
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 517
EP  - 534
VL  - 26
IS  - 3
KW  - Antineoplastic Agents
KW  - 0
KW  - Chelating Agents
KW  - Organometallic Compounds
KW  - copper (N-2-hydroxyacetophenone)glycinate
KW  - Glutathione
KW  - GAN16C9B8O
KW  - Glycine
KW  - TE7660XO1C
KW  - Index Medicus
KW  - Drug Screening Assays, Antitumor
KW  - Animals
KW  - Cell Survival -- drug effects
KW  - HeLa Cells
KW  - Dose-Response Relationship, Drug
KW  - Cells, Cultured
KW  - Humans
KW  - HEK293 Cells
KW  - Mice
KW  - HCT116 Cells
KW  - K562 Cells
KW  - NIH 3T3 Cells
KW  - Structure-Activity Relationship
KW  - Glycine -- chemistry
KW  - Chelating Agents -- pharmacology
KW  - Chelating Agents -- chemistry
KW  - Organometallic Compounds -- pharmacology
KW  - Glycine -- pharmacology
KW  - Glutathione -- metabolism
KW  - Apoptosis -- drug effects
KW  - Glycine -- analogs & derivatives
KW  - Antineoplastic Agents -- chemistry
KW  - Antineoplastic Agents -- pharmacology
KW  - Organometallic Compounds -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367878366?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biometals+%3A+an+international+journal+on+the+role+of+metal+ions+in+biology%2C+biochemistry%2C+and+medicine&rft.atitle=Selective+induction+of+apoptosis+in+various+cancer+cells+irrespective+of+drug+sensitivity+through+a+copper+chelate%2C+copper+N-%282+hydroxy+acetophenone%29+glycinate%3A+crucial+involvement+of+glutathione.&rft.au=Chatterjee%2C+Shilpak%3BChakraborty%2C+Paramita%3BBanerjee%2C+Kaushik%3BSinha%2C+Abhinaba%3BAdhikary%2C+Arghya%3BDas%2C+Tanya%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Chatterjee&rft.aufirst=Shilpak&rft.date=2013-06-01&rft.volume=26&rft.issue=3&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Biometals+%3A+an+international+journal+on+the+role+of+metal+ions+in+biology%2C+biochemistry%2C+and+medicine&rft.issn=1572-8773&rft_id=info:doi/10.1007%2Fs10534-013-9637-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-12-22
N1  - Date created - 2013-06-13
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s10534-013-9637-z
ER  - 



TY  - JOUR
T1  - Electrocardiographic studies of romidepsin demonstrate its safety and identify a potential role for K(ATP) channel.
AN  - 1365051453; 23589175
AB  - Romidepsin is a histone deacetylase inhibitor (HDI) approved for the treatment of both cutaneous and peripheral T-cell lymphoma (CTCL and PTCL). During development, a thorough assessment of cardiac toxicity was conducted.
          A phase II single-agent nonrandomized study of romidepsin was conducted in patients with CTCL or PTCL who had progressed after at least 1 prior systemic therapy. Results for the first 42 patients enrolled on the NCI 1312 phase II study of romidepsin in CTCL or PTCL showed no cardiac toxicity based on serial electrocardiograms (ECG), troponins, and MUGA scans/echocardiograms. The cardiac assessments reported herein confirm the safety of romidepsin among 131 enrolled patients, while supporting a role for electrolyte replacement. Heart rate increased an average 11 bpm following romidepsin infusion; there was no evidence of increased arrhythmia. Criteria for potassium/magnesium replacement were met before 55% of 1365 romidepsin doses; an association with hypoalbuminemia was confirmed. We propose a mechanism for ST segment flattening and depression, the most common ECG abnormalities observed: HDI-induced alteration of the activity or expression of KATP channels. In addition, examination of the variants of the active transporter of romidepsin, ABCB1, showed a trend toward smaller heart rate changes in the peri-infusion period among wild-type than variant diplotypes.
          We conclude that in the context of appropriate attention to electrolyte levels, the data support the cardiac safety of romidepsin. ©2013 AACR
JF  - Clinical cancer research : an official journal of the American Association for Cancer Research
AU  - Noonan, Anne M
AU  - Eisch, Robin A
AU  - Liewehr, David J
AU  - Sissung, Tristan M
AU  - Venzon, David J
AU  - Flagg, Thomas P
AU  - Haigney, Mark C
AU  - Steinberg, Seth M
AU  - Figg, William D
AU  - Piekarz, Richard L
AU  - Bates, Susan E
AD  - Medical Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.
Y1  - 2013/06/01/
PY  - 2013
DA  - 2013 Jun 01
SP  - 3095
EP  - 3104
VL  - 19
IS  - 11
SN  - 1078-0432, 1078-0432
KW  - ABCB1 protein, human
KW  - 0
KW  - Antibiotics, Antineoplastic
KW  - Depsipeptides
KW  - Histone Deacetylase Inhibitors
KW  - P-Glycoprotein
KW  - P-Glycoproteins
KW  - romidepsin
KW  - CX3T89XQBK
KW  - Magnesium
KW  - I38ZP9992A
KW  - Potassium
KW  - RWP5GA015D
KW  - Index Medicus
KW  - Lymphoma, T-Cell, Peripheral -- genetics
KW  - Magnesium -- blood
KW  - Humans
KW  - Lymphoma, T-Cell, Cutaneous -- genetics
KW  - Aged
KW  - Lymphoma, T-Cell, Cutaneous -- drug therapy
KW  - Genotype
KW  - Lymphoma, T-Cell, Cutaneous -- metabolism
KW  - Heart Rate -- drug effects
KW  - P-Glycoprotein -- genetics
KW  - Aged, 80 and over
KW  - Adult
KW  - Lymphoma, T-Cell, Peripheral -- drug therapy
KW  - Potassium -- blood
KW  - Middle Aged
KW  - Male
KW  - Lymphoma, T-Cell, Peripheral -- metabolism
KW  - Female
KW  - Histone Deacetylase Inhibitors -- adverse effects
KW  - Depsipeptides -- adverse effects
KW  - Antibiotics, Antineoplastic -- adverse effects
KW  - Electrocardiography -- drug effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1365051453?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Electrocardiographic+studies+of+romidepsin+demonstrate+its+safety+and+identify+a+potential+role+for+K%28ATP%29+channel.&rft.au=Noonan%2C+Anne+M%3BEisch%2C+Robin+A%3BLiewehr%2C+David+J%3BSissung%2C+Tristan+M%3BVenzon%2C+David+J%3BFlagg%2C+Thomas+P%3BHaigney%2C+Mark+C%3BSteinberg%2C+Seth+M%3BFigg%2C+William+D%3BPiekarz%2C+Richard+L%3BBates%2C+Susan+E&rft.aulast=Noonan&rft.aufirst=Anne&rft.date=2013-06-01&rft.volume=19&rft.issue=11&rft.spage=3095&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-13-0109
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-08
N1  - Date created - 2013-06-04
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1158/1078-0432.CCR-13-0109
ER  - 



TY  - JOUR
T1  - Phase II clinical trial of cediranib in patients with metastatic castration-resistant prostate cancer.
AN  - 1356954677; 23419134
AB  - To assess the efficacy and toxicity of cediranib, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, in patients with metastatic castration-resistant prostate cancer (CRPC) previously treated with docetaxel-based therapy.
          The study used a Simon two-stage trial design, which required at least two of 12 patients in the first cohort to be progression-free at 6 months. We enrolled a total of 35 evaluable patients who all received cediranib 20 mg orally daily. In a second cohort, 23 additional patients received prednisone 10 mg daily with cediranib. Endpoints included tumour response, progression-free survival (PFS), overall survival (OS), vascular permeability via dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), and toxicity.
          A total of 59 patients were enrolled, of whom 67% had received two or more previous chemotherapy regimens. Six of 39 patients with measurable disease had confirmed partial responses and one had an unconfirmed partial response. At 6 months, 43.9% of patients were progression-free; the median PFS and OS periods for all patients were 3.7 months and 10.1 months, respectively. We found that the DCE-MRI variables baseline transport constant (Ktrans ) and rate constant at day 28 were significantly associated with PFS in univariate analyses, but only baseline Ktrans remained significant when considered jointly. The most frequent toxicities were hypertension, fatigue, anorexia and weight loss; the addition of prednisone reduced the incidence of constitutional toxicities. This study demonstrated that cediranib was generally well tolerated with some anti-tumour activity in highly pretreated patients with metastatic CRPC who had progressive disease after docetaxel-based therapy.
          Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
JF  - BJU international
AU  - Dahut, William L
AU  - Madan, Ravi A
AU  - Karakunnel, Joyson J
AU  - Adelberg, David
AU  - Gulley, James L
AU  - Turkbey, Ismail B
AU  - Chau, Cindy H
AU  - Spencer, Shawn D
AU  - Mulquin, Marcia
AU  - Wright, John
AU  - Parnes, Howard L
AU  - Steinberg, Seth M
AU  - Choyke, Peter L
AU  - Figg, William D
AD  - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 1269
EP  - 1280
VL  - 111
IS  - 8
KW  - Protein Kinase Inhibitors
KW  - 0
KW  - Quinazolines
KW  - cediranib
KW  - NQU9IPY4K9
KW  - Index Medicus
KW  - Magnetic Resonance Imaging
KW  - Administration, Oral
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Protein Kinase Inhibitors -- administration & dosage
KW  - Treatment Outcome
KW  - Neoplasm Metastasis
KW  - Aged
KW  - Middle Aged
KW  - Follow-Up Studies
KW  - Time Factors
KW  - Male
KW  - Quinazolines -- administration & dosage
KW  - Prostatic Neoplasms -- pathology
KW  - Prostatic Neoplasms -- surgery
KW  - Prostatic Neoplasms -- drug therapy
KW  - Adenocarcinoma -- drug therapy
KW  - Adenocarcinoma -- surgery
KW  - Orchiectomy
KW  - Adenocarcinoma -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1356954677?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BJU+international&rft.atitle=Phase+II+clinical+trial+of+cediranib+in+patients+with+metastatic+castration-resistant+prostate+cancer.&rft.au=Dahut%2C+William+L%3BMadan%2C+Ravi+A%3BKarakunnel%2C+Joyson+J%3BAdelberg%2C+David%3BGulley%2C+James+L%3BTurkbey%2C+Ismail+B%3BChau%2C+Cindy+H%3BSpencer%2C+Shawn+D%3BMulquin%2C+Marcia%3BWright%2C+John%3BParnes%2C+Howard+L%3BSteinberg%2C+Seth+M%3BChoyke%2C+Peter+L%3BFigg%2C+William+D&rft.aulast=Dahut&rft.aufirst=William&rft.date=2013-06-01&rft.volume=111&rft.issue=8&rft.spage=1269&rft.isbn=&rft.btitle=&rft.title=BJU+international&rft.issn=1464-410X&rft_id=info:doi/10.1111%2Fj.1464-410X.2012.11667.x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-30
N1  - Date created - 2013-05-29
N1  - Date revised - 2017-01-14
N1  - Genetic sequence - NCT00436956; ClinicalTrials.gov
N1  - SuppNotes - Cited By:
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437]
J Clin Oncol. 2012 May 1;30(13):1534-40 [22454414]
Invest New Drugs. 2002 May;20(2):183-94 [12099578]
Cancer Metastasis Rev. 2002;21(1):93-106 [12400998]
N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213]
Control Clin Trials. 1989 Mar;10(1):1-10 [2702835]
J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243]
J Urol. 1997 Jun;157(6):2329-33 [9146665]
Urology. 1999 Sep;54(3):523-7 [10475365]
Cancer Res. 2005 May 15;65(10):4389-400 [15899831]
J Clin Oncol. 2005 Nov 1;23(31):7811-9 [16258083]
Histol Histopathol. 2006 Aug;21(8):857-65 [16691538]
Clin Cancer Res. 2007 May 15;13(10):3051-7 [17505008]
J Clin Oncol. 2007 Jul 20;25(21):3045-54 [17634482]
Invest New Drugs. 2007 Oct;25(5):445-51 [17458505]
J Clin Oncol. 2008 Mar 1;26(7):1148-59 [18309951]
J Clin Oncol. 2008 Oct 1;26(28):4572-8 [18824708]
Clin Colorectal Cancer. 2009 Jan;8(1):59-60 [19203899]
BJU Int. 2009 Jun;103(12):1636-40 [19154507]
Expert Opin Investig Drugs. 2009 Oct;18(10):1549-57 [19671039]
J Clin Oncol. 2009 Nov 20;27(33):5601-6 [19826113]
J Clin Oncol. 2010 Jan 1;28(1):49-55 [19917841]
Ann Oncol. 2010 Feb;21(2):319-24 [19633050]
J Clin Oncol. 2010 Jun 10;28(17):2817-23 [20458050]
J Thorac Oncol. 2010 Aug;5(8):1279-84 [20559150]
N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862]
CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300 [20610543]
Lancet. 2010 Oct 2;376(9747):1147-54 [20888992]
Cancer Res. 2010 Nov 1;70(21):8662-73 [20959486]
JAMA. 2011 Feb 2;305(5):487-94 [21285426]
Clin Cancer Res. 2011 Mar 1;17(5):1190-9 [21224376]
N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468]
Eur J Cancer. 2012 Mar;48(4):527-37 [22285180]
Expert Opin Ther Targets. 2012 Apr;16(4):365-76 [22413953]
Cancer Invest. 2001;19(2):181-91 [11296622]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/j.1464-410X.2012.11667.x
ER  - 



TY  - JOUR
T1  - Prior Exposure to THC Increases the Addictive Effects of Nicotine in Rats
AN  - 1356932206; 18039475
AB  - Although it is more common for drug abuse to progress from tobacco to cannabis, in many cases cannabis use develops before tobacco use. Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due to cannabis exposure per se, in addition to any genetic, social, or environmental factors that might contribute, we extended our series of studies on 'gateway drug' effects in animal models of drug abuse. Rats were exposed to THC, the main psychoactive constituent of cannabis, for 3 days (two intraperitoneal injections/day). Then, starting 1 week later, they were allowed to self-administer nicotine intravenously. THC exposure increased the likelihood of acquiring the nicotine self-administration response from 65% in vehicle-exposed rats to 94% in THC-exposed rats. When the price of nicotine was manipulated by increasing the response requirement, THC-exposed rats maintained higher levels of intake than vehicle-exposed rats, indicating that THC exposure increased the value of nicotine reward. These results contrast sharply with our earlier findings that prior THC exposure did not increase the likelihood of rats acquiring either heroin or cocaine self-administration, nor did it increase the reward value of these drugs. The findings obtained here suggest that a history of cannabis exposure might have lasting effects that increase the risk of becoming addicted to nicotine.
JF  - Neuropsychopharmacology
AU  - Panlilio, Leigh V
AU  - Zanettini, Claudio
AU  - Barnes, Chanel
AU  - Solinas, Marcelo
AU  - Goldberg, Steven R
AD  - Preclinical Pharmacology Section, Behavioral Neuroscience Research Branch, Intramural Research Program, Department of Health and Human Services, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1198
EP  - 1208
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 38
IS  - 7
SN  - 0893-133X, 0893-133X
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - Tetrahydrocannabinol
KW  - Nicotine
KW  - Heroin
KW  - Cannabis
KW  - Tobacco
KW  - Reinforcement
KW  - Animal models
KW  - Drug abuse
KW  - Environmental factors
KW  - Drug self-administration
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/1356932206?accountid=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=Neuropsychopharmacology&rft.atitle=Prior+Exposure+to+THC+Increases+the+Addictive+Effects+of+Nicotine+in+Rats&rft.au=Panlilio%2C+Leigh+V%3BZanettini%2C+Claudio%3BBarnes%2C+Chanel%3BSolinas%2C+Marcelo%3BGoldberg%2C+Steven+R&rft.aulast=Panlilio&rft.aufirst=Leigh&rft.date=2013-06-01&rft.volume=38&rft.issue=7&rft.spage=1198&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology&rft.issn=0893133X&rft_id=info:doi/10.1038%2Fnpp.2013.16
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2013-08-23
N1  - SubjectsTermNotLitGenreText - Tetrahydrocannabinol; Heroin; Nicotine; Animal models; Reinforcement; Tobacco; Cannabis; Drug abuse; Environmental factors; Drug self-administration
DO  - http://dx.doi.org/10.1038/npp.2013.16
ER  - 



TY  - JOUR
T1  - Relationship Between Alcohol Consumption Prior to Sex, Unprotected Sex and Prevalence of STI/HIV Among Socially Marginalized Men in Three Coastal Cities of Peru
AN  - 1354685130; 23054035
AB  - This article presents data about the relationship between alcohol consumption prior to sex and unprotected sex and the prevalence of at least one sexually transmitted infection (STI) including HIV among socially marginalized men in three coastal Peruvians cities. During an epidemiological survey with 2,146 men, we assessed their STI prevalence, frequency of alcohol consumption prior to sex, unprotected sex and other sexual risk behaviors. The overall prevalence of at least one STI/HIV was 8.5 % (95 % CI 7.3-9.7), the prevalence of unprotected sex was 79.1 % (95 % CI 77.8-80.3) and alcohol consumption prior to sex with any of the last five sex partners in the previous 6 months was 68.9 % (95 % CI 66.9-70.9). Bivariate and multivariate analysis showed that alcohol consumption of participants or their partners prior to sex were associated with the prevalence of at least one STI, adjusted Prevalence Ratio (aPR) = 1.3 (95 % CI 1.01-1.68). Unprotected sex was significantly associated with alcohol consumption prior to sex when both partners used alcohol, aPR = 1.15 (95 % CI 1.10-1.20) or when either one of them used alcohol aPR = 1.14 (95 % CI 1.09-1.18). These findings concur with previous literature suggesting a relationship between alcohol consumption prior to sex and STI and HIV. These data improve our understanding of this relationship in this context and could be used to enhance STI and HIV prevention strategies for socially marginalized men in Peru.[PUBLICATION ABSTRACT]
JF  - AIDS and Behavior
AU  - Maguiña, Jorge L
AU  - Konda, Kelika A
AU  - Leon, Segundo R
AU  - Lescano, Andrés G
AU  - Clark, Jesse L
AU  - Hall, Eric R
AU  - Klausner, Jeffrey D
AU  - Coates, Tom J
AU  - Caceres, Carlos F
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 1724
EP  - 33
CY  - New York
PB  - Springer Science & Business Media
VL  - 17
IS  - 5
SN  - 10907165
KW  - Psychology
KW  - Alcohol use
KW  - Sexual behavior
KW  - Sexually transmitted diseases--STD
KW  - Human immunodeficiency virus--HIV
KW  - Condoms
KW  - Men
KW  - Peru
KW  - Sexually Transmitted Diseases -- psychology
KW  - Young Adult
KW  - Humans
KW  - Alcohol Drinking -- epidemiology
KW  - Multivariate Analysis
KW  - Peru -- epidemiology
KW  - Cross-Sectional Studies
KW  - Adult
KW  - Unsafe Sex -- statistics & numerical data
KW  - HIV Infections -- psychology
KW  - Sexual Behavior -- psychology
KW  - Male
KW  - Prevalence
KW  - Sexual Behavior -- statistics & numerical data
KW  - Unsafe Sex -- psychology
KW  - Alcohol Drinking -- psychology
KW  - HIV Infections -- epidemiology
KW  - Social Marginalization -- psychology
KW  - Sexually Transmitted Diseases -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1354685130?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acriminaljusticeperiodicals&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+and+Behavior&rft.atitle=Relationship+Between+Alcohol+Consumption+Prior+to+Sex%2C+Unprotected+Sex+and+Prevalence+of+STI%2FHIV+Among+Socially+Marginalized+Men+in+Three+Coastal+Cities+of+Peru&rft.au=Magui%C3%B1a%2C+Jorge+L%3BKonda%2C+Kelika+A%3BLeon%2C+Segundo+R%3BLescano%2C+Andr%C3%A9s+G%3BClark%2C+Jesse+L%3BHall%2C+Eric+R%3BKlausner%2C+Jeffrey+D%3BCoates%2C+Tom+J%3BCaceres%2C+Carlos+F&rft.aulast=Magui%C3%B1a&rft.aufirst=Jorge&rft.date=2013-06-01&rft.volume=17&rft.issue=5&rft.spage=1724&rft.isbn=&rft.btitle=&rft.title=AIDS+and+Behavior&rft.issn=10907165&rft_id=info:doi/10.1007%2Fs10461-012-0310-2
LA  - English
DB  - ProQuest Central
N1  - Copyright - Springer Science+Business Media New York 2013
N1  - Document feature - References
N1  - Last updated - 2014-08-29
N1  - CODEN - AIBEFC
N1  - SubjectsTermNotLitGenreText - Peru
DO  - http://dx.doi.org/10.1007/s10461-012-0310-2
ER  - 



TY  - JOUR
T1  - Comparison of automated versus manual neutrophil counts for the detection of cellular abnormalities in dogs receiving chemotherapy: 50 cases (May to June 2008).
AN  - 1353480358; 23683019
AB  - To determine the frequency of clinically relevant abnormalities missed by failure to perform a blood smear evaluation in a specific subset of dogs receiving chemotherapy and to compare automated and manual neutrophil counts in the same population.
          Retrospective case series. 50 dogs receiving chemotherapy with a total nucleated cell count > 4,000 nucleated cells/μL.
          50 blood smears were evaluated for abnormalities that have strong potential to change the medical plan for a patient: presence of blast cells, band neutrophils, nucleated RBCs, toxic change, hemoparasites, schistocytes, and spherocytes. Automated and manual neutrophil counts were compared. Blood smears from 10 (20%) patients had ≥ 1 abnormalities. Blast cells were identified on 4 (8%) blood smears, increased nucleated RBCs were identified on 5 (10%), and very mild toxic change was identified on 2 (4%). Correlation coefficient of the neutrophil counts was 0.96. Analysis revealed a slight bias between the automated and manual neutrophil counts (mean ± SD difference, -0.43 × 10(3)/μL ± 1.10 × 10(3)/μL).
          In this series of patients, neutrophil count correlation was very good. Clinically relevant abnormalities were found on 20% of the blood smears. An automated CBC appears to be accurate for neutrophil counts, but a microscopic examination of the corresponding blood smear is still recommended; further studies are needed to determine whether the detection or frequency of these abnormalities would differ dependent on chemotherapy protocol, neoplastic disease, and decision thresholds used by the oncologist in the ordering of a CBC without a blood smear evaluation.
JF  - Journal of the American Veterinary Medical Association
AU  - Cora, Michelle C
AU  - Neel, Jennifer A
AU  - Grindem, Carol B
AU  - Kissling, Grace E
AU  - Hess, Paul R
AD  - Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, USA. coramc@niehs.nih.gov
Y1  - 2013/06/01/
PY  - 2013
DA  - 2013 Jun 01
SP  - 1539
EP  - 1543
VL  - 242
IS  - 11
KW  - Antineoplastic Agents
KW  - 0
KW  - Index Medicus
KW  - Neoplasms -- veterinary
KW  - Neoplasms -- drug therapy
KW  - Animals
KW  - Retrospective Studies
KW  - Dogs
KW  - Neutropenia -- chemically induced
KW  - Dog Diseases -- drug therapy
KW  - Neutrophils -- physiology
KW  - Dog Diseases -- blood
KW  - Neutropenia -- diagnosis
KW  - Antineoplastic Agents -- therapeutic use
KW  - Neutropenia -- veterinary
KW  - Antineoplastic Agents -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1353480358?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Veterinary+Medical+Association&rft.atitle=Comparison+of+automated+versus+manual+neutrophil+counts+for+the+detection+of+cellular+abnormalities+in+dogs+receiving+chemotherapy%3A+50+cases+%28May+to+June+2008%29.&rft.au=Cora%2C+Michelle+C%3BNeel%2C+Jennifer+A%3BGrindem%2C+Carol+B%3BKissling%2C+Grace+E%3BHess%2C+Paul+R&rft.aulast=Cora&rft.aufirst=Michelle&rft.date=2013-06-01&rft.volume=242&rft.issue=11&rft.spage=1539&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Veterinary+Medical+Association&rft.issn=1943-569X&rft_id=info:doi/10.2460%2Fjavma.242.11.1539
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-26
N1  - Date created - 2013-05-20
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.2460/javma.242.11.1539
ER  - 



TY  - JOUR
T1  - The absence of ER-β results in altered gene expression in ovarian granulosa cells isolated from in vivo preovulatory follicles.
AN  - 1353476696; 23580569
AB  - Determining the spatial and temporal expression of genes involved in the ovulatory pathway is critical for the understanding of the role of each estrogen receptor in the modulation of folliculogenesis and ovulation. Estrogen receptor (ER)-β is highly expressed in ovarian granulosa cells, and mice lacking ER-β are subfertile due to inefficient ovulation. Previous work has focused on isolated granulosa cells or cultured follicles and, although informative, provides confounding results due to the heterogeneous cell types present including granulosa and theca cells and oocytes and exposure to in vitro conditions. Herein we isolated preovulatory granulosa cells from wild-type (WT) and ERβ-null mice using laser capture microdissection to examine the genomic transcriptional response downstream of pregnant mare serum gonadotropin (mimicking FSH) and pregnant mare serum gonadotropin/human chorionic gonadotropin (mimicking LH) stimulation. This allows for a direct comparison of in vivo granulosa cells at the same stage of development from both WT and ERβ-null ovaries. ERβ-null granulosa cells showed altered expression of genes known to be regulated by FSH (Akap12 and Runx2) as well as not previously reported (Arnt2 and Pou5f1) in WT granulosa cells. Our analysis also identified 304 genes not previously associated with ERβ in granulosa cells. LH-responsive genes including Abcb1b and Fam110c show reduced expression in ERβ-null granulosa cells; however, novel genes including Rassf2 and Megf10 were also identified as being downstream of LH signaling in granulosa cells. Collectively, our data suggest that granulosa cells from ERβ-null ovaries may not be appropriately differentiated and are unable to respond properly to gonadotropin stimulation.
JF  - Endocrinology
AU  - Binder, April K
AU  - Rodriguez, Karina F
AU  - Hamilton, Katherine J
AU  - Stockton, Patricia S
AU  - Reed, Casey E
AU  - Korach, Kenneth S
AD  - National Institute of Environmental Health Sciences, Laboratory of Reproduction and Developmental Toxicology, 111 TW Alexander Drive, MD B3-02, Research Triangle Park, North Carolina 27709, USA.
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 2174
EP  - 2187
VL  - 154
IS  - 6
KW  - Chorionic Gonadotropin
KW  - 0
KW  - Estrogen Receptor beta
KW  - Gonadotropins, Equine
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Animals
KW  - Ovulation -- genetics
KW  - Oligonucleotide Array Sequence Analysis
KW  - Chorionic Gonadotropin -- pharmacology
KW  - Cells, Cultured
KW  - Humans
KW  - Horses
KW  - Gonadotropins, Equine -- pharmacology
KW  - Mice
KW  - Time Factors
KW  - Female
KW  - Pregnancy
KW  - Mice, Knockout
KW  - Ovary -- metabolism
KW  - Gene Expression Profiling
KW  - Ovary -- cytology
KW  - Granulosa Cells -- drug effects
KW  - Ovarian Follicle -- metabolism
KW  - Estrogen Receptor beta -- deficiency
KW  - Granulosa Cells -- metabolism
KW  - Ovarian Follicle -- cytology
KW  - Estrogen Receptor beta -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1353476696?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+absence+of+ER-%CE%B2+results+in+altered+gene+expression+in+ovarian+granulosa+cells+isolated+from+in+vivo+preovulatory+follicles.&rft.au=Binder%2C+April+K%3BRodriguez%2C+Karina+F%3BHamilton%2C+Katherine+J%3BStockton%2C+Patricia+S%3BReed%2C+Casey+E%3BKorach%2C+Kenneth+S&rft.aulast=Binder&rft.aufirst=April&rft.date=2013-06-01&rft.volume=154&rft.issue=6&rft.spage=2174&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/10.1210%2Fen.2012-2256
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-25
N1  - Date created - 2013-05-20
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - GSE44651; GEO
N1  - SuppNotes - Cited By:
Biol Reprod. 2000 Feb;62(2):310-7 [10642567]
Proc Natl Acad Sci U S A. 2012 Oct 30;109(44):E2979-88 [23045700]
Science. 2004 Aug 20;305(5687):1157-9 [15326356]
Carcinogenesis. 2004 Oct;25(10):2005-13 [15142886]
Biol Reprod. 1985 Jun;32(5):1038-50 [2990583]
Endocrinology. 1985 Sep;117(3):1156-61 [2990868]
Mol Cell Endocrinol. 1994 Sep;104(2):133-8 [7527351]
Recent Prog Horm Res. 1995;50:223-54 [7740159]
Biol Reprod. 1996 Mar;54(3):523-30 [8835372]
Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15677-82 [9861029]
Mol Cell Endocrinol. 1998 Oct 25;145(1-2):47-54 [9922098]
Mol Endocrinol. 1999 Jun;13(6):1035-48 [10379900]
Reproduction. 2005 Apr;129(4):473-80 [15798022]
Mol Cell Endocrinol. 2005 Apr 29;234(1-2):75-9 [15836955]
Endocrinology. 2005 Jun;146(6):2817-26 [15731357]
Endocrinology. 2005 Aug;146(8):3247-62 [15831568]
Cancer Res. 2006 Feb 15;66(4):1964-73 [16488995]
Mol Endocrinol. 2006 Apr;20(4):715-23 [16051667]
J Biol Chem. 2006 Aug 11;281(32):22429-33 [16793760]
Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12435-40 [16895991]
Development. 2006 Nov;133(22):4527-37 [17050619]
J Biol Chem. 2006 Nov 24;281(47):35747-56 [16997917]
Front Biosci. 2007;12:1804-13 [17127422]
Toxicol Appl Pharmacol. 2007 Aug 15;223(1):66-72 [17594909]
Mol Endocrinol. 2008 Aug;22(8):1842-52 [18535249]
Mol Reprod Dev. 2009 Jun;76(6):537-47 [18951380]
Reproduction. 2009 May;137(5):843-55 [19225042]
Endocrinology. 2009 Jul;150(7):3291-300 [19342459]
Mol Endocrinol. 2009 Jul;23(7):955-65 [19324971]
Environ Health Perspect. 2009 Jul;117(7):1155-61 [19654927]
Trends Endocrinol Metab. 2010 Jan;21(1):25-32 [19875303]
J Clin Invest. 2010 Apr;120(4):963-72 [20364094]
Endocrinology. 2010 Jun;151(6):2826-34 [20378682]
Reproduction. 2010 Aug;140(2):287-94 [20501789]
Handb Exp Pharmacol. 2010;(198):37-44 [20839085]
Endocrinology. 2010 Oct;151(10):4994-5006 [20739397]
FASEB J. 2010 Dec;24(12):4660-7 [20667977]
Mol Hum Reprod. 2011 Feb;17(2):104-14 [20823264]
Mol Endocrinol. 2011 Feb;25(2):253-68 [21177758]
Mol Endocrinol. 2011 Mar;25(3):445-59 [21212137]
Mol Hum Reprod. 2011 Jul;17(7):399-404 [21307090]
Mol Reprod Dev. 2011 Jun;78(6):391-402 [21520325]
PLoS One. 2012;7(1):e29937 [22253831]
Nature. 2012 Mar 22;483(7390):465-9 [22407321]
Biol Reprod. 2012 Mar;86(3):86 [22190699]
Mol Endocrinol. 2012 May;26(5):887-98 [22446102]
Biol Reprod. 2012 Jun;86(6):185 [22460667]
Reproduction. 2012 Nov;144(5):595-602 [22956516]
Biol Reprod. 2002 Dec;67(6):1662-70 [12444039]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1210/en.2012-2256
ER  - 



TY  - JOUR
T1  - Late acyltransferase genes lpxX and lpxL jointly contribute to the biological activities of Moraxella catarrhalis.
AN  - 1352281693; 23475908
AB  - Lipo-oligosaccharide (LOS) is a major surface component and virulence factor of the human respiratory pathogen Moraxella catarrhalis. Two late acyltransferase genes, lpxX and lpxL, have been identified involved in the incorporation of acyloxyacyl-linked secondary acyl chains into lipid A during M. catarrhalis LOS biosynthesis. In this study, a double mutant with a deletion of both the lpxX and lpxL genes in M. catarrhalis strain O35E was constructed and named O35ElpxXL. Structural analysis of lipid A showed that the O35ElpxXL mutant lacked two decanoic acids (10 : 0) and one dodecanoic (lauric) acid (12 : 0). In comparison with the O35E parental strain and the single mutants O35ElpxX and O35ElpxL, the double mutant O35ElpxXL displayed prominently decreased endotoxin content, reduced resistance to normal human serum and accelerated bacterial clearance at 0, 3 and 6 h after an aerosol challenge in a mouse model of bacterial pulmonary clearance. These results indicate that these two genes encoding late acyltransferases responsible for lipid A biosynthesis jointly contribute to the biological activities and pathogenicity of M. catarrhalis. The double mutant O35ElpxXL with dramatically reduced toxicity is proposed as a potential vaccine candidate against M. catarrhalis infections for further investigation.
JF  - Journal of medical microbiology
AU  - Gao, Song
AU  - Ren, Dabin
AU  - Peng, Daxin
AU  - Zhang, Wenhong
AU  - Muszyński, Artur
AU  - Carlson, Russell W
AU  - Gu, Xin-Xing
AD  - Vaccine Research Section, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Rockville, MD 20850, USA.
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 807
EP  - 812
VL  - 62
KW  - Antibodies, Bacterial
KW  - 0
KW  - Bacterial Proteins
KW  - Lipid A
KW  - Lipopolysaccharides
KW  - Virulence Factors
KW  - Acyltransferases
KW  - EC 2.3.-
KW  - LpxL protein, bacteria
KW  - Index Medicus
KW  - Animals
KW  - Lipid A -- genetics
KW  - Blood Bactericidal Activity
KW  - Humans
KW  - Lipopolysaccharides -- metabolism
KW  - Lipid A -- chemistry
KW  - Antibodies, Bacterial -- immunology
KW  - Mice
KW  - Lipopolysaccharides -- chemistry
KW  - Mice, Inbred BALB C
KW  - Virulence
KW  - Lipopolysaccharides -- immunology
KW  - Lipid A -- biosynthesis
KW  - Antibodies, Bacterial -- blood
KW  - Mutation
KW  - Female
KW  - Bacterial Proteins -- genetics
KW  - Moraxellaceae Infections -- microbiology
KW  - Acyltransferases -- genetics
KW  - Bacterial Proteins -- metabolism
KW  - Moraxella (Branhamella) catarrhalis -- genetics
KW  - Acyltransferases -- metabolism
KW  - Moraxella (Branhamella) catarrhalis -- enzymology
KW  - Moraxellaceae Infections -- immunology
KW  - Moraxella (Branhamella) catarrhalis -- pathogenicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352281693?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medical+microbiology&rft.atitle=Late+acyltransferase+genes+lpxX+and+lpxL+jointly+contribute+to+the+biological+activities+of+Moraxella+catarrhalis.&rft.au=Gao%2C+Song%3BRen%2C+Dabin%3BPeng%2C+Daxin%3BZhang%2C+Wenhong%3BMuszy%C5%84ski%2C+Artur%3BCarlson%2C+Russell+W%3BGu%2C+Xin-Xing&rft.aulast=Gao&rft.aufirst=Song&rft.date=2013-06-01&rft.volume=62&rft.issue=&rft.spage=807&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+microbiology&rft.issn=1473-5644&rft_id=info:doi/10.1099%2Fjmm.0.056846-0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-15
N1  - Date created - 2013-05-15
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Infect Immun. 2005 Nov;73(11):7569-77 [16239560]
Am J Respir Crit Care Med. 2005 Jul 15;172(2):195-9 [15805178]
Adv Exp Med Biol. 2011;780:125-41 [21842370]
J Exp Med. 2000 Mar 20;191(6):949-60 [10727457]
Microbes Infect. 2000 Apr;2(5):547-59 [10865200]
Infect Immun. 2000 Sep;68(9):4980-5 [10948114]
J Bacteriol. 2002 May;184(9):2379-88 [11948150]
Microb Pathog. 2003 Mar;34(3):121-30 [12631473]
Anal Biochem. 1982 Jan 1;119(1):115-9 [6176137]
Carbohydr Res. 1988 Apr 15;175(2):273-82 [2900066]
J Clin Microbiol. 1990 Feb;28(2):182-7 [2107197]
Eur J Biochem. 1994 Feb 15;220(1):209-16 [8119289]
Carbohydr Res. 1994 May 5;257(2):269-84 [7516823]
J Biol Chem. 1998 Jan 30;273(5):2747-57 [9446581]
Infect Immun. 1998 May;66(5):1891-7 [9573066]
Eur J Biochem. 1999 Oct;265(2):524-9 [10504382]
Infect Immun. 2005 Jul;73(7):4222-30 [15972513]
FEBS J. 2008 Oct;275(20):5201-14 [18795947]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1099/jmm.0.056846-0
ER  - 



TY  - JOUR
T1  - Adolescent transformations of behavioral and neural processes as potential targets for prevention
AN  - 1350888694; 4437107
AB  - Adolescence is a transitional period in development that is marked by a distinct, typical behavioral profile of high rates of exploration, novelty-seeking, and emotional lability. While these behaviors generally assist the adolescent transition to independence, they can also confer vulnerability for excessive risk-taking and psychopathology, particularly in the context of specific environmental or genetic influences. As prevention research depends on the identification of targets of vulnerability, the following review will discuss the interplay among motivational systems including reward-related, avoidance-related, and regulatory processes in typical and atypical adolescent development. Each set of processes will be discussed in relation to their underlying neural correlates and distinct developmental trajectories. Evidence suggests that typical adolescent behavior and the risk for atypical development are mediated by heightened adolescent responsiveness of reward-related and avoidance-related systems under specific conditions, concurrent with poor modulation by immature regulatory processes. Finally, we will propose strategies to exploit heightened reward processing to reinforce inhibitory control, which is an essential component of regulatory processes in prevention interventions. Reprinted by permission of Springer
JF  - Prevention science
AU  - Eldreth, Dana
AU  - Hardin, Michael G
AU  - Pavletic, Nevia
AU  - Ernst, Monique
AD  - RTI International ; National Institute of Mental Health
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 257
EP  - 266
VL  - 14
IS  - 3
SN  - 1389-4986, 1389-4986
KW  - Sociology
KW  - Risk
KW  - Prevention
KW  - Psychopathology
KW  - Development
KW  - Children
KW  - Adolescents
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1350888694?accountid=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=Adolescent+transformations+of+behavioral+and+neural+processes+as+potential+targets+for+prevention&rft.au=Eldreth%2C+Dana%3BHardin%2C+Michael+G%3BPavletic%2C+Nevia%3BErnst%2C+Monique&rft.aulast=Eldreth&rft.aufirst=Dana&rft.date=2013-06-01&rft.volume=14&rft.issue=3&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-012-0322-1
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 3483; 593; 2212; 10072; 10409; 11035
DO  - http://dx.doi.org/10.1007/s11121-012-0322-1
ER  - 



TY  - JOUR
T1  - A call to address complexity in prevention science research
AN  - 1350888022; 4437109
AB  - The problems targeted by preventive interventions are often complex, embedded in multiple levels of social and environmental context, and span the developmental lifespan. Despite this appreciation for multiple levels and systems of influence, prevention science has yet to apply analytic approaches that can satisfactorily address the complexities with which it is faced. In this article, we introduce a systems science approach to problem solving and methods especially equipped to handle complex relationships and their evolution over time. Progress in prevention science may be significantly enhanced by applying approaches that can examine a wide array of complex systems interactions among biology, behavior, and environment that jointly yield unique combinations of developmental risk and protective factors and outcomes. To illustrate the potential utility of a systems science approach, we present examples of current prevention research challenges, and propose how to complement traditional methods and augment research objectives by applying systems science methodologies. Reprinted by permission of Springer
JF  - Prevention science
AU  - Lich, Kristen Hassmiller
AU  - Ginexi, Elizabeth M
AU  - Osgood, Nathaniel D
AU  - Mabry, Patricia L
AD  - University of North Carolina, Chapel Hill ; National Institutes of Health ; University of Saskatchewan
Y1  - 2013/06//
PY  - 2013
DA  - Jun 2013
SP  - 279
EP  - 289
VL  - 14
IS  - 3
SN  - 1389-4986, 1389-4986
KW  - Sociology
KW  - Life cycles
KW  - Scientific research
KW  - Prevention
KW  - Problem solving
KW  - Biology
KW  - Methodology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1350888022?accountid=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=A+call+to+address+complexity+in+prevention+science+research&rft.au=Lich%2C+Kristen+Hassmiller%3BGinexi%2C+Elizabeth+M%3BOsgood%2C+Nathaniel+D%3BMabry%2C+Patricia+L&rft.aulast=Lich&rft.aufirst=Kristen&rft.date=2013-06-01&rft.volume=14&rft.issue=3&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-012-0285-2
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 10072; 10220; 7994; 11347 10902; 7396 3245 971; 1615 8573 11325
DO  - http://dx.doi.org/10.1007/s11121-012-0285-2
ER  - 



TY  - JOUR
T1  - Exemestane: one part of the chemopreventive spectrum for ER-positive breast cancer.
AN  - 1349093326; 23535509
AB  - Development of drugs to prevent breast cancer has focused largely on anti-estrogenic agents, leading to approval by the US FDA of two such agents for this purpose: tamoxifen and raloxifene. However, the uptake of these drugs by high-risk women and their primary care physicians has been limited, due in large part to a perceived unfavorable risk:benefit balance. The current focus is on aromatase inhibitors, which appear to have more acceptable side effects in addition to being more efficacious in reducing breast cancer risk in high-risk women. The placebo-controlled phase III MAP.3 trial tested the AI exemestane in high-risk women and documented a 65% relative reduction in total and a 73% reduction in ER-positive breast cancers in the intervention compared to the placebo group. Toxicities centered around musculoskeletal side effects, but in the relatively short 35-month median follow-up period, these did not impair quality-of-life. A bone study nested within MAP.3 demonstrated significant decreases in bone mineral density (BMD) and in structural parameters of bone quality. The strengths and weaknesses of preventive exemestane as evaluated in the MAP.3 trial are discussed as are relevant areas for future consideration: influence of obesity, alternative dosing, and biomarker use in phase III prevention trials of aromatase inhibitors.
          Copyright © 2013. Published by Elsevier Ltd.
JF  - Breast (Edinburgh, Scotland)
AU  - Dunn, Barbara K
AU  - Cazzaniga, Massimiliano
AU  - DeCensi, Andrea
AD  - Division of Cancer Prevention, Chemoprevention Agent Development Research Group,National Institutes of Health, National Cancer Institute, Bethesda, MD 20892, USA.
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 225
EP  - 237
VL  - 22
IS  - 3
KW  - Androstadienes
KW  - 0
KW  - Anticarcinogenic Agents
KW  - Aromatase Inhibitors
KW  - Receptors, Estrogen
KW  - exemestane
KW  - NY22HMQ4BX
KW  - Index Medicus
KW  - Humans
KW  - Receptors, Estrogen -- analysis
KW  - Androstadienes -- adverse effects
KW  - Anticarcinogenic Agents -- therapeutic use
KW  - Androstadienes -- therapeutic use
KW  - Breast Neoplasms -- prevention & control
KW  - Breast Neoplasms -- chemistry
KW  - Aromatase Inhibitors -- therapeutic use
KW  - Anticarcinogenic Agents -- adverse effects
KW  - Aromatase Inhibitors -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349093326?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%28Edinburgh%2C+Scotland%29&rft.atitle=Exemestane%3A+one+part+of+the+chemopreventive+spectrum+for+ER-positive+breast+cancer.&rft.au=Dunn%2C+Barbara+K%3BCazzaniga%2C+Massimiliano%3BDeCensi%2C+Andrea&rft.aulast=Dunn&rft.aufirst=Barbara&rft.date=2013-06-01&rft.volume=22&rft.issue=3&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Breast+%28Edinburgh%2C+Scotland%29&rft.issn=1532-3080&rft_id=info:doi/10.1016%2Fj.breast.2013.02.015
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-05
N1  - Date created - 2013-05-06
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.breast.2013.02.015
ER  - 



TY  - JOUR
T1  - Second solid cancers after radiation therapy: a systematic review of the epidemiologic studies of the radiation dose-response relationship.
AN  - 1349092666; 23102695
AB  - Rapid innovations in radiation therapy techniques have resulted in an urgent need for risk projection models for second cancer risks from high-dose radiation exposure, because direct observation of the late effects of newer treatments will require patient follow-up for a decade or more. However, the patterns of cancer risk after fractionated high-dose radiation are much less well understood than those after lower-dose exposures (0.1-5 Gy). In particular, there is uncertainty about the shape of the dose-response curve at high doses and about the magnitude of the second cancer risk per unit dose. We reviewed the available evidence from epidemiologic studies of second solid cancers in organs that received high-dose exposure (>5 Gy) from radiation therapy where dose-response curves were estimated from individual organ-specific doses. We included 28 eligible studies with 3434 second cancer patients across 11 second solid cancers. Overall, there was little evidence that the dose-response curve was nonlinear in the direction of a downturn in risk, even at organ doses of ≥60 Gy. Thyroid cancer was the only exception, with evidence of a downturn after 20 Gy. Generally the excess relative risk per Gray, taking account of age and sex, was 5 to 10 times lower than the risk from acute exposures of <2 Gy among the Japanese atomic bomb survivors. However, the magnitude of the reduction in risk varied according to the second cancer. The results of our review provide insights into radiation carcinogenesis from fractionated high-dose exposures and are generally consistent with current theoretical models. The results can be used to refine the development of second solid cancer risk projection models for novel radiation therapy techniques.
          Published by Elsevier Inc.
JF  - International journal of radiation oncology, biology, physics
AU  - Berrington de Gonzalez, Amy
AU  - Gilbert, Ethel
AU  - Curtis, Rochelle
AU  - Inskip, Peter
AU  - Kleinerman, Ruth
AU  - Morton, Lindsay
AU  - Rajaraman, Preetha
AU  - Little, Mark P
AD  - Radiation Epidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. berringtona@mail.nih.gov
Y1  - 2013/06/01/
PY  - 2013
DA  - 2013 Jun 01
SP  - 224
EP  - 233
VL  - 86
IS  - 2
KW  - Radioactive Fallout
KW  - 0
KW  - Index Medicus
KW  - Lung Neoplasms -- etiology
KW  - Dose Fractionation
KW  - Humans
KW  - Case-Control Studies
KW  - Breast Neoplasms -- etiology
KW  - Thyroid Neoplasms -- etiology
KW  - Dose-Response Relationship, Radiation
KW  - Survivors
KW  - Sarcoma -- etiology
KW  - Male
KW  - Female
KW  - Risk Assessment
KW  - Radioactive Fallout -- adverse effects
KW  - Brain Neoplasms -- etiology
KW  - Organs at Risk -- radiation effects
KW  - Neoplasms, Radiation-Induced -- etiology
KW  - Neoplasms, Second Primary -- etiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349092666?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Second+solid+cancers+after+radiation+therapy%3A+a+systematic+review+of+the+epidemiologic+studies+of+the+radiation+dose-response+relationship.&rft.au=Berrington+de+Gonzalez%2C+Amy%3BGilbert%2C+Ethel%3BCurtis%2C+Rochelle%3BInskip%2C+Peter%3BKleinerman%2C+Ruth%3BMorton%2C+Lindsay%3BRajaraman%2C+Preetha%3BLittle%2C+Mark+P&rft.aulast=Berrington+de+Gonzalez&rft.aufirst=Amy&rft.date=2013-06-01&rft.volume=86&rft.issue=2&rft.spage=224&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=1879-355X&rft_id=info:doi/10.1016%2Fj.ijrobp.2012.09.001
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-26
N1  - Date created - 2013-05-06
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Int J Radiat Oncol Biol Phys. 2009 Jun 1;74(2):616-22 [19427561]
Radiother Oncol. 2009 Apr;91(1):132-7 [19147246]
Radiat Environ Biophys. 2009 Aug;48(3):275-86 [19499238]
J Clin Oncol. 2009 Aug 20;27(24):3901-7 [19620485]
Int J Radiat Oncol Biol Phys. 2009 Dec 1;75(5):1420-9 [19931732]
Phys Med Biol. 2010 Dec 7;55(23):7055-65 [21076199]
Radiat Res. 2010 Dec;174(6):741-52 [21128798]
J Clin Oncol. 2010 Dec 20;28(36):5287-93 [21079138]
Radiat Prot Dosimetry. 2011 Jul;146(1-3):263-7 [21561937]
Theor Biol Med Model. 2011;8:27 [21791103]
J Radiol Prot. 2012 Sep;32(3):205-22 [22810503]
Ann Oncol. 2012 Dec;23(12):3081-91 [22745217]
Arch Intern Med. 1999 Dec 13-27;159(22):2713-9 [10597762]
Int J Radiat Biol. 2000 May;76(5):699-710 [10866293]
Radiat Environ Biophys. 2000 Dec;39(4):241-52 [11200968]
Int J Radiat Biol. 2001 Apr;77(4):431-64 [11304437]
Radiat Res. 2002 Aug;158(2):220-35 [12105993]
Int J Radiat Oncol Biol Phys. 1996 Jan 1;34(1):251-66 [12118559]
J Natl Cancer Inst. 2002 Oct 16;94(20):1555-63 [12381708]
Radiat Res. 2003 Feb;159(2):161-73 [12537521]
Int J Radiat Oncol Biol Phys. 2003 May 1;56(1):83-8 [12694826]
JAMA. 2003 Jul 23;290(4):465-75 [12876089]
Int J Cancer. 2004 May 20;110(1):87-93 [15054872]
N Engl J Med. 1987 Sep 3;317(10):588-93 [3475572]
J Natl Cancer Inst. 1987 Dec;79(6):1295-311 [3480381]
Radiat Res. 1988 Oct;116(1):3-55 [3186929]
Radiat Res. 1990 Sep;123(3):275-84 [2217725]
Cancer Res. 1991 Jun 1;51(11):2885-8 [1851664]
J Natl Cancer Inst. 1994 Jul 6;86(13):983-8 [8007020]
Radiat Res. 1995 Mar;141(3):259-77 [7871153]
J Natl Cancer Inst. 1996 Mar 6;88(5):270-8 [8614005]
Int J Radiat Biol. 1996 Jul;70(1):83-94 [8691040]
JAMA. 1997 Oct 15;278(15):1262-7 [9333268]
Int J Cancer. 1998 Jul 29;77(3):370-7 [9663598]
Int J Cancer. 1998 Oct 29;78(3):269-75 [9766556]
Radiat Res. 1999 Sep;152(3):280-92 [10453089]
J Clin Oncol. 2005 Jan 1;23(1):197-204 [15625374]
Breast Cancer Res Treat. 2005 Feb;89(3):277-88 [15754127]
Radiat Res. 2006 Jul;166(1 Pt 2):141-57 [16808603]
Radiat Res. 2006 Jul;166(1 Pt 2):303-12 [16808615]
J Natl Cancer Inst. 2006 Nov 1;98(21):1528-37 [17077355]
J Natl Cancer Inst. 2006 Dec 20;98(24):1794-806 [17179481]
Radiat Res. 2007 Jan;167(1):12-42 [17214511]
J Theor Biol. 2007 Mar 7;245(1):83-97 [17092522]
Radiat Res. 2007 Jul;168(1):1-64 [17722996]
Radiat Res. 2008 Jun;169(6):660-76 [18494541]
Med Phys. 2009 Apr;36(4):1138-43 [19472619]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.ijrobp.2012.09.001
ER  - 



TY  - JOUR
T1  - Nicotinamide forestalls pathology and cognitive decline in Alzheimer mice: evidence for improved neuronal bioenergetics and autophagy procession.
AN  - 1317405118; 23273573
AB  - Impaired brain energy metabolism and oxidative stress are implicated in cognitive decline and the pathologic accumulations of amyloid β-peptide (Aβ) and hyperphosphorylated tau in Alzheimer's disease (AD). To determine whether improving brain energy metabolism will forestall disease progress in AD, the impact of the β-nicotinamide adenine dinucleotide precursor nicotinamide on brain cell mitochondrial function and macroautophagy, bioenergetics-related signaling, and cognitive performance were studied in cultured neurons and in a mouse model of AD. Oxidative stress resulted in decreased mitochondrial mass, mitochondrial degeneration, and autophagosome accumulation in neurons. Nicotinamide preserved mitochondrial integrity and autophagy function, and reduced neuronal vulnerability to oxidative/metabolic insults and Aβ toxicity. β-Nicotinamide adenine dinucleotide biosynthesis, autophagy, and phosphatidylinositol-3-kinase signaling were required for the neuroprotective action of nicotinamide. Treatment of 3xTgAD mice with nicotinamide for 8 months resulted in improved cognitive performance, and reduced Aβ and hyperphosphorylated tau pathologies in hippocampus and cerebral cortex. Nicotinamide treatment preserved mitochondrial integrity, and improved autophagy-lysosome procession by enhancing lysosome/autolysosome acidification to reduce autophagosome accumulation. Treatment of 3xTgAD mice with nicotinamide resulted in elevated levels of activated neuroplasticity-related kinases (protein kinase B [Akt] and extracellular signal-regulated kinases) and the transcription factor cyclic adenosine monophosphate (AMP) response element-binding protein in the hippocampus and cerebral cortex. Thus, nicotinamide suppresses AD pathology and cognitive decline in a mouse model of AD by a mechanism involving improved brain bioenergetics with preserved functionality of mitochondria and the autophagy system. Published by Elsevier Inc.
JF  - Neurobiology of aging
AU  - Liu, Dong
AU  - Pitta, Michael
AU  - Jiang, Haiyang
AU  - Lee, Jong-Hwan
AU  - Zhang, Guofeng
AU  - Chen, Xinzhi
AU  - Kawamoto, Elisa M
AU  - Mattson, Mark P
AD  - Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA.
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 1564
EP  - 1580
VL  - 34
IS  - 6
KW  - Vitamin B Complex
KW  - 12001-76-2
KW  - Niacinamide
KW  - 25X51I8RD4
KW  - Index Medicus
KW  - Vitamin B Complex -- therapeutic use
KW  - Animals
KW  - Neurons -- metabolism
KW  - Neurons -- drug effects
KW  - Mice
KW  - Mice, Transgenic
KW  - Neurons -- pathology
KW  - Rats
KW  - Oxidative Stress -- physiology
KW  - Vitamin B Complex -- pharmacology
KW  - Cells, Cultured
KW  - Mice, Inbred C57BL
KW  - Oxidative Stress -- drug effects
KW  - Autophagy -- drug effects
KW  - Niacinamide -- pharmacology
KW  - Cognition Disorders -- metabolism
KW  - Niacinamide -- therapeutic use
KW  - Energy Metabolism -- physiology
KW  - Energy Metabolism -- drug effects
KW  - Cognition Disorders -- drug therapy
KW  - Alzheimer Disease -- drug therapy
KW  - Disease Models, Animal
KW  - Cognition Disorders -- pathology
KW  - Alzheimer Disease -- metabolism
KW  - Autophagy -- physiology
KW  - Alzheimer Disease -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1317405118?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nicotinamide+forestalls+pathology+and+cognitive+decline+in+Alzheimer+mice%3A+evidence+for+improved+neuronal+bioenergetics+and+autophagy+procession.&rft.au=Liu%2C+Dong%3BPitta%2C+Michael%3BJiang%2C+Haiyang%3BLee%2C+Jong-Hwan%3BZhang%2C+Guofeng%3BChen%2C+Xinzhi%3BKawamoto%2C+Elisa+M%3BMattson%2C+Mark+P&rft.aulast=Liu&rft.aufirst=Dong&rft.date=2013-06-01&rft.volume=34&rft.issue=6&rft.spage=1564&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+aging&rft.issn=1558-1497&rft_id=info:doi/10.1016%2Fj.neurobiolaging.2012.11.020
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-11
N1  - Date created - 2013-03-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Neurosci. 2003 Nov 26;23(34):10756-64 [14645467]
Mol Biol Cell. 2004 Mar;15(3):1101-11 [14699058]
Nat Genet. 2004 Jun;36(6):585-95 [15146184]
Nature. 2004 Aug 5;430(7000):631-9 [15295589]
Dev Cell. 2004 Aug;7(2):167-78 [15296714]
Curr Biol. 2004 Sep 21;14(18):1650-6 [15380067]
J Biol Chem. 1971 Apr 25;246(8):2425-9 [5553400]
J Biol Chem. 1991 Sep 15;266(26):17707-12 [1832676]
Neurosci Lett. 1995 Feb 15;186(1):17-20 [7783942]
Methods Cell Biol. 1995;46:187-216 [7541884]
J Neurosci. 1996 Jan;16(1):186-99 [8613784]
Science. 1997 Jan 31;275(5300):661-5 [9005851]
J Neurosci Methods. 1996 Dec 28;70(2):195-200 [9007759]
J Biol Chem. 2004 Dec 3;279(49):50754-63 [15381699]
Curr Drug Targets CNS Neurol Disord. 2005 Feb;4(1):41-50 [15723612]
J Cell Biol. 2005 Oct 10;171(1):87-98 [16203860]
Nature. 2006 Jun 15;441(7095):885-9 [16625204]
Nature. 2006 Jun 15;441(7095):880-4 [16625205]
J Alzheimers Dis. 2006 Jul;9(2):101-10 [16873957]
J Neurosci. 2006 Aug 16;26(33):8484-91 [16914673]
EMBO J. 2006 Aug 23;25(16):3900-11 [16874299]
Genes Dev. 2006 Nov 1;20(21):2913-21 [17079682]
Trends Biochem Sci. 2007 Jan;32(1):12-9 [17161604]
J Biol Chem. 2007 Apr 13;282(15):11590-601 [17308309]
Exp Neurol. 2007 May;205(1):166-76 [17368447]
Cell. 2007 Jul 13;130(1):165-78 [17632063]
J Neurochem. 2007 Oct;103(2):425-38 [17645457]
Trends Cell Biol. 2007 Sep;17(9):422-7 [17804237]
Autophagy. 2008 Feb;4(2):176-84 [18059160]
J Neurotrauma. 2008 Feb;25(2):130-9 [18260796]
J Pharmacol Exp Ther. 2008 Mar;324(3):883-93 [18165311]
J Neurosci. 2008 Nov 5;28(45):11500-10 [18987186]
Aging Cell. 2008 Dec;7(6):920-3 [18691181]
Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19318-23 [19050078]
Ann N Y Acad Sci. 2008 Dec;1147:275-82 [19076449]
Curr Pharm Des. 2009;15(1):20-8 [19149599]
Methods Enzymol. 2009;452:199-213 [19200884]
Neuromolecular Med. 2009;11(1):28-42 [19288225]
Cell Metab. 2011 May 4;13(5):495-504 [21531332]
Eur J Neurosci. 2008 Jul;28(1):137-47 [18662339]
Autophagy. 2009 May;5(4):502-10 [19270530]
Neuromolecular Med. 2009;11(2):97-100 [19554482]
Autophagy. 2009 Nov;5(8):1229-31 [19855187]
Biochim Biophys Acta. 2010 Jan;1802(1):122-34 [19715758]
J Alzheimers Dis. 2010;19(1):341-53 [20061649]
Antioxid Redox Signal. 2010 Apr;12(4):503-35 [19650712]
J Neurosci. 2010 Feb 24;30(8):2967-78 [20181594]
BMC Neurosci. 2010;11:21 [20167092]
Endocr Rev. 2010 Apr;31(2):194-223 [20007326]
Neuropathol Appl Neurobiol. 2010 Apr;36(2):125-32 [20202120]
J Biol Chem. 2010 Jun 11;285(24):18737-48 [20404319]
Neurodegener Dis. 2010;7(4):265-71 [20551691]
Nature. 2010 Jun 17;465(7300):942-6 [20526321]
Nat Neurosci. 2010 Jul;13(7):805-11 [20581817]
Expert Rev Neurother. 2010 Jul;10(7):1209-18 [20586699]
Cell. 2010 Jun 25;141(7):1146-58 [20541250]
Science. 2010 Jul 9;329(5988):229-32 [20522742]
Dev Cell. 2010 Jun 15;18(6):1041-52 [20627085]
J Neurosci. 2010 Jul 14;30(28):9402-10 [20631169]
Trends Endocrinol Metab. 2010 Oct;21(10):589-98 [20638297]
Trends Neurosci. 2010 Dec;33(12):541-9 [20947179]
Neurobiol Dis. 2011 Jan;41(1):43-50 [20736066]
J Alzheimers Dis. 2010;22(2):443-57 [20847430]
J Neurochem. 2011 Jan;116(1):1-9 [21044077]
Brain. 2011 Jan;134(Pt 1):258-77 [21186265]
Lancet Neurol. 2011 Feb;10(2):187-98 [21147038]
Science. 2011 Jan 28;331(6016):456-61 [21205641]
J Cereb Blood Flow Metab. 2011 Feb;31(2):680-92 [20736962]
Biochim Biophys Acta. 2011 Apr;1812(4):507-13 [21241801]
Neurobiol Dis. 2011 Jul;43(1):46-51 [20887789]
J Neurosci. 2011 May 25;31(21):7817-30 [21613495]
Hum Mol Genet. 2011 Jul 1;20(13):2495-509 [21459773]
Free Radic Biol Med. 2011 Sep 1;51(5):1014-26 [21130159]
Cell. 2011 Sep 2;146(5):682-95 [21884931]
EMBO Rep. 2011 Oct;12(10):1069-76 [21836635]
PLoS One. 2011;6(9):e25416 [21980451]
Neurochem Res. 2011 Dec;36(12):2270-7 [21833846]
Hum Mol Genet. 2011 Dec 1;20(23):4515-29 [21873260]
Autophagy. 2012 Jan;8(1):77-87 [22113203]
J Neurosci. 2012 Apr 25;32(17):5821-32 [22539844]
J Biol Chem. 2012 Jun 1;287(23):19304-14 [22493485]
Cell Metab. 2012 Jun 6;15(6):838-47 [22682224]
Biol Psychiatry. 2012 Oct 1;72(7):528-36 [22592058]
J Alzheimers Dis. 2012;32(1):57-76 [22785397]
Neurosignals. 2013;21(1-2):75-88 [22572473]
Science. 2009 Apr 3;324(5923):102-5 [19342591]
J Neurosci. 2000 May 1;20(9):3139-46 [10777777]
EMBO J. 2000 Nov 1;19(21):5720-8 [11060023]
Diabetologia. 2000 Nov;43(11):1337-45 [11126400]
Free Radic Biol Med. 2001 Feb 15;30(4):447-50 [11182300]
J Neurosci. 2001 May 1;21(9):3017-23 [11312286]
J Neuropathol Exp Neurol. 2001 Aug;60(8):759-67 [11487050]
Mol Biol Cell. 2001 Aug;12(8):2245-56 [11514614]
Annu Rev Biochem. 2001;70:81-120 [11395403]
Exp Neurol. 2002 Jul;176(1):163-74 [12093093]
J Alzheimers Dis. 2002 Jun;4(3):225-32 [12226541]
Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13217-21 [12244210]
Neuron. 2003 Jul 31;39(3):409-21 [12895417]
J Neurochem. 2003 Sep;86(5):1101-7 [12911618]
Annu Rev Neurosci. 2003;26:299-330 [12598680]
Cancer Res. 2003 Nov 1;63(21):7436-42 [14612543]
Erratum In:
Neurobiol Aging. 2013 Sep;34(9):e3
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.neurobiolaging.2012.11.020
ER  - 



TY  - JOUR
T1  - Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells.
AN  - 1312851401; 23129342
AB  - Human Cripto-1 (CR-1) plays an important role in regulating embryonic development while also regulating various stages of tumor progression. However, mechanisms that regulate CR-1 expression during embryogenesis and tumorigenesis are still not well defined. In the present study, we investigated the effects of two nuclear receptors, liver receptor homolog (LRH)-1 and germ cell nuclear factor receptor (GCNF) and epigenetic modifications on CR-1 gene expression in NTERA-2 human embryonal carcinoma cells and in breast cancer cells. CR-1 expression in NTERA-2 cells was positively regulated by LRH-1 through direct binding to a DR0 element within the CR-1 promoter, while GCNF strongly suppressed CR-1 expression in these cells. In addition, the CR-1 promoter was unmethylated in NTERA-2 cells, while T47D, ZR75-1, and MCF7 breast cancer cells showed high levels of CR-1 promoter methylation and low CR-1 mRNA and protein expression. Treatment of breast cancer cells with a demethylating agent and histone deacetylase inhibitors reduced methylation of the CR-1 promoter and reactivated CR-1 mRNA and protein expression in these cells, promoting migration and invasion of breast cancer cells. Analysis of a breast cancer tissue array revealed that CR-1 was highly expressed in the majority of human breast tumors, suggesting that CR-1 expression in breast cancer cell lines might not be representative of in vivo expression. Collectively, these findings offer some insight into the transcriptional regulation of CR-1 gene expression and its critical role in the pathogenesis of human cancer.
          Copyright © 2012 Wiley Periodicals, Inc.
JF  - Journal of cellular physiology
AU  - Bianco, Caterina
AU  - Castro, Nadia P
AU  - Baraty, Christina
AU  - Rollman, Kelly
AU  - Held, Natalie
AU  - Rangel, Maria Cristina
AU  - Karasawa, Hideaki
AU  - Gonzales, Monica
AU  - Strizzi, Luigi
AU  - Salomon, David S
AD  - Laboratory of Cancer Prevention, Frederick National Laboratory for Cancer Research, Frederick, MD, USA. biancoc@mail.nih.gov
Y1  - 2013/06//
PY  - 2013
DA  - June 2013
SP  - 1174
EP  - 1188
VL  - 228
IS  - 6
KW  - GPI-Linked Proteins
KW  - 0
KW  - Histone Deacetylase Inhibitors
KW  - Hydroxamic Acids
KW  - Intercellular Signaling Peptides and Proteins
KW  - NR5A2 protein, human
KW  - NR6A1 protein, human
KW  - Neoplasm Proteins
KW  - Nuclear Receptor Subfamily 6, Group A, Member 1
KW  - RNA, Messenger
KW  - Receptors, Cytoplasmic and Nuclear
KW  - TDGF1 protein, human
KW  - trichostatin A
KW  - 3X2S926L3Z
KW  - Tretinoin
KW  - 5688UTC01R
KW  - Valproic Acid
KW  - 614OI1Z5WI
KW  - decitabine
KW  - 776B62CQ27
KW  - Luciferases
KW  - EC 1.13.12.-
KW  - DNA Modification Methylases
KW  - EC 2.1.1.-
KW  - Azacitidine
KW  - M801H13NRU
KW  - Index Medicus
KW  - Tretinoin -- pharmacology
KW  - DNA Modification Methylases -- metabolism
KW  - Azacitidine -- pharmacology
KW  - Azacitidine -- analogs & derivatives
KW  - Humans
KW  - Embryonal Carcinoma Stem Cells -- metabolism
KW  - Transcription, Genetic
KW  - Valproic Acid -- pharmacology
KW  - Gene Expression Regulation, Neoplastic
KW  - Tissue Array Analysis
KW  - Genes, Reporter
KW  - MCF-7 Cells
KW  - Luciferases -- genetics
KW  - RNA Interference
KW  - Hydroxamic Acids -- pharmacology
KW  - Time Factors
KW  - Cell Movement
KW  - Neoplasm Invasiveness
KW  - Histone Deacetylase Inhibitors -- pharmacology
KW  - Dose-Response Relationship, Drug
KW  - DNA Modification Methylases -- antagonists & inhibitors
KW  - Binding Sites
KW  - Luciferases -- biosynthesis
KW  - RNA, Messenger -- metabolism
KW  - Transfection
KW  - Embryonal Carcinoma Stem Cells -- pathology
KW  - Gene Expression Regulation, Developmental
KW  - Female
KW  - Breast Neoplasms -- genetics
KW  - Carcinoma, Ductal, Breast -- pathology
KW  - Carcinoma, Embryonal -- genetics
KW  - Breast Neoplasms -- metabolism
KW  - Receptors, Cytoplasmic and Nuclear -- genetics
KW  - Nuclear Receptor Subfamily 6, Group A, Member 1 -- metabolism
KW  - Nuclear Receptor Subfamily 6, Group A, Member 1 -- genetics
KW  - Intercellular Signaling Peptides and Proteins -- genetics
KW  - Promoter Regions, Genetic
KW  - Carcinoma, Embryonal -- metabolism
KW  - GPI-Linked Proteins -- metabolism
KW  - Breast Neoplasms -- pathology
KW  - Receptors, Cytoplasmic and Nuclear -- metabolism
KW  - Carcinoma, Ductal, Breast -- metabolism
KW  - Neoplasm Proteins -- genetics
KW  - DNA Methylation -- drug effects
KW  - Carcinoma, Embryonal -- pathology
KW  - Neoplasm Proteins -- metabolism
KW  - Carcinoma, Ductal, Breast -- genetics
KW  - Intercellular Signaling Peptides and Proteins -- metabolism
KW  - GPI-Linked Proteins -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312851401?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Regulation+of+human+Cripto-1+expression+by+nuclear+receptors+and+DNA+promoter+methylation+in+human+embryonal+and+breast+cancer+cells.&rft.au=Bianco%2C+Caterina%3BCastro%2C+Nadia+P%3BBaraty%2C+Christina%3BRollman%2C+Kelly%3BHeld%2C+Natalie%3BRangel%2C+Maria+Cristina%3BKarasawa%2C+Hideaki%3BGonzales%2C+Monica%3BStrizzi%2C+Luigi%3BSalomon%2C+David+S&rft.aulast=Bianco&rft.aufirst=Caterina&rft.date=2013-06-01&rft.volume=228&rft.issue=6&rft.spage=1174&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24271
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-18
N1  - Date created - 2013-02-26
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Am J Pathol. 2008 Feb;172(2):345-57 [18202186]
Eur J Surg Oncol. 2007 May;33(4):438-43 [17125961]
Cell Cycle. 2008 Jul 1;7(13):1931-5 [18604175]
Science. 2008 Aug 1;321(5889):699-702 [18276851]
Biochem Biophys Res Commun. 2008 Dec 5;377(1):215-20 [18835250]
Nat Biotechnol. 2008 Nov;26(11):1276-84 [18931654]
Development. 2009 Apr;136(8):1339-49 [19279133]
Stem Cells. 2009 May;27(5):1042-9 [19415770]
Nat Med. 2009 Aug;15(8):907-13 [19648928]
Am J Pathol. 2009 Nov;175(5):2146-58 [19834060]
Future Oncol. 2010 Jul;6(7):1127-42 [20624125]
Am J Pathol. 2010 Aug;177(2):532-40 [20616345]
Nat Genet. 2006 Apr;38(4):431-40 [16518401]
Biochem Biophys Res Commun. 2006 Jun 9;344(3):845-51 [16631596]
Clin Cancer Res. 2006 Sep 1;12(17):5158-64 [16951234]
Cancer Lett. 2006 Nov 28;244(1):24-33 [16427184]
J Biol Chem. 2006 Nov 3;281(44):33497-504 [16954206]
Mol Cell Biol. 2006 Dec;26(24):9471-83 [17030610]
Biochem Biophys Res Commun. 2007 Mar 30;355(1):240-4 [17291450]
Stem Cells. 2007 Apr;25(4):961-73 [17204602]
Stem Cells. 2010 Aug;28(8):1303-14 [20549704]
Endocr Relat Cancer. 2010 Dec;17(4):965-75 [20817789]
Breast Cancer Res Treat. 2011 Jun;127(2):385-96 [20607599]
Stem Cells. 2011 Jul;29(7):1041-51 [21608077]
Cell Stem Cell. 2011 Oct 4;9(4):330-44 [21982233]
Growth Factors. 2012 Feb;30(1):13-21 [22149969]
Am J Pathol. 2012 Jun;180(6):2188-200 [22542493]
Mol Cell. 2001 May;7(5):949-57 [11389842]
Mol Cell Biol. 2002 Apr;22(8):2586-97 [11909953]
J Cell Physiol. 2004 Jan;198(1):31-9 [14584041]
Mol Cell Endocrinol. 2004 Feb 27;215(1-2):39-44 [15026173]
Dev Biol. 1998 Apr 15;196(2):237-47 [9576836]
Nature. 1998 Oct 15;395(6703):702-7 [9790191]
J Natl Cancer Inst. 2005 Jan 19;97(2):132-41 [15657343]
Stem Cells. 2005 Feb;23(2):166-85 [15671141]
Mol Cell Biol. 2005 May;25(9):3492-505 [15831456]
J Neuroendocrinol. 2005 Apr;17(4):197-207 [15842231]
Mol Cell Biol. 2005 Oct;25(19):8507-19 [16166633]
Oncogene. 2005 Dec 8;24(55):8167-75 [16091743]
J Cell Physiol. 2008 Apr;215(1):192-203 [17941089]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/jcp.24271
ER  - 



TY  - JOUR
T1  - Structure of RSV Fusion Glycoprotein Trimer Bound to a Prefusion-Specific Neutralizing Antibody
AN  - 1559682190; 20373881
AB  - Building Better VaccinesVaccines are one of the most effective tools to protect against infectious diseases. Unfortunately, vaccines for diseases with the highest global health burdens, such as HIV, malaria, and tuberculosis, are not yet available. Koff et al. (p. 1064) review the latest advances in vaccine development and why these particular diseases remain such a challenge. Respiratory syncytial virus (RSV) is a serious cause of morbidity and mortality in infants and young children worldwide. Although a prophylactic antibody is available for children at high risk, a vaccine is much needed. As a potential step toward this goal, McLellan et al. (p. 1113, published online 25 April) solved the cocrystal structure of a neutralizing antibody (D25) bound to the prefusion F protein of RSV. Knowledge of the structure of the prefusion protein should help to guide vaccine design and the development of additional therapeutics.
JF  - Science
AU  - McLellan, Jason S
AU  - Chen, Man
AU  - Leung, Sherman
AU  - Graepel, Kevin W
AU  - Du, Xiulian
AU  - Yang, Yongping
AU  - Zhou, Tongqing
AU  - Baxa, Ulrich
AU  - Yasuda, Etsuko
AU  - Beaumont, Tim
AU  - Kumar, Azad
AU  - Modjarrad, Kayvon
AU  - Zheng, Zizheng
AU  - Zhao, Min
AU  - Xia, Ningshao
AU  - Kwong, Peter D
AU  - Graham, Barney S
AD  - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA, mclellanja@niaid.nih.gov
Y1  - 2013/05/31/
PY  - 2013
DA  - 2013 May 31
SP  - 1113
EP  - 1117
PB  - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States
VL  - 340
IS  - 6136
SN  - 0036-8075, 0036-8075
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW  - Mycobacterium
KW  - Respiration
KW  - Disease control
KW  - Public health
KW  - Respiratory syncytial virus
KW  - Antibodies
KW  - Infectious diseases
KW  - Human immunodeficiency virus
KW  - Tuberculosis
KW  - Vaccines
KW  - Mortality causes
KW  - Metabolism
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/1559682190?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science&rft.atitle=Structure+of+RSV+Fusion+Glycoprotein+Trimer+Bound+to+a+Prefusion-Specific+Neutralizing+Antibody&rft.au=McLellan%2C+Jason+S%3BChen%2C+Man%3BLeung%2C+Sherman%3BGraepel%2C+Kevin+W%3BDu%2C+Xiulian%3BYang%2C+Yongping%3BZhou%2C+Tongqing%3BBaxa%2C+Ulrich%3BYasuda%2C+Etsuko%3BBeaumont%2C+Tim%3BKumar%2C+Azad%3BModjarrad%2C+Kayvon%3BZheng%2C+Zizheng%3BZhao%2C+Min%3BXia%2C+Ningshao%3BKwong%2C+Peter+D%3BGraham%2C+Barney+S&rft.aulast=McLellan&rft.aufirst=Jason&rft.date=2013-05-31&rft.volume=340&rft.issue=6136&rft.spage=1113&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1234914
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-10-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Antibodies; Infectious diseases; Respiration; Disease control; Tuberculosis; Vaccines; Metabolism; Mortality causes; Public health; Respiratory syncytial virus; Mycobacterium; Human immunodeficiency virus
DO  - http://dx.doi.org/10.1126/science.1234914
ER  - 



TY  - JOUR
T1  - Downregulation of splicing factor SRSF3 induces p53β, an alternatively spliced isoform of p53 that promotes cellular senescence.
AN  - 1357495869; 22777358
AB  - Most human pre-mRNA transcripts are alternatively spliced, but the significance and fine-tuning of alternative splicing in different biological processes is only starting to be understood. SRSF3 (SRp20) is a member of a highly conserved family of splicing factors that have critical roles in key biological processes, including tumor progression. Here, we show that SRSF3 regulates cellular senescence, a p53-mediated process to suppress tumorigenesis, through TP53 alternative splicing. Downregulation of SRSF3 was observed in normal human fibroblasts undergoing replicative senescence, and was associated with the upregulation of p53β, an alternatively spliced isoform of p53 that promotes p53-mediated senescence. Knockdown of SRSF3 by short interfering RNA (siRNA) in early-passage fibroblasts induced senescence, which was associated with elevated expression of p53β at mRNA and protein levels. Knockdown of p53 partially rescued SRSF3-knockdown-induced senescence, suggesting that SRSF3 acts on p53-mediated cellular senescence. RNA pulldown assays demonstrated that SRSF3 binds to an alternatively spliced exon uniquely included in p53β mRNA through the consensus SRSF3-binding sequences. RNA crosslinking and immunoprecipitation assays (CLIP) also showed that SRSF3 in vivo binds to endogenous p53 pre-mRNA at the region containing the p53β-unique exon. Splicing assays using a transfected TP53 minigene in combination with siRNA knockdown of SRSF3 showed that SRSF3 functions to inhibit the inclusion of the p53β-unique exon in splicing of p53 pre-mRNA. These data suggest that downregulation of SRSF3 represents an endogenous mechanism for cellular senescence that directly regulates the TP53 alternative splicing to generate p53β. This study uncovers the role for general splicing machinery in tumorigenesis, and suggests that SRSF3 is a direct regulator of p53.
JF  - Oncogene
AU  - Tang, Y
AU  - Horikawa, I
AU  - Ajiro, M
AU  - Robles, A I
AU  - Fujita, K
AU  - Mondal, A M
AU  - Stauffer, J K
AU  - Zheng, Z-M
AU  - Harris, C C
AD  - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4258, USA.
Y1  - 2013/05/30/
PY  - 2013
DA  - 2013 May 30
SP  - 2792
EP  - 2798
VL  - 32
IS  - 22
KW  - Protein Isoforms
KW  - 0
KW  - RNA Precursors
KW  - RNA, Messenger
KW  - RNA, Small Interfering
KW  - RNA-Binding Proteins
KW  - SRSF3 protein, human
KW  - Tumor Suppressor Protein p53
KW  - Serine-Arginine Splicing Factors
KW  - 170974-22-8
KW  - Index Medicus
KW  - RNA, Messenger -- metabolism
KW  - Down-Regulation
KW  - Humans
KW  - Up-Regulation
KW  - RNA Interference
KW  - RNA Precursors -- genetics
KW  - Cell Aging -- genetics
KW  - Cell Transformation, Neoplastic
KW  - Cell Line
KW  - Fibroblasts
KW  - RNA-Binding Proteins -- metabolism
KW  - RNA-Binding Proteins -- genetics
KW  - Alternative Splicing -- genetics
KW  - Protein Isoforms -- metabolism
KW  - Tumor Suppressor Protein p53 -- genetics
KW  - Protein Isoforms -- genetics
KW  - Tumor Suppressor Protein p53 -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1357495869?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Downregulation+of+splicing+factor+SRSF3+induces+p53%CE%B2%2C+an+alternatively+spliced+isoform+of+p53+that+promotes+cellular+senescence.&rft.au=Tang%2C+Y%3BHorikawa%2C+I%3BAjiro%2C+M%3BRobles%2C+A+I%3BFujita%2C+K%3BMondal%2C+A+M%3BStauffer%2C+J+K%3BZheng%2C+Z-M%3BHarris%2C+C+C&rft.aulast=Tang&rft.aufirst=Y&rft.date=2013-05-30&rft.volume=32&rft.issue=22&rft.spage=2792&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2012.288
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-29
N1  - Date created - 2013-05-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/onc.2012.288
ER  - 



TY  - JOUR
T1  - CD97 amplifies LPA receptor signaling and promotes thyroid cancer progression in a mouse model.
AN  - 1357495862; 22797060
AB  - CD97, a member of the adhesion family of G-protein-coupled receptors (GPCRs), complexes with and potentiates lysophosphatidic acid (LPA) receptor signaling to the downstream effector RHOA. We show here that CD97 was expressed in a majority of thyroid cancers but not normal thyroid epithelium and that the level of CD97 expression was further elevated with progression to poorly differentiated and undifferentiated carcinoma. Intratumoral progression also showed that CD97 expression correlates with invasiveness and dedifferentiation. To determine the functional role of CD97, we produced a transgenic model of thyroglobulin promoter-driven CD97 expression. Transgenic CD97 in combination with Thrb(PV), an established mouse model of thyroid follicular cell carcinogenesis, significantly increased the occurrence of vascular invasion and lung metastasis. Expression of transgenic CD97 in thyroid epithelium led to elevated ERK phosphorylation and increased numbers of Ki67+ cells in developing tumors. In addition, tumor cell cultures derived from CD97 transgenic as compared with non-transgenic mice demonstrated enhanced, constitutive and LPA-stimulated ERK activation. In human thyroid cancer cell lines, CD97 depletion reduced RHO-GTP and decreased LPA-stimulated invasion but not EGF-stimulated invasion, further suggesting that CD97 influences an LPA-associated mechanism of progression. Consistent with the above, CD97 expression in human thyroid cancers correlated with LPA receptor and markers of aggressiveness including Ki67 and pAKT. This study shows an autonomous effect of CD97 on thyroid cancer progression and supports the investigation of this GPCR as a therapeutic target for these cancers.
JF  - Oncogene
AU  - Ward, Y
AU  - Lake, R
AU  - Martin, P L
AU  - Killian, K
AU  - Salerno, P
AU  - Wang, T
AU  - Meltzer, P
AU  - Merino, M
AU  - Cheng, S-y
AU  - Santoro, M
AU  - Garcia-Rostan, G
AU  - Kelly, K
AD  - Cell and Cancer Biology Branch, Center for Cancer Research, NCI, Bethesda, MD 20892, USA.
Y1  - 2013/05/30/
PY  - 2013
DA  - 2013 May 30
SP  - 2726
EP  - 2738
VL  - 32
IS  - 22
KW  - Cd97 protein, mouse
KW  - 0
KW  - Ki-67 Antigen
KW  - Membrane Glycoproteins
KW  - Receptors, G-Protein-Coupled
KW  - Receptors, Lysophosphatidic Acid
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  - rhoA GTP-Binding Protein
KW  - EC 3.6.5.2
KW  - Index Medicus
KW  - rhoA GTP-Binding Protein -- metabolism
KW  - Neoplasm Invasiveness
KW  - Animals
KW  - rhoA GTP-Binding Protein -- genetics
KW  - Humans
KW  - Lung Neoplasms -- secondary
KW  - Disease Progression
KW  - Cell Differentiation
KW  - Disease Models, Animal
KW  - Cell Line, Tumor
KW  - Mice
KW  - Extracellular Signal-Regulated MAP Kinases -- metabolism
KW  - Mice, Transgenic
KW  - Gene Expression Regulation, Neoplastic
KW  - Phosphorylation
KW  - Signal Transduction
KW  - Thyroid Neoplasms -- metabolism
KW  - Receptors, G-Protein-Coupled -- metabolism
KW  - Receptors, Lysophosphatidic Acid -- metabolism
KW  - Membrane Glycoproteins -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1357495862?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=CD97+amplifies+LPA+receptor+signaling+and+promotes+thyroid+cancer+progression+in+a+mouse+model.&rft.au=Ward%2C+Y%3BLake%2C+R%3BMartin%2C+P+L%3BKillian%2C+K%3BSalerno%2C+P%3BWang%2C+T%3BMeltzer%2C+P%3BMerino%2C+M%3BCheng%2C+S-y%3BSantoro%2C+M%3BGarcia-Rostan%2C+G%3BKelly%2C+K&rft.aulast=Ward&rft.aufirst=Y&rft.date=2013-05-30&rft.volume=32&rft.issue=22&rft.spage=2726&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2012.301
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-29
N1  - Date created - 2013-05-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/onc.2012.301
ER  - 



TY  - JOUR
T1  - The Human Malaria Parasite Pfs47 Gene Mediates Evasion of the Mosquito Immune System
AN  - 1551627948; 20373864
AB  - Malaria Cloak and DaggerMosquitoes have a complex immune system capable of effective antiparasite responses; however, malaria transmission is still highly efficient. Molina-Cruz et al. (p. 984, published online 9 May; see the Perspective by ) show that Plasmodium falciparum has a gene product, Pfs47, that makes the parasite's ookinetes "invisible" to the mosquito immune system. Disruption of this mechanism could potentially be used to block malaria transmission.
JF  - Science
AU  - Molina-Cruz, Alvaro
AU  - Garver, Lindsey S
AU  - Alabaster, Amy
AU  - Bangiolo, Lois
AU  - Haile, Ashley
AU  - Winikor, Jared
AU  - Ortega, Corrie
AU  - van Schaijk, Ben CL
AU  - Sauerwein, Robert W
AU  - Taylor-Salmon, Emma
AU  - Barillas-Mury, Carolina
AD  - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20892, USA, cbarillas@niaid.nih.gov
Y1  - 2013/05/24/
PY  - 2013
DA  - 2013 May 24
SP  - 984
EP  - 987
PB  - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States
VL  - 340
IS  - 6135
SN  - 0036-8075, 0036-8075
KW  - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Parasites
KW  - Human diseases
KW  - Zygotes
KW  - Immune system
KW  - Culicidae
KW  - Malaria
KW  - Gene products
KW  - Plasmodium falciparum
KW  - Public health
KW  - Genes
KW  - Aquatic insects
KW  - Internet
KW  - G 07720:Immunogenetics
KW  - K 03350:Immunology
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/1551627948?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science&rft.atitle=The+Human+Malaria+Parasite+Pfs47+Gene+Mediates+Evasion+of+the+Mosquito+Immune+System&rft.au=Molina-Cruz%2C+Alvaro%3BGarver%2C+Lindsey+S%3BAlabaster%2C+Amy%3BBangiolo%2C+Lois%3BHaile%2C+Ashley%3BWinikor%2C+Jared%3BOrtega%2C+Corrie%3Bvan+Schaijk%2C+Ben+CL%3BSauerwein%2C+Robert+W%3BTaylor-Salmon%2C+Emma%3BBarillas-Mury%2C+Carolina&rft.aulast=Molina-Cruz&rft.aufirst=Alvaro&rft.date=2013-05-24&rft.volume=340&rft.issue=6135&rft.spage=984&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1235264
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Genes; Gene products; Malaria; Aquatic insects; Public health; Zygotes; Immune system; Internet; Culicidae; Plasmodium falciparum
DO  - http://dx.doi.org/10.1126/science.1235264
ER  - 



TY  - CPAPER
T1  - Remodeling E. coli Nucleoid by RNA Polymerase
T2  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AN  - 1412148928; 6226353
JF  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AU  - Cagliero, C
AU  - Zhou, Y
AU  - Jin, D
Y1  - 2013/05/18/
PY  - 2013
DA  - 2013 May 18
KW  - DNA-directed RNA polymerase
KW  - Nucleoids
KW  - Escherichia coli
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412148928?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.atitle=Remodeling+E.+coli+Nucleoid+by+RNA+Polymerase&rft.au=Cagliero%2C+C%3BZhou%2C+Y%3BJin%2C+D&rft.aulast=Cagliero&rft.aufirst=C&rft.date=2013-05-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.abstractsonline.com/plan/start.aspx?mkey={15C31F4D-CBA9-43A6-B6E1-2F312E144DB4}
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-30
N1  - Last updated - 2013-07-25
ER  - 



TY  - CPAPER
T1  - Surfing the Bacterial Nucleoid on a Protein Wave: A key role for Spatial Confinement in Partition and Transport in Bacteria
T2  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AN  - 1412148712; 6226350
JF  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AU  - Vecchiarelli, A
AU  - Neuman, K
AU  - Mizuuchi, K
Y1  - 2013/05/18/
PY  - 2013
DA  - 2013 May 18
KW  - Surfing
KW  - Waves
KW  - Nucleoids
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412148712?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.atitle=Surfing+the+Bacterial+Nucleoid+on+a+Protein+Wave%3A+A+key+role+for+Spatial+Confinement+in+Partition+and+Transport+in+Bacteria&rft.au=Vecchiarelli%2C+A%3BNeuman%2C+K%3BMizuuchi%2C+K&rft.aulast=Vecchiarelli&rft.aufirst=A&rft.date=2013-05-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.abstractsonline.com/plan/start.aspx?mkey={15C31F4D-CBA9-43A6-B6E1-2F312E144DB4}
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-30
N1  - Last updated - 2013-07-25
ER  - 



TY  - CPAPER
T1  - Surface Proteins of the Lyme Disease Spirochete: How to Dress for Success Session Title: Microbial Transmission: Getting from Here to There
T2  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AN  - 1412146789; 6226221
JF  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AU  - Rosa, Patricia
Y1  - 2013/05/18/
PY  - 2013
DA  - 2013 May 18
KW  - Spirochetes
KW  - Disease transmission
KW  - Lyme disease
KW  - Borrelia
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412146789?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.atitle=Surface+Proteins+of+the+Lyme+Disease+Spirochete%3A+How+to+Dress+for+Success+Session+Title%3A+Microbial+Transmission%3A+Getting+from+Here+to+There&rft.au=Rosa%2C+Patricia&rft.aulast=Rosa&rft.aufirst=Patricia&rft.date=2013-05-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.abstractsonline.com/plan/start.aspx?mkey={15C31F4D-CBA9-43A6-B6E1-2F312E144DB4}
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-30
N1  - Last updated - 2013-07-25
ER  - 



TY  - CPAPER
T1  - Major Changes in Nomenclature and Taxonomy of Medically Important Fungi: "What's in a Name?"
T2  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AN  - 1412146640; 6226238
JF  - 113th General Meeting of the American Society for Microbiology (ASM 2013)
AU  - Kwon-chung, June
Y1  - 2013/05/18/
PY  - 2013
DA  - 2013 May 18
KW  - Nomenclature
KW  - Fungi
KW  - Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412146640?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.atitle=Major+Changes+in+Nomenclature+and+Taxonomy+of+Medically+Important+Fungi%3A+%22What%27s+in+a+Name%3F%22&rft.au=Kwon-chung%2C+June&rft.aulast=Kwon-chung&rft.aufirst=June&rft.date=2013-05-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=113th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.abstractsonline.com/plan/start.aspx?mkey={15C31F4D-CBA9-43A6-B6E1-2F312E144DB4}
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-30
N1  - Last updated - 2013-07-25
ER  - 



TY  - JOUR
T1  - Recruitment of Normal Stem Cells to an Oncogenic Phenotype by Noncontiguous Carcinogen-Transformed Epithelia Depends on the Transforming Carcinogen
AN  - 1427013249; 18418174
AB  - Background: Cancer stem cells (CSCs) drive tumor initiation, progression, and metastasis. The microenvironment is critical to the fate of CSCs. We have found that a normal stem cell (NSC) line from human prostate (WPE-stem) is recruited into CSC-like cells by nearby, but noncontiguous, arsenic-transformed isogenic malignant epithelial cells (MECs). Objective: It is unknown whether this recruitment of NSCs into CSCs by noncontact co-culture is specific to arsenic-transformed MECs. Thus, we used co-culture to examine the effects of neighboring noncontiguous cadmium-transformed MECs (Cd-MECs) and N-methyl-N-nitrosourea-transformed MECs (MNU-MECs) on NSCs. Results: After 2 weeks of noncontact Cd-MEC co-culture, NSCs showed elevated metalloproteinase-9 (MMP-9) and MMP-2 secretion, increased invasiveness, increased colony formation, decreased PTEN expression, and formation of aggressive, highly branched duct-like structures from single cells in Matrigel, all characteristics typical of cancer cells. These oncogenic characteristics did not occur in NSCs co-cultured with MNU-MECs. The NSCs co-cultured with Cd-MECs retained self-renewal capacity, as evidenced by multiple passages (> 3) of structures formed in Matrigel. Cd-MEC-co-cultured NSCs also showed molecular (increased VIM, SNAIL1, and TWIST1 expression; decreased E-CAD expression) and morphologic evidence of epithelial-to-mesenchymal transition typical for conversion to CSCs. Dysregulated expression of SC-renewal genes, including ABCG2, OCT-4, and WNT-3, also occurred in NSCs during oncogenic transformation induced by noncontact co-culture with Cd-MECs. Conclusions: These data indicate that Cd-MECs can recruit nearby NSCs into a CSC-like phenotype, but MNU-MECs do not. Thus, the recruitment of NSCs into CSCs by nearby MECs is dependent on the carcinogen originally used to malignantly transform the MECs.
JF  - Environmental Health Perspectives
AU  - Xu, Yuanyuan
AU  - Tokar, Erik J
AU  - Person, Rachel J
AU  - Orihuela, Ruben G
AU  - Ngalame, Ntube NO
AU  - Waalkes, Michael P
AD  - National Toxicology Program Laboratory, 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  - 2013/05/17/
PY  - 2013
DA  - 2013 May 17
SP  - 944
EP  - 950
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 8
SN  - 0091-6765, 0091-6765
KW  - Toxicology Abstracts; Oncogenes & Growth Factors Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - cadmium
KW  - cancer stem cells
KW  - inflammatory factors
KW  - prostate
KW  - stem cells
KW  - Transformation
KW  - Epithelial cells
KW  - Invasiveness
KW  - Secretion
KW  - PTEN protein
KW  - Carcinogens
KW  - Metastases
KW  - Colonies
KW  - Stem cells
KW  - Oct-4 protein
KW  - Data processing
KW  - Recruitment
KW  - Tumors
KW  - Cancer
KW  - Microenvironments
KW  - Gelatinase A
KW  - Gelatinase B
KW  - Prostate
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - X 24370:Natural Toxins
KW  - B 26670:Tumor Suppressors
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427013249?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Recruitment+of+Normal+Stem+Cells+to+an+Oncogenic+Phenotype+by+Noncontiguous+Carcinogen-Transformed+Epithelia+Depends+on+the+Transforming+Carcinogen&rft.au=Xu%2C+Yuanyuan%3BTokar%2C+Erik+J%3BPerson%2C+Rachel+J%3BOrihuela%2C+Ruben+G%3BNgalame%2C+Ntube+NO%3BWaalkes%2C+Michael+P&rft.aulast=Xu&rft.aufirst=Yuanyuan&rft.date=2013-05-17&rft.volume=121&rft.issue=8&rft.spage=944&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306714
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Transformation; Epithelial cells; Invasiveness; Data processing; Secretion; Carcinogens; PTEN protein; Tumors; Cancer; Metastases; Stem cells; Colonies; Microenvironments; Gelatinase A; Gelatinase B; Oct-4 protein; Prostate; Recruitment
DO  - http://dx.doi.org/10.1289/ehp.1306714
ER  - 



TY  - JOUR
T1  - Modulation of Mycobacterial-Specific Th1 and Th17 Cells in Latent Tuberculosis by Coincident Hookworm Infection
AN  - 1551623168; 20354570
AB  - Hookworm infections and tuberculosis (TB) are coendemic in many parts of the world. It has been suggested that infection with helminth parasites could suppress the predominant Th1 (IFN- gamma -mediated) response needed to control Mycobacterium tuberculosis infection and enhance susceptibility to infection and/or disease. To determine the role of coincident hookworm infection on responses at steady-state and on M. tuberculosis-specific immune responses in latent TB (LTB), we examined the cellular responses in individuals with LTB with or without concomitant hookworm infection. By analyzing the expression of Th1, Th2, and Th17 subsets of CD4+ T cells, we were able to demonstrate that the presence of coincident hookworm infection significantly diminished both spontaneously expressed and M. tuberculosis-specific mono- and dual-functional Th1 and Th17 cells. Hookworm infection, in contrast, was associated with expanded frequencies of mono- and dual-functional Th2 cells at both steady-state and upon Ag stimulation. This differential induction of CD4+ T cell subsets was abrogated upon mitogen stimulation. Additionally, coincident hookworm infection was associated with increased adaptive T regulatory cells but not natural regulatory T cells in LTB. Finally, the CD4+ T cell cytokine expression pattern was also associated with alterations in the systemic levels of Th1 and Th2 cytokines. Thus, coincident hookworm infection exerts a profound inhibitory effect on protective Th1 and Th17 responses in LTB and may predispose toward the development of active tuberculosis in humans.
JF  - Journal of Immunology
AU  - George, Parakkal Jovvian
AU  - Anuradha, Rajamanickam
AU  - Kumaran, Paramasivam Paul
AU  - Chandrasekaran, Vedachalam
AU  - Nutman, Thomas B
AU  - Babu, Subash
AD  - National Institutes of Health-International Center for Excellence in Research, Chennai 600031, India
Y1  - 2013/05/15/
PY  - 2013
DA  - 2013 May 15
SP  - 5161
EP  - 5168
PB  - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States
VL  - 190
IS  - 10
SN  - 0022-1767, 0022-1767
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Immunoregulation
KW  - gamma -Interferon
KW  - Parasites
KW  - CD4 antigen
KW  - Helper cells
KW  - Lymphocytes T
KW  - Cytokines
KW  - Mitogens
KW  - Tuberculosis
KW  - Infection
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/1551623168?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=Modulation+of+Mycobacterial-Specific+Th1+and+Th17+Cells+in+Latent+Tuberculosis+by+Coincident+Hookworm+Infection&rft.au=George%2C+Parakkal+Jovvian%3BAnuradha%2C+Rajamanickam%3BKumaran%2C+Paramasivam+Paul%3BChandrasekaran%2C+Vedachalam%3BNutman%2C+Thomas+B%3BBabu%2C+Subash&rft.aulast=George&rft.aufirst=Parakkal&rft.date=2013-05-15&rft.volume=190&rft.issue=10&rft.spage=5161&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1203311
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-10-02
N1  - SubjectsTermNotLitGenreText - Parasites; gamma -Interferon; Immunoregulation; CD4 antigen; Helper cells; Lymphocytes T; Mitogens; Cytokines; Tuberculosis; Infection; Mycobacterium tuberculosis
DO  - http://dx.doi.org/10.4049/jimmunol.1203311
ER  - 



TY  - JOUR
T1  - Network-guided sparse regression modeling for detection of gene-by-gene interactions
AN  - 1367492041; 18082595
AB  - Motivation: Genetic variants identified by genome-wide association studies to date explain only a small fraction of total heritability. Gene-by-gene interaction is one important potential source of unexplained total heritability. We propose a novel approach to detect such interactions that uses penalized regression and sparse estimation principles, and incorporates outside biological knowledge through a network-based penalty.Results: We tested our new method on simulated and real data. Simulation showed that with reasonable outside biological knowledge, our method performs noticeably better than stage-wise strategies (i.e. selecting main effects first, and interactions second, from those main effects selected) in finding true interactions, especially when the marginal strength of main effects is weak. We applied our method to Framingham Heart Study data on total plasma immunoglobulin E (IgE) concentrations and found a number of interactions among different classes of human leukocyte antigen genes that may interact to influence the risk of developing IgE dysregulation and allergy.Availability: The proposed method is implemented in R and available at http://math.bu.edu/people/kolaczyk/software.html.Contact: chenluu.eduSupplementary information: Supplementary data are available at Bioinformatics online.
JF  - Bioinformatics
AU  - Lu, Chen
AU  - Latourelle, Jeanne
AU  - O'Connor, George T
AU  - Dupuis, Josee
AU  - Kolaczyk, Eric D
AD  - super(1)Department of Biostatistics, Boston University School of Public Health, super(2)Pulmonary Center, Department of Medicine and super(3)Department of Neurology, Boston University School of Medicine, Boston, MA, USA, super(4)The NHLBI's Framingham Heart Study, Framingham, MA, USA, super(5)Program in Bioinformatics and super(6)Department of Mathematics and Statistics, Boston University, Boston, MA, USA
Y1  - 2013/05/15/
PY  - 2013
DA  - 2013 May 15
SP  - 1241
EP  - 1249
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 10
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Histocompatibility antigen HLA
KW  - Heart
KW  - Data processing
KW  - Immunoglobulin E
KW  - Bioinformatics
KW  - Heritability
KW  - Internet
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367492041?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Network-guided+sparse+regression+modeling+for+detection+of+gene-by-gene+interactions&rft.au=Lu%2C+Chen%3BLatourelle%2C+Jeanne%3BO%27Connor%2C+George+T%3BDupuis%2C+Josee%3BKolaczyk%2C+Eric+D&rft.aulast=Lu&rft.aufirst=Chen&rft.date=2013-05-15&rft.volume=29&rft.issue=10&rft.spage=1241&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt139
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2015-03-19
N1  - SubjectsTermNotLitGenreText - Heart; Histocompatibility antigen HLA; Data processing; Immunoglobulin E; Bioinformatics; Internet; Heritability
DO  - http://dx.doi.org/10.1093/bioinformatics/btt139
ER  - 



TY  - JOUR
T1  - Extracting drug indication information from structured product labels using natural language processing
AN  - 1551620333; 20322327
AB  - ObjectiveTo extract drug indications from structured drug labels and represent the information using codes from standard medical terminologies.Materials and methodsWe used MetaMap and other publicly available resources to extract information from the indications section of drug labels. Drugs and indications were encoded by RxNorm and UMLS identifiers respectively. A sample was manually reviewed. We also compared the results with two independent information sources: National Drug File-Reference Terminology and the Semantic Medline project.ResultsA total of 6797 drug labels were processed, resulting in 19473 unique drug-indication pairs. Manual review of 298 most frequently prescribed drugs by seven physicians showed a recall of 0.95 and precision of 0.77. Inter-rater agreement (Fleiss Kappa ) was 0.713. The precision of the subset of results corroborated by Semantic Medline extractions increased to 0.93.DiscussionCorrelation of a patient's medical problems and drugs in an electronic health record has been used to improve data quality and reduce medication errors. Authoritative drug indication information is available from drug labels, but not in a format readily usable by computer applications. Our study shows that it is feasible to use publicly available natural language processing resources to extract drug indications from drug labels. The same method can be applied to other sections of the drug label-for example, adverse effects, contraindications.ConclusionsIt is feasible to use publicly available natural language processing tools to extract indication information from freely available drug labels. Named entity recognition sources (eg, MetaMap) provide reasonable recall. Combination with other data sources provides higher precision.
JF  - Journal of the American Medical Informatics Association
AU  - Fung, Kin Wah
AU  - Jao, Chiang S
AU  - Demner-Fushman, Dina
AD  - Lister Hill National Center for Biomedical Communications, National Library of Medicine, US National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2013/05/09/
PY  - 2013
DA  - 2013 May 09
SP  - 482
EP  - 488
PB  - American Medical Informatics Association, 4915 St. Elmo Ave. Bethesda MD 20814 United States
VL  - 20
IS  - 3
SN  - 1067-5027, 1067-5027
KW  - Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - Informatics
KW  - Information processing
KW  - Reviews
KW  - Language
KW  - Computer applications
KW  - Drugs
KW  - Side effects
KW  - Semantics
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551620333?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Medical+Informatics+Association&rft.atitle=Extracting+drug+indication+information+from+structured+product+labels+using+natural+language+processing&rft.au=Fung%2C+Kin+Wah%3BJao%2C+Chiang+S%3BDemner-Fushman%2C+Dina&rft.aulast=Fung&rft.aufirst=Kin&rft.date=2013-05-09&rft.volume=20&rft.issue=3&rft.spage=482&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Medical+Informatics+Association&rft.issn=10675027&rft_id=info:doi/10.1136%2Famiajnl-2012-001291
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-08-21
N1  - SubjectsTermNotLitGenreText - Data processing; Informatics; Reviews; Information processing; Language; Computer applications; Drugs; Side effects; Semantics
DO  - http://dx.doi.org/10.1136/amiajnl-2012-001291
ER  - 



TY  - JOUR
T1  - MicroRNA-24 regulates XIAP to reduce the apoptosis threshold in cancer cells.
AN  - 1350151186; 22733138
AB  - MicroRNAs have been implicated as important mediators of cancer cell homeostasis, and accumulating data suggest compelling roles for them in the apoptosis pathway. X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor and an important barrier to apoptotic cell death, but the mechanisms that determine the diverse range of XIAP expression seen in cancer remains unclear. In this study, we present evidence that miR-24 directly targets the 3'UTR of the XIAP messenger RNA (mRNA) to exert translational repression. Using a heuristic algorithm of bioinformatics analysis and in vitro screening, we identified miR-24 as a candidate regulator of XIAP expression. Array comparative genomic hybridization and spectral karyotype analysis reveal that genomic copy number loss at the miR-24 locus is concordant with the loss of endogenous miR-24 in cancer cells. Using a luciferase construct of the XIAP 3'UTR, we showed that miR-24 specifically coordinates to the XIAP mRNA. Interference with miR-24's binding of the critical seed region, resulting from site-directed mutagenesis of the 3'UTR, significantly abrogated miR-24's effects on XIAP expression. Moreover, miR-24 overexpression can overcome apoptosis resistance in cancer cells via downregulation of XIAP expression, and the resulting cancer cell death induced by tumor necrosis factor-related apoptosis-inducing ligand is executed by the canonical caspase-mediated apoptosis pathway. In summary, our data suggest a novel mechanism by which miR-24 directly modulates XIAP expression level and consequently the apoptosis threshold in cancer cells.
JF  - Oncogene
AU  - Xie, Y
AU  - Tobin, L A
AU  - Camps, J
AU  - Wangsa, D
AU  - Yang, J
AU  - Rao, M
AU  - Witasp, E
AU  - Awad, K S
AU  - Yoo, N
AU  - Ried, T
AU  - Kwong, K F
AD  - Section of Thoracic Oncology, Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/05/09/
PY  - 2013
DA  - 2013 May 09
SP  - 2442
EP  - 2451
VL  - 32
IS  - 19
KW  - 3' Untranslated Regions
KW  - 0
KW  - MIRN24 microRNA, human
KW  - MicroRNAs
KW  - X-Linked Inhibitor of Apoptosis Protein
KW  - XIAP protein, human
KW  - Index Medicus
KW  - Down-Regulation
KW  - Transfection
KW  - HeLa Cells
KW  - Cell Growth Processes -- physiology
KW  - Humans
KW  - Cell Line, Tumor
KW  - Cell Growth Processes -- genetics
KW  - Apoptosis -- genetics
KW  - Neoplasms -- pathology
KW  - MicroRNAs -- metabolism
KW  - MicroRNAs -- genetics
KW  - Apoptosis -- physiology
KW  - X-Linked Inhibitor of Apoptosis Protein -- metabolism
KW  - X-Linked Inhibitor of Apoptosis Protein -- genetics
KW  - Neoplasms -- genetics
KW  - Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1350151186?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=MicroRNA-24+regulates+XIAP+to+reduce+the+apoptosis+threshold+in+cancer+cells.&rft.au=Xie%2C+Y%3BTobin%2C+L+A%3BCamps%2C+J%3BWangsa%2C+D%3BYang%2C+J%3BRao%2C+M%3BWitasp%2C+E%3BAwad%2C+K+S%3BYoo%2C+N%3BRied%2C+T%3BKwong%2C+K+F&rft.aulast=Xie&rft.aufirst=Y&rft.date=2013-05-09&rft.volume=32&rft.issue=19&rft.spage=2442&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2012.258
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-30
N1  - Date created - 2013-05-09
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Chemother Pharmacol. 2012 Mar;69(3):723-31 [21993663]
Cancer Res. 2011 Oct 1;71(19):6208-19 [21852381]
Hum Gene Ther. 2008 Jan;19(1):17-26 [18211225]
Nature. 2008 Sep 4;455(7209):64-71 [18668037]
Nature. 1999 Oct 21;401(6755):818-22 [10548111]
Nature. 2001 Mar 1;410(6824):112-6 [11242052]
Cell. 2001 Mar 9;104(5):769-80 [11257230]
Cell. 2001 Mar 9;104(5):791-800 [11257232]
Science. 2001 Oct 26;294(5543):853-8 [11679670]
Genes Dev. 2002 Mar 15;16(6):720-8 [11914277]
Mol Cell. 2003 Feb;11(2):519-27 [12620238]
Ann N Y Acad Sci. 2003 Dec;1010:249-58 [15033729]
Cancer Genet Cytogenet. 2004 Jul 1;152(1):15-22 [15193437]
EMBO J. 2004 Oct 13;23(20):4051-60 [15372072]
Nature. 1998 Feb 19;391(6669):806-11 [9486653]
EMBO J. 1998 Mar 16;17(6):1675-87 [9501089]
Cancer Res. 1999 Jan 1;59(1):141-50 [9892199]
Genes Dev. 1999 Feb 1;13(3):239-52 [9990849]
PLoS Biol. 2004 Nov;2(11):e363 [15502875]
J Neurosci. 2004 Dec 1;24(48):10963-73 [15574746]
Science. 2005 Sep 2;309(5740):1573-6 [16081698]
Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262]
Proc Natl Acad Sci U S A. 2005 Nov 22;102(47):16961-6 [16287976]
Mol Cell. 2006 Feb 17;21(4):533-42 [16483934]
Drug Resist Updat. 2005 Dec;8(6):339-43 [16338161]
Science. 2006 Apr 7;312(5770):75-9 [16484454]
Mol Cell. 2006 May 19;22(4):553-60 [16713585]
Nucleic Acids Res. 2006 Jul 1;34(Web Server issue):W451-4 [16845047]
EMBO Rep. 2006 Oct;7(10):988-94 [17016456]
Cancer Treat Rev. 2007 Apr;33(2):203-12 [17210228]
Nat Protoc. 2006;1(6):3129-42 [17406576]
Mol Cell. 2007 Jul 6;27(1):91-105 [17612493]
Proc Natl Acad Sci U S A. 2007 Aug 14;104(33):13513-8 [17686970]
Cancer Genet Cytogenet. 2008 Jan 1;180(1):6-13 [18068526]
Blood. 2008 Jan 15;111(2):588-95 [17906079]
PLoS One. 2008;3(3):e1864 [18365017]
Nature. 2008 Sep 4;455(7209):58-63 [18668040]
Cell Cycle. 2008 Aug 15;7(16):2485-92 [18719380]
Cancer Immunol Immunother. 2009 Apr;58(4):589-601 [18791715]
Genes Dev. 2009 May 1;23(9):1046-51 [19372388]
Nat Struct Mol Biol. 2009 May;16(5):492-8 [19377482]
Cancer Res. 2009 May 15;69(10):4443-53 [19435910]
PLoS One. 2009;4(6):e5848 [19513126]
Nucleic Acids Res. 2009 Jul;37(Web Server issue):W273-6 [19406924]
Mol Cell. 2009 Sep 11;35(5):610-25 [19748357]
Brain Res Bull. 2009 Oct 28;80(4-5):268-73 [19683563]
PLoS One. 2010;5(2):e9429 [20195546]
Nucleic Acids Res. 2010 Aug;38(14):4665-74 [20385593]
Biochem Biophys Res Commun. 2010 Sep 17;400(2):236-40 [20727858]
FEBS Lett. 2010 Sep 24;584(18):4048-52 [20728447]
Int J Cancer. 2010 Dec 1;127(11):2520-9 [20162574]
Blood. 2010 Dec 2;116(23):4885-93 [20807887]
Cancer Res. 2011 Mar 15;71(6):2381-91 [21385904]
Tumori. 2011 Mar-Apr;97(2):248-51 [21617726]
Blood. 2011 Jun 2;117(22):5953-62 [21478427]
Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11662-7 [21709246]
Clin Cancer Res. 2011 Aug 15;17(16):5287-98 [21159887]
Cancer Immunol Immunother. 2011 Sep;60(9):1299-307 [21626030]
Arthritis Rheum. 2012 Jun;64(6):1771-9 [22161761]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/onc.2012.258
ER  - 



TY  - JOUR
T1  - Measures of Thyroid Function among Belarusian Children and Adolescents Exposed to Iodine-131 from the Accident at the Chernobyl Nuclear Plant
AN  - 1660071530; 18970799
AB  - Background: Thyroid dysfunction after exposure to low or moderate doses of radioactive iodine-131 (131I) at a young age is a public health concern. However, quantitative data are sparse concerning 131I-related risk of these common diseases. Objective: Our goal was to assess the prevalence of thyroid dysfunction in association with 131I exposure during childhood ( less than or equal to 18 years) due to fallout from the Chernobyl accident. Methods: We conducted a cross-sectional analysis of hypothyroidism, hyperthyroidism, autoimmune thyroiditis (AIT), serum concentrations of thyroid-stimulating hormone (TSH), and autoantibodies to thyroperoxidase (ATPO) in relation to measurement-based 131I dose estimates in a Belarusian cohort of 10,827 individuals screened for various thyroid diseases. Results: Mean age at exposure ( plus or minus SD) was 8.2 plus or minus 5.0 years. Mean (median) estimated 131I thyroid dose was 0.54 (0.23) Gy (range, 0.001-26.6 Gy). We found significant positive associations of 131I dose with hypothyroidism (mainly subclinical and antibody-negative) and serum TSH concentration. The excess odds ratio per 1 Gy for hypothyroidism was 0.34 (95% CI: 0.15, 0.62) and varied significantly by age at exposure and at examination, presence of goiter, and urban/rural residency. We found no evidence of positive associations with antibody-positive hypothyroidism, hyperthyroidism, AIT, or elevated ATPO. Conclusions: The association between 131I dose and hypothyroidism in the Belarusian cohort is consistent with that previously reported for a Ukrainian cohort and strengthens evidence of the effect of environmental 131I exposure during childhood on hypothyroidism, but not other thyroid outcomes.
JF  - Environmental Health Perspectives
AU  - Ostroumova, Evgenia
AU  - Rozhko, Alexander
AU  - Hatch, Maureen
AU  - Furukawa, Kyoji
AU  - Polyanskaya, Olga
AU  - McConnell, Robert J
AU  - Nadyrov, Eldar
AU  - Petrenko, Sergey
AU  - Romanov, George
AU  - Yauseyenka, Vasilina
AU  - Drozdovitch, Vladimir
AU  - Minenko, Viktor
AU  - Prokopovich, Alexander
AU  - Savasteeva, Irina
AU  - Zablotska, Lydia B
AU  - Mabuchi, Kiyohiko
AU  - Brenner, Alina V
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
Y1  - 2013/05/07/
PY  - 2013
DA  - 2013 May 07
SP  - 865
EP  - 871
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 7
SN  - 0091-6765, 0091-6765
KW  - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - antithyroid antibodies
KW  - autoimmune thyroiditis
KW  - Chernobyl
KW  - Chornobyl
KW  - dose response
KW  - hyperthyroidism
KW  - hypothyroidism
KW  - radioiodine
KW  - thyroid gland
KW  - Belarus
KW  - Risk
KW  - Age
KW  - Accidents
KW  - Iodine-131
KW  - Diseases
KW  - Background radiation
KW  - Serums
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660071530?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Measures+of+Thyroid+Function+among+Belarusian+Children+and+Adolescents+Exposed+to+Iodine-131+from+the+Accident+at+the+Chernobyl+Nuclear+Plant&rft.au=Ostroumova%2C+Evgenia%3BRozhko%2C+Alexander%3BHatch%2C+Maureen%3BFurukawa%2C+Kyoji%3BPolyanskaya%2C+Olga%3BMcConnell%2C+Robert+J%3BNadyrov%2C+Eldar%3BPetrenko%2C+Sergey%3BRomanov%2C+George%3BYauseyenka%2C+Vasilina%3BDrozdovitch%2C+Vladimir%3BMinenko%2C+Viktor%3BProkopovich%2C+Alexander%3BSavasteeva%2C+Irina%3BZablotska%2C+Lydia+B%3BMabuchi%2C+Kiyohiko%3BBrenner%2C+Alina+V&rft.aulast=Ostroumova&rft.aufirst=Evgenia&rft.date=2013-05-07&rft.volume=121&rft.issue=7&rft.spage=865&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205783
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-05-04
DO  - http://dx.doi.org/10.1289/ehp.1205783
ER  - 



TY  - JOUR
T1  - Evaluation of the Association between Persistent Organic Pollutants (POPs) and Diabetes in Epidemiological Studies: A National Toxicology Program Workshop Review
AN  - 1492649605; 18970798
AB  - Background: Diabetes is a major threat to public health in the United States and worldwide. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. Objective: We assessed the epidemiologic literature for evidence of associations between persistent organic pollutants (POPs) and type 2 diabetes. Methods: Using a PubMed search and reference lists from relevant studies or review articles, we identified 72 epidemiological studies that investigated associations of persistent organic pollutants (POPs) with diabetes. We evaluated these studies for consistency, strengths and weaknesses of study design (including power and statistical methods), clinical diagnosis, exposure assessment, study population characteristics, and identification of data gaps and areas for future research. Conclusions: Heterogeneity of the studies precluded conducting a meta-analysis, but the overall evidence is sufficient for a positive association of some organochlorine POPs with type 2 diabetes. Collectively, these data are not sufficient to establish causality. Initial data mining revealed that the strongest positive correlation of diabetes with POPs occurred with organochlorine compounds, such as trans-nonachlor, dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCBs), and dioxins and dioxin-like chemicals. There is less indication of an association between other nonorganochlorine POPs, such as perfluoroalkyl acids and brominated compounds, and type 2 diabetes. Experimental data are needed to confirm the causality of these POPs, which will shed new light on the pathogenesis of diabetes. This new information should be considered by governmental bodies involved in the regulation of environmental contaminants.
JF  - Environmental Health Perspectives
AU  - Taylor, Kyla W
AU  - Novak, Raymond F
AU  - Anderson, Henry A
AU  - Birnbaum, Linda S
AU  - Blystone, Chad
AU  - DeVito, Michael
AU  - Jacobs, David
AU  - Kohrle, Josef
AU  - Lee, Duk-Hee
AU  - Rylander, Lars
AU  - Rignell-Hydbom, Anna
AU  - Tornero-Velez, Rogelio
AU  - Turyk, Mary E
AU  - Boyles, Abee L
AU  - Thayer, Kristina A
AU  - Lind, Lars
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  - 2013/05/07/
PY  - 2013
DA  - 2013 May 07
SP  - 774
EP  - 783
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 7
SN  - 0091-6765, 0091-6765
KW  - Pollution Abstracts; Toxicology Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - chemically induced
KW  - diabetes
KW  - environment
KW  - epidemiology
KW  - glucose
KW  - hormone
KW  - insulin
KW  - metabolic syndrome
KW  - obesity
KW  - persistent organic pollutants
KW  - pollution
KW  - toxicology
KW  - Chemicals
KW  - Statistics
KW  - Organochlorine compounds
KW  - Environmental health
KW  - Dioxins
KW  - Public health
KW  - Insecticides
KW  - Nitrous oxide
KW  - Pollutants
KW  - PCB compounds
KW  - Toxicology
KW  - PCB
KW  - Data processing
KW  - Population characteristics
KW  - Conferences
KW  - DDE
KW  - Population studies
KW  - Diabetes mellitus
KW  - USA
KW  - polychlorinated biphenyls
KW  - Reviews
KW  - Acids
KW  - Persistent organic pollutants
KW  - Contaminants
KW  - Dioxin
KW  - H 11000:Diseases/Injuries/Trauma
KW  - X 24330:Agrochemicals
KW  - P 6000:TOXICOLOGY AND HEALTH
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492649605?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Evaluation+of+the+Association+between+Persistent+Organic+Pollutants+%28POPs%29+and+Diabetes+in+Epidemiological+Studies%3A+A+National+Toxicology+Program+Workshop+Review&rft.au=Taylor%2C+Kyla+W%3BNovak%2C+Raymond+F%3BAnderson%2C+Henry+A%3BBirnbaum%2C+Linda+S%3BBlystone%2C+Chad%3BDeVito%2C+Michael%3BJacobs%2C+David%3BKohrle%2C+Josef%3BLee%2C+Duk-Hee%3BRylander%2C+Lars%3BRignell-Hydbom%2C+Anna%3BTornero-Velez%2C+Rogelio%3BTuryk%2C+Mary+E%3BBoyles%2C+Abee+L%3BThayer%2C+Kristina+A%3BLind%2C+Lars&rft.aulast=Taylor&rft.aufirst=Kyla&rft.date=2013-05-07&rft.volume=121&rft.issue=7&rft.spage=774&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205502
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Data processing; Organochlorine compounds; Statistics; Conferences; DDE; Population studies; Public health; Diabetes mellitus; polychlorinated biphenyls; Pollutants; Acids; Reviews; Contaminants; PCB; Dioxin; Chemicals; Population characteristics; Environmental health; Dioxins; Insecticides; Nitrous oxide; Persistent organic pollutants; PCB compounds; Toxicology; USA
DO  - http://dx.doi.org/10.1289/ehp.1205502
ER  - 



TY  - JOUR
T1  - Identifying residues that cause pH-dependent reduction potentials.
AN  - 1349401178; 23607577
AB  - The pH dependence of the reduction potential E° for a metalloprotein indicates that the protonation state of at least one residue near the redox site changes and may be important for its activity. The responsible residue is usually identified by site-specific mutagenesis, which may be time-consuming. Here, the titration of E° for Chromatium vinosum high-potential iron-sulfur protein is predicted to be in good agreement with experiment using density functional theory and Poisson-Boltzmann calculations if only the sole histidine undergoes changes in protonation. The implementation of this approach into CHARMMing, a user-friendly web-based portal, allows users to identify residues in other proteins causing similar pH dependence.
JF  - Biochemistry
AU  - Perrin, B Scott
AU  - Ichiye, Toshiko
AD  - Laboratory of Computational Biology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/05/07/
PY  - 2013
DA  - 2013 May 07
SP  - 3022
EP  - 3024
VL  - 52
IS  - 18
KW  - Index Medicus
KW  - Oxidation-Reduction
KW  - Models, Molecular
KW  - Chromatium -- chemistry
KW  - Hydrogen-Ion Concentration
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349401178?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Identifying+residues+that+cause+pH-dependent+reduction+potentials.&rft.au=Perrin%2C+B+Scott%3BIchiye%2C+Toshiko&rft.aulast=Perrin&rft.aufirst=B&rft.date=2013-05-07&rft.volume=52&rft.issue=18&rft.spage=3022&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=1520-4995&rft_id=info:doi/10.1021%2Fbi4002858
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-05
N1  - Date created - 2013-05-07
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Proteins. 2010 Oct;78(13):2798-808 [20635418]
J Phys Chem A. 2011 Apr 28;115(16):4042-53 [21428436]
J Comput Chem. 2013 Mar 15;34(7):576-82 [23115132]
Acta Crystallogr D Biol Crystallogr. 1999 Nov;55(Pt 11):1773-84 [10531472]
Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10037-41 [11517324]
J Chem Inf Model. 2009 Sep;49(9):2013-33 [19702243]
J Mol Biol. 1985 Sep 20;185(2):389-404 [2414450]
Biochemistry. 1986 Dec 30;25(26):8368-72 [2435316]
Biochemistry. 1990 Nov 6;29(44):10219-25 [2271649]
Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5804-8 [2062860]
Proteins. 1993 Mar;15(3):252-65 [7681210]
J Chem Inf Model. 2008 Sep;48(9):1920-9 [18698840]
Biochemistry. 1980 Oct 14;19(21):4727-33 [7426625]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1021/bi4002858
ER  - 



TY  - JOUR
T1  - Long-Term Follow-up of Foamy Viral Vector-Mediated Gene Therapy for Canine Leukocyte Adhesion Deficiency
AN  - 1668268268; PQ0001244750
AB  - The development of leukemia following gammaretroviral vector-mediated gene therapy for X-linked severe combined immunodeficiency disease and chronic granulomatous disease (CGD) has emphasized the need for long-term follow-up in animals treated with hematopoietic stem cell gene therapy. In this study, we report the long-term follow-up (4-7 years) of four dogs with canine leukocyte adhesion deficiency (CLAD) treated with foamy viral (FV) vector-mediated gene therapy. All four CLAD dogs previously received nonmyeloablative conditioning with 200 cGy total body irradiation followed by infusion of autologous, CD34 super(+) hematopoietic stem cells transduced by a FV vector expressing canine CD18 from an internal Murine Stem Cell Virus (MSCV) promoter. CD18 super(+) leukocyte levels were >2% following infusion of vector-transduced cells leading to ongoing reversal of the CLAD phenotype for >4 years. There was no clinical development of lymphoid or myeloid leukemia in any of the four dogs and integration site analysis did not reveal insertional oncogenesis. These results showing disease correction/amelioration of disease in CLAD without significant adverse events provide support for the use of a FV vector to treat children with leukocyte adhesion deficiency type 1 (LAD-1) in a human gene therapy clinical trial.
JF  - Molecular Therapy
AU  - Bauer, Thomas R, Jr
AU  - Tuschong, Laura M
AU  - Calvo, Katherine R
AU  - Shive, Heather R
AU  - Burkholder, Tanya H
AU  - Karlsson, Eleanor K
AU  - West, Robert R
AU  - Russell, David W
AU  - Hickstein, Dennis D
AD  - Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA, hicksted@mail.nihi.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 964
EP  - 972
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 5
SN  - 1525-0016, 1525-0016
KW  - Genetics Abstracts; Virology & AIDS Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Autografts
KW  - Gene therapy
KW  - Myeloid leukemia
KW  - Tumorigenesis
KW  - X chromosome
KW  - Leukocytes
KW  - CD34 antigen
KW  - Children
KW  - Clinical trials
KW  - CD18 antigen
KW  - Fv
KW  - Expression vectors
KW  - Integration
KW  - Promoters
KW  - Stem cells
KW  - Radiation
KW  - Severe combined immunodeficiency
KW  - Chronic granulomatous disease
KW  - W 30905:Medical Applications
KW  - F 06950:Immunogenetics, MHC, HLA
KW  - G 07760:Viruses & Phages
KW  - V 22370:Oncology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668268268?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-Term+Follow-up+of+Foamy+Viral+Vector-Mediated+Gene+Therapy+for+Canine+Leukocyte+Adhesion+Deficiency&rft.au=Bauer%2C+Thomas+R%2C+Jr%3BTuschong%2C+Laura+M%3BCalvo%2C+Katherine+R%3BShive%2C+Heather+R%3BBurkholder%2C+Tanya+H%3BKarlsson%2C+Eleanor+K%3BWest%2C+Robert+R%3BRussell%2C+David+W%3BHickstein%2C+Dennis+D&rft.aulast=Bauer&rft.aufirst=Thomas&rft.date=2013-05-01&rft.volume=21&rft.issue=5&rft.spage=964&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2013.34
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Autografts; Gene therapy; Myeloid leukemia; Leukocytes; X chromosome; Tumorigenesis; CD34 antigen; Children; CD18 antigen; Clinical trials; Fv; Expression vectors; Promoters; Integration; Stem cells; Radiation; Severe combined immunodeficiency; Chronic granulomatous disease
DO  - http://dx.doi.org/10.1038/mt.2013.34
ER  - 



TY  - JOUR
T1  - Numerical processing efficiency improved in experienced mental abacus children
AN  - 1663900887; 4654262
AB  - Experienced mental abacus (MA) users are able to perform mental arithmetic calculations with unusual speed and accuracy. However, it remains unclear whether their extraordinary gains in mental arithmetic ability are accompanied by an improvement in numerical processing efficiency. To address this question, the present study, using a numerical Stroop paradigm, examined the numerical processing efficiency of experienced MA children, MA beginners and their respective peers. The results showed that experienced MA children were less influenced than their peers by physical size information when intentionally processing numerical magnitude information, but they were more influenced than their peers by numerical magnitude information when intentionally processing physical size information. By contrast, MA beginners and peers showed no differences in the reciprocal influences between the two conflicting dimensions. These findings indicate that substantial gains in numerical processing efficiency could be achieved through long-term intensive MA training. Implications for numerical magnitude representations and for training students with mathematical learning disabilities are discussed. All rights reserved, Elsevier
JF  - Cognition
AU  - Hu, Yuzheng
AU  - Du, Fenglei
AU  - Chen, Feiyan
AU  - Wang, Yunqi
AU  - Geng, Fengji
AD  - Zhejiang University ; National Institutes of Health, Baltimore
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 149
EP  - 158
VL  - 127
IS  - 2
SN  - 0010-0277, 0010-0277
KW  - Sociology
KW  - Arithmetic
KW  - Learning
KW  - Training
KW  - Intellectual ability
KW  - Information processing
KW  - Numbers
KW  - Students
KW  - Children
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1663900887?accountid=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=Cognition&rft.atitle=Numerical+processing+efficiency+improved+in+experienced+mental+abacus+children&rft.au=Hu%2C+Yuzheng%3BDu%2C+Fenglei%3BChen%2C+Feiyan%3BWang%2C+Yunqi%3BGeng%2C+Fengji&rft.aulast=Hu&rft.aufirst=Yuzheng&rft.date=2013-05-01&rft.volume=127&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Cognition&rft.issn=00100277&rft_id=info:doi/10.1016%2Fj.cognition.2012.12.004
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2015-03-16
N1  - Last updated - 2015-03-17
N1  - SubjectsTermNotLitGenreText - 8790 8795 2588 2572 11659; 6527; 2212; 1252 7824; 12894; 7278 12929 7073; 12334 4049; 6602 491
DO  - http://dx.doi.org/10.1016/j.cognition.2012.12.004
ER  - 



TY  - JOUR
T1  - New Sylvatic Hosts of Trypanosoma cruzi and Their Reservoir Competence in the Humid Chaco of Argentina: A Longitudinal Study
AN  - 1647005553; 21172075
AB  - A four-year longitudinal study of the structure of sylvatic transmission cycles of Trypanosoma cruzi, reservoir host competence and parasite discrete typing units was conducted in a disturbed rural area of the humid Chaco in Argentina. Among 190 mammals examined by xenodiagnosis and polymerase chain reaction amplification, the composite prevalence of infection was substantially higher in Dasypus novemcinctus armadillos (57.7%) and Didelphis albiventris opossums (38.1%) than in Euphractus sexcinctus (20.0%), Tolypeutes matacus (12.5%), and Chaetophractus vellerosus (6.3%) armadillos. Trypanosoma cruzi was detected for the first time in Thylamys pusilla small opossums and in two unidentified small rodents. Infection was spatially aggregated only in armadillos. All Didelphis were infected with T. cruzi I and all armadillo species were infected with T. cruzi III, implying two distinct sylvatic cycles with no inputs from the domestic cycle. Dasypus armadillos and Didelphis opossums were much more infectious to vectors than other armadillos, small opossums, or rodents.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Orozco, M Marcela
AU  - Enriquez, Gustavo F
AU  - Alvarado-Otegui, Julia A
AU  - Cardinal, M Victoria
AU  - Schijman, Alejandro G
AU  - Kitron, Uriel
AU  - Gurtler, Ricardo E
AD  - Laboratory of Eco-Epidemiology, Department of Ecology, Genetics and Evolution, Universidad de Buenos Aires, Buenos Aires, Argentina; Laboratorio de Biologi Molecular de la Enfermedad de Chagas, Instituto de Investigaciones en Ingenieri Genetica y Biologi Molecular, Buenos Aires, Argentina; Department of Environmental Studies, Emory University, Atlanta, Georgia; Fogarty International Center, National Institutes of Health, Bethesda, Maryland, gurtler@ege.fcen.uba.ar
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 872
EP  - 882
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 88
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  - Trypanosoma cruzi
KW  - Reservoir
KW  - Parasites
KW  - Didelphis albiventris
KW  - Nucleotide sequence
KW  - Vectors
KW  - Didelphis
KW  - Hosts
KW  - Infection
KW  - Disease transmission
KW  - Argentina, Chaco
KW  - Typing
KW  - Argentina
KW  - Dasypus
KW  - Dasypus novemcinctus
KW  - Polymerase chain reaction
KW  - Xenodiagnosis
KW  - Hygiene
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
KW  - K 03310:Genetics & Taxonomy
KW  - J 02300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647005553?accountid=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=New+Sylvatic+Hosts+of+Trypanosoma+cruzi+and+Their+Reservoir+Competence+in+the+Humid+Chaco+of+Argentina%3A+A+Longitudinal+Study&rft.au=Orozco%2C+M+Marcela%3BEnriquez%2C+Gustavo+F%3BAlvarado-Otegui%2C+Julia+A%3BCardinal%2C+M+Victoria%3BSchijman%2C+Alejandro+G%3BKitron%2C+Uriel%3BGurtler%2C+Ricardo+E&rft.aulast=Orozco&rft.aufirst=M&rft.date=2013-05-01&rft.volume=88&rft.issue=5&rft.spage=872&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0519
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Parasites; Reservoir; Nucleotide sequence; Polymerase chain reaction; Hosts; Hygiene; Typing; Vectors; Xenodiagnosis; Infection; Disease transmission; Trypanosoma cruzi; Didelphis albiventris; Dasypus; Dasypus novemcinctus; Didelphis; Argentina, Chaco; Argentina
DO  - http://dx.doi.org/10.4269/ajtmh.12-0519
ER  - 



TY  - JOUR
T1  - One thousand genomes imputation in the national cancer institute breast and prostate cancer cohort consortium aggressive prostate cancer genome-wide association study
AN  - 1636453386; 23255287
AB  - BACKGROUND  
Genotype imputation substantially increases available markers for analysis in genome-wide association studies (GWAS) by leveraging linkage disequilibrium from a reference panel. We sought to (i) investigate the performance of imputation from the August 2010 release of the 1000 Genomes Project (1000GP) in an existing GWAS of prostate cancer, (ii) look for novel associations with prostate cancer risk, (iii) fine-map known prostate cancer susceptibility regions using an approximate Bayesian framework and stepwise regression, and (iv) compare power and efficiency of imputation and de novo sequencing.  
METHODS  
We used 2,782 aggressive prostate cancer cases and 4,458 controls from the NCI Breast and Prostate Cancer Cohort Consortium aggressive prostate cancer GWAS to infer 5.8 million well-imputed autosomal single nucleotide polymorphisms (SNPs).  
RESULTS  
Imputation quality, as measured by correlation between imputed and true allele counts, was higher among common variants than rare variants. We found no novel prostate cancer associations among a subset of 1.2 million well-imputed low-frequency variants. At a genome-wide sequencing cost of $2,500, imputation from SNP arrays is a more powerful strategy than sequencing for detecting disease associations of SNPs with minor allele frequencies (MAF) above 1%.  
CONCLUSIONS  
1000GP imputation provided dense coverage of previously identified prostate cancer susceptibility regions, highlighting its potential as an inexpensive first-pass approach to fine mapping in regions such as 5p15 and 8q24. Our study shows 1000GP imputation can accurately identify low-frequency variants and stresses the importance of large sample size when studying these variants. Prostate 73: 677-689, 2013. © 2012 Wiley Periodicals, Inc.
JF  - The Prostate
AU  - Machiela, Mitchell J
AU  - Chen, Constance
AU  - Liang, Liming
AU  - Diver, W Ryan
AU  - Stevens, Victoria L
AU  - Tsilidis, Konstantinos K
AU  - Haiman, Christopher A
AU  - Chanock, Stephen J
AU  - Hunter, David J
AU  - Kraft, Peter
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 677
EP  - 89
CY  - Hoboken
PB  - Wiley Subscription Services, Inc.
VL  - 73
IS  - 7
SN  - 02704137
KW  - Medical Sciences--Urology And Nephrology
KW  - United States
KW  - Humans
KW  - Chromosome Mapping
KW  - Male
KW  - Female
KW  - Genome-Wide Association Study
KW  - Breast Neoplasms -- genetics
KW  - Genome, Human
KW  - National Cancer Institute (U.S.)
KW  - Prostatic Neoplasms -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1636453386?accountid=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=The+Prostate&rft.atitle=One+thousand+genomes+imputation+in+the+national+cancer+institute+breast+and+prostate+cancer+cohort+consortium+aggressive+prostate+cancer+genome-wide+association+study&rft.au=Machiela%2C+Mitchell+J%3BChen%2C+Constance%3BLiang%2C+Liming%3BDiver%2C+W+Ryan%3BStevens%2C+Victoria+L%3BTsilidis%2C+Konstantinos+K%3BHaiman%2C+Christopher+A%3BChanock%2C+Stephen+J%3BHunter%2C+David+J%3BKraft%2C+Peter&rft.aulast=Machiela&rft.aufirst=Mitchell&rft.date=2013-05-01&rft.volume=73&rft.issue=7&rft.spage=677&rft.isbn=&rft.btitle=&rft.title=The+Prostate&rft.issn=02704137&rft_id=info:doi/10.1002%2Fpros.22608
LA  - English
DB  - ProQuest Central
N1  - Copyright - Copyright © 2012 Wiley Periodicals, Inc.
N1  - Last updated - 2014-12-16
N1  - CODEN - PRSTDS
DO  - http://dx.doi.org/10.1002/pros.22608
ER  - 



TY  - JOUR
T1  - Sensitivity to First-Order Relations of Facial Elements in Infant Rhesus Macaques
AN  - 1512195851; 201406666
AB  - Faces are visually attractive to both human and nonhuman primates. Human neonates are thought to have a broad template for faces at birth and prefer face-like to non-face-like stimuli. To better compare developmental trajectories of face processing phylogenetically, here, we investigated preferences for face-like stimuli in infant rhesus macaques using photographs of real faces. We presented infant macaques aged 15-25 days with human, macaque and abstract faces with both normal and linear arrangements of facial features and measured infants' gaze durations, number of fixations and latency to look to each face using eye-tracking technology. There was an overall preference for normal over linear facial arrangements for abstract and monkey faces but not human faces. Moreover, infant macaques looked less at monkey faces than at abstract or human faces. These results suggest that species and facial configurations affect face processing in infant macaques, and we discuss potential explanations for these findings. Further, carefully controlled studies are required to ascertain whether infant macaques' face template can be considered as broad as human infants' face template. [Copyright John Wiley and Sons, Ltd.]
JF  - Infant and Child Development
AU  - Paukner, Annika
AU  - Bower, Seth
AU  - Simpson, Elizabeth A
AU  - Suomi, Stephen J
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development, Laboratory of Comparative Ethology, Maryland, USA pauknera@mail.nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 320
EP  - 330
PB  - John Wiley, Chichester UK
VL  - 22
IS  - 3
SN  - 1522-7227, 1522-7227
KW  - rhesus macaque
KW  - infant
KW  - face perception
KW  - first order relations
KW  - eye tracking
KW  - Latency
KW  - Sensitivity
KW  - Monkeys
KW  - Preferences
KW  - Photographs
KW  - Infants
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512195851?accountid=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=Infant+and+Child+Development&rft.atitle=Sensitivity+to+First-Order+Relations+of+Facial+Elements+in+Infant+Rhesus+Macaques&rft.au=Paukner%2C+Annika%3BBower%2C+Seth%3BSimpson%2C+Elizabeth+A%3BSuomi%2C+Stephen+J&rft.aulast=Paukner&rft.aufirst=Annika&rft.date=2013-05-01&rft.volume=22&rft.issue=3&rft.spage=320&rft.isbn=&rft.btitle=&rft.title=Infant+and+Child+Development&rft.issn=15227227&rft_id=info:doi/10.1002%2Ficd.1793
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-04-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Infants; Monkeys; Preferences; Latency; Sensitivity; Photographs
DO  - http://dx.doi.org/10.1002/icd.1793
ER  - 



TY  - JOUR
T1  - RET/PTC and PAX8/PPAR[gamma] chromosomal rearrangements in post-Chernobyl thyroid cancer and their association with iodine-131 radiation dose and other characteristics
AN  - 1492621665; 18486681
AB  - BACKGROUND: Childhood exposure to iodine-131 from the 1986 nuclear accident in Chernobyl, Ukraine, led to a sharp increase in papillary thyroid carcinoma (PTC) incidence in regions surrounding the reactor. Data concerning the association between genetic mutations in PTCs and individual radiation doses are limited. METHODS: Mutational analysis was performed on 62 PTCs diagnosed in a Ukrainian cohort of patients who were < 18 years old in 1986 and received 0.008 to 8.6 Gy of super(131)I to the thyroid. Associations between mutation types and super(131)I dose and other characteristics were explored. RESULTS: RET/PTC (ret proto-oncogene/papillary thyroid carcinoma) rearrangements were most common (35%), followed by BRAF (15%) and RAS (8%) point mutations. Two tumors carrying PAX8/PPAR[gamma] (paired box 8/peroxisome proliferator-activated receptor gamma) rearrangement were identified. A significant negative association with super(131)I dose for BRAF and RAS point mutations and a significant concave association with super(131)I dose, with an inflection point at 1.6 Gy and odds ratio of 2.1, based on a linear-quadratic model for RET/PTC and PAX8/PPAR[gamma] rearrangements were found. The trends with dose were significantly different between tumors with point mutations and rearrangements. Compared with point mutations, rearrangements were associated with residence in the relatively iodine-deficient Zhytomyr region, younger age at exposure or surgery, and male sex. CONCLUSIONS: These results provide the first demonstration of PAX8/PPAR[gamma] rearrangements in post-Chernobyl tumors and show different associations for point mutations and chromosomal rearrangements with super(131)I dose and other factors. These data support the relationship between chromosomal rearrangements, but not point mutations, and super(131)I exposure and point to a possible role of iodine deficiency in generation of RET/PTC rearrangements in these patients. Cancer 2013. [copy 2013 American Cancer Society. This study of papillary thyroid carcinomas in populations exposed to the 1986 accident in Chernobyl, Ukraine, provides the first documentation of PAX8/PPAR[gamma] rearrangements in post-Chernobyl thyroid cancer; demonstrates a link between chromosomal rearrangements, but not point mutations, and individual iodine-131 dose received; and points to a possible role of iodine deficiency in generation of RET/PTC rearrangements in these patients.
JF  - Cancer
AU  - Leeman-Neill, Rebecca J
AU  - Brenner, Alina V
AU  - Little, Mark P
AU  - Bogdanova, Tetiana I
AU  - Hatch, Maureen
AU  - Zurnadzy, Liudmyla Y
AU  - Mabuchi, Kiyohiko
AU  - Tronko, Mykola D
AU  - Nikiforov, Yuri E
AD  - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland., nikiforovye@upmc.edu
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1792
EP  - 1799
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 10
SN  - 0008-543X, 0008-543X
KW  - Genetics Abstracts; Toxicology Abstracts
KW  - Accidents
KW  - Point mutation
KW  - X 24390:Radioactive Materials
KW  - G 07880:Human Genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492621665?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=RET%2FPTC+and+PAX8%2FPPAR%5Bgamma%5D+chromosomal+rearrangements+in+post-Chernobyl+thyroid+cancer+and+their+association+with+iodine-131+radiation+dose+and+other+characteristics&rft.au=Leeman-Neill%2C+Rebecca+J%3BBrenner%2C+Alina+V%3BLittle%2C+Mark+P%3BBogdanova%2C+Tetiana+I%3BHatch%2C+Maureen%3BZurnadzy%2C+Liudmyla+Y%3BMabuchi%2C+Kiyohiko%3BTronko%2C+Mykola+D%3BNikiforov%2C+Yuri+E&rft.aulast=Leeman-Neill&rft.aufirst=Rebecca&rft.date=2013-05-01&rft.volume=119&rft.issue=10&rft.spage=1792&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27893
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Point mutation
DO  - http://dx.doi.org/10.1002/cncr.27893
ER  - 



TY  - JOUR
T1  - Synthesis, Bifunctionalization, and Remarkable Adsorption Performance of Benzene-Bridged Periodic Mesoporous Organosilicas Functionalized with High Loadings of Carboxylic Acids
AN  - 1464508954; 18485123
AB  - Highly ordered benzene-bridged periodic mesoporous organosilicas (PMOs) that were functionalized with exceptionally high loadings of carboxylic acid groups (COOH), up to 80mol% based on silica, have been synthesized and their use as adsorbents for the adsorption of methylene blue (MB), a basic dye pollutant, and for the loading and release of doxorubicin (DOX), an anticancer drug, is demonstrated. These COOH-functionalized benzene-silicas were synthesized by the co-condensation of 1,4-bis(triethoxysilyl) benzene (BTEB) and carboxyethylsilanetriol sodium salt (CES), an organosilane that contained a carboxylic acid group, in the presence of non-ionic oligomeric surfactant Brij76 in acidic medium. The materials thus obtained were characterized by a variety of techniques, including powder X-ray diffraction (XRD), nitrogen-adsorption/desorption isotherms, TEM, and super(13)C and super(29)Si solid-state NMR spectroscopy. Owing to the exceptionally high loadings of COOH groups, their high surface areas, and possible pi - pi -stacking interactions, these adsorbents have very high adsorption capacities and extremely rapid adsorption rates for MB removal and for the controlled loading/release of DOX, thus manifesting their great potential for environmental and biomedical applications. Functionalization matters! Highly ordered benzene-bridged periodic mesoporous silicas with extremely high loadings (up to 80mol%) of COOH groups have been synthesized and used as adsorbents for the removal of methylene blue (MB) and the delivery of an anticancer drug, doxorubicin (DOX). These materials exhibited high adsorption capacities, rapid adsorption rates for methylene blue removal, and an excellent loading/release profile for doxorubicin.
JF  - Chemistry: A European Journal
AU  - Wu, Hao-Yiang
AU  - Shieh, Fa-Kuen
AU  - Kao, Hsien-Ming
AU  - Chen, Yi-Wen
AU  - Deka, Juti Rani
AU  - Liao, Shih-Hsiang
AU  - Wu, Kevin C-W
AD  - Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, 325, Sec. 2, Cheng-Kung Rd, Nei-Hu Dist, Taipei 11490, Taiwan (ROC)., hmkao@cc.ncu.edu.tw
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 6358
EP  - 6367
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 19
IS  - 20
SN  - 0947-6539, 0947-6539
KW  - Pollution Abstracts
KW  - carboxylic acids
KW  - doxorubicin
KW  - drug delivery
KW  - mesoporous materials
KW  - methylene blue
KW  - Desorption
KW  - Surface area
KW  - Spectroscopy
KW  - X-ray diffraction
KW  - Benzene
KW  - Sodium
KW  - Salts
KW  - Silica
KW  - Carboxylic acids
KW  - Adsorption
KW  - NMR
KW  - Surfactants
KW  - Drugs
KW  - P 9999:GENERAL POLLUTION
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464508954?accountid=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=Chemistry%3A+A+European+Journal&rft.atitle=Synthesis%2C+Bifunctionalization%2C+and+Remarkable+Adsorption+Performance+of+Benzene-Bridged+Periodic+Mesoporous+Organosilicas+Functionalized+with+High+Loadings+of+Carboxylic+Acids&rft.au=Wu%2C+Hao-Yiang%3BShieh%2C+Fa-Kuen%3BKao%2C+Hsien-Ming%3BChen%2C+Yi-Wen%3BDeka%2C+Juti+Rani%3BLiao%2C+Shih-Hsiang%3BWu%2C+Kevin+C-W&rft.aulast=Wu&rft.aufirst=Hao-Yiang&rft.date=2013-05-01&rft.volume=19&rft.issue=20&rft.spage=6358&rft.isbn=&rft.btitle=&rft.title=Chemistry%3A+A+European+Journal&rft.issn=09476539&rft_id=info:doi/10.1002%2Fchem.201204400
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2016-03-30
N1  - SubjectsTermNotLitGenreText - Desorption; Surface area; X-ray diffraction; Spectroscopy; Benzene; Sodium; Salts; Silica; Adsorption; Carboxylic acids; NMR; Drugs; Surfactants
DO  - http://dx.doi.org/10.1002/chem.201204400
ER  - 



TY  - JOUR
T1  - Treatment for Substance Use Disorder: Opportunities and Challenges under the Affordable Care Act
AN  - 1448999205; 201308729
AB  - Addiction is a chronic brain disease with consequences that remain problematic years after discontinuation of use. Despite this, treatment models focus on acute interventions and are carved out from the main health care system. The Patient Protection and Affordable Care Act (2010) brings the opportunity to change the way substance use disorder (SUD) is treated in the United States. The treatment of SUD must adapt to a chronic care model offered in an integrated care system that screens for at-risk patients and includes services needed to prevent relapses. The partnering of the health care system with substance abuse treatment programs could dramatically expand the benefits of prevention and treatment of SUD. Expanding roles of health information technology and nonphysician workforces, such as social workers, are essential to the success of a chronic care model. Adapted from the source document.
JF  - Social Work in Public Health
AU  - Tai, Betty
AU  - Volkow, Nora D
AD  - Center for the Clinical Trials Network, National Institute on Drug Abuse, National Institutes of Health, 6001 Executive Boulevard, Bethesda, MD 20892, USA btai@nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 165
EP  - 174
PB  - Taylor & Francis, Philadelphia PA
VL  - 28
IS  - 3-4
SN  - 1937-1918, 1937-1918
KW  - Substance use disorder, Affordable Care Act, chronic care model, health information technology, social workforce, screening brief intervention and referral to treatment
KW  - Relapse
KW  - Prevention
KW  - Substance Abuse
KW  - Brain
KW  - Intervention
KW  - Patients
KW  - Addiction
KW  - Treatment
KW  - Health Care Services
KW  - article
KW  - 6124: health care promotion/education
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448999205?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Work+in+Public+Health&rft.atitle=Treatment+for+Substance+Use+Disorder%3A+Opportunities+and+Challenges+under+the+Affordable+Care+Act&rft.au=Tai%2C+Betty%3BVolkow%2C+Nora+D&rft.aulast=Tai&rft.aufirst=Betty&rft.date=2013-05-01&rft.volume=28&rft.issue=3-4&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Social+Work+in+Public+Health&rft.issn=19371918&rft_id=info:doi/10.1080%2F19371918.2013.758975
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2014-02-21
N1  - Number of references - 53
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Health Care Services; Substance Abuse; Patients; Addiction; Brain; Intervention; Treatment; Prevention; Relapse
DO  - http://dx.doi.org/10.1080/19371918.2013.758975
ER  - 



TY  - JOUR
T1  - The Impact of Alcohol on Society: A Brief Overview
AN  - 1448997778; 201308721
AB  - Alcohol is the most common drug used among adults in the United States. The use of alcohol is associated with an increased risk of injuries and accidents. Even a single episode of excessive drinking can lead to a negative outcome. Alcoholism and chronic use of alcohol are associated with numerous medical, psychiatric, social, and family problems. Family members, including children, exposed to a first-degree relative's alcohol problem are at risk for problems. Children of parents with alcohol addiction, for example, show higher rates of alcoholism than children who do not have parents with an alcohol addiction. It is important for social workers to keep in mind that alcohol and alcohol problems affect the health, safety, and well-being of people. Adapted from the source document.
JF  - Social Work in Public Health
AU  - Moss, Howard B
AD  - Associate Director, Clinical and Translational Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5635 Fishers Lane, Bethesda, MD 20892, USA mossh@mail.nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 175
EP  - 177
PB  - Taylor & Francis, Philadelphia PA
VL  - 28
IS  - 3-4
SN  - 1937-1918, 1937-1918
KW  - Alcohol, health, epidemiology, social factors
KW  - Risk
KW  - Accidents
KW  - Alcohol Abuse
KW  - Well Being
KW  - Health Problems
KW  - Alcoholism
KW  - Parents
KW  - Children
KW  - Psychiatry
KW  - article
KW  - 6124: health care promotion/education
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448997778?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Work+in+Public+Health&rft.atitle=The+Impact+of+Alcohol+on+Society%3A+A+Brief+Overview&rft.au=Moss%2C+Howard+B&rft.aulast=Moss&rft.aufirst=Howard&rft.date=2013-05-01&rft.volume=28&rft.issue=3-4&rft.spage=175&rft.isbn=&rft.btitle=&rft.title=Social+Work+in+Public+Health&rft.issn=19371918&rft_id=info:doi/10.1080%2F19371918.2013.758987
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2013-11-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Alcohol Abuse; Alcoholism; Children; Well Being; Health Problems; Parents; Risk; Psychiatry; Accidents
DO  - http://dx.doi.org/10.1080/19371918.2013.758987
ER  - 



TY  - JOUR
T1  - Blending Research and Practice: An Evolving Dissemination Strategy in Substance Abuse
AN  - 1448997666; 201308720
AB  - Substance abuse is a leading cause of death and disability throughout the world. The mission of the National Institute on Drug Abuse (NIDA) is to lead the United States in bringing the power of science to bear on drug abuse and addiction. This charge has two critical components: (a) strategic support of research across a broad range of disciplines and (b) rapid, effective dissemination of research results that can improve prevention and treatment efforts, with potential to inform policy. The NIDA Clinical Trials Network and the Blending Initiative are critical elements of this strategy, and the social work field is poised to use these resources to expand its role in the dissemination and implementation of NIDA's mission. Adapted from the source document.
JF  - Social Work in Public Health
AU  - Michel, Mary Ellen
AU  - Pintello, Denise A
AU  - Subramaniam, Geetha
AD  - Deputy Director, Center for the Clinical Trials Network, National Institute on Drug Abuse, NIH, 6001 Executive Blvd, Room 3119, Rockville, MD 20852, USA
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 302
EP  - 312
PB  - Taylor & Francis, Philadelphia PA
VL  - 28
IS  - 3-4
SN  - 1937-1918, 1937-1918
KW  - Blending Initiative, National Institute on Drug Abuse, dissemination, community practice, clinical trials
KW  - Prevention
KW  - Drug Addiction
KW  - Substance Abuse
KW  - Power
KW  - Information Dissemination
KW  - United States of America
KW  - Medical Research
KW  - Social Work
KW  - Drug Abuse
KW  - article
KW  - 6124: health care promotion/education
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448997666?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Work+in+Public+Health&rft.atitle=Blending+Research+and+Practice%3A+An+Evolving+Dissemination+Strategy+in+Substance+Abuse&rft.au=Michel%2C+Mary+Ellen%3BPintello%2C+Denise+A%3BSubramaniam%2C+Geetha&rft.aulast=Michel&rft.aufirst=Mary&rft.date=2013-05-01&rft.volume=28&rft.issue=3-4&rft.spage=302&rft.isbn=&rft.btitle=&rft.title=Social+Work+in+Public+Health&rft.issn=19371918&rft_id=info:doi/10.1080%2F19371918.2013.774660
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2014-02-21
N1  - Number of references - 16
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Drug Abuse; Substance Abuse; Information Dissemination; Drug Addiction; Medical Research; Prevention; Social Work; United States of America; Power
DO  - http://dx.doi.org/10.1080/19371918.2013.774660
ER  - 



TY  - JOUR
T1  - Quiescent Innate Response to Infective Filariae by Human Langerhans Cells Suggests a Strategy of Immune Evasion
AN  - 1443375692; 18642803
AB  - Filarial infection is initiated by mosquito-derived third-stage larvae (L3) deposited on the skin that transit through the epidermis, which contains Langerhans cells (LC) and keratinocytes (KC), among other cells. This earliest interaction between L3 and the LC likely conditions the priming of the immune system to the parasite. To determine the nature of this interaction, human LC (langerin+ E-cadherin+ CD1a+) were generated in vitro and exposed to live L3. LC exposed to live L3 for 48 h showed no alterations in the cell surface markers CD14, CD86, CD83, CD207, E-cadherin, CD80, CD40, and HLA-DR or in mRNA expression of inflammation-associated genes, such as those for interleukin 18 (IL-18), IL-18BP, and caspase 1. In contrast to L3, live tachyzoites of Toxoplasma gondii, an intracellular parasite, induced production of CXCL9, IP-10, and IL-6 in LC. Furthermore, preexposure of LC to L3 did not alter Toll-like receptor 3 (TLR3)- or TLR4-mediated expression of the proinflammatory cytokines IL-1 beta , gamma interferon (IFN- gamma ), IL-6, or IL-10. Interestingly, cocultures of KC and LC produced significantly more IL-18, IL-1 alpha , and IL-8 than did cultures of LC alone, although exposure of the cocultures to live L3 did not result in altered cytokine production. Microarray examination of ex vivo LC from skin blisters that were exposed to live L3 also showed few significant changes in gene expression compared with unexposed blisters, further underscoring the relatively muted response of LC to L3. Our data suggest that failure by LC to initiate an inflammatory response to the invasive stage of filarial parasites may be a strategy for immune evasion by the filarial parasite.
JF  - Infection and Immunity
AU  - Boyd, Alexis
AU  - Bennuru, Sasisekhar
AU  - Wang, Yuanyuan
AU  - Sanprasert, Vivornpun
AU  - Law, Melissa
AU  - Chaussabel, Damien
AU  - Nutman, Thomas B
AU  - Semnani, Roshanak Tolouei
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1420
EP  - 1429
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 5
SN  - 0019-9567, 0019-9567
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Immunology Abstracts
KW  - Histocompatibility antigen HLA
KW  - Interleukin 6
KW  - gamma -Interferon
KW  - Cell surface
KW  - Parasites
KW  - CD83 antigen
KW  - CD86 antigen
KW  - Immune system
KW  - Interleukin 1
KW  - Cell culture
KW  - CD14 antigen
KW  - Infection
KW  - Interleukin 8
KW  - Interleukin 10
KW  - Gene expression
KW  - TLR3 protein
KW  - IP-10 protein
KW  - Interleukin 18
KW  - CD80 antigen
KW  - Keratinocytes
KW  - CD40 antigen
KW  - Aquatic insects
KW  - Data processing
KW  - Skin
KW  - Larvae
KW  - Receptors
KW  - Immunity
KW  - Inflammation
KW  - Langerhans cells
KW  - Epidermis
KW  - Toxoplasma gondii
KW  - tachyzoites
KW  - Caspase-1
KW  - Toll-like receptors
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443375692?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Quiescent+Innate+Response+to+Infective+Filariae+by+Human+Langerhans+Cells+Suggests+a+Strategy+of+Immune+Evasion&rft.au=Boyd%2C+Alexis%3BBennuru%2C+Sasisekhar%3BWang%2C+Yuanyuan%3BSanprasert%2C+Vivornpun%3BLaw%2C+Melissa%3BChaussabel%2C+Damien%3BNutman%2C+Thomas+B%3BSemnani%2C+Roshanak+Tolouei&rft.aulast=Boyd&rft.aufirst=Alexis&rft.date=2013-05-01&rft.volume=81&rft.issue=5&rft.spage=1420&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01301-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 35
N1  - Last updated - 2014-12-11
N1  - SubjectsTermNotLitGenreText - Parasites; Skin; Receptors; Immunity; Aquatic insects; Interleukin 6; Histocompatibility antigen HLA; Cell surface; gamma -Interferon; CD83 antigen; Immune system; CD86 antigen; Interleukin 1; Cell culture; Infection; CD14 antigen; Interleukin 10; Interleukin 8; Gene expression; TLR3 protein; IP-10 protein; Interleukin 18; CD80 antigen; Keratinocytes; CD40 antigen; Data processing; Larvae; Inflammation; Langerhans cells; Epidermis; tachyzoites; Caspase-1; Toll-like receptors; Toxoplasma gondii
DO  - http://dx.doi.org/10.1128/IAI.01301-12
ER  - 



TY  - JOUR
T1  - Susceptibility of Intact Germinating Arabidopsis thaliana to Human Fungal Pathogens Cryptococcus neoformans and C. gattii
AN  - 1443375458; 18642752
AB  - The fungus Cryptococcus contributes a large global burden of infectious death in both HIV-infected and healthy individuals. As Cryptococcus is an opportunistic pathogen, much of the evolutionary pressure shaping virulence occurs in environments in contact with plants and soil. The present studies investigated inoculation of intact seeds of the common weed Arabidopsis thaliana with fungal cells over a 21-day period. C. gattii was the more virulent plant pathogen, resulting in disrupted germination as well as increased stem lodging, fungal burden, and plant tissue colocalization. C. neoformans was a less virulent plant pathogen but exhibited prolonged tissue residence within the cuticle and vascular spaces. Arabidopsis mutants of the PRN1 gene, which is involved in abiotic and biotic signaling affecting phenylalanine-derived flavonoids, showed altered susceptibility to cryptoccocal infections, suggesting roles for this pathway in cryptococcal defense. The fungal virulence factor laccase was also implicated in plant pathogenesis, as a cryptococcal lac1 Delta strain was less virulent than wild-type fungi and was unable to colonize seedlings. In conclusion, these studies expand knowledge concerning the ecological niche of Cryptococcus by demonstrating the pathogenic capacity of the anamorphic form of cryptococcal cells against healthy seedlings under physiologically relevant conditions. In addition, an important role of laccase in plant as well as human virulence may suggest mechanisms for laccase retention and optimization during evolution of this fungal pathogen.
JF  - Applied and Environmental Microbiology
AU  - Warpeha, Katherine M
AU  - Park, Yoon-Dong
AU  - Williamson, Peter R
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 2979
EP  - 2988
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 79
IS  - 9
SN  - 0099-2240, 0099-2240
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Cuticles
KW  - Arabidopsis thaliana
KW  - Pathogens
KW  - K:03320
KW  - A:01380
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443375458?accountid=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=Applied+and+Environmental+Microbiology&rft.atitle=Susceptibility+of+Intact+Germinating+Arabidopsis+thaliana+to+Human+Fungal+Pathogens+Cryptococcus+neoformans+and+C.+gattii&rft.au=Warpeha%2C+Katherine+M%3BPark%2C+Yoon-Dong%3BWilliamson%2C+Peter+R&rft.aulast=Warpeha&rft.aufirst=Katherine&rft.date=2013-05-01&rft.volume=79&rft.issue=9&rft.spage=2979&rft.isbn=&rft.btitle=&rft.title=Applied+and+Environmental+Microbiology&rft.issn=00992240&rft_id=info:doi/10.1128%2FAEM.03697-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Pathogens; Arabidopsis thaliana
DO  - http://dx.doi.org/10.1128/AEM.03697-12
ER  - 



TY  - JOUR
T1  - Overcoming Allelic Specificity by Immunization with Five Allelic Forms of Plasmodium falciparum Apical Membrane Antigen 1
AN  - 1443375422; 18642816
AB  - Apical membrane antigen 1 (AMA1) is a leading vaccine candidate, but the allelic polymorphism is a stumbling block for vaccine development. We previously showed that a global set of AMA1 haplotypes could be grouped into six genetic populations. Using this information, six recombinant AMA1 proteins representing each population were produced. Rabbits were immunized with either a single recombinant AMA1 protein or mixtures of recombinant AMA1 proteins (mixtures of 4, 5, or 6 AMA1 proteins). Antibody levels were measured by enzyme-linked immunosorbent assay (ELISA), and purified IgG from each rabbit was used for growth inhibition assay (GIA) with 12 different clones of parasites (a total of 108 immunogen-parasite combinations). Levels of antibodies to all six AMA1 proteins were similar when the antibodies were tested against homologous antigens. When the percent inhibitions in GIA were plotted against the number of ELISA units measured with homologous AMA1, all data points followed a sigmoid curve, regardless of the immunogen. In homologous combinations, there were no differences in the percent inhibition between the single-allele and allele mixture groups. However, all allele mixture groups showed significantly higher percent inhibition than the single-allele groups in heterologous combinations. The 5-allele-mixture group showed significantly higher inhibition to heterologous parasites than the 4-allele-mixture group. On the other hand, there was no difference between the 5- and 6-allele-mixture groups. These data indicate that mixtures with a limited number of alleles may cover a majority of the parasite population. In addition, using the data from 72 immunogen-parasite combinations, we mathematically identified 13 amino acid polymorphic sites which significantly impact GIA activities. These results could be a foundation for the rational design of a future AMA1 vaccine.
JF  - Infection and Immunity
AU  - Miura, Kazutoyo
AU  - Herrera, Raul
AU  - Diouf, Ababacar
AU  - Zhou, Hong
AU  - Mu, Jianbing
AU  - Hu, Zonghui
AU  - MacDonald, Nicholas J
AU  - Reiter, Karine
AU  - Nguyen, Vu
AU  - Shimp, Richard L, Jr
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1491
EP  - 1501
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 5
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts
KW  - Apical membrane antigen 1
KW  - Parasites
KW  - Enzyme-linked immunosorbent assay
KW  - Data processing
KW  - Amino acids
KW  - Allelles
KW  - Disease control
KW  - Plasmodium falciparum
KW  - Biopolymorphism
KW  - Immunization
KW  - AmA1 protein
KW  - Recombinants
KW  - Population genetics
KW  - Antibodies
KW  - Antigens
KW  - Haplotypes
KW  - Immunoglobulin G
KW  - Vaccines
KW  - K 03410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443375422?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Overcoming+Allelic+Specificity+by+Immunization+with+Five+Allelic+Forms+of+Plasmodium+falciparum+Apical+Membrane+Antigen+1&rft.au=Miura%2C+Kazutoyo%3BHerrera%2C+Raul%3BDiouf%2C+Ababacar%3BZhou%2C+Hong%3BMu%2C+Jianbing%3BHu%2C+Zonghui%3BMacDonald%2C+Nicholas+J%3BReiter%2C+Karine%3BNguyen%2C+Vu%3BShimp%2C+Richard+L%2C+Jr&rft.aulast=Miura&rft.aufirst=Kazutoyo&rft.date=2013-05-01&rft.volume=81&rft.issue=5&rft.spage=1491&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01414-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 39
N1  - Last updated - 2014-11-12
N1  - SubjectsTermNotLitGenreText - Recombinants; Parasites; Population genetics; Antibodies; Antigens; Allelles; Disease control; Vaccines; Biopolymorphism; Apical membrane antigen 1; Enzyme-linked immunosorbent assay; Amino acids; Data processing; Haplotypes; Immunoglobulin G; Immunization; AmA1 protein; Plasmodium falciparum
DO  - http://dx.doi.org/10.1128/IAI.01414-12
ER  - 



TY  - JOUR
T1  - Nanoparticles and the blood coagulation system. Part I: benefits of nanotechnology
AN  - 1443374118; 18678613
AB  - Nanotechnology is proven to provide certain benefits in drug delivery by improving solubility, increasing uptake to target sites and changing pharmacokinetics profiles of traditional drugs. Since properties of many materials change tremendously at the nanoscale levels, nanotechnology is also being explored in various industrial applications. As such, nanoparticles are rapidly entering various areas of industry, biology and medicine. The benefits of using nanotechnology for industrial and biomedical applications are often tempered by concerns about the safety of these new materials. One such area of concern includes their effect on the immune system. While nanoparticle interactions with various constituents of the immune system have been reviewed before, little attention was given to nanoparticle effects on the blood coagulation system. Nanoparticle interface with the blood coagulation system may lead to either benefits to the host or adverse reactions. This article reviews recent advances in our understanding of nanoparticle interactions with plasma coagulation factors, platelets, endothelial cells and leukocytes. Part I is focused on desirable interactions between nanoparticles and the coagulation system, and discusses benefits of using nanotechnology to intervene in coagulation disorders. Undesirable interactions posing safety concerns are covered in part II, which will be published in the June issue of Nanomedicine.
JF  - Nanomedicine
AU  - Ilinskaya, Anna N
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, marina@mail.nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 773
EP  - 784
PB  - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL  - 8
IS  - 5
SN  - 1743-5889, 1743-5889
KW  - Biotechnology and Bioengineering Abstracts
KW  - Drug delivery
KW  - Solubility
KW  - Immune system
KW  - Leukocytes
KW  - Coagulation factors
KW  - Pharmacokinetics
KW  - Endothelial cells
KW  - Blood coagulation
KW  - Industrial applications
KW  - Reviews
KW  - Platelets
KW  - nanoparticles
KW  - Side effects
KW  - nanotechnology
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443374118?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nanoparticles+and+the+blood+coagulation+system.+Part+I%3A+benefits+of+nanotechnology&rft.au=Ilinskaya%2C+Anna+N%3BDobrovolskaia%2C+Marina+A&rft.aulast=Ilinskaya&rft.aufirst=Anna&rft.date=2013-05-01&rft.volume=8&rft.issue=5&rft.spage=773&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/10.2217%2Fnnm.13.48
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 91
N1  - Last updated - 2013-11-04
N1  - SubjectsTermNotLitGenreText - Drug delivery; Solubility; Immune system; Leukocytes; Coagulation factors; Pharmacokinetics; Endothelial cells; Blood coagulation; Industrial applications; Reviews; Platelets; nanoparticles; Side effects; nanotechnology
DO  - http://dx.doi.org/10.2217/nnm.13.48
ER  - 



TY  - JOUR
T1  - Induction of the Yersinia pestis PhoP-PhoQ Regulatory System in the Flea and Its Role in Producing a Transmissible Infection
AN  - 1443372721; 18642994
AB  - Transmission of Yersinia pestis is greatly enhanced after it forms a bacterial biofilm in the foregut of the flea vector that interferes with normal blood feeding. Here we report that the ability to produce a normal foregut-blocking infection depends on induction of the Y. pestis PhoP-PhoQ two-component regulatory system in the flea. Y. pestis phoP-negative mutants achieved normal infection rates and bacterial loads in the flea midgut but produced a less cohesive biofilm both in vitro and in the flea and had a greatly reduced ability to localize to and block the flea foregut. Thus, not only is the PhoP-PhoQ system induced in the flea gut environment, but also this induction is required to produce a normal transmissible infection. The altered biofilm phenotype in the flea was not due to lack of PhoPQ-dependent or PmrAB-dependent addition of aminoarabinose to the Y. pestis lipid A, because an aminoarabinose-deficient mutant that is highly sensitive to cationic antimicrobial peptides had a normal phenotype in the flea digestive tract. In addition to enhancing transmissibility, induction of the PhoP-PhoQ system in the arthropod vector prior to transmission may preadapt Y. pestis to resist the initial encounter with the mammalian innate immune response.
JF  - Journal of Bacteriology
AU  - Rebeil, Roberto
AU  - Jarrett, Clayton O
AU  - Driver, James D
AU  - Ernst, Robert K
AU  - Oyston, Petra CF
AU  - Hinnebusch, B Joseph
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1920
EP  - 1930
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 195
IS  - 9
SN  - 0021-9193, 0021-9193
KW  - Microbiology Abstracts B: Bacteriology
KW  - Feeding
KW  - Yersinia pestis
KW  - Vectors
KW  - Infection
KW  - Disease transmission
KW  - Blood
KW  - Arthropoda
KW  - Digestive tract
KW  - cationic antimicrobial peptides
KW  - Lipid A
KW  - Biofilms
KW  - Midgut
KW  - Immune response
KW  - Foregut
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443372721?accountid=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=Induction+of+the+Yersinia+pestis+PhoP-PhoQ+Regulatory+System+in+the+Flea+and+Its+Role+in+Producing+a+Transmissible+Infection&rft.au=Rebeil%2C+Roberto%3BJarrett%2C+Clayton+O%3BDriver%2C+James+D%3BErnst%2C+Robert+K%3BOyston%2C+Petra+CF%3BHinnebusch%2C+B+Joseph&rft.aulast=Rebeil&rft.aufirst=Roberto&rft.date=2013-05-01&rft.volume=195&rft.issue=9&rft.spage=1920&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.02000-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 88
N1  - Last updated - 2016-08-03
N1  - SubjectsTermNotLitGenreText - Blood; Feeding; cationic antimicrobial peptides; Digestive tract; Vectors; Lipid A; Immune response; Midgut; Biofilms; Infection; Foregut; Disease transmission; Arthropoda; Yersinia pestis
DO  - http://dx.doi.org/10.1128/JB.02000-12
ER  - 



TY  - JOUR
T1  - Potential effect of the risk of ovarian cancer algorithm (ROCA) on the mortality outcome of the Prostate, Lung, Colorectal and Ovarian (PLCO) trial
AN  - 1443366933; 18602627
AB  - Recently, the Prostate, Lung, Colorectal and Ovarian (PLCO) Trial reported no mortality benefit for annual screening with CA-125 and transvaginal ultrasound (TVU). Currently ongoing is the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS), which utilizes the risk of ovarian cancer algorithm (ROCA), a statistical tool that considers current and past CA125 values to determine ovarian cancer risk. In contrast, PLCO used a single cutoff for CA125, based on current levels alone. We investigated whether having had used ROCA in PLCO could have, under optimal assumptions, resulted in a significant mortality benefit by applying ROCA to PLCO CA125 screening values. A best-case scenario assumed that all cancers showing a positive screen result earlier with ROCA than under the PLCO protocol would have avoided mortality; under a stage-shift scenario, such women were assigned survival equivalent to Stage I/II screen-detected cases. Updated PLCO data show 132 intervention arm ovarian cancer deaths versus 119 in usual care (relative risk, RR = 1.11). Forty-three ovarian cancer cases, 25 fatal, would have been detected earlier with ROCA, with a median (minimum) advance time for fatal cases of 344 (147) days. Best-case and stage-shift scenarios gave 25 and 19 deaths prevented with ROCA, for RRs of 0.90 (95% CI: 0.69-1.17) and 0.95 (95% CI: 0.74-1.23), respectively. Having utilized ROCA in PLCO would not have led to a significant mortality benefit of screening. However, ROCA could still show a significant effect in other screening trials, including UKCTOCS. What's new The Prostate, Lung, Colorectal and Ovarian (PLCO) trial found no mortality benefit for ovarian cancer screening using a single cutoff value for the biomarker CA125. PLCO, however, did not incorporate the potential impact of ROCA (Risk of Ovarian Cancer Algorithm), which evaluates serial CA125 values. Here, in a best-case scenario analysis, ROCA was found to have little impact on mortality in the context of PLCO. The findings do not rule out possible benefits from ROCA in the ongoing UK Collaborative Trial of Ovarian Cancer Screening.
JF  - International Journal of Cancer
AU  - Pinsky, Paul F
AU  - Zhu, Claire
AU  - Skates, Steve J
AU  - Black, Amanda
AU  - Partridge, Edward
AU  - Buys, Saundra S
AU  - Berg, Christine D
AD  - Massachusetts General Hospital, Boston, MA., pp4f@nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 2127
EP  - 2133
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 9
SN  - 0020-7136, 0020-7136
KW  - Risk Abstracts
KW  - British Isles
KW  - Bioindicators
KW  - Mortality
KW  - Health risks
KW  - Lung
KW  - Intervention
KW  - Survival
KW  - Ovarian carcinoma
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443366933?accountid=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=Potential+effect+of+the+risk+of+ovarian+cancer+algorithm+%28ROCA%29+on+the+mortality+outcome+of+the+Prostate%2C+Lung%2C+Colorectal+and+Ovarian+%28PLCO%29+trial&rft.au=Pinsky%2C+Paul+F%3BZhu%2C+Claire%3BSkates%2C+Steve+J%3BBlack%2C+Amanda%3BPartridge%2C+Edward%3BBuys%2C+Saundra+S%3BBerg%2C+Christine+D&rft.aulast=Pinsky&rft.aufirst=Paul&rft.date=2013-05-01&rft.volume=132&rft.issue=9&rft.spage=2127&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27909
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Bioindicators; Health risks; Mortality; Lung; Survival; Intervention; Ovarian carcinoma; Cancer; British Isles
DO  - http://dx.doi.org/10.1002/ijc.27909
ER  - 



TY  - JOUR
T1  - Efficient Generation of Astrocytes from Human Pluripotent Stem Cells in Defined Conditions
AN  - 1434026153; 18501526
AB  - Astrocytes can be generated from various tissue sources including human pluripotent stem cells (PSC). In this manuscript, we describe a chemically defined xeno-free medium culture system for rapidly generating astrocytes from neural stem cells derived from PSC. We show that astrocyte development in vitro, mimics normal development in vivo, and also passes through a CD44 super(+) astrocyte precursor stage. Astrocytes generated by our method display similar gene expression patterns, morphological characteristics and functional properties to primary astrocytes, and they survive and integrate after xenotransplantation. Whole genome expression profiling of astrocyte differentiation was performed at several time points of differentiation, and the results indicate the importance of known regulators and identify potential novel regulators and stage-specific lineage markers. STEM CELLS 2013; 31:941-952
JF  - Stem Cells
AU  - Shaltouki, Atossa
AU  - Peng, Jun
AU  - Liu, Qiuyue
AU  - Rao, Mahendra S
AU  - Zeng, Xianmin
AD  - National Center of Regenerative Medicine, National Institutes of Health, Bethesda, Maryland, USA., xzeng@buckinstitute.org
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 941
EP  - 952
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 31
IS  - 5
SN  - 1066-5099, 1066-5099
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Gene expression
KW  - Genomes
KW  - Differentiation
KW  - Stem cells
KW  - Astrocytes
KW  - Xenografts
KW  - Neural stem cells
KW  - N3 11023:Neurogenetics
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434026153?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Efficient+Generation+of+Astrocytes+from+Human+Pluripotent+Stem+Cells+in+Defined+Conditions&rft.au=Shaltouki%2C+Atossa%3BPeng%2C+Jun%3BLiu%2C+Qiuyue%3BRao%2C+Mahendra+S%3BZeng%2C+Xianmin&rft.aulast=Shaltouki&rft.aufirst=Atossa&rft.date=2013-05-01&rft.volume=31&rft.issue=5&rft.spage=941&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1334
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Genomes; Gene expression; Differentiation; Stem cells; Astrocytes; Xenografts; Neural stem cells
DO  - http://dx.doi.org/10.1002/stem.1334
ER  - 



TY  - JOUR
T1  - EPR oxygen imaging and hyperpolarized super(13)C MRI of pyruvate metabolism as noninvasive biomarkers of tumor treatment response to a glycolysis inhibitor 3-bromopyruvate
AN  - 1434015066; 18496093
AB  - The hypoxic nature of tumors results in treatment resistance and poor prognosis. To spare limited oxygen for more crucial pathways, hypoxic cancerous cells suppress mitochondrial oxidative phosphorylation and promote glycolysis for energy production. Thereby, inhibition of glycolysis has the potential to overcome treatment resistance of hypoxic tumors. Here, EPR imaging was used to evaluate oxygen dependent efficacy on hypoxia-sensitive drug. The small molecule 3-bromopyruvate blocks glycolysis pathway by inhibiting hypoxia inducible enzymes and enhanced cytotoxicity of 3-bromopyruvate under hypoxic conditions has been reported in vitro. However, the efficacy of 3-bromopyruvate was substantially attenuated in hypoxic tumor regions (pO sub(2) < 10 mmHg) in vivo using squamous cell carcinoma (SCCVII)-bearing mouse model. Metabolic MRI studies using hyperpolarized super(13)C-labeled pyruvate showed that monocarboxylate transporter-1 is the major transporter for pyruvate and the analog 3-bromopyruvate in SCCVII tumor. The discrepant results between in vitro and in vivo data were attributed to biphasic oxygen dependent expression of monocarboxylate transporter-1 in vivo. Expression of monocarboxylate transporter-1 was enhanced in moderately hypoxic (8-15 mmHg) tumor regions but down regulated in severely hypoxic (<5 mmHg) tumor regions. These results emphasize the importance of noninvasive imaging biomarkers to confirm the action of hypoxia-activated drugs. Magn Reson Med, 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Magnetic Resonance in Medicine
AU  - Matsumoto, Shingo
AU  - Saito, Keita
AU  - Yasui, Hironobu
AU  - Morris, HDouglas
AU  - Munasinghe, Jeeva P
AU  - Lizak, Martin
AU  - Merkle, Hellmut
AU  - Ardenkjaer-Larsen, Jan Henrik
AU  - Choudhuri, Rajani
AU  - Devasahayam, Nallathamby
AU  - Subramanian, Sankaran
AU  - Koretsky, Alan P
AU  - Mitchell, James B
AU  - Krishna, Murali C
AD  - Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan., murali@helix.nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1443
EP  - 1450
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 5
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - Oxidative phosphorylation
KW  - Magnetic resonance imaging
KW  - Animal models
KW  - Prognosis
KW  - Mitochondria
KW  - Enzymes
KW  - squamous cell carcinoma
KW  - Tumors
KW  - biomarkers
KW  - Oxygen
KW  - Cytotoxicity
KW  - Pyruvic acid
KW  - Hypoxia
KW  - N.M.R.
KW  - Drugs
KW  - Glycolysis
KW  - Metabolism
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434015066?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=EPR+oxygen+imaging+and+hyperpolarized+super%2813%29C+MRI+of+pyruvate+metabolism+as+noninvasive+biomarkers+of+tumor+treatment+response+to+a+glycolysis+inhibitor+3-bromopyruvate&rft.au=Matsumoto%2C+Shingo%3BSaito%2C+Keita%3BYasui%2C+Hironobu%3BMorris%2C+HDouglas%3BMunasinghe%2C+Jeeva+P%3BLizak%2C+Martin%3BMerkle%2C+Hellmut%3BArdenkjaer-Larsen%2C+Jan+Henrik%3BChoudhuri%2C+Rajani%3BDevasahayam%2C+Nallathamby%3BSubramanian%2C+Sankaran%3BKoretsky%2C+Alan+P%3BMitchell%2C+James+B%3BKrishna%2C+Murali+C&rft.aulast=Matsumoto&rft.aufirst=Shingo&rft.date=2013-05-01&rft.volume=69&rft.issue=5&rft.spage=1443&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24355
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Data processing; Oxidative phosphorylation; Magnetic resonance imaging; Prognosis; Animal models; Enzymes; Mitochondria; squamous cell carcinoma; Tumors; biomarkers; Oxygen; Cytotoxicity; Pyruvic acid; Hypoxia; N.M.R.; Glycolysis; Drugs; Metabolism
DO  - http://dx.doi.org/10.1002/mrm.24355
ER  - 



TY  - JOUR
T1  - Circulating Biomarkers of Pulmonary and Extrapulmonary Tuberculosis in Children
AN  - 1419368822; 18280311
AB  - Tuberculosis (TB) in children is not only more likely to cause more severe disease than that seen in adults, it is also more likely to be extrapulmonary. Moreover, pediatric TB is very difficult to diagnose and suffers from a lack of understanding of host biomarkers for monitoring the progression of disease. Hence, we sought to identify the expression patterns of a variety of biomarkers in the plasma of children with pulmonary TB (PTB) and extrapulmonary TB (ETB), as well as in healthy control (HC) children. Thus, we examined a variety of circulating markers reflecting tissue inflammation, oxidative stress, innate immune activation, fibrosis, and the cytokine response. Children with active TB, compared to HC children, showed markedly elevated plasma levels of matrix metalloproteinases and their endogenous inhibitors. In addition, children with active TB had significantly elevated levels of C-reactive protein, alpha -2 macroglobulin, and haptoglobin, as well as hemoxygenase 1. Markers of innate immune activation (lipopolysaccharide [LPS] and lipopolysaccharide-binding protein [LBP]) were significantly lower in ETB than in PTB children. Although there were no significant differences between the two groups in their levels of cytokines (type 1 [gamma interferon (IFN- gamma ), tumor necrosis factor alpha (TNF- alpha ), interleukin 2 (IL-2), and IL-12], type 2 [IL-4, IL-5, IL-13, and IL-33], and most type 17 [IL-17A, IL-22, IL-1 beta , and IL-6] and type 1 interferons [IFN- alpha and IFN- beta ]) or most of the cytokines associated with immune modulation (IL-10 and IL-20), pediatric TB was associated with elevated plasma transforming growth factor beta (TGF- beta ), IL-21, and IL-23 levels. Thus, pediatric TB is characterized by elevated levels of a variety of biomarkers at homeostasis, suggesting that these responses may play a crucial role in disease pathogenesis.
JF  - Clinical and Vaccine Immunology
AU  - Kumar, Nathella Pavan
AU  - Anuradha, R
AU  - Andrade, Bruno B
AU  - Suresh, N
AU  - Ganesh, R
AU  - Shankar, Janani
AU  - Kumaraswami, V
AU  - Nutman, Thomas B
AU  - Babu, Subash
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 704
EP  - 711
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 20
IS  - 5
SN  - 1556-679X, 1556-679X
KW  - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Interleukin 6
KW  - gamma -Interferon
KW  - Interleukin 4
KW  - Interleukin 5
KW  - Interleukin 2
KW  - Mycobacterium
KW  - Fibrosis
KW  - Interleukin 1
KW  - Matrix metalloproteinase
KW  - Homeostasis
KW  - Lipopolysaccharide-binding protein
KW  - Immunomodulation
KW  - Macroglobulins
KW  - Interleukin 10
KW  - Interleukin 12
KW  - Interleukin 13
KW  - Haptoglobin
KW  - Cytokines
KW  - Lipopolysaccharides
KW  - Tuberculosis
KW  - beta -Interferon
KW  - Pediatrics
KW  - Children
KW  - biomarkers
KW  - Inflammation
KW  - Lung
KW  - Transforming growth factor- beta
KW  - alpha -Interferon
KW  - Immune response
KW  - Tumor necrosis factor- alpha
KW  - C-reactive protein
KW  - F 06905:Vaccines
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419368822?accountid=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=Circulating+Biomarkers+of+Pulmonary+and+Extrapulmonary+Tuberculosis+in+Children&rft.au=Kumar%2C+Nathella+Pavan%3BAnuradha%2C+R%3BAndrade%2C+Bruno+B%3BSuresh%2C+N%3BGanesh%2C+R%3BShankar%2C+Janani%3BKumaraswami%2C+V%3BNutman%2C+Thomas+B%3BBabu%2C+Subash&rft.aulast=Kumar&rft.aufirst=Nathella&rft.date=2013-05-01&rft.volume=20&rft.issue=5&rft.spage=704&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=1556679X&rft_id=info:doi/10.1128%2FCVI.00038-13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 51
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Interleukin 6; gamma -Interferon; Interleukin 4; Interleukin 5; Interleukin 2; Fibrosis; Interleukin 1; Matrix metalloproteinase; Homeostasis; Immunomodulation; Lipopolysaccharide-binding protein; Interleukin 10; Macroglobulins; Interleukin 12; Interleukin 13; Haptoglobin; Lipopolysaccharides; Cytokines; Tuberculosis; beta -Interferon; Pediatrics; Children; biomarkers; Inflammation; Lung; alpha -Interferon; Transforming growth factor- beta; Tumor necrosis factor- alpha; Immune response; C-reactive protein; Mycobacterium
DO  - http://dx.doi.org/10.1128/CVI.00038-13
ER  - 



TY  - JOUR
T1  - GRL-0519, a Novel Oxatricyclic Ligand-Containing Nonpeptidic HIV-1 Protease Inhibitor (PI), Potently Suppresses Replication of a Wide Spectrum of Multi-PI-Resistant HIV-1 Variants In Vitro
AN  - 1419365224; 18280097
AB  - We report that GRL-0519, a novel nonpeptidic human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PI) containing tris-tetrahydrofuranylurethane (tris-THF) and a sulfonamide isostere, is highly potent against laboratory HIV-1 strains and primary clinical isolates (50% effective concentration [EC50], 0.0005 to 0.0007 mu M) with minimal cytotoxicity (50% cytotoxic concentration [CC50], 44.6 mu M). GRL-0519 blocked the infectivity and replication of HIV-1NL4-3 variants selected by up to a 5 mu M concentration of ritonavir, lopinavir, or atazanavir (EC50, 0.0028 to 0.0033 mu M). GRL-0519 was also potent against multi-PI-resistant clinical HIV-1 variants isolated from patients who no longer responded to existing antiviral regimens after long-term antiretroviral therapy, highly darunavir (DRV)-resistant variants, and HIV-2ROD. The development of resistance against GRL-0519 was substantially delayed compared to other PIs, including amprenavir (APV) and DRV. The effects of nonspecific binding of human serum proteins on GRL-0519's antiviral activity were insignificant. Our analysis of the crystal structures of GRL-0519 (3OK9) and DRV (2IEN) with protease suggested that the tris-THF moiety, compared to the bis-THF moiety present in DRV, has greater water-mediated polar interactions with key active-site residues of protease and that the tris-THF moiety and paramethoxy group effectively fill the S2 and S2' binding pockets, respectively, of the protease. The present data demonstrate that GRL-0519 has highly favorable features as a potential therapeutic agent for treating patients infected with wild-type and/or multi-PI-resistant variants and that the tris-THF moiety is critical for strong binding of GRL-0519 to the HIV protease substrate binding site and appears to be responsible for its favorable antiretroviral characteristics.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Amano, Masayuki
AU  - Tojo, Yasushi
AU  - Salcedo-Gomez, Pedro Miguel
AU  - Campbell, Joseph Richard
AU  - Das, Debananda
AU  - Aoki, Manabu
AU  - Xu, Chun-Xiao
AU  - Rao, Kalapala Venkateswara
AU  - Ghosh, Arun K
AU  - Mitsuya, Hiroaki
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 2036
EP  - 2046
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 5
SN  - 0066-4804, 0066-4804
KW  - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Clinical isolates
KW  - Data processing
KW  - Replication
KW  - antiretroviral therapy
KW  - Proteinase inhibitors
KW  - Antiviral activity
KW  - Serum proteins
KW  - Infectivity
KW  - Cytotoxicity
KW  - Antiviral agents
KW  - Lopinavir
KW  - Ritonavir
KW  - Human immunodeficiency virus 1
KW  - Crystal structure
KW  - Sulfonamides
KW  - amprenavir
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22360:AIDS and HIV
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419365224?accountid=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=GRL-0519%2C+a+Novel+Oxatricyclic+Ligand-Containing+Nonpeptidic+HIV-1+Protease+Inhibitor+%28PI%29%2C+Potently+Suppresses+Replication+of+a+Wide+Spectrum+of+Multi-PI-Resistant+HIV-1+Variants+In+Vitro&rft.au=Amano%2C+Masayuki%3BTojo%2C+Yasushi%3BSalcedo-Gomez%2C+Pedro+Miguel%3BCampbell%2C+Joseph+Richard%3BDas%2C+Debananda%3BAoki%2C+Manabu%3BXu%2C+Chun-Xiao%3BRao%2C+Kalapala+Venkateswara%3BGhosh%2C+Arun+K%3BMitsuya%2C+Hiroaki&rft.aulast=Amano&rft.aufirst=Masayuki&rft.date=2013-05-01&rft.volume=57&rft.issue=5&rft.spage=2036&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.02189-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 38
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Clinical isolates; Data processing; Replication; Proteinase inhibitors; antiretroviral therapy; Antiviral activity; Serum proteins; Cytotoxicity; Infectivity; Lopinavir; Antiviral agents; Ritonavir; Crystal structure; Sulfonamides; amprenavir; Human immunodeficiency virus 1
DO  - http://dx.doi.org/10.1128/AAC.02189-12
ER  - 



TY  - JOUR
T1  - Theoretical innovations in social and personality psychology and implications for health: Introduction to special issue.
AN  - 1373490192; 201313411
AB  - The goal of this special issue was to highlight major areas of innovation in recent social/personality psychology that hold promise for synergistic integration with health psychology and related fields in the pursuit of adequate health promotion, health care, and population health. The desired outcome is to excite interest and new ways of thinking that, in turn, spawn programs of research poised to advance both theory and practice. Each of the articles reinforces a culture of science in which psychologists of all stripes (social, personality, health, clinical, and others) can work collaboratively to develop stronger models and testable hypotheses with clear applications to enduring health problems. Undergirding this ethos is the observation that much work in the health arena is carried out by multidisciplinary research teams, buttressed by concomitant evidence that "team science" can produce superior outcomes (Hall et al., 2012). [Copyright The American Psychological Association.]
JF  - Health Psychology
AU  - Klein, William M P
AU  - Rothman, Alexander J
AU  - Cameron, Linda D
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 457
EP  - 459
PB  - American Psychological Association, Washington DC
VL  - 32
IS  - 5
SN  - 0278-6133, 0278-6133
KW  - social psychology
KW  - personality psychology
KW  - health psychology
KW  - innovations
KW  - Interdisciplinary team work
KW  - Social psychology
KW  - Occupational health and safety
KW  - Personality
KW  - Health
KW  - Innovations
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373490192?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Psychology&rft.atitle=Theoretical+innovations+in+social+and+personality+psychology+and+implications+for+health%3A+Introduction+to+special+issue.&rft.au=Klein%2C+William+M+P%3BRothman%2C+Alexander+J%3BCameron%2C+Linda+D&rft.aulast=Klein&rft.aufirst=William+M&rft.date=2013-05-01&rft.volume=32&rft.issue=5&rft.spage=457&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fa0032386
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-07-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Health; Personality; Interdisciplinary team work; Social psychology; Innovations; Occupational health and safety
DO  - http://dx.doi.org/10.1037/a0032386
ER  - 



TY  - JOUR
T1  - The Strengths and Difficulties Questionnaire (SDQ): the Factor Structure and Scale Validation in U.S. Adolescents
AN  - 1373489814; 201313143
AB  - The Strengths and Difficulties Questionnaire (SDQ) is one of the most commonly used instruments for screening psychopathology in children and adolescents. This study evaluated the hypothesized five-factor structure of the SDQ and examined its convergent validity against comprehensive clinical diagnostic assessments. Data were derived from the National Comorbidity Survey -- Adolescent Supplement (NCS-A), a nationally representative sample of U.S. adolescents aged 13 to 18 years. Parents/parent surrogates (n=6,483) was asked to complete a self-administered questionnaire including the SDQ and DSM-IV comprehensive diagnostic information on the participating adolescents. Confirmatory factor analysis (CFA) was conducted to assess the factor structure of the SDQ. The five-factor solution of the SDQ (including emotional, conduct, hyperactivity-inattention, peer relationship, and prosocial) provided a satisfactory fit to the data, and was invariant across sex, age, race/ethnicity and income subgroups. SDQ scores predicted a significantly increased probability of meeting criteria for a DSM-IV disorder, with better prediction for behavior disorders than for mood disorders. Decreasing the SDQ cutoffs to the 80th percentile significantly increased the sensitivity from 39% to 63% for the SDQ Total Difficulties Score, with an expected decrease in specificity from 93% to 87%. This work confirms the five-factor structure of the SDQ in an ethnically and sociodemogrpahically diverse community sample of adolescents. Our findings strengthen empirical evidence for the use of the parent-reported SDQ as a screening tool for DSM-IV behavioral and emotional disorders in adolescents identified in the general population.
JF  - Journal of Abnormal Child Psychology
AU  - He, Jian-Ping
AU  - Burstein, Marcy
AU  - Schmitz, Anja
AU  - Merikangas, Kathleen R
AD  - Genetic Epidemiology Research Branch, Intramural Research Program, National Institute of Mental Health, Building 35, Room 1A201, 35 Convent Drive, MSC #3720, Bethesda, MD, 20892, USA
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 583
EP  - 595
PB  - Springer, Dordrecht The Netherlands
VL  - 41
IS  - 4
SN  - 0091-0627, 0091-0627
KW  - Screening
KW  - Clinical assessment
KW  - Prosocial behaviour
KW  - Parents
KW  - Adolescents
KW  - Factor structures
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373489814?accountid=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=The+Strengths+and+Difficulties+Questionnaire+%28SDQ%29%3A+the+Factor+Structure+and+Scale+Validation+in+U.S.+Adolescents&rft.au=He%2C+Jian-Ping%3BBurstein%2C+Marcy%3BSchmitz%2C+Anja%3BMerikangas%2C+Kathleen+R&rft.aulast=He&rft.aufirst=Jian-Ping&rft.date=2013-05-01&rft.volume=41&rft.issue=4&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-012-9696-6
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-07-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JAPCAC
N1  - SubjectsTermNotLitGenreText - Adolescents; Clinical assessment; Parents; Factor structures; Screening; Prosocial behaviour
DO  - http://dx.doi.org/10.1007/s10802-012-9696-6
ER  - 



TY  - JOUR
T1  - Modulating the endocannabinoid system in human health and disease - successes and failures
AN  - 1367486161; 17981031
AB  - The discovery of the endocannabinoid system, comprising the G-protein coupled cannabinoid 1 and 2 receptors (CB1/2), their endogenous lipid ligands or endocannabinoids, and synthetic and metabolizing enzymes, has triggered an avalanche of experimental studies implicating the endocannabinoid system in a growing number of physiological/pathological functions. These studies have also suggested that modulating the activity of the endocannabinoid system holds therapeutic promise for a broad range of diseases, including neurodegenerative, cardiovascular and inflammatory disorders; obesity/metabolic syndrome; cachexia; chemotherapy-induced nausea and vomiting; and tissue injury and pain, amongst others. However, clinical trials with globally acting CB1 antagonists in obesity/metabolic syndrome, and other studies with peripherally-restricted CB1/2 agonists and inhibitors of the endocannabinoid metabolizing enzyme in pain, have introduced unexpected complexities, suggesting that a better understanding of the pathophysiological role of the endocannabinoid system is required to devise clinically successful treatment strategies. Modulating the endocannabinoid system (ECS) holds therapeutic potential in a broad range of diseases affecting humans. However, the successful translation of preclinical findings to clinical practice depends on finding the right balance between desirable and undesirable consequences of targeting this system, and on precise understanding the pathological role of the ECS in various diseases and of endocannabinoid pharmacology.
JF  - FEBS Journal
AU  - Pacher, Pal
AU  - Kunos, George
AD  - Laboratory of Physiologic Studies. National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1918
EP  - 1943
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 280
IS  - 9
SN  - 1742-464X, 1742-464X
KW  - Health & Safety Science Abstracts
KW  - Obesity
KW  - Avalanches
KW  - Pharmacology
KW  - Metabolic disorders
KW  - Lipids
KW  - Enzymes
KW  - Pain
KW  - Clinical trials
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367486161?accountid=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=FEBS+Journal&rft.atitle=Modulating+the+endocannabinoid+system+in+human+health+and+disease+-+successes+and+failures&rft.au=Pacher%2C+Pal%3BKunos%2C+George&rft.aulast=Pacher&rft.aufirst=Pal&rft.date=2013-05-01&rft.volume=280&rft.issue=9&rft.spage=1918&rft.isbn=&rft.btitle=&rft.title=FEBS+Journal&rft.issn=1742464X&rft_id=info:doi/10.1111%2Ffebs.12260
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-08-17
N1  - SubjectsTermNotLitGenreText - Obesity; Avalanches; Pharmacology; Lipids; Metabolic disorders; Enzymes; Pain; Clinical trials
DO  - http://dx.doi.org/10.1111/febs.12260
ER  - 



TY  - JOUR
T1  - The relationship between large cavum septum pellucidum and antisocial behavior, callous-unemotional traits and psychopathy in adolescents
AN  - 1364767743; 201311908
AB  - Background: The presence of a large cavum septum pellucidum (CSP) has been previously associated with antisocial behavior/psychopathic traits in an adult community sample. Aims: The current study investigated the relationship between a large CSP and symptom severity in disruptive behavior disorders (DBD; conduct disorder and oppositional defiant disorder). Method: Structural MRI scans of youth with DBDs (N=32) and healthy comparison youth (N=27) were examined for the presence of a large CSP and if this was related to symptom severity. Results: Replicating previous results, a large CSP was associated with DBD diagnosis, proactive aggression, and level of psychopathic traits in youth. However, the presence of a large CSP was unrelated to aggression or psychopathic traits within the DBD sample. Conclusions: Early brain mal-development may increase the risk of a DBD diagnosis, but does not mark a particularly severe form of DBD within patients receiving these diagnoses. Adapted from the source document.
JF  - The Journal of Child Psychology and Psychiatry
AU  - White, Stuart F
AU  - Brislin, Sarah
AU  - Sinclair, Stephen
AU  - Fowler, Katherine A
AU  - Pope, Kayla
AU  - Blair, R James R
AD  - Unit on Affective Cognitive Neuroscience, National Institute of Mental Health, NIH, Bethesda, MD, USA
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 575
EP  - 581
PB  - Blackwell Publishing, Oxford UK
VL  - 54
IS  - 5
SN  - 0021-9630, 0021-9630
KW  - Symptoms
KW  - Severity
KW  - Diagnosis
KW  - Psychopathy
KW  - Antisocial behaviour
KW  - Aggression
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364767743?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Child+Psychology+and+Psychiatry&rft.atitle=The+relationship+between+large+cavum+septum+pellucidum+and+antisocial+behavior%2C+callous-unemotional+traits+and+psychopathy+in+adolescents&rft.au=White%2C+Stuart+F%3BBrislin%2C+Sarah%3BSinclair%2C+Stephen%3BFowler%2C+Katherine+A%3BPope%2C+Kayla%3BBlair%2C+R+James+R&rft.aulast=White&rft.aufirst=Stuart&rft.date=2013-05-01&rft.volume=54&rft.issue=5&rft.spage=575&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2012.02603.x
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JPPDAI
N1  - SubjectsTermNotLitGenreText - Psychopathy; Aggression; Symptoms; Antisocial behaviour; Diagnosis; Severity
DO  - http://dx.doi.org/10.1111/j.1469-7610.2012.02603.x
ER  - 



TY  - JOUR
T1  - Basic traits predict the prevalence of personality disorder across the life span: the example of psychopathy
AN  - 1364721991; 4444779
AB  - Personality disorders (PDs) may be better understood in terms of dimensions of general personality functioning rather than as discrete categorical conditions. Personality-trait descriptions of PDs are robust across methods and settings, and PD assessments based on trait measures show good construct validity. The study reported here extends research showing that basic traits (e.g., impulsiveness, warmth, straightforwardness, modesty, and deliberation) can re-create the epidemiological characteristics associated with PDs. Specifically, we used normative changes in absolute trait levels to simulate age-related differences in the prevalence of psychopathy in a forensic setting. Results demonstrated that trait information predicts the rate of decline for psychopathy over the life span; discriminates the decline of psychopathy from that of a similar disorder, antisocial PD; and accurately predicts the differential decline of subfactors of psychopathy. These findings suggest that basic traits provide a parsimonious account of PD prevalence across the life span. Reprinted by permission of Sage Publications
JF  - Psychological science
AU  - Vachon, David D
AU  - Lynam, Donald R
AU  - Widiger, Thomas A
AU  - Miller, Joshua D
AU  - McCrae, Robert R
AU  - Costa, Paul T
AD  - Purdue University ; University of Kentucky ; University of Georgia ; National Institutes of Health ; Johns Hopkins University
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 698
EP  - 705
VL  - 24
IS  - 5
SN  - 0956-7976, 0956-7976
KW  - Sociology
KW  - Anti-social behaviour
KW  - Epidemiology
KW  - Personality traits
KW  - Personality
KW  - Psychopathology
KW  - Personality disorders
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364721991?accountid=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=Psychological+science&rft.atitle=Basic+traits+predict+the+prevalence+of+personality+disorder+across+the+life+span%3A+the+example+of+psychopathy&rft.au=Vachon%2C+David+D%3BLynam%2C+Donald+R%3BWidiger%2C+Thomas+A%3BMiller%2C+Joshua+D%3BMcCrae%2C+Robert+R%3BCosta%2C+Paul+T&rft.aulast=Vachon&rft.aufirst=David&rft.date=2013-05-01&rft.volume=24&rft.issue=5&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=Psychological+science&rft.issn=09567976&rft_id=info:doi/10.1177%2F0956797612460249
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 9423 10412 7951 6220 7954; 9416 2153; 1121 11776; 10409; 4357 7894; 9429 9416 2153
DO  - http://dx.doi.org/10.1177/0956797612460249
ER  - 



TY  - JOUR
T1  - Inhibition of TGF- beta signaling in genetically engineered tumor antigen-reactive T cells significantly enhances tumor treatment efficacy
AN  - 1356929406; 18014295
AB  - Transforming growth factor beta (TGF- beta ) is a cytokine with complex biological functions that may involve tumor promotion or tumor suppression. It has been reported that multiple types of tumors secrete TGF- beta , which can inhibit tumor-specific cellular immunity and may represent a major obstacle to the success of tumor immunotherapy. In this study, we sought to enhance tumor immunotherapy using genetically modified antigen-specific T cells by interfering with TGF- beta signaling. We constructed three gamma -retroviral vectors, one that expressed TGF- beta -dominant-negative receptor II (DNRII) or two that secreted soluble TGF- beta receptors: soluble TGF- beta receptor II (sRII) and the sRII fused with mouse IgG Fc domain (sRIIFc). We demonstrated that T cells genetically modified with these viral vectors were resistant to exogenous TGF- beta -induced smad-2 phosphorylation in vitro. The functionality of antigen-specific T cells engineered to resist TGF- beta signaling was further evaluated in vivo using the B16 melanoma tumor model. Antigen-specific CD8+ T cells (pmel-1) or CD4+ T cells (tyrosinase-related protein-1) expressing DNRII dramatically improved tumor treatment efficacy. There was no enhancement in the B16 tumor treatment using cells secreting soluble receptors. Our data support the potential application of the blockade of TGF- beta signaling in tumor-specific T cells for cancer immunotherapy.
JF  - Gene Therapy
AU  - Zhang, L
AU  - Yu, Z
AU  - Muranski, P
AU  - Palmer, D C
AU  - Restifo, N P
AU  - Rosenberg, S A
AU  - Morgan, R A
AD  - Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 575
EP  - 580
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 20
IS  - 5
SN  - 0969-7128, 0969-7128
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - Gene therapy
KW  - Immunotherapy
KW  - Tumorigenesis
KW  - Animal models
KW  - CD8 antigen
KW  - Cancer
KW  - Fc receptors
KW  - Melanoma
KW  - CD4 antigen
KW  - Immunity (cell-mediated)
KW  - Phosphorylation
KW  - Genetic engineering
KW  - Transforming growth factor- beta
KW  - Lymphocytes T
KW  - Immunoglobulin G
KW  - Cytokines
KW  - G 07720:Immunogenetics
KW  - W 30905:Medical Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1356929406?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+TGF-+beta+signaling+in+genetically+engineered+tumor+antigen-reactive+T+cells+significantly+enhances+tumor+treatment+efficacy&rft.au=Zhang%2C+L%3BYu%2C+Z%3BMuranski%2C+P%3BPalmer%2C+D+C%3BRestifo%2C+N+P%3BRosenberg%2C+S+A%3BMorgan%2C+R+A&rft.aulast=Zhang&rft.aufirst=L&rft.date=2013-05-01&rft.volume=20&rft.issue=5&rft.spage=575&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2012.75
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2017-02-01
N1  - SubjectsTermNotLitGenreText - Data processing; Gene therapy; Immunotherapy; Tumorigenesis; Animal models; CD8 antigen; Cancer; Melanoma; Fc receptors; CD4 antigen; Phosphorylation; Immunity (cell-mediated); Genetic engineering; Transforming growth factor- beta; Immunoglobulin G; Lymphocytes T; Cytokines
DO  - http://dx.doi.org/10.1038/gt.2012.75
ER  - 



TY  - JOUR
T1  - Arsenic Exposure and Incidence of Type 2 Diabetes in Southwestern American Indians
AN  - 1356928725; 17998511
AB  - Association of urinary arsenic concentration with incident diabetes was examined in American Indians from Arizona who have a high prevalence of type 2 diabetes and were screened for diabetes between 1982 and 2007. The population resides where drinking water contains arsenic at concentrations above federally recommended limits. A total of 150 nondiabetic subjects aged greater than or equal to 25 years who subsequently developed type 2 diabetes were matched by year of examination and sex to 150 controls who remained nondiabetic for greater than or equal to 10 years. Total urinary arsenic concentration, adjusted for urinary creatinine level, ranged from 6.6 mu g/L to 123.1 mu g/L, and inorganic arsenic concentration ranged from 0.1 mu g/L to 36.0 mu g/L. In logistic regression models adjusted for age, sex, body mass index, and urinary creatinine level, the odds ratios for incident diabetes were 1.11 (95% confidence interval (CI): 0.79, 1.57) and 1.16 (95% CI: 0.89, 1.53) for a 2-fold increase in total arsenic and inorganic arsenic, respectively. Categorical analyses suggested a positive relationship between quartiles of inorganic arsenic and incident diabetes (P = 0.056); post-hoc comparison of quartiles 2-4 with quartile 1 revealed 2-fold higher odds of diabetes in the upper quartiles (OR = 2.14, 95% CI: 1.19, 3.85). Modestly elevated exposure to inorganic arsenic may predict type 2 diabetes in American Indians. Larger studies that include measures of speciated arsenic are required for confirmation.
JF  - American Journal of Epidemiology
AU  - Kim, Nan Hee
AU  - Mason, Clinton C
AU  - Nelson, Robert G
AU  - Afton, Scott E
AU  - Essader, Amal S
AU  - Medlin, James E
AU  - Levine, Keith E
AU  - Hoppin, Jane A
AU  - Lin, Cynthia
AU  - Knowler, William C
AU  - Sandler, Dale P
AD  - Correspondence to Dr. Robert G. Nelson, National Institutes of Health, 1550 East Indian School Road, Phoenix, AZ 85014-4972., rnelson@nih.gov
Y1  - 2013/05/01/
PY  - 2013
DA  - 2013 May 01
SP  - 962
EP  - 969
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 9
SN  - 0002-9262, 0002-9262
KW  - Toxicology Abstracts; Health & Safety Science Abstracts
KW  - arsenic
KW  - diabetes mellitus, type 2
KW  - incidence
KW  - Indians, North American
KW  - nested case-control studies
KW  - Age
KW  - Arsenic
KW  - Body mass
KW  - Models
KW  - Diabetes mellitus
KW  - Creatinine
KW  - Urine
KW  - Regression analysis
KW  - USA, Arizona
KW  - Drinking water
KW  - Body mass index
KW  - Ethnic groups
KW  - Sex
KW  - H 3000:Environment and Ecology
KW  - X 24360:Metals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1356928725?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Arsenic+Exposure+and+Incidence+of+Type+2+Diabetes+in+Southwestern+American+Indians&rft.au=Kim%2C+Nan+Hee%3BMason%2C+Clinton+C%3BNelson%2C+Robert+G%3BAfton%2C+Scott+E%3BEssader%2C+Amal+S%3BMedlin%2C+James+E%3BLevine%2C+Keith+E%3BHoppin%2C+Jane+A%3BLin%2C+Cynthia%3BKnowler%2C+William+C%3BSandler%2C+Dale+P&rft.aulast=Kim&rft.aufirst=Nan&rft.date=2013-05-01&rft.volume=177&rft.issue=9&rft.spage=962&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws329
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Diabetes mellitus; Arsenic; Creatinine; Regression analysis; Body mass index; Drinking water; Models; Sex; Age; Urine; Body mass; Ethnic groups; USA, Arizona
DO  - http://dx.doi.org/10.1093/aje/kws329
ER  - 



TY  - JOUR
T1  - Information seeking from media and family/friends increases the likelihood of engaging in healthy lifestyle behaviors
AN  - 1353279849; 4439637
AB  - The amount of cancer-related information available to the general population continues to grow; yet, its effects are unclear. This study extends previous cross-sectional research establishing that cancer information seeking across a variety of sources is extensive and positively associated with engaging in health-related behaviors. The authors studied how active information seeking about cancer prevention influenced three healthy lifestyle behaviors using a 2-round nationally representative sample of adults ages 40-70 years (n = 1,795), using propensity scoring to control for potential confounders including baseline behavior. The adjusted odds of dieting at follow-up were 1.51 (95% CI: 1.05, 2.19) times higher for those who reported baseline seeking from media and interpersonal sources relative to nonseekers. Baseline seekers ate 0.59 (95% CI: 0.28, 0.91) more fruits and vegetable servings per day and exercised 0.36 (95% CI: 0.12, 0.60) more days per week at 1-year follow-up compared with nonseekers. The effects of seeking from media and friends/family on eating fruits and vegetables and exercising were independent of seeking from physicians. The authors offer several explanations for why information seeking predicts healthy lifestyle behaviors: information obtained motivates these behaviors; information sought teaches specific techniques; and the act of information seeking may reinforce a psychological commitment to dieting, eating fruits and vegetables, and exercising. Reprinted by permission of Taylor & Francis Ltd.
JF  - Journal of health communication
AU  - Ramírez, A Susana
AU  - Freres, Derek
AU  - Martinez, Lourdes S
AU  - Lewis, Nehama
AU  - Bourgoin, Angel
AU  - Kelly, Bridget J
AU  - Lee, Chul-joo
AU  - Nagler, Rebekah
AU  - Schwartz, J Sanford
AU  - Hornik, Robert C
AD  - National Cancer Institute ; University of Pennsylvania ; Michigan State University ; Florida International University ; RTI International ; Ohio State University ; Dana-Farber Cancer Institute
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 527
EP  - 542
VL  - 18
IS  - 5
SN  - 1081-0730, 1081-0730
KW  - Sociology
KW  - Media
KW  - Health
KW  - Cross-sectional analysis
KW  - Adults
KW  - Life styles
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1353279849?accountid=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=Information+seeking+from+media+and+family%2Ffriends+increases+the+likelihood+of+engaging+in+healthy+lifestyle+behaviors&rft.au=Ram%C3%ADrez%2C+A+Susana%3BFreres%2C+Derek%3BMartinez%2C+Lourdes+S%3BLewis%2C+Nehama%3BBourgoin%2C+Angel%3BKelly%2C+Bridget+J%3BLee%2C+Chul-joo%3BNagler%2C+Rebekah%3BSchwartz%2C+J+Sanford%3BHornik%2C+Robert+C&rft.aulast=Ram%C3%ADrez&rft.aufirst=A&rft.date=2013-05-01&rft.volume=18&rft.issue=5&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2012.743632
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 7862 2572; 1939 3617 6220; 3063 971; 5772; 603; 7404
DO  - http://dx.doi.org/10.1080/10810730.2012.743632
ER  - 



TY  - JOUR
T1  - Cancer patient and survivor research from the cancer information service research consortium: a preview of three large randomized trials and initial lessons learned
AN  - 1353279679; 4439635
AB  - The authors describe 3 large randomized trials from the Cancer Information Service Research Consortium. Three web-based multimedia programs are being tested to help newly diagnosed prostate (Project 1) and breast cancer patients (Project 2) make informed treatment decisions and breast cancer patients prepare for life after treatment (Project 3). Project 3 also tests a telephone callback intervention delivered by a cancer information specialist. All participants receive standard print material specific to each project. Preliminary results from the 2-month follow-up interviews are reported for the initial wave of enrolled participants, most of whom were recruited from the Cancer Information Service (1-800-4-CANCER) telephone information program (Project 1: n =208; Project 2: n =340; Project 3: n =792). Self- reported use of the multimedia program was 51%, 52%, and 67% for Projects 1, 2, and 3, respectively. Self-reported use of the print materials (read all, most, or some) was 90%, 85%, and 83% for Projects 1, 2, and 3, respectively. The callback intervention was completed by 92% of Project 3 participants. Among those using the Cancer Information Service Research Consortium interventions, perceived usefulness and benefit was high, and more than 90% reported that they would recommend them to other cancer patients. The authors present 5 initial lessons learned that may help inform future cancer communications research. Reprinted by permission of Taylor & Francis Ltd.
JF  - Journal of health communication
AU  - Marcus, Alfred C
AU  - Diefenbach, Michael A
AU  - Stanton, Annette L
AU  - Miller, Suzanne M
AU  - Fleisher, Linda
AU  - Raich, Peter C
AU  - Morra, Marion E
AU  - Perocchia, Rosemarie Slevin
AU  - Tran, Zung Vu
AU  - Bright, Mary Anne
AD  - University of Colorado ; Icahn School of Medicine ; University of California, Los Angeles ; Fox Chase Cancer Center ; Denver Health and Hospital Authority ; Yale University ; Memorial Sloan-Kettering Cancer Center ; National Cancer Institute
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 543
EP  - 562
VL  - 18
IS  - 5
SN  - 1081-0730, 1081-0730
KW  - Sociology
KW  - Telephone
KW  - Information services
KW  - Patients
KW  - Interviews
KW  - Communication research
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1353279679?accountid=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=Cancer+patient+and+survivor+research+from+the+cancer+information+service+research+consortium%3A+a+preview+of+three+large+randomized+trials+and+initial+lessons+learned&rft.au=Marcus%2C+Alfred+C%3BDiefenbach%2C+Michael+A%3BStanton%2C+Annette+L%3BMiller%2C+Suzanne+M%3BFleisher%2C+Linda%3BRaich%2C+Peter+C%3BMorra%2C+Marion+E%3BPerocchia%2C+Rosemarie+Slevin%3BTran%2C+Zung+Vu%3BBright%2C+Mary+Anne&rft.aulast=Marcus&rft.aufirst=Alfred&rft.date=2013-05-01&rft.volume=18&rft.issue=5&rft.spage=543&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2012.743629
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 1939 3617 6220; 9271 7890 5792 10484; 2582 10902; 6532 6515; 12647 12641 2572; 6832 10919
DO  - http://dx.doi.org/10.1080/10810730.2012.743629
ER  - 



TY  - JOUR
T1  - The Simmune Modeler visual interface for creating signaling networks based on bi-molecular interactions
AN  - 1352292889; 17998533
AB  - Motivation: Biochemical modeling efforts now frequently take advantage of the possibility to automatically create reaction networks based on the specification of pairwise molecular interactions. Even though a variety of tools exist to visualize the resulting networks, defining the rules for the molecular interactions typically requires writing scripts, which impacts the non-specialist accessibility of those approaches. We introduce the Simmune Modeler that allows users to specify molecular complexes and their interactions as well as the reaction-induced modifications of the molecules through a flexible visual interface. It can take into account the positions of the components of trans-membrane complexes relative to the embedding membranes as well as symmetry aspects affecting the reactions of multimeric molecular structures. Models created with this tool can be simulated using the Simmune Simulator or be exported as SBML code or as files describing the reaction networks as systems of ODEs for import into Matlab.
JF  - Bioinformatics
AU  - Zhang, Fengkai
AU  - Angermann, Bastian R
AU  - Meier-Schellersheim, Martin
AD  - Computational Biology Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA
Y1  - 2013/05/01/
PY  - 2013
DA  - 2013 May 01
SP  - 1229
EP  - 1230
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 9
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Computer programs
KW  - Data processing
KW  - Bioinformatics
KW  - Embedding
KW  - Internet
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352292889?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+Simmune+Modeler+visual+interface+for+creating+signaling+networks+based+on+bi-molecular+interactions&rft.au=Zhang%2C+Fengkai%3BAngermann%2C+Bastian+R%3BMeier-Schellersheim%2C+Martin&rft.aulast=Zhang&rft.aufirst=Fengkai&rft.date=2013-05-01&rft.volume=29&rft.issue=9&rft.spage=1229&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt134
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Computer programs; Data processing; Bioinformatics; Embedding; Internet
DO  - http://dx.doi.org/10.1093/bioinformatics/btt134
ER  - 



TY  - JOUR
T1  - Structural equation modeling of the inflammatory response to traffic air pollution
AN  - 1352285603; 17945113
AB  - Several epidemiological studies have reported conflicting results on the effect of traffic-related pollutants on markers of inflammation. In a Bayesian framework, we examined the effect of traffic pollution on inflammation using structural equation models (SEMs). We studied measurements of C-reactive protein (CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble intracellular adhesion molecule-1 (sICAM-1) for 749 elderly men from the Normative Aging Study. Using repeated measures SEMs, we fit a latent variable for traffic pollution that is reflected by levels of black carbon, carbon monoxide, nitrogen monoxide and nitrogen dioxide to estimate its effect on a latent variable for inflammation that included sICAM-1, sVCAM-1 and CRP. Exposure periods were assessed using 1-, 2-, 3-, 7-, 14- and 30-day moving averages previsit. We compared our findings using SEMs with those obtained using linear mixed models. Traffic pollution was related to increased inflammation for 3-, 7-, 14- and 30-day exposure periods. An inter-quartile range increase in traffic pollution was associated with a 2.3% (95% posterior interval (PI): 0.0-4.7%) increase in inflammation for the 3-day moving average, with the most significant association observed for the 30-day moving average (23.9%; 95% PI: 13.9-36.7%). Traffic pollution adversely impacts inflammation in the elderly. SEMs in a Bayesian framework can comprehensively incorporate multiple pollutants and health outcomes simultaneously in air pollution-cardiovascular epidemiological studies.
JF  - Journal of Exposure Science and Environmental Epidemiology
AU  - Baja, Emmanuel S
AU  - Schwartz, Joel D
AU  - Coull, Brent A
AU  - Wellenuis, Gregory A
AU  - Vokonas, Pantel S
AU  - Suh, Helen H
AD  - 1] Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA [2] Institute of Clinical Epidemiology, National Institutes of Health University of the Philippines, Manila, Philippines
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 268
EP  - 274
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 23
IS  - 3
SN  - 1559-0631, 1559-0631
KW  - Pollution Abstracts; Meteorological & Geoastrophysical Abstracts; Toxicology Abstracts; Health & Safety Science Abstracts
KW  - Adhesion
KW  - Atmospheric pollution models
KW  - Traffic
KW  - Inflammation
KW  - P 0000:AIR POLLUTION
KW  - X:24300
KW  - M2:551.510.42
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352285603?accountid=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=Structural+equation+modeling+of+the+inflammatory+response+to+traffic+air+pollution&rft.au=Baja%2C+Emmanuel+S%3BSchwartz%2C+Joel+D%3BCoull%2C+Brent+A%3BWellenuis%2C+Gregory+A%3BVokonas%2C+Pantel+S%3BSuh%2C+Helen+H&rft.aulast=Baja&rft.aufirst=Emmanuel&rft.date=2013-05-01&rft.volume=23&rft.issue=3&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2012.106
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Inflammation; Atmospheric pollution models; Traffic
DO  - http://dx.doi.org/10.1038/jes.2012.106
ER  - 



TY  - JOUR
T1  - Ordinal latent variable models and their application in the study of newly licensed teenage drivers
AN  - 1349395169; 4434636
AB  - Summary. In a unique longitudinal study of teen driving, risky driving behaviour and the occurrence of crashes or near crashes are measured prospectively over the first 18 months of licensure. Of scientific interest is relating the two processes and developing a predictor of crashes from previous risky driving behaviour. In this work, we propose two latent class models for relating risky driving behaviour to the occurrence of a crash or near-crash event. The first approach models the binary longitudinal crash or near-crash outcome by using a binary latent variable which depends on risky driving covariates and previous outcomes. A random-effects model introduces heterogeneity among subjects in modelling the mean value of the latent state. The second approach extends the first model to the ordinal case where the latent state is composed of K ordinal classes. Additionally, we discuss an alternative hidden Markov model formulation. Estimation is performed by using the expectation-maximization algorithm and Monte Carlo expectation-maximization. We illustrate the importance of using these latent class modelling approaches through the analysis of the teen driving behaviour. Reprinted by permission of Blackwell Publishers
JF  - Journal of the Royal Statistical Society
AU  - Zhang, Zhiwei
AU  - Simons-Morton, Bruce
AU  - Jackson, John C
AU  - Albert, Paul S
AD  - United States Military Academy at West Point ; National Institutes of Health
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 435
EP  - 450
VL  - 62
IS  - 3
SN  - 0035-9254, 0035-9254
KW  - Sociology
KW  - Monte Carlo simulation
KW  - Longitudinal studies
KW  - Stochastic models
KW  - Algorithms
KW  - Human behaviour
KW  - Adolescents
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349395169?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=Ordinal+latent+variable+models+and+their+application+in+the+study+of+newly+licensed+teenage+drivers&rft.au=Zhang%2C+Zhiwei%3BSimons-Morton%2C+Bruce%3BJackson%2C+John+C%3BAlbert%2C+Paul+S&rft.aulast=Zhang&rft.aufirst=Zhiwei&rft.date=2013-05-01&rft.volume=62&rft.issue=3&rft.spage=435&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=00359254&rft_id=info:doi/10.1111%2Fj.1467-9876.2012.01065.x
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 593; 7541 7537 971; 918 7824; 12263 8163; 8268 12265 3865 4025 10214 12224 971 12228 10919; 6071 1542 11325
DO  - http://dx.doi.org/10.1111/j.1467-9876.2012.01065.x
ER  - 



TY  - JOUR
T1  - Genetic variants in sex hormone metabolic pathway genes and risk of esophageal squamous cell carcinoma.
AN  - 1349093406; 23358850
AB  - In China, esophageal cancer is the fourth leading cause of cancer death where essentially all cases are histologically esophageal squamous cell carcinoma (ESCC), in contrast to esophageal adenocarcinoma in the West. Globally, ESCC is 2.4 times more common among men than women and recently it has been suggested that sex hormones may be associated with the risk of ESCC. We examined the association between genetic variants in sex hormone metabolic genes and ESCC risk in a population from north central China with high-incidence rates. A total of 1026 ESCC cases and 1452 controls were genotyped for 797 unique tag single-nucleotide polymorphisms (SNPs) in 51 sex hormone metabolic genes. SNP-, gene- and pathway-based associations with ESCC risk were evaluated using unconditional logistic regression adjusted for age, sex and geographical location and the adaptive rank truncated product (ARTP) method. Statistical significance was determined through use of permutation for pathway- and gene-based associations. No associations were observed for the overall sex hormone metabolic pathway (P = 0.14) or subpathways (androgen synthesis: P = 0.30, estrogen synthesis: P = 0.15 and estrogen removal: P = 0.19) with risk of ESCC. However, six individual genes (including SULT2B1, CYP1B1, CYP3A7, CYP3A5, SHBG and CYP11A1) were significantly associated with ESCC risk (P < 0.05). Our examination of genetic variation in the sex hormone metabolic pathway is consistent with a potential association with risk of ESCC. These positive findings warrant further evaluation in relation to ESCC risk and replication in other populations.
JF  - Carcinogenesis
AU  - Hyland, Paula L
AU  - Freedman, Neal D
AU  - Hu, Nan
AU  - Tang, Ze-Zhong
AU  - Wang, Lemin
AU  - Wang, Chaoyu
AU  - Ding, Ti
AU  - Fan, Jin-Hu
AU  - Qiao, You-Lin
AU  - Golozar, Asieh
AU  - Wheeler, William
AU  - Yu, Kai
AU  - Yuenger, Jeff
AU  - Burdett, Laurie
AU  - Chanock, Stephen J
AU  - Dawsey, Sanford M
AU  - Tucker, Margaret A
AU  - Goldstein, Alisa M
AU  - Abnet, Christian C
AU  - Taylor, Philip R
AD  - Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Institutes of Health, Rockville, MA 20852, USA.hylandpl@mail.nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1062
EP  - 1068
VL  - 34
IS  - 5
KW  - Gonadal Steroid Hormones
KW  - 0
KW  - Index Medicus
KW  - Metabolic Networks and Pathways -- genetics
KW  - Polymorphism, Single Nucleotide
KW  - Stomach Neoplasms -- metabolism
KW  - Humans
KW  - Genotype
KW  - Stomach Neoplasms -- genetics
KW  - Risk Factors
KW  - Case-Control Studies
KW  - Incidence
KW  - Middle Aged
KW  - Genetic Predisposition to Disease
KW  - Stomach Neoplasms -- etiology
KW  - China
KW  - Female
KW  - Male
KW  - Gonadal Steroid Hormones -- genetics
KW  - Carcinoma, Squamous Cell -- etiology
KW  - Esophageal Neoplasms -- metabolism
KW  - Esophageal Neoplasms -- genetics
KW  - Carcinoma, Squamous Cell -- genetics
KW  - Gonadal Steroid Hormones -- metabolism
KW  - Carcinoma, Squamous Cell -- metabolism
KW  - Esophageal Neoplasms -- etiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349093406?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+variants+in+sex+hormone+metabolic+pathway+genes+and+risk+of+esophageal+squamous+cell+carcinoma.&rft.au=Hyland%2C+Paula+L%3BFreedman%2C+Neal+D%3BHu%2C+Nan%3BTang%2C+Ze-Zhong%3BWang%2C+Lemin%3BWang%2C+Chaoyu%3BDing%2C+Ti%3BFan%2C+Jin-Hu%3BQiao%2C+You-Lin%3BGolozar%2C+Asieh%3BWheeler%2C+William%3BYu%2C+Kai%3BYuenger%2C+Jeff%3BBurdett%2C+Laurie%3BChanock%2C+Stephen+J%3BDawsey%2C+Sanford+M%3BTucker%2C+Margaret+A%3BGoldstein%2C+Alisa+M%3BAbnet%2C+Christian+C%3BTaylor%2C+Philip+R&rft.aulast=Hyland&rft.aufirst=Paula&rft.date=2013-05-01&rft.volume=34&rft.issue=5&rft.spage=1062&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt030
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-30
N1  - Date created - 2013-05-06
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Natl Cancer Inst. 1992 May 20;84(10):771-6 [1573663]
Cancer Res. 1990 Nov 15;50(22):7212-5 [2224855]
Cancer Causes Control. 1993 May;4(3):195-202 [8318635]
Cancer Res. 1994 Apr 1;54(7 Suppl):2029s-2031s [8137333]
Ann Epidemiol. 1993 Nov;3(6):577-85 [7921303]
Int J Cancer. 2005 Jan 20;113(3):456-63 [15455378]
Endocr Rev. 2004 Dec;25(6):947-70 [15583024]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078]
World J Gastroenterol. 2005 May 7;11(17):2531-8 [15849806]
Gut. 2005 Jun;54(6):759-63 [15888779]
Cancer Lett. 2005 Jul 28;225(2):275-82 [15978331]
Pharmacogenomics. 2005 Jun;6(4):357-71 [16004554]
Eur J Cancer. 2007 May;43(7):1188-99 [17383866]
Clin Cancer Res. 2007 Jul 15;13(14):4046-50 [17634528]
J Pharmacol Exp Ther. 2007 Aug;322(2):529-40 [17496163]
Int J Cancer. 2007 Oct 15;121(8):1643-58 [17674367]
Curr Protoc Bioinformatics. 2005 Oct;Chapter 1:Unit 1.12 [18428742]
Dis Esophagus. 2008;21(4):298-303 [18477250]
Endocr Dev. 2008;13:1-18 [18493130]
Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3490-8 [19064566]
Carcinogenesis. 2009 Jan;30(1):71-7 [19015200]
Clin Endocrinol (Oxf). 2009 Feb;70(2):303-10 [18681858]
J Clin Endocrinol Metab. 2009 Mar;94(3):1033-41 [19116238]
Gastroenterology. 2009 Apr;136(4):1215-24, e1-2 [19250648]
J Natl Cancer Inst. 2009 Apr 1;101(7):507-18 [19318634]
Clin Chim Acta. 2010 Jan;411(1-2):53-8 [19818337]
Genet Epidemiol. 2009 Dec;33(8):700-9 [19333968]
Cytogenet Genome Res. 2009;126(3):243-52 [20068295]
Biochem Biophys Res Commun. 2010 Jan 29;392(1):29-35 [20043878]
World J Surg Oncol. 2010;8:9 [20146809]
Cancer. 2010 Mar 15;116(6):1572-81 [20186831]
Carcinogenesis. 2010 May;31(5):827-33 [20053928]
Breast Cancer Res. 2010;12(2):R19 [20214802]
Dis Esophagus. 2010 Jul;23(5):392-7 [19903195]
Nat Genet. 2010 Sep;42(9):764-7 [20729852]
Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269]
Med Oncol. 2011 Mar;28(1):188-93 [20195802]
Cancer Prev Res (Phila). 2011 Jun;4(6):840-50 [21505180]
Endocr Relat Cancer. 2011 Jun;18(3):371-84 [21490239]
Cancer Epidemiol. 2011 Dec;35(6):e91-9 [21846596]
Am J Hum Genet. 2000 Jul;67(1):110-9 [10841811]
Cancer Res. 2000 Jul 1;60(13):3440-4 [10910054]
Nat Genet. 2001 Apr;27(4):383-91 [11279519]
Br J Cancer. 2001 Aug 3;85(3):341-5 [11487262]
Anticancer Res. 2001 Jul-Aug;21(4B):3107-14 [11712819]
Adv Drug Deliv Rev. 2002 Nov 18;54(10):1271-94 [12406645]
Jpn J Surg. 1989 Mar;19(2):195-202 [2724718]
Cancer Res. 1990 Apr 1;50(7):2113-8 [2317801]
Int J Epidemiol. 1992 Oct;21(5):877-82 [1468848]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/carcin/bgt030
ER  - 



TY  - JOUR
T1  - Blockage of melatonin receptors impairs p53-mediated prevention of DNA damage accumulation.
AN  - 1349093392; 23354312
AB  - Melatonin has been known to be a chemopreventive agent since its levels inversely correlate with the risk of developing cancer. We have recently shown that melatonin induces p38-dependent phosphorylation of both p53 and histone H2AX. This is associated with a p53-mediated increase in repair of both endogenous and chemotherapy-induced DNA damage. In addition, the inhibition of p38 activities impairs melatonin's capability to induce a p53-dependent DNA damage response and thus its ability to maintain genome integrity. Since melatonin-induced p53 phosphorylation requires an intact p38 phosphorylation cascade and p38 can be activated by G proteins, we supposed that melatonin's activities could be mediated by its G-protein-coupled membrane receptors, MT1 and MT2. Here, we show that the activation of the p53-dependent DNA damage response by melatonin is indeed mediated by MT1 and MT2. As a result, the absence of either receptor impairs melatonin's ability to reduce both cell proliferation and clonogenic potential of cancer cells. In addition, this causes an impairment of the p53-dependent DNA damage response. By providing molecular insight, our findings might have translational impact, suggesting the involvement of melatonin receptors in tumorigenesis.
JF  - Carcinogenesis
AU  - Santoro, Raffaela
AU  - Mori, Federica
AU  - Marani, Marina
AU  - Grasso, Giuseppe
AU  - Cambria, Maria Anna
AU  - Blandino, Giovanni
AU  - Muti, Paola
AU  - Strano, Sabrina
AD  - Molecular Chemoprevention Group, Molecular Medicine Area, Regina Elena National Cancer Institute, Rome 00144, Italy.
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1051
EP  - 1061
VL  - 34
IS  - 5
KW  - MMP15 protein, human
KW  - 0
KW  - Receptors, G-Protein-Coupled
KW  - Receptors, Melatonin
KW  - Tumor Suppressor Protein p53
KW  - Matrix Metalloproteinase 15
KW  - EC 3.4.24.-
KW  - MMP14 protein, human
KW  - EC 3.4.24.80
KW  - Matrix Metalloproteinase 14
KW  - Melatonin
KW  - JL5DK93RCL
KW  - Index Medicus
KW  - Cell Proliferation -- drug effects
KW  - Animals
KW  - Matrix Metalloproteinase 15 -- genetics
KW  - Cell Transformation, Neoplastic -- metabolism
KW  - Humans
KW  - Matrix Metalloproteinase 15 -- metabolism
KW  - Cell Transformation, Neoplastic -- drug effects
KW  - Mice, Nude
KW  - Mice
KW  - Cell Line, Tumor
KW  - HCT116 Cells
KW  - Matrix Metalloproteinase 14 -- metabolism
KW  - Receptors, G-Protein-Coupled -- metabolism
KW  - MCF-7 Cells
KW  - Transplantation, Heterologous
KW  - Receptors, G-Protein-Coupled -- genetics
KW  - Cell Transformation, Neoplastic -- genetics
KW  - Matrix Metalloproteinase 14 -- genetics
KW  - Melatonin -- pharmacology
KW  - DNA Damage
KW  - Receptors, Melatonin -- antagonists & inhibitors
KW  - Receptors, Melatonin -- genetics
KW  - Tumor Suppressor Protein p53 -- genetics
KW  - Receptors, Melatonin -- metabolism
KW  - Tumor Suppressor Protein p53 -- metabolism
KW  - Melatonin -- metabolism
KW  - Melatonin -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1349093392?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Blockage+of+melatonin+receptors+impairs+p53-mediated+prevention+of+DNA+damage+accumulation.&rft.au=Santoro%2C+Raffaela%3BMori%2C+Federica%3BMarani%2C+Marina%3BGrasso%2C+Giuseppe%3BCambria%2C+Maria+Anna%3BBlandino%2C+Giovanni%3BMuti%2C+Paola%3BStrano%2C+Sabrina&rft.aulast=Santoro&rft.aufirst=Raffaela&rft.date=2013-05-01&rft.volume=34&rft.issue=5&rft.spage=1051&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt025
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-30
N1  - Date created - 2013-05-06
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/carcin/bgt025
ER  - 



TY  - JOUR
T1  - The Exposome - Exciting Opportunities for Discoveries in Reproductive and Perinatal Epidemiology
AN  - 1348489247; 17926075
AB  - Understanding the mechanisms that underlie successful human reproduction and development is an ambitious goal, given the many unique methodological challenges surrounding such study. These challenges are well understood by reproductive and perinatal epidemiologists and include its conditional nature, unobservable yet informative outcomes such as conception, multi-scale missing data, correlated or non-independent outcomes, interval censoring and a hierarchical data structure. Novel methodologies for overcoming these challenges and for answering critical data gaps are needed if we are to better understand the inefficiency that currently characterises human reproduction with the goal of improving population health. The exposome is an emerging paradigm that offers promise for understanding the natural history of human reproduction and development, and its many associated impairments that develop later in child- or adulthood. This novel paradigm recognises the need to identify and measure the totality of environmental (non-genetic) exposures from preconception through sensitive windows, and to identify patterns associated with healthy and adverse outcomes. The exposome accommodates research focusing on unique subpopulations, such as couples undergoing assisted reproductive technologies, so that methodological limitations such as unobservable and conditional outcomes can be better addressed. Reproductive and perinatal epidemiology is uniquely suited for proof-of-concept exposome research, given the intricate relations between fecundity, gravid health and later onset disease and the narrow and interrelated sensitive windows that characterise the conditional nature of human reproduction and development. Bold new conceptual frameworks such as the exposome are needed for designing research that may lead to discovery and improve population health.
JF  - Paediatric and Perinatal Epidemiology
AU  - Buck Louis, Germaine M
AU  - Yeung, Edwina
AU  - Sundaram, Rajeshwari
AU  - Laughon, SKatherine
AU  - Zhang, Cuilin
AD  - Division of Epidemiology, Statistics and Prevention Research. National Institutes of Health
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 229
EP  - 236
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 27
IS  - 3
SN  - 0269-5022, 0269-5022
KW  - Health & Safety Science Abstracts
KW  - Epidemiology
KW  - Reproduction
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1348489247?accountid=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=Paediatric+and+Perinatal+Epidemiology&rft.atitle=The+Exposome+-+Exciting+Opportunities+for+Discoveries+in+Reproductive+and+Perinatal+Epidemiology&rft.au=Buck+Louis%2C+Germaine+M%3BYeung%2C+Edwina%3BSundaram%2C+Rajeshwari%3BLaughon%2C+SKatherine%3BZhang%2C+Cuilin&rft.aulast=Buck+Louis&rft.aufirst=Germaine&rft.date=2013-05-01&rft.volume=27&rft.issue=3&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+Perinatal+Epidemiology&rft.issn=02695022&rft_id=info:doi/10.1111%2Fppe.12040
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Reproduction
DO  - http://dx.doi.org/10.1111/ppe.12040
ER  - 



TY  - JOUR
T1  - Cost analyses of peer health worker and mhealth support interventions for improving AIDS care in Rakai, Uganda
AN  - 1346796444; 4432773
AB  - A cost analysis study calculates resources needed to deliver an intervention and can provide useful information on affordability for service providers and policy-makers. We conducted cost analyses of both a peer health worker (PHW) and a mHealth (mobile phone) support intervention. Excluding supervisory staffing costs, total yearly costs for the PHW intervention was $8475, resulting in a yearly cost per patient of $8.74, per virologic failure averted cost of $189, and per patient lost to follow-up averted cost of $1025. Including supervisory staffing costs increased total yearly costs to $14,991. Yearly costs of the mHealth intervention were an additional $1046, resulting in a yearly cost per patient of $2.35. In a threshold analysis, the PHW intervention was found to be cost saving if it was able to avert 1.50 patients per year from switching to second-line antiretroviral therapy. Other AIDS care programs may find these intervention costs affordable. Reprinted by permission of Routledge, Taylor & Francis Ltd.
JF  - AIDS care
AU  - Chang, Larry W
AU  - Kagaayi, Joseph
AU  - Nakigozi, Gertrude
AU  - Serwada, David
AU  - Quinn, Thomas C
AU  - Gray, Ronald H
AU  - Bollinger, Robert C
AU  - Reynolds, Steven J
AU  - Holtgrave, David
AD  - Johns Hopkins University ; National Institutes of Health
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 652
EP  - 656
VL  - 25
IS  - 5
SN  - 0954-0121, 0954-0121
KW  - Sociology
KW  - AIDS
KW  - Cost analysis
KW  - Uganda
KW  - Policy making
KW  - Medical personnel
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1346796444?accountid=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=Cost+analyses+of+peer+health+worker+and+mhealth+support+interventions+for+improving+AIDS+care+in+Rakai%2C+Uganda&rft.au=Chang%2C+Larry+W%3BKagaayi%2C+Joseph%3BNakigozi%2C+Gertrude%3BSerwada%2C+David%3BQuinn%2C+Thomas+C%3BGray%2C+Ronald+H%3BBollinger%2C+Robert+C%3BReynolds%2C+Steven+J%3BHoltgrave%2C+David&rft.aulast=Chang&rft.aufirst=Larry&rft.date=2013-05-01&rft.volume=25&rft.issue=5&rft.spage=652&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2012.722600
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 2920 971 2934 3883; 7884 13682; 482 3617 6220; 9625 9628; 435 115 2
DO  - http://dx.doi.org/10.1080/09540121.2012.722600
ER  - 



TY  - JOUR
T1  - Alcohol use predicts sexual risk behavior with HIV-negative or partners of unknown status among young HIV-positive men who have sex with men
AN  - 1346796416; 4432770
AB  - Although the relationship between substance use and heightened sexual risk behaviors have been documented in samples of young men who have sex with men (YMSM) and HIV-positive adult men who have sex with men (MSM), there is a dearth of research on the role of substance use in the sexual risk behaviors of HIV-positive YMSM. We examined associations between alcohol and other drug use with sexual risk behaviors among a sample of HIV-positive YMSM (N=200). There were no significant predictors of either receptive or insertive unprotected anal intercourse (UAI) with HIV-positive partners among the substance use variables. Failure to use a condom after drinking alcohol (β=2.00, p<0.01) was significantly associated with insertive UAI with HIV- negative partners or partners of unknown status. Failure to use a condom after drinking alcohol (β=1.36, p<0.05) and age (β=0.35, p<0.05) were significantly associated with receptive UAI with HIV-negative partners or partners of unknown status. Findings from this article underscore the role of alcohol in facilitating UAI among HIV-positive YMSM and their HIV-negative and status-unknown partners. Reprinted by permission of Routledge, Taylor & Francis Ltd.
JF  - AIDS care
AU  - Bruce, Douglas
AU  - Kahana, Shoshana
AU  - Harper, Gary W
AU  - Fernández, M Isabel
AD  - DePaul University ; National Institute on Drug Abuse ; Nova Southeastern University
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 559
EP  - 565
VL  - 25
IS  - 5
SN  - 0954-0121, 0954-0121
KW  - Sociology
KW  - Alcohol
KW  - Sexual behaviour
KW  - Alcoholism
KW  - Drug abuse
KW  - HIV
KW  - Youth
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1346796416?accountid=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=Alcohol+use+predicts+sexual+risk+behavior+with+HIV-negative+or+partners+of+unknown+status+among+young+HIV-positive+men+who+have+sex+with+men&rft.au=Bruce%2C+Douglas%3BKahana%2C+Shoshana%3BHarper%2C+Gary+W%3BFern%C3%A1ndez%2C+M+Isabel&rft.aulast=Bruce&rft.aufirst=Douglas&rft.date=2013-05-01&rft.volume=25&rft.issue=5&rft.spage=559&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2012.720363
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 13779 652 5676 646 6091; 909; 913 561 6220; 11563 1025 1542 11325 6071; 5703 3617 6220; 3742 1121 11776 3753 3755
DO  - http://dx.doi.org/10.1080/09540121.2012.720363
ER  - 



TY  - JOUR
T1  - Eosinophils mediate the pathogenesis of halothane-induced liver injury in mice.
AN  - 1345512944; 23238640
AB  - Drug-induced liver injury (DILI) is a major health issue, as it remains difficult to predict which new drugs will cause injury and who will be susceptible to this disease. This is due in part to the lack of animal models and knowledge of susceptibility factors that predispose individuals to DILI. In this regard, liver eosinophilia has often been associated with DILI, although its role remains unclear. We decided to investigate this problem in a murine model of halothane-induced liver injury (HILI). When female Balb/cJ mice were administered halothane, eosinophils were detected by flow cytometry in the liver within 12 hours and increased thereafter proportionally to liver damage. Chemokines, eotaxin-1 (CCL11) and eotaxin-2 (CCL24), which are known to attract eosinophils, increased in response to halothane treatment. The severity of HILI was decreased significantly when the study was repeated in wildtype mice made deficient in eosinophils with a depleting antibody and in eosinophil lineage-ablated ΔdblGata(-/-) mice. Moreover, depletion of neutrophils by pretreating animals with Gr-1 antibody prior to halothane administration failed to reduce the severity of HILI at antibody concentrations that did not affect hepatic eosinophils. Immunohistochemical staining for the granule protein, major basic protein, revealed that eosinophils accumulated exclusively around areas of hepatocellular necrosis. Our findings indicate that eosinophils have a pathologic role in HILI in mice and suggest that they may contribute similarly in many clinical cases of DILI.
          Copyright © 2012 American Association for the Study of Liver Diseases.
JF  - Hepatology (Baltimore, Md.)
AU  - Proctor, William R
AU  - Chakraborty, Mala
AU  - Chea, Lynette S
AU  - Morrison, Jeffrey C
AU  - Berkson, Julia D
AU  - Semple, Kenrick
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, USA. william.proctor@nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 2026
EP  - 2036
VL  - 57
IS  - 5
KW  - Ccl11 protein, mouse
KW  - 0
KW  - Ccl24 protein, mouse
KW  - Chemokine CCL11
KW  - Chemokine CCL24
KW  - Halothane
KW  - UQT9G45D1P
KW  - Index Medicus
KW  - Cell Movement
KW  - Animals
KW  - Chemokine CCL24 -- metabolism
KW  - Liver -- pathology
KW  - Chemokine CCL11 -- metabolism
KW  - Disease Models, Animal
KW  - Liver -- metabolism
KW  - Mice
KW  - Mice, Inbred BALB C
KW  - Comorbidity
KW  - Mice, Knockout
KW  - Eosinophilia -- epidemiology
KW  - Female
KW  - Prevalence
KW  - Chemical and Drug Induced Liver Injury -- etiology
KW  - Eosinophils -- physiology
KW  - Chemical and Drug Induced Liver Injury -- pathology
KW  - Eosinophils -- pathology
KW  - Halothane -- adverse effects
KW  - Chemical and Drug Induced Liver Injury -- physiopathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1345512944?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Eosinophils+mediate+the+pathogenesis+of+halothane-induced+liver+injury+in+mice.&rft.au=Proctor%2C+William+R%3BChakraborty%2C+Mala%3BChea%2C+Lynette+S%3BMorrison%2C+Jeffrey+C%3BBerkson%2C+Julia+D%3BSemple%2C+Kenrick%3BBourdi%2C+Mohammed%3BPohl%2C+Lance+R&rft.aulast=Proctor&rft.aufirst=William&rft.date=2013-05-01&rft.volume=57&rft.issue=5&rft.spage=2026&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.26196
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-05
N1  - Date created - 2013-04-23
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Exp Med. 2008 Jun 9;205(6):1285-92 [18490489]
Chem Res Toxicol. 2007 May;20(5):734-44 [17439248]
J Viral Hepat. 2008 Jul;15(7):523-30 [18266647]
Biochem Pharmacol. 2009 Jan 15;77(2):277-84 [18940183]
Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056]
J Allergy Clin Immunol. 2009 Sep;124(3):573-82, 582.e1-9 [19539982]
Toxicol Sci. 2009 Oct;111(2):302-10 [19633216]
J Immunol. 2009 Oct 15;183(8):5333-41 [19783675]
J Pharmacol Exp Ther. 2010 May;333(2):364-72 [20124411]
Biochem Pharmacol. 2010 Jul 15;80(2):255-61 [20359463]
Clin Respir J. 2010 May;4 Suppl 1:15-9 [20500605]
J Gastrointestin Liver Dis. 2010 Jun;19(2):187-90 [20593053]
Toxicol Sci. 2011 Apr;120(2):507-18 [21245496]
J Immunol Methods. 2011 Jun 30;369(1-2):91-7 [21565196]
Immunol Rev. 2011 Jul;242(1):161-77 [21682744]
Clin Rev Allergy Immunol. 2011 Dec;41(3):298-310 [21249468]
Aliment Pharmacol Ther. 2007 Jun 15;25(12):1411-21 [17539980]
N Engl J Med. 2000 Feb 3;342(5):359-60 [10660405]
J Immunol. 2000 Nov 15;165(10):5509-17 [11067904]
Chem Res Toxicol. 2001 Apr;14(4):362-70 [11304124]
J Hepatol. 2001 Apr;34(4):537-47 [11394653]
J Exp Med. 2002 Jun 3;195(11):1387-95 [12045237]
Gastroenterology. 2002 Jun;122(7):2001-10 [12055605]
Eur J Gastroenterol Hepatol. 2002 Aug;14(8):887-90 [12172412]
J Immunol. 2003 Sep 15;171(6):3233-44 [12960353]
Hepatology. 2004 May;39(5):1430-40 [15122773]
Gastroenterology. 1975 Aug;69(2):289-302 [1150039]
J Allergy Clin Immunol. 1985 Oct;76(4):595-604 [4056248]
Proc Natl Acad Sci U S A. 1989 Jan;86(1):322-6 [2911577]
J Immunol. 1993 Sep 1;151(5):2399-408 [8360469]
Hepatology. 1994 Sep;20(3):654-62 [7521317]
J Immunol Methods. 1996 Oct 16;197(1-2):139-50 [8890901]
J Hepatol. 1998 Feb;28(2):356-7 [9514552]
Hepatology. 2006 Jun;43(6):1220-30 [16729305]
J Leukoc Biol. 2006 Aug;80(2):330-41 [16731772]
Infect Immun. 2006 Sep;74(9):5236-43 [16926417]
Blood. 2006 Oct 1;108(7):2420-7 [16772607]
Hepatology. 2006 Dec;44(6):1421-31 [17133481]
J Hepatol. 2008 Jul;49(1):107-14 [18485518]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1002/hep.26196
ER  - 



TY  - JOUR
T1  - The emerging issue of cardiac dysfunction induced by antineoplastic angiogenesis inhibitors.
AN  - 1345512920; 23325019
AB  - Left ventricular dysfunction from anticancer drugs has emerged as a relevant problem in the clinical and scientific communities. Anthracycline toxicity has always been the most relevant, but with the increasing use of biological targeted therapies in treatment protocols, with an increasing number of cancer survivors, new toxicities have been increasing in more recent years. Cardiomyopathy after ErbB2 inhibitors has been intensively studied. Another important class of biological anticancer drugs are vascular endothelial growth factor (VEGF) inhibitors. VEGF signalling is crucial for vascular growth, but it also has a major impact on myocardial function. Also, it is important to note that such angiogenesis inhibitors are multitargeted in most cases, and can produce a broad spectrum of cardiovascular side effects. Here we review the mechanisms and pathophysiology of the most significant cardiotoxic effects of antiangiogenic drugs, and particular attention is drawn to LV dysfunction, discussing the assessment and management on the basis of the most recent cardio-oncological findings and heart failure guidelines.
JF  - European journal of heart failure
AU  - Tocchetti, Carlo G
AU  - Gallucci, Giuseppina
AU  - Coppola, Carmela
AU  - Piscopo, Giovanna
AU  - Cipresso, Clemente
AU  - Maurea, Carlo
AU  - Giudice, Aldo
AU  - Iaffaioli, Rosario V
AU  - Arra, Claudio
AU  - Maurea, Nicola
AD  - Division of Cardiology, National Cancer Institute, Pascale Foundation, Naples, Italy. cgtocchetti@iol.it
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 482
EP  - 489
VL  - 15
IS  - 5
KW  - Angiogenesis Inhibitors
KW  - 0
KW  - Antineoplastic Agents
KW  - Vascular Endothelial Growth Factor A
KW  - Index Medicus
KW  - Vascular Endothelial Growth Factor A -- antagonists & inhibitors
KW  - Risk Factors
KW  - Humans
KW  - Cardiovascular System -- physiopathology
KW  - Cardiovascular System -- drug effects
KW  - Angiogenesis Inhibitors -- adverse effects
KW  - Ventricular Dysfunction, Left -- physiopathology
KW  - Ventricular Dysfunction, Left -- chemically induced
KW  - Antineoplastic Agents -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1345512920?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+heart+failure&rft.atitle=The+emerging+issue+of+cardiac+dysfunction+induced+by+antineoplastic+angiogenesis+inhibitors.&rft.au=Tocchetti%2C+Carlo+G%3BGallucci%2C+Giuseppina%3BCoppola%2C+Carmela%3BPiscopo%2C+Giovanna%3BCipresso%2C+Clemente%3BMaurea%2C+Carlo%3BGiudice%2C+Aldo%3BIaffaioli%2C+Rosario+V%3BArra%2C+Claudio%3BMaurea%2C+Nicola&rft.aulast=Tocchetti&rft.aufirst=Carlo&rft.date=2013-05-01&rft.volume=15&rft.issue=5&rft.spage=482&rft.isbn=&rft.btitle=&rft.title=European+journal+of+heart+failure&rft.issn=1879-0844&rft_id=info:doi/10.1093%2Feurjhf%2Fhft008
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-26
N1  - Date created - 2013-04-23
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/eurjhf/hft008
ER  - 



TY  - JOUR
T1  - Integrated metabolite and gene expression profiles identify lipid biomarkers associated with progression of hepatocellular carcinoma and patient outcomes.
AN  - 1338392703; 23376425
AB  - We combined gene expression and metabolic profiling analyses to identify factors associated with outcomes of patients with hepatocellular carcinoma (HCC).
          We compared metabolic and gene expression patterns between paired tumor and nontumor tissues from 30 patients with HCC, and validated the results using samples from 356 patients with HCC. A total of 469 metabolites were measured using liquid chromatography/mass spectrometry and gas chromatography/mass spectrometry. Metabolic and genomic data were integrated, and Kaplan-Meier and Cox proportional hazards analyses were used to associate specific patterns with patient outcomes. Associated factors were evaluated for their effects on cancer cells in vitro and tumor formation in nude mice. We identified 28 metabolites and 169 genes associated with aggressive HCC. Lipid metabolites of stearoyl-CoA-desaturase (SCD) activity were associated with aberrant palmitate signaling in aggressive HCC samples. Expression of gene products associated with these metabolites, including SCD, were associated independently with survival times and tumor recurrence in the test and validation sets. Combined expression of SCD and α-fetoprotein were associated with outcomes of patients with early-stage HCC. Levels of monounsaturated palmitic acid, the product of SCD activity, were increased in aggressive HCCs; monounsaturated palmitic acid increased migration and invasion of cultured HCC cells and colony formation by HCC cells. HCC cells that expressed small interfering RNA against SCD had decreased cell migration and colony formation in culture and reduced tumorigenicity in mice.
          By using a combination of gene expression and metabolic profile analysis, we identified a lipogenic network that involves SCD and palmitate signaling and was associated with HCC progression and patient outcomes. The microarray platform and data have been submitted to the Gene Expression Omnibus public database at NCBI following MIAME guidelines. Accession numbers: GPL4700 (platform), and GSE6857 (samples). Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.
JF  - Gastroenterology
AU  - Budhu, Anuradha
AU  - Roessler, Stephanie
AU  - Zhao, Xuelian
AU  - Yu, Zhipeng
AU  - Forgues, Marshonna
AU  - Ji, Junfang
AU  - Karoly, Edward
AU  - Qin, Lun-Xiu
AU  - Ye, Qing-Hai
AU  - Jia, Hu-Liang
AU  - Fan, Jia
AU  - Sun, Hui-Chuan
AU  - Tang, Zhao-You
AU  - Wang, Xin Wei
AD  - Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 1066
EP  - 1075.e1
VL  - 144
IS  - 5
KW  - Biomarkers, Tumor
KW  - 0
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Survival Rate -- trends
KW  - Liver Neoplasms, Experimental -- genetics
KW  - Animals
KW  - Liver Neoplasms, Experimental -- mortality
KW  - Liver Neoplasms, Experimental -- metabolism
KW  - Humans
KW  - China -- epidemiology
KW  - Signal Transduction -- genetics
KW  - Disease Progression
KW  - Mice, Nude
KW  - Mice
KW  - Female
KW  - Gene Expression Regulation, Neoplastic
KW  - Biomarkers, Tumor -- genetics
KW  - Liver Neoplasms -- metabolism
KW  - Carcinoma, Hepatocellular -- metabolism
KW  - Carcinoma, Hepatocellular -- genetics
KW  - Liver Neoplasms -- mortality
KW  - Carcinoma, Hepatocellular -- pathology
KW  - Lipid Metabolism -- genetics
KW  - Biomarkers, Tumor -- biosynthesis
KW  - Liver Neoplasms -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1338392703?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Integrated+metabolite+and+gene+expression+profiles+identify+lipid+biomarkers+associated+with+progression+of+hepatocellular+carcinoma+and+patient+outcomes.&rft.au=Budhu%2C+Anuradha%3BRoessler%2C+Stephanie%3BZhao%2C+Xuelian%3BYu%2C+Zhipeng%3BForgues%2C+Marshonna%3BJi%2C+Junfang%3BKaroly%2C+Edward%3BQin%2C+Lun-Xiu%3BYe%2C+Qing-Hai%3BJia%2C+Hu-Liang%3BFan%2C+Jia%3BSun%2C+Hui-Chuan%3BTang%2C+Zhao-You%3BWang%2C+Xin+Wei&rft.aulast=Budhu&rft.aufirst=Anuradha&rft.date=2013-05-01&rft.volume=144&rft.issue=5&rft.spage=1066&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2013.01.054
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-11
N1  - Date created - 2013-04-22
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - GSE6857; GEO; GPL4700
N1  - SuppNotes - Cited By:
Curr Opin Biotechnol. 2011 Feb;22(1):26-31 [20934866]
Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642]
Nat Rev Gastroenterol Hepatol. 2011 Apr;8(4):224-38 [21386810]
Diabetes. 2011 May;60(5):1493-503 [21478464]
Cell Cycle. 2010 Mar 15;9(6):1057-64 [20305377]
Mol Cell Proteomics. 2011 Jul;10(7):M110.004945 [21518826]
Cell. 2000 Jan 7;100(1):57-70 [10647931]
Gastroenterology. 2001 Jun;120(7):1763-73 [11375957]
Nature. 2001 Nov 1;414(6859):105-11 [11689955]
Carcinogenesis. 2002 Nov;23(11):1933-6 [12419843]
Nat Med. 2003 Apr;9(4):416-23 [12640447]
Prog Lipid Res. 2004 Mar;43(2):91-104 [14654089] Int J Cancer. 1999 Nov 26;83(5):585-90 [10521790]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078]
J Natl Cancer Inst. 2005 Aug 17;97(16):1180-4 [16106022]
Trends Biotechnol. 2005 Nov;23(11):544-6 [16154652]
Nat Med. 2006 Apr;12(4):410-6 [16532004]
Apoptosis. 2006 Jul;11(7):1231-8 [16703263]
Cancer Cell. 2006 Aug;10(2):99-111 [16904609]
Clin Cancer Res. 2007 Feb 15;13(4):1133-9 [17317821]
Hepatology. 2007 Apr;45(4):938-47 [17393520]
Cancer Res. 2008 Mar 1;68(5):1451-61 [18316609]
Pharmacogenomics. 2008 Apr;9(4):383-97 [18384253]
J Lipid Res. 2008 Oct;49(10):2124-34 [18599738]
Cell. 2008 Sep 19;134(6):933-44 [18805087]
J Appl Toxicol. 2008 Nov;28(8):1021-6 [18626905]
Nature. 2009 Feb 12;457(7231):910-4 [19212411]
Gastroenterology. 2009 Mar;136(3):1012-24 [19150350]
Expert Rev Gastroenterol Hepatol. 2009 Apr;3(2):101-3 [19351279]
Nat Genet. 2002 Aug;31(4):339-46 [12149612]
J Biol Chem. 2009 May 1;284(18):11755-9 [19117948]
Anal Chim Acta. 2009 Aug 19;648(1):98-104 [19616694]
Hepatology. 2009 Aug;50(2):472-80 [19585654]
Expert Opin Ther Pat. 2009 Sep;19(9):1169-91 [19691439]
Lancet Oncol. 2010 Feb;11(2):193-203 [20152771]
Anal Chem. 2009 Aug 15;81(16):6656-67 [19624122]
J Hepatol. 2010 May;52(5):690-7 [20338660]
Carcinogenesis. 2010 Sep;31(9):1509-15 [20595235]
Cell. 2010 Dec 10;143(6):1005-17 [21129771]
Gastroenterology. 2011 Mar;140(3):1071-83 [21147110]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1053/j.gastro.2013.01.054
ER  - 



TY  - JOUR
T1  - Pertuzumab : evolving therapeutic strategies in the management of HER2-overexpressing breast cancer.
AN  - 1324959467; 23530718
AB  - HER2 overexpression or amplification is present in approximately one-fifth of breast cancers and historically was associated with aggressive disease and poorer prognosis. The introduction of the humanized monoclonal antibody trastuzumab dramatically improved disease-free survival (DFS) and overall survival (OS) in this subgroup. As the majority of patients with metastatic disease ultimately develop resistance to trastuzumab, a need exists for more effective targeted therapies. Pertuzumab is an anti-HER2/neu-targeted therapy in the late stages of clinical development. The combination of pertuzumab, trastuzumab and docetaxel has been found to have an OS benefit in patients with HER2 positive metastatic breast cancer (MBC) when used in the first-line setting. This reflects a new standard of care, and pertuzumab was recently approved for this indication by the Food and Drug Administration (FDA). The efficacy of pertuzumab and trastuzumab in conjunction with chemotherapy is currently being evaluated in the adjuvant setting.
          This article provides an overview of preclinical investigations in addition to reviewing pertinent Phase I, Phase II and Phase III clinical trials. Pertuzumab, in combination with the humanized monoclonal antibody trastuzumab, and docetaxel is a standard of care for patients with previously untreated metastatic breast cancer based on the CLEOPATRA study showing a survival benefit. There is no increase in cardiac toxicity with the combined HER2-targeted therapy. Future issues will address appropriate sequencing and combination with other anti-HER2-targeted therapies and/or chemotherapy.
JF  - Expert opinion on biological therapy
AU  - O'Sullivan, Ciara C
AU  - Swain, Sandra M
AD  - Medical Oncology Branch, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 779
EP  - 790
VL  - 13
IS  - 5
KW  - Antibodies, Monoclonal, Humanized
KW  - 0
KW  - ERBB2 protein, human
KW  - EC 2.7.10.1
KW  - Receptor, ErbB-2
KW  - pertuzumab
KW  - K16AIQ8CTM
KW  - Index Medicus
KW  - Gene Expression Regulation, Neoplastic
KW  - Clinical Trials, Phase II as Topic
KW  - Clinical Trials, Phase III as Topic
KW  - Humans
KW  - Drug Approval
KW  - Clinical Trials, Phase I as Topic
KW  - Neoadjuvant Therapy
KW  - Product Surveillance, Postmarketing
KW  - Drug Evaluation, Preclinical
KW  - Female
KW  - Breast Neoplasms -- genetics
KW  - Breast Neoplasms -- drug therapy
KW  - Antibodies, Monoclonal, Humanized -- pharmacokinetics
KW  - Receptor, ErbB-2 -- genetics
KW  - Antibodies, Monoclonal, Humanized -- adverse effects
KW  - Antibodies, Monoclonal, Humanized -- therapeutic use
KW  - Receptor, ErbB-2 -- metabolism
KW  - Antibodies, Monoclonal, Humanized -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1324959467?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+biological+therapy&rft.atitle=Pertuzumab+%3A+evolving+therapeutic+strategies+in+the+management+of+HER2-overexpressing+breast+cancer.&rft.au=O%27Sullivan%2C+Ciara+C%3BSwain%2C+Sandra+M&rft.aulast=O%27Sullivan&rft.aufirst=Ciara&rft.date=2013-05-01&rft.volume=13&rft.issue=5&rft.spage=779&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+biological+therapy&rft.issn=1744-7682&rft_id=info:doi/10.1517%2F14712598.2013.783007
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-25
N1  - Date created - 2013-04-08
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1517/14712598.2013.783007
ER  - 



TY  - JOUR
T1  - Prostate cancer prevention: strategies for agent development.
AN  - 1323794947; 23518594
AB  - This article provides an update of clinical research supported by the National Cancer Institute's Phase I/II prostate cancer chemoprevention agent development program.
          Numerous clinical trials of pharmacologic interventions to delay, prevent or reverse carcinogenesis ('chemoprevention') with the ultimate goal of reducing cancer incidence have been conducted over the past decade. These trials range from relatively small, short-duration studies with biomarker endpoints to very large, long-term, general population trials with definitive cancer endpoints. Two large, population-based, Phase III prostate cancer prevention trials have shown a significant benefit for 5-α-reductase inhibitors. However, this class of agents was also associated with increased detection of high-grade prostate cancer. Another large, Phase III prostate cancer prevention trial showed no benefit for either selenium or vitamin E, given individually or in combination; in fact, a significant increase in prostate cancer was observed among men randomized to the vitamin E alone arm. A number of early phase trials and three definitive Phase III trials have been conducted in the field of prostate cancer prevention over the past decade. Although a great deal has been learned from these studies, significant work remains to be done to fully realize the potential of chemoprevention in this disease.
JF  - Current opinion in oncology
AU  - Parnes, Howard L
AU  - House, Margaret G
AU  - Tangrea, Joseph A
AD  - Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland 20892, USA. parnesh@mail.nih.gov
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 242
EP  - 251
VL  - 25
IS  - 3
KW  - Anticarcinogenic Agents
KW  - 0
KW  - Index Medicus
KW  - Drug Discovery
KW  - Humans
KW  - Clinical Trials as Topic
KW  - Male
KW  - Prostatic Neoplasms -- prevention & control
KW  - Anticarcinogenic Agents -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323794947?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prostate+cancer+prevention%3A+strategies+for+agent+development.&rft.au=Parnes%2C+Howard+L%3BHouse%2C+Margaret+G%3BTangrea%2C+Joseph+A&rft.aulast=Parnes&rft.aufirst=Howard&rft.date=2013-05-01&rft.volume=25&rft.issue=3&rft.spage=242&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0b013e32835fc8d4
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-05
N1  - Date created - 2013-04-03
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1097/CCO.0b013e32835fc8d4
ER  - 



TY  - JOUR
T1  - Biological determinants of health disparities in prostate cancer.
AN  - 1323794656; 23399519
AB  - Prostate cancer mortality rates are highest among men of African ancestry in the United States and globally. Environmental exposures and ancestry-related factors may influence tumor biology and induce a more aggressive disease in this population. Here, we summarize the most recent advances in our understanding of race/ethnic differences in the tumor biology of prostate cancer with an emphasis on the excess disease burden among African-Americans.
          Results from several DNA methylation studies showed an increased prevalence in DNA hypermethylation at disease-related loci in tumors from African-American patients compared with tumors from European-American patients. Analyses of genome-wide gene expression in prostate tumors revealed frequent alterations in the expression of genes related to immunobiology among the African-American patients, consistent with immune response differences between them and their European-American counterparts. Lastly, population differences in the frequency of oncogenic erythroblast transformation-specific family of transcription factors (ETS)-related gene rearrangements were evaluated in three studies that showed that these alterations manifest themselves most commonly in tumors from men of European ancestry, but are significantly less frequent in men of African ancestry, whereas least common in men of Asian ancestry. Analysis of tumor markers indicates that tumor biological differences may exist between prostate cancer patients of African ancestry and those of European or Asian ancestry. These differences could affect disease aggressiveness and response to therapy.
JF  - Current opinion in oncology
AU  - Martin, Damali N
AU  - Starks, Adrienne M
AU  - Ambs, Stefan
AD  - Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4258, USA.
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 235
EP  - 241
VL  - 25
IS  - 3
KW  - Index Medicus
KW  - Oncogenes
KW  - DNA Methylation
KW  - Humans
KW  - Male
KW  - Genome-Wide Association Study
KW  - Prostatic Neoplasms -- pathology
KW  - Prostatic Neoplasms -- immunology
KW  - African Continental Ancestry Group -- genetics
KW  - Prostatic Neoplasms -- ethnology
KW  - Prostatic Neoplasms -- genetics
KW  - Health Status Disparities
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323794656?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Biological+determinants+of+health+disparities+in+prostate+cancer.&rft.au=Martin%2C+Damali+N%3BStarks%2C+Adrienne+M%3BAmbs%2C+Stefan&rft.aulast=Martin&rft.aufirst=Damali&rft.date=2013-05-01&rft.volume=25&rft.issue=3&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0b013e32835eb5d1
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-05
N1  - Date created - 2013-04-03
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1097/CCO.0b013e32835eb5d1
ER  - 



TY  - JOUR
T1  - Myeloid derived suppressor cells (MDSCs) can induce the generation of Th17 response from naïve CD4+ T cells.
AN  - 1322730260; 22995935
AB  - IL-17 producing CD4(+) T cells (Th17) are identified as a subset of proinflammatory T cells present at the tumor site of various murine and human cancer cases and plays a crucial role in shaping the neoplastic process through fostering tumor angiogenesis and metastasis. However, the development of Th17 response in the tumor microenvironment has not yet been fully elucidated. Herein, we make an attempt to disclose the involvement of tumor infiltrating antigen presenting cells (APCs), especially tumor associated macrophages (TAMs) and myeloid derived suppressor cells (MDSCs) to polarize naïve CD4(+) T cells toward IL-17(+) T cells. We have found that MDSCs either isolated from the tumor site or generated in vitro are superior over TAMs to induce IL-17 production by naïve CD4(+) T cells. Furthermore, we have shown that MDSCs mediated induction of IL-17(+) T cell response is independent of MDSCs-T cell contact but crucially depends on the cytokines secreted by MDSCs. Our study will help to develop potential therapeutic strategies by harnessing the ability of MDSCs to induce IL-17 production by CD4(+) T cells and thus restrict the generation of inflammatory Th17 population at the disease site.
          Copyright © 2012 Elsevier GmbH. All rights reserved.
JF  - Immunobiology
AU  - Chatterjee, Shilpak
AU  - Das, Satyajit
AU  - Chakraborty, Paramita
AU  - Manna, Alak
AU  - Chatterjee, Mitali
AU  - Choudhuri, Soumitra Kumar
AD  - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India.
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 718
EP  - 724
VL  - 218
IS  - 5
KW  - Interleukin-17
KW  - 0
KW  - Index Medicus
KW  - Animals
KW  - Interleukin-17 -- biosynthesis
KW  - Tumor Cells, Cultured
KW  - Interleukin-17 -- immunology
KW  - Cell Differentiation
KW  - Cell Communication
KW  - Mice
KW  - Signal Transduction
KW  - Macrophages -- pathology
KW  - Macrophages -- immunology
KW  - Th17 Cells -- pathology
KW  - Carcinoma, Ehrlich Tumor -- pathology
KW  - Antigen-Presenting Cells -- pathology
KW  - Myeloid Cells -- immunology
KW  - Carcinoma, Ehrlich Tumor -- immunology
KW  - Antigen-Presenting Cells -- immunology
KW  - Tumor Microenvironment -- immunology
KW  - Th17 Cells -- immunology
KW  - Myeloid Cells -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1322730260?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunobiology&rft.atitle=Myeloid+derived+suppressor+cells+%28MDSCs%29+can+induce+the+generation+of+Th17+response+from+na%C3%AFve+CD4%2B+T+cells.&rft.au=Chatterjee%2C+Shilpak%3BDas%2C+Satyajit%3BChakraborty%2C+Paramita%3BManna%2C+Alak%3BChatterjee%2C+Mitali%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Chatterjee&rft.aufirst=Shilpak&rft.date=2013-05-01&rft.volume=218&rft.issue=5&rft.spage=718&rft.isbn=&rft.btitle=&rft.title=Immunobiology&rft.issn=1878-3279&rft_id=info:doi/10.1016%2Fj.imbio.2012.08.271
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-05
N1  - Date created - 2013-04-01
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.imbio.2012.08.271
ER  - 



TY  - JOUR
T1  - Sputum analysis: non-invasive early lung cancer detection.
AN  - 1282517767; 23086732
AB  - Lung cancer is the leading cause of cancer-related deaths over the world, characterized by a very high mortality rate. Molecular technique development tries to focus on early detection of cancers by studying molecular alterations that characterize cancer cells. Worldwide lung cancer research has focused on an ever-increasing number of molecular elements of carcinogenesis at genetic, epigenetic and protein levels. The non-invasiveness is the characteristic that all clinical trials on cancer detection should have. Abnormal chest imaging and/or non-specific symptoms are initial signals of lung cancer that appear in an advanced stage of disease. This fact represents the cause of the low 5-year survival rate: over 90% of patients dying within 5 years of diagnosis. Since smokers have higher quantity of sputum containing exfoliated cells from the bronchial tree, and the sputum represents the most easily accessible biological fluid and its collection is non-invasive, analysis of this sample represents a good area of research in early lung cancer diagnosis. Continued cigarette smoking is the cause of chronic obstructive pulmonary disease (COPD), with an estimated attributable risk factor exceeding 80% in smoking affected individuals. Lung cancer is found in 40-70% of patients with COPD, particularly in severe disease, and it is a common cause of death in these patients. A large prospective trial of almost half a million non-smokers showed as lung cancer is also common in patients with COPD who have never smoked. This review describes issues related to early lung cancer screening using non-invasive methods.
          Copyright © 2012 Wiley Periodicals, Inc.
JF  - Journal of cellular physiology
AU  - D'Urso, Vittorio
AU  - Doneddu, Valentina
AU  - Marchesi, Irene
AU  - Collodoro, Angelo
AU  - Pirina, Pietro
AU  - Giordano, Antonio
AU  - Bagella, Luigi
AD  - INT-CROM, Pascale Foundation National Cancer Institute, Cancer Research Center, Mercogliano, Italy.
Y1  - 2013/05//
PY  - 2013
DA  - May 2013
SP  - 945
EP  - 951
VL  - 228
IS  - 5
KW  - Index Medicus
KW  - Smoking
KW  - Survival Rate
KW  - Pulmonary Disease, Chronic Obstructive -- epidemiology
KW  - Risk Factors
KW  - Humans
KW  - Pulmonary Disease, Chronic Obstructive -- diagnosis
KW  - Sputum -- cytology
KW  - Lung Neoplasms -- diagnosis
KW  - Lung Neoplasms -- epidemiology
KW  - Early Detection of Cancer
KW  - Sputum -- metabolism
KW  - Lung Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282517767?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sputum+analysis%3A+non-invasive+early+lung+cancer+detection.&rft.au=D%27Urso%2C+Vittorio%3BDoneddu%2C+Valentina%3BMarchesi%2C+Irene%3BCollodoro%2C+Angelo%3BPirina%2C+Pietro%3BGiordano%2C+Antonio%3BBagella%2C+Luigi&rft.aulast=D%27Urso&rft.aufirst=Vittorio&rft.date=2013-05-01&rft.volume=228&rft.issue=5&rft.spage=945&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24263
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-03
N1  - Date created - 2013-01-28
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/jcp.24263
ER  - 



TY  - JOUR
T1  - β-Arrestin-2 deficiency attenuates abdominal aortic aneurysm formation in mice.
AN  - 1346577520; 23524589
AB  - Abdominal aortic aneurysms (AAAs) are a chronic inflammatory vascular disease for which pharmacological treatments are not available. A mouse model of AAA formation involves chronic infusion of angiotensin II (AngII), and previous studies indicated a primary role for the AngII type 1a receptor in AAA formation. β-arrestin (βarr)-2 is a multifunctional scaffolding protein that binds G-protein-coupled receptors such as AngII type 1a and regulates numerous signaling pathways and pathophysiological processes. However, a role for βarr2 in AngII-induced AAA formation is currently unknown.
          To determine whether βarr2 played a role in AngII-induced AAA formation in mice. Treatment of βarr2(+/+) and βarr2(-/-) mice on the hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) background or on normolipidemic C57BL/6 background with AngII for 28 days indicated that βarr2 deficiency significantly attenuated AAA formation. βarr2 deficiency attenuated AngII-induced expression of cyclooxygenase-2, monocyte chemoattractant protein-1, macrophage inflammatory protein 1α, and macrophage infiltration. AngII also increased the levels of phosphorylated extracellular signal-regulated kinase 1/2 in apoE(-/-)/βarr2(+/+) aortas, whereas βarr2 deficiency diminished this increase. Furthermore, inhibition of extracellular signal-regulated kinase 1/2 activation with CI1040 (100 mg/kg per day) reduced the level of AngII-induced cyclooxygenase-2 expression in apoE(-/-)/βarr2(+/+) mice to the level observed in apoE(-/-)/βarr2(-/-) mice. AngII treatment also increased matrix metalloproteinase expression and disruption of the elastic layer in apoE(-/-)/βarr2(+/+) aortas, and βarr2 deficiency reduced these effects. βarr2 contributes to AngII-induced AAA formation in mice by phosphorylated extracellular signal-regulated kinase 1/2-mediated cyclooxygenase-2 induction and increased inflammation. These studies suggest that for the AngII type 1a receptor, G-protein-independent, βarr2-dependent signaling plays a major role in AngII-induced AAA formation.
JF  - Circulation research
AU  - Trivedi, Darshini B
AU  - Loftin, Charles D
AU  - Clark, James
AU  - Myers, Page
AU  - DeGraff, Laura M
AU  - Cheng, Jennifer
AU  - Zeldin, Darryl C
AU  - Langenbach, Robert
AD  - Laboratory of Toxicology and Pharmacology, Comparative Medicine Branch, and Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Y1  - 2013/04/26/
PY  - 2013
DA  - 2013 Apr 26
SP  - 1219
EP  - 1229
VL  - 112
IS  - 9
KW  - 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide
KW  - 0
KW  - Apolipoproteins E
KW  - Arrb2 protein, mouse
KW  - Arrestins
KW  - Benzamides
KW  - Ccl2 protein, mouse
KW  - Ccl3 protein, mouse
KW  - Chemokine CCL2
KW  - Chemokine CCL3
KW  - Protein Kinase Inhibitors
KW  - beta-Arrestin 2
KW  - beta-Arrestins
KW  - Angiotensin II
KW  - 11128-99-7
KW  - Ptgs2 protein, mouse
KW  - EC 1.14.99.-
KW  - Cyclooxygenase 2
KW  - EC 1.14.99.1
KW  - Calcium-Calmodulin-Dependent Protein Kinases
KW  - EC 2.7.11.17
KW  - Mapk1 protein, mouse
KW  - EC 2.7.11.24
KW  - Mitogen-Activated Protein Kinase 1
KW  - Mitogen-Activated Protein Kinase 3
KW  - Matrix Metalloproteinase 2
KW  - EC 3.4.24.24
KW  - Mmp2 protein, mouse
KW  - Matrix Metalloproteinase 9
KW  - EC 3.4.24.35
KW  - Mmp9 protein, mouse
KW  - Index Medicus
KW  - Apolipoproteins E -- deficiency
KW  - Animals
KW  - Disease Models, Animal
KW  - Matrix Metalloproteinase 2 -- metabolism
KW  - Mice, Knockout
KW  - Matrix Metalloproteinase 9 -- metabolism
KW  - Phosphorylation
KW  - Benzamides -- pharmacology
KW  - Chemokine CCL3 -- metabolism
KW  - Calcium-Calmodulin-Dependent Protein Kinases -- antagonists & inhibitors
KW  - Cyclooxygenase 2 -- metabolism
KW  - Time Factors
KW  - Signal Transduction
KW  - Male
KW  - Apolipoproteins E -- genetics
KW  - Macrophages -- metabolism
KW  - Calcium-Calmodulin-Dependent Protein Kinases -- metabolism
KW  - Elastic Tissue -- metabolism
KW  - Protein Kinase Inhibitors -- pharmacology
KW  - Blood Pressure
KW  - Elastic Tissue -- pathology
KW  - Mice
KW  - Chemokine CCL2 -- metabolism
KW  - Mitogen-Activated Protein Kinase 3 -- metabolism
KW  - Macrophages -- pathology
KW  - Mitogen-Activated Protein Kinase 1 -- metabolism
KW  - Mice, Inbred C57BL
KW  - Aortic Aneurysm, Abdominal -- genetics
KW  - Aorta, Abdominal -- metabolism
KW  - Aortic Aneurysm, Abdominal -- prevention & control
KW  - Aortic Aneurysm, Abdominal -- metabolism
KW  - Arrestins -- genetics
KW  - Arrestins -- deficiency
KW  - Aortic Aneurysm, Abdominal -- pathology
KW  - Aorta, Abdominal -- drug effects
KW  - Aortic Aneurysm, Abdominal -- chemically induced
KW  - Aorta, Abdominal -- pathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1346577520?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=%CE%B2-Arrestin-2+deficiency+attenuates+abdominal+aortic+aneurysm+formation+in+mice.&rft.au=Trivedi%2C+Darshini+B%3BLoftin%2C+Charles+D%3BClark%2C+James%3BMyers%2C+Page%3BDeGraff%2C+Laura+M%3BCheng%2C+Jennifer%3BZeldin%2C+Darryl+C%3BLangenbach%2C+Robert&rft.aulast=Trivedi&rft.aufirst=Darshini&rft.date=2013-04-26&rft.volume=112&rft.issue=9&rft.spage=1219&rft.isbn=&rft.btitle=&rft.title=Circulation+research&rft.issn=1524-4571&rft_id=info:doi/10.1161%2FCIRCRESAHA.112.280399
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-20
N1  - Date created - 2013-04-26
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Circ Res. 2000 Apr 28;86(8):906-14 [10785514]
Arterioscler Thromb Vasc Biol. 2007 Feb;27(2):380-6 [17158350]
J Clin Invest. 2000 Jun;105(11):1605-12 [10841519]
Am J Pathol. 2001 Oct;159(4):1455-64 [11583973]
Br J Pharmacol. 2001 Oct;134(4):865-70 [11606327]
J Vasc Surg. 2001 Oct;34(4):730-8 [11668331]
J Clin Invest. 2002 Sep;110(5):625-32 [12208863]
Physiol Genomics. 2002 Oct 2;11(1):21-30 [12361987]
J Pharmacol Exp Ther. 2002 Nov;303(2):563-73 [12388637]
Arterioscler Thromb Vasc Biol. 2003 Mar 1;23(3):483-8 [12615694]
Circ Res. 2003 Mar 21;92(5):510-7 [12600880]
J Clin Invest. 2003 Aug;112(4):566-74 [12925697]
Annu Rev Physiol. 2007;69:483-510 [17305471]
Circulation. 2008 Mar 11;117(10):1302-9 [18285567]
Circ Res. 2008 Jul 3;103(1):70-9 [18519945]
Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1660-5 [19252100]
J Pharmacol Exp Ther. 2009 Jul;330(1):118-24 [19351865]
Nat Rev Cardiol. 2009 Jul;6(7):464-74 [19468292]
Nat Rev Cardiol. 2009 Aug;6(8):543-52 [19546866]
Carcinogenesis. 2009 Sep;30(9):1620-7 [19587094]
Arterioscler Thromb Vasc Biol. 2009 Nov;29(11):1764-71 [19729613]
Dev Cell. 2009 Oct;17(4):443-58 [19853559]
J Cell Physiol. 2010 Nov;225(2):406-16 [20589830]
Science. 1999 Dec 24;286(5449):2495-8 [10617462]
FASEB J. 2010 Oct;24(10):3770-81 [20495177]
J Zhejiang Univ Sci B. 2011 Aug;12(8):624-8 [21796801]
Am J Pathol. 2011 Sep;179(3):1542-8 [21763672]
Trends Biochem Sci. 2011 Sep;36(9):457-69 [21764321]
Hypertension. 2000 Jan;35(1 Pt 1):68-75 [10642277]
Adv Pharmacol. 2011;62:79-107 [21907907]
Arterioscler Thromb Vasc Biol. 2011 Dec;31(12):2845-52 [21868698]
PLoS One. 2012;7(5):e36724 [22570740]
Am J Pathol. 2012 Jul;181(1):313-21 [22595380]
J Hypertens. 2011 Mar;29(3):529-36 [21169864]
Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1621-6 [12855482]
J Clin Invest. 2003 Nov;112(9):1318-31 [14597759]
Hypertension. 2004 Feb;43(2):364-9 [14718360]
J Biol Chem. 2004 Feb 27;279(9):7807-11 [14711824]
Arterioscler Thromb Vasc Biol. 2004 Mar;24(3):429-34 [14739119]
Nat Med. 2004 Sep;10(9):966-73 [15322539]
Biochem Biophys Res Commun. 1992 May 29;185(1):253-9 [1599461]
J Clin Invest. 1995 Jul;96(1):318-26 [7615801]
Arterioscler Thromb Vasc Biol. 1995 Aug;15(8):1145-51 [7627708]
J Vasc Surg. 1997 May;25(5):810-5 [9152308]
Arterioscler Thromb Vasc Biol. 1998 Oct;18(10):1625-33 [9763536]
Circulation. 1999 Jul 6;100(1):48-54 [10393680]
Ann N Y Acad Sci. 1999 Jun 30;878:159-78 [10415728]
Br J Pharmacol. 2005 Feb;144(3):443-8 [15655500]
Circulation. 2005 May 3;111(17):2219-26 [15851596]
Atherosclerosis. 2006 Feb;184(2):312-21 [16023123]
Arterioscler Thromb Vasc Biol. 2006 May;26(5):1137-43 [16514081]
Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16284-9 [17060617]
Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2605-13 [16973970]
Mol Cell. 2006 Dec 8;24(5):643-52 [17157248]
Cardiovasc Res. 2007 Jan 1;73(1):227-36 [17137566]
Pharmacol Ther. 2007 Jan;113(1):210-26 [17125841]
Am J Physiol Cell Physiol. 2007 Jan;292(1):C82-97 [16870827]
J Appl Physiol (1985). 2000 May;88(5):1537-44 [10797109]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1161/CIRCRESAHA.112.280399
ER  - 



TY  - CPAPER
T1  - Regulation of myelination by action potentials and an introduction to neuron-glia interactions
T2  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AN  - 1510098227; 6271997
JF  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AU  - Fields, R
Y1  - 2013/04/20/
PY  - 2013
DA  - 2013 Apr 20
KW  - Action potential
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510098227?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.atitle=Regulation+of+myelination+by+action+potentials+and+an+introduction+to+neuron-glia+interactions&rft.au=Fields%2C+R&rft.aulast=Fields&rft.aufirst=R&rft.date=2013-04-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aspet.org/EB2013/program/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Research funder perspective: PhD graduate attributes - future needs
T2  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AN  - 1510098025; 6272008
JF  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AU  - Hall, Alison
Y1  - 2013/04/20/
PY  - 2013
DA  - 2013 Apr 20
KW  - Experimental biology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510098025?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.atitle=Research+funder+perspective%3A+PhD+graduate+attributes+-+future+needs&rft.au=Hall%2C+Alison&rft.aulast=Hall&rft.aufirst=Alison&rft.date=2013-04-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aspet.org/EB2013/program/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Danger, tissue injury and immunity
T2  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AN  - 1510097699; 6271929
JF  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AU  - Matzinger, Polly
Y1  - 2013/04/20/
PY  - 2013
DA  - 2013 Apr 20
KW  - Injuries
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510097699?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.atitle=Danger%2C+tissue+injury+and+immunity&rft.au=Matzinger%2C+Polly&rft.aulast=Matzinger&rft.aufirst=Polly&rft.date=2013-04-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aspet.org/EB2013/program/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Identification of substituted benzazepines as functionally selective ligands of the D1dopamine receptor
T2  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AN  - 1510097431; 6271991
JF  - 2013 Conference on Experimental Biology of the American Society for Pharmacology and Experimental Therapeutics (EB 2013)
AU  - Conroy, Jennie
Y1  - 2013/04/20/
PY  - 2013
DA  - 2013 Apr 20
KW  - Ligands
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510097431?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.atitle=Identification+of+substituted+benzazepines+as+functionally+selective+ligands+of+the+D1dopamine+receptor&rft.au=Conroy%2C+Jennie&rft.aulast=Conroy&rft.aufirst=Jennie&rft.date=2013-04-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Conference+on+Experimental+Biology+of+the+American+Society+for+Pharmacology+and+Experimental+Therapeutics+%28EB+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aspet.org/EB2013/program/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - JOUR
T1  - Improving the Human Hazard Characterization of Chemicals: A Tox21 Update
AN  - 1660060476; 18970790
AB  - Background: In 2008, the National Institute of Environmental Health Sciences/National Toxicology Program, the U.S. Environmental Protection Agency's National Center for Computational Toxicology, and the National Human Genome Research Institute/National Institutes of Health Chemical Genomics Center entered into an agreement on "high throughput screening, toxicity pathway profiling, and biological interpretation of findings." In 2010, the U.S. Food and Drug Administration (FDA) joined the collaboration, known informally as Tox21. Objectives: The Tox21 partners agreed to develop a vision and devise an implementation strategy to shift the assessment of chemical hazards away from traditional experimental animal toxicology studies to one based on target-specific, mechanism-based, biological observations largely obtained using in vitro assays. Discussion: Here we outline the efforts of the Tox21 partners up to the time the FDA joined the collaboration, describe the approaches taken to develop the science and technologies that are currently being used, assess the current status, and identify problems that could impede further progress as well as suggest approaches to address those problems. Conclusion: Tox21 faces some very difficult issues. However, we are making progress in integrating data from diverse technologies and end points into what is effectively a systems-biology approach to toxicology. This can be accomplished only when comprehensive knowledge is obtained with broad coverage of chemical and biological/toxicological space. The efforts thus far reflect the initial stage of an exceedingly complicated program, one that will likely take decades to fully achieve its goals. However, even at this stage, the information obtained has attracted the attention of the international scientific community, and we believe these efforts foretell the future of toxicology.
JF  - Environmental Health Perspectives
AU  - Tice, Raymond R
AU  - Austin, Christopher P
AU  - Kavlock, Robert J
AU  - Bucher, John R
AD  - 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  - 2013/04/19/
PY  - 2013
DA  - 2013 Apr 19
SP  - 756
EP  - 765
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 7
SN  - 0091-6765, 0091-6765
KW  - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - chemical hazard characterization
KW  - computational biology
KW  - high throughput testing
KW  - in vitro models
KW  - systems biology
KW  - Tox21
KW  - Hazards
KW  - Assessments
KW  - Human
KW  - Biological
KW  - Health
KW  - Toxicity
KW  - Drugs
KW  - Toxicology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660060476?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Improving+the+Human+Hazard+Characterization+of+Chemicals%3A+A+Tox21+Update&rft.au=Tice%2C+Raymond+R%3BAustin%2C+Christopher+P%3BKavlock%2C+Robert+J%3BBucher%2C+John+R&rft.aulast=Tice&rft.aufirst=Raymond&rft.date=2013-04-19&rft.volume=121&rft.issue=7&rft.spage=756&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205784
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-05-04
DO  - http://dx.doi.org/10.1289/ehp.1205784
ER  - 



TY  - JOUR
T1  - Expedient synthesis of highly potent antagonists of inhibitor of apoptosis proteins (IAPs) with unique selectivity for ML-IAP.
AN  - 1331089546; 23323685
AB  - A series of novel, potent antagonists of the inhibitor of apoptosis proteins (IAPs) were synthesized in a highly convergent and rapid fashion (≤6 steps) using the Ugi four-component reaction as the key step, thus enabling rapid optimization of binding potency. These IAP antagonists compete with caspases 3, 7, and 9 for inhibition by X chromosome-linked IAP (XIAP) and bind strongly (nanomolar binding constants) to several crucial members of the IAP family of cancer pro-survival proteins to promote apoptosis, with a particularly unique selectivity for melanoma IAP (ML-IAP). Experiments in cell culture revealed powerful cancer cell growth inhibitory activity in multiple (breast, ovarian, and prostate) cell lines with single agent toxicity at low nanomolar levels against SKOV-3 human ovarian carcinoma cells. Administration of the compounds to human foreskin fibroblast cells revealed no general toxicity to normal cells. Furthermore, computational modeling was performed, revealing key contacts between the IAP proteins and antagonists, suggesting a structural basis for the observed potency.
JF  - ACS chemical biology
AU  - Vamos, Mitchell
AU  - Welsh, Kate
AU  - Finlay, Darren
AU  - Lee, Pooi San
AU  - Mace, Peter D
AU  - Snipas, Scott J
AU  - Gonzalez, Monica L
AU  - Ganji, Santhi Reddy
AU  - Ardecky, Robert J
AU  - Riedl, Stefan J
AU  - Salvesen, Guy S
AU  - Vuori, Kristiina
AU  - Reed, John C
AU  - Cosford, Nicholas D P
AD  - Program in Apoptosis and Cell Death and NCI Designated Cancer Center, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Y1  - 2013/04/19/
PY  - 2013
DA  - 2013 Apr 19
SP  - 725
EP  - 732
VL  - 8
IS  - 4
KW  - Caspase Inhibitors
KW  - 0
KW  - Inhibitor of Apoptosis Proteins
KW  - Index Medicus
KW  - Fluorescence Polarization
KW  - Caspase Inhibitors -- pharmacology
KW  - Models, Molecular
KW  - Drug Design
KW  - Inhibitor of Apoptosis Proteins -- antagonists & inhibitors
KW  - Melanoma -- metabolism
KW  - Inhibitor of Apoptosis Proteins -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1331089546?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+chemical+biology&rft.atitle=Expedient+synthesis+of+highly+potent+antagonists+of+inhibitor+of+apoptosis+proteins+%28IAPs%29+with+unique+selectivity+for+ML-IAP.&rft.au=Vamos%2C+Mitchell%3BWelsh%2C+Kate%3BFinlay%2C+Darren%3BLee%2C+Pooi+San%3BMace%2C+Peter+D%3BSnipas%2C+Scott+J%3BGonzalez%2C+Monica+L%3BGanji%2C+Santhi+Reddy%3BArdecky%2C+Robert+J%3BRiedl%2C+Stefan+J%3BSalvesen%2C+Guy+S%3BVuori%2C+Kristiina%3BReed%2C+John+C%3BCosford%2C+Nicholas+D+P&rft.aulast=Vamos&rft.aufirst=Mitchell&rft.date=2013-04-19&rft.volume=8&rft.issue=4&rft.spage=725&rft.isbn=&rft.btitle=&rft.title=ACS+chemical+biology&rft.issn=1554-8937&rft_id=info:doi/10.1021%2Fcb3005512
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-17
N1  - Date created - 2013-04-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Biol Chem. 2001 Feb 2;276(5):3238-46 [11024045]
Biochem Biophys Res Commun. 2000 Dec 29;279(3):820-31 [11162435]
J Med Chem. 2004 Aug 26;47(18):4417-26 [15317454]
Anal Biochem. 2004 Sep 15;332(2):261-73 [15325294]
J Med Chem. 1997 May 23;40(11):1570-7 [9171867]
Chemistry. 2004 Nov 5;10(22):5681-8 [15470696]
EMBO J. 2005 Feb 9;24(3):645-55 [15650747]
Chem Rev. 2005 May;105(5):1735-66 [15884788]
J Am Chem Soc. 2006 Oct 25;128(42):13761-71 [17044704]
ACS Chem Biol. 2006 Sep 19;1(8):525-33 [17168540]
J Org Chem. 2007 Mar 16;72(6):1871-82 [17346029]
Cancer Cell. 2007 Nov;12(5):445-56 [17996648]
Cell Death Differ. 2008 May;15(5):920-8 [18239672]
Mol Cancer Ther. 2008 Dec;7(12):3661-9 [19074843]
J Med Chem. 2009 Mar 26;52(6):1723-30 [19228017]
Cancer Res. 2009 Jul 1;69(13):5475-80 [19549891]
J Biol Chem. 2009 Aug 14;284(33):21777-81 [19473994]
Bioorg Med Chem Lett. 2010 Apr 1;20(7):2229-33 [20189383]
Protein Sci. 2010 Dec;19(12):2418-29 [20954235]
Curr Top Microbiol Immunol. 2011;348:89-113 [21072626]
J Med Chem. 2011 Apr 28;54(8):2714-26 [21443232]
Bioorg Med Chem Lett. 2011 Jul 15;21(14):4332-6 [21680182]
Mol Cancer Ther. 2012 Jan;11(1):3-13 [22234808]
Nat Rev Drug Discov. 2012 Feb;11(2):109-24 [22293567]
PLoS One. 2012;7(4):e35073 [22558117]
J Med Chem. 2012 May 10;55(9):4101-13 [22413863]
Curr Biol. 2000 Nov 2;10(21):1359-66 [11084335]
Cell. 2000 Jan 7;100(1):57-70 [10647931]
Biochem J. 2012 Nov 1;447(3):427-36 [22853455]
Nature. 2000 Dec 21-28;408(6815):1004-8 [11140637]
Annu Rev Med. 2002;53:615-27 [11818492]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1021/cb3005512
ER  - 



TY  - JOUR
T1  - Biological profile of the less lipophilic and synthetically more accessible bryostatin 7 closely resembles that of bryostatin 1.
AN  - 1331087827; 23369356
AB  - The bryostatins are a group of 20 macrolides isolated by Pettit and co-workers from the marine organism Bugula neritina. Bryostatin 1, the flagship member of the family, has been the subject of intense chemical and biological investigations due to its remarkably diverse biological activities, including promising indications as therapy for cancer, Alzheimer's disease, and HIV. Other bryostatins, however, have attracted far less attention, most probably due to their relatively low natural abundance and associated scarcity of supply. Among all macrolides in this family, bryostatin 7 is biologically the most potent protein kinase C (PKC) ligand (in terms of binding affinity) and also the first bryostatin to be synthesized in the laboratory. Nonetheless, almost no biological studies have been carried out on this agent. We describe herein the total synthesis of bryostatin 7 based on our pyran annulation technology, which allows for the first detailed biological characterizations of bryostatin 7 with side-by-side comparisons to bryostatin 1. The results suggest that the more easily synthesized and less lipophilic bryostatin 7 may be an effective surrogate for bryostatin 1.
JF  - ACS chemical biology
AU  - Kedei, Noemi
AU  - Lewin, Nancy E
AU  - Géczy, Tamás
AU  - Selezneva, Julia
AU  - Braun, Derek C
AU  - Chen, Jinqiu
AU  - Herrmann, Michelle A
AU  - Heldman, Madeleine R
AU  - Lim, Langston
AU  - Mannan, Poonam
AU  - Garfield, Susan H
AU  - Poudel, Yam B
AU  - Cummins, Thomas J
AU  - Rudra, Arnab
AU  - Blumberg, Peter M
AU  - Keck, Gary E
AD  - Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Y1  - 2013/04/19/
PY  - 2013
DA  - 2013 Apr 19
SP  - 767
EP  - 777
VL  - 8
IS  - 4
KW  - Bryostatins
KW  - 0
KW  - Isoenzymes
KW  - Lipids
KW  - bryostatin 7
KW  - bryostatin 1
KW  - 37O2X55Y9E
KW  - Protein Kinase C
KW  - EC 2.7.11.13
KW  - Index Medicus
KW  - Real-Time Polymerase Chain Reaction
KW  - Protein Kinase C -- metabolism
KW  - Membrane Potential, Mitochondrial -- drug effects
KW  - Down-Regulation
KW  - Humans
KW  - Cell Line, Tumor
KW  - Subcellular Fractions -- enzymology
KW  - Male
KW  - Isoenzymes -- metabolism
KW  - U937 Cells
KW  - Lipids -- chemistry
KW  - Bryostatins -- chemical synthesis
KW  - Bryostatins -- chemistry
KW  - Bryostatins -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1331087827?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+chemical+biology&rft.atitle=Biological+profile+of+the+less+lipophilic+and+synthetically+more+accessible+bryostatin+7+closely+resembles+that+of+bryostatin+1.&rft.au=Kedei%2C+Noemi%3BLewin%2C+Nancy+E%3BG%C3%A9czy%2C+Tam%C3%A1s%3BSelezneva%2C+Julia%3BBraun%2C+Derek+C%3BChen%2C+Jinqiu%3BHerrmann%2C+Michelle+A%3BHeldman%2C+Madeleine+R%3BLim%2C+Langston%3BMannan%2C+Poonam%3BGarfield%2C+Susan+H%3BPoudel%2C+Yam+B%3BCummins%2C+Thomas+J%3BRudra%2C+Arnab%3BBlumberg%2C+Peter+M%3BKeck%2C+Gary+E&rft.aulast=Kedei&rft.aufirst=Noemi&rft.date=2013-04-19&rft.volume=8&rft.issue=4&rft.spage=767&rft.isbn=&rft.btitle=&rft.title=ACS+chemical+biology&rft.issn=1554-8937&rft_id=info:doi/10.1021%2Fcb300671s
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-17
N1  - Date created - 2013-04-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Eur J Cell Biol. 2000 Nov;79(11):824-33 [11139146]
Clin Cancer Res. 2000 Apr;6(4):1498-507 [10778982]
Cancer Chemother Pharmacol. 2002 Jan;49(1):69-77 [11855754]
Org Lett. 2002 Apr 4;4(7):1189-92 [11922815]
Mol Pharmacol. 2003 Jan;63(1):232-42 [12488556]
Acc Chem Res. 2003 Jun;36(6):434-43 [12809530]
J Biol Chem. 2004 Feb 13;279(7):5788-801 [14638691]
Cancer Res. 2004 May 1;64(9):3243-55 [15126366]
Proc Natl Acad Sci U S A. 2004 Jul 27;101(30):11141-6 [15263077]
Cancer Res. 1968 Nov;28(11):2338-49 [5723975]
Planta Med. 1984 Feb;50(1):65-9 [6739574]
Biochem Biophys Res Commun. 1985 Sep 30;131(3):1109-16 [2996535]
Biochim Biophys Acta. 1987 Jun 15;929(1):40-6 [3036247]
Proc Natl Acad Sci U S A. 1988 Oct;85(19):7197-201 [3174627]
Biochem Biophys Res Commun. 1989 Aug 15;162(3):1207-13 [2764930]
Cancer Res. 1992 Jun 1;52(11):3119-24 [1591725]
Cancer Res. 1992 Oct 1;52(19):5353-8 [1394140]
Cancer Res. 1993 Jun 1;53(11):2507-12 [8495413]
Mol Pharmacol. 1993 Aug;44(2):298-307 [8355667]
Mol Pharmacol. 1994 Aug;46(2):374-9 [8078499]
Cell. 1995 Jun 16;81(6):917-24 [7781068]
Anticancer Drugs. 1995 Jun;6(3):384-91 [7670135]
Science. 1996 May 3;272(5262):728-31 [8614835]
AIDS. 1996 Jul;10(8):819-26 [8828738]
Blood. 1997 May 1;89(9):3402-11 [9129048]
Cancer Res. 1998 Apr 1;58(7):1423-8 [9537243]
Differentiation. 1998 May;63(1):33-42 [9615391]
Biosci Biotechnol Biochem. 1998 Aug;62(8):1568-73 [9757563]
Biochem Pharmacol. 1998 Oct 1;56(7):861-9 [9774148]
Cardiol Rev. 2005 Jan-Feb;13(1):3-12 [15596021]
J Biol Chem. 2005 Mar 4;280(9):8164-71 [15611119]
Eur J Pharmacol. 2005 Apr 4;512(1):43-51 [15814089]
Biol Bull. 2006 Jun;210(3):201-14 [16801495]
Clin Cancer Res. 2006 Sep 15;12(18):5336-45 [17000666]
Nat Rev Cancer. 2007 Apr;7(4):281-94 [17384583]
Nat Rev Cancer. 2007 Jul;7(7):554-62 [17585335]
Eur J Pharmacol. 2008 Apr 28;584(2-3):328-37 [18313045]
J Am Chem Soc. 2008 May 28;130(21):6660-1 [18452293]
Curr Drug Targets. 2008 Aug;9(8):614-25 [18691009]
PLoS One. 2010;5(6):e11160 [20585398]
Mol Pharmacol. 2010 Sep;78(3):325-32 [20516369]
J Am Chem Soc. 2011 Feb 2;133(4):744-7 [21175177]
J Biol Chem. 2011 Apr 1;286(13):11254-64 [21252239]
Biochem Pharmacol. 2011 Jun 1;81(11):1296-308 [21458422]
Chembiochem. 2011 May 16;12(8):1242-51 [21542090]
Biochem Pharmacol. 2013 Feb 1;85(3):313-24 [23146662]
J Biol Chem. 1999 Dec 24;274(52):37233-9 [10601287]
J Biol Chem. 2000 Apr 21;275(16):12136-46 [10766849]
Clin Cancer Res. 2000 Dec;6(12):4950-6 [11156256]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1021/cb300671s
ER  - 



TY  - JOUR
T1  - Effectiveness of Monovalent 2009 Pandemic Influenza A Virus Subtype H1N1 and 2010-2011 Trivalent Inactivated Influenza Vaccines in Wisconsin During the 2010-2011 Influenza Season
AN  - 1622602725; 20900182
AB  - Background. The 2009 influenza A virus subtype H1N1 (A[H1N1]pdm09) did not exhibit antigenic drift during the 2010-2011 influenza season, providing an opportunity to investigate the duration of protection after vaccination. We estimated the independent effects of 2010-2011 seasonal trivalent inactivated influenza vaccine (TIV) and A (H1N1)pdm09 vaccine for preventing medically attended influenza A virus infection during the 2010-2011 season. Methods. Individuals were tested for influenza A virus by real-time reverse transcription polymerase chain reaction (rRT-PCR) after a clinical encounter for acute respiratory illness. Case-control analyses compared participants with rRT-PCR-confirmed influenza A virus infection and test-negative controls. Vaccine effectiveness was estimated separately for monovalent pandemic vaccine and TIV and was calculated as 100 x [1 - adjusted odds ratio], where the odds ratio was adjusted for potential confounders. Results. The effectiveness of TIV against influenza A virus infection was 63% (95% confidence interval [CI], 37%-78%). The effectiveness of TIV against A(H1N1)pdm09 infection was 77% (95% CI, 44%-90%). Monovalent vaccine administered between October 2009 and April 2010 was not protective during the 2010-2011 season, with an effectiveness of -1% (95% CI, -146% to 59%) against A(H1N1)pdm09 infection. Conclusions. Monovalent vaccine provided no sustained protection against A(H1N1)pdm09 infection during the 2010-2011 season. This waning effectiveness supports the need for annual revaccination, even in the absence of antigenic drift in A(H1N1)pdm09.
JF  - Journal of Infectious Diseases
AU  - Bateman, Allen C
AU  - Kieke, Burney A
AU  - Irving, Stephanie A
AU  - Meece, Jennifer K
AU  - Shay, David K
AU  - Belongia, Edward A
AD  - Marshfield Clinic Research Foundation, Marshfield, Wisconsin; National Institutes of Health Fogarty Global Health post-doctoral fellow, Centre for Infectious Disease Research, Zambia, belongia.edward@marshfieldclinic.org
Y1  - 2013/04/15/
PY  - 2013
DA  - 2013 Apr 15
SP  - 1262
EP  - 1269
PB  - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 207
IS  - 8
SN  - 0022-1899, 0022-1899
KW  - Virology & AIDS Abstracts; Health & Safety Science Abstracts
KW  - case-control studies
KW  - effectiveness
KW  - epidemiology
KW  - influenza
KW  - vaccine
KW  - USA, Wisconsin
KW  - Infection
KW  - Reverse transcription
KW  - Influenza
KW  - pandemics
KW  - Sulfur dioxide
KW  - Antigenic drift
KW  - Infectious diseases
KW  - Influenza A virus
KW  - Polymerase chain reaction
KW  - Vaccines
KW  - Seasonal variations
KW  - H 1000:Occupational Safety and Health
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622602725?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Effectiveness+of+Monovalent+2009+Pandemic+Influenza+A+Virus+Subtype+H1N1+and+2010-2011+Trivalent+Inactivated+Influenza+Vaccines+in+Wisconsin+During+the+2010-2011+Influenza+Season&rft.au=Bateman%2C+Allen+C%3BKieke%2C+Burney+A%3BIrving%2C+Stephanie+A%3BMeece%2C+Jennifer+K%3BShay%2C+David+K%3BBelongia%2C+Edward+A&rft.aulast=Bateman&rft.aufirst=Allen&rft.date=2013-04-15&rft.volume=207&rft.issue=8&rft.spage=1262&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjit020
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Last updated - 2016-04-13
N1  - SubjectsTermNotLitGenreText - pandemics; Antigenic drift; Polymerase chain reaction; Vaccines; Infection; Reverse transcription; Influenza; Sulfur dioxide; Infectious diseases; Seasonal variations; Influenza A virus; USA, Wisconsin
DO  - http://dx.doi.org/10.1093/infdis/jit020
ER  - 



TY  - JOUR
T1  - A Prospective Study of Medical Diagnostic Radiography and Risk of Thyroid Cancer
AN  - 1352285149; 17938929
AB  - Although diagnostic x-ray procedures provide important medical benefits, cancer risks associated with their exposure are also possible, but not well characterized. The US Radiologic Technologists Study (1983-2006) is a nationwide, prospective cohort study with extensive questionnaire data on history of personal diagnostic imaging procedures collected prior to cancer diagnosis. We used Cox proportional hazard regressions to estimate thyroid cancer risks related to the number and type of selected procedures. We assessed potential modifying effects of age and calendar year of the first x-ray procedure in each category of procedures. Incident thyroid cancers (n = 251) were diagnosed among 75,494 technologists (1.3 million person-years; mean follow-up = 17 years). Overall, there was no clear evidence of thyroid cancer risk associated with diagnostic x-rays except for dental x-rays. We observed a 13% increase in thyroid cancer risk for every 10 reported dental radiographs (hazard ratio = 1.13, 95% confidence interval: 1.01, 1.26), which was driven by dental x-rays first received before 1970, but we found no evidence that the relationship between dental x-rays and thyroid cancer was associated with childhood or adolescent exposures as would have been anticipated. The lack of association of thyroid cancer with x-ray procedures that expose the thyroid to higher radiation doses than do dental x-rays underscores the need to conduct a detailed radiation exposure assessment to enable quantitative evaluation of risk.
JF  - American Journal of Epidemiology
AU  - Neta, Gila
AU  - Rajaraman, Preetha
AU  - Berrington de Gonzalez, Amy
AU  - Doody, Michele M
AU  - Alexander, Bruce H
AU  - Preston, Dale
AU  - Simon, Steven L
AU  - Melo, Dunstana
AU  - Miller, Jeremy
AU  - Freedman, D Michal
AU  - Linet, Martha S
AU  - Sigurdson, Alice J
AD  - Correspondence to Dr. Gila Neta, Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, EPS 7049, MSC 7238, Bethesda, MD 20892-7238., netagil@mail.nih.gov
Y1  - 2013/04/15/
PY  - 2013
DA  - 2013 Apr 15
SP  - 800
EP  - 809
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 8
SN  - 0002-9262, 0002-9262
KW  - Risk Abstracts
KW  - Historical account
KW  - Age
KW  - Thyroid
KW  - Radiography
KW  - Children
KW  - Cancer
KW  - Adolescents
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352285149?accountid=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=A+Prospective+Study+of+Medical+Diagnostic+Radiography+and+Risk+of+Thyroid+Cancer&rft.au=Neta%2C+Gila%3BRajaraman%2C+Preetha%3BBerrington+de+Gonzalez%2C+Amy%3BDoody%2C+Michele+M%3BAlexander%2C+Bruce+H%3BPreston%2C+Dale%3BSimon%2C+Steven+L%3BMelo%2C+Dunstana%3BMiller%2C+Jeremy%3BFreedman%2C+D+Michal%3BLinet%2C+Martha+S%3BSigurdson%2C+Alice+J&rft.aulast=Neta&rft.aufirst=Gila&rft.date=2013-04-15&rft.volume=177&rft.issue=8&rft.spage=800&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws315
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2013-11-04
N1  - SubjectsTermNotLitGenreText - Historical account; Age; Thyroid; Radiography; Children; Adolescents; Cancer
DO  - http://dx.doi.org/10.1093/aje/kws315
ER  - 



TY  - JOUR
T1  - Body Mass Index and Physical Activity at Different Ages and Risk of Multiple Myeloma in the NIH-AARP Diet and Health Study
AN  - 1352282584; 17938935
AB  - Several studies have reported an increased risk of multiple myeloma associated with excess body weight. We investigated the risk of multiple myeloma in relation to separate measures of adiposity and energy balance at different ages in the National Institutes of Health-AARP Diet and Health Study, a large prospective cohort study in the United States. Participants completed a baseline questionnaire (1995-1996; n = 485,049), and a subset of participants completed a second questionnaire (1996-1997; n = 305,618) in which we solicited more detailed exposure information. Hazard ratios and 95% confidence intervals were estimated for the risk of multiple myeloma (overall, n = 813; subset, n = 489) in relation to several measures of obesity and leisure time physical activity. Multiple myeloma risk was associated with increasing body mass index (BMI) at cohort entry (per 5-kg/m super(2) increase, hazard ratio (HR) = 1.10, 95% confidence interval (CI): 1.00, 1.22); similar associations were observed for BMI at age 50 years (HR = 1.14, 95% CI: 1.02, 1.28), age 35 years (HR = 1.20, 95% CI: 1.05, 1.36), and age 18 years (HR = 1.13, 95% CI: 0.98, 1.32) without adjustment for baseline BMI. Risk of multiple myeloma was not associated with physical activity level at any age. These findings support the hypothesis that excess body weight, both in early adulthood and later in life, is a risk factor for multiple myeloma and suggest that maintaining a healthy body weight throughout life may reduce multiple myeloma risk.
JF  - American Journal of Epidemiology
AU  - Hofmann, Jonathan N
AU  - Moore, Steven C
AU  - Lim, Unhee
AU  - Park, Yikyung
AU  - Baris, Dalsu
AU  - Hollenbeck, Albert R
AU  - Matthews, Charles E
AU  - Gibson, Todd M
AU  - Hartge, Patricia
AU  - Purdue, Mark P
AD  - Correspondence to Dr. Jonathan N. Hofmann, Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, EPS 8109, Bethesda, MD 20892-7240., hofmannjn@mail.nih.gov
Y1  - 2013/04/15/
PY  - 2013
DA  - 2013 Apr 15
SP  - 776
EP  - 786
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 8
SN  - 0002-9262, 0002-9262
KW  - Physical Education Index; Health & Safety Science Abstracts; Risk Abstracts
KW  - Diets
KW  - Obesity
KW  - Age
KW  - Physical activity
KW  - Body mass
KW  - Diet (weight control)
KW  - Surveys
KW  - Health
KW  - Exercise
KW  - USA
KW  - Multiple myeloma
KW  - Body weight
KW  - Risk factors
KW  - R2 23060:Medical and environmental health
KW  - H 12000:Epidemiology and Public Health
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352282584?accountid=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=Body+Mass+Index+and+Physical+Activity+at+Different+Ages+and+Risk+of+Multiple+Myeloma+in+the+NIH-AARP+Diet+and+Health+Study&rft.au=Hofmann%2C+Jonathan+N%3BMoore%2C+Steven+C%3BLim%2C+Unhee%3BPark%2C+Yikyung%3BBaris%2C+Dalsu%3BHollenbeck%2C+Albert+R%3BMatthews%2C+Charles+E%3BGibson%2C+Todd+M%3BHartge%2C+Patricia%3BPurdue%2C+Mark+P&rft.aulast=Hofmann&rft.aufirst=Jonathan&rft.date=2013-04-15&rft.volume=177&rft.issue=8&rft.spage=776&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws295
LA  - English
DB  - Physical Education Index; ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Obesity; Risk factors; Body mass; Diet (weight control); Surveys; Health; Exercise; Diets; Age; Body weight; Multiple myeloma; Physical activity; USA
DO  - http://dx.doi.org/10.1093/aje/kws295
ER  - 



TY  - JOUR
T1  - PleioGRiP: genetic risk prediction with pleiotropy
AN  - 1352282558; 17938957
AB  - Motivation: Although several studies have used Bayesian classifiers for risk prediction using genome-wide single nucleotide polymorphism (SNP) datasets, no software can efficiently perform these analyses on massive genetic datasets and can accommodate multiple traits.Results: We describe the program PleioGRiP that performs a genome-wide Bayesian model search to identify SNPs associated with a discrete phenotype and uses SNPs ranked by Bayes factor to produce nested Bayesian classifiers. These classifiers can be used for genetic risk prediction, either selecting the classifier with optimal number of features or using an ensemble of classifiers. In addition, PleioGRiP implements an extension to the Bayesian search and classification and can search for pleiotropic relationships in which SNPs are simultaneosly associated with two or more distinct phenotypes. These relationships can be used to generate connected Bayesian classifiers to predict the phenotype of interest either using genetic data alone or in combination with the secondary phenotype(s).
JF  - Bioinformatics
AU  - Hartley, Stephen W
AU  - Sebastiani, Paola
AD  - super(1)National Institutes of Health/National Human Genome Research Institute, 5625 Fishers Lane, Suite 5 N-01, Rockville, MD 20850, USA and super(2)Department of Biostatistics, Boston University School of Public Health, 801 Massachusetts Avenue, Boston MA 02118, USA
Y1  - 2013/04/15/
PY  - 2013
DA  - 2013 Apr 15
SP  - 1086
EP  - 1088
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 8
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Computer programs
KW  - pleiotropy
KW  - software
KW  - Data processing
KW  - Mathematical models
KW  - Bayesian analysis
KW  - Single-nucleotide polymorphism
KW  - Bioinformatics
KW  - Internet
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352282558?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=PleioGRiP%3A+genetic+risk+prediction+with+pleiotropy&rft.au=Hartley%2C+Stephen+W%3BSebastiani%2C+Paola&rft.aulast=Hartley&rft.aufirst=Stephen&rft.date=2013-04-15&rft.volume=29&rft.issue=8&rft.spage=1086&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt081
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Computer programs; software; pleiotropy; Mathematical models; Data processing; Single-nucleotide polymorphism; Bayesian analysis; Bioinformatics; Internet
DO  - http://dx.doi.org/10.1093/bioinformatics/btt081
ER  - 



TY  - JOUR
T1  - Genetic Simulation Resources: a website for the registration and discovery of genetic data simulators
AN  - 1352282520; 17938955
AB  - Summary: Many simulation methods and programs have been developed to simulate genetic data of the human genome. These data have been widely used, for example, to predict properties of populations retrospectively or prospectively according to mathematically intractable genetic models, and to assist the validation, statistical inference and power analysis of a variety of statistical models. However, owing to the differences in type of genetic data of interest, simulation methods, evolutionary features, input and output formats, terminologies and assumptions for different applications, choosing the right tool for a particular study can be a resource-intensive process that usually involves searching, downloading and testing many different simulation programs. Genetic Simulation Resources (GSR) is a website provided by the National Cancer Institute (NCI) that aims to help researchers compare and choose the appropriate simulation tools for their studies. This website allows authors of simulation software to register their applications and describe them with well-defined attributes, thus allowing site users to search and compare simulators according to specified features.
JF  - Bioinformatics
AU  - Peng, Bo
AU  - Chen, Huann-Sheng
AU  - Mechanic, Leah E
AU  - Racine, Ben
AU  - Clarke, John
AU  - Clarke, Lauren
AU  - Gillanders, Elizabeth
AU  - Feuer, Eric J
AD  - super(1)Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, super(2)Statistical Methodology and Applications Branch, Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20892, super(3)Host Susceptibility Factors Branch, Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, NCI, NIH, Bethesda, MD 20892 and super(4)Cornerstone Systems Northwest, Inc. Lynden, WA 98264
Y1  - 2013/04/15/
PY  - 2013
DA  - 2013 Apr 15
SP  - 1101
EP  - 1102
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 8
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Genomes
KW  - Computer programs
KW  - software
KW  - Data processing
KW  - Mathematical models
KW  - Statistics
KW  - Statistical analysis
KW  - Bioinformatics
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352282520?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+Simulation+Resources%3A+a+website+for+the+registration+and+discovery+of+genetic+data+simulators&rft.au=Peng%2C+Bo%3BChen%2C+Huann-Sheng%3BMechanic%2C+Leah+E%3BRacine%2C+Ben%3BClarke%2C+John%3BClarke%2C+Lauren%3BGillanders%2C+Elizabeth%3BFeuer%2C+Eric+J&rft.aulast=Peng&rft.aufirst=Bo&rft.date=2013-04-15&rft.volume=29&rft.issue=8&rft.spage=1101&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt094
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2015-03-19
N1  - SubjectsTermNotLitGenreText - Genomes; Computer programs; software; Statistics; Mathematical models; Data processing; Statistical analysis; Bioinformatics
DO  - http://dx.doi.org/10.1093/bioinformatics/btt094
ER  - 



TY  - CPAPER
T1  - Inflammation and lung and colorectal cancer disparities
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102954; 6271012
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Harris, Curtis
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Colorectal carcinoma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102954?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Inflammation+and+lung+and+colorectal+cancer+disparities&rft.au=Harris%2C+Curtis&rft.aulast=Harris&rft.aufirst=Curtis&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Biopharmaceutical development
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102951; 6270981
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Gaum, Douglas
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102951?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Biopharmaceutical+development&rft.au=Gaum%2C+Douglas&rft.aulast=Gaum&rft.aufirst=Douglas&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Human papillomavirus immunology
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102944; 6270982
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Pinto, Ligia
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Immunology
KW  - Human papillomavirus
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102944?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Human+papillomavirus+immunology&rft.au=Pinto%2C+Ligia&rft.aulast=Pinto&rft.aufirst=Ligia&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - The leap from bench to "deskside": One PhD's transition from academia to the government
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102931; 6271088
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Hamlet, Michelle
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102931?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=The+leap+from+bench+to+%22deskside%22%3A+One+PhD%27s+transition+from+academia+to+the+government&rft.au=Hamlet%2C+Michelle&rft.aulast=Hamlet&rft.aufirst=Michelle&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Prevention of noncervical HPV-associated cancers
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102914; 6270987
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Kreimer, Aimee
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Prevention
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102914?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Prevention+of+noncervical+HPV-associated+cancers&rft.au=Kreimer%2C+Aimee&rft.aulast=Kreimer&rft.aufirst=Aimee&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Evaluating career paths
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102874; 6271091
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Conlan, Lori
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Careers
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102874?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Evaluating+career+paths&rft.au=Conlan%2C+Lori&rft.aulast=Conlan&rft.aufirst=Lori&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Antibody characterization
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102862; 6270979
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Whiteley, Gordon
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Antibodies
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102862?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Antibody+characterization&rft.au=Whiteley%2C+Gordon&rft.aulast=Whiteley&rft.aufirst=Gordon&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Overview of ADCs and what makes a good ADC target
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510102837; 6271190
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Teicher, Beverly
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510102837?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Overview+of+ADCs+and+what+makes+a+good+ADC+target&rft.au=Teicher%2C+Beverly&rft.aulast=Teicher&rft.aufirst=Beverly&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Short-term and long-term approaches to the prevention of HPV-associated cancers
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101746; 6271079
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Lowy, Douglas
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Prevention
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101746?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Short-term+and+long-term+approaches+to+the+prevention+of+HPV-associated+cancers&rft.au=Lowy%2C+Douglas&rft.aulast=Lowy&rft.aufirst=Douglas&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Targeting the genetic and metabolic basis of kidney cancer
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101722; 6271194
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Linehan, W
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Kidneys
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101722?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Targeting+the+genetic+and+metabolic+basis+of+kidney+cancer&rft.au=Linehan%2C+W&rft.aulast=Linehan&rft.aufirst=W&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Microenvironmental regulation of human glioblastoma radiosensitivity
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101719; 6271181
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Tofilon, Philip
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Glioblastoma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101719?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Microenvironmental+regulation+of+human+glioblastoma+radiosensitivity&rft.au=Tofilon%2C+Philip&rft.aulast=Tofilon&rft.aufirst=Philip&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Development of combination targeted therapy in Ewing's sarcoma: What we need for future success
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101702; 6271209
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Helman, Lee
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Sarcoma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101702?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Development+of+combination+targeted+therapy+in+Ewing%27s+sarcoma%3A+What+we+need+for+future+success&rft.au=Helman%2C+Lee&rft.aulast=Helman&rft.aufirst=Lee&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Molecular mechanisms that modulate oncogenic Ras/Raf signaling
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101626; 6270945
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Morrison, Deborah
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - RAS
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101626?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Molecular+mechanisms+that+modulate+oncogenic+Ras%2FRaf+signaling&rft.au=Morrison%2C+Deborah&rft.aulast=Morrison&rft.aufirst=Deborah&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Center for Advanced Preclinical Research
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101186; 6270980
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Kozlov, Serguei
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101186?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Center+for+Advanced+Preclinical+Research&rft.au=Kozlov%2C+Serguei&rft.aulast=Kozlov&rft.aufirst=Serguei&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Candidate targets and the treatment of EBV-positive and -negative Burkitt lymphomas
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510101104; 6271078
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Schmitz, Roland
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Lymphoma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510101104?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Candidate+targets+and+the+treatment+of+EBV-positive+and+-negative+Burkitt+lymphomas&rft.au=Schmitz%2C+Roland&rft.aulast=Schmitz&rft.aufirst=Roland&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - PLCO biorepository resource for cancer etiology and early detection research
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510094095; 6270749
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Zhu, Claire
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Etiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094095?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=PLCO+biorepository+resource+for+cancer+etiology+and+early+detection+research&rft.au=Zhu%2C+Claire&rft.aulast=Zhu&rft.aufirst=Claire&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Genome-wide detection of enhancer and promoter interactions
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510094067; 6270489
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Zhao, Keji
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Promoters
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094067?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Genome-wide+detection+of+enhancer+and+promoter+interactions&rft.au=Zhao%2C+Keji&rft.aulast=Zhao&rft.aufirst=Keji&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Dendritic cell dysfunction in cancer
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510094042; 6270418
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Hurwitz, Arthur
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Dendritic cells
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094042?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Dendritic+cell+dysfunction+in+cancer&rft.au=Hurwitz%2C+Arthur&rft.aulast=Hurwitz&rft.aufirst=Arthur&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Next-generation genomics enabling nextgeneration medicine: The promise and the challenges
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510094029; 6270393
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Khan, Javed
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - genomics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094029?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Next-generation+genomics+enabling+nextgeneration+medicine%3A+The+promise+and+the+challenges&rft.au=Khan%2C+Javed&rft.aulast=Khan&rft.aufirst=Javed&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - An overview of dbGaP content, format, and access
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510094009; 6270653
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Sherry, Stephen
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094009?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=An+overview+of+dbGaP+content%2C+format%2C+and+access&rft.au=Sherry%2C+Stephen&rft.aulast=Sherry&rft.aufirst=Stephen&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Reprogrammimg human cancer cells in vivo in the mouse mammary gland
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510093668; 6270545
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Smith, Gilbert
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Glands
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510093668?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Reprogrammimg+human+cancer+cells+in+vivo+in+the+mouse+mammary+gland&rft.au=Smith%2C+Gilbert&rft.aulast=Smith&rft.aufirst=Gilbert&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Trapping of PARP: DNA complexes: A previously unsuspected mechanism for the anticancer activity of PARP inhibitors
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510093642; 6270415
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Pommier, Yves
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Inhibitors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510093642?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Trapping+of+PARP%3A+DNA+complexes%3A+A+previously+unsuspected+mechanism+for+the+anticancer+activity+of+PARP+inhibitors&rft.au=Pommier%2C+Yves&rft.aulast=Pommier&rft.aufirst=Yves&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - The range of cancers treatable by genetically modified cells
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510093597; 6270566
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Rosenberg, Steven
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510093597?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=The+range+of+cancers+treatable+by+genetically+modified+cells&rft.au=Rosenberg%2C+Steven&rft.aulast=Rosenberg&rft.aufirst=Steven&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Alliance of Glycobiologists for Detection of Cancer
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091190; 6270975
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Krueger, Karl
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091190?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Alliance+of+Glycobiologists+for+Detection+of+Cancer&rft.au=Krueger%2C+Karl&rft.aulast=Krueger&rft.aufirst=Karl&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Collaborative opportunity for biomarker research at NCI
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091185; 6270976
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Srivastava, Sudhir
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Bioindicators
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091185?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Collaborative+opportunity+for+biomarker+research+at+NCI&rft.au=Srivastava%2C+Sudhir&rft.aulast=Srivastava&rft.aufirst=Sudhir&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Problems, successes, and challenges in the research realm as we move into an era of ever more sophisticated clinical trials
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091169; 6270905
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Abrams, Jeffrey
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Clinical trials
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091169?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Problems%2C+successes%2C+and+challenges+in+the+research+realm+as+we+move+into+an+era+of+ever+more+sophisticated+clinical+trials&rft.au=Abrams%2C+Jeffrey&rft.aulast=Abrams&rft.aufirst=Jeffrey&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - NCI context: The evolution of the CRN Research Resource
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091154; 6270916
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Doria-Rose, Vincent
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Evolution
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091154?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=NCI+context%3A+The+evolution+of+the+CRN+Research+Resource&rft.au=Doria-Rose%2C+Vincent&rft.aulast=Doria-Rose&rft.aufirst=Vincent&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - NIGMS glycomics initiatives
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091111; 6270977
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Marino, Pamela
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091111?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=NIGMS+glycomics+initiatives&rft.au=Marino%2C+Pamela&rft.aulast=Marino&rft.aufirst=Pamela&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - DUCs and DARs and data, oh my!
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091037; 6270651
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Gillanders, Elizabeth
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Data processing
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091037?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=DUCs+and+DARs+and+data%2C+oh+my%21&rft.au=Gillanders%2C+Elizabeth&rft.aulast=Gillanders&rft.aufirst=Elizabeth&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Biospecimen resources supported by NCI Division of Cancer Control and Population Sciences
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091014; 6270748
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Mechanic, Leah
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091014?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Biospecimen+resources+supported+by+NCI+Division+of+Cancer+Control+and+Population+Sciences&rft.au=Mechanic%2C+Leah&rft.aulast=Mechanic&rft.aufirst=Leah&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Programs of Excellence in Glycosciences
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510091007; 6270978
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Sarkar, Rita
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091007?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Programs+of+Excellence+in+Glycosciences&rft.au=Sarkar%2C+Rita&rft.aulast=Sarkar&rft.aufirst=Rita&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Implementing point localization microscopy methods to define the organization of assembling virions
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510090872; 6270486
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - van Engelenburg, Schuyler
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Microscopy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510090872?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Implementing+point+localization+microscopy+methods+to+define+the+organization+of+assembling+virions&rft.au=van+Engelenburg%2C+Schuyler&rft.aulast=van+Engelenburg&rft.aufirst=Schuyler&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Therapeutic targets and clinical trials in lymphoma from genomics
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510090853; 6270604
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Staudt, Louis
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Lymphoma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510090853?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Therapeutic+targets+and+clinical+trials+in+lymphoma+from+genomics&rft.au=Staudt%2C+Louis&rft.aulast=Staudt&rft.aufirst=Louis&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - CPAPER
T1  - Rational combination therapy of lymphoma using the BTK inhibitor ibrutinib as a platform
T2  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AN  - 1510090822; 6270573
JF  - 2013 American Association for Cancer Research Annual Meeting (AACR 2013)
AU  - Staudt, Louis
Y1  - 2013/04/06/
PY  - 2013
DA  - 2013 Apr 06
KW  - Lymphoma
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510090822?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.atitle=Rational+combination+therapy+of+lymphoma+using+the+BTK+inhibitor+ibrutinib+as+a+platform&rft.au=Staudt%2C+Louis&rft.aulast=Staudt&rft.aufirst=Louis&rft.date=2013-04-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+American+Association+for+Cancer+Research+Annual+Meeting+%28AACR+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/previous-annual-meetings/annual-meeting-2013/program.aspx
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-24
N1  - Last updated - 2014-03-26
ER  - 



TY  - JOUR
T1  - Validation of Different Instruments for Caffeine Measurement Among Premenopausal Women in the BioCycle Study
AN  - 1837317067; 17910804
AB  - Effects of caffeine on women's health are inconclusive, in part because of inadequate exposure assessment. In this study we determined 1) validity of a food frequency questionnaire compared with multiple 24-hour dietary recalls (24HDRs) for measuring monthly caffeine and caffeinated beverage intakes; and 2) validity of the 24HDR compared with the prior day's diary record for measuring daily caffeinated coffee intake. BioCycle Study (2005-2007) participants, women (n = 259) aged 18-44 years from western New York State, were followed for 2 menstrual cycles. Participants completed a food frequency questionnaire at the end of each cycle, four 24HDRs per cycle, and daily diaries. Caffeine intakes reported for the food frequency questionnaires were greater than those reported for the 24HDRs (mean = 114.1 vs. 92.6mg/day, P = 0.01) but showed high correlation (r = 0.73, P < 0.001) and moderate agreement (К = 0.51, 95% confidence interval: 0.43, 0.57). Women reported less caffeinated coffee intake in their 24HDRs compared with their corresponding diary days (mean = 0.51 vs. 0.80 cups/day, P < 0.001) (1 cup = 237 mL). Although caffeine and coffee exposures were highly correlated, absolute intakes differed significantly between measurement tools. These results highlight the importance of considering potential misclassification of caffeine exposure.
JF  - American Journal of Epidemiology
AU  - Schliep, Karen C
AU  - Schisterman, Enrique F
AU  - Mumford, Sunni L
AU  - Perkins, Neil J
AU  - Ye, Aijun
AU  - Pollack, Anna Z
AU  - Zhang, Cuilin
AU  - Porucznik, Christina A
AU  - VanDerslice, James A
AU  - Stanford, Joseph B
AU  - Wactawski-Wende, Jean
AD  - Correspondence to Dr. Enrique F. Schisterman, Epidemiology Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Boulevard, 7B03M, Rockville, MD 20852 (e-mail: schisteeail.nih.gov)., schistee@mail.nih.gov
Y1  - 2013/04/01/
PY  - 2013
DA  - 2013 Apr 01
SP  - 690
EP  - 699
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 7
SN  - 0002-9262, 0002-9262
KW  - Toxicology Abstracts
KW  - beverages
KW  - caffeine
KW  - diet
KW  - mental recall
KW  - nutrition assessment
KW  - questionnaires
KW  - validation studies
KW  - women
KW  - Coffee
KW  - Inventories
KW  - Beverages
KW  - Food
KW  - Caffeine
KW  - X 24380:Social Poisons & Drug Abuse
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837317067?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Validation+of+Different+Instruments+for+Caffeine+Measurement+Among+Premenopausal+Women+in+the+BioCycle+Study&rft.au=Schliep%2C+Karen+C%3BSchisterman%2C+Enrique+F%3BMumford%2C+Sunni+L%3BPerkins%2C+Neil+J%3BYe%2C+Aijun%3BPollack%2C+Anna+Z%3BZhang%2C+Cuilin%3BPorucznik%2C+Christina+A%3BVanDerslice%2C+James+A%3BStanford%2C+Joseph+B%3BWactawski-Wende%2C+Jean&rft.aulast=Schliep&rft.aufirst=Karen&rft.date=2013-04-01&rft.volume=177&rft.issue=7&rft.spage=690&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws283
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Coffee; Inventories; Beverages; Food; Caffeine
DO  - http://dx.doi.org/10.1093/aje/kws283
ER  - 



TY  - JOUR
T1  - Social cognitive influences on physical activity participation in long-term breast cancer survivors
AN  - 1665158480
AB  - Background Although physical activity is beneficial for breast cancer survivors, the majority do not meet public health physical activity recommendations. The purpose of this study was to test a social cognitive theory model of physical activity behavior in a sample of long-term breast cancer survivors using both self-report and objective measures of physical activity. Methods Participants ( N=1527) completed measures of physical activity, self-efficacy, goals, outcome expectations, fatigue, and social support at baseline and 6-month follow-up. A subsample ( n=370) was randomly selected to wear an accelerometer. It was hypothesized that self-efficacy directly and indirectly influences physical activity through goals, social support, fatigue, and outcome expectations. Relationships were examined using panel analysis within a covariance modeling framework. Results The hypothesized model provided a good model-data fit ( χ<sup>2</sup>=1168.73, df=271, p=<0.001, CFI=0.96, SRMR=0.04) in the full sample when controlling for covariates. At baseline, self-efficacy directly and indirectly, via goals, outcome expectations, and social support, influenced physical activity. These relationships were also supported across time. Additionally, the hypothesized model was supported in the subsample with accelerometer data ( χ2=656.88, df=330, p<0.001, CFI=0.95, SRMR=0.05). Conclusions This study validates a social cognitive model for understanding physical activity behavior in long-term breast cancer survivors. Future studies should be designed to replicate this model in other breast cancer survivor populations, and the findings should be applied to the development of future physical activity programs and studies for this population. Copyright © 2012 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Phillips, Siobhan M
AU  - McAuley, Edward
AD  - Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, Bethesda, MD, 20892, USA., Department of Kinesiology and Community Health, University of Illinois Urbana Champaign, Urbana, USA. ; Department of Kinesiology and Community Health, University of Illinois Urbana Champaign, Urbana, USA. ; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, Bethesda, MD, 20892, USA.; Department of Kinesiology and Community Health, University of Illinois Urbana Champaign, Urbana, USA.
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 783
EP  - 791
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 4
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Breast cancer
KW  - Activities
KW  - Behaviour
KW  - Cognitive modelling
KW  - Cognitive-Behavioural factors
KW  - Time use
KW  - Cancer
KW  - Efficacy
KW  - Fatigue
KW  - Goals
KW  - Health status
KW  - Physical activity
KW  - Public health
KW  - Selfefficacy
KW  - Selfreport
KW  - Social cognitive theory
KW  - Social support
KW  - Survivors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665158480?accountid=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+cognitive+influences+on+physical+activity+participation+in+long-term+breast+cancer+survivors&rft.au=Phillips%2C+Siobhan+M%3BMcAuley%2C+Edward&rft.aulast=Phillips&rft.aufirst=Siobhan&rft.date=2013-04-01&rft.volume=22&rft.issue=4&rft.spage=783&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3074
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.3074
ER  - 



TY  - JOUR
T1  - Economic survivorship stress is associated with poor health-related quality of life among distressed survivors of hematopoietic stem cell transplantation
AN  - 1665153866
AB  - Background Hematopoietic stem cell transplantation is a demanding cancer treatment associated with enduring physical and psychological complications. Survivorsʼ well-being may be further compromised by exposure to chronic stressors common to this population, including difficulties arising from costly medical care, changes in employment status, and health insurance coverage. Thus, we hypothesized that financial, employment, and insurance stressors (collectively referred to as economic survivorship stressors) would be associated with poorer health-related quality of life (HRQOL) among hematopoietic stem cell transplantation survivors. Methods Survivors ( n=181; M=640 days post-transplant) completed the measures of study variables through mailed questionnaires and telephone interviews. Hierarchical regression analyses were conducted to test the hypothesized associations between economic survivorship stressors and HRQOL, and to examine whether social and situational factors interact with survivorsʼ stress perceptions to predict HRQOL. Results Greater financial and employment stress were associated with poorer functioning across multiple HRQOL domains, even after controlling for the effects of possible confounding sociodemographic and medical variables. Insurance stress was not associated with HRQOL. Some associations were moderated by situational factors including timing of the current financial crisis and portion of the transplant paid for by health insurance. Conclusions Hematopoietic stem cell transplantation survivors can face serious economic challenges during recovery. Results suggest the value of viewing these challenges as chronic stressors capable of reducing survivorsʼ mental and physical well-being. Identifying resources and skills that help survivors cope with these demands is an important goal for clinicians and researchers. Copyright © 2012 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Hamilton, Jada G
AU  - Wu, Lisa M
AU  - Austin, Jane E
AU  - Valdimarsdottir, Heiddis
AU  - Basmajian, Katie
AU  - Vu, AnnaMarie
AU  - Rowley, Scott D
AU  - Isola, Luis
AU  - Redd, William H
AU  - Rini, Christine
AD  - Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, Rockville, MD, USA. ; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY, USA. ; Department of Psychology, William Paterson University, Wayne, NJ, USA. ; The John Theurer Cancer Center, Hackensack University Medical Center, Hackensack, NJ, USA. ; Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA. ; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY, USA., Department of Health Behavior and Health Education, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, Rockville, MD, USA.
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 911
EP  - 921
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 4
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Cancer
KW  - Recovery
KW  - Situational factors
KW  - Sociodemographic aspects
KW  - Stress
KW  - Survivors
KW  - Timing
KW  - Wellbeing
KW  - Coverage
KW  - Economic crisis
KW  - Economic recovery
KW  - Employment
KW  - Employment status
KW  - Health care
KW  - Health insurance
KW  - Health problems
KW  - Health status
KW  - Insurance
KW  - Moderated
KW  - Perceptions
KW  - Psychological wellbeing
KW  - Quality of life
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665153866?accountid=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=Economic+survivorship+stress+is+associated+with+poor+health-related+quality+of+life+among+distressed+survivors+of+hematopoietic+stem+cell+transplantation&rft.au=Hamilton%2C+Jada+G%3BWu%2C+Lisa+M%3BAustin%2C+Jane+E%3BValdimarsdottir%2C+Heiddis%3BBasmajian%2C+Katie%3BVu%2C+AnnaMarie%3BRowley%2C+Scott+D%3BIsola%2C+Luis%3BRedd%2C+William+H%3BRini%2C+Christine&rft.aulast=Hamilton&rft.aufirst=Jada&rft.date=2013-04-01&rft.volume=22&rft.issue=4&rft.spage=911&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3091
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.3091
ER  - 



TY  - JOUR
T1  - Reduction of Aedes aegypti Vector Competence for Dengue Virus under Large Temperature Fluctuations
AN  - 1647018064; 21172044
AB  - Diurnal temperature fluctuations can fundamentally alter mosquito biology and mosquito-virus interactions in ways that impact pathogen transmission. We investigated the effect of two daily fluctuating temperature profiles on Aedes aegypti vector competence for dengue virus (DENV) serotype-1. A large diurnal temperature range of 18.6 [degrees]C around a 26[degrees]C mean, corresponding with the low DENV transmission season in northwestern Thailand, reduced midgut infection rates and tended to extend the virus extrinsic incubation period. Dissemination was first observed at day 7 under small fluctuations (7.6 [degrees]C; corresponding with high DENV transmission) and constant control temperature, but not until Day 11 for the large diurnal temperature range. Results indicate that female Ae. aegypti in northwest Thailand are less likely to transmit DENV during the low than high transmission season because of reduced DENV susceptibility and extended virus extrinsic incubation period. Better understanding of DENV transmission dynamics will come with improved knowledge of temperature effects on mosquito-virus interactions.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Carrington, Lauren B
AU  - Seifert, Stephanie N
AU  - Armijos, M Veronica
AU  - Lambrechts, Louis
AU  - Scott, Thomas W
AD  - Insects and Infectious Diseases, Centre National de la Recherche Scientifique, Unite de Recherche Associee 3012, Institut Pasteur, Paris, France; Fogarty International Center, National Institutes of Health, Bethesda, Maryland; Department of Entomology, University of California, 1 Shields Avenue, Davis, CA 95616, lbcarrington@ucdavis.edu
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 689
EP  - 697
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 88
IS  - 4
SN  - 0002-9637, 0002-9637
KW  - Entomology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Health & Safety Science Abstracts
KW  - Dengue virus
KW  - Temperature effects
KW  - Diurnal variations
KW  - Aedes aegypti
KW  - Human diseases
KW  - Thailand
KW  - Temperature
KW  - Vectors
KW  - Pest control
KW  - Hosts
KW  - Pathogens
KW  - Infection
KW  - Public health
KW  - Disease transmission
KW  - Dengue
KW  - Midgut
KW  - Hygiene
KW  - Aquatic insects
KW  - K 03410:Animal Diseases
KW  - J 02410:Animal Diseases
KW  - V 22410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Z 05350:Medical, Veterinary, and Agricultural Entomology
KW  - Q5 08502:Methods and instruments
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647018064?accountid=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=Reduction+of+Aedes+aegypti+Vector+Competence+for+Dengue+Virus+under+Large+Temperature+Fluctuations&rft.au=Carrington%2C+Lauren+B%3BSeifert%2C+Stephanie+N%3BArmijos%2C+M+Veronica%3BLambrechts%2C+Louis%3BScott%2C+Thomas+W&rft.aulast=Carrington&rft.aufirst=Lauren&rft.date=2013-04-01&rft.volume=88&rft.issue=4&rft.spage=689&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0488
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Temperature effects; Human diseases; Pest control; Pathogens; Hosts; Hygiene; Aquatic insects; Disease transmission; Public health; Vectors; Midgut; Infection; Diurnal variations; Dengue; Temperature; Dengue virus; Aedes aegypti; Thailand
DO  - http://dx.doi.org/10.4269/ajtmh.12-0488
ER  - 



TY  - JOUR
T1  - Smoking as a risk factor for oral candidiasis in HIV-infected adults
AN  - 1464514154; 17880697
AB  - We aimed to examine if smoking is an independent predictor of oral candidiasis (OC) among HIV-1 infected persons. The cross-sectional part of this study evaluated 631 adult dentate HIV-1 seropositive persons examined for OC from 1995-2000 at the University of North Carolina Hospitals in Chapel Hill, NC. In the second part, from the above sample, a total of 283 individuals who were free of HIV-associated oral diseases at baseline were followed up for 2 years to assess incident OC events. Data collected from medical record review, interview questionnaires, and clinical examinations were analyzed using chi-squared tests and t-tests. Logistic regression models were developed for prevalent OC employing the likelihood ratio test, whereas Poisson regression models were developed for assessing cumulative incidence of OC. These models included a variety of independent variables to adjust for confounding. Thirteen percent of participants had OC only; 4.6% had OC with Oral Hairy Leukoplakia; and 69.7% had neither. Smoking was associated with OC in all models [prevalent OC - current smokers: logistic regression - Odd ratio (95% CI) = 2.5 (1.3, 4.8); Incident OC - current smokers: Poisson regression (main effects model) - Incidence rate ratio (95% CI) = 1.9 (1.1, 3.8)]. Other Poisson regression models suggested evidence for effect modification between CD4 cell count and incident OC by smoking. Smoking is an independent risk factor for the development of OC in HIV-1 infected persons, and the risk of OC is modified by CD4 cell count which measures strength of the immune system.
JF  - Journal of Oral Pathology and Medicine
AU  - Chattopadhyay, Amit
AU  - Patton, Lauren L
AD  - Office of Science Policy and Analysis. NIH-NIDCR
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 302
EP  - 308
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 42
IS  - 4
SN  - 0904-2512, 0904-2512
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Risk assessment
KW  - USA, North Carolina
KW  - Smoking
KW  - Pathology
KW  - Risk factors
KW  - Reviews
KW  - Immune system
KW  - Human immunodeficiency virus 1
KW  - Hospitals
KW  - H 13000:Medical Safety
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464514154?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Oral+Pathology+and+Medicine&rft.atitle=Smoking+as+a+risk+factor+for+oral+candidiasis+in+HIV-infected+adults&rft.au=Chattopadhyay%2C+Amit%3BPatton%2C+Lauren+L&rft.aulast=Chattopadhyay&rft.aufirst=Amit&rft.date=2013-04-01&rft.volume=42&rft.issue=4&rft.spage=302&rft.isbn=&rft.btitle=&rft.title=Journal+of+Oral+Pathology+and+Medicine&rft.issn=09042512&rft_id=info:doi/10.1111%2Fjop.12019
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Risk assessment; Smoking; Pathology; Immune system; Reviews; Risk factors; Hospitals; Human immunodeficiency virus 1; USA, North Carolina
DO  - http://dx.doi.org/10.1111/jop.12019
ER  - 



TY  - JOUR
T1  - Pulmonary vein morphology by free-breathing whole heart magnetic resonance imaging at 3 tesla versus breathhold multi-detector computed tomography
AN  - 1458540655; 18492284
AB  - Purpose: To compare pulmonary vein and left atrial anatomy using three-dimensional free-breathing whole-heart magnetic resonance imaging (MR) at 3 Tesla (T) and multi-detector computed tomography (MDCT). Materials and Methods: Thirty-three subjects (19 male, age 49 plus or minus 12 years) underwent free-breathing 3T MR and contrast-enhanced MDCT during inspiratory breath hold. Pulmonary vein parameters (ostial areas, diameters, angles) were measured. Results: All pulmonary veins and anomalies were identified by 3T MR and by MDCT. The right-sided pulmonary veins were directed more posteriorly, the right superior pulmonary vein more inferiorly, and the right inferior pulmonary vein more superiorly by 3T MR when compared with MDCT. The cross-sectional area, perimeters and minimum diameters of right-sided pulmonary vein ostia were significantly larger by MR, as were the maximum diameters of right and left inferior pulmonary veins. There were no significant differences between techniques in distance to first pulmonary vein branch. Conclusion: Pulmonary vein measurements demonstrated significant differences in angulations and dimensions when 3T MR is compared with MDCT. These differences likely represent hemodynamic and respiratory variation during free-breathing with MR versus breath-holding with MDCT. MR imaging at 3T during free-breathing offers an alternate method to define pulmonary vein and left atrial anatomy without exposure to radiation. J. Magn. Reson. Imaging 2013; 37:846-852. [copy 2012 Wiley Periodicals, Inc.
JF  - Journal of Magnetic Resonance Imaging
AU  - Fodi, Eszter
AU  - McAreavey, Dorothea
AU  - Abd-Elmoniem, Khaled Z
AU  - Ohayon, Jacques
AU  - Saba, Magdi
AU  - Elagha, Abdalla
AU  - Pettigrew, Roderic I
AU  - Gharib, Ahmed M
AD  - NIH Clinical Center, National Institutes of Health, Bethesda, Maryland, USA., agharib@niddk.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 846
EP  - 852
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 37
IS  - 4
SN  - 1053-1807, 1053-1807
KW  - Biotechnology and Bioengineering Abstracts
KW  - Heart
KW  - Age
KW  - Veins
KW  - Radiation
KW  - Lung
KW  - Respiration
KW  - Magnetic resonance imaging
KW  - Computed tomography
KW  - Hemodynamics
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458540655?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Magnetic+Resonance+Imaging&rft.atitle=Pulmonary+vein+morphology+by+free-breathing+whole+heart+magnetic+resonance+imaging+at+3+tesla+versus+breathhold+multi-detector+computed+tomography&rft.au=Fodi%2C+Eszter%3BMcAreavey%2C+Dorothea%3BAbd-Elmoniem%2C+Khaled+Z%3BOhayon%2C+Jacques%3BSaba%2C+Magdi%3BElagha%2C+Abdalla%3BPettigrew%2C+Roderic+I%3BGharib%2C+Ahmed+M&rft.aulast=Fodi&rft.aufirst=Eszter&rft.date=2013-04-01&rft.volume=37&rft.issue=4&rft.spage=846&rft.isbn=&rft.btitle=&rft.title=Journal+of+Magnetic+Resonance+Imaging&rft.issn=10531807&rft_id=info:doi/10.1002%2Fjmri.23865
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Heart; Age; Veins; Radiation; Lung; Respiration; Computed tomography; Magnetic resonance imaging; Hemodynamics
DO  - http://dx.doi.org/10.1002/jmri.23865
ER  - 



TY  - JOUR
T1  - An international comparison of male and female breast cancer incidence rates
AN  - 1443369510; 18602602
AB  - Global international trends in female breast cancer incidence have been described previously but no comparable analysis of male breast cancer incidence rates has been conducted. We obtained male and female case and population data using Cancer Incidence in Five Continents (CI5). We calculated age-adjusted, sex-specific incidence rates and female-to-male incidence rate ratios (FMIRRs) and compared trends of such for the period 1988-2002. This analysis included 8,681 male breast cancer cases and 1.14 million female breast cancer cases. The highest male incidence rate was observed in Israel at 1.24 per 100,000 man-years, and the highest female incidence rate was observed in the United States at 90.7 per 100,000 woman-years. The lowest incidence rates for males (0.16) and females (18.0) were observed in Thailand. In general, male breast cancer incidence trends were variable; a minority of countries displayed evidence for an increase. In contrast, female incidence rates have been increasing in a majority of countries. The Pearson correlation coefficient (r) for male and female breast cancer incidence rates by country during 1988-2002 was 0.69. Male breast cancer rates were generally less than 1 per 100,000 man-years, in contrast to the much higher rates of female breast cancer, providing for an overall FMIRR of 122. The differences in both incidence rates and time trends between males and females may reflect sex differences in underlying risk factors, pathogenesis, and/or overdiagnosis. Conversely, the high correlation between male and female breast cancer incidences may indicate that both sexes share some common risk factors for breast cancer. What's new? Are the causes of breast cancer in men similar to those in women? Is male breast cancer a different disease entity, or is it the same in men and women? In this study, the authors have compiled the first epidemiologic analysis comparing international trends for male and female breast-cancer incidence. They conclude that, while incidence patterns are similar, there may also be sex-specific processes that play a role in the pathogenesis of this disease.
JF  - International Journal of Cancer
AU  - Ly, Diana
AU  - Forman, David
AU  - Ferlay, Jacques
AU  - Brinton, Louise A
AU  - Cook, Michael B
AD  - Section of Cancer Information, International Agency for Research on Cancer, Lyon, Cedex 08, France., michael.cook@nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 1918
EP  - 1926
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 8
SN  - 0020-7136, 0020-7136
KW  - Risk Abstracts
KW  - Health risks
KW  - Comparative studies
KW  - USA
KW  - Continents
KW  - Thailand
KW  - Risk factors
KW  - Males
KW  - Breast cancer
KW  - Israel
KW  - Females
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443369510?accountid=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=An+international+comparison+of+male+and+female+breast+cancer+incidence+rates&rft.au=Ly%2C+Diana%3BForman%2C+David%3BFerlay%2C+Jacques%3BBrinton%2C+Louise+A%3BCook%2C+Michael+B&rft.aulast=Ly&rft.aufirst=Diana&rft.date=2013-04-01&rft.volume=132&rft.issue=8&rft.spage=1918&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27841
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Comparative studies; Health risks; Continents; Males; Risk factors; Breast cancer; Females; USA; Thailand; Israel
DO  - http://dx.doi.org/10.1002/ijc.27841
ER  - 



TY  - JOUR
T1  - Chronic inhalation of biomass smoke is associated with DNA damage in airway cells: involvement of particulate pollutants and benzene
AN  - 1439228079; 18615982
AB  - This study examined whether indoor air pollution from biomass fuel burning induces DNA damage in airway cells. For this, sputum cells were collected from 56 premenopausal rural women who cooked with biomass (wood, dung, crop residues) and 49 age-matched controls who cooked with cleaner liquefied petroleum gas. The levels of particulate matters with diameters of less than 10 and 2.5 mu m (PM sub(10) and PM sub(2.5)) in indoor air were measured using a real-time aerosol monitor. Benzene exposure was monitored by measuring trans,trans-muconic acid (t,t-MA) in urine by HPLC-UV. DNA damage was examined by alkaline comet assay in sputum cells. Generation of reactive oxygen species (ROS) and level of superoxide dismutase (SOD) in sputum cells were measured by flow cytometry and spectrophotometry, respectively. Compared with controls, biomass users had 4 times higher tail percentage DNA, 37% more comet tail length and 5 times more Olive tail moment (p<0.001) in inflammatory and epithelial cells in sputum, suggesting extensive DNA damage. In addition, women who cooked with biomass had 6 times higher levels of urinary t,t-MA and 2-fold higher levels of ROS generation concomitant with 28% depletion of SOD. Indoor air of biomass-using households had 2-4 times more PM sub(10) and PM sub(2.5) than that of controls sub(.) After controlling potential confounders, positive association was found between DNA damage parameters, particulate pollution, urinary t,t-MA and ROS. Thus, long-term exposure to biomass smoke induces DNA damage in airway cells and the effect was probably mediated, at least in part, by oxidative stress generated by inhaled particulate matter and benzene. Copyright [copy 2011 John Wiley & Sons, Ltd. The possibility of DNA damage in sputum cells was examined in 56 premenopausal women who cooked with biomass and 49 matched control who cooked with cleaner fuel. DNA damage was upregulated in biomass users in association with elevated level of urinary t,t-MA, increased ROS generation and depleted SOD along with elevated PM sub(10) and PM sub(2.5) in cooking areas. Thus, biomass smoke causes DNA damage in airway cells, possibly by oxidative stress generated by inhaled pollutants including PM and benzene.
JF  - Journal of Applied Toxicology
AU  - Mukherjee, Bidisha
AU  - Dutta, Anindita
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.
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 281
EP  - 289
PB  - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801
VL  - 33
IS  - 4
SN  - 0260-437X, 0260-437X
KW  - Pollution Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Health & Safety Science Abstracts; Toxicology Abstracts
KW  - biomass fuel
KW  - particulate matter
KW  - benzene
KW  - oxidative stress
KW  - comet assay
KW  - airway cells
KW  - Inhalation
KW  - Olea
KW  - Epithelial cells
KW  - Fuels
KW  - Particulate matter
KW  - Particulate pollution
KW  - Particulates
KW  - Benzene
KW  - Flow cytometry
KW  - Reactive oxygen species
KW  - Pollutants
KW  - Superoxide dismutase
KW  - Oxidative stress
KW  - Petroleum
KW  - Cooking
KW  - Spectrophotometry
KW  - Respiratory tract
KW  - Particle size
KW  - Aerosols
KW  - Crop residues
KW  - Biomass
KW  - Inflammation
KW  - Air pollution
KW  - Smoke
KW  - DNA damage
KW  - Urine
KW  - DNA
KW  - Dung
KW  - Burning
KW  - Comet assay
KW  - Sputum
KW  - Indoor environments
KW  - P 0000:AIR POLLUTION
KW  - N 14820:DNA Metabolism & Structure
KW  - H 14000:Toxicology
KW  - X 24350:Industrial Chemicals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439228079?accountid=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+Applied+Toxicology&rft.atitle=Chronic+inhalation+of+biomass+smoke+is+associated+with+DNA+damage+in+airway+cells%3A+involvement+of+particulate+pollutants+and+benzene&rft.au=Mukherjee%2C+Bidisha%3BDutta%2C+Anindita%3BRoychoudhury%2C+Sanghita%3BRay%2C+Manas+Ranjan&rft.aulast=Mukherjee&rft.aufirst=Bidisha&rft.date=2013-04-01&rft.volume=33&rft.issue=4&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Journal+of+Applied+Toxicology&rft.issn=0260437X&rft_id=info:doi/10.1002%2Fjat.1748
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - Inhalation; Epithelial cells; Fuels; Particulate matter; Particulate pollution; Benzene; Flow cytometry; Pollutants; Reactive oxygen species; Oxidative stress; Superoxide dismutase; Petroleum; Cooking; Spectrophotometry; Respiratory tract; Aerosols; Crop residues; Biomass; Inflammation; Smoke; Air pollution; DNA damage; Urine; Dung; Sputum; Comet assay; Burning; Particle size; DNA; Particulates; Indoor environments; Olea
DO  - http://dx.doi.org/10.1002/jat.1748
ER  - 



TY  - JOUR
T1  - Developmental Pathways Among Adaptive Functioning and Externalizing and Internalizing Behavioral Problems: Cascades From Childhood Into Adolescence
AN  - 1438605312; 2011-437351
AB  - Here, a 3-wave multivariate design and developmental cascade analysis were used to investigate pathways among adaptive functioning and externalizing and internalizing behavioral problems in a community sample of 134 children seen at 4, 10, and 14 years. Adaptive functioning in early adolescence was predicted by early childhood adaptive functioning and externalizing behavioral problems, with both effects mediated by late childhood adaptive functioning and internalizing behavioral problems; externalizing behavioral problems in early adolescence were predicted by early childhood internalizing behavioral problems with the effect mediated by late childhood externalizing behavioral problems. These developmental cascades were obtained independent of child intelligence. Strategically timed and targeted interventions designed to address young children's behavioral problems may return investment in terms of an enhanced epidemiology of adaptively functioning teens. Adapted from the source document.
JF  - Applied Developmental Science
AU  - Bornstein, Marc H
AU  - Hahn, Chun-Shin
AU  - Suwalsky, Joan T D
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 76
EP  - 87
PB  - Taylor & Francis, Philadelphia PA
VL  - 17
IS  - 2
SN  - 1088-8691, 1088-8691
KW  - Population groups, population policy, and demographics - Children and youth
KW  - Social conditions and policy - Psychology
KW  - Education and education policy - Educational psychology and learning ability
KW  - Banking and public and private finance - Investments and securities
KW  - Health conditions and policy - Medicine and health care
KW  - Intelligence
KW  - Investments
KW  - Epidemiology
KW  - Children
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1438605312?accountid=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=Applied+Developmental+Science&rft.atitle=Developmental+Pathways+Among+Adaptive+Functioning+and+Externalizing+and+Internalizing+Behavioral+Problems%3A+Cascades+From+Childhood+Into+Adolescence&rft.au=Bornstein%2C+Marc+H%3BHahn%2C+Chun-Shin%3BSuwalsky%2C+Joan+T+D&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2013-04-01&rft.volume=17&rft.issue=2&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=Applied+Developmental+Science&rft.issn=10888691&rft_id=info:doi/10.1080%2F10888691.2013.774875
LA  - English
DB  - PAIS Index
N1  - Date revised - 2013-10-01
N1  - Last updated - 2016-09-28
N1  - CODEN - ADSCFM
N1  - SubjectsTermNotLitGenreText - Children; Intelligence; Investments; Epidemiology
DO  - http://dx.doi.org/10.1080/10888691.2013.774875
ER  - 



TY  - JOUR
T1  - Soft constraints in nonlinear spectral fitting with regularized lineshape deconvolution
AN  - 1434035472; 18496055
AB  - This article presents a novel method for incorporating a priori knowledge into regularized nonlinear spectral fitting as soft constraints. Regularization was recently introduced to lineshape deconvolution as a method for correcting spectral distortions. Here, the deconvoluted lineshape was described by a new type of lineshape model and applied to spectral fitting. The nonlinear spectral fitting was carried out in two steps that were subject to hard constraints and soft constraints, respectively. The hard constraints step provided a starting point and, therefore, only the changes of the relevant variables were constrained in the soft constraints step and incorporated into the linear substeps of the Levenberg-Marquardt algorithm. The method was demonstrated using localized averaged echo time point resolved spectroscopy proton spectroscopy of human brains. Magn Reson Med 69:912-919, 2013. [copy 2012 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  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 912
EP  - 919
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 4
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - Protons
KW  - Algorithms
KW  - Brain
KW  - N.M.R.
KW  - Spectroscopy
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434035472?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Soft+constraints+in+nonlinear+spectral+fitting+with+regularized+lineshape+deconvolution&rft.au=Zhang%2C+Yan%3BShen%2C+Jun&rft.aulast=Zhang&rft.aufirst=Yan&rft.date=2013-04-01&rft.volume=69&rft.issue=4&rft.spage=912&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24337
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Protons; Brain; Algorithms; N.M.R.; Spectroscopy
DO  - http://dx.doi.org/10.1002/mrm.24337
ER  - 



TY  - JOUR
T1  - Chromatin structure outside and inside the nucleus
AN  - 1434016916; 18483835
AB  - The structure of the 30-nm chromatin fiber has provided, over the years, an important reference in chromatin studies. Originally derived from electron microscopic studies of soluble chromatin fibers released by restriction digestion, the gross structural features of such fragments have been supported by biophysical methods such as low angle X-ray and neutron scattering, sedimentation, light scattering, and electric dichroism. Electron microscopy and sedimentation velocity measurements demonstrated that reconstituted chromatin fibers, prepared from repeating arrays of high affinity nucleosome positioning sequences, retain the same overall features as observed for native chromatin fibers. It had been suggested that the 30 nm fiber might be the form assumed in vivo by transcriptionally silent chromatin, but individual gene or genome-wide studies of chromatin released from nuclei do not reveal any such simple correlation. Furthermore, even though the 30 nm fiber has been thought to represent an intermediate in the hierarchical folding of DNA into chromosomes, most analyses of chromatin folding within the nucleus do not detect any regular extended compact structures. However, there are important exceptions in chicken erythroid cell nuclei as well as in transcribed regions that form extended loops. Localized domains within the nucleus, either at the surface of chromosome domains or constrained as a specialized kind of constitutive heterochromatin by specific DNA binding proteins, may adopt 30 nm fiber-like structures. [copy 2012 Wiley Periodicals, Inc. Biopolymers 99: 225-232, 2013.
JF  - Biopolymers
AU  - Ghirlando, Rodolfo
AU  - Felsenfeld, Gary
AD  - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0540., gary.felsenfeld@nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 225
EP  - 232
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 99
IS  - 4
SN  - 0006-3525, 0006-3525
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - chromatin
KW  - nuclear organization
KW  - 30 nm fiber
KW  - Heterochromatin
KW  - Chromatin
KW  - DNA-binding protein
KW  - Erythroid cells
KW  - Biopolymers
KW  - Light scattering
KW  - Transcription
KW  - Electric dichroism
KW  - Fibers
KW  - Nucleosomes
KW  - Chromosomes
KW  - Neutron scattering
KW  - Ionizing radiation
KW  - Sedimentation
KW  - Nuclei
KW  - Electron microscopy
KW  - W 30950:Waste Treatment & Pollution Clean-up
KW  - N 14820:DNA Metabolism & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434016916?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chromatin+structure+outside+and+inside+the+nucleus&rft.au=Ghirlando%2C+Rodolfo%3BFelsenfeld%2C+Gary&rft.aulast=Ghirlando&rft.aufirst=Rodolfo&rft.date=2013-04-01&rft.volume=99&rft.issue=4&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22157
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Heterochromatin; Chromatin; DNA-binding protein; Erythroid cells; Light scattering; Biopolymers; Transcription; Fibers; Electric dichroism; Chromosomes; Nucleosomes; Neutron scattering; Ionizing radiation; Nuclei; Sedimentation; Electron microscopy
DO  - http://dx.doi.org/10.1002/bip.22157
ER  - 



TY  - JOUR
T1  - Quantitative assessment of the relative contributions of steric repulsion and chemical interactions to macromolecular crowding
AN  - 1434016243; 18483836
AB  - The term "macromolecular crowding" denotes the combined effects of high volume fractions of nominally unrelated macromolecules upon the equilibrium and transport properties of all macrosolutes, dilute as well as concentrated, in the crowded medium. We present a formal partitioning of the total crowding effect into contributions from steric exclusion (excluded volume) and weak, nonspecific attractive interactions between a concentrated "crowding agent" and reactant and product species present at trace concentration. A numerical example of the combined effect of both steric and chemical interactions between crowder and tracer upon the reversible dimerization of tracer is presented, based upon reasonable estimates of the magnitude of both repulsive and attractive interactions between tracer and crowder species. [copy 2012Wiley Periodicals, Inc. Biopolymers 99: 239-244, 2013.
JF  - Biopolymers
AU  - Minton, Allen P
AD  - Section on Physical Biochemistry, Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, U.S. Department of Health and Human Services, Bethesda, MD., minton@helix.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 239
EP  - 244
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 99
IS  - 4
SN  - 0006-3525, 0006-3525
KW  - Biotechnology and Bioengineering Abstracts
KW  - excluded volume
KW  - steric repulsion
KW  - weak binding
KW  - equivalent hard particle model
KW  - Tracers
KW  - Macromolecules
KW  - Crowding
KW  - Biopolymers
KW  - W 30935:Food Biotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434016243?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quantitative+assessment+of+the+relative+contributions+of+steric+repulsion+and+chemical+interactions+to+macromolecular+crowding&rft.au=Minton%2C+Allen+P&rft.aulast=Minton&rft.aufirst=Allen&rft.date=2013-04-01&rft.volume=99&rft.issue=4&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22163
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Tracers; Macromolecules; Crowding; Biopolymers
DO  - http://dx.doi.org/10.1002/bip.22163
ER  - 



TY  - JOUR
T1  - Feasibility and safety of sequential research-related tumor core biopsies in clinical trials
AN  - 1434015859; 18486944
AB  - BACKGROUND: There has been increasing interest in serial research biopsies in studies of targeted therapies. Definition of patient characteristics and optimal target tissue for safe research tumor biopsy in the era of antiangiogenic and targeted agents is needed. METHODS: This institutional review board-approved, retrospective study included chart and interventional radiology case review from 6 phase 1/2 studies at the National Cancer Institute. RESULTS: One hundred forty-two of 150 protocol patients who were approached gave consent for research biopsies. Patients' median age was 56 years (range, 27-78 years), their median body mass index was 25.8 kg/m super(2) (range, 14.4-46.2 kg/m super(2)), they had an Eastern Cooperative Oncology Group performance status of 0 or 1, and they had normal end-organ function. Baseline biopsies were collected from 138 of 142 patients (97%), and paired specimens were collected from 96 (70%). Most patients had metastatic gynecologic cancers (85%), and 78% had target disease below the diaphragm with a median size of 2.7 cm (range, 1-14.5 cm). Protocol therapies included kinase inhibitors (35%), angiogenesis inhibitors (54%), and olaparib/carboplatin (11%); therapy was not interrupted for biopsies. All adverse events were uncomplicated and were observed in 4 patients (liver subcapsular hematoma in 1 patient, vasovagal syncope in 2 patients, and pneumothorax in 1 patient). The complication rate in obese patients was similar to that in nonobese patients (3 of 108 patients vs 1 of 34 patients, respectively). Sixty-seven patients (48%) were receiving bevacizumab at the time of subsequent biopsies. The complication rate was not different between patients who were and were not receiving bevacizumab (3 of 67 patients vs 1 of 71 patients, respectively). Ninety-five percent of biopsies yielded useable material. CONCLUSIONS: Serial percutaneous core-needle biopsies can be obtained safely and yield material applicable for multiple translational applications. Obesity and/or concomitant antiangiogenic therapy and depth of disease did not increase the risk or preclude the successful acquisition of useful tissue. Cancer 2013. [copy 2012 American Cancer Society. Good-quality, sequential, percutaneous core-needle biopsies can be obtained safely in patients who are receiving targeted therapies. Obesity, depth of lesion, and concomitant receipt of antiangiogenic agents do not increase the risk or reduce the successful acquisition of useful tissue.
JF  - Cancer
AU  - Lee, Jung-min
AU  - Hays, John L
AU  - Noonan, Anne M
AU  - Squires, Jennifer
AU  - Minasian, Lori
AU  - Annunziata, Christina
AU  - Wood, Bradford J
AU  - Yu, Minshu
AU  - Calvo, Katherine R
AU  - Houston, Nicole
AU  - Azad, Nilofer
AU  - Kohn, Elise C
AD  - Center for Interventional Radiology, Radiology and Imaging Sciences, National Institutes of Health, Bethesda, Maryland., leej6@mail.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 1357
EP  - 1364
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 7
SN  - 0008-543X, 0008-543X
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Feasibility studies
KW  - Obesity
KW  - Complications
KW  - Body mass
KW  - Tumors
KW  - Radiology
KW  - Clinical trials
KW  - Cancer
KW  - Health risks
KW  - Reviews
KW  - Liver
KW  - Lesions
KW  - Cooperatives
KW  - Side effects
KW  - R2 23060:Medical and environmental health
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434015859?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Feasibility+and+safety+of+sequential+research-related+tumor+core+biopsies+in+clinical+trials&rft.au=Lee%2C+Jung-min%3BHays%2C+John+L%3BNoonan%2C+Anne+M%3BSquires%2C+Jennifer%3BMinasian%2C+Lori%3BAnnunziata%2C+Christina%3BWood%2C+Bradford+J%3BYu%2C+Minshu%3BCalvo%2C+Katherine+R%3BHouston%2C+Nicole%3BAzad%2C+Nilofer%3BKohn%2C+Elise+C&rft.aulast=Lee&rft.aufirst=Jung-min&rft.date=2013-04-01&rft.volume=119&rft.issue=7&rft.spage=1357&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27916
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-12-04
N1  - SubjectsTermNotLitGenreText - Feasibility studies; Obesity; Complications; Body mass; Tumors; Radiology; Clinical trials; Cancer; Health risks; Reviews; Liver; Cooperatives; Lesions; Side effects
DO  - http://dx.doi.org/10.1002/cncr.27916
ER  - 



TY  - JOUR
T1  - The risk of developing invasive breast cancer in Hispanic women
AN  - 1434013502; 18486952
AB  - BACKGROUND: Current evidence on breast cancer among US Hispanic women indicates a significant public health threat, although few studies have assessed the heterogeneity in breast cancer risk among Hispanics of different origin. METHODS: The 2000 and 2005 National Health Interview Survey Cancer Control Modules were used to examine the Breast Cancer Risk Assessment Tool (BCRAT) 5-year risk and lifetime risk of invasive breast cancer among Mexican/Mexican American, Puerto Rican, Cuban/Cuban American, Dominican (Republic), Central/South American, Other Hispanic, and non-Hispanic white (NHW) women ages 35 to 84 years. Multiple linear regression models were used to compare the BCRAT 5-year and lifetime breast cancer risk between 1) Hispanics and NHWs and 2) Hispanic subgroups. RESULTS: Hispanic women had significantly lower mean BCRAT 5-year and lifetime breast cancer risk compared with NHW women (P < .001). Among Hispanic subgroups, Cuban/Cuban Americans had a higher BCRAT 5-year risk (P < .05), whereas Dominicans had a higher lifetime risk (P < .001) compared with Mexican/Mexican Americans. Approximately 2.6% of Hispanic women were at high risk for breast cancer (BCRAT 5-year risk greater than or equal to 1.67%), ranging from 1% of Central/South Americans to 3.7% of Puerto Ricans; few Hispanics (0.2%) had a lifetime risk greater than or equal to 20%. CONCLUSIONS: The current findings indicate that Hispanic women have a significantly lower risk of breast cancer compared with NHW women, although the risk according to BCRAT differed significantly between specific Hispanic subgroups. We provide estimates of the number of US Hispanic women from six subgroups who may be eligible for prophylactic breast cancer chemoprevention. The authors concluded that future studies should further investigate the heterogeneity in breast cancer risk and risk factors between Hispanic women of different origins. Cancer 2013. [copy 2012 American Cancer Society. Findings from this study indicate that Hispanic women have a significantly lower risk of breast cancer compared with non-Hispanic white women, and that breast cancer risk significantly differs between specific Hispanic subgroups, based on the Breast Cancer Risk Assessment Tool (BCRAT). Approximately 2.6% of Hispanic women, ranging from 1% of Central/South Americans to 3.7% of Puerto Ricans, are at high risk for breast cancer (BCRAT 5-year risk greater than or equal to 1.67%) and may be eligible for prophylactic breast cancer chemoprevention.
JF  - Cancer
AU  - Banegas, Matthew P
AU  - Leng, Mei
AU  - Graubard, Barry I
AU  - Morales, Leo S
AD  - Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., banegasmp@mail.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 1373
EP  - 1380
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 7
SN  - 0008-543X, 0008-543X
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Health risks
KW  - Age
KW  - Chemotherapy
KW  - Risk factors
KW  - Breast cancer
KW  - Females
KW  - ASW, Caribbean Sea, Greater Antilles, Dominican Rep.
KW  - Ethnic groups
KW  - Public health
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/1434013502?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=The+risk+of+developing+invasive+breast+cancer+in+Hispanic+women&rft.au=Banegas%2C+Matthew+P%3BLeng%2C+Mei%3BGraubard%2C+Barry+I%3BMorales%2C+Leo+S&rft.aulast=Banegas&rft.aufirst=Matthew&rft.date=2013-04-01&rft.volume=119&rft.issue=7&rft.spage=1373&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27896
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Health risks; Age; Risk factors; Chemotherapy; Breast cancer; Females; Ethnic groups; Public health; ASW, Caribbean Sea, Greater Antilles, Dominican Rep.
DO  - http://dx.doi.org/10.1002/cncr.27896
ER  - 



TY  - JOUR
T1  - Reports on the 2012 AAAI Fall Symposium Series
AN  - 1429844346; 201308788
AB  - The Association for the Advancement of Artificial Intelligence was pleased to present the 2012 Fall Symposium Series, held Friday through Sunday, November 2-4, at the Westin Arlington Gateway in Arlington, Virginia. The titles of the eight symposia were as follows: AI for Gerontechnology (FS-12-01), Artificial Intelligence of Humor (FS-12-02), Discovery Informatics: The Role of AI Research in Innovating Scientific Processes (FS-12-03), Human Control of Bio-Inspired Swarms (FS-12-04), Information Retrieval and Knowledge Discovery in Biomedical Text (FS-12-05), Machine Aggregation of Human Judgment (FS-12-06), Robots Learning Interactively from Human Teachers (FS-12-07), and Social Networks and Social Contagion (FS-12-08). The highlights of each symposium are presented in this report. Adapted from the source document.
JF  - AI Magazine
AU  - Dogan, Rezarta Islamaj
AU  - Gil, Yolanda
AU  - Hirsh, Haym
AU  - Krishnan, Narayanan C
AU  - Lewis, Michael
AU  - Mericli, Cetin
AU  - Rashidi, Parisa
AU  - Raskin, Victor
AU  - Swarup, Samarth
AU  - Sun, Wei
AU  - Taylor, Julia M
AU  - Yeganova, Lana
AD  - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 93
EP  - 100
PB  - American Association for Artificial Intelligence
VL  - 34
IS  - 1
SN  - 0738-4602, 0738-4602
KW  - Artificial intelligence
KW  - Conferences
KW  - article
KW  - 14.19: COMPUTER APPLICATIONS
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1429844346?accountid=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=AI+Magazine&rft.atitle=Reports+on+the+2012+AAAI+Fall+Symposium+Series&rft.au=Dogan%2C+Rezarta+Islamaj%3BGil%2C+Yolanda%3BHirsh%2C+Haym%3BKrishnan%2C+Narayanan+C%3BLewis%2C+Michael%3BMericli%2C+Cetin%3BRashidi%2C+Parisa%3BRaskin%2C+Victor%3BSwarup%2C+Samarth%3BSun%2C+Wei%3BTaylor%2C+Julia+M%3BYeganova%2C+Lana&rft.aulast=Dogan&rft.aufirst=Rezarta&rft.date=2013-04-01&rft.volume=34&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=AI+Magazine&rft.issn=07384602&rft_id=info:doi/
LA  - English
DB  - Library & Information Science Abstracts (LISA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Artificial intelligence; Conferences
ER  - 



TY  - JOUR
T1  - Predictors of Latent Trajectory Classes of Physical Dating Violence Victimization
AN  - 1417523230; 201333943
AB  - This study identified classes of developmental trajectories of physical dating violence victimization from grades 8 to 12 and examined theoretically-based risk factors that distinguished among trajectory classes. Data were from a multi-wave longitudinal study spanning 8th through 12th grade (n = 2,566; 51.9 % female). Growth mixture models were used to identify trajectory classes of physical dating violence victimization separately for girls and boys. Logistic and multinomial logistic regressions were used to identify situational and target vulnerability factors associated with the trajectory classes. For girls, three trajectory classes were identified: a low/non-involved class; a moderate class where victimization increased slightly until the 10th grade and then decreased through the 12th grade; and a high class where victimization started at a higher level in the 8th grade, increased substantially until the 10th grade, and then decreased until the 12th grade. For males, two classes were identified: a low/non-involved class, and a victimized class where victimization increased slightly until the 9th grade, decreased until the 11th grade, and then increased again through the 12th grade. In bivariate analyses, almost all of the situational and target vulnerability risk factors distinguished the victimization classes from the non-involved classes. However, when all risk factors and control variables were in the model, alcohol use (a situational vulnerability) was the only factor that distinguished membership in the moderate trajectory class from the non-involved class for girls; anxiety and being victimized by peers (target vulnerability factors) were the factors that distinguished the high from the non-involved classes for the girls; and victimization by peers was the only factor distinguishing the victimized from the non-involved class for boys. These findings contribute to our understanding of the heterogeneity in physical dating violence victimization during adolescence and the malleable risk factors associated with each trajectory class for boys and girls. Adapted from the source document.
JF  - Journal of Youth and Adolescence
AU  - Brooks-Russell, Ashley
AU  - Foshee, Vangie A
AU  - Ennett, Susan T
AD  - Prevention Research Branch, Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA ashley.russell@nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 566
EP  - 580
PB  - Springer, Dordrecht, The Netherlands
VL  - 42
IS  - 4
SN  - 0047-2891, 0047-2891
KW  - Peers
KW  - Alcohol Abuse
KW  - Males
KW  - Membership
KW  - Risk Factors
KW  - Victims
KW  - Females
KW  - Vulnerability
KW  - Victimization
KW  - article
KW  - 1939: the family and socialization; adolescence & youth
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1417523230?accountid=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=Journal+of+Youth+and+Adolescence&rft.atitle=Predictors+of+Latent+Trajectory+Classes+of+Physical+Dating+Violence+Victimization&rft.au=Brooks-Russell%2C+Ashley%3BFoshee%2C+Vangie+A%3BEnnett%2C+Susan+T&rft.aulast=Brooks-Russell&rft.aufirst=Ashley&rft.date=2013-04-01&rft.volume=42&rft.issue=4&rft.spage=566&rft.isbn=&rft.btitle=&rft.title=Journal+of+Youth+and+Adolescence&rft.issn=00472891&rft_id=info:doi/10.1007%2Fs10964-012-9876-2
LA  - English
DB  - Sociological Abstracts
N1  - Date revised - 2013-08-01
N1  - Last updated - 2016-09-28
N1  - CODEN - JYADA6
N1  - SubjectsTermNotLitGenreText - Victims; Victimization; Vulnerability; Females; Risk Factors; Peers; Membership; Alcohol Abuse; Males
DO  - http://dx.doi.org/10.1007/s10964-012-9876-2
ER  - 



TY  - JOUR
T1  - Russia's Energy Policy and the Middle East?
TT  - Quelle politique energetique pour la Russie au Moyen-Orient?
AN  - 1373424050; 201322009
AB  - Its relationship with the Middle East is a central element of Russia's energy calculations. The power held by OPEC in determining oil pricing has pushed Moscow to strengthen its ties with countries dominant within the cartel -- Saudi Arabia, for example. The uncertainty of the regional situation (development of the Arab Spring, crisis in Syria, problems in Iran, etc.) could still disrupt Russia's strategy and its position in the Middle East. Adapted from the source document.
JF  - Politique etrangere
AU  - Nocetti, Julien
AD  - Chercheur associe au centre Russie/NEI de l'Ifri
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 93
EP  - 105
PB  - IFRI, Paris France
IS  - 1
SN  - 0032-342X, 0032-342X
KW  - Iran
KW  - Saudi Arabia
KW  - Energy
KW  - Petroleum
KW  - Syria
KW  - Russia
KW  - Energy Policy
KW  - International Economic Organizations
KW  - Middle East
KW  - article
KW  - 9141: political economy; political economy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373424050?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awpsa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Politique+etrangere&rft.atitle=Russia%27s+Energy+Policy+and+the+Middle+East%3F&rft.au=Nocetti%2C+Julien&rft.aulast=Nocetti&rft.aufirst=Julien&rft.date=2013-04-01&rft.volume=&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Politique+etrangere&rft.issn=0032342X&rft_id=info:doi/
LA  - French
DB  - Worldwide Political Science Abstracts
N1  - Date revised - 2013-07-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Russia; Middle East; Petroleum; Iran; Saudi Arabia; Syria; International Economic Organizations; Energy Policy; Energy
ER  - 



TY  - JOUR
T1  - File: Russia in the Middle East: Introduction
TT  - Dossier: La Russie Au Moyen-Orient: Introduction
AN  - 1373423585; 201320824
AB  - Abstract not available.
JF  - Politique etrangere
AU  - Nocetti, Julien
AD  - Chercheur au centre Russie/NEI, Ifri
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 76
EP  - 78
PB  - IFRI, Paris France
IS  - 1
SN  - 0032-342X, 0032-342X
KW  - Russia
KW  - Foreign Policy
KW  - Middle East
KW  - article
KW  - 9063: international relations; international relations
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373423585?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awpsa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Politique+etrangere&rft.atitle=File%3A+Russia+in+the+Middle+East%3A+Introduction&rft.au=Nocetti%2C+Julien&rft.aulast=Nocetti&rft.aufirst=Julien&rft.date=2013-04-01&rft.volume=&rft.issue=1&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=Politique+etrangere&rft.issn=0032342X&rft_id=info:doi/
LA  - French
DB  - Worldwide Political Science Abstracts
N1  - Date revised - 2013-07-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Foreign Policy; Russia; Middle East
ER  - 



TY  - JOUR
T1  - A new generation of human artificial chromosomes for functional genomics and gene therapy
AN  - 1367483550; 17820840
AB  - Since their description in the late 1990s, human artificial chromosomes (HACs) carrying a functional kinetochore were considered as a promising system for gene delivery and expression with a potential to overcome many problems caused by the use of viral-based gene transfer systems. Indeed, HACs avoid the limited cloning capacity, lack of copy number control and insertional mutagenesis due to integration into host chromosomes that plague viral vectors. Nevertheless, until recently, HACs have not been widely recognized because of uncertainties of their structure and the absence of a unique gene acceptor site. The situation changed a few years ago after engineering of HACs with a single loxP gene adopter site and a defined structure. In this review, we summarize recent progress made in HAC technology and concentrate on details of two of the most advanced HACs, 21HAC generated by truncation of human chromosome 21 and alphoid super(tetO)-HAC generated de novo using a synthetic tetO-alphoid DNA array. Multiple potential applications of the HAC vectors are discussed, specifically the unique features of two of the most advanced HAC cloning systems.
JF  - Cellular and Molecular Life Sciences
AU  - Kouprina, Natalay
AU  - Earnshaw, William C
AU  - Masumoto, Hiroshi
AU  - Larionov, Vladimir
AD  - Laboratory of Molecular Pharmacology, NCI, NIH, Bethesda, MD, USA, kouprinn@mail.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 1135
EP  - 1148
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 70
IS  - 7
SN  - 1420-682X, 1420-682X
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - Cloning vectors
KW  - W 30905:Medical Applications
KW  - G 07730:Development & Cell Cycle
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367483550?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+and+Molecular+Life+Sciences&rft.atitle=A+new+generation+of+human+artificial+chromosomes+for+functional+genomics+and+gene+therapy&rft.au=Kouprina%2C+Natalay%3BEarnshaw%2C+William+C%3BMasumoto%2C+Hiroshi%3BLarionov%2C+Vladimir&rft.aulast=Kouprina&rft.aufirst=Natalay&rft.date=2013-04-01&rft.volume=70&rft.issue=7&rft.spage=1135&rft.isbn=&rft.btitle=&rft.title=Cellular+and+Molecular+Life+Sciences&rft.issn=1420682X&rft_id=info:doi/10.1007%2Fs00018-012-1113-3
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Cloning vectors
DO  - http://dx.doi.org/10.1007/s00018-012-1113-3
ER  - 



TY  - JOUR
T1  - Judging risk for multiple diseases: The role of disease worry
AN  - 1364766409; 201311265
AB  - Risk perceptions and disease worry of 1,959 healthy adults were measured in a telephone-based survey. In the model for each of eight health conditions, people's perceived risk was related to their worry for that condition (p < .0001) and their worry for the other seven conditions (p < .001). There was also an interaction indicating that the less people were worried about a certain condition, the more their worry about the other seven conditions increased their risk perception for that condition (p < .0001). The results are important for preventing biased risk perceptions in multiple-disease contexts. [Copyright Sage Publications Ltd.]
JF  - Journal of Health Psychology
AU  - Senay, Ibrahim
AU  - Hensley-Alford, Sharon
AU  - Kaphingst, Kimberly A
AD  - National Institutes of Health, USA
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 554
EP  - 560
PB  - Sage Publications, London UK
VL  - 18
IS  - 4
SN  - 1359-1053, 1359-1053
KW  - Disease risk disease worry affect heuristic genetic testing
KW  - Telephone services
KW  - Worry
KW  - Health
KW  - Risk perception
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364766409?accountid=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=Judging+risk+for+multiple+diseases%3A+The+role+of+disease+worry&rft.au=Senay%2C+Ibrahim%3BHensley-Alford%2C+Sharon%3BKaphingst%2C+Kimberly+A&rft.aulast=Senay&rft.aufirst=Ibrahim&rft.date=2013-04-01&rft.volume=18&rft.issue=4&rft.spage=554&rft.isbn=&rft.btitle=&rft.title=Journal+of+Health+Psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105312437263
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JHPSFC
N1  - SubjectsTermNotLitGenreText - Worry; Risk perception; Telephone services; Health
DO  - http://dx.doi.org/10.1177/1359105312437263
ER  - 



TY  - JOUR
T1  - Short-term outcome of take-home prescriptions for opioid dependence: a clinic-based study
AN  - 1364764321; 201308638
AB  - Introduction & Aim: To evaluate in a real-world setting the short-term outcome among opioid-dependent patients receiving take-home medications. Methods: A total of 102 opioid-dependent patients who formed part of this study received either naltrexone or buprenorphine as long-term treatment for relapse prevention. Following the initiation of treatment in a hospital-based setting, a family member supervised the treatment at home. Measurements included assessment of demographic and clinical variables, retention in treatment, drug use at baseline and follow-up. Results: Majority of patients (69, 67.6%) were dependent on pharmaceutical opioids. Thirty-two (32%) received naltrexone and 70 (68%) were put on buprenorphine maintenance treatment. Follow-up information was available for 67.5% for 3 months, 63% for 6 months and 58% for 1 year. At the end of 6 months, 40% patients were abstinent. This rate decreased to 37.8% at the end of 1 year. Discussion & Conclusions: Buprenorphine was found to be more effective with greater retention rates compared with naltrexone (68% vs. 42%). Buprenorphine maintenance was also found to be useful for patients with pharmaceutical opioid dependence. Adapted from the source document.
JF  - Journal of Substance Use
AU  - Chand, Prabhat
AU  - Murthy, Pratima
AD  - Department of Psychiatry, Centre for Addiction Medicine, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore, India prabhatkumarchand@gmail.com
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 108
EP  - 118
PB  - Taylor & Francis, Basingstoke UK
VL  - 18
IS  - 2
SN  - 1465-9891, 1465-9891
KW  - Opioid dependence, buprenorphine, naltrexone, outcome
KW  - Short term
KW  - Buprenorphine
KW  - Naltrexone
KW  - Retention
KW  - Drug industry
KW  - Drug dependency
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364764321?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Substance+Use&rft.atitle=Short-term+outcome+of+take-home+prescriptions+for+opioid+dependence%3A+a+clinic-based+study&rft.au=Chand%2C+Prabhat%3BMurthy%2C+Pratima&rft.aulast=Chand&rft.aufirst=Prabhat&rft.date=2013-04-01&rft.volume=18&rft.issue=2&rft.spage=108&rft.isbn=&rft.btitle=&rft.title=Journal+of+Substance+Use&rft.issn=14659891&rft_id=info:doi/10.3109%2F14659891.2011.615882
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Drug dependency; Buprenorphine; Naltrexone; Short term; Drug industry; Retention
DO  - http://dx.doi.org/10.3109/14659891.2011.615882
ER  - 



TY  - JOUR
T1  - Celtic Initial Mutation: Pattern Extraction and Subcategorisation
AN  - 1364739092; 201308199
AB  - In this paper I argue that initial consonant mutation in the Celtic languages does not involve synchronically derived phonological alternation, nor is it the product of full lexical listing of alternant wordforms. Rather, Celtic initial mutation involves associations of consonants represented in the lexicon which relate a specific initial consonant of a radical form to its associated mutation reflexes. Together with subcategorisation, which ensures that the correct mutation reflex of a wordform appears in the correct environment, the appropriate initial consonant is selected from an association of consonants extracted by the speaker from the recurring patterns in the language. It is these consonant associations, not full alternant wordforms, that are listed in the lexicon. The advantages to this approach are threefold: broad patterns are identified which full lexical listing obscures, the participation of neologisms in mutation is accounted for straightforwardly, and some of the motivation for diachronic reanalysis within the mutation system is made more apparent. Adapted from the source document
JF  - Word Structure
AU  - Hannahs, S J
AD  - School of English Literature, Language & Linguistics, Newcastle University, Newcastle upon Tyne, NEI 7RU, United Kingdom s.j.hannahs@ncl.ac.uk
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 1
EP  - 20
VL  - 6
IS  - 1
SN  - 1750-1245, 1750-1245
KW  - Neologisms (56850)
KW  - Language Patterns (43300)
KW  - Celtic Languages (11250)
KW  - Consonants (14900)
KW  - Phonology (65250)
KW  - Lexicon (47150)
KW  - Etymology (23250)
KW  - Motivation (55580)
KW  - article
KW  - 5113: descriptive linguistics; computational/mathematical linguistics and machine translation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364739092?accountid=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=Word+Structure&rft.atitle=Celtic+Initial+Mutation%3A+Pattern+Extraction+and+Subcategorisation&rft.au=Hannahs%2C+S+J&rft.aulast=Hannahs&rft.aufirst=S&rft.date=2013-04-01&rft.volume=6&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Word+Structure&rft.issn=17501245&rft_id=info:doi/
LA  - English
DB  - Linguistics and Language Behavior Abstracts (LLBA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Consonants (14900); Celtic Languages (11250); Lexicon (47150); Motivation (55580); Etymology (23250); Phonology (65250); Neologisms (56850); Language Patterns (43300)
ER  - 



TY  - JOUR
T1  - Correlates and Geographic Patterns of Knowledge That Physical Activity Decreases Cancer Risk
AN  - 1356933690; 18040267
AB  - While many lifestyle-related cancer risk factors including tobacco use, poor diet, and sun exposure are well recognized by the general public, the role of physical activity in decreasing cancer risk is less recognized. Studies have demonstrated gender-, race/ethnicity-, and age-based disparities in cancer risk factor knowledge; however, beliefs and geographic factors that may be related to knowledge are under-examined. In this study, we analyzed data from the 2008 Health Information National Trends Survey to determine correlates of knowledge of the relationship between physical activity and reduced cancer risk in the adult US population. We generated geographic information system maps to examine the geographic distribution of this knowledge. Results revealed that there is confusion among US adults about the relationship between physical activity and cancer risk: Respondents who believed that cancer is not preventable had significantly lower odds of knowing that physical activity reduces cancer risk (p < .001) whereas respondents who believed that cancer is caused by one's behavior had almost two times the odds of knowing that physical activity reduces cancer risk (p < .001). Those who were aware of current physical activity guidelines were also significantly more likely to know that physical activity reduces cancer risk (p < .01). Observed geographic variability in knowledge was consistent with geographic trends in obesity and physical inactivity. Correlates of cancer risk factor knowledge point to opportunities for targeted interventions.
JF  - Journal of Primary Prevention
AU  - Ramirez, ASusana
AU  - Finney Rutten, Lila J
AU  - Vanderpool, Robin C
AU  - Moser, Richard P
AU  - Hesse, Bradford W
AD  - National Cancer Institute, 6130 Executive Blvd., Suite 4051A, MSC 7150, Rockville, MD, 20892-7105, USA, ramirezas@mail.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 31
EP  - 39
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 34
IS  - 1-2
SN  - 0278-095X, 0278-095X
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Diets
KW  - Obesity
KW  - Prevention
KW  - Physical activity
KW  - Risk factors
KW  - Guidelines
KW  - Tobacco
KW  - Intervention
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/1356933690?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Primary+Prevention&rft.atitle=Correlates+and+Geographic+Patterns+of+Knowledge+That+Physical+Activity+Decreases+Cancer+Risk&rft.au=Ramirez%2C+ASusana%3BFinney+Rutten%2C+Lila+J%3BVanderpool%2C+Robin+C%3BMoser%2C+Richard+P%3BHesse%2C+Bradford+W&rft.aulast=Ramirez&rft.aufirst=ASusana&rft.date=2013-04-01&rft.volume=34&rft.issue=1-2&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Journal+of+Primary+Prevention&rft.issn=0278095X&rft_id=info:doi/10.1007%2Fs10935-012-0289-5
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Number of references - 30
N1  - Last updated - 2013-07-26
N1  - SubjectsTermNotLitGenreText - Diets; Obesity; Prevention; Risk factors; Physical activity; Guidelines; Tobacco; Intervention; Cancer
DO  - http://dx.doi.org/10.1007/s10935-012-0289-5
ER  - 



TY  - JOUR
T1  - The simplified SART embryo scoring system is highly correlated to implantation and live birth in single blastocyst transfers
AN  - 1352292483; 18006959
AB  - Objective: Prior studies have validated the ability of the SART embryo scoring system to correlate with outcomes in cleavage stage embryo transfers. However, this scoring system has not been evaluated in blastocyst transfers. The objective of this study was to estimate the correlation between the simplified SART embryo scoring system and ART cycle outcomes in single blastocyst transfers. Materials and methods: All fresh, autologous single blastocyst transfers cycles from a large ART center from 2010 were analyzed. Blastocysts were given a single grade of good, fair, or poor based upon SART criteria which combines the grading of the inner cell mass and trophectoderm. Multiple logistic regression assessed the predictive value of the SART grade on embryo implantation and live birth. Results: Seven hundred seventeen fresh, autologous single blastocyst transfers cycles were included in the analysis. The live birth rate was 52 % and included both elective and non-elective SBT. Chi square analysis showed higher live birth in good grade embryos as compared to fair (p=0.03) and poor (p=0.02). Univariate binary logistic regression analysis demonstrated SART embryo grading to be significantly correlated with both implantation and live birth (p<0.01). This significance persisted when patient age, BMI, and the stage of the blastocyst were controlled for with multiple logistic regression. In five patients with a poor blastocyst score, there were no live births. Conclusion: These data demonstrate that the SART embryo scoring system is highly correlated to implantation and live birth in single blastocyst transfers. Patients with a good grade embryo are excellent candidates for a single blastocyst transfer.
JF  - Journal of Assisted Reproduction and Genetics
AU  - Heitmann, Ryan J
AU  - Hill, Micah J
AU  - Richter, Kevin S
AU  - DeCherney, Alan H
AU  - Widra, Eric A
AD  - Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA, eric.widra@integramed.com
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 563
EP  - 567
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 30
IS  - 4
SN  - 1058-0468, 1058-0468
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - blastocysts
KW  - Age
KW  - Data processing
KW  - Regression analysis
KW  - trophectoderm
KW  - Embryo transfer
KW  - G 07730:Development & Cell Cycle
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352292483?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Assisted+Reproduction+and+Genetics&rft.atitle=The+simplified+SART+embryo+scoring+system+is+highly+correlated+to+implantation+and+live+birth+in+single+blastocyst+transfers&rft.au=Heitmann%2C+Ryan+J%3BHill%2C+Micah+J%3BRichter%2C+Kevin+S%3BDeCherney%2C+Alan+H%3BWidra%2C+Eric+A&rft.aulast=Heitmann&rft.aufirst=Ryan&rft.date=2013-04-01&rft.volume=30&rft.issue=4&rft.spage=563&rft.isbn=&rft.btitle=&rft.title=Journal+of+Assisted+Reproduction+and+Genetics&rft.issn=10580468&rft_id=info:doi/10.1007%2Fs10815-013-9932-1
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Number of references - 18
N1  - Last updated - 2013-07-15
N1  - SubjectsTermNotLitGenreText - Age; blastocysts; Data processing; Regression analysis; trophectoderm; Embryo transfer
DO  - http://dx.doi.org/10.1007/s10815-013-9932-1
ER  - 



TY  - JOUR
T1  - Semiparametric inference on the absolute risk reduction and the restricted mean survival difference
AN  - 1352289343; 17949379
AB  - For time-to-event data, when the hazards are non-proportional, in addition to the hazard ratio, the absolute risk reduction and the restricted mean survival difference can be used to describe the time-dependent treatment effect. The absolute risk reduction measures the direct impact of the treatment on event rate or survival, and the restricted mean survival difference provides a way to evaluate the cumulative treatment effect. However, in the literature, available methods are limited for flexibly estimating these measures and making inference on them. In this article, point estimates, pointwise confidence intervals and simultaneous confidence bands of the absolute risk reduction and the restricted mean survival difference are established under a semiparametric model that can be used in a sufficiently wide range of applications. These methods are motivated by and illustrated for data from the Women's Health Initiative estrogen plus progestin clinical trial.
JF  - Lifetime Data Analysis
AU  - Yang, Song
AD  - Office of Biostatistics Research, National Heart, Lung, and Blood Institute, 6701 Rockledge Dr. MSC 7913, Bethesda, MD, 20892, USA, yangso@nhlbi.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 219
EP  - 241
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 19
IS  - 2
SN  - 1380-7870, 1380-7870
KW  - Risk Abstracts
KW  - Estrogens
KW  - Survival
KW  - Risk reduction
KW  - Clinical trials
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352289343?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lifetime+Data+Analysis&rft.atitle=Semiparametric+inference+on+the+absolute+risk+reduction+and+the+restricted+mean+survival+difference&rft.au=Yang%2C+Song&rft.aulast=Yang&rft.aufirst=Song&rft.date=2013-04-01&rft.volume=19&rft.issue=2&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Lifetime+Data+Analysis&rft.issn=13807870&rft_id=info:doi/10.1007%2Fs10985-013-9243-y
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Number of references - 24
N1  - Last updated - 2013-05-31
N1  - SubjectsTermNotLitGenreText - Estrogens; Survival; Risk reduction; Clinical trials
DO  - http://dx.doi.org/10.1007/s10985-013-9243-y
ER  - 



TY  - JOUR
T1  - A U-shaped relationship between haematocrit and mortality in a large prospective cohort study
AN  - 1348487561; 17910914
AB  - Background Only a limited number of studies have investigated the correlation between haematocrit (HCT) and mortality in the general population, and few of those studies have had data on a wide range of low and high levels of HCT. We investigated the association between baseline HCT and mortality in a prospective cohort study of 49 983 adult subjects in Iran with a broad spectrum of HCT values.Methods Data on socio-demographic and life-style factors, past medical history, and levels of HCT were collected at enrollment. During a mean follow-up of 5 years (follow-up success rate similar to 99%), 2262 deaths were reported. Cox proportional hazards regression models were used to estimate hazard ratios and corresponding 95% confidence intervals.Results There was a U-shaped relationship between categories of HCT and mortality in both sexes: both low and high levels of HCT were associated with increased overall mortality and mortality from cardiovascular disease. The U-shaped relationship persisted after several sensitivity analyses were done, including analyses restricted to non-smokers and non-users of opium; analyses excluding deaths from accidents and other external causes as well as deaths of persons with self-reported ischemic heart disease at the baseline interview for the study; and analyses excluding the first 2 years of follow-up. Self-reported past medical history and lack of data about lipids and other cellular blood components were the major limitations of the study.Conclusions Low and high levels of HCT are associated with increased mortality in the general population. The findings in the present study can be of particular importance for low- and middle-income countries in which a substantial proportion of the population lives with suboptimal levels of HCT.
JF  - International Journal of Epidemiology
AU  - Boffetta, Paolo
AU  - Islami, Farhad
AU  - Vedanthan, Rajesh
AU  - Pourshams, Akram
AU  - Kamangar, Farin
AU  - Khademi, Hooman
AU  - Etemadi, Arash
AU  - Salahi, Rasool
AU  - Semnani, Shahryar
AU  - Emadi, Ashkan
AU  - Abnet, Christian C
AU  - Brennan, Paul
AU  - Pharoah, Paul D
AU  - Dawsey, Sanford M
AU  - Malekzadeh, Reza
AD  - super(1)Institute for Transitional Epidemiology and the Tisch Cancer Institute, Mount Sinai School of Medicine, New York, NY, USA, super(2)International Prevention Research Institute, Lyon, France, super(3)Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran, super(4)The Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY, USA, super(5)Department of Public Health Analysis, School of Community Health and Policy, Morgan State University, Baltimore, MD, USA, super(6)International Agency for Research on Cancer, Lyon, France, super(7)Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, super(8)Golestan Research Center of Gastroenterology and Hepatology, Golestan University of Medi, paolo.boffetta@mssm.edu
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 601
EP  - 615
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 42
IS  - 2
SN  - 0300-5771, 0300-5771
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Iran
KW  - Mortality
KW  - Historical account
KW  - Accidents
KW  - Sensitivity analysis
KW  - Lipids
KW  - Cardiovascular diseases
KW  - Heart diseases
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/1348487561?accountid=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+Epidemiology&rft.atitle=A+U-shaped+relationship+between+haematocrit+and+mortality+in+a+large+prospective+cohort+study&rft.au=Boffetta%2C+Paolo%3BIslami%2C+Farhad%3BVedanthan%2C+Rajesh%3BPourshams%2C+Akram%3BKamangar%2C+Farin%3BKhademi%2C+Hooman%3BEtemadi%2C+Arash%3BSalahi%2C+Rasool%3BSemnani%2C+Shahryar%3BEmadi%2C+Ashkan%3BAbnet%2C+Christian+C%3BBrennan%2C+Paul%3BPharoah%2C+Paul+D%3BDawsey%2C+Sanford+M%3BMalekzadeh%2C+Reza&rft.aulast=Boffetta&rft.aufirst=Paolo&rft.date=2013-04-01&rft.volume=42&rft.issue=2&rft.spage=601&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Epidemiology&rft.issn=03005771&rft_id=info:doi/10.1093%2Fije%2Fdyt013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2013-11-04
N1  - SubjectsTermNotLitGenreText - Historical account; Mortality; Accidents; Sensitivity analysis; Lipids; Cardiovascular diseases; Heart diseases; Iran
DO  - http://dx.doi.org/10.1093/ije/dyt013
ER  - 



TY  - JOUR
T1  - In vivo phosphorylation dynamics of the Bordetella pertussis virulence-controlling response regulator BvgA
AN  - 1348483734; 17873408
AB  - We have used protein electrophoresis through polyacrylamide gels derivatized with the proprietary ligand Phos-tag(TM)to separate the response regulator BvgAfrom its phosphorylated counterpart BvgA similar to P. This approach has allowed us to readily ascertain the degree of phosphorylation of BvgAin in vitro reactions, or in crude lysates of Bordetella pertussis grown under varying laboratory conditions. We have used this technique to examine the kinetics of BvgAphosphorylation after shift of B. pertussis cultures from non-permissive to permissive conditions, or of its dephosphorylation following a shift from permissive to non-permissive conditions. Our results provide the first direct evidence that levels of BvgA similar to Pin vivo correspond temporally to the expression of early and late BvgA-regulated virulence genes. We have also examined a number of other aspects of BvgA function predicted from previous studies and by analogy with other two-component response regulators. These include the site of BvgA phosphorylation, the exclusive role of the cognate BvgS sensor kinase in its phosphorylation in Bordetella pertussis, and the effect of the T194M mutation on phosphorylation. We also detected the phosphorylation of a small but consistent fraction of BvgA purified after expression in Escherichia coli.
JF  - Molecular Microbiology
AU  - Boulanger, Alice
AU  - Chen, Qing
AU  - Hinton, Deborah M
AU  - Stibitz, Scott
AD  - Gene Expression and Regulation Section Laboratory of Cell and Molecular Biology NIDDK. National Institutes of Health
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 156
EP  - 172
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 88
IS  - 1
SN  - 0950-382X, 0950-382X
KW  - Microbiology Abstracts B: Bacteriology
KW  - Virulence
KW  - Gels
KW  - Pertussis
KW  - Bordetella pertussis
KW  - Electrophoresis
KW  - Phosphorylation
KW  - Kinetics
KW  - Dephosphorylation
KW  - Escherichia coli
KW  - Mutation
KW  - J 02410:Animal Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1348483734?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=In+vivo+phosphorylation+dynamics+of+the+Bordetella+pertussis+virulence-controlling+response+regulator+BvgA&rft.au=Boulanger%2C+Alice%3BChen%2C+Qing%3BHinton%2C+Deborah+M%3BStibitz%2C+Scott&rft.aulast=Boulanger&rft.aufirst=Alice&rft.date=2013-04-01&rft.volume=88&rft.issue=1&rft.spage=156&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fmmi.12177
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2016-04-29
N1  - SubjectsTermNotLitGenreText - Gels; Virulence; Pertussis; Electrophoresis; Phosphorylation; Kinetics; Dephosphorylation; Mutation; Bordetella pertussis; Escherichia coli
DO  - http://dx.doi.org/10.1111/mmi.12177
ER  - 



TY  - JOUR
T1  - Malaria parasites tolerate a broad range of ionic environments and do not require host cation remodelling
AN  - 1348483724; 17873407
AB  - Malaria parasites grow within erythrocytes, but are also free in host plasma between cycles of asexual replication. As a result, the parasite is exposed to fluctuating levels of Na+ and K+, ions assumed to serve important roles for the human pathogen, Plasmodium falciparum. We examined these assumptions and the parasite's ionic requirements by establishing continuous culture in novel sucrose-based media. With sucrose as the primary osmoticant and K+ and Cl- as the main extracellular ions, we obtained parasite growth and propagation at rates indistinguishable from those in physiological media. These conditions abolish long-known increases in intracellular Na+ via parasite-induced channels, excluding a requirement for erythrocyte cation remodelling. We also dissected Na+, K+ and Cl- requirements and found that unexpectedly low concentrations of each ion meet the parasite's demands. Surprisingly, growth was not adversely affected by up to 148 mM K+, suggesting that low extracellular K+ is not an essential trigger for erythrocyte invasion. At the same time, merozoite egress and invasion required a threshold ionic strength, suggesting critical electrostatic interactions between macromolecules at these stages. These findings provide insights into transmembrane signalling in malaria and reveal fundamental differences between host and parasite ionic requirements.
JF  - Molecular Microbiology
AU  - Pillai, Ajay D
AU  - Addo, Rachel
AU  - Sharma, Paresh
AU  - Nguitragool, Wang
AU  - Srinivasan, Prakash
AU  - Desai, Sanjay A
AD  - Laboratory of Malaria and Vector Research National Institute of Allergy and Infectious Diseases. National Institutes of Health
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 20
EP  - 34
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 88
IS  - 1
SN  - 0950-382X, 0950-382X
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Parasites
KW  - Macromolecules
KW  - Human diseases
KW  - Erythrocytes
KW  - Electrostatic properties
KW  - Chloride
KW  - Malaria
KW  - Hosts
KW  - Public health
KW  - Sucrose
KW  - Media (culture)
KW  - Ions
KW  - Ionic strength
KW  - Replication
KW  - Potassium
KW  - Plasmodium falciparum
KW  - Pathogens
KW  - Continuous culture
KW  - Cations
KW  - Microbiology
KW  - Merozoites
KW  - Propagation
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
KW  - K 03310:Genetics & Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1348483724?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Malaria+parasites+tolerate+a+broad+range+of+ionic+environments+and+do+not+require+host+cation+remodelling&rft.au=Pillai%2C+Ajay+D%3BAddo%2C+Rachel%3BSharma%2C+Paresh%3BNguitragool%2C+Wang%3BSrinivasan%2C+Prakash%3BDesai%2C+Sanjay+A&rft.aulast=Pillai&rft.aufirst=Ajay&rft.date=2013-04-01&rft.volume=88&rft.issue=1&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fmmi.12159
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2016-04-29
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Replication; Microbiology; Erythrocytes; Malaria; Pathogens; Hosts; Public health; Ions; Macromolecules; Ionic strength; Potassium; Chloride; Electrostatic properties; Continuous culture; Cations; Sucrose; Merozoites; Propagation; Media (culture); Plasmodium falciparum
DO  - http://dx.doi.org/10.1111/mmi.12159
ER  - 



TY  - JOUR
T1  - Extensions of criteria for evaluating risk prediction models for public health applications
AN  - 1323806449; 17803837
AB  - We recently proposed two novel criteria to assess the usefulness of risk prediction models for public health applications. The proportion of cases followed, PCF(p), is the proportion of individuals who will develop disease who are included in the proportion p of individuals in the population at highest risk. The proportion needed to follow-up, PNF(q), is the proportion of the general population at highest risk that one needs to follow in order that a proportion q of those destined to become cases will be followed (Pfeiffer, R.M. and Gail, M.H., 2011. Two criteria for evaluating risk prediction models. Biometrics 67, 1057-1065). Here, we extend these criteria in two ways. First, we introduce two new criteria by integrating PCF and PNF over a range of values of q or p to obtain iPCF, the integrated PCF, and iPNF, the integrated PNF. A key assumption in the previous work was that the risk model is well calibrated. This assumption also underlies novel estimates of iPCF and iPNF based on observed risks in a population alone. The second extension is to propose and study estimates of PCF, PNF, iPCF, and iPNF that are consistent even if the risk models are not well calibrated. These new estimates are obtained from case-control data when the outcome prevalence in the population is known, and from cohort data, with baseline covariates and observed health outcomes. We study the efficiency of the various estimates and propose and compare tests for comparing two risk models, both of which were evaluated in the same validation data.
JF  - Biostatistics
AU  - Pfeiffer, Ruth M
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 366
EP  - 381
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 14
IS  - 2
SN  - 1465-4644, 1465-4644
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Prediction models
KW  - Biometrics
KW  - Public health
KW  - H 12000:Epidemiology and Public Health
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323806449?accountid=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=Biostatistics&rft.atitle=Extensions+of+criteria+for+evaluating+risk+prediction+models+for+public+health+applications&rft.au=Pfeiffer%2C+Ruth+M&rft.aulast=Pfeiffer&rft.aufirst=Ruth&rft.date=2013-04-01&rft.volume=14&rft.issue=2&rft.spage=366&rft.isbn=&rft.btitle=&rft.title=Biostatistics&rft.issn=14654644&rft_id=info:doi/10.1093%2Fbiostatistics%2Fkxs037
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2013-05-17
N1  - SubjectsTermNotLitGenreText - Prediction models; Biometrics; Public health
DO  - http://dx.doi.org/10.1093/biostatistics/kxs037
ER  - 



TY  - JOUR
T1  - Clinical and molecular features of POLG-related mitochondrial disease.
AN  - 1323280685; 23545419
AB  - The inability to replicate mitochondrial genomes (mtDNA) by the mitochondrial DNA polymerase (pol γ) leads to a subset of mitochondrial diseases. Many mutations in POLG, the gene that encodes pol γ, have been associated with mitochondrial diseases such as myocerebrohepatopathy spectrum (MCHS) disorders, Alpers-Huttenlocher syndrome, myoclonic epilepsy myopathy sensory ataxia (MEMSA), ataxia neuropathy spectrum (ANS), and progressive external ophthalmoplegia (PEO). This chapter explores five important topics in POLG-related disease: (1) clinical symptoms that identify and distinguish POLG-related diseases, (2) molecular characterization of defects in polymerase activity by POLG disease variants, (3) the importance of holoenzyme formation in disease presentation, (4) the role of pol γ exonuclease activity and mutagenesis in disease and aging, and (5) novel approaches to therapy and avoidance of toxicity based on primary research in pol γ replication.
JF  - Cold Spring Harbor perspectives in biology
AU  - Stumpf, Jeffrey D
AU  - Saneto, Russell P
AU  - Copeland, William C
AD  - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Y1  - 2013/04/01/
PY  - 2013
DA  - 2013 Apr 01
SP  - 1
VL  - 5
IS  - 4
KW  - DNA, Mitochondrial
KW  - 0
KW  - POLG protein, human
KW  - EC 2.7.7.-
KW  - DNA-Directed DNA Polymerase
KW  - EC 2.7.7.7
KW  - Index Medicus
KW  - Phenotype
KW  - Animals
KW  - Humans
KW  - Oxidative Stress
KW  - Mice
KW  - Crystallography, X-Ray
KW  - Genetic Predisposition to Disease
KW  - Mutation
KW  - DNA Replication
KW  - Mutagenesis
KW  - Mitochondrial Diseases -- genetics
KW  - DNA-Directed DNA Polymerase -- physiology
KW  - Mitochondrial Diseases -- metabolism
KW  - Gene Expression Regulation
KW  - DNA-Directed DNA Polymerase -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323280685?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cold+Spring+Harbor+perspectives+in+biology&rft.atitle=Clinical+and+molecular+features+of+POLG-related+mitochondrial+disease.&rft.au=Stumpf%2C+Jeffrey+D%3BSaneto%2C+Russell+P%3BCopeland%2C+William+C&rft.aulast=Stumpf&rft.aufirst=Jeffrey&rft.date=2013-04-01&rft.volume=5&rft.issue=4&rft.spage=a011395&rft.isbn=&rft.btitle=&rft.title=Cold+Spring+Harbor+perspectives+in+biology&rft.issn=1943-0264&rft_id=info:doi/10.1101%2Fcshperspect.a011395
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-30
N1  - Date created - 2013-04-02
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Ther. 2000 Jun;22(6):685-708 [10929917]
Genomics. 2000 Oct 15;69(2):151-61 [11031098]
Nat Genet. 2001 Jul;28(3):211-2 [11431686]
J Biol Chem. 2002 May 3;277(18):15225-8 [11897778]
Ann Neurol. 2002 Aug;52(2):211-9 [12210792]
Hum Mol Genet. 2005 Jul 15;14(14):1907-20 [15917273]
J Biol Chem. 2005 Sep 9;280(36):31341-6 [16024923]
DNA Repair (Amst). 2005 Dec 8;4(12):1381-9 [16181814]
Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):17993-8 [16332961]
Arch Neurol. 2006 Jan;63(1):107-11 [16401742]
Hum Mol Genet. 2006 Jan 15;15(2):363-74 [16368709]
Cell Cycle. 2006 May;5(9):958-62 [16687920]
J Hepatol. 2006 Jul;45(1):108-16 [16545482]
Brain. 2006 Jul;129(Pt 7):1674-84 [16621917]
Brain. 2006 Jul;129(Pt 7):1685-92 [16638794]
Hum Mol Genet. 2006 Oct 1;15(19):2846-55 [16940310]
Hum Reprod. 2006 Oct;21(10):2467-73 [16595552]
Hum Mol Genet. 2006 Dec 1;15(23):3473-83 [17088268]
Eur J Pediatr. 2007 Mar;166(3):229-34 [16957900]
Lab Invest. 2007 Apr;87(4):326-35 [17310215]
Nat Genet. 2007 Apr;39(4):540-3 [17334366]
J Infect Dis. 2007 May 15;195(10):1419-25 [17436221]
J Pediatr. 2007 May;150(5):531-4, 534.e1-6 [17452231]
Nat Genet. 2007 Jun;39(6):776-80 [17486094]
Pediatrics. 2007 Dec;120(6):1326-33 [18055683]
Seizure. 2010 Apr;19(3):140-6 [20138553]
Science. 2005 Jul 15;309(5733):481-4 [16020738]
Am J Hum Genet. 2005 Sep;77(3):430-41 [16080118]
Gene. 2005 Jul 18;354:125-31 [15913923]
Hum Mol Genet. 2010 Jun 1;19(11):2123-33 [20185557]
Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1159-62 [20388490]
Clin Chem. 2010 Jul;56(7):1119-27 [20448188]
Hum Mutat. 2008 Sep;29(9):E150-72 [18546365]
Aging Cell. 2010 Aug;9(4):536-44 [20456298]
Methods. 2010 Aug;51(4):364-73 [20558295]
J Neurol. 2010 Sep;257(9):1517-23 [20405137]
Hum Mol Genet. 2010 Sep 15;19(18):3516-29 [20601675]
J Biol Chem. 2010 Sep 3;285(36):28105-16 [20513922]
Dev Disabil Res Rev. 2010;16(2):163-74 [20818731]
J Biol Chem. 2010 Sep 24;285(39):29690-702 [20659899]
Cell Metab. 2010 Dec 1;12(6):675-82 [21109200]
Mitochondrion. 2011 Jan;11(1):182-90 [20883824]
Cell Mol Life Sci. 2011 Jan;68(2):219-33 [20927567]
Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4135-40 [21368114]
PLoS Genet. 2011 Mar;7(3):e1002028 [21455489]
Bioorg Med Chem Lett. 2011 Jun 15;21(12):3693-8 [21600768]
J Med Genet. 2011 Oct;48(10):669-81 [21880868]
Mitochondrion. 2011 Nov;11(6):929-34 [21856450]
Neuromuscul Disord. 2003 Feb;13(2):133-42 [12565911]
Hum Mutat. 2003 Dec;22(6):498-9 [14635118]
Neurology. 2003 Dec 23;61(12):1811-3 [14694057]
Ann Neurol. 2004 May;55(5):706-12 [15122711]
Nature. 2004 May 27;429(6990):417-23 [15164064]
Nat Struct Mol Biol. 2004 Aug;11(8):770-6 [15258572]
Lancet. 2004 Sep 4-10;364(9437):875-82 [15351195]
Neurology. 2004 Oct 12;63(7):1251-7 [15477547]
J Child Neurol. 1990 Oct;5(4):273-87 [2246481]
Brain Dev. 1991 May;13(3):167-73 [1928609]
J Biol Chem. 1992 Mar 25;267(9):5835-41 [1556099]
Ann Neurol. 1992 Dec;32(6):767-75 [1471867]
Neurology. 1994 Apr;44(4):721-7 [8164833]
Mol Gen Genet. 1995 Nov 1;249(1):1-7 [8552025]
Neurology. 1997 Jul;49(1):239-45 [9222196]
Biochemistry. 1998 Jul 21;37(29):10529-39 [9671525]
Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12244-8 [9770471]
Ann Neurol. 1999 Jan;45(1):54-8 [9894877]
Brain. 2005 Apr;128(Pt 4):723-31 [15689359]
Neurology. 2005 Apr 12;64(7):1204-8 [15824347]
Hum Mol Genet. 2005 Jul 1;14(13):1775-83 [15888483]
Biochim Biophys Acta. 2007 Dec;1772(11-12):1225-35 [17980715]
Annu Rev Med. 2008;59:131-46 [17892433]
Brain. 2008 Mar;131(Pt 3):818-28 [18238797]
Nat Genet. 2008 Apr;40(4):392-4 [18311139]
Neuromuscul Disord. 2008 Mar;18(3):259-67 [18160290]
Mol Genet Metab. 2008 May;94(1):16-37 [18243024]
Epilepsia. 2008 Jun;49(6):1038-45 [18294203]
Neuromuscul Disord. 2008 Aug;18(8):626-32 [18585914]
Nucleic Acids Res. 2009 Apr;37(7):2327-35 [19244310]
Neurology. 2009 May 5;72(18):e86-90 [19414717]
Biochim Biophys Acta. 2009 May;1787(5):312-9 [19010300]
Antimicrob Agents Chemother. 2009 Jun;53(6):2610-2 [19364868]
J Biol Chem. 2009 Jul 17;284(29):19501-10 [19478085]
Epilepsia. 2009 Jun;50(6):1596-607 [19054397]
Cell Metab. 2009 Aug;10(2):131-8 [19656491]
Cell. 2009 Oct 16;139(2):312-24 [19837034]
J Med Genet. 2009 Nov;46(11):776-85 [19578034]
Cell Metab. 2009 Dec;10(6):437 [19945399]
J Biol Chem. 2010 Jan 8;285(2):1490-9 [19858216]
Mitochondrion. 2010 Mar;10(2):183-7 [19887119]
J Biol Chem. 1999 Dec 31;274(53):38197-203 [10608893]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1101/cshperspect.a011395
ER  - 



TY  - JOUR
T1  - Are women who smoke at higher risk for lung cancer than men who smoke?
AN  - 1323279056; 23425629
AB  - Worldwide lung cancer incidence is decreasing or leveling off among men, but rising among women. Sex differences in associations of tobacco carcinogens with lung cancer risk have been hypothesized, but the epidemiologic evidence is conflicting. We tested sex-smoking interaction in association with lung cancer risk within a population-based case-control study, the Environment and Genetics in Lung Cancer Etiology (EAGLE) Study (Lombardy, Italy, 2002-2005). Detailed lifetime smoking histories were collected by personal interview in 2,100 cases with incident lung cancer and 2,120 controls. Odds ratios and 95% confidence intervals for pack-years of cigarette smoking were estimated by logistic regression, adjusted for age, residence area, and time since quitting smoking. To assess sex-smoking interaction, we compared the slopes of odds ratios for logarithm of pack-years in a model for men and women combined. Overall, the slope for pack-years was steeper in men (odds ratio for female-smoking interaction = 0.39, 95% confidence interval: 0.24, 0.62; P < 0.0001); after restriction to ever smokers, the difference in slopes was much smaller (odds ratio for interaction = 0.63, 95% confidence interval: 0.29, 1.37; P = 0.24). Similar results were found by histological type. Results were unchanged when additional confounders were evaluated (e.g., tobacco type, inhalation depth, Fagerström-assessed nicotine dependence). These findings do not support a higher female susceptibility to tobacco-related lung cancer.
JF  - American journal of epidemiology
AU  - De Matteis, Sara
AU  - Consonni, Dario
AU  - Pesatori, Angela C
AU  - Bergen, Andrew W
AU  - Bertazzi, Pier Alberto
AU  - Caporaso, Neil E
AU  - Lubin, Jay H
AU  - Wacholder, Sholom
AU  - Landi, Maria Teresa
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA.
Y1  - 2013/04/01/
PY  - 2013
DA  - 2013 Apr 01
SP  - 601
EP  - 612
VL  - 177
IS  - 7
KW  - Index Medicus
KW  - Sociobiology
KW  - Odds Ratio
KW  - Sex Factors
KW  - Risk Factors
KW  - Humans
KW  - Confounding Factors (Epidemiology)
KW  - Adult
KW  - Case-Control Studies
KW  - Algorithms
KW  - Aged
KW  - Middle Aged
KW  - Time Factors
KW  - Male
KW  - Female
KW  - Lung Neoplasms -- epidemiology
KW  - Smoking -- adverse effects
KW  - Lung Neoplasms -- chemically induced
KW  - Smoking -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323279056?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+epidemiology&rft.atitle=Are+women+who+smoke+at+higher+risk+for+lung+cancer+than+men+who+smoke%3F&rft.au=De+Matteis%2C+Sara%3BConsonni%2C+Dario%3BPesatori%2C+Angela+C%3BBergen%2C+Andrew+W%3BBertazzi%2C+Pier+Alberto%3BCaporaso%2C+Neil+E%3BLubin%2C+Jay+H%3BWacholder%2C+Sholom%3BLandi%2C+Maria+Teresa&rft.aulast=De+Matteis&rft.aufirst=Sara&rft.date=2013-04-01&rft.volume=177&rft.issue=7&rft.spage=601&rft.isbn=&rft.btitle=&rft.title=American+journal+of+epidemiology&rft.issn=1476-6256&rft_id=info:doi/10.1093%2Faje%2Fkws445
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-05-28
N1  - Date created - 2013-04-02
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Epidemiology. 1998 Jan;9(1):79-83 [9430273]
Cancer Causes Control. 2004 May;15(4):341-8 [15141135]
Am J Epidemiol. 1999 Jun 15;149(12):1077-86 [10369501]
Jpn J Clin Oncol. 2006 May;36(5):309-24 [16735374]
Int J Cancer. 2006 Aug 15;119(4):741-4 [16557573]
JAMA. 2006 Jul 12;296(2):180-4 [16835423]
J Clin Oncol. 2007 Feb 10;25(5):561-70 [17290066]
Prev Med. 2007 Aug-Sep;45(2-3):198-201 [17477965]
Lancet Oncol. 2008 Jul;9(7):649-56 [18556244]
BMC Public Health. 2008;8:203 [18538025]
Carcinogenesis. 2009 Apr;30(4):626-35 [19174490]
Gend Med. 2010 Oct;7(5):381-401 [21056866]
CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855]
Int J Occup Environ Health. 1998 Oct-Dec;4(4):236-40 [9876632]
J Natl Cancer Inst. 2004 Jun 2;96(11):812-3 [15173256]
J Natl Cancer Inst. 2004 Jun 2;96(11):826-34 [15173266]
J Natl Cancer Inst. 2004 Jun 16;96(12):898-900 [15199103]
J Natl Cancer Inst. 2004 Oct 20;96(20):1560; author reply 1560-1 [15494607]
Environ Health Perspect. 1990 Jul;87:19-26 [2269225]
Br J Addict. 1991 Sep;86(9):1119-27 [1932883]
Epidemiology. 1992 Jan;3(1):61-4 [1313311]
Int J Cancer. 1993 Apr 22;54(1):44-8 [8386708]
Am J Epidemiol. 1993 Sep 1;138(5):281-93 [8395141]
Int J Epidemiol. 1993 Aug;22(4):592-9 [8225730]
Am J Public Health. 1995 Sep;85(9):1223-30 [7661229]
J Natl Cancer Inst. 1996 Feb 21;88(3-4):183-92 [8632492]
Cancer Epidemiol Biomarkers Prev. 1997 Nov;6(11):863-73 [9367058]
Br J Cancer. 2000 Jan;82(1):227-33 [10638994]
Int J Cancer. 2001 Mar 15;91(6):876-87 [11275995]
Int J Epidemiol. 2001 Aug;30(4):787-92 [11511603]
J Epidemiol Community Health. 2001 Nov;55(11):825-30 [11604439]
J Natl Cancer Inst. 2001 Nov 7;93(21):1600-2 [11698563]
Carcinogenesis. 2002 Feb;23(2):227-9 [11872626]
J Natl Cancer Inst. 2003 Mar 19;95(6):470-8 [12644540]
JAMA. 2004 Apr 14;291(14):1763-8 [15082704]
Comment In:
Am J Epidemiol. 2013 Apr 1;177(7):613-6 [23425628]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/aje/kws445
ER  - 



TY  - JOUR
T1  - A large-scale zebrafish gene knockout resource for the genome-wide study of gene function.
AN  - 1323278620; 23382537
AB  - With the completion of the zebrafish genome sequencing project, it becomes possible to analyze the function of zebrafish genes in a systematic way. The first step in such an analysis is to inactivate each protein-coding gene by targeted or random mutation. Here we describe a streamlined pipeline using proviral insertions coupled with high-throughput sequencing and mapping technologies to widely mutagenize genes in the zebrafish genome. We also report the first 6144 mutagenized and archived F1's predicted to carry up to 3776 mutations in annotated genes. Using in vitro fertilization, we have rescued and characterized ~0.5% of the predicted mutations, showing mutation efficacy and a variety of phenotypes relevant to both developmental processes and human genetic diseases. Mutagenized fish lines are being made freely available to the public through the Zebrafish International Resource Center. These fish lines establish an important milestone for zebrafish genetics research and should greatly facilitate systematic functional studies of the vertebrate genome.
JF  - Genome research
AU  - Varshney, Gaurav K
AU  - Lu, Jing
AU  - Gildea, Derek E
AU  - Huang, Haigen
AU  - Pei, Wuhong
AU  - Yang, Zhongan
AU  - Huang, Sunny C
AU  - Schoenfeld, David
AU  - Pho, Nam H
AU  - Casero, David
AU  - Hirase, Takashi
AU  - Mosbrook-Davis, Deborah
AU  - Zhang, Suiyuan
AU  - Jao, Li-En
AU  - Zhang, Bo
AU  - Woods, Ian G
AU  - Zimmerman, Steven
AU  - Schier, Alexander F
AU  - Wolfsberg, Tyra G
AU  - Pellegrini, Matteo
AU  - Burgess, Shawn M
AU  - Lin, Shuo
AD  - Developmental Genomics Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 727
EP  - 735
VL  - 23
IS  - 4
KW  - Index Medicus
KW  - Phenotype
KW  - Animals
KW  - Alleles
KW  - Gammaretrovirus -- physiology
KW  - Computational Biology -- methods
KW  - Virus Integration
KW  - Chromosome Mapping -- methods
KW  - Mutation
KW  - Mutagenesis, Insertional
KW  - Molecular Sequence Annotation
KW  - Gene Knockout Techniques
KW  - Zebrafish -- genetics
KW  - Genomics
KW  - Genome-Wide Association Study
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323278620?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+research&rft.atitle=A+large-scale+zebrafish+gene+knockout+resource+for+the+genome-wide+study+of+gene+function.&rft.au=Varshney%2C+Gaurav+K%3BLu%2C+Jing%3BGildea%2C+Derek+E%3BHuang%2C+Haigen%3BPei%2C+Wuhong%3BYang%2C+Zhongan%3BHuang%2C+Sunny+C%3BSchoenfeld%2C+David%3BPho%2C+Nam+H%3BCasero%2C+David%3BHirase%2C+Takashi%3BMosbrook-Davis%2C+Deborah%3BZhang%2C+Suiyuan%3BJao%2C+Li-En%3BZhang%2C+Bo%3BWoods%2C+Ian+G%3BZimmerman%2C+Steven%3BSchier%2C+Alexander+F%3BWolfsberg%2C+Tyra+G%3BPellegrini%2C+Matteo%3BBurgess%2C+Shawn+M%3BLin%2C+Shuo&rft.aulast=Varshney&rft.aufirst=Gaurav&rft.date=2013-04-01&rft.volume=23&rft.issue=4&rft.spage=727&rft.isbn=&rft.btitle=&rft.title=Genome+research&rft.issn=1549-5469&rft_id=info:doi/10.1101%2Fgr.151464.112
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-17
N1  - Date created - 2013-04-02
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nature. 2004 Oct 21;431(7011):931-45 [15496913]
Science. 2003 Jun 13;300(5626):1749-51 [12805549]
J Virol. 1990 Jun;64(6):3056-8 [2335826]
Genetics. 1994 Apr;136(4):1401-20 [8013916]
Curr Biol. 1994 Mar 1;4(3):189-202 [7922324]
Nucleic Acids Res. 1995 May 11;23(9):1644-5 [7784225]
Nature. 1996 Oct 31;383(6603):829-32 [8893009]
Methods Cell Biol. 1999;60:87-98 [9891332]
Methods Cell Biol. 1999;60:259-86 [9891342]
Methods Cell Biol. 2004;77:305-29 [15602919]
Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13188-93 [16129827]
Proc Natl Acad Sci U S A. 2007 Jul 24;104(30):12428-33 [17640903]
Mol Ther. 2008 Sep;16(9):1617-23 [18578011]
Brief Funct Genomic Proteomic. 2008 Nov;7(6):427-43 [18977782]
Methods Mol Biol. 2009;546:13-30 [19378095]
Methods. 2009 Apr;47(4):261-8 [19038346]
Genome Biol. 2009;10(3):R25 [19261174]
Plant J. 2010 Jul 1;63(1):167-77 [20409008]
Plant Cell. 2011 Apr;23(4):1273-92 [21498682]
Nat Biotechnol. 2011 Aug;29(8):699-700 [21822242]
Methods Cell Biol. 2011;104:453-78 [21924177]
Nature. 2012 Nov 1;491(7422):114-8 [23000899]
Nucleic Acids Res. 2013 Jan;41(Database issue):D861-4 [23180778]
Nature. 2002 Dec 5;420(6915):520-62 [12466850]
J Virol. 1990 Feb;64(2):907-12 [2296087]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1101/gr.151464.112
ER  - 



TY  - JOUR
T1  - Worry and risk perceptions as independent and interacting predictors of health protective behaviors
AN  - 1322727698; 4424374
AB  - Worry and risk perceptions are generally found to be independently associated with health- promoting behaviors, although it is unknown whether they interact in ways that potentially dampen the effect of either construct on behavior. In this hypothesis- generating study, cancer-related worry and risk perception, and their interaction, were used to predict odds of meeting 5-a-day fruit and vegetable consumption guidelines and engaging in any exercise using data from a nationally representative sample (N = 10,230). Risk perception was not associated with either behavior; worry was associated only with exercise (OR = 1.77, 95% CI: 1.16, 2.70, p < .01). More important, their interaction was associated with these behaviors in a counterintuitive manner; among those higher in worry, higher levels of risk perception were associated with lower vegetable consumption (OR = 0.79, 95% CI: 0.62, 1.00, p < .05) and exercise (OR = 0.77, 95% CI: 0.63, 0.95, p = .01). These results suggest the hypothesis that, among people high in worry, attempts to increase risk perception could be counterproductive. These and related findings suggest the importance of distinguishing worry from risk perception, and future research is necessary to determine the causal nature of these associations. Reprinted by permission of Taylor & Francis Ltd.
JF  - Journal of health communication
AU  - Ferrer, Rebecca A
AU  - Portnoy, David B
AU  - Klein, William M.P.
AD  - US National Institutes of Health
Y1  - 2013/04//
PY  - 2013
DA  - Apr 2013
SP  - 397
EP  - 409
VL  - 18
IS  - 4
SN  - 1081-0730, 1081-0730
KW  - Sociology
KW  - Risk aversion
KW  - Food consumption
KW  - Fruits and vegetables
KW  - Behavioural psychology
KW  - Health management
KW  - Cancer
KW  - Health promotion
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1322727698?accountid=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=Worry+and+risk+perceptions+as+independent+and+interacting+predictors+of+health+protective+behaviors&rft.au=Ferrer%2C+Rebecca+A%3BPortnoy%2C+David+B%3BKlein%2C+William+M.P.&rft.aulast=Ferrer&rft.aufirst=Rebecca&rft.date=2013-04-01&rft.volume=18&rft.issue=4&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2012.727954
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 11036 11040 11035; 5790 5772; 5785 7625; 1939 3617 6220; 5120 2805 3872 554 971; 5333 5136 10286; 1540 1543 10404
DO  - http://dx.doi.org/10.1080/10810730.2012.727954
ER  - 



TY  - JOUR
T1  - Hospitalizations for suicide-related drug poisonings and co-occurring alcohol overdoses in adolescents (ages 12-17) and young adults (ages 18-24) in the United States, 1999-2008: results from the Nationwide Inpatient Sample.
AN  - 1320165210; 23356834
AB  - Drug poisoning is the leading method of suicide-related deaths among females and third among males in the United States. Alcohol can increase the severity of drug poisonings, yet the prevalence of alcohol overdoses in suicide-related drug poisonings (SRDP) remains unclear. Data from the Nationwide Inpatient Sample was examined to determine rates of inpatient hospital stays for SRDP and co-occurring alcohol overdoses in adolescents (ages 12-17) and young adults (ages 18-24) between 1999 and 2008. Among adolescents, there were 14,615 hospitalizations for drug poisonings in 2008, of which 72% (10,462) were suicide-related at a cost of $43 million. Rates of SRDP in this age group decreased between 1999 and 2008. The prevalence of co-occurring alcohol overdoses increased from 5% in 1999 to 7% in 2008. Among young adults, there were 32,471 hospitalizations for drug poisonings in 2008, of which 64% (20,746) were suicide-related at a cost of $110 million. Rates of SRDP did not change significantly between 1999 and 2008. The prevalence of co-occurring alcohol overdoses increased from 14% in 1999 to 20% in 2008. Thus, while rates of SRDP decreased for adolescents and remained unchanged for young adults, the prevalence of co-occurring alcohol overdoses increased for both age groups. Such hospitalizations provide important opportunities to employ intervention techniques to prevent further suicide attempts.
          © 2013 The American Association of Suicidology.
JF  - Suicide & life-threatening behavior
AU  - White, Aaron M
AU  - MacInnes, Erin
AU  - Hingson, Ralph W
AU  - Pan, I-Jen
AD  - Division of Epidemiology and Prevention Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892-9304, USA. whitea4@mail.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 198
EP  - 212
VL  - 43
IS  - 2
KW  - Index Medicus
KW  - Humans
KW  - Confidence Intervals
KW  - Hospital Costs
KW  - Child
KW  - Adolescent
KW  - United States -- epidemiology
KW  - Male
KW  - Female
KW  - Alcoholic Intoxication -- psychology
KW  - Alcoholic Intoxication -- epidemiology
KW  - Suicide, Attempted -- statistics & numerical data
KW  - Drug Overdose -- epidemiology
KW  - Suicide, Attempted -- trends
KW  - Hospitalization -- statistics & numerical data
KW  - Drug Overdose -- psychology
KW  - Hospitalization -- trends
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1320165210?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Suicide+%26+life-threatening+behavior&rft.atitle=Hospitalizations+for+suicide-related+drug+poisonings+and+co-occurring+alcohol+overdoses+in+adolescents+%28ages+12-17%29+and+young+adults+%28ages+18-24%29+in+the+United+States%2C+1999-2008%3A+results+from+the+Nationwide+Inpatient+Sample.&rft.au=White%2C+Aaron+M%3BMacInnes%2C+Erin%3BHingson%2C+Ralph+W%3BPan%2C+I-Jen&rft.aulast=White&rft.aufirst=Aaron&rft.date=2013-04-01&rft.volume=43&rft.issue=2&rft.spage=198&rft.isbn=&rft.btitle=&rft.title=Suicide+%26+life-threatening+behavior&rft.issn=1943-278X&rft_id=info:doi/10.1111%2Fsltb.12008
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-30
N1  - Date created - 2013-03-26
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1111/sltb.12008
ER  - 



TY  - JOUR
T1  - A multi-histology trial of fostamatinib in patients with advanced colorectal, non-small cell lung, head and neck, thyroid, and renal cell carcinomas, and pheochromocytomas.
AN  - 1320162655; 23404627
AB  - A multi-cohort phase II study of fostamatinib, an oral multi-kinase inhibitor, was conducted to determine the response rate in patients with advanced colorectal (CRC), thyroid, non-small cell lung, head and neck, and renal cell carcinomas, and pheochromocytomas.
          Patients received 200 mg fostamatinib BID in 4-week cycles with response assessed every 2 cycles. Blood was collected for pharmacokinetic analysis and measurements of circulating tumor cells and circulating endothelial (progenitor) cells (CE(P)Cs). A total of 37 patients (22 CRC), median of 4 prior therapies, were enrolled. Due to toxicities in four of the first five patients, the study was amended to incorporate a dose escalation phase for each histology. The maximum-tolerated dose was established at 50 mg BID in CRC but was not established for the other cancers. Common grade 3/4 toxicities included transaminitis, hyperbilirubinemia, and hypertension. Pharmacokinetic profile was similar to previous reports. Seventy-three percent of CRC patients had liver involvement and 91 % had prior anti-angiogenic therapy. Patients with abnormal liver tests at baseline were more likely to experience grade ≥ 2 hepatotoxicity than those with normal tests (44 vs. 0 %). No responses were observed; disease stabilization rate was 27 % in CRC. Reduction in CECs following treatment was associated with a better disease stabilization rate (75 vs. 0 %) in CRC.
          Fostamatinib had limited anti-tumor activity in this first clinical trial in patients with advanced refractory solid tumors; reduction in CECs and CEPs was indicative of anti-angiogenic effects. Abnormal liver testing at baseline appeared to influence drug tolerability.
JF  - Cancer chemotherapy and pharmacology
AU  - Park, Sook Ryun
AU  - Speranza, Giovanna
AU  - Piekarz, Richard
AU  - Wright, John J
AU  - Kinders, Robert J
AU  - Wang, Lihua
AU  - Pfister, Thomas
AU  - Trepel, Jane B
AU  - Lee, Min-Jung
AU  - Alarcon, Sylvia
AU  - Steinberg, Seth M
AU  - Collins, Jerry
AU  - Doroshow, James H
AU  - Kummar, Shivaani
AD  - Division of Cancer Treatment and Diagnosis, National Cancer Institute, 31 Center Drive, 3A44, Bethesda, MD 20892, USA.
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 981
EP  - 990
VL  - 71
IS  - 4
KW  - Oxazines
KW  - 0
KW  - Protein Kinase Inhibitors
KW  - Pyridines
KW  - fostamatinib
KW  - SQ8A3S5101
KW  - Index Medicus
KW  - Kidney Neoplasms -- drug therapy
KW  - Humans
KW  - Lung Neoplasms -- drug therapy
KW  - Aged
KW  - Carcinoma, Renal Cell -- drug therapy
KW  - Colorectal Neoplasms -- drug therapy
KW  - Head and Neck Neoplasms -- drug therapy
KW  - Aged, 80 and over
KW  - Adult
KW  - Cohort Studies
KW  - Thyroid Neoplasms -- drug therapy
KW  - Pheochromocytoma -- drug therapy
KW  - Middle Aged
KW  - Carcinoma, Non-Small-Cell Lung -- drug therapy
KW  - Endothelial Cells -- pathology
KW  - Male
KW  - Female
KW  - Adrenal Gland Neoplasms -- drug therapy
KW  - Neoplasms -- drug therapy
KW  - Neoplasms -- pathology
KW  - Protein Kinase Inhibitors -- therapeutic use
KW  - Oxazines -- therapeutic use
KW  - Pyridines -- therapeutic use
KW  - Pyridines -- adverse effects
KW  - Oxazines -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1320162655?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+multi-histology+trial+of+fostamatinib+in+patients+with+advanced+colorectal%2C+non-small+cell+lung%2C+head+and+neck%2C+thyroid%2C+and+renal+cell+carcinomas%2C+and+pheochromocytomas.&rft.au=Park%2C+Sook+Ryun%3BSperanza%2C+Giovanna%3BPiekarz%2C+Richard%3BWright%2C+John+J%3BKinders%2C+Robert+J%3BWang%2C+Lihua%3BPfister%2C+Thomas%3BTrepel%2C+Jane+B%3BLee%2C+Min-Jung%3BAlarcon%2C+Sylvia%3BSteinberg%2C+Seth+M%3BCollins%2C+Jerry%3BDoroshow%2C+James+H%3BKummar%2C+Shivaani&rft.aulast=Park&rft.aufirst=Sook&rft.date=2013-04-01&rft.volume=71&rft.issue=4&rft.spage=981&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=1432-0843&rft_id=info:doi/10.1007%2Fs00280-013-2091-3
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-13
N1  - Date created - 2013-03-26
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Stem Cell Rev. 2008 Sep;4(3):169-77 [18607782]
Leukemia. 2012 Apr;26(4):795-805 [21926965]
J Clin Oncol. 2008 Oct 20;26(30):4899-905 [18794539]
Arthritis Rheum. 2008 Nov;58(11):3309-18 [18975322]
Br J Cancer. 2008 Nov 18;99(10):1564-71 [18941458]
Crit Rev Oncol Hematol. 2009 Feb;69(2):108-24 [18768327]
Birth Defects Res A Clin Mol Teratol. 2009 Feb;85(2):130-6 [19107952]
Blood. 2009 Apr 2;113(14):3154-60 [19096013]
Biochim Biophys Acta. 2009 Jul;1793(7):1115-27 [19306898]
J Clin Oncol. 2009 Jun 20;27(18):3020-6 [19470921]
J Clin Oncol. 2009 Jun 20;27(18):3027-35 [19470923]
Autoimmunity. 2010 Feb;43(1):48-55 [20001666]
Blood. 2010 Apr 1;115(13):2578-85 [19965662]
Drug Metab Dispos. 2010 Jul;38(7):1166-76 [20371637]
N Engl J Med. 2010 Sep 30;363(14):1303-12 [20879879]
Ann Oncol. 2010 Dec;21(12):2382-9 [20497963]
Eur J Cancer. 2011 May;47(7):997-1005 [21247755]
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437]
J Clin Pharmacol. 2011 Sep;51(9):1310-8 [21209239]
Control Clin Trials. 1989 Mar;10(1):1-10 [2702835]
Cancer Cell. 2005 Jan;7(1):101-11 [15652753]
Science. 2006 Sep 22;313(5794):1785-7 [16990548]
J Pharmacol Exp Ther. 2006 Dec;319(3):998-1008 [16946104]
J Pharmacol Exp Ther. 2012 Feb;340(2):277-85 [22031919]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1007/s00280-013-2091-3
ER  - 



TY  - JOUR
T1  - Farletuzumab in lung cancer.
AN  - 1316053437; 23357463
AB  - Folate is essential for proliferating cells and folate transport pathways and folate-dependent metabolic processes show promise as targets for anti-neoplastic therapy. Folate receptor α (FOLR1), a folate transporter, is an attractive target for anti-neoplastic therapy due to its high affinity for folate, restricted range of expression in normal tissue and differential over-expression in malignant tissue. FOLR1 is expressed in non-small cell lung cancer, with a higher expression in adenocarcinoma compared with squamous cell carcinoma. Farletuzumab is a monoclonal antibody targeting FOLR1 which in pre-clinical studies led to cytotoxicity of FOLR1-expressing cells, inhibited tumor growth in animal models and showed limited reactivity with normal tissue. In phase I/II trials, farletuzumab was well tolerated as a single-agent and in combination, without additive toxicity with chemotherapy. An ongoing phase II, double blind, placebo-controlled study is evaluating farletuzumab in patients with FOLR1 expressing metastatic adenocarcinoma of lung.
          Published by Elsevier Ireland Ltd.
JF  - Lung cancer (Amsterdam, Netherlands)
AU  - Thomas, Anish
AU  - Maltzman, Julia
AU  - Hassan, Raffit
AD  - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA.
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 15
EP  - 18
VL  - 80
IS  - 1
KW  - Antibodies, Monoclonal, Humanized
KW  - 0
KW  - FOLR1 protein, human
KW  - Folate Receptor 1
KW  - farletuzumab
KW  - Folic Acid
KW  - 935E97BOY8
KW  - Index Medicus
KW  - Animals
KW  - Folic Acid -- metabolism
KW  - Humans
KW  - Clinical Trials as Topic
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW  - Folate Receptor 1 -- antagonists & inhibitors
KW  - Carcinoma, Non-Small-Cell Lung -- metabolism
KW  - Antibodies, Monoclonal, Humanized -- therapeutic use
KW  - Carcinoma, Non-Small-Cell Lung -- genetics
KW  - Lung Neoplasms -- drug therapy
KW  - Lung Neoplasms -- genetics
KW  - Folate Receptor 1 -- metabolism
KW  - Antibodies, Monoclonal, Humanized -- administration & dosage
KW  - Folate Receptor 1 -- genetics
KW  - Carcinoma, Non-Small-Cell Lung -- drug therapy
KW  - Lung Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1316053437?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Farletuzumab+in+lung+cancer.&rft.au=Thomas%2C+Anish%3BMaltzman%2C+Julia%3BHassan%2C+Raffit&rft.aulast=Thomas&rft.aufirst=Anish&rft.date=2013-04-01&rft.volume=80&rft.issue=1&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.issn=1872-8332&rft_id=info:doi/10.1016%2Fj.lungcan.2012.12.021
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-30
N1  - Date created - 2013-03-11
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Oncotarget. 2012 Apr;3(4):414-25 [22547449]
Adv Drug Deliv Rev. 2004 Apr 29;56(8):1067-84 [15094207]
Cancer Chemother Pharmacol. 2012 Jul;70(1):113-20 [22644798]
J Thorac Oncol. 2012 May;7(5):833-40 [22729036]
Oncogene. 2003 Apr 10;22(14):2192-205 [12687021]
Adv Drug Deliv Rev. 2002 Sep 13;54(5):675-93 [12204598]
N Engl J Med. 2002 Jan 10;346(2):92-8 [11784875]
Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13784-9 [11707590]
Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567]
J Thorac Cardiovasc Surg. 2001 Feb;121(2):225-33 [11174727]
Ann Oncol. 2011 Dec;22(12):2616-24 [22071650]
Clin Cancer Res. 2010 Nov 1;16(21):5288-95 [20855460]
CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300 [20610543]
N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680]
Int J Cancer. 2008 Oct 1;123(7):1699-703 [18646191]
Nucl Med Biol. 2008 Apr;35(3):343-51 [18355690]
Ann Surg Oncol. 2008 Mar;15(3):889-99 [18181001]
J Thorac Oncol. 2007 Aug;2(8):706-14 [17762336]
Int J Cancer. 2007 Sep 1;121(5):938-42 [17487842]
Cancer Metastasis Rev. 2007 Mar;26(1):111-28 [17334909]
Cancer Immun. 2007;7:6 [17346028]
Ann N Y Acad Sci. 2005 Nov;1059:86-96 [16382047]
Oncologist. 2005 Jun-Jul;10(6):363-8 [15967829]
Anal Biochem. 2005 Mar 15;338(2):284-93 [15745749]
Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):775-82 [10498396]
Int J Cancer. 1998 Apr 17;79(2):121-6 [9583724]
BMJ. 1995 Oct 7;311(7010):899-909 [7580546]
Eur J Cancer. 1994;30A(3):363-9 [8204360]
Int J Cancer Suppl. 1994;8:89-95 [8194901]
Am J Pathol. 1993 Feb;142(2):557-67 [8434649]
Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5572-6 [2062838]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.lungcan.2012.12.021
ER  - 



TY  - JOUR
T1  - Propylisopropylacetic acid (PIA), a constitutional isomer of valproic acid, uncompetitively inhibits arachidonic acid acylation by rat acyl-CoA synthetase 4: a potential drug for bipolar disorder.
AN  - 1314710972; 23354024
AB  - Mood stabilizers used for treating bipolar disorder (BD) selectively downregulate arachidonic acid (AA) turnover (deacylation-reacylation) in brain phospholipids, when given chronically to rats. In vitro studies suggest that one of these, valproic acid (VPA), which is teratogenic, reduces AA turnover by inhibiting the brain long-chain acyl-CoA synthetase (Acsl)4 mediated acylation of AA to AA-CoA. We tested whether non-teratogenic VPA analogues might also inhibit Acsl4 catalyzed acylation, and thus have a potential anti-BD action.
          Rat Acsl4-flag protein was expressed in Escherichia coli, and the ability of three VPA analogues, propylisopropylacetic acid (PIA), propylisopropylacetamide (PID) and N-methyl-2,2,3,3-tetramethylcyclopropanecarboxamide (MTMCD), and of sodium butyrate, to inhibit conversion of AA to AA-CoA by Acsl4 was quantified using Michaelis-Menten kinetics. Acsl4-mediated conversion of AA to AA-CoA in vitro was inhibited uncompetitively by PIA, with a Ki of 11.4mM compared to a published Ki of 25mM for VPA, while PID, MTMCD and sodium butyrate had no inhibitory effect.
          PIA's ability to inhibit conversion of AA to AA-CoA by Acsl4 in vitro suggests that, like VPA, PIA may reduce AA turnover in brain phospholipids in unanesthetized rats, and if so, may be effective as a non-teratogenic mood stabilizer in BD patients. Published by Elsevier B.V.
JF  - Biochimica et biophysica acta
AU  - Modi, Hiren R
AU  - Basselin, Mireille
AU  - Taha, Ameer Y
AU  - Li, Lei O
AU  - Coleman, Rosalind A
AU  - Bialer, Meir
AU  - Rapoport, Stanley I
AD  - Brain Physiology and Metabolism Section, National Institute on Aging, Laboratory of Neurosciences, National Institutes of Health, Bethesda, MD, USA. modihr@mail.nih.gov
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 880
EP  - 886
VL  - 1831
IS  - 4
SN  - 0006-3002, 0006-3002
KW  - Antimanic Agents
KW  - 0
KW  - Arachidonic Acid
KW  - 27YG812J1I
KW  - Valproic Acid
KW  - 614OI1Z5WI
KW  - Acsl4 protein, rat
KW  - EC 6.2.1.-
KW  - Coenzyme A Ligases
KW  - Index Medicus
KW  - Rats
KW  - Molecular Structure
KW  - Animals
KW  - Antimanic Agents -- pharmacology
KW  - Antimanic Agents -- chemistry
KW  - Valproic Acid -- pharmacology
KW  - Valproic Acid -- chemistry
KW  - Coenzyme A Ligases -- metabolism
KW  - Acylation -- drug effects
KW  - Bipolar Disorder -- metabolism
KW  - Arachidonic Acid -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314710972?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Propylisopropylacetic+acid+%28PIA%29%2C+a+constitutional+isomer+of+valproic+acid%2C+uncompetitively+inhibits+arachidonic+acid+acylation+by+rat+acyl-CoA+synthetase+4%3A+a+potential+drug+for+bipolar+disorder.&rft.au=Modi%2C+Hiren+R%3BBasselin%2C+Mireille%3BTaha%2C+Ameer+Y%3BLi%2C+Lei+O%3BColeman%2C+Rosalind+A%3BBialer%2C+Meir%3BRapoport%2C+Stanley+I&rft.aulast=Modi&rft.aufirst=Hiren&rft.date=2013-04-01&rft.volume=1831&rft.issue=4&rft.spage=880&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbalip.2013.01.008
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-11
N1  - Date created - 2013-03-04
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Neurochem. 2007 Sep;102(6):1918-27 [17550430]
J Med Chem. 2007 Dec 13;50(25):6419-27 [17994680]
J Lipid Res. 2008 Jan;49(1):162-8 [17957090]
Exp Biol Med (Maywood). 2008 May;233(5):507-21 [18375835]
Clin Ther. 2008 Jul;30(7):1180-95 [18691980]
Neurochem Res. 2008 Nov;33(11):2318-23 [18500552]
J Biol Chem. 2008 Oct 31;283(44):30235-45 [18772128]
Prostaglandins Leukot Essent Fatty Acids. 2008 Sep-Nov;79(3-5):153-6 [18973997]
Neuroscience. 2009 Mar 17;159(2):657-69 [19166906]
Neuropharmacology. 2009 Mar;56(4):831-7 [19705552]
Brain Res Rev. 2009 Oct;61(2):185-209 [19555719]
J Immunol. 2010 Jan 15;184(2):1071-8 [20018618]
Lancet. 2010 Jan 30;375(9712):385-95 [20092882]
Neurobiol Dis. 2010 Mar;37(3):596-603 [19945534]
Am J Med Genet A. 2010 Mar;152A(3):713-7 [20186809]
Mol Psychiatry. 2010 Apr;15(4):384-92 [19488045]
J Lipid Res. 2010 May;51(5):1049-56 [20040630]
J Affect Disord. 2010 Aug;124(3):319-23 [20060174]
J Lipid Res. 2010 Aug;51(8):2334-40 [20388940]
Biochim Biophys Acta. 2011 Mar;1811(3):163-9 [21184843]
Mol Psychiatry. 2011 Apr;16(4):419-28 [20038946]
Neuropharmacology. 2011 Dec;61(8):1256-64 [21839100]
Prostaglandins Leukot Essent Fatty Acids. 2012 Aug-Sep;87(2-3):71-7 [22841517]
FEBS Lett. 2000 Feb 11;467(2-3):263-7 [10675551]
J Pharmacol Exp Ther. 2000 Mar;292(3):968-73 [10688611]
J Nutr. 2000 Feb;130(2S Suppl):294S-298S [10721891]
Arch Gen Psychiatry. 2000 May;57(5):481-9 [10807488]
Brain Res. 2000 Nov 24;884(1--2):77-86 [11082489]
Biol Psychiatry. 2001 Jan 15;49(2):97-109 [11164756]
J Neurochem. 2001 May;77(3):796-803 [11331408]
J Biol Chem. 2001 Sep 28;276(39):36734-41 [11473107]
Mol Psychiatry. 2002;7 Suppl 1:S57-63 [11986996]
Arch Gen Psychiatry. 2002 Jul;59(7):592-6 [12090811]
Mol Psychiatry. 2002;7(8):845-50 [12232777]
J Neurochem. 2003 May;85(3):690-6 [12694395]
Neurochem Res. 2003 Jun;28(6):861-6 [12718439]
J Neurochem. 2004 Mar;88(5):1168-78 [15009672]
J Biol Chem. 2004 Jul 23;279(30):31717-26 [15145952]
Biol Psychiatry. 2004 Aug 15;56(4):248-54 [15312812]
Anal Biochem. 1976 May 7;72:248-54 [942051]
Psychopharmacology (Berl). 1980;67(3):297-305 [6155678]
Hepatology. 1982 Sep-Oct;2(5):591-7 [6811394]
Hepatology. 1982 Nov-Dec;2(6):870-3 [6815046]
Biochem Soc Trans. 1985 Feb;13(1):75-7 [3922822]
Science. 1987 Sep 4;237(4819):1171-6 [2820055]
Ann N Y Acad Sci. 1989;559:37-55 [2672943]
J Pharmacol Exp Ther. 1989 Sep;250(3):1067-78 [2506334]
Pharm Res. 1989 Aug;6(8):683-9 [2510141]
J Neurochem. 1990 Jul;55(1):1-15 [2113081]
Drug Metab Dispos. 1992 Jul-Aug;20(4):578-84 [1356738]
Epilepsy Res. 1993 Jun;15(2):113-31 [8370349]
Chem Res Toxicol. 1996 Jul-Aug;9(5):866-70 [8828922]
Pharm Res. 1996 Feb;13(2):284-9 [8932450]
Neurosci Lett. 1996 Dec 20;220(3):171-4 [8994220]
Exp Toxicol Pathol. 1997 Aug;49(3-4):225-32 [9314057]
Epilepsia. 1997 Sep;38(9):981-90 [9579936]
Neurotoxicology. 1998 Jun;19(3):357-70 [9621342]
Neurochem Res. 1999 Mar;24(3):399-406 [10215514]
Chirality. 1999;11(8):645-50 [10467316]
Biochemistry. 2005 Feb 8;44(5):1635-42 [15683247]
Biochem Pharmacol. 2005 May 15;69(10):1501-8 [15857614]
Neurochem Res. 2005 May;30(5):597-601 [16176062]
Neurochem Res. 2005 May;30(5):677-83 [16176072]
Psychopharmacology (Berl). 2005 Oct;182(1):180-5 [15986187]
Cytogenet Genome Res. 2006;112(1-2):170-5 [16276108]
Psychopharmacology (Berl). 2006 Jan;184(1):122-9 [16344985]
Bipolar Disord. 2006 Feb;8(1):15-27 [16411977]
Biol Psychiatry. 2006 Mar 1;59(5):401-7 [16182257]
Neuropsychopharmacology. 2006 Aug;31(8):1659-74 [16292331]
Mol Pharmacol. 2007 Mar;71(3):884-92 [17167030]
J Neurochem. 2007 Aug;102(3):761-72 [17488274]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.bbalip.2013.01.008
ER  - 



TY  - JOUR
T1  - Functional activity and tumor-specific expression of dual oxidase 2 in pancreatic cancer cells and human malignancies characterized with a novel monoclonal antibody.
AN  - 1314336587; 23404210
AB  - Dual oxidase 2 (Duox2), one of the seven members of the NADPH oxidase gene family, plays a critical role in generating H2O2 for thyroid hormone biosynthesis and as an integral part of the host defense system of the respiratory epithelium and the gastrointestinal tract. Recent evidence suggests that the regulation of Duox2 expression is under the control of pro-inflammatory cytokines and that Duox2-induced reactive oxygen species (ROS) contribute to the inflammation-related tissue injury that occurs in two pre-malignant, inflammatory conditions: chronic pancreatitis and inflammatory bowel disease. Because no reliable Duox antibodies are commercially available, we report the development of a murine monoclonal antibody (MAb) to Duox2 (clone Duox S-12) and its use for the characterization of Duox2 expression in human tumors, tumor cell lines and normal tissues. Duox S-12 specifically detected both endogenously- and ectopically-expressed Duox2 protein by immunoblotting, immunofluorescence microscopy and immunohistochemistry (where both membranous and cytoplasmic staining were present). Duox2 expression detected by Duox S-12 was functionally coupled to the generation of H(2)O(2) in pancreatic cancer cells that expressed Duox2 and its cognate maturation factor DuoxA2. Although Duox S-12 recognizes ectopically expressed Duox1 protein because of the extensive amino acid homology between Duox1 and Duox2, the lack of substantial Duox1 mRNA expression in human tumors (except thyroid cancer) allowed us to evaluate Duox2 expression across a wide range of normal and malignant tissues by immuno-histochemistry. Duox2 was expressed at elevated levels in many human cancers, most notably tumors of the prostate, lung, colon and breast while brain tumors and lymphomas demonstrated the lowest frequency of expression. The Duox-specific monoclonal antibody described here provides a promising tool for the further examination of the role of Duox-dependent reactive oxygen production in inflammation-related carcinogenesis, where alterations in oxidant tone play a critical role in cell growth and proliferation.
JF  - International journal of oncology
AU  - Wu, Yonghzong
AU  - Antony, Smitha
AU  - Hewitt, Stephen M
AU  - Jiang, Guojian
AU  - Yang, Sherry X
AU  - Meitzler, Jennifer L
AU  - Juhasz, Agnes
AU  - Lu, Jiamo
AU  - Liu, Han
AU  - Doroshow, James H
AU  - Roy, Krishnendu
AD  - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/04//
PY  - 2013
DA  - April 2013
SP  - 1229
EP  - 1238
VL  - 42
IS  - 4
KW  - Antibodies, Monoclonal, Murine-Derived
KW  - 0
KW  - DUOXA2 protein, human
KW  - Membrane Proteins
KW  - Hydrogen Peroxide
KW  - BBX060AN9V
KW  - DUOX2 protein, human
KW  - EC 1.6.3.1
KW  - NADPH Oxidase
KW  - Index Medicus
KW  - Animals
KW  - Hybridomas
KW  - COS Cells
KW  - Membrane Proteins -- metabolism
KW  - Humans
KW  - Hydrogen Peroxide -- metabolism
KW  - Mice
KW  - Amino Acid Sequence
KW  - Cell Line, Tumor
KW  - Mice, Inbred BALB C
KW  - Antibody Specificity
KW  - Tissue Array Analysis
KW  - Cercopithecus aethiops
KW  - Molecular Sequence Data
KW  - Immunohistochemistry
KW  - Female
KW  - Male
KW  - NADPH Oxidase -- metabolism
KW  - Adenocarcinoma -- enzymology
KW  - Antibodies, Monoclonal, Murine-Derived -- immunology
KW  - Pancreatic Neoplasms -- enzymology
KW  - NADPH Oxidase -- immunology
KW  - Breast Neoplasms -- enzymology
KW  - Antibodies, Monoclonal, Murine-Derived -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314336587?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+oncology&rft.atitle=Functional+activity+and+tumor-specific+expression+of+dual+oxidase+2+in+pancreatic+cancer+cells+and+human+malignancies+characterized+with+a+novel+monoclonal+antibody.&rft.au=Wu%2C+Yonghzong%3BAntony%2C+Smitha%3BHewitt%2C+Stephen+M%3BJiang%2C+Guojian%3BYang%2C+Sherry+X%3BMeitzler%2C+Jennifer+L%3BJuhasz%2C+Agnes%3BLu%2C+Jiamo%3BLiu%2C+Han%3BDoroshow%2C+James+H%3BRoy%2C+Krishnendu&rft.aulast=Wu&rft.aufirst=Yonghzong&rft.date=2013-04-01&rft.volume=42&rft.issue=4&rft.spage=1229&rft.isbn=&rft.btitle=&rft.title=International+journal+of+oncology&rft.issn=1791-2423&rft_id=info:doi/10.3892%2Fijo.2013.1821
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-19
N1  - Date created - 2013-03-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Clin Endocrinol Metab. 2001 Jul;86(7):3351-8 [11443211]
Cancer Cell. 2011 Jun 14;19(6):728-39 [21665147]
Surg Oncol. 2002 May;10(4):153-69 [12020670]
Mol Cell Endocrinol. 2004 Feb 12;214(1-2):53-62 [15062544]
Cancer Res. 1987 Sep 15;47(18):4771-5 [3040230]
Mol Cell Biochem. 1988 Dec;84(2):189-98 [3231222]
Cancer Res. 1991 Feb 1;51(3):794-8 [1846317]
Arch Biochem Biophys. 1993 Aug 1;304(2):314-21 [8394053]
Am J Physiol Gastrointest Liver Physiol. 2005 May;288(5):G933-42 [15591162]
Am J Respir Cell Mol Biol. 2005 May;32(5):462-9 [15677770]
Mod Pathol. 2005 Jun;18(6):779-87 [15791284]
Philos Trans R Soc Lond B Biol Sci. 2005 Dec 29;360(1464):2301-8 [16321800]
J Biol Chem. 2006 Jul 7;281(27):18269-72 [16651268]
J Gastroenterol. 2006 Nov;41(11):1053-63 [17160516]
Physiol Rev. 2007 Jan;87(1):245-313 [17237347]
Free Radic Biol Med. 2007 Aug 1;43(3):332-47 [17602948]
Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G99-G108 [17962358]
Cancer Res. 2008 Feb 15;68(4):1037-45 [18281478]
Free Radic Res. 2009 Jun;43(6):523-32 [19431059]
Cancer Sci. 2009 Aug;100(8):1382-8 [19493276]
J Cell Sci. 2009 Oct 1;122(Pt 19):3522-30 [19759286]
Trends Immunol. 2010 Jul;31(7):278-87 [20579935]
Inflamm Bowel Dis. 2010 Oct;16(10):1649-57 [20155851]
J Biol Chem. 2011 Apr 8;286(14):12245-56 [21321110]
Thyroid. 2001 Nov;11(11):1017-23 [11762710]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.3892/ijo.2013.1821
ER  - 



TY  - JOUR
T1  - Assessing biomarkers for brain diseases: progress and gaps
AN  - 1516752362; 19529864
AB  - A report on the 2nd Wellcome Trust Scientific Conference on Biomarkers for Brain Disorders: Challenges and Opportunities, held at the Moller Centre, Cambridge, UK, February 3-5, 2013.
JF  - Genome Medicine
AU  - Brady, Linda S
AD  - Division of Neuroscience and Basic Behavioral Science, National Institute of Mental Health, 6001 Executive Boulevard, Bethesda, MD 20892, USA, lbrady@mail.nih.gov
Y1  - 2013/03/20/
PY  - 2013
DA  - 2013 Mar 20
SP  - 23
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 5
IS  - 3
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - Conferences
KW  - Brain
KW  - biomarkers
KW  - G 07880:Human Genetics
KW  - W 30970:Book & Conference Notices
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516752362?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+Medicine&rft.atitle=Assessing+biomarkers+for+brain+diseases%3A+progress+and+gaps&rft.au=Brady%2C+Linda+S&rft.aulast=Brady&rft.aufirst=Linda&rft.date=2013-03-20&rft.volume=5&rft.issue=3&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Genome+Medicine&rft.issn=1756-994X&rft_id=info:doi/10.1186%2Fgm427
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Conferences; Brain; biomarkers
DO  - http://dx.doi.org/10.1186/gm427
ER  - 



TY  - JOUR
T1  - Contrasting the epidemiological and evolutionary dynamics of influenza spatial transmission
AN  - 1551637498; 20369680
AB  - In the past decade, rapid increases in the availability of high-resolution molecular and epidemiological data, combined with developments in statistical and computational methods to simulate and infer migration patterns, have provided key insights into the spatial dynamics of influenza A viruses in humans. In this review, we contrast findings from epidemiological and molecular studies of influenza virus transmission at different spatial scales. We show that findings are broadly consistent in large-scale studies of inter-regional or inter-hemispheric spread in temperate regions, revealing intense epidemics associated with multiple viral introductions, followed by deep troughs driven by seasonal bottlenecks. However, aspects of the global transmission dynamics of influenza viruses are still debated, especially with respect to the existence of tropical source populations experiencing high levels of genetic diversity and the extent of prolonged viral persistence between epidemics. At the scale of a country or community, epidemiological studies have revealed spatially structured diffusion patterns in seasonal and pandemic outbreaks, which were not identified in molecular studies. We discuss the role of sampling issues in generating these conflicting results, and suggest strategies for future research that may help to fully integrate the epidemiological and evolutionary dynamics of influenza virus over space and time.
JF  - Philosophical Transactions of the Royal Society of London, Series B: Biological Sciences
AU  - Viboud, Cecile
AU  - Nelson, Martha I
AU  - Tan, Yi
AU  - Holmes, Edward C
AD  - Fogarty International Center, National Institutes of Health, , Bethesda, MD 20892, USA, viboudc@mail.nih.gov
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
SP  - 20120199
PB  - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom
VL  - 368
IS  - 1614
SN  - 0962-8436, 0962-8436
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - influenza
KW  - spatial diffusion
KW  - human mobility
KW  - phylogeography
KW  - source population
KW  - viral persistence
KW  - Epidemics
KW  - Statistics
KW  - Data processing
KW  - Spatial distribution
KW  - Influenza A
KW  - Viruses
KW  - Genetic diversity
KW  - Computer applications
KW  - Migration
KW  - Disease transmission
KW  - Influenza
KW  - pandemics
KW  - Influenza virus
KW  - Sulfur dioxide
KW  - Reviews
KW  - Diffusion
KW  - Outbreaks
KW  - Sampling
KW  - Seasonal variations
KW  - Evolution
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/1551637498?accountid=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=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=Contrasting+the+epidemiological+and+evolutionary+dynamics+of+influenza+spatial+transmission&rft.au=Viboud%2C+Cecile%3BNelson%2C+Martha+I%3BTan%2C+Yi%3BHolmes%2C+Edward+C&rft.aulast=Viboud&rft.aufirst=Cecile&rft.date=2013-03-19&rft.volume=368&rft.issue=1614&rft.spage=20120199&rft.isbn=&rft.btitle=&rft.title=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628436&rft_id=info:doi/10.1098%2Frstb.2012.0199
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2015-04-02
N1  - SubjectsTermNotLitGenreText - pandemics; Data processing; Statistics; Epidemics; Influenza A; Genetic diversity; Diffusion; Sampling; Computer applications; Migration; Evolution; Disease transmission; Influenza; Sulfur dioxide; Spatial distribution; Reviews; Viruses; Outbreaks; Seasonal variations; Influenza virus
DO  - http://dx.doi.org/10.1098/rstb.2012.0199
ER  - 



TY  - CPAPER
T1  - The Phenotype-Genotype Integrator (PheGenI): Synthesizing genome-wide association study data with existing genomic resources
T2  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AN  - 1420114746; 6230955
JF  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AU  - Ramos, Erin
AU  - Hoffman, Douglas
AU  - Junkins, Heather
AU  - Kimura, Masato
AU  - Maglott, Donna
AU  - Phan, Lon
AU  - Feolo, Michael
AU  - Hindorff, Lucia
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
KW  - Data processing
KW  - genomics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420114746?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.atitle=The+Phenotype-Genotype+Integrator+%28PheGenI%29%3A+Synthesizing+genome-wide+association+study+data+with+existing+genomic+resources&rft.au=Ramos%2C+Erin%3BHoffman%2C+Douglas%3BJunkins%2C+Heather%3BKimura%2C+Masato%3BMaglott%2C+Donna%3BPhan%2C+Lon%3BFeolo%2C+Michael%3BHindorff%2C+Lucia&rft.aulast=Ramos&rft.aufirst=Erin&rft.date=2013-03-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ww2.aievolution.com/acm1301/index.cfm?do=abs.pubSearchAbstracts&style=0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-31
N1  - Last updated - 2013-08-14
ER  - 



TY  - CPAPER
T1  - Medical Variation and Phenotypes at NCBI: GTR, MedGen, and ClinVar
T2  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AN  - 1420114617; 6230967
JF  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AU  - Rubinstein, Wendy
AU  - Maglott, Donna
AU  - Malheiro, Adriana
AU  - Kattman, Brandi
AU  - Lee, Jennifer
AU  - Riley, George
AU  - Landrum, Melissa
AU  - Hoffman, Douglas
AU  - Chitipiralla, Shanmuga
AU  - Ovetsky, Michael
AU  - Gorelenkov, Viatcheslav
AU  - Hem, Vichet
AU  - Song, Guangfeng
AU  - Wallin, Craig
AU  - Katz, Kenneth
AU  - Jang, Wonhee
AU  - Halavi, Maryam
AU  - Fomous, Cathy
AU  - Church, Deanna
AU  - Ostell, James
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
KW  - Phenotypes
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420114617?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.atitle=Medical+Variation+and+Phenotypes+at+NCBI%3A+GTR%2C+MedGen%2C+and+ClinVar&rft.au=Rubinstein%2C+Wendy%3BMaglott%2C+Donna%3BMalheiro%2C+Adriana%3BKattman%2C+Brandi%3BLee%2C+Jennifer%3BRiley%2C+George%3BLandrum%2C+Melissa%3BHoffman%2C+Douglas%3BChitipiralla%2C+Shanmuga%3BOvetsky%2C+Michael%3BGorelenkov%2C+Viatcheslav%3BHem%2C+Vichet%3BSong%2C+Guangfeng%3BWallin%2C+Craig%3BKatz%2C+Kenneth%3BJang%2C+Wonhee%3BHalavi%2C+Maryam%3BFomous%2C+Cathy%3BChurch%2C+Deanna%3BOstell%2C+James&rft.aulast=Rubinstein&rft.aufirst=Wendy&rft.date=2013-03-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ww2.aievolution.com/acm1301/index.cfm?do=abs.pubSearchAbstracts&style=0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-31
N1  - Last updated - 2013-08-14
ER  - 



TY  - CPAPER
T1  - 'Double Trouble': Diagnostic Challenges in DMD in Patients with an Additional Hereditary Skeletal Dysplasia
T2  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AN  - 1420114117; 6230705
JF  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AU  - Donkervoort, Sandra
AU  - Schindler, Alice
AU  - Schreiber, Allison
AU  - Wagner, Kathryn
AU  - Friedman, Neil
AU  - Bonnemann, Carsten
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
KW  - Bone dysplasia
KW  - Skeleton
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420114117?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.atitle=%27Double+Trouble%27%3A+Diagnostic+Challenges+in+DMD+in+Patients+with+an+Additional+Hereditary+Skeletal+Dysplasia&rft.au=Donkervoort%2C+Sandra%3BSchindler%2C+Alice%3BSchreiber%2C+Allison%3BWagner%2C+Kathryn%3BFriedman%2C+Neil%3BBonnemann%2C+Carsten&rft.aulast=Donkervoort&rft.aufirst=Sandra&rft.date=2013-03-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ww2.aievolution.com/acm1301/index.cfm?do=abs.pubSearchAbstracts&style=0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-31
N1  - Last updated - 2013-08-14
ER  - 



TY  - CPAPER
T1  - An Unusual Case of Mosaicism for a Trisomic Imbalance of 21q and 14q
T2  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AN  - 1420114103; 6230747
JF  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AU  - Banks, Nicole
AU  - Raygada, Margarita
AU  - Christacos, Nicole
AU  - Schonberg, Steven
AU  - Charalsawadi, Chariyawan
AU  - Jackson-Cook, Colleen
AU  - Rennert, Owen
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
KW  - Mosaicism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420114103?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.atitle=An+Unusual+Case+of+Mosaicism+for+a+Trisomic+Imbalance+of+21q+and+14q&rft.au=Banks%2C+Nicole%3BRaygada%2C+Margarita%3BChristacos%2C+Nicole%3BSchonberg%2C+Steven%3BCharalsawadi%2C+Chariyawan%3BJackson-Cook%2C+Colleen%3BRennert%2C+Owen&rft.aulast=Banks&rft.aufirst=Nicole&rft.date=2013-03-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ww2.aievolution.com/acm1301/index.cfm?do=abs.pubSearchAbstracts&style=0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-31
N1  - Last updated - 2013-08-14
ER  - 



TY  - CPAPER
T1  - Ocular and Systemic Findings in Patients with Uveal Coloboma
T2  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AN  - 1420114101; 6230750
JF  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AU  - Blain, Delphine
AU  - Huynh, Nancy
AU  - Hadsall, Casey
AU  - Rowan, John
AU  - Alur, Ramakrishna
AU  - Lang, David
AU  - Sran, Pushpa
AU  - Khan, Lynn
AU  - Zein, Wadih
AU  - Bardakjian, Tanya
AU  - Schneider, Adele
AU  - Traboulsi, Elias
AU  - Weleber, Richard
AU  - Doss, Lauren
AU  - Glaser, Tanya
AU  - Pinto, Natasha
AU  - Sarchet, Jennifer
AU  - Brooks, Brian
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
KW  - Genetics
KW  - Medicine
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420114101?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.atitle=Ocular+and+Systemic+Findings+in+Patients+with+Uveal+Coloboma&rft.au=Blain%2C+Delphine%3BHuynh%2C+Nancy%3BHadsall%2C+Casey%3BRowan%2C+John%3BAlur%2C+Ramakrishna%3BLang%2C+David%3BSran%2C+Pushpa%3BKhan%2C+Lynn%3BZein%2C+Wadih%3BBardakjian%2C+Tanya%3BSchneider%2C+Adele%3BTraboulsi%2C+Elias%3BWeleber%2C+Richard%3BDoss%2C+Lauren%3BGlaser%2C+Tanya%3BPinto%2C+Natasha%3BSarchet%2C+Jennifer%3BBrooks%2C+Brian&rft.aulast=Blain&rft.aufirst=Delphine&rft.date=2013-03-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ww2.aievolution.com/acm1301/index.cfm?do=abs.pubSearchAbstracts&style=0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-31
N1  - Last updated - 2013-08-14
ER  - 



TY  - CPAPER
T1  - Broad Variability in Skeletal Dysplasia in Children with GM1 Gangliosidosis: Implications for Management
T2  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AN  - 1420114067; 6230659
JF  - 2013 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2013)
AU  - Regier, Debra
AU  - Johnston, Jean
AU  - Golas, Gretchen
AU  - Tifft, Cynthia
AU  - Spranger, Jurgen
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
KW  - Gangliosidosis
KW  - Bone dysplasia
KW  - Children
KW  - Skeleton
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1420114067?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.atitle=Broad+Variability+in+Skeletal+Dysplasia+in+Children+with+GM1+Gangliosidosis%3A+Implications+for+Management&rft.au=Regier%2C+Debra%3BJohnston%2C+Jean%3BGolas%2C+Gretchen%3BTifft%2C+Cynthia%3BSpranger%2C+Jurgen&rft.aulast=Regier&rft.aufirst=Debra&rft.date=2013-03-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://ww2.aievolution.com/acm1301/index.cfm?do=abs.pubSearchAbstracts&style=0
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-31
N1  - Last updated - 2013-08-14
ER  - 



TY  - JOUR
T1  - Flavonoid intake and risk of pancreatic cancer in the National Institutes of Health-AARP Diet and Health Study Cohort.
AN  - 1318689198; 23299536
AB  - Limited epidemiological studies show inverse associations between dietary flavonoid intake and pancreatic cancer risk, but results are inconsistent and are based on few cases. We examined the association between intake of flavonoids and pancreatic cancer risk in the large, prospective National Institutes of Health-AARP Diet and Health Study Cohort.
          During follow-up through 2006 (median follow-up 10.6 years), 2379 pancreatic cancer cases were identified. We used Cox proportional hazards modelling to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). We found no association between total flavonoid intake (Q5 vs Q1 HR=1.09, 95% CI: 0.96-1.24) or any flavonoid subtypes and pancreatic cancer risk. Significant interactions were not observed by age, sex, smoking status, BMI or diabetes.
          Our results do not support the hypothesis that flavonoids have a protective role in pancreatic cancer carcinogenesis.
JF  - British journal of cancer
AU  - Arem, H
AU  - Bobe, G
AU  - Sampson, J
AU  - Subar, A F
AU  - Park, Y
AU  - Risch, H
AU  - Hollenbeck, A
AU  - Mayne, S T
AU  - Stolzenberg-Solomon, R Z
AD  - Yale School of Public Health, New Haven, CT, USA. Aremhe2@mail.nih.gov
Y1  - 2013/03/19/
PY  - 2013
DA  - 2013 Mar 19
SP  - 1168
EP  - 1172
VL  - 108
IS  - 5
KW  - Flavonoids
KW  - 0
KW  - Index Medicus
KW  - Risk Factors
KW  - Humans
KW  - Cohort Studies
KW  - Aged
KW  - Middle Aged
KW  - United States -- epidemiology
KW  - Male
KW  - Female
KW  - Pancreatic Neoplasms -- epidemiology
KW  - Diet
KW  - Flavonoids -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318689198?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Flavonoid+intake+and+risk+of+pancreatic+cancer+in+the+National+Institutes+of+Health-AARP+Diet+and+Health+Study+Cohort.&rft.au=Arem%2C+H%3BBobe%2C+G%3BSampson%2C+J%3BSubar%2C+A+F%3BPark%2C+Y%3BRisch%2C+H%3BHollenbeck%2C+A%3BMayne%2C+S+T%3BStolzenberg-Solomon%2C+R+Z&rft.aulast=Arem&rft.aufirst=H&rft.date=2013-03-19&rft.volume=108&rft.issue=5&rft.spage=1168&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2012.584
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-05-21
N1  - Date created - 2013-03-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biomed Pharmacother. 2002 Aug;56(6):276-82 [12224598]
Cancer Causes Control. 2002 May;13(4):373-82 [12074507]
Carcinogenesis. 1992 Apr;13(4):605-8 [1315626]
Am J Clin Nutr. 1997 Apr;65(4 Suppl):1220S-1228S; discussion 1229S-1231S [9094926]
Am J Clin Nutr. 2005 Jan;81(1 Suppl):268S-276S [15640490]
Mol Cancer. 2006;5:76 [17196098]
J Nutr. 2007 May;137(5):1244-52 [17449588]
Am J Epidemiol. 2007 Oct 15;166(8):924-31 [17690219]
Public Health Nutr. 2008 Feb;11(2):183-95 [17610761]
Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):553-62 [18349272]
Mol Nutr Food Res. 2008 May;52(5):507-26 [18435439]
Arch Biochem Biophys. 2008 Aug 15;476(2):107-12 [18284912]
Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275]
J Am Coll Nutr. 2001 Oct;20(5 Suppl):464S-472S; discussion 473S-475S [11603657]
Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517]
Int J Cancer. 2002 Apr 10;98(5):761-9 [11920648]
J Biol Chem. 2004 Aug 13;279(33):34643-54 [15155719]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/bjc.2012.584
ER  - 



TY  - CPAPER
T1  - Biomarkers of Hepatocellular Cancer Risk and Diagnosis
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369227319; 6212690
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Santella, R
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Bioindicators
KW  - Biomarkers
KW  - biomarkers
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369227319?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Biomarkers+of+Hepatocellular+Cancer+Risk+and+Diagnosis&rft.au=Santella%2C+R&rft.aulast=Santella&rft.aufirst=R&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Metabolomics Identifies an Oxidative Stress- Mediated Signal Transduction Cascade Involved in Dioxin-Induced Hepatotoxicity
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226982; 6212659
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Gonzalez, F
AU  - Matsubara, T
AU  - Tanaka, N
AU  - Krausz, K
AU  - Patterson, A
AU  - Shah, Y
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Hepatotoxicity
KW  - metabolomics
KW  - hepatotoxicity
KW  - Transduction
KW  - Signal transduction
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226982?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Metabolomics+Identifies+an+Oxidative+Stress-+Mediated+Signal+Transduction+Cascade+Involved+in+Dioxin-Induced+Hepatotoxicity&rft.au=Gonzalez%2C+F%3BMatsubara%2C+T%3BTanaka%2C+N%3BKrausz%2C+K%3BPatterson%2C+A%3BShah%2C+Y&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Periconception Parental Metal Exposures, Couple Fecundity, and Child Health: Delineating the Chicken and Egg Question
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226961; 6212462
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Louis, G
AU  - Sundaram, R
AU  - Maisog, J
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Metals
KW  - Chickens
KW  - Fecundity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226961?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Periconception+Parental+Metal+Exposures%2C+Couple+Fecundity%2C+and+Child+Health%3A+Delineating+the+Chicken+and+Egg+Question&rft.au=Louis%2C+G%3BSundaram%2C+R%3BMaisog%2C+J&rft.aulast=Louis&rft.aufirst=G&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Application of Cancer Toxicoepigenomics in Identifying High-Risk Populations
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226955; 6212592
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Verma, M
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Risk groups
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226955?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Application+of+Cancer+Toxicoepigenomics+in+Identifying+High-Risk+Populations&rft.au=Verma%2C+M&rft.aulast=Verma&rft.aufirst=M&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - The Use of Population-Based Inbred Panels and Diversity Outbred Mouse Models to Explore Individual Variability and Toxicity to Benzene
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226926; 6212735
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - French, J
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Species diversity
KW  - Animal models
KW  - Inbreeding
KW  - Toxicity
KW  - Benzene
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226926?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=The+Use+of+Population-Based+Inbred+Panels+and+Diversity+Outbred+Mouse+Models+to+Explore+Individual+Variability+and+Toxicity+to+Benzene&rft.au=French%2C+J&rft.aulast=French&rft.aufirst=J&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Integrated Genetic and Genomic Approaches to Understand Susceptibility to Toxicant-Induced Lung Disease
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226907; 6212375
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Kleeberger., S
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Lung diseases
KW  - genomics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226907?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Integrated+Genetic+and+Genomic+Approaches+to+Understand+Susceptibility+to+Toxicant-Induced+Lung+Disease&rft.au=Kleeberger.%2C+S&rft.aulast=Kleeberger.&rft.aufirst=S&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Modeling Human Genetic Variability and Susceptibility in the Laboratory
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226881; 6212733
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Woychik, R
AU  - Threadgill, D
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Genetic isolation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226881?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Modeling+Human+Genetic+Variability+and+Susceptibility+in+the+Laboratory&rft.au=Woychik%2C+R%3BThreadgill%2C+D&rft.aulast=Woychik&rft.aufirst=R&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Antioxidants and Oxidative Modification of Biomolecules: Can They Identify a Biomarker of Ozone Oxidative Stress?
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226846; 6212479
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Kadiiska, M
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Bioindicators
KW  - Antioxidants
KW  - Oxidative stress
KW  - Biomarkers
KW  - biomarkers
KW  - Ozone
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226846?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Antioxidants+and+Oxidative+Modification+of+Biomolecules%3A+Can+They+Identify+a+Biomarker+of+Ozone+Oxidative+Stress%3F&rft.au=Kadiiska%2C+M&rft.aulast=Kadiiska&rft.aufirst=M&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Microglia Heterogeneity in Neuroinflammation and Neurotoxicity
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226348; 6212511
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Harry, G
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Neurotoxicity
KW  - Microglia
KW  - Inflammation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226348?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Microglia+Heterogeneity+in+Neuroinflammation+and+Neurotoxicity&rft.au=Harry%2C+G&rft.aulast=Harry&rft.aufirst=G&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - The Dynamics of Neuroinflammation and Inflammatory Cell Responses in Neurologic Disease
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226341; 6212510
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Harry, G
AU  - Curran, C
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Neurological diseases
KW  - Inflammation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226341?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=The+Dynamics+of+Neuroinflammation+and+Inflammatory+Cell+Responses+in+Neurologic+Disease&rft.au=Harry%2C+G%3BCurran%2C+C&rft.aulast=Harry&rft.aufirst=G&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Mechanistic Insights into the Toxicity of Multiwalled Carbon Nanotubes and Cerium Dioxide Nanoparticles in Primary Human Bronchial Epithelial Cells
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226251; 6212495
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Hussain, S
AU  - Snyder, R
AU  - Anderson, S
AU  - Marshburn, J
AU  - Rice, A
AU  - Walker, N
AU  - Garantziotis, S
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Epithelial cells
KW  - Carbon
KW  - Cerium
KW  - nanotubes
KW  - Toxicity
KW  - nanoparticles
KW  - Nanotechnology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226251?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Mechanistic+Insights+into+the+Toxicity+of+Multiwalled+Carbon+Nanotubes+and+Cerium+Dioxide+Nanoparticles+in+Primary+Human+Bronchial+Epithelial+Cells&rft.au=Hussain%2C+S%3BSnyder%2C+R%3BAnderson%2C+S%3BMarshburn%2C+J%3BRice%2C+A%3BWalker%2C+N%3BGarantziotis%2C+S&rft.aulast=Hussain&rft.aufirst=S&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Liver Effects in CD1 Mice Prenatally-Exposed to Low Doses of Perfluorooctanoic Acid (PFOA): Novel Modes of Action
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226233; 6212484
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Fenton, S
AU  - Filgo, A
AU  - Cummings, C
AU  - Hoenerhoff, M
AU  - Malarkey, D
AU  - Quist, E
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Liver
KW  - perfluorooctanoic acid
KW  - Mice
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226233?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Liver+Effects+in+CD1+Mice+Prenatally-Exposed+to+Low+Doses+of+Perfluorooctanoic+Acid+%28PFOA%29%3A+Novel+Modes+of+Action&rft.au=Fenton%2C+S%3BFilgo%2C+A%3BCummings%2C+C%3BHoenerhoff%2C+M%3BMalarkey%2C+D%3BQuist%2C+E&rft.aulast=Fenton&rft.aufirst=S&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Overview of Concepts and Strategies Needed for Assessing the Safety of Nanoscale Materials
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226215; 6212728
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Walker, N
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226215?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Overview+of+Concepts+and+Strategies+Needed+for+Assessing+the+Safety+of+Nanoscale+Materials&rft.au=Walker%2C+N&rft.aulast=Walker&rft.aufirst=N&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Biomarkers of Testicular Injury: Where Have We Been.
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226181; 6212384
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - McIntyre, B
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Testes
KW  - Bioindicators
KW  - Injuries
KW  - Biomarkers
KW  - biomarkers
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226181?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Biomarkers+of+Testicular+Injury%3A+Where+Have+We+Been.&rft.au=McIntyre%2C+B&rft.aulast=McIntyre&rft.aufirst=B&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Exposure Science in the 21st Century: Perspectives from the NAS and What It Means for Toxicology
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369226067; 6212712
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Birnbaum, L
AU  - Orme-Zavaleta, J
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Toxicology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226067?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Exposure+Science+in+the+21st+Century%3A+Perspectives+from+the+NAS+and+What+It+Means+for+Toxicology&rft.au=Birnbaum%2C+L%3BOrme-Zavaleta%2C+J&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Low Dose and Nonmonotonic Dose-Response Curves for Endocrine Disruptors
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369225901; 6212547
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Birnbaum, L
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - endocrine disruptors
KW  - Endocrinology
KW  - Endocrine disruptors
KW  - Dose-response effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369225901?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Low+Dose+and+Nonmonotonic+Dose-Response+Curves+for+Endocrine+Disruptors&rft.au=Birnbaum%2C+L&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Perinatal Toxicity and Carcinogenicity Studies of Styrene Acrylonitrile Trimer, a Ground Water Contaminant
T2  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AN  - 1369225779; 6212411
JF  - 52nd Annual Meeting of the Society of Toxicology (SOT 2013)
AU  - Behl, M
AU  - Elmore, S
AU  - Hejtmancik, M
AU  - Gerken, D
AU  - Chhabra, R
Y1  - 2013/03/10/
PY  - 2013
DA  - 2013 Mar 10
KW  - Styrene
KW  - Carcinogenicity
KW  - Groundwater pollution
KW  - Toxicity
KW  - Contaminants
KW  - Acrylonitrile
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369225779?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.atitle=Perinatal+Toxicity+and+Carcinogenicity+Studies+of+Styrene+Acrylonitrile+Trimer%2C+a+Ground+Water+Contaminant&rft.au=Behl%2C+M%3BElmore%2C+S%3BHejtmancik%2C+M%3BGerken%2C+D%3BChhabra%2C+R&rft.aulast=Behl&rft.aufirst=M&rft.date=2013-03-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.toxicology.org/AI/PUB/Prog/2013Program.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - A Developing Drug Development: Meet the Expert
T2  - 114th Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2013)
AN  - 1369227081; 6212820
JF  - 114th Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2013)
AU  - Collins, Jerry
Y1  - 2013/03/06/
PY  - 2013
DA  - 2013 Mar 06
KW  - Drug development
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369227081?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Annual+Meeting+of+the+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2013%29&rft.atitle=A+Developing+Drug+Development%3A+Meet+the+Expert&rft.au=Collins%2C+Jerry&rft.aulast=Collins&rft.aufirst=Jerry&rft.date=2013-03-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+Annual+Meeting+of+the+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.ascpt.org/Portals/8/docs/Meetings/2013%20Annual%20Meeting/ASCPT-Online-030113_website.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Physiological Model of Body Weight Regulation and Application for Development of Weight Loss Therapies
T2  - 114th Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2013)
AN  - 1369226659; 6212800
JF  - 114th Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2013)
AU  - Hall, Kevin
Y1  - 2013/03/06/
PY  - 2013
DA  - 2013 Mar 06
KW  - Body weight
KW  - Physiology
KW  - Therapy
KW  - Models
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226659?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Annual+Meeting+of+the+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2013%29&rft.atitle=Physiological+Model+of+Body+Weight+Regulation+and+Application+for+Development+of+Weight+Loss+Therapies&rft.au=Hall%2C+Kevin&rft.aulast=Hall&rft.aufirst=Kevin&rft.date=2013-03-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+Annual+Meeting+of+the+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://www.ascpt.org/Portals/8/docs/Meetings/2013%20Annual%20Meeting/ASCPT-Online-030113_website.pdf
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - JOUR
T1  - Prediagnosis Body Mass Index, Physical Activity, and Mortality in Endometrial Cancer Patients
AN  - 1323814673; 17785581
AB  - Background Higher body mass index (BMI) and inactivity have been associated with a higher risk of developing endometrial cancer, but the impact on endometrial cancer survival is unclear. Methods Among incident endometrial cancer case subjects in the National Institutes of Health-AARP Diet and Health Study, we examined associations of prediagnosis BMI (n = 1400) and physical activity (n = 875) with overall and disease-specific 5- and 10-year mortality. Using Cox proportional hazards regression, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for tumor characteristics, treatment, and other risk factors. All statistical tests were two-sided. Results Compared with women with a BMI in the range of 18.5 to less than 25kg/m super(2), the hazard ratios for 5-year all-cause mortality were 1.74 (95% CI = 1.13 to 2.66) for BMI in the range of 25 to less than 30kg/m super(2), 1.84 (95% CI = 1.17 to 2.88) for BMI in the range of 30 to less than 35kg/m super(2), and 2.35 (95% CI = 1.48 to 3.73) for BMI greater than or equal to 35kg/m super(2) (P sub(trend) 7 hours/week vs never/rarely), but the association was attenuated after adjustment for BMI (HR = 0.64, 95% CI = 0.37 to 1.12). No association was observed between physical activity and disease-specific mortality. Conclusions Our findings suggest that higher prediagnosis BMI increases risk of overall and disease-specific mortality among women diagnosed with endometrial cancer, whereas physical activity lowers risk. Intervention studies of the effect of these modifiable lifestyle factors on mortality are needed.
JF  - Journal of the National Cancer Institute
AU  - Arem, Hannah
AU  - Park, Yikyung
AU  - Pelser, Colleen
AU  - Ballard-Barbash, Rachel
AU  - Irwin, Melinda L
AU  - Hollenbeck, Albert
AU  - Gierach, Gretchen L
AU  - Brinton, Louise A
AU  - Pfeiffer, Ruth M
AU  - Matthews, Charles E
AD  - Affiliations of authors.Yale School of Public Health (HA, MLI) and Yale Cancer Center (MLI), New Haven, CT; Division of Cancer Epidemiology and Genetics (HA, YP, CP, GLG, LAB, RMP, CEM) and Division of Cancer Control and Population Sciences (RBB), National Cancer Institute, Bethesda, MD; AARP, Washington, DC (AH)., aremhe2@mail.nih.gov
Y1  - 2013/03/06/
PY  - 2013
DA  - 2013 Mar 06
SP  - 342
EP  - 349
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 5
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Body mass
KW  - Cancer
KW  - Cardiovascular diseases
KW  - Diets
KW  - Intervention
KW  - Mortality
KW  - Physical activity
KW  - Risk factors
KW  - Survival
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323814673?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Prediagnosis+Body+Mass+Index%2C+Physical+Activity%2C+and+Mortality+in+Endometrial+Cancer+Patients&rft.au=Arem%2C+Hannah%3BPark%2C+Yikyung%3BPelser%2C+Colleen%3BBallard-Barbash%2C+Rachel%3BIrwin%2C+Melinda+L%3BHollenbeck%2C+Albert%3BGierach%2C+Gretchen+L%3BBrinton%2C+Louise+A%3BPfeiffer%2C+Ruth+M%3BMatthews%2C+Charles+E&rft.aulast=Arem&rft.aufirst=Hannah&rft.date=2013-03-06&rft.volume=105&rft.issue=5&rft.spage=342&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs530
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2013-05-06
N1  - SubjectsTermNotLitGenreText - Diets; Mortality; Risk factors; Body mass; Physical activity; Intervention; Survival; Cardiovascular diseases; Cancer
DO  - http://dx.doi.org/10.1093/jnci/djs530
ER  - 



TY  - JOUR
T1  - Temporal Variability of Pesticide Concentrations in Homes and Implications for Attenuation Bias in Epidemiologic Studies
AN  - 1399920386; 18211235
AB  - Background: Residential pesticide exposure has been linked to adverse health outcomes in adults and children. High-quality exposure estimates are critical for confirming these associations. Past epidemiologic studies have used one measurement of pesticide concentrations in carpet dust to characterize an individual's average long-term exposure. If concentrations vary over time, this approach could substantially misclassify exposure and attenuate risk estimates. Objectives: We assessed the repeatability of pesticide concentrations in carpet dust samples and the potential attenuation bias in epidemiologic studies relying on one sample. Methods: We collected repeated carpet dust samples (median = 3; range, 1-7) from 21 homes in Fresno County, California, during 2003-2005. Dust was analyzed for 13 pesticides using gas chromatography-mass spectrometry. We used mixed-effects models to estimate between- and within-home variance. For each pesticide, we computed intraclass correlation coefficients (ICCs) and the estimated attenuation of regression coefficients in a hypothetical case-control study collecting a single dust sample. Results: The median ICC was 0.73 (range, 0.37-0.95), demonstrating higher between-home than within-home variability for most pesticides. The expected magnitude of attenuation bias associated with using a single dust sample was estimated to be less than or equal to 30% for 7 of the 13 compounds evaluated. Conclusions: For several pesticides studied, use of one dust sample to represent an exposure period of approximately 2 years would not be expected to substantially attenuate odds ratios. Further study is needed to determine if our findings hold for longer exposure periods and for other pesticides.
JF  - Environmental Health Perspectives
AU  - Deziel, Nicole C
AU  - Ward, Mary H
AU  - Bell, Erin M
AU  - Whitehead, Todd P
AU  - Gunier, Robert B
AU  - Friesen, Melissa C
AU  - Nuckols, John R
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  - 2013/03/05/
PY  - 2013
DA  - 2013 Mar 05
SP  - 565
EP  - 571
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 5
SN  - 0091-6765, 0091-6765
KW  - Risk Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - dust
KW  - environmental exposure
KW  - pesticides
KW  - reliability
KW  - USA, California, Fresno Cty.
KW  - Pesticides
KW  - USA, California
KW  - Children
KW  - Dust
KW  - Spectrometry
KW  - H 5000:Pesticides
KW  - R2 23060:Medical and environmental health
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399920386?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Temporal+Variability+of+Pesticide+Concentrations+in+Homes+and+Implications+for+Attenuation+Bias+in+Epidemiologic+Studies&rft.au=Deziel%2C+Nicole+C%3BWard%2C+Mary+H%3BBell%2C+Erin+M%3BWhitehead%2C+Todd+P%3BGunier%2C+Robert+B%3BFriesen%2C+Melissa+C%3BNuckols%2C+John+R&rft.aulast=Deziel&rft.aufirst=Nicole&rft.date=2013-03-05&rft.volume=121&rft.issue=5&rft.spage=565&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205811
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Pesticides; Children; Dust; Spectrometry; USA, California, Fresno Cty.; USA, California
DO  - http://dx.doi.org/10.1289/ehp.1205811
ER  - 



TY  - JOUR
T1  - Targeting pathological B cell receptor signalling in lymphoid malignancies
AN  - 1842509591; 17761433
AB  - Signalling through the B cell receptor (BCR) is central to the development and maintenance of B cells. In light of the numerous proliferative and survival pathways activated downstream of the BCR, it comes as no surprise that malignant B cells would co-opt this receptor to promote their own growth and survival. However, direct evidence for BCR signalling in human lymphoma has only come to light recently. Roles for antigen-dependent and antigen-independent, or tonic, BCR signalling have now been described for several different lymphoma subtypes. Furthermore, correlative data implicate antigen-dependent BCR signalling in many other forms of lymphoma. A host of therapeutic agents targeting effectors of the BCR signalling pathway are now in clinical trials and have shown initial success against multiple forms of lymphoma.
JF  - Nature Reviews: Drug Discovery
AU  - Young, Ryan M
AU  - Staudt, Louis M
AD  - Metabolism Branch, Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 229
EP  - 243
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 12
IS  - 3
SN  - 1474-1776, 1474-1776
KW  - Toxicology Abstracts
KW  - B-cell receptor
KW  - Cell survival
KW  - Malignancy
KW  - Data processing
KW  - Lymphocytes B
KW  - Lymphoma
KW  - Clinical trials
KW  - Signal transduction
KW  - X 24500:Reviews, Legislation, Book & Conference Notices
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842509591?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+Reviews%3A+Drug+Discovery&rft.atitle=Targeting+pathological+B+cell+receptor+signalling+in+lymphoid+malignancies&rft.au=Young%2C+Ryan+M%3BStaudt%2C+Louis+M&rft.aulast=Young&rft.aufirst=Ryan&rft.date=2013-03-01&rft.volume=12&rft.issue=3&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Nature+Reviews%3A+Drug+Discovery&rft.issn=14741776&rft_id=info:doi/10.1038%2Fnrd3937
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Cell survival; B-cell receptor; Malignancy; Data processing; Lymphocytes B; Clinical trials; Lymphoma; Signal transduction
DO  - http://dx.doi.org/10.1038/nrd3937
ER  - 



TY  - JOUR
T1  - microRNA Regulation and Its Consequences in Cancer.
AN  - 1826565513; 23420713
AB  - MicroRNA (miRNA) function has been studied extensively in the last two decades. These short, non-coding RNAs influence a variety of cellular processes through repression of target genes. With the number of genes that a single miRNA can target, the biological effects of one miRNA alone can be vast. In cancer, aberrant miRNA expression is ubiquitous and consequently it can provoke progression of the disease. Though much is known about the downstream effects of miRNA, the mechanisms that control the level of miRNA expression itself are not well documented. In this review, we will focus on how miRNAs are regulated as well as potential therapeutic targets that can be exploited for cancer therapy.
JF  - Current pathobiology reports
AU  - Parpart, Sonya
AU  - Wang, Xin Wei
AD  - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892 ; Department of Oncology, Lombardi Cancer Center, Georgetown University, Washington, DC 20057.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 71
EP  - 79
VL  - 1
IS  - 1
KW  - Single nucleotide polymorphisms
KW  - RNA structure
KW  - Transcriptional
KW  - Post-transcriptional
KW  - miRNA
KW  - SNPs
KW  - microRNA
KW  - Regulation
KW  - Pathobiology
KW  - Epigenetic
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826565513?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pathobiology+reports&rft.atitle=microRNA+Regulation+and+Its+Consequences+in+Cancer.&rft.au=Parpart%2C+Sonya%3BWang%2C+Xin+Wei&rft.aulast=Parpart&rft.aufirst=Sonya&rft.date=2013-03-01&rft.volume=1&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Current+pathobiology+reports&rft.issn=&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date created - 2013-02-19
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
ER  - 



TY  - JOUR
T1  - Trajectories of kinematic risky driving among novice teenagers
AN  - 1746882864; PQ0002257353
AB  - Objectives Elevated gravitational force event rates are associated with the likelihood of a crash or near crash and provide an objective measure of risky driving. The purpose of this research is to examine the patterns over time of kinematic measures of risky driving among novice teenage drivers. Methods Driving data were collected from 42 newly licensed teenage drivers during the first 18 months of licensure. Data recording systems installed in participants' vehicles provided information on driving performance and driver characteristics. Latent class and logistic regression models were used to analyze trajectories of elevated gravitational-force (g-force) event rates, called kinematic risky driving, with respect to risk groups and associated factors. Results Kinematic risky driving over the 18-month study period was best characterized as two classes, a higher-risk and a lower-risk class. The rate of kinematic risky driving during the first 6 months generally maintained over 18 months. Indeed, of those classified by latent class analysis as higher risk, 88.9%, 94.4% and 94.4% had average event rates above the median in the 1st, 2nd, and 3rd 6-month periods, respectively, indicating substantial tracking over time. Friends' risky driving, friends' risky behavior, self-reported risky driving, and perceptions about risky driving and driving privileges were associated with trip-level rates of kinematic risky driving. However, none of these factors was associated with trip-level rates after stratifying by overall risk in a latent class model, although friend's risky driving was marginally significant. Conclusion Kinematic risky driving tended to track over time within the lower and higher risky driving groups. Self-reported risky driving and having risky friends were predictors of kinematic risky driving rates, but these variables did not explain the heterogeneity within higher and lower classes of risky drivers.
JF  - Accident Analysis & Prevention
AU  - Simons-Morton, Bruce G
AU  - Cheon, Kyeongmi
AU  - Guo, Feng
AU  - Albert, Paul
AD  - Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Bethesda, MD 20892-7510, United States
PY  - 2013
SP  - 27
EP  - 32
PB  - Elsevier B.V., P.O. Box 800 Kidlington Oxford OX5 1DX United Kingdom
VL  - 51
SN  - 0001-4575, 0001-4575
KW  - Risk Abstracts
KW  - Adolescence
KW  - Risk taking
KW  - Motor vehicle crashes
KW  - Naturalistic driving
KW  - Prevention
KW  - Accidents
KW  - Driving ability
KW  - Behavior
KW  - Perception
KW  - Risk factors
KW  - Adolescents
KW  - Recording
KW  - R2 23010:General: Models, forecasting
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746882864?accountid=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=Accident+Analysis+%26+Prevention&rft.atitle=Trajectories+of+kinematic+risky+driving+among+novice+teenagers&rft.au=Simons-Morton%2C+Bruce+G%3BCheon%2C+Kyeongmi%3BGuo%2C+Feng%3BAlbert%2C+Paul&rft.aulast=Simons-Morton&rft.aufirst=Bruce&rft.date=2013-03-01&rft.volume=51&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Accident+Analysis+%26+Prevention&rft.issn=00014575&rft_id=info:doi/10.1016%2Fj.aap.2012.10.011
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-12-01
N1  - Last updated - 2015-12-23
N1  - SubjectsTermNotLitGenreText - Accidents; Prevention; Driving ability; Behavior; Perception; Risk factors; Risk taking; Adolescents; Recording
DO  - http://dx.doi.org/10.1016/j.aap.2012.10.011
ER  - 



TY  - JOUR
T1  - Lactobacillus priming of the respiratory tract: Heterologous immunity and protection against lethal pneumovirus infection
AN  - 1676347375; PQ0001393032
AB  - We showed previously that wild-type mice primed via intranasal inoculation with live or heat-inactivated Lactobacillus species were fully (100%) protected against the lethal sequelae of infection with the virulent pathogen, pneumonia virus of mice (PVM), a response that is associated with diminished expression of proinflammatory cytokines and diminished virus recovery. We show here that 40% of the mice primed with live Lactobacillus survived when PVM challenge was delayed for 5months. This robust and sustained resistance to PVM infection resulting from prior interaction with an otherwise unrelated microbe is a profound example of heterologous immunity. We undertook the present study in order to understand the nature and unique features of this response. We found that intranasal inoculation with L. reuteri elicited rapid, transient neutrophil recruitment in association with proinflammatory mediators (CXCL1, CCL3, CCL2, CXCL10, TNF-alpha and IL-17A) but not Th1 cytokines. IFN gamma does not contribute to survival promoted by Lactobacillus-priming. Live L. reuteri detected in lung tissue underwent rapid clearance, and was undetectable at 24h after inoculation. In contrast, L. reuteri peptidoglycan (PGN) and L. reuteri genomic DNA (gDNA) were detected at 24 and 48h after inoculation, respectively. In contrast to live bacteria, intranasal inoculation with isolated L. reuteri gDNA elicited no neutrophil recruitment, had minimal impact on virus recovery and virus-associated production of CCL3, and provided no protection against the negative sequelae of virus infection. Isolated PGN elicited neutrophil recruitment and proinflammatory cytokines but did not promote sustained survival in response to subsequent PVM infection. Overall, further evaluation of the responses leading to Lactobacillus-mediated heterologous immunity may provide insight into novel antiviral preventive modalities.
JF  - Antiviral Research
AU  - Garcia-Crespo, Katia E
AU  - Chan, Calvin C
AU  - Gabryszewski, Stanislaw J
AU  - Percopo, Caroline M
AU  - Rigaux, Peter
AU  - Dyer, Kimberly D
AU  - Domachowske, Joseph B
AU  - Rosenberg, Helene F
AD  - Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 270
EP  - 279
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 97
IS  - 3
SN  - 0166-3542, 0166-3542
KW  - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Cytokines
KW  - Neutrophils
KW  - Peptidoglycan
KW  - Genomic DNA
KW  - Heterologous immunity
KW  - Cell survival
KW  - Helper cells
KW  - peptidoglycans
KW  - Infection
KW  - Lactobacillus
KW  - Lymphocytes T
KW  - Pneumonia virus of mice
KW  - genomics
KW  - Respiratory tract
KW  - Pneumovirus
KW  - Monocyte chemoattractant protein 1
KW  - Complications
KW  - CCL3 protein
KW  - Leukocytes (neutrophilic)
KW  - Immunity
KW  - Pathogens
KW  - Inflammation
KW  - CXCL10 protein
KW  - Lung
KW  - Inoculation
KW  - DNA
KW  - Tumor necrosis factor- alpha
KW  - Pneumonia
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22410:Animal Diseases
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676347375?accountid=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=Antiviral+Research&rft.atitle=Lactobacillus+priming+of+the+respiratory+tract%3A+Heterologous+immunity+and+protection+against+lethal+pneumovirus+infection&rft.au=Garcia-Crespo%2C+Katia+E%3BChan%2C+Calvin+C%3BGabryszewski%2C+Stanislaw+J%3BPercopo%2C+Caroline+M%3BRigaux%2C+Peter%3BDyer%2C+Kimberly+D%3BDomachowske%2C+Joseph+B%3BRosenberg%2C+Helene+F&rft.aulast=Garcia-Crespo&rft.aufirst=Katia&rft.date=2013-03-01&rft.volume=97&rft.issue=3&rft.spage=270&rft.isbn=&rft.btitle=&rft.title=Antiviral+Research&rft.issn=01663542&rft_id=info:doi/10.1016%2Fj.antiviral.2012.12.022
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-04-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Cell survival; Monocyte chemoattractant protein 1; Complications; Helper cells; CCL3 protein; Leukocytes (neutrophilic); peptidoglycans; Pathogens; Immunity; Infection; Inflammation; CXCL10 protein; Lung; DNA; Inoculation; Lymphocytes T; Cytokines; genomics; Tumor necrosis factor- alpha; Pneumonia; Respiratory tract; Pneumovirus; Lactobacillus; Pneumonia virus of mice
DO  - http://dx.doi.org/10.1016/j.antiviral.2012.12.022
ER  - 



TY  - JOUR
T1  - Oral Vaccination With Adeno-associated Virus Vectors Expressing the Neu Oncogene Inhibits the Growth of Murine Breast Cancer
AN  - 1668268756; PQ0001244918
AB  - Recombinant adeno-associated viruses (AAV) have been used for therapeutic gene transfer. These vectors offer a number of advantages including resistance to the effects of pH, a broad cellular tropism, efficient gene transfer, persistence of gene expression, and little toxicity. AAV vectors; however, at high doses can induce humoral and cellular immune responses. While potentially problematic for replacement gene therapy, this effect may be advantageous for antitumor vaccination. We examined the activity of an oral and intramuscular antitumor vaccination using AAV serotypes 5 and 6 expressing a truncated neu oncogene in a neu-positive murine TUBO breast cancer model. Mice receiving a single oral administration of AAV5-neu or AAV6-neu demonstrated improved survival. Oral vaccination significantly improved survivals compared with intramuscular vaccination. Mice vaccinated with AAV6-neu survived longer than those treated with AAV5-neu. Vaccination with AAV5-neu or AAV6-neu induced both humoral and cellular immune responses against the NEU antigen. These responses were more robust in the mice undergoing oral vaccination compared with mice receiving the intramuscular vaccination. Protection from tumor was long lasting with 80% of the animals treated with oral AAV6-neu surviving a re-challenge with TUBO cells at 120 and 320 days post-vaccination. Further evaluation of AAV-based vectors as tumor vaccines is warranted.
JF  - Molecular Therapy
AU  - Steel, Jason C
AU  - Di Pasquale, Giovanni
AU  - Ramlogan, Charmaine A
AU  - Patel, Vyomesh
AU  - Chiorini, John A
AU  - Morris, John C
AD  - Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA; Division of Hematology-Oncology, Department of Medicine, University of Cincinnati, Cincinnati, Ohio, USA, morri2j7@uc.edu
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 680
EP  - 687
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 3
SN  - 1525-0016, 1525-0016
KW  - Oncogenes & Growth Factors Abstracts; Virology & AIDS Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Cancer vaccines
KW  - Serotypes
KW  - ErbB-2 protein
KW  - Gene therapy
KW  - Tropism
KW  - Oral administration
KW  - Animal models
KW  - Tumors
KW  - Toxicity
KW  - Adeno-associated virus
KW  - Expression vectors
KW  - Oncogenes
KW  - Breast cancer
KW  - Immune response (humoral)
KW  - pH effects
KW  - W 30905:Medical Applications
KW  - B 26660:Miscellaneous Oncogenes & Growth Factors
KW  - V 22350:Immunology
KW  - F 06915:Cancer Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668268756?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oral+Vaccination+With+Adeno-associated+Virus+Vectors+Expressing+the+Neu+Oncogene+Inhibits+the+Growth+of+Murine+Breast+Cancer&rft.au=Steel%2C+Jason+C%3BDi+Pasquale%2C+Giovanni%3BRamlogan%2C+Charmaine+A%3BPatel%2C+Vyomesh%3BChiorini%2C+John+A%3BMorris%2C+John+C&rft.aulast=Steel&rft.aufirst=Jason&rft.date=2013-03-01&rft.volume=21&rft.issue=3&rft.spage=680&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.260
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Cancer vaccines; ErbB-2 protein; Serotypes; Gene therapy; Tropism; Animal models; Oral administration; Toxicity; Tumors; Expression vectors; Oncogenes; Breast cancer; Immune response (humoral); pH effects; Adeno-associated virus
DO  - http://dx.doi.org/10.1038/mt.2012.260
ER  - 



TY  - JOUR
T1  - Parental trust in health care—a prospective study from the Childrenʼs Cancer Hospital in Egypt
AN  - 1665157804
AB  - Objective Patient–physician communication and patient satisfaction are important elements of cancer care. Trust is considered to be crucial for the patient–physician relationship, yet little is to be found in the literature regarding what factors may influence trust. Methods We assessed predictors of trust in health-care professionals and in the medical care by administering two questionnaires, one at start of chemotherapy treatment and one at the time of the third chemotherapy cycle, to 304 parents of children with newly diagnosed cancer at the Childrenʼs Cancer Hospital in Cairo, Egypt. Results Parentsʼ trust in the medical care at the time of the childʼs third chemotherapy cycle was significantly associated with the following at the start of treatment: having received at least moderate information about the disease (relative risk (RR) 13.2; 95% CI 7.8–22.3) and the treatment (RR 17.2; 95% CI 9.5–31.4), having the opportunity to communicate with the childʼs physicians (RR 21.3; 95% CI 11.7–38.8), being satisfied with the physicians conversation style (RR 30.6; 95% CI 14.4–64.9), having the emotional needs met (RR 22.2; 95% CI 11.8–41.9), and being met with care by the childʼs physicians (RR 32.0; 95% CI 15.2–67.7). After multivariable model selection, the strongest predictor of trust at the time of the third chemotherapy cycle was to be met with care at the start of treatment. Conclusion Parents being met with care by the childʼs physicians at the beginning of the childʼs chemotherapy treatment develop an increased trust in the medical care. Copyright © 2012 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - El Malla, Hanan
AU  - Kreicbergs, Ulrika
AU  - Steineck, Gunnar
AU  - Wilderäng, Ulrica
AU  - El Sayed Elborai, Yasser
AU  - Ylitalo, Nathalie
AD  - Department of Oncology, Division of Clinical Cancer Epidemiology, Sahlgrenska University Hospital, Gothenburg, Sweden. ; Department of Women and Childʼs Health, Karolinska Institutet, Stockholm, Sweden., Sophiahemmet University College, Stockholm, Sweden. ; Department of Oncology, Division of Clinical Cancer Epidemiology, Sahlgrenska University Hospital, Gothenburg, Sweden., Department of Oncology and Pathology, Division of Clinical Cancer Epidemiology, Karolinska Institute, Stockholm, Sweden. ; Cairo University Hospital, Childrenʼs Cancer Hospital, Cairo, Egypt., National Cancer Institute, Cairo, Egypt. ; Department of Oncology, Division of Clinical Cancer Epidemiology, Sahlgrenska University Hospital, Gothenburg, Sweden., Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden. ; Department of Oncology, Division of Clinical Cancer Epidemiology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 548
EP  - 554
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 3
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Cancer
KW  - Chemotherapy
KW  - Children
KW  - Doctor-Patient communication
KW  - Doctors
KW  - Health care
KW  - Health professional-Patient communication
KW  - Health professionals
KW  - Newly diagnosed
KW  - Parents
KW  - Patient satisfaction
KW  - Sick children
KW  - Egypt
KW  - Cairo Egypt
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665157804?accountid=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=Parental+trust+in+health+care%E2%80%94a+prospective+study+from+the+Children%CA%BCs+Cancer+Hospital+in+Egypt&rft.au=El+Malla%2C+Hanan%3BKreicbergs%2C+Ulrika%3BSteineck%2C+Gunnar%3BWilder%C3%A4ng%2C+Ulrica%3BEl+Sayed+Elborai%2C+Yasser%3BYlitalo%2C+Nathalie&rft.aulast=El+Malla&rft.aufirst=Hanan&rft.date=2013-03-01&rft.volume=22&rft.issue=3&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3028
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2015-01-09
N1  - Last updated - 2016-08-17
N1  - SubjectsTermNotLitGenreText - Cairo Egypt; Egypt
DO  - http://dx.doi.org/10.1002/pon.3028
ER  - 



TY  - JOUR
T1  - A Blueprint for Genomic Nursing Science
AN  - 1665156684
AB  - Purpose: This article reports on recommendations arising from an invitational workshop series held at the National Institutes of Health for the purposes of identifying critical genomics problems important to the health of the public that can be addressed through nursing science. The overall purpose of the Genomic Nursing State of the Science Initiative is to establish a nursing research blueprint based on gaps in the evidence and expert evaluation of the current state of the science and through public comment. Organizing Constructs: A Genomic Nursing State of the Science Advisory Panel was convened in 2012 to develop the nursing research blueprint. The Advisory Panel, which met via two webinars and two in-person meetings, considered existing evidence from evidence reviews, testimony from key stakeholder groups, presentations from experts in research synthesis, and public comment. Findings: The genomic nursing science blueprint arising from the Genomic Nursing State of Science Advisory Panel focuses on biologic plausibility studies as well as interventions likely to improve a variety of outcomes (e.g., clinical, economic, environmental). It also includes all care settings and diverse populations. The focus is on (a) the client, defined as person, family, community, or population; (b) the context, targeting informatics support systems, capacity building, education, and environmental influences; and (c) cross-cutting themes. It was agreed that building capacity to measure the impact of nursing actions on costs, quality, and outcomes of patient care is a strategic and scientific priority if findings are to be synthesized and aggregated to inform practice and policy. Conclusions: The genomic nursing science blueprint provides the framework for furthering genomic nursing science to improve health outcomes. This blueprint is an independent recommendation of the Advisory Panel with input from the public and is not a policy statement of the National Institutes of Health or the federal government. Clinical Relevance: This genomic nursing science blueprint targets research to build the evidence base to inform integration of genomics into nursing practice and regulation (such as nursing licensure requirements, institutional accreditation, and academic nursing school accreditation).
JF  - Journal of Nursing Scholarship
AU  - Calzone, Kathleen A
AU  - Jenkins, Jean
AU  - Bakos, Alexis D
AU  - Cashion, Ann K
AU  - Donaldson, Nancy
AU  - Feero, W Gregory
AU  - Feetham, Suzanne
AU  - Grady, Patricia A
AU  - Hinshaw, Ada Sue
AU  - Knebel, Ann R
AU  - Robinson, Nellie
AU  - Ropka, Mary E
AU  - Seibert, Diane
AU  - Stevens, Kathleen R
AU  - Tully, Lois A
AU  - Webb, Jo Ann
AD  - Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD. ; Senior Clinical Advisor, National Institutes of Health, National Human Genome Research Institute, Bethesda, MD. ; Deputy Director, Division of Nursing, Bureau of Health Professions, Health Resources and Services Administration, Rockville, MD. ; Scientific Director for the NINR Intramural Research Program, National Institutes of Health, National Institute of Nursing Research, Bethesda, MD. ; Clinical Professor, Department of Physiological Nursing, UCSF School of Nursing, San Francisco, CA; Senior Scientist, Collaborative Alliance for Nursing Outcomes (CALNOC); Member, NQF Common Formats Expert Panel. ; Special Advisor to the Director for Genomic Medicine, Genomic Healthcare Branch, National Human Genome Research Institute, Bethesda, MD. ; Nursing Research Consultant, Childrenʼs National Medical Center, Bethesda, MD and Visiting Professor, University of Wisconsin-Milwaukee. ; Director, National Institutes of Health, National Institute of Nursing Research, Bethesda, MD. ; Dean and Professor, Graduate School of Nursing, Uniformed Services University of the Health Sciences, Bethesda, MD. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Deputy Director, National Institutes of Health, National Institute of Nursing Research, Bethesda MD. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Executive Vice President of Patient Care Services, Chief Nursing Officer, Childrenʼs National Medical Center, Washington, DC. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Beta Kappa , Professor of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, VA. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Associate Professor and Director of the Family Nurse Practitioner Program in the Graduate School of Nursing, Uniformed Services University of the Health Sciences, Bethesda, MD. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Professor and Director, Academic Center for Evidence-Based Practice, University of Texas Health Science Center San Antonio, San Antonio, TX. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Program Director, Division of Extramural Activities, National Institute of Nursing Research, Bethesda, MD. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD., Senior Director, Federal Relations and Policy, American Organization of Nurse Executives, Washington, DC. ; Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 96
EP  - 104
CY  - Indianapolis
PB  - Wiley Subscription Services, Inc.
VL  - 45
IS  - 1
SN  - 1527-6546
KW  - Medical Sciences--Nurses And Nursing
KW  - Capacity building approach
KW  - Nursing
KW  - Patient care
KW  - Professional practices
KW  - Clinical guidelines
KW  - Clinical nursing
KW  - Clinical outcomes
KW  - Environmental aspects
KW  - Experts
KW  - Health costs
KW  - Health status
KW  - Interventions
KW  - Licensing
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665156684?accountid=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+Nursing+Scholarship&rft.atitle=A+Blueprint+for+Genomic+Nursing+Science&rft.au=Calzone%2C+Kathleen+A%3BJenkins%2C+Jean%3BBakos%2C+Alexis+D%3BCashion%2C+Ann+K%3BDonaldson%2C+Nancy%3BFeero%2C+W+Gregory%3BFeetham%2C+Suzanne%3BGrady%2C+Patricia+A%3BHinshaw%2C+Ada+Sue%3BKnebel%2C+Ann+R%3BRobinson%2C+Nellie%3BRopka%2C+Mary+E%3BSeibert%2C+Diane%3BStevens%2C+Kathleen+R%3BTully%2C+Lois+A%3BWebb%2C+Jo+Ann&rft.aulast=Calzone&rft.aufirst=Kathleen&rft.date=2013-03-01&rft.volume=45&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nursing+Scholarship&rft.issn=15276546&rft_id=info:doi/10.1111%2Fjnu.12007
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Name - National Institutes of Health
N1  - Date revised - 2015-09-22
N1  - Last updated - 2016-05-13
DO  - http://dx.doi.org/10.1111/jnu.12007
ER  - 



TY  - JOUR
T1  - Long-term effect of the self-management comprehensive coping strategy program on quality of life in patients with breast cancer treated with high-dose chemotherapy
AN  - 1665153247
AB  - Background This study aims to examine the effectiveness of a self-management multimodal comprehensive coping strategy program (CCSP) on quality of life (QOL) among breast cancer patients 1year after treatment. Methods Patients ( n=110) with stage II, III, or IV breast cancer scheduled to receive high dose chemotherapy and autologous hematopoietic stem cell transplantation were randomized to either CCSP treatment or control group. The CCSP intervention was taught 2week before hospital admission with reinforcement at specified times during treatment and 3months after discharge. The CCSP components included educational information, cognitive restructuring, coping skills enhancement, and relaxation with guided imagery. Instruments administered at baseline included the following: Quality of Life Index—Cancer Version (QOLI-CV), State–Trait Anxiety Inventory, Beck Depression Inventory, and Coping Strategies Questionnaire. At 1-year follow-up, patients ( n=73) completed and returned the follow-up QOLI-CV. Results Patients were mainly ≥40years of age, married, Caucasian, and diagnosed with advanced breast cancer. A model measuring effectiveness of CCSP on QOL (total and subscale) at 1-year follow-up showed that the CCSP group ( n=38) had significant improvement in overall QOL ( p<0.01), health and functioning ( p<0.05), and socioeconomic ( p<0.05) and psychological/spiritual well-being ( p<0.01) compared with the control group ( n=35). The CCSP patients frequently used the CCSP to manage psychological (51%) and sleep problems (60%). Conclusions The CCSP improved QOL for patients at 1-year follow-up. Patients overwhelmingly reported that CCSP was beneficial. The CCSP as an effective coping intervention has potential as a self-management program for breast cancer survivors. Copyright © 2012 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Gaston-Johansson, Fannie
AU  - Fall-Dickson, Jane M
AU  - Nanda, Joy P
AU  - Sarenmalm, Elisabeth Kenne
AU  - Browall, Maria
AU  - Goldstein, Nancy
AD  - Johns Hopkins University, Department of Acute and Chronic Care, School of Nursing, Baltimore, MD, USA. ; National Institute of Health, Symptom Management Branch, National Institute of Nursing, Research, Bethesda, MD, USA. ; Johns Hopkins Medical Institutions, Baltimore, MD, USA. ; Skaraborg Hospital, Department of Research and Development Centre, Skövde, Sweden. ; Universtiy of Skövde, School of Life Sciences, Skövde, Sweden. ; Johns Hopkins University, Department of Acute and Chronic Care, School of Nursing, Baltimore, MD, USA.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 530
EP  - 539
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 3
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Anxiety
KW  - Hospitalization
KW  - Relaxation
KW  - Self
KW  - Selfmanagement
KW  - Sleep problems
KW  - Spiritual wellbeing
KW  - Survivors
KW  - Trait anxiety
KW  - Wellbeing
KW  - Anxiety-Depression
KW  - Breast cancer
KW  - Cancer
KW  - Chemotherapy
KW  - Cognitive restructuring
KW  - Coping
KW  - Coping skills
KW  - Coping strategies
KW  - Depression
KW  - Guided imagery
KW  - Imagery
KW  - Psychological wellbeing
KW  - Quality of life
KW  - Reinforcement
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665153247?accountid=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=Long-term+effect+of+the+self-management+comprehensive+coping+strategy+program+on+quality+of+life+in+patients+with+breast+cancer+treated+with+high-dose+chemotherapy&rft.au=Gaston-Johansson%2C+Fannie%3BFall-Dickson%2C+Jane+M%3BNanda%2C+Joy+P%3BSarenmalm%2C+Elisabeth+Kenne%3BBrowall%2C+Maria%3BGoldstein%2C+Nancy&rft.aulast=Gaston-Johansson&rft.aufirst=Fannie&rft.date=2013-03-01&rft.volume=22&rft.issue=3&rft.spage=530&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3031
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.3031
ER  - 



TY  - JOUR
T1  - Short Report: Leishmania major, the Predominant Leishmania Species Responsible for Cutaneous Leishmaniasis in Mali
AN  - 1647011369; 21210953
AB  - Leishmania major is the only species of Leishmania known to cause cutaneous leishmanisis (CL) in Mali. We amplified Leishmania DNA stored on archived Giemsa-stained dermal scraping slides obtained from self-referral patients with clinically suspected CL seen in the Center National d'Appui A La Lutte Contre La Maladie (CNAM) in Bamako, Mali, to determine if any other Leishmania species were responsible for CL in Mali and evaluate its geographic distribution. Polymerase chain reaction (PCR) amplification was performed using a Leishmania species-specific primer pair that can amplify DNA from L. major, L. tropica, L. infantum, and L. donovani parasites, possible causative agents of CL in Mali. L. major was the only species detected in 41 microscopically confirmed cases of CL from five regions of Mali (Kayes, Koulikoro, Segou, Mopti, and Tombouctou). These results implicate L. major as the predominant, possibly exclusive species responsible for CL in Mali.
JF  - American Journal of Tropical Medicine and Hygiene
AU  - Paz, Carlos
AU  - Samake, Sibiry
AU  - Anderson, Jennifer M
AU  - Faye, Ousmane
AU  - Traore, Pierre
AU  - Tall, Koureishi
AU  - Cisse, Moumine
AU  - Keita, Somita
AU  - Valenzuela, Jesus G
AU  - Doumbia, Seydou
AD  - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville, Maryland; International Center of Excellence in Research (ICER-Mali), Faculty of Medicine, University of Sciences, Techniques and Technologies of Bamako (USTTB), Bamako, Mali; Centre National D'Appui A La Lutte Contre La Maladie (CNAM), Bamako, Mali, sdoumbia@icermali.org
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 583
EP  - 585
PB  - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL  - 88
IS  - 3
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  - Geographical distribution
KW  - Mali
KW  - Skin
KW  - Nucleotide sequence
KW  - Population genetics
KW  - Dominant species
KW  - DNA
KW  - Polymerase chain reaction
KW  - Primers
KW  - Archives
KW  - Hygiene
KW  - Leishmania major
KW  - Cutaneous leishmaniasis
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08502:Methods and instruments
KW  - J 02400:Human Diseases
KW  - K 03310:Genetics & Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647011369?accountid=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=Short+Report%3A+Leishmania+major%2C+the+Predominant+Leishmania+Species+Responsible+for+Cutaneous+Leishmaniasis+in+Mali&rft.au=Paz%2C+Carlos%3BSamake%2C+Sibiry%3BAnderson%2C+Jennifer+M%3BFaye%2C+Ousmane%3BTraore%2C+Pierre%3BTall%2C+Koureishi%3BCisse%2C+Moumine%3BKeita%2C+Somita%3BValenzuela%2C+Jesus+G%3BDoumbia%2C+Seydou&rft.aulast=Paz&rft.aufirst=Carlos&rft.date=2013-03-01&rft.volume=88&rft.issue=3&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0434
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-01-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Parasites; Dominant species; Population genetics; Geographical distribution; Nucleotide sequence; DNA; Polymerase chain reaction; Archives; Hygiene; Skin; Primers; Cutaneous leishmaniasis; Leishmania major; Mali
DO  - http://dx.doi.org/10.4269/ajtmh.12-0434
ER  - 



TY  - JOUR
T1  - Age- and Sex-Specific Mortality Associated With the 1918-1919 Influenza Pandemic in Kentucky
AN  - 1622602409; 20881899
AB  - Background. The reasons for the unusual age-specific mortality patterns of the 1918-1919 influenza pandemic remain unknown. Here we characterize pandemic-related mortality by single year of age in a unique statewide Kentucky data set and explore breakpoints in the age curves. Methods. Individual death certificates from Kentucky during 1911-1919 were abstracted by medically trained personnel. Pandemic-associated excess mortality rates were calculated by subtracting observed rates during pandemic months from rates in previous years, separately for each single year of age and by sex. Results. The age profile of excess mortality risk in fall 1918 was characterized by a maximum among infants, a minimum at ages 9-10 years, a maximum at ages 24-26 years, and a second minimum at ages 56-59 years. The excess mortality risk in young adults had been greatly attenuated by winter 1919. The age breakpoints of mortality risk did not differ between males and females. Conclusions. The observed mortality breakpoints in male and female cohorts born during 1859-1862, 1892-1894, and 1908-1909 did not coincide with known dates of historical pandemics. The atypical age mortality patterns of the 1918-1919 pandemic cannot be explained by military crowding, war-related factors, or prior immunity alone and likely result from a combination of unknown factors.
JF  - Journal of Infectious Diseases
AU  - Viboud, Cecile
AU  - Eisenstein, Jana
AU  - Reid, Ann H
AU  - Janczewski, Thomas A
AU  - Morens, David M
AU  - Taubenberger, Jeffery K
AD  - Fogarty International Center, taubenbergerj@niaid.nih.gov
Y1  - 2013/03/01/
PY  - 2013
DA  - 2013 Mar 01
SP  - 721
EP  - 729
PB  - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 207
IS  - 5
SN  - 0022-1899, 0022-1899
KW  - Virology & AIDS Abstracts; Risk Abstracts; Health & Safety Science Abstracts
KW  - pandemic
KW  - influenza
KW  - mortality
KW  - age patterns
KW  - gender
KW  - immunity
KW  - military
KW  - Historical account
KW  - Age
KW  - Winter
KW  - Influenza
KW  - Breakpoints
KW  - pandemics
KW  - Infectious diseases
KW  - Personnel
KW  - Risk factors
KW  - Military
KW  - Sex
KW  - Mortality
KW  - Data processing
KW  - Crowding
KW  - Immunity
KW  - Mortality patterns
KW  - USA, Kentucky
KW  - Young adults
KW  - Infants
KW  - R2 23060:Medical and environmental health
KW  - H 1000:Occupational Safety and Health
KW  - V 22400:Human Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622602409?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Age-+and+Sex-Specific+Mortality+Associated+With+the+1918-1919+Influenza+Pandemic+in+Kentucky&rft.au=Viboud%2C+Cecile%3BEisenstein%2C+Jana%3BReid%2C+Ann+H%3BJanczewski%2C+Thomas+A%3BMorens%2C+David+M%3BTaubenberger%2C+Jeffery+K&rft.aulast=Viboud&rft.aufirst=Cecile&rft.date=2013-03-01&rft.volume=207&rft.issue=5&rft.spage=721&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjis745
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-11-01
N1  - Last updated - 2016-04-13
N1  - SubjectsTermNotLitGenreText - Influenza; Breakpoints; Mortality; pandemics; Age; Data processing; Crowding; Personnel; Immunity; Sex; Infants; Historical account; Infectious diseases; Risk factors; Young adults; Military; Mortality patterns; Winter; USA, Kentucky
DO  - http://dx.doi.org/10.1093/infdis/jis745
ER  - 



TY  - JOUR
T1  - Lessons Learned From Field-Testing a Brief Behavioral Intervention Package for African American Women at Risk for HIV/STDs
AN  - 1541982729; 201418817
AB  - This article describes how Sister to Sister, an evidence-based HIV/STD intervention for African American women in clinical settings, was prepared for national dissemination using the Centers for Disease Control and Prevention's Replicating Effective Programs research translation process. To test the feasibility of the intervention in the "real world," Sister to Sister's original research team collaborated with community partners to field-test the intervention in three clinical settings. Experiences from field-testing and input from a community advisory board were used to translate research protocols into a package of user-friendly materials that could be easily adopted by frontline clinic staff throughout the nation. Process monitoring and evaluation data demonstrated that Sister to Sister could be implemented successfully by a variety of practitioners including nurses, health educators, and HIV test counselors. "Buy-in" from clinic administrators and providers was a prerequisite to the success of the intervention. Replicating Effective Programs provided a useful process that can be applied by others to successfully prepare evidence-based interventions such as Sister to Sister for national dissemination. [Reprinted by permission of Sage Publications Inc., copyright holder.]
JF  - Health Promotion Practice
AU  - Jones, Patricia L
AU  - Baker, Jillian L
AU  - Gelaude, Deborah
AU  - King, Winifred
AU  - Jemmott, Loretta
AD  - National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 168
EP  - 173
PB  - Sage Publications, Thousand Oaks CA
VL  - 14
IS  - 2
SN  - 1524-8399, 1524-8399
KW  - HIV/STD evidence-based interventions field-testing implementation science knowledge translation African American women clinic-based prevention interventions
KW  - Sisters
KW  - Black American people
KW  - Women
KW  - Brief interventions
KW  - HIV
KW  - Dissemination
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541982729?accountid=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=Lessons+Learned+From+Field-Testing+a+Brief+Behavioral+Intervention+Package+for+African+American+Women+at+Risk+for+HIV%2FSTDs&rft.au=Jones%2C+Patricia+L%3BBaker%2C+Jillian+L%3BGelaude%2C+Deborah%3BKing%2C+Winifred%3BJemmott%2C+Loretta&rft.aulast=Jones&rft.aufirst=Patricia&rft.date=2013-03-01&rft.volume=14&rft.issue=2&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Health+Promotion+Practice&rft.issn=15248399&rft_id=info:doi/10.1177%2F1524839912474276
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2014-07-01
N1  - Number of references - 8
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Sisters; HIV; Dissemination; Women; Black American people; Brief interventions
DO  - http://dx.doi.org/10.1177/1524839912474276
ER  - 



TY  - JOUR
T1  - Quantifying spillover spreading for comparing instrument performance and aiding in multicolor panel design
AN  - 1492650667; 18967110
AB  - After compensation, the measurement errors arising from multiple fluorescences spilling into each detector become evident by the spreading of nominally negative distributions. Depending on the instrument configuration and performance, and reagents used, this "spillover spreading" (SS) affects sensitivity in any given parameter. The degree of SS had been predicted theoretically to increase with measurement error, i.e., by the square root of fluorescence intensity, as well as directly related to the spectral overlap matrix coefficients. We devised a metric to quantify SS between any pair of detectors. This metric is intrinsic, as it is independent of fluorescence intensity. The combination of all such values for one instrument can be represented as a spillover spreading matrix (SSM). Single-stained controls were used to determine the SSM on multiple instruments over time, and under various conditions of signal quality. SSM values reveal fluorescence spectrum interactions that can limit the sensitivity of a reagent in the presence of brightly-stained cells on a different color. The SSM was found to be highly reproducible; its non-trivial values show a CV of less than 30% across a 2-month time frame. In addition, the SSM is comparable between similarly-configured instruments; instrument-specific differences in the SSM reveal underperforming detectors. Quantifying and monitoring the SSM can be a useful tool in instrument quality control to ensure consistent sensitivity and performance. In addition, the SSM is a key element for predicting the performance of multicolor immunofluorescence panels, which will aid in the optimization and development of new panels. We propose that the SSM is a critical component of QA/QC in evaluation of flow cytometer performance. Published 2013 Wiley- Periodicals, Inc.
JF  - Cytometry Part A
AU  - Nguyen, Richard
AU  - Perfetto, Stephen
AU  - Mahnke, Yolanda D
AU  - Chattopadhyay, Pratip
AU  - Roederer, Mario
AD  - Flow Cytometry Core, Vaccine Research Center, NIAID, NIH, Bethesda, Maryland., roederer@nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 306
EP  - 315
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 83A
IS  - 3
SN  - 1552-4922, 1552-4922
KW  - Biotechnology and Bioengineering Abstracts
KW  - Color
KW  - Spreading
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492650667?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quantifying+spillover+spreading+for+comparing+instrument+performance+and+aiding+in+multicolor+panel+design&rft.au=Nguyen%2C+Richard%3BPerfetto%2C+Stephen%3BMahnke%2C+Yolanda+D%3BChattopadhyay%2C+Pratip%3BRoederer%2C+Mario&rft.aulast=Nguyen&rft.aufirst=Richard&rft.date=2013-03-01&rft.volume=83A&rft.issue=3&rft.spage=306&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22251
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Spreading
DO  - http://dx.doi.org/10.1002/cyto.a.22251
ER  - 



TY  - JOUR
T1  - The effects of jaspamide on human cardiomyocyte function and cardiac ion channel activity
AN  - 1492636013; 18918497
AB  - Jaspamide (jasplakinolide; NSC-613009) is a cyclodepsipeptide that has antitumor activity. A narrow margin of safety was observed between doses required for efficacy in mouse tumor models and doses that caused severe acute toxicity in rats and dogs. We explored the hypothesis that the observed toxicity was due to cardiotoxicity. Jaspamide was tested in a patch clamp assay to determine its effect on selected cardiac ion channels. Jaspamide (10 mu M) inhibited Kv1.5 activity by 98.5%. Jaspamide also inhibited other channels including Cav1.2, Cav3.2, and HCN2; however, the Kv11.1 (hERG) channel was minimally affected. Using spontaneously contracting human cardiomyocytes derived from induced pluripotent stem cells, effects on cardiomyocyte contraction and viability were also examined. Jaspamide (30 nM to 30 mu M) decreased cardiomyocyte cell indices and beat amplitude, putative measurements of cell viability and cardiac contractility, respectively. Concentration-dependent increases in rhythmic beating rate were noted at less than or equal to 6 h of treatment, followed by dose-dependent decreases after 6 and 72 h exposure. The toxic effects of jaspamide were compared with that of the known cardiotoxicant mitoxantrone, and confirmed by multiparameter fluorescence imaging analysis. These results support the hypothesis that the toxicity observed in rats and dogs is due to toxic effects of jaspamide on cardiomyocytes.
JF  - Toxicology In Vitro
AU  - Schweikart, K
AU  - Guo, L
AU  - Shuler, Z
AU  - Abrams, R
AU  - Chiao, E T
AU  - Kolaja, K L
AU  - Davis, M
AD  - Developmental Therapeutics Program, National Cancer Institute, Bethesda, MD 20892, United States, schweikk@mail.nih.gov
PY  - 2013
VL  - 27
IS  - 2
SN  - 0887-2333, 0887-2333
KW  - Toxicology Abstracts
KW  - HERG protein
KW  - Heart
KW  - Muscle contraction
KW  - Fluorescence
KW  - Animal models
KW  - Tumors
KW  - Acute toxicity
KW  - Calcium channels (voltage-gated)
KW  - cardiomyocytes
KW  - imaging
KW  - Jasplakinolide
KW  - Stem cells
KW  - Ion channels
KW  - Potassium channels (voltage-gated)
KW  - ion channels (cyclic nucleotide-gated)
KW  - Rhythms
KW  - mitoxantrone
KW  - Antitumor activity
KW  - X 24300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492636013?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+In+Vitro&rft.atitle=The+effects+of+jaspamide+on+human+cardiomyocyte+function+and+cardiac+ion+channel+activity&rft.au=Schweikart%2C+K%3BGuo%2C+L%3BShuler%2C+Z%3BAbrams%2C+R%3BChiao%2C+E+T%3BKolaja%2C+K+L%3BDavis%2C+M&rft.aulast=Schweikart&rft.aufirst=K&rft.date=2013-03-01&rft.volume=27&rft.issue=2&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Toxicology+In+Vitro&rft.issn=08872333&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Heart; HERG protein; Muscle contraction; Fluorescence; Animal models; cardiomyocytes; Calcium channels (voltage-gated); Acute toxicity; Tumors; imaging; Stem cells; Jasplakinolide; Ion channels; ion channels (cyclic nucleotide-gated); Potassium channels (voltage-gated); Rhythms; mitoxantrone; Antitumor activity
ER  - 



TY  - JOUR
T1  - Evaluating Environmental Change Strategies: Challenges and Solutions
AN  - 1463019353; 201309513
AB  - In this introductory article we define environmental change strategies (ECS), summarize the primary challenges associated with evaluating ECS, and provide an overview of the methods researchers have employed to begin to address these challenges. This special issue provides a range of examples, from researchers and practitioners in the field, of different approaches for addressing these challenges. These articles present new methods to understand and test how ECS are implemented and propose methods to evaluate their implementation. The content of the articles covers multiple public health issues, including substance abuse prevention, tobacco control, HIV prevention, and obesity prevention. This special issue is intended to build the evidence base for effective ECS, generate compelling discussion, critical analyses, and spur future research that will help improve the implementation and evaluation of ECS. Adapted from the source document.
JF  - American Journal of Community Psychology
AU  - Pettibone, Kristianna G
AU  - Friend, Karen B
AU  - Nargiso, Jessica E
AU  - Florin, Paul
AD  - National Institute of Environmental Health Sciences, National Institutes of Health pettibonekg@niehs.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 217
EP  - 221
PB  - Springer, Dordrecht The Netherlands
VL  - 51
IS  - 1-2
SN  - 0091-0562, 0091-0562
KW  - Obesity
KW  - Prevention
KW  - Substance Abuse
KW  - Public Health
KW  - Acquired Immune Deficiency Syndrome
KW  - Environmental Factors
KW  - article
KW  - 6140: illness & health care
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463019353?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Community+Psychology&rft.atitle=Evaluating+Environmental+Change+Strategies%3A+Challenges+and+Solutions&rft.au=Pettibone%2C+Kristianna+G%3BFriend%2C+Karen+B%3BNargiso%2C+Jessica+E%3BFlorin%2C+Paul&rft.aulast=Pettibone&rft.aufirst=Kristianna&rft.date=2013-03-01&rft.volume=51&rft.issue=1-2&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Community+Psychology&rft.issn=00910562&rft_id=info:doi/10.1007%2Fs10464-012-9556-0
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-09-28
N1  - CODEN - AJCPCK
N1  - SubjectsTermNotLitGenreText - Prevention; Public Health; Environmental Factors; Obesity; Acquired Immune Deficiency Syndrome; Substance Abuse
DO  - http://dx.doi.org/10.1007/s10464-012-9556-0
ER  - 



TY  - JOUR
T1  - Associations of insulin-like growth factor and insulin-like growth factor binding protein-3 with mortality in women with breast cancer
AN  - 1443372698; 18602509
AB  - Elevated circulating insulin-like growth factor-1 (IGF-1), a breast epithelial cell mitogen, is associated with breast cancer development. However, its association with breast cancer survival is not established. Circulating concentrations of IGF-1 are controlled via binding proteins, including IGF Binding Protein-3 (IGFBP-3), that may modulate the association of IGF-1 with breast-cancer outcomes. We measured IGF-1 and IGFBP-3 concentrations in serum from 600 women enrolled in the health, eating, activity, and lifestyle (HEAL) study, a multiethnic, prospective cohort study of women diagnosed with stage I-IIIA breast cancer. We evaluated the association between IGF-1 and IGFBP-3, and as a ratio, modeled using quintile cut-points, with risk of breast cancer-specific (n = 42 deaths) and all-cause mortality (n = 87 deaths) using Cox proportional hazards models. In models adjusted for body mass index, ethnicity, tamoxifen use at time of blood draw, treatment received at diagnosis and IGFBP-3, women in the highest quintile of IGF-1 level had an increased risk of all-cause mortality (Hazard Ratio (HR) = 3.10, 95% CI 1.21-7.93, p = 0.02), although no dose-response association was evident. The IGF-1/IGFBP-3 ratio, an indicator of free IGF-I levels, was significantly associated with increasing risk of all-cause mortality (HR = 2.83, 95% CI 1.25-6.36 p sub(trend) = 0.01, upper vs. lower quintile) in a fully adjusted model. In conclusion, high serum levels of IGF-1 and the IGF-1/IGFBP-3 ratio were associated with increased risk of all-cause mortality in women with breast cancer. These results need to be confirmed in larger breast cancer survivor cohorts. What's new? Despite known associations with breast cancer risk, whether high serum levels of insulin-like growth factor-1 (IGF-1) also iinfluences prognosis of the disease remains unclear. In this analysis of 600 breast cancer patients, increases in IGF-1 and the ratio of IGF-1 to its binding protein IGFBP-3 were associated with all-cause mortality. The relationship appeared to involve a threshold effect in which IGFBP-3 production eventually failed to keep pace with production of IGF-1, resulting in conditions favorable for tumor growth.
JF  - International Journal of Cancer
AU  - Duggan, Catherine
AU  - Wang, Ching-Yun
AU  - Neuhouser, Marian L
AU  - Xiao, Liren
AU  - Smith, Ashley Wilder
AU  - Reding, Kerryn W
AU  - Baumgartner, Richard N
AU  - Baumgartner, Kathy B
AU  - Bernstein, Leslie
AU  - Ballard-Barbash, Rachel
AU  - McTiernan, Anne
AD  - Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD., cduggan@fhcrc.org
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 1191
EP  - 1200
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 5
SN  - 0020-7136, 0020-7136
KW  - Risk Abstracts
KW  - Health risks
KW  - Mortality
KW  - Dose-response effects
KW  - Breast cancer
KW  - Proteins
KW  - Survival
KW  - Growth factors
KW  - Females
KW  - Ethnic groups
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443372698?accountid=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=Associations+of+insulin-like+growth+factor+and+insulin-like+growth+factor+binding+protein-3+with+mortality+in+women+with+breast+cancer&rft.au=Duggan%2C+Catherine%3BWang%2C+Ching-Yun%3BNeuhouser%2C+Marian+L%3BXiao%2C+Liren%3BSmith%2C+Ashley+Wilder%3BReding%2C+Kerryn+W%3BBaumgartner%2C+Richard+N%3BBaumgartner%2C+Kathy+B%3BBernstein%2C+Leslie%3BBallard-Barbash%2C+Rachel%3BMcTiernan%2C+Anne&rft.aulast=Duggan&rft.aufirst=Catherine&rft.date=2013-03-01&rft.volume=132&rft.issue=5&rft.spage=1191&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27753
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Mortality; Health risks; Dose-response effects; Survival; Proteins; Breast cancer; Females; Growth factors; Ethnic groups
DO  - http://dx.doi.org/10.1002/ijc.27753
ER  - 



TY  - JOUR
T1  - High-throughput RNA sequencing of a formalin-fixed, paraffin-embedded autopsy lung tissue sample from the 1918 influenza pandemic
AN  - 1434014891; 18497079
AB  - Most biopsy and autopsy tissues are formalin-fixed and paraffin-embedded ( FFPE ), but this process leads to RNA degradation that limits gene expression analysis. The RNA genome of the 1918 pandemic influenza virus was previously determined in a 9-year effort by overlapping RT-PCR from post-mortem samples. Here, the full genome of the 1918 virus at 3000 coverage was determined in one high-throughput sequencing run of a library derived from total RNA of a 1918 FFPE sample after duplex-specific nuclease treatments. Bacterial sequences associated with secondary bacterial pneumonias were also detected. Host transcripts were well represented in the library. Compared to a 2009 pandemic influenza virus FFPE post-mortem library, the 1918 sample showed significant enrichment for host defence and cell death response genes, concordant with prior animal studies. This methodological approach should assist in the analysis of FFPE tissue samples isolated over the past century from a variety of diseases.
JF  - Journal of Pathology
AU  - Xiao, Yong-Li
AU  - Kash, John C
AU  - Beres, Stephen B
AU  - Sheng, Zong-Mei
AU  - Musser, James M
AU  - Taubenberger, Jeffery K
AD  - Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 535
EP  - 545
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 229
IS  - 4
SN  - 0022-3417, 0022-3417
KW  - Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Health & Safety Science Abstracts
KW  - Autopsy
KW  - Influenza
KW  - Influenza virus
KW  - RNA
KW  - N 14810:Methods
KW  - H 0500:General
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434014891?accountid=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+Pathology&rft.atitle=High-throughput+RNA+sequencing+of+a+formalin-fixed%2C+paraffin-embedded+autopsy+lung+tissue+sample+from+the+1918+influenza+pandemic&rft.au=Xiao%2C+Yong-Li%3BKash%2C+John+C%3BBeres%2C+Stephen+B%3BSheng%2C+Zong-Mei%3BMusser%2C+James+M%3BTaubenberger%2C+Jeffery+K&rft.aulast=Xiao&rft.aufirst=Yong-Li&rft.date=2013-03-01&rft.volume=229&rft.issue=4&rft.spage=535&rft.isbn=&rft.btitle=&rft.title=Journal+of+Pathology&rft.issn=00223417&rft_id=info:doi/10.1002%2Fpath.4145
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - RNA; Influenza; Influenza virus
DO  - http://dx.doi.org/10.1002/path.4145
ER  - 



TY  - JOUR
T1  - Prediction, refinement, and persistency of transmembrane helix dimers in lipid bilayers using implicit and explicit solvent/lipid representations: Microsecond molecular dynamics simulations of ErbB1/B2 and EphA1
AN  - 1434014617; 18498810
AB  - All-atom simulations are carried out on ErbB1/B2 and EphA1 transmembrane helix dimers in lipid bilayers starting from their solution/DMPC bicelle NMR structures. Over the course of microsecond trajectories, the structures remain in close proximity to the initial configuration and satisfy the majority of experimental tertiary contact restraints. These results further validate CHARMM protein/lipid force fields and simulation protocols on Anton. Separately, dimer conformations are generated using replica exchange in conjunction with an implicit solvent and lipid representation. The implicit model requires further improvement, and this study investigates whether lengthy all-atom molecular dynamics simulations can alleviate the shortcomings of the initial conditions. The simulations correct many of the deficiencies. For example, excessive helix twisting is eliminated over a period of hundreds of nanoseconds. The helix tilt, crossing angles, and dimer contacts approximate those of the NMR-derived structure, although the detailed contact surface remains off-set for one of two helices in both systems. Hence, even microsecond simulations are not long enough for extensive helix rotations. The alternate structures can be rationalized with reference to interaction motifs and may represent still sought after receptor states that are important in ErbB1/B2 and EphA1 signaling. Proteins 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Proteins: Structure, Function and Bioinformatics
AU  - Zhang, Liqun
AU  - Sodt, Alexander J
AU  - Venable, Richard M
AU  - Pastor, Richard W
AU  - Buck, Matthias
AD  - Laboratory of Computational Biology, National Heart Lung Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-9314., matthias.buck@case.edu
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 365
EP  - 376
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States
VL  - 81
IS  - 3
SN  - 0887-3585, 0887-3585
KW  - Biotechnology and Bioengineering Abstracts
KW  - Protein structure
KW  - Molecular modelling
KW  - Lipid bilayers
KW  - Solvents
KW  - N.M.R.
KW  - Bioinformatics
KW  - ErbB-1 protein
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434014617?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prediction%2C+refinement%2C+and+persistency+of+transmembrane+helix+dimers+in+lipid+bilayers+using+implicit+and+explicit+solvent%2Flipid+representations%3A+Microsecond+molecular+dynamics+simulations+of+ErbB1%2FB2+and+EphA1&rft.au=Zhang%2C+Liqun%3BSodt%2C+Alexander+J%3BVenable%2C+Richard+M%3BPastor%2C+Richard+W%3BBuck%2C+Matthias&rft.aulast=Zhang&rft.aufirst=Liqun&rft.date=2013-03-01&rft.volume=81&rft.issue=3&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24192
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Protein structure; Molecular modelling; Lipid bilayers; Solvents; N.M.R.; Bioinformatics; ErbB-1 protein
DO  - http://dx.doi.org/10.1002/prot.24192
ER  - 



TY  - JOUR
T1  - The impact of influenza hemagglutinin fusion peptide length and viral subtype on its structure and dynamics
AN  - 1434013374; 18483833
AB  - A peptide comprising no fewer than the first 20 residues of the influenza hemagglutinin HA2 subunit suffices to induce lipid mixing between the membranes of different unilamellar vesicles. This 20-residue peptide was previously reported to adopt an open "boomerang" structure that differs significantly from the closed helical-hairpin structure of a fusion peptide consisting of the first 23 residues of the HA2 sequence. This study investigates the structural and dynamic features of fusion peptides of different length and subtype. Lacking key interactions that stabilize the closed, helical-hairpin structure, the 20-residue peptide is in a dynamic equilibrium between closed and open states, adopting a ca. 11% population of the former when solubilized by DPC micelles. Peptides shorter than 20 residues would have even fewer interactions to stabilize a helical hairpin fold, resulting in a vanishing hairpin population. Considering the conserved nature of hairpin-stabilizing interactions across all serotypes, and the minimum of 20 residues needed for fusion, we postulate that the closed state plays an essential role in the fusion process. However, opening of this hairpin structure may be essential to the formation of a membrane pore at the final stage of the fusion process. Published 2012 Wiley Periodicals, Inc. Biopolymers 99: 189-195, 2013.
JF  - Biopolymers
AU  - Lorieau, Justin L
AU  - Louis, John M
AU  - Bax, Ad
AD  - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892., bax@nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 189
EP  - 195
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 99
IS  - 3
SN  - 0006-3525, 0006-3525
KW  - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts
KW  - NMR
KW  - chemical shift
KW  - dynamics
KW  - boomerang
KW  - hairpin
KW  - Influenza
KW  - Pores
KW  - Serotypes
KW  - Micelles
KW  - Hemagglutinins
KW  - Lipids
KW  - Biopolymers
KW  - Vesicles
KW  - W 30935:Food Biotechnology
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434013374?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+impact+of+influenza+hemagglutinin+fusion+peptide+length+and+viral+subtype+on+its+structure+and+dynamics&rft.au=Lorieau%2C+Justin+L%3BLouis%2C+John+M%3BBax%2C+Ad&rft.aulast=Lorieau&rft.aufirst=Justin&rft.date=2013-03-01&rft.volume=99&rft.issue=3&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22102
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Influenza; Pores; Serotypes; Micelles; Lipids; Hemagglutinins; Biopolymers; Vesicles
DO  - http://dx.doi.org/10.1002/bip.22102
ER  - 



TY  - JOUR
T1  - Endocrine Disruptors and the Breast: Early Life Effects and Later Life Disease
AN  - 1427006073; 17740698
AB  - Breast cancer risk has both heritable and environment/lifestyle components. The heritable component is a small contribution (5-27 %), leaving the majority of risk to environment (e.g., applied chemicals, food residues, occupational hazards, pharmaceuticals, stress) and lifestyle (e.g., physical activity, cosmetics, water source, alcohol, smoking). However, these factors are not well-defined, primarily due to the enormous number of factors to be considered. In both humans and rodent models, environmental factors that act as endocrine disrupting compounds (EDCs) have been shown to disrupt normal mammary development and lead to adverse lifelong consequences, especially when exposures occur during early life. EDCs can act directly or indirectly on mammary tissue to increase sensitivity to chemical carcinogens or enhance development of hyperplasia, beaded ducts, or tumors. Protective effects have also been reported. The mechanisms for these changes are not well understood. Environmental agents may also act as carcinogens in adult rodent models, directly causing or promoting tumor development, typically in more than one organ. Many of the environmental agents that act as EDCs and are known to affect the breast are discussed. Understanding the mechanism(s) of action for these compounds will be critical to prevent their effects on the breast in the future.
JF  - Journal of Mammary Gland Biology and Neoplasia
AU  - Macon, Madisa B
AU  - Fenton, Suzanne E
AD  - Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC, USA, fentonse@niehs.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 43
EP  - 61
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 18
IS  - 1
SN  - 1083-3021, 1083-3021
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Chemicals
KW  - Alcohol
KW  - Endocrine disruptors
KW  - Physical activity
KW  - Cosmetics
KW  - Tumors
KW  - Carcinogens
KW  - Organs
KW  - Rodents
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/1427006073?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Mammary+Gland+Biology+and+Neoplasia&rft.atitle=Endocrine+Disruptors+and+the+Breast%3A+Early+Life+Effects+and+Later+Life+Disease&rft.au=Macon%2C+Madisa+B%3BFenton%2C+Suzanne+E&rft.aulast=Macon&rft.aufirst=Madisa&rft.date=2013-03-01&rft.volume=18&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Journal+of+Mammary+Gland+Biology+and+Neoplasia&rft.issn=10833021&rft_id=info:doi/10.1007%2Fs10911-013-9275-7
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 168
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Chemicals; Alcohol; Physical activity; Endocrine disruptors; Cosmetics; Carcinogens; Tumors; Organs; Rodents
DO  - http://dx.doi.org/10.1007/s10911-013-9275-7
ER  - 



TY  - JOUR
T1  - Callous-Unemotional Traits and Response to Functional Family Therapy in Adolescent Offenders
AN  - 1417548815; 201316671
AB  - Objective: The current study examined whether callous-unemotional (CU) traits moderated the effectiveness of Functional Family Therapy for juvenile justice involved adolescents. Method: Participants were all youths (n = 134) who had been arrested and participated in an FFT program provided in a community mental health center over a 20-month period (mean age 15.34, 71.6% males, 59% African-American). Parent and self-report ratings of emotional, behavioral, and social functioning, multi-informant ratings of treatment progress, and probation/arrest records were used as outcome indicators. Results: CU traits were associated with poorer behavioral, emotional, and social adjustment prior to treatment but they were also associated with greater improvements in adjustment over the course of treatment. CU traits were not associated with significantly lower rates of participation or higher rates of treatment dropout, and the association between CU traits and risk for violent charges decreased after treatment at 6- and 12-month follow-ups. However, CU traits were still correlated with poorer levels of adjustment post-treatment, less perceived change over treatment by youth and their parents, and increased likelihood of violent offending during treatment. Conclusions: The results of this study indicate that FFT can lead to improvements in youth with CU traits; however, they enter treatment with a greater number of symptoms and are at higher risk for committing violence during treatment than other youth. [Copyright John Wiley and Sons, Ltd.]
JF  - Behavioral Sciences & the Law
AU  - White, Stuart F
AU  - Frick, Paul J
AU  - Lawing, Kathryn
AU  - Bauer, Daliah
AD  - The National Institute of Mental Health, 9000 Rockville Pike, Bldg. 15k, Room 300-C, Bethesda, MD 20892, U.S.A whitesf@mail.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 271
EP  - 285
PB  - John Wiley & Sons, Chichester UK
VL  - 31
IS  - 2
SN  - 0735-3936, 0735-3936
KW  - Violent offenders
KW  - Community mental health services
KW  - Parents
KW  - Adjustment
KW  - Family therapy
KW  - Adolescents
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1417548815?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavioral+Sciences+%26+the+Law&rft.atitle=Callous-Unemotional+Traits+and+Response+to+Functional+Family+Therapy+in+Adolescent+Offenders&rft.au=White%2C+Stuart+F%3BFrick%2C+Paul+J%3BLawing%2C+Kathryn%3BBauer%2C+Daliah&rft.aulast=White&rft.aufirst=Stuart&rft.date=2013-03-01&rft.volume=31&rft.issue=2&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Behavioral+Sciences+%26+the+Law&rft.issn=07353936&rft_id=info:doi/10.1002%2Fbsl.2041
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-08-01
N1  - Last updated - 2016-09-27
N1  - CODEN - BSLADR
N1  - SubjectsTermNotLitGenreText - Adolescents; Family therapy; Parents; Violent offenders; Adjustment; Community mental health services
DO  - http://dx.doi.org/10.1002/bsl.2041
ER  - 



TY  - JOUR
T1  - Forgoing Debriefing in Deceptive Research: Is It Ever Ethical
AN  - 1373490315; 201314425
AB  - The use of deception in research is generally permitted so long as participants are debriefed at the conclusion of their participation. Several authoritative research ethics guidelines allow investigators to omit debriefing under certain circumstances, however. Here we examine various justifications for forgoing debriefing in deceptive research, including concerns about subject pool contamination, the risk that revealing the deception will be harmful or distressing to participants, and issues of practicability. We conclude that, contrary to current practice, omitting debriefing is ethically acceptable only when debriefing is impracticable, the deception is innocuous, and no reasonable person would object to involvement in the research. Adapted from the source document.
JF  - Ethics & Behavior
AU  - Sommers, Roseanna
AU  - Miller, Franklin G
AD  - National Institutes of Health, Clinical Center Department of Bioethics
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 98
EP  - 116
PB  - Taylor & Francis, Philadelphia PA
VL  - 23
IS  - 2
SN  - 1050-8422, 1050-8422
KW  - Justification
KW  - Contamination
KW  - Ethics
KW  - Deception
KW  - Debriefing
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373490315?accountid=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=Ethics+%26+Behavior&rft.atitle=Forgoing+Debriefing+in+Deceptive+Research%3A+Is+It+Ever+Ethical&rft.au=Sommers%2C+Roseanna%3BMiller%2C+Franklin+G&rft.aulast=Sommers&rft.aufirst=Roseanna&rft.date=2013-03-01&rft.volume=23&rft.issue=2&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=Ethics+%26+Behavior&rft.issn=10508422&rft_id=info:doi/10.1080%2F10508422.2012.732505
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-07-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Debriefing; Deception; Contamination; Justification; Ethics
DO  - http://dx.doi.org/10.1080/10508422.2012.732505
ER  - 



TY  - JOUR
T1  - Gender differences in the psychological impact of tsunami
AN  - 1364767375; 201311776
AB  - Aim: The aim of this observational study was to explore gender-related differences in psychiatric morbidity during the initial three months following the December 2004 earthquake and tsunami involving the Andaman and Nicobar Islands, India. Methods: There were 12,784 survivors sheltered across 74 relief camps with 4,684 displaced survivors in Port Blair and 8,100 non-displaced survivors in Car-Nicobar Island. All persons who accessed mental health assistance within the camps constituted the study sample. Diagnoses were made by qualified psychiatrists using the ICD-10. There were 475 patients: 188 (40%) men and 287 (60%) women. Results: There were significant gender differences in terms of displacement. There were significantly higher levels of panic disorder, unspecified anxiety disorder and somatic complaints in the displaced women while the non-displaced population showed more adjustment disorder. Conclusions: Displacement was a significant factor in the manifestations of observed pathology. Displaced women had greater psychiatric morbidity. In addition, the fact that adjustment disorder (a self-limiting disorder form of psychopathology) was more prevalent in the non-displaced group may be a reflection of the findings of overall lesser morbidity in non-displaced women. Hence, women may have to be rehabilitated in their own habitats after major disasters. [Reprinted by permission of Sage Publications Ltd., copyright holder.]
JF  - International Journal of Social Psychiatry
AU  - Viswanath, Biju
AU  - Maroky, Ami S
AU  - Math, Suresh B
AU  - John, John P
AU  - Cherian, Anish V
AU  - Girimaji, Satish C
AU  - Benegal, Vivek
AU  - Hamza, Ameer
AU  - Chaturvedi, Santosh K
AD  - Department of Psychiatry, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore, India
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 130
EP  - 136
PB  - Sage Publications, London UK
VL  - 59
IS  - 2
SN  - 0020-7640, 0020-7640
KW  - Disaster gender tsunami high-risk population mental health
KW  - Displacement
KW  - Adjustment disorder
KW  - Psychiatric morbidity
KW  - Women
KW  - Gender differences
KW  - Survivors
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364767375?accountid=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=Gender+differences+in+the+psychological+impact+of+tsunami&rft.au=Viswanath%2C+Biju%3BMaroky%2C+Ami+S%3BMath%2C+Suresh+B%3BJohn%2C+John+P%3BCherian%2C+Anish+V%3BGirimaji%2C+Satish+C%3BBenegal%2C+Vivek%3BHamza%2C+Ameer%3BChaturvedi%2C+Santosh+K&rft.aulast=Viswanath&rft.aufirst=Biju&rft.date=2013-03-01&rft.volume=59&rft.issue=2&rft.spage=130&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764011423469
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - CODEN - IJSPAG
N1  - SubjectsTermNotLitGenreText - Survivors; Adjustment disorder; Gender differences; Psychiatric morbidity; Women; Displacement
DO  - http://dx.doi.org/10.1177/0020764011423469
ER  - 



TY  - JOUR
T1  - A Blueprint for Genomic Nursing Science
AN  - 1364764094; 201308564
AB  - Purpose: This article reports on recommendations arising from an invitational workshop series held at the National Institutes of Health for the purposes of identifying critical genomics problems important to the health of the public that can be addressed through nursing science. The overall purpose of the Genomic Nursing State of the Science Initiative is to establish a nursing research blueprint based on gaps in the evidence and expert evaluation of the current state of the science and through public comment. Organizing Constructs: A Genomic Nursing State of the Science Advisory Panel was convened in 2012 to develop the nursing research blueprint. The Advisory Panel, which met via two webinars and two in-person meetings, considered existing evidence from evidence reviews, testimony from key stakeholder groups, presentations from experts in research synthesis, and public comment. Findings: The genomic nursing science blueprint arising from the Genomic Nursing State of Science Advisory Panel focuses on biologic plausibility studies as well as interventions likely to improve a variety of outcomes (e.g., clinical, economic, environmental). It also includes all care settings and diverse populations. The focus is on (a) the client, defined as person, family, community, or population; (b) the context, targeting informatics support systems, capacity building, education, and environmental influences; and (c) cross-cutting themes. It was agreed that building capacity to measure the impact of nursing actions on costs, quality, and outcomes of patient care is a strategic and scientific priority if findings are to be synthesized and aggregated to inform practice and policy. Conclusions: The genomic nursing science blueprint provides the framework for furthering genomic nursing science to improve health outcomes. This blueprint is an independent recommendation of the Advisory Panel with input from the public and is not a policy statement of the National Institutes of Health or the federal government. Clinical Relevance: This genomic nursing science blueprint targets research to build the evidence base to inform integration of genomics into nursing practice and regulation (such as nursing licensure requirements, institutional accreditation, and academic nursing school accreditation). Adapted from the source document.
JF  - Journal of Nursing Scholarship
AU  - Calzone, Kathleen A
AU  - Jenkins, Jean
AU  - Bakos, Alexis D
AU  - Cashion, Ann K
AU  - Donaldson, Nancy
AU  - Feero, W Gregory
AU  - Feetham, Suzanne
AU  - Grady, Patricia A
AU  - Hinshaw, Ada Sue
AU  - Knebel, Ann R
AU  - Robinson, Nellie
AU  - Ropka, Mary E
AU  - Seibert, Diane
AU  - Stevens, Kathleen R
AU  - Tully, Lois A
AU  - Webb, Jo Ann
AD  - Xi, Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 96
EP  - 104
PB  - Wiley-Blackwell, UK
VL  - 45
IS  - 1
SN  - 1527-6546, 1527-6546
KW  - Clinical nursing
KW  - Nursing
KW  - Capacity building approach
KW  - Health
KW  - Professional practices
KW  - Patient care
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364764094?accountid=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+Nursing+Scholarship&rft.atitle=A+Blueprint+for+Genomic+Nursing+Science&rft.au=Calzone%2C+Kathleen+A%3BJenkins%2C+Jean%3BBakos%2C+Alexis+D%3BCashion%2C+Ann+K%3BDonaldson%2C+Nancy%3BFeero%2C+W+Gregory%3BFeetham%2C+Suzanne%3BGrady%2C+Patricia+A%3BHinshaw%2C+Ada+Sue%3BKnebel%2C+Ann+R%3BRobinson%2C+Nellie%3BRopka%2C+Mary+E%3BSeibert%2C+Diane%3BStevens%2C+Kathleen+R%3BTully%2C+Lois+A%3BWebb%2C+Jo+Ann&rft.aulast=Calzone&rft.aufirst=Kathleen&rft.date=2013-03-01&rft.volume=45&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nursing+Scholarship&rft.issn=15276546&rft_id=info:doi/10.1111%2Fjnu.12007
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - SubjectsTermNotLitGenreText - Nursing; Clinical nursing; Health; Capacity building approach; Professional practices; Patient care
DO  - http://dx.doi.org/10.1111/jnu.12007
ER  - 



TY  - JOUR
T1  - Racial/Ethnic Differences in Cancer Risk After Kidney Transplantation
AN  - 1323810814; 17779152
AB  - Transplant recipients have elevated cancer risk, but it is unknown if cancer risk differs across race and ethnicity as in the general population. US kidney recipients (N = 87,895) in the Transplant Cancer Match Study between 1992 and 2008 were evaluated for racial/ethnic differences in risk for six common cancers after transplantation. Compared to white recipients, black recipients had lower incidence of non-Hodgkin lymphoma (NHL) (adjusted incidence rate ratio [aIRR] 0.60, p<0.001) and higher incidence of kidney (aIRR 2.09, p<0.001) and prostate cancer (aIRR 2.14, p<0.001); Hispanic recipients had lower incidence of NHL (aIRR 0.64, p = 0.001), lung (aIRR 0.41, p < 0.001), breast (aIRR 0.53, p = 0.003) and prostate cancer (aIRR 0.72, p = 0.05). Colorectal cancer incidence was similar across groups. Standardized incidence ratios (SIRs) measured the effect of transplantation on cancer risk and were similar for most cancers (p greater than or equal to 0.1). However, black and Hispanic recipients had larger increases in kidney cancer risk with transplantation (SIRs: 8.96 in blacks, 5.95 in Hispanics vs. 4.44 in whites), and only blacks had elevated prostate cancer risk following transplantation (SIR: 1.21). Racial/ethnic differences in cancer risk after transplantation mirror general population patterns, except for kidney and prostate cancers where differences reflect the effects of end-stage renal disease or transplantation. Among US kidney recipients, cancer incidence varies by race/ethnicity, reflecting both background differences in the general population and, for some cancers, differing effects of transplantation on risk.
JF  - American Journal of Transplantation
AU  - Hall, E C
AU  - Segev, D L
AU  - Engels, E A
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 714
EP  - 720
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 13
IS  - 3
SN  - 1600-6135, 1600-6135
KW  - Immunology Abstracts; Risk Abstracts
KW  - Non-Hodgkin's lymphoma
KW  - Transplantation
KW  - Prostate cancer
KW  - Kidney transplantation
KW  - Kidney
KW  - Colorectal carcinoma
KW  - Standards
KW  - Cancer
KW  - Ethnic groups
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323810814?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Transplantation&rft.atitle=Racial%2FEthnic+Differences+in+Cancer+Risk+After+Kidney+Transplantation&rft.au=Hall%2C+E+C%3BSegev%2C+D+L%3BEngels%2C+E+A&rft.aulast=Hall&rft.aufirst=E&rft.date=2013-03-01&rft.volume=13&rft.issue=3&rft.spage=714&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Transplantation&rft.issn=16006135&rft_id=info:doi/10.1111%2Fajt.12066
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2016-05-13
N1  - SubjectsTermNotLitGenreText - Non-Hodgkin's lymphoma; Prostate cancer; Transplantation; Kidney transplantation; Kidney; Colorectal carcinoma; Standards; Ethnic groups; Cancer
DO  - http://dx.doi.org/10.1111/ajt.12066
ER  - 



TY  - JOUR
T1  - Identification of VAR2CSA Domain-Specific Inhibitory Antibodies of the Plasmodium falciparum Erythrocyte Membrane Protein 1 Using a Novel Flow Cytometry Assay
AN  - 1323809202; 17819215
AB  - VAR2CSA, a member of the Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) family, is a leading candidate for use in vaccines to protect first-time mothers from placental malaria (PM). VAR2CSA, which is comprised of a series of six Duffy binding-like (DBL) domains, binds chondroitin sulfate A (CSA) on placental syncytiotrophoblast. Several recombinant DBL domains have been shown to bind CSA. In order to identify and develop recombinant proteins suitable for clinical development, DBL2X and DBL3X, as well as their respective third subdomain (S3) from the FCR3 parasite clone, were expressed in Escherichia coli, refolded, and purified. All but DBL3X-S3 recombinant proteins bound to CSA expressed on Chinese hamster ovary (CHO)-K1 cells but not to CHO-pgsA745 cells, which are CSA negative as determined by flow cytometry. All but DBL3X-S3 bound to CSA on chondroitin sulfate proteoglycan (CSPG) as determined by surface plasmon resonance (SPR) analysis. Purified IgG from rats and rabbits immunized with these four recombinant proteins bound homologous and some heterologous parasite-infected erythrocytes (IE). Using a novel flow cytometry inhibition-of-binding assay (flow-IBA), antibodies against DBL3X-S3 inhibited 35% and 45% of IE binding to CSA on CHO-K1 cells compared to results for soluble CSA (sCSA) and purified multigravida (MG) IgG, respectively, from areas in Tanzania to which malaria is endemic. Antibodies generated against the other domains provided little or no inhibition of IE binding to CSA on CHO-K1 cells as determined by the flow cytometry inhibition-of-binding assay. These results demonstrate for the first time the ability to identify antibodies to VAR2CSA DBL domains and subdomains capable of inhibiting VAR2CSA parasite-IE binding to CSA by flow cytometry. The flow cytometry inhibition-of-binding assay was robust and provided an accurate, reproducible, and reliable means to identify blocking of IE binding to CSA and promises to be significant in the development of a vaccine to protect pregnant women.
JF  - Clinical and Vaccine Immunology
AU  - Obiakor, Harold
AU  - Avril, Marion
AU  - MacDonald, Nicholas J
AU  - Srinivasan, Prakash
AU  - Reiter, Karine
AU  - Anderson, Charles
AU  - Holmes, Kevin L
AU  - Fried, Michal
AU  - Duffy, Patrick E
AU  - Smith, Joseph D
AD  - Laboratory of Malaria Immunology and Vaccinology, NIAID/NIH, Rockville, Maryland, USA, DavidL.Narum,dnarum{at}niaid.nih.gov,andLouisH.Miller,lmiller{at}niaid.nih.gov.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 433
EP  - 442
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 20
IS  - 3
SN  - 1556-679X, 1556-679X
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts
KW  - Parasites
KW  - Human diseases
KW  - Tanzania
KW  - Erythrocytes
KW  - Disease control
KW  - Malaria
KW  - Public health
KW  - Flow cytometry
KW  - Placenta
KW  - Escherichia coli
KW  - Chondroitin sulfate
KW  - Plasmodium falciparum
KW  - Pregnancy
KW  - Proteoglycans
KW  - Recombinants
KW  - Antibodies
KW  - surface plasmon resonance
KW  - Immunoglobulin G
KW  - erythrocyte membrane protein 1
KW  - Vaccines
KW  - K 03350:Immunology
KW  - F 06905:Vaccines
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323809202?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+and+Vaccine+Immunology&rft.atitle=Identification+of+VAR2CSA+Domain-Specific+Inhibitory+Antibodies+of+the+Plasmodium+falciparum+Erythrocyte+Membrane+Protein+1+Using+a+Novel+Flow+Cytometry+Assay&rft.au=Obiakor%2C+Harold%3BAvril%2C+Marion%3BMacDonald%2C+Nicholas+J%3BSrinivasan%2C+Prakash%3BReiter%2C+Karine%3BAnderson%2C+Charles%3BHolmes%2C+Kevin+L%3BFried%2C+Michal%3BDuffy%2C+Patrick+E%3BSmith%2C+Joseph+D&rft.aulast=Obiakor&rft.aufirst=Harold&rft.date=2013-03-01&rft.volume=20&rft.issue=3&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=1556679X&rft_id=info:doi/10.1128%2FCVI.00638-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Number of references - 44
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Recombinants; Flow cytometry; Parasites; Human diseases; Antibodies; Erythrocytes; Disease control; Vaccines; Public health; Proteoglycans; surface plasmon resonance; Chondroitin sulfate; Placenta; Immunoglobulin G; Malaria; erythrocyte membrane protein 1; Pregnancy; Escherichia coli; Plasmodium falciparum; Tanzania
DO  - http://dx.doi.org/10.1128/CVI.00638-12
ER  - 



TY  - JOUR
T1  - Essential Staphylococcus aureus toxin export system
AN  - 1323805540; 17782010
AB  - Widespread antibiotic resistance among important bacterial pathogens such as Staphylococcus aureus calls for alternative routes of drug development. Interfering with crucial virulence determinants is considered a promising new approach to control bacterial infection. Phenol-soluble modulins (PSMs) are peptide toxins with multiple key roles in pathogenesis and have a major impact on the ability of highly virulent S. aureus to cause disease. However, targeting PSMs for therapeutic intervention is hampered by their multitude and diversity. Here we report that an ATP-binding cassette transporter with previously unknown function is responsible for the export of all PSMs, thus representing a single target for complete obstruction of PSM production. The transporter had a strong effect on virulence phenotypes, such as neutrophil lysis, and the extent of its effect on the development of S. aureus infection was similar to that of the sum of all PSMs. Notably, the transporter was essential for bacterial growth. Furthermore, it contributed to producer immunity toward secreted PSMs and defense against PSM-mediated bacterial interference. Our study reveals a noncanonical, dedicated secretion mechanism for an important class of toxins and identifies this mechanism as a comprehensive potential target for the development of drugs to efficiently inhibit the growth and virulence of pathogenic staphylococci.
JF  - Nature Medicine
AU  - Chatterjee, Som S
AU  - Joo, Hwang-Soo
AU  - Duong, Anthony C
AU  - Dieringer, Thomas D
AU  - Tan, Vee Y
AU  - Song, Yan
AU  - Fischer, Elizabeth R
AU  - Cheung, Gordon Y C
AU  - Li, Min
AU  - Otto, Michael
AD  - Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 364
EP  - 367
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 19
IS  - 3
SN  - 1078-8956, 1078-8956
KW  - Microbiology Abstracts B: Bacteriology
KW  - Virulence
KW  - ATP-binding protein
KW  - Leukocytes (neutrophilic)
KW  - Therapeutic applications
KW  - Drug development
KW  - Pathogens
KW  - Immunity
KW  - Staphylococcus aureus
KW  - Infection
KW  - Toxins
KW  - Antibiotic resistance
KW  - J 02300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323805540?accountid=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=Nature+Medicine&rft.atitle=Essential+Staphylococcus+aureus+toxin+export+system&rft.au=Chatterjee%2C+Som+S%3BJoo%2C+Hwang-Soo%3BDuong%2C+Anthony+C%3BDieringer%2C+Thomas+D%3BTan%2C+Vee+Y%3BSong%2C+Yan%3BFischer%2C+Elizabeth+R%3BCheung%2C+Gordon+Y+C%3BLi%2C+Min%3BOtto%2C+Michael&rft.aulast=Chatterjee&rft.aufirst=Som&rft.date=2013-03-01&rft.volume=19&rft.issue=3&rft.spage=364&rft.isbn=&rft.btitle=&rft.title=Nature+Medicine&rft.issn=10788956&rft_id=info:doi/10.1038%2Fnm.3047
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Virulence; ATP-binding protein; Leukocytes (neutrophilic); Therapeutic applications; Drug development; Immunity; Pathogens; Infection; Antibiotic resistance; Toxins; Staphylococcus aureus
DO  - http://dx.doi.org/10.1038/nm.3047
ER  - 



TY  - JOUR
T1  - MRI roadmap-guided transendocardial delivery of exon-skipping recombinant adeno-associated virus restores dystrophin expression in a canine model of Duchenne muscular dystrophy
AN  - 1323802375; 17782002
AB  - Duchenne muscular dystrophy (DMD) cardiomyopathy patients currently have no therapeutic options. We evaluated catheter-based transendocardial delivery of a recombinant adeno-associated virus (rAAV) expressing a small nuclear U7 RNA (U7smOPT) complementary to specific cis-acting splicing signals. Eliminating specific exons restores the open reading frame resulting in translation of truncated dystrophin protein. To test this approach in a clinically relevant DMD model, golden retriever muscular dystrophy (GRMD) dogs received serotype 6 rAAV-U7smOPT via the intracoronary or transendocardial route. Transendocardial injections were administered with an injection-tipped catheter and fluoroscopic guidance using X-ray fused with magnetic resonance imaging (XFM) roadmaps. Three months after treatment, tissues were analyzed for DNA, RNA, dystrophin protein, and histology. Whereas intracoronary delivery did not result in effective transduction, transendocardial injections, XFM guidance, enabled 30 plus or minus 10 non-overlapping injections per animal. Vector DNA was detectable in all samples tested and ranged from 3000 vector genome copies per cell. RNA analysis, western blot analysis, and immunohistology demonstrated extensive expression of skipped RNA and dystrophin protein in the treated myocardium. Left ventricular function remained unchanged over a 3-month follow-up. These results demonstrated that effective transendocardial delivery of rAAV-U7smOPT was achieved using XFM. This approach restores an open reading frame for dystrophin in affected dogs and has potential clinical utility.
JF  - Gene Therapy
AU  - Barbash, I M
AU  - Cecchini, S
AU  - Faranesh, A Z
AU  - Virag, T
AU  - Li, L
AU  - Yang, Y
AU  - Hoyt, R F
AU  - Kornegay, J N
AU  - Bogan, J R
AU  - Garcia, L
AU  - Lederman, R J
AU  - Kotin, R M
AD  - Cardiovascular and Pulmonary Branch, Division of Intramural Research, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 274
EP  - 282
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 20
IS  - 3
SN  - 0969-7128, 0969-7128
KW  - Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Cardiomyopathy
KW  - Dystrophin
KW  - Adeno-associated virus
KW  - W 30905:Medical Applications
KW  - G:07730
KW  - N:14810
KW  - V:22410
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323802375?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MRI+roadmap-guided+transendocardial+delivery+of+exon-skipping+recombinant+adeno-associated+virus+restores+dystrophin+expression+in+a+canine+model+of+Duchenne+muscular+dystrophy&rft.au=Barbash%2C+I+M%3BCecchini%2C+S%3BFaranesh%2C+A+Z%3BVirag%2C+T%3BLi%2C+L%3BYang%2C+Y%3BHoyt%2C+R+F%3BKornegay%2C+J+N%3BBogan%2C+J+R%3BGarcia%2C+L%3BLederman%2C+R+J%3BKotin%2C+R+M&rft.aulast=Barbash&rft.aufirst=I&rft.date=2013-03-01&rft.volume=20&rft.issue=3&rft.spage=274&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2012.38
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Dystrophin; Adeno-associated virus
DO  - http://dx.doi.org/10.1038/gt.2012.38
ER  - 



TY  - JOUR
T1  - Pan-PCR, a Computational Method for Designing Bacterium-Typing Assays Based on Whole-Genome Sequence Data
AN  - 1323800600; 17760260
AB  - With increasing rates of antibiotic resistance, bacterial infections have become more difficult to treat, elevating the importance of surveillance and prevention. Effective surveillance relies on the availability of rapid, cost-effective, and informative typing methods to monitor bacterial isolates. PCR-based typing assays are fast and inexpensive, but their utility is limited by the lack of targets which are capable of distinguishing between strains within a species. To identify highly informative PCR targets from the growing base of publicly available bacterial genome sequences, we developed pan-PCR. This computer algorithm uses existing genome sequences for isolates of a species of interest and identifies a set of genes whose patterns of presence or absence provide the best discrimination between strains in this species. A set of PCR primers targeting the identified genes is then designed, with each PCR product being of a different size to allow multiplexing. These target DNA regions and PCR primers can then be utilized to type bacterial isolates. To evaluate pan-PCR, we designed an assay for the emerging pathogen Acinetobacter baumannii. Taking as input a set of 29 previously sequenced genomes, pan-PCR identified 6 genetic loci whose presence or absence was capable of distinguishing all the input strains. This assay was applied to a set of patient isolates, and its discriminatory power was compared to that of multilocus sequence typing (MLST) and whole-genome optical maps. We found that the pan-PCR assay was capable of making clinically relevant distinctions between strains with identical MLST profiles and showed a discriminatory power similar to that of optical maps. Pan-PCR represents a tool capable of exploiting available genome sequence data to design highly discriminatory PCR assays. The ease of design and implementation makes this approach feasible for diagnostic facilities of all sizes.
JF  - Journal of Clinical Microbiology
AU  - Yang, Joy Y
AU  - Brooks, Shelise
AU  - Meyer, Jennifer A
AU  - Blakesley, Robert R
AU  - Zelazny, Adrian M
AU  - Segre, Julia A
AU  - Snitkin, Evan S
AD  - Genetics and Molecular Biology Branch, National Human Genome Research Institute, Bethesda, Maryland, USA, JuliaA.Segre,jsegre{at}nhgri.nih.gov,orEvanS.Snitkin,snitkines{at}mail.nih.gov.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 752
EP  - 758
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 51
IS  - 3
SN  - 0095-1137, 0095-1137
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology
KW  - Genomes
KW  - Bacteria
KW  - Data processing
KW  - Nucleotide sequence
KW  - Computers
KW  - Algorithms
KW  - Pathogens
KW  - Computer applications
KW  - Infection
KW  - multilocus sequence typing
KW  - Acinetobacter baumannii
KW  - Typing
KW  - Polymerase chain reaction
KW  - Primers
KW  - Antibiotic resistance
KW  - Gene mapping
KW  - J 02310:Genetics & Taxonomy
KW  - A 01340:Antibiotics & Antimicrobials
KW  - N 14810:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323800600?accountid=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=Pan-PCR%2C+a+Computational+Method+for+Designing+Bacterium-Typing+Assays+Based+on+Whole-Genome+Sequence+Data&rft.au=Yang%2C+Joy+Y%3BBrooks%2C+Shelise%3BMeyer%2C+Jennifer+A%3BBlakesley%2C+Robert+R%3BZelazny%2C+Adrian+M%3BSegre%2C+Julia+A%3BSnitkin%2C+Evan+S&rft.aulast=Yang&rft.aufirst=Joy&rft.date=2013-03-01&rft.volume=51&rft.issue=3&rft.spage=752&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.02671-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Number of references - 41
N1  - Last updated - 2013-11-04
N1  - SubjectsTermNotLitGenreText - Genomes; Data processing; Computers; Nucleotide sequence; Algorithms; Pathogens; Infection; Computer applications; multilocus sequence typing; Typing; Polymerase chain reaction; Primers; Antibiotic resistance; Gene mapping; Bacteria; Acinetobacter baumannii
DO  - http://dx.doi.org/10.1128/JCM.02671-12
ER  - 



TY  - JOUR
T1  - What Does It Mean to "Employ" the RE-AIM Model
AN  - 1323338236; 201304242
AB  - Many grant proposals identify the use of a given evaluation model or framework but offer little about how such models are implemented. The authors discuss what it means to employ a specific model, RE-AIM, and key dimensions from this model for program planning, implementation, evaluation, and reporting. The authors report both conceptual and content specifications for the use of the RE-AIM model and a content review of 42 recent dissemination and implementation grant applications to National Institutes of Health that proposed the use of this model. Outcomes include the extent to which proposals addressed the overall RE-AIM model and specific items within the five dimensions in their methods or evaluation plans. The majority of grants used only some elements of the model (less than 10% contained thorough measures across all RE-AIM dimensions). Few met criteria for "fully developed use" of RE-AIM and the percentage of key issues addressed varied from, on average, 45% to 78% across the RE-AIM dimensions. The results and discussion of key criteria should help investigators in their use of RE-AIM and illuminate the broader issue of comprehensive use of evaluation models. [Reprinted by permission of Sage Publications Inc., copyright holder.]
JF  - Evaluation & the Health Professions
AU  - Kessler, Rodger S
AU  - Purcell, E Peyton
AU  - Glasgow, Russell E
AU  - Klesges, Lisa M
AU  - Benkeser, Rachel M
AU  - Peek, C J
AD  - Department of Family Medicine, University of Vermont, Burlington, VT, USA
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 44
EP  - 66
PB  - Sage Publications, Thousand Oaks CA
VL  - 36
IS  - 1
SN  - 0163-2787, 0163-2787
KW  - RE-AIM evaluation fidelity model testing methodology review criteria
KW  - Grants
KW  - Specification
KW  - Health
KW  - Dissemination
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323338236?accountid=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=Evaluation+%26+the+Health+Professions&rft.atitle=What+Does+It+Mean+to+%22Employ%22+the+RE-AIM+Model&rft.au=Kessler%2C+Rodger+S%3BPurcell%2C+E+Peyton%3BGlasgow%2C+Russell+E%3BKlesges%2C+Lisa+M%3BBenkeser%2C+Rachel+M%3BPeek%2C+C+J&rft.aulast=Kessler&rft.aufirst=Rodger&rft.date=2013-03-01&rft.volume=36&rft.issue=1&rft.spage=44&rft.isbn=&rft.btitle=&rft.title=Evaluation+%26+the+Health+Professions&rft.issn=01632787&rft_id=info:doi/10.1177%2F0163278712446066
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-04-01
N1  - Last updated - 2016-09-27
N1  - CODEN - EHPRDK
N1  - SubjectsTermNotLitGenreText - Grants; Health; Dissemination; Specification
DO  - http://dx.doi.org/10.1177/0163278712446066
ER  - 



TY  - JOUR
T1  - Federalizing medical campaigns against alcoholism and drug abuse
AN  - 1322727566; 4424721
AB  - The formation of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the Special Action Office for Drug Abuse Prevention (SAODAP) in the early 1970s dramatically expanded scientific and medical efforts to control alcoholism and drug abuse in the United States. Drawing on a variety of primary, secondary, and archival sources, this article describes the creation and early years of these agencies. I show that while the agencies appeared at roughly the same time, their creation involved separate sets of issues and actors. In addition, I show that SAODAP received more money and resources, even though advocates for alcoholics mobilized a stronger lobbying campaign. Two factors explain this discrepancy in money and resources: (1) alcoholism was framed as a public health problem, whereas drug abuse was drawn into broader debates about crime and social decline; and (2) alcohol programs relied on congressional support, whereas drug programs found champions at high levels of the Nixon administration. These political and cultural factors help explain why current programs for illegal drugs receive more federal support, despite alcohol's greater public health burden. Reprinted by permission of Blackwell Publishers
JF  - Milbank quarterly
AU  - Metlay, Grischa
AD  - National Institutes of Health
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 123
EP  - 162
VL  - 91
IS  - 1
SN  - 0887-378X, 0887-378X
KW  - Economics
KW  - Lobbying
KW  - Crime
KW  - Money
KW  - Alcoholism
KW  - U.S.A.
KW  - Cultural factors
KW  - Drug abuse
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1322727566?accountid=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=Milbank+quarterly&rft.atitle=Federalizing+medical+campaigns+against+alcoholism+and+drug+abuse&rft.au=Metlay%2C+Grischa&rft.aulast=Metlay&rft.aufirst=Grischa&rft.date=2013-03-01&rft.volume=91&rft.issue=1&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=Milbank+quarterly&rft.issn=0887378X&rft_id=info:doi/10.1111%2Fmilq.12004
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 913 561 6220; 3742 1121 11776 3753 3755; 8235; 3015 11881; 10449 5772; 3141 3198; 7490 9716; 433 293 14
DO  - http://dx.doi.org/10.1111/milq.12004
ER  - 



TY  - JOUR
T1  - Injury prevention and care: an important public health agenda for health, survival and safety of children.
AN  - 1320177236; 22718091
AB  - Injuries affect the lives of thousands of young people and their families each year in India. With the gradual decline of communicable and nutritional diseases, injuries will be a leading cause of mortality, morbidity and disabilities and the success achieved so far in child health and survival is in jeopardy. Available data indicate that among children less than 18 y, 10-15 % of deaths, 20-30 % of hospital registrations and 20 % of disabilities are due to injuries. Based on available data, it is estimated that injuries result in death of nearly 1, 00,000 children every year in India and hospitalisations among 2 million children. Road Traffic Injuries (RTI's), drowning, falls, burns and poisoning are leading injury causes in India. Drowning and burns are major causes of mortality in less than 5 y, while RTIs, falls and poisoning are leading causes in 5-18 y. A shift in the occurrence of suicides to younger age groups of 15-20 y is a matter of serious concern in recent years. More number of males, those in rural areas, and majority of poor income households are affected due to injuries.Child injuries are predictable and preventable. Children have limitations of size, development, vision, hearing and risk perceptions as compared to adults and hence are more susceptible and vulnerable to injuries. Thus, it is important to make products and home - road and school environments safer along with greater supervision by parents and care givers. The key approaches include vehicle and product safety, environmental modification, legislation and enforcement, education and skills development along with availability of quality trauma care. Child injury prevention and care requires good quality data, building human and financial resources, strengthening policies and programmes based on evidence and integrated implementation of countermeasures along with monitoring and evaluation. Child injury prevention and control is crucial and should be an integral part of child health and survival.
JF  - Indian journal of pediatrics
AU  - Gururaj, Gopalkrishna
AD  - Department of Epidemiology, WHO Collaborating Centre for Injury Prevention and Safety Promotion, National Institute of Mental Health and Neuro Sciences, Bangalore, 560029, India. epiguru@yahoo.com
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - S100
EP  - S108
VL  - 80 Suppl 1
KW  - Index Medicus
KW  - Humans
KW  - Child
KW  - Health Policy
KW  - Cause of Death
KW  - Child, Preschool
KW  - India
KW  - Infant
KW  - Cross-Sectional Studies
KW  - Risk Factors
KW  - Health Promotion -- organization & administration
KW  - Education, Nonprofessional
KW  - Adolescent
KW  - Male
KW  - Female
KW  - Wounds and Injuries -- therapy
KW  - Public Health
KW  - Safety
KW  - Developing Countries
KW  - Wounds and Injuries -- prevention & control
KW  - Wounds and Injuries -- mortality
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1320177236?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+pediatrics&rft.atitle=Injury+prevention+and+care%3A+an+important+public+health+agenda+for+health%2C+survival+and+safety+of+children.&rft.au=Gururaj%2C+Gopalkrishna&rft.aulast=Gururaj&rft.aufirst=Gopalkrishna&rft.date=2013-03-01&rft.volume=80+Suppl+1&rft.issue=&rft.spage=S100&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+pediatrics&rft.issn=0973-7693&rft_id=info:doi/10.1007%2Fs12098-012-0783-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-11
N1  - Date created - 2013-03-13
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/s12098-012-0783-z
ER  - 



TY  - JOUR
T1  - Orthologous Gene Clusters and Taxon Signature Genes for Viruses of Prokaryotes
AN  - 1315624424; 17709877
AB  - Viruses are the most abundant biological entities on earth and encompass a vast amount of genetic diversity. The recent rapid increase in the number of sequenced viral genomes has created unprecedented opportunities for gaining new insight into the structure and evolution of the virosphere. Here, we present an update of the phage orthologous groups (POGs), a collection of 4,542 clusters of orthologous genes from bacteriophages that now also includes viruses infecting archaea and encompasses more than 1,000 distinct virus genomes. Analysis of this expanded data set shows that the number of POGs keeps growing without saturation and that a substantial majority of the POGs remain specific to viruses, lacking homologues in prokaryotic cells, outside known proviruses. Thus, the great majority of virus genes apparently remains to be discovered. A complementary observation is that numerous viral genomes remain poorly, if at all, covered by POGs. The genome coverage by POGs is expected to increase as more genomes are sequenced. Taxon-specific, single-copy signature genes that are not observed in prokaryotic genomes outside detected proviruses were identified for two-thirds of the 57 taxa (those with genomes available from at least 3 distinct viruses), with half of these present in all members of the respective taxon. These signatures can be used to specifically identify the presence and quantify the abundance of viruses from particular taxa in metagenomic samples and thus gain new insights into the ecology and evolution of viruses in relation to their hosts.
JF  - Journal of Bacteriology
AU  - Kristensen, David M
AU  - Waller, Alison S
AU  - Yamada, Takuji
AU  - Bork, Peer
AU  - Mushegian, Arcady R
AU  - Koonin, Eugene V
AD  - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland, USA, EugeneV.Koonin,koonin{at}ncbi.nlm.nih.gov.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 941
EP  - 950
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 195
IS  - 5
SN  - 0021-9193, 0021-9193
KW  - Virology & AIDS Abstracts; Genetics Abstracts; Water Resources Abstracts; Aqualine Abstracts; Microbiology Abstracts B: Bacteriology
KW  - Abundance
KW  - Genomes
KW  - Archaea
KW  - Viruses
KW  - SW 5040:Data acquisition
KW  - J:02430
KW  - AQ 00005:Underground Services and Water Use
KW  - V:22310
KW  - G:07760
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315624424?accountid=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=Journal+of+Bacteriology&rft.atitle=Orthologous+Gene+Clusters+and+Taxon+Signature+Genes+for+Viruses+of+Prokaryotes&rft.au=Kristensen%2C+David+M%3BWaller%2C+Alison+S%3BYamada%2C+Takuji%3BBork%2C+Peer%3BMushegian%2C+Arcady+R%3BKoonin%2C+Eugene+V&rft.aulast=Kristensen&rft.aufirst=David&rft.date=2013-03-01&rft.volume=195&rft.issue=5&rft.spage=941&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01801-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Genomes; Viruses; Archaea
DO  - http://dx.doi.org/10.1128/JB.01801-12
ER  - 



TY  - JOUR
T1  - Reduction of Cellular Stress by TolC-Dependent Efflux Pumps in Escherichia coli Indicated by BaeSR and CpxARP Activation of spy in Efflux Mutants
AN  - 1315623436; 17709881
AB  - Escherichia coli has nine inner membrane efflux pumps which complex with the outer membrane protein TolC and cognate membrane fusion proteins to form tripartite transperiplasmic pumps with diverse functions, including the expulsion of antibiotics. We recently observed that tolC mutants have elevated activities for three stress response regulators, MarA, SoxS, and Rob, and we suggested that TolC-dependent efflux is required to prevent the accumulation of stressful cellular metabolites. Here, we used spy::lacZ fusions to show that two systems for sensing/repairing extracytoplasmic stress, BaeRS and CpxARP, are activated in the absence of TolC-dependent efflux. In either tolC mutants or bacteria with mutations in the genes for four TolC-dependent efflux pumps, spy expression was increased 6- to 8-fold. spy encodes a periplasmic chaperone regulated by the BaeRS and CpxARP stress response systems. The overexpression of spy in tolC or multiple efflux pump mutants also depended on these systems. spy overexpression was not due to acetate, ethanol, or indole accumulation, since external acetate had only a minor effect on wild-type cells, ethanol had a large effect that was not CpxA dependent, and a tolC tnaA mutant which cannot accumulate internal indole overexpressed spy. We propose that, unless TolC-dependent pumps excrete certain metabolites, the metabolites accumulate and activate at least five different stress response systems.
JF  - Journal of Bacteriology
AU  - Rosner, Judah L
AU  - Martin, Robert G
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 1042
EP  - 1050
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 195
IS  - 5
SN  - 0021-9193, 0021-9193
KW  - Water Resources Abstracts; Aqualine Abstracts; Microbiology Abstracts B: Bacteriology
KW  - Accumulation
KW  - Escherichia coli
KW  - Pumps
KW  - Metabolites
KW  - SW 5010:Network design
KW  - J:02310
KW  - AQ 00008:Effects of Pollution
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315623436?accountid=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=Journal+of+Bacteriology&rft.atitle=Reduction+of+Cellular+Stress+by+TolC-Dependent+Efflux+Pumps+in+Escherichia+coli+Indicated+by+BaeSR+and+CpxARP+Activation+of+spy+in+Efflux+Mutants&rft.au=Rosner%2C+Judah+L%3BMartin%2C+Robert+G&rft.aulast=Rosner&rft.aufirst=Judah&rft.date=2013-03-01&rft.volume=195&rft.issue=5&rft.spage=1042&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01996-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Metabolites; Pumps; Escherichia coli
DO  - http://dx.doi.org/10.1128/JB.01996-12
ER  - 



TY  - JOUR
T1  - Increased cardiovascular risk in association with chronic airflow obstruction among premenopausal rural women of India who cook exclusively with biomass
AN  - 1315621697; 17740061
AB  - We aimed to compare the cardiovascular risk in biomass-using women with or without chronic obstructive pulmonary disease (COPD). A total of 22 biomass-using married women with COPD and 24 matched controls with normal lung function were enrolled for this purpose. Platelet P-selectin (P-sel) expression and platelet-leukocyte aggregation were determined using flow cytometry. Platelet aggregation by collagen was measured by aggregometer. Soluble P-selectin (sP-sel), tumor necrosis factor-alpha (TNF- alpha ), interleukin-8, -6, -10 (IL-8, IL-6, IL-10), neutrophil-activating protein-2 (NAP-2), C-reactive protein (CRP), oxidized low density lipoprotein (oxLDL) in plasma were measured by enzyme-linked immunosorbent assay. Generation of reactive oxygen species (ROS) by leukocytes was measured by flow cytometry, and erythrocyte content of superoxide dismutase (SOD) was measured by spectrophotometry. Particulate matter with a diameter of less than 2.5 mu m (PM sub(2.5)) in indoor air was measured by real-time aerosol monitor. Compared with control, biomass users with COPD had increased expression of platelet P-selectin, elevated levels of sP-sel, oxLDL, TNF- alpha , IL-8, IL-6, NAP-2, CRP, lowered IL-10 and more circulating platelet-neutrophil (p<0.0001) and platelet-monocyte (p<0.0001) aggregates. ROS generation was increased by 19.5% while SOD was depleted by 32% in women with COPD. Biomass smoke-induced COPD is associated with excess cardiovascular risk via oxidative stress, platelet activation, and inflammation.
JF  - Air Quality, Atmosphere and Health
AU  - Dutta, Anindita
AU  - Ray, Manas Ranjan
AU  - Mukherjee, Bidisha
AU  - Chowdhury, Saswati
AD  - Chittaranjan National Cancer Institute, Kolkata, India, anidu14@gmail.com
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 307
EP  - 315
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 6
IS  - 1
SN  - 1873-9318, 1873-9318
KW  - Health & Safety Science Abstracts; Risk Abstracts; Pollution Abstracts; Meteorological & Geoastrophysical Abstracts
KW  - Aerosols
KW  - Atmospheric pollution
KW  - Biomass
KW  - India
KW  - P 0000:AIR POLLUTION
KW  - R2 23060:Medical and environmental health
KW  - M2:551.510.42
KW  - H 0500:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315621697?accountid=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=Air+Quality%2C+Atmosphere+and+Health&rft.atitle=Increased+cardiovascular+risk+in+association+with+chronic+airflow+obstruction+among+premenopausal+rural+women+of+India+who+cook+exclusively+with+biomass&rft.au=Dutta%2C+Anindita%3BRay%2C+Manas+Ranjan%3BMukherjee%2C+Bidisha%3BChowdhury%2C+Saswati&rft.aulast=Dutta&rft.aufirst=Anindita&rft.date=2013-03-01&rft.volume=6&rft.issue=1&rft.spage=307&rft.isbn=&rft.btitle=&rft.title=Air+Quality%2C+Atmosphere+and+Health&rft.issn=18739318&rft_id=info:doi/10.1007%2Fs11869-012-0173-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Atmospheric pollution; Biomass; India
DO  - http://dx.doi.org/10.1007/s11869-012-0173-8
ER  - 



TY  - JOUR
T1  - Chlamydia trachomatis Plasmid-Encoded Pgp4 Is a Transcriptional Regulator of Virulence-Associated Genes
AN  - 1315620871; 17720536
AB  - Chlamydia trachomatis causes chronic inflammatory diseases of the eye and genital tract and has global medical importance. The chlamydial plasmid plays an important role in the pathophysiology of these diseases, as plasmid-deficient organisms are highly attenuated. The cryptic plasmid carries noncoding RNAs and eight conserved open reading frames (ORFs). To understand plasmid gene function, we generated plasmid shuttle vectors with deletions in each of the eight ORFs. The individual deletion mutants were used to transform chlamydiae and the transformants were characterized phenotypically and at the transcriptional level. We show that pgp1, -2, -6, and -8 are essential for plasmid maintenance, while the other ORFs can be deleted and the plasmid stably maintained. We further show that a pgp4 knockout mutant exhibits an in vitro phenotype similar to its isogenic plasmidless strain, in terms of abnormal inclusion morphology and lack of glycogen accumulation. Microarray and qRT-PCR analysis revealed that Pgp4 is a transcriptional regulator of plasmid-encoded pgp3 and multiple chromosomal genes, including the glycogen synthase gene glgA, that are likely important in chlamydial virulence. Our findings have major implications for understanding the plasmid's role in chlamydial pathogenesis at the molecular level.
JF  - Infection and Immunity
AU  - Song, Lihua
AU  - Carlson, John H
AU  - Whitmire, William M
AU  - Kari, Laszlo
AU  - Virtaneva, Kimmo
AU  - Sturdevant, Daniel E
AU  - Watkins, Heather
AU  - Zhou, Bing
AU  - Sturdevant, Gail L
AU  - Porcella, Stephen F
AD  - Laboratory of Intracellular Parasites, HarlanD.Caldwell,hcaldwell{at}niaid.nih.gov.
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 636
EP  - 644
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 3
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Immunology Abstracts
KW  - Deletion mutant
KW  - Eye
KW  - Chlamydia trachomatis
KW  - Medical importance
KW  - Transcription
KW  - Glycogen synthase
KW  - shuttle vectors
KW  - Plasmids
KW  - DNA microarrays
KW  - Glycogen
KW  - Virulence
KW  - Gene deletion
KW  - Inflammatory diseases
KW  - Genital tract
KW  - Open reading frames
KW  - J 02350:Immunology
KW  - F 06910:Microorganisms & Parasites
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315620871?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Chlamydia+trachomatis+Plasmid-Encoded+Pgp4+Is+a+Transcriptional+Regulator+of+Virulence-Associated+Genes&rft.au=Song%2C+Lihua%3BCarlson%2C+John+H%3BWhitmire%2C+William+M%3BKari%2C+Laszlo%3BVirtaneva%2C+Kimmo%3BSturdevant%2C+Daniel+E%3BWatkins%2C+Heather%3BZhou%2C+Bing%3BSturdevant%2C+Gail+L%3BPorcella%2C+Stephen+F&rft.aulast=Song&rft.aufirst=Lihua&rft.date=2013-03-01&rft.volume=81&rft.issue=3&rft.spage=636&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01305-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 53
N1  - Last updated - 2013-07-15
N1  - SubjectsTermNotLitGenreText - Deletion mutant; Eye; Transcription; Medical importance; shuttle vectors; Glycogen synthase; Plasmids; DNA microarrays; Glycogen; Virulence; Gene deletion; Inflammatory diseases; Genital tract; Open reading frames; Chlamydia trachomatis
DO  - http://dx.doi.org/10.1128/IAI.01305-12
ER  - 



TY  - JOUR
T1  - Full-Length Plasmodium falciparum Circumsporozoite Protein Administered with Long-Chain Poly(I.C) or the Toll-Like Receptor 4 Agonist Glucopyranosyl Lipid Adjuvant-Stable Emulsion Elicits Potent Antibody and CD4+ T Cell Immunity and Protection in Mice
AN  - 1315615011; 17720523
AB  - The Plasmodium falciparum circumsporozoite (CS) protein (CSP) is a major vaccine target for preventing malaria infection. Thus, developing strong and durable antibody and T cell responses against CSP with novel immunogens and potent adjuvants may improve upon the success of current approaches. Here, we compare four distinct full-length P. falciparum CS proteins expressed in Escherichia coli or Pichia pastoris for their ability to induce immunity and protection in mice when administered with long-chain poly(I.C) [poly(I.C)LC] as an adjuvant. CS proteins expressed in E. coli induced high-titer antibody responses against the NANP repeat region and potent CSP-specific CD4+ T cell responses. Moreover, E. coli-derived CS proteins in combination with poly(I.C)LC induced potent multifunctional (interleukin 2-positive [IL-2+], tumor necrosis factor alpha-positive [TNF- alpha +], gamma interferon-positive [IFN- gamma +]) CD4+ effector T cell responses in blood, in spleen, and particularly in liver. Using transgenic Plasmodium berghei expressing the repeat region of P. falciparum CSP [Pb-CS(Pf)], we showed that there was a 1- to 4-log decrease in malaria rRNA in the liver following a high-dose challenge and similar to 50% sterilizing protection with a low-dose challenge compared to control levels. Protection was directly correlated with high-level antibody titers but not CD4+ T cell responses. Finally, protective immunity was also induced using the Toll-like receptor 4 agonist glucopyranosyl lipid adjuvant-stable emulsion (GLA-SE) as the adjuvant, which also correlated with high antibody titers yet CD4+ T cell immunity that was significantly less potent than that with poly(I.C)LC. Overall, these data suggest that full-length CS proteins and poly(I.C)LC or GLA-SE offer a simple vaccine formulation to be used alone or in combination with other vaccines for preventing malaria infection.
JF  - Infection and Immunity
AU  - Kastenmueller, Kathrin
AU  - Espinosa, Diego A
AU  - Trager, Lauren
AU  - Stoyanov, Cristina
AU  - Salazar, Andres M
AU  - Pokalwar, Santosh
AU  - Singh, Sanjay
AU  - Dutta, Sheetij
AU  - Ockenhouse, Christian F
AU  - Zavala, Fidel
AD  - Vaccine Research Center and Cellular Immunology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, rseder@mail.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 789
EP  - 800
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 3
SN  - 0019-9567, 0019-9567
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts
KW  - gamma -Interferon
KW  - Parasites
KW  - Human diseases
KW  - Lipids
KW  - Tumor necrosis factor
KW  - Disease control
KW  - Malaria
KW  - Adjuvants
KW  - Infection
KW  - Public health
KW  - circumsporozoite protein
KW  - rRNA
KW  - CD4 antigen
KW  - Escherichia coli
KW  - Lymphocytes T
KW  - TLR4 protein
KW  - Data processing
KW  - Spleen
KW  - Plasmodium falciparum
KW  - Immunity
KW  - Emulsions
KW  - Plasmodium berghei
KW  - Blood
KW  - Antibodies
KW  - Liver
KW  - Vaccines
KW  - Pichia pastoris
KW  - Toll-like receptors
KW  - K 03350:Immunology
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315615011?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Full-Length+Plasmodium+falciparum+Circumsporozoite+Protein+Administered+with+Long-Chain+Poly%28I.C%29+or+the+Toll-Like+Receptor+4+Agonist+Glucopyranosyl+Lipid+Adjuvant-Stable+Emulsion+Elicits+Potent+Antibody+and+CD4%2B+T+Cell+Immunity+and+Protection+in+Mice&rft.au=Kastenmueller%2C+Kathrin%3BEspinosa%2C+Diego+A%3BTrager%2C+Lauren%3BStoyanov%2C+Cristina%3BSalazar%2C+Andres+M%3BPokalwar%2C+Santosh%3BSingh%2C+Sanjay%3BDutta%2C+Sheetij%3BOckenhouse%2C+Christian+F%3BZavala%2C+Fidel&rft.aulast=Kastenmueller&rft.aufirst=Kathrin&rft.date=2013-03-01&rft.volume=81&rft.issue=3&rft.spage=789&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01108-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 71
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Antibodies; Disease control; Malaria; Vaccines; Immunity; Emulsions; Public health; gamma -Interferon; Data processing; Tumor necrosis factor; Lipids; Spleen; Adjuvants; Infection; circumsporozoite protein; Blood; rRNA; CD4 antigen; Lymphocytes T; Liver; TLR4 protein; Toll-like receptors; Escherichia coli; Plasmodium falciparum; Pichia pastoris; Plasmodium berghei
DO  - http://dx.doi.org/10.1128/IAI.01108-12
ER  - 



TY  - JOUR
T1  - Pharmacokinetics of intravenous voriconazole in obese patients: implications of CYP2C19 homozygous poor metabolizer genotype.
AN  - 1314714363; 23400848
AB  - There is a paucity of pharmacokinetic studies describing weight-based dosing of intravenous voriconazole in obese patients. In this case report, we describe the pharmacokinetics of intravenous voriconazole in an obese CYP2C19 homozygous poor metabolizer and review previously reported data regarding the use of intravenous voriconazole in obese patients. A 17-year-old obese Hispanic male patient (body mass index 35 kg/m(2) ) received intravenous voriconazole for the treatment of suspected aspergillosis. After 2.5 days of voriconazole 4 mg/kg intravenously every 12 hours based on adjusted body weight, the voriconazole area under the serum concentration-time curve over the course of a single (12-hr) dosing interval and trough concentration were 86,100 ng · hr/ml and 6.2 µg/ml, respectively. Six days later, the voriconazole dosage was decreased. A trough concentration measured just before the dosage reduction (after 8.5 days of voriconazole 4 mg/kg intravenously every 12 hours based on adjusted body weight) remained elevated at 5.8 µg/ml. Genotyping revealed a CYP2C19 homozygous poor metabolizer (CYP2C19*2/*2). Voriconazole was subsequently discontinued due to QTc prolongation. These data and those from two recent publications suggest that voriconazole does not distribute extensively into human adipose tissue and that obese patients should be dosed on an adjusted body weight basis. If an obese patient dosed on total body weight is also a CYP2C19 poor metabolizer, serum voriconazole concentrations will be further elevated, potentially leading to drug-induced toxicity.
          © 2013 Pharmacotherapy Publications, Inc.
JF  - Pharmacotherapy
AU  - Moriyama, Brad
AU  - Jarosinski, Paul F
AU  - Figg, William D
AU  - Henning, Stacey A
AU  - Danner, Robert L
AU  - Penzak, Scott R
AU  - Wayne, Alan S
AU  - Walsh, Thomas J
AD  - Pharmacy Department, National Institutes of Health Clinical Center, Bethesda, MD 20892, USA. bmoriyama@cc.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - e19
EP  - e22
VL  - 33
IS  - 3
KW  - Antifungal Agents
KW  - 0
KW  - Pyrimidines
KW  - Triazoles
KW  - Aryl Hydrocarbon Hydroxylases
KW  - EC 1.14.14.1
KW  - CYP2C19 protein, human
KW  - Cytochrome P-450 CYP2C19
KW  - Voriconazole
KW  - JFU09I87TR
KW  - Index Medicus
KW  - Aspergillosis -- metabolism
KW  - Drug Administration Schedule
KW  - Injections, Intravenous
KW  - Area Under Curve
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Aspergillosis -- drug therapy
KW  - Body Weight
KW  - Genotype
KW  - Aspergillosis -- complications
KW  - Aspergillosis -- blood
KW  - Adolescent
KW  - Male
KW  - Pyrimidines -- therapeutic use
KW  - Triazoles -- blood
KW  - Pyrimidines -- blood
KW  - Pyrimidines -- administration & dosage
KW  - Antifungal Agents -- blood
KW  - Antifungal Agents -- therapeutic use
KW  - Obesity -- blood
KW  - Obesity -- complications
KW  - Obesity -- metabolism
KW  - Obesity -- enzymology
KW  - Antifungal Agents -- administration & dosage
KW  - Triazoles -- therapeutic use
KW  - Aryl Hydrocarbon Hydroxylases -- genetics
KW  - Triazoles -- administration & dosage
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314714363?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacokinetics+of+intravenous+voriconazole+in+obese+patients%3A+implications+of+CYP2C19+homozygous+poor+metabolizer+genotype.&rft.au=Moriyama%2C+Brad%3BJarosinski%2C+Paul+F%3BFigg%2C+William+D%3BHenning%2C+Stacey+A%3BDanner%2C+Robert+L%3BPenzak%2C+Scott+R%3BWayne%2C+Alan+S%3BWalsh%2C+Thomas+J&rft.aulast=Moriyama&rft.aufirst=Brad&rft.date=2013-03-01&rft.volume=33&rft.issue=3&rft.spage=e19&rft.isbn=&rft.btitle=&rft.title=Pharmacotherapy&rft.issn=1875-9114&rft_id=info:doi/10.1002%2Fphar.1192
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-23
N1  - Date created - 2013-03-04
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Mol Diagn Ther. 2006;10(3):135-51 [16771600]
J Clin Pharmacol. 2012 Feb;52(2):195-203 [21383338]
Ther Drug Monit. 2008 Apr;30(2):167-72 [18367976]
Pharmacogenomics. 2008 May;9(5):561-84 [18466103]
J Clin Pharmacol. 2009 Feb;49(2):196-204 [19033450]
Ann Pharmacother. 2009 Apr;43(4):726-31 [19299322]
Antimicrob Agents Chemother. 2011 Jun;55(6):2601-5 [21422207]
Pharmacogenomics. 2011 Jun;12(6):861-72 [21692616]
Clin Infect Dis. 2011 Oct;53(7):745 [21846833]
Mycoses. 2011 Nov;54(6):e877-9 [21615537]
JAMA. 2012 Feb 1;307(5):491-7 [22253363]
JAMA. 2012 Feb 1;307(5):483-90 [22253364]
Clin Infect Dis. 2012 Aug;55(3):391-3 [22610924]
Clin Infect Dis. 2012 Aug;55(3):381-90 [22610925]
Pharmacotherapy. 2007 Aug;27(8):1081-91 [17655508]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1002/phar.1192
ER  - 



TY  - JOUR
T1  - Increased cancer burden among pesticide applicators and others due to pesticide exposure.
AN  - 1314709101; 23322675
AB  - A growing number of well-designed epidemiological and molecular studies provide substantial evidence that the pesticides used in agricultural, commercial, and home and garden applications are associated with excess cancer risk. This risk is associated both with those applying the pesticide and, under some conditions, those who are simply bystanders to the application. In this article, the epidemiological, molecular biology, and toxicological evidence emerging from recent literature assessing the link between specific pesticides and several cancers including prostate cancer, non-Hodgkin lymphoma, leukemia, multiple myeloma, and breast cancer are integrated. Although the review is not exhaustive in its scope or depth, the literature does strongly suggest that the public health problem is real. If we are to avoid the introduction of harmful chemicals into the environment in the future, the integrated efforts of molecular biology, pesticide toxicology, and epidemiology are needed to help identify the human carcinogens and thereby improve our understanding of human carcinogenicity and reduce cancer risk. Copyright © 2013 American Cancer Society, Inc.
JF  - CA: a cancer journal for clinicians
AU  - Alavanja, Michael C R
AU  - Ross, Matthew K
AU  - Bonner, Matthew R
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, North Bethesda, MD 20892, USA. alavanjm@mail.nih.gov
PY  - 2013
SP  - 120
EP  - 142
VL  - 63
IS  - 2
KW  - Carcinogens
KW  - 0
KW  - Carcinogens, Environmental
KW  - Pesticides
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Public Health
KW  - Risk Factors
KW  - Humans
KW  - Carcinogens, Environmental -- toxicity
KW  - Male
KW  - Female
KW  - Occupational Exposure -- statistics & numerical data
KW  - Environmental Exposure -- statistics & numerical data
KW  - Neoplasms -- chemically induced
KW  - Neoplasms -- epidemiology
KW  - Carcinogens -- toxicity
KW  - Pesticides -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314709101?accountid=14244
L2  - http://onlinelibrary.wiley.com/doi/10.3322/caac.21170/full
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-17
N1  - Date created - 2013-03-04
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Comment In:
CA Cancer J Clin. 2013 Sep;63(5):366-7 [23722636]
CA Cancer J Clin. 2013 Sep;63(5):364-6 [23722713]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.3322/caac.21170
ER  - 



TY  - JOUR
T1  - Inhibition of radiation-induced skin fibrosis with imatinib.
AN  - 1314705346; 23083077
AB  - Dermal fibrosis is a disabling late toxicity of radiotherapy. Several lines of evidence suggest that overactive signaling via the Platelet-derived growth factor receptor-beta (PDGFR-β) and V-abl Abelson murine leukemia viral oncogene homolog 1 (cAbl) may be etiologic factors in the development of radiation-induced fibrosis. We tested the hypothesis that imatinib, a clinically available inhibitor of PDGFR-β, Mast/stem cell growth factor receptor (c-kit) and cAbl, would reduce the severity of dermal fibrosis in a murine model.
          The right hind legs of female C3H/HeN mice were exposed to 35 Gy of X-rays. Cohorts of mice were maintained on chow formulated with imatinib 0.5 mg/g or control chow for the duration of the experiment. Bilateral hind limb extension was measured serially to assess fibrotic contracture. Immunohistochemistry and biochemical assays were used to evaluate the levels of collagen and cytokines implicated in radiation-induced fibrosis. Imatinib treatment significantly reduced hind limb contracture and dermal thickness after irradiation. Immunohistochemical studies demonstrated a substantial reduction in PDGFR-β phosphorylation. We also observed reduced Transforming Growth factor-β (TGF-β) and collagen expression in irradiated skin of imatinib-treated mice, suggesting that imatinib may suppress the fibrotic process by interrupting cross-talk between these pathways.
          Taken together, these results support that imatinib may be a useful agent in the prevention and treatment of radiation-induced dermal fibrosis.
JF  - International journal of radiation biology
AU  - Horton, Jason A
AU  - Chung, Eun Joo
AU  - Hudak, Kathryn E
AU  - Sowers, Anastasia
AU  - Thetford, Angela
AU  - White, Ayla O
AU  - Mitchell, James B
AU  - Citrin, Deborah E
AD  - Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 162
EP  - 170
VL  - 89
IS  - 3
KW  - Benzamides
KW  - 0
KW  - Piperazines
KW  - Pyrimidines
KW  - Radiation-Protective Agents
KW  - Transforming Growth Factor beta1
KW  - Imatinib Mesylate
KW  - 8A1O1M485B
KW  - Proto-Oncogene Proteins c-kit
KW  - EC 2.7.10.1
KW  - Receptor, Platelet-Derived Growth Factor beta
KW  - Proto-Oncogene Proteins c-abl
KW  - EC 2.7.10.2
KW  - Index Medicus
KW  - Space life sciences
KW  - Animals
KW  - Transforming Growth Factor beta1 -- metabolism
KW  - Fibrosis
KW  - Receptor, Platelet-Derived Growth Factor beta -- metabolism
KW  - Mice
KW  - Radiation-Protective Agents -- pharmacology
KW  - Signal Transduction -- radiation effects
KW  - Proto-Oncogene Proteins c-abl -- antagonists & inhibitors
KW  - Phosphorylation
KW  - Signal Transduction -- drug effects
KW  - Mice, Inbred C3H
KW  - Proto-Oncogene Proteins c-kit -- antagonists & inhibitors
KW  - Female
KW  - Receptor, Platelet-Derived Growth Factor beta -- antagonists & inhibitors
KW  - Radiation Injuries, Experimental -- pathology
KW  - Radiation Injuries, Experimental -- metabolism
KW  - Skin -- radiation effects
KW  - Skin -- drug effects
KW  - Skin -- metabolism
KW  - Skin -- pathology
KW  - Pyrimidines -- pharmacology
KW  - Piperazines -- pharmacology
KW  - Radiation Injuries, Experimental -- prevention & control
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314705346?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+biology&rft.atitle=Inhibition+of+radiation-induced+skin+fibrosis+with+imatinib.&rft.au=Horton%2C+Jason+A%3BChung%2C+Eun+Joo%3BHudak%2C+Kathryn+E%3BSowers%2C+Anastasia%3BThetford%2C+Angela%3BWhite%2C+Ayla+O%3BMitchell%2C+James+B%3BCitrin%2C+Deborah+E&rft.aulast=Horton&rft.aufirst=Jason&rft.date=2013-03-01&rft.volume=89&rft.issue=3&rft.spage=162&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+biology&rft.issn=1362-3095&rft_id=info:doi/10.3109%2F09553002.2013.741281
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-24
N1  - Date created - 2013-03-04
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.3109/09553002.2013.741281
ER  - 



TY  - JOUR
T1  - Refocusing the responsiveness requirement
AN  - 1314699895; 4412688
AB  - Many guidelines for international research require that studies be responsive to host community health needs or health priorities. Although responsiveness possesses great intuitive and rhetorical appeal, existing conceptions are confusing and difficult to apply. Not only are there few examples of what research the responsiveness requirement permits and what it rejects, but its application can lead to contradictory results. Because of the practical difficulties in applying responsiveness and the danger that misapplying responsiveness could harm the interests of developing countries, we argue that responsiveness should be refocused in three ways: in terms of (1) who enforces it, (2) under what standard, and (3) in what cases. We conclude that responsiveness should be applied by host country officials at the policy level with the exercise of judgment when externally funded research threatens to displace scarce local resources. Reprinted by permission of Blackwell Publishers
JF  - Bioethics
AU  - Emanuel, Ezekiel
AU  - Shah, Seema
AU  - Wolitz, Rebecca
AD  - National Institutes of Health ; Yale University
Y1  - 2013/03//
PY  - 2013
DA  - Mar 2013
SP  - 151
EP  - 159
VL  - 27
IS  - 3
SN  - 0269-9702, 0269-9702
KW  - Sociology
KW  - Bioethics
KW  - Developing countries
KW  - Judgement
KW  - Public health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314699895?accountid=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=Bioethics&rft.atitle=Refocusing+the+responsiveness+requirement&rft.au=Emanuel%2C+Ezekiel%3BShah%2C+Seema%3BWolitz%2C+Rebecca&rft.aulast=Emanuel&rft.aufirst=Ezekiel&rft.date=2013-03-01&rft.volume=27&rft.issue=3&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Bioethics&rft.issn=02699702&rft_id=info:doi/10.1111%2Fj.1467-8519.2011.01903.x
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 1603 4408 8282 8281 6085; 10449 5772; 3480 2958 12092; 7007 3322 6071 1542 11325 4551
DO  - http://dx.doi.org/10.1111/j.1467-8519.2011.01903.x
ER  - 



TY  - JOUR
T1  - A coordinated proteomic approach for identifying proteins that interact with the E. coli ribosomal protein S12.
AN  - 1314338052; 23305560
AB  - The bacterial ribosomal protein S12 contains a universally conserved D88 residue on a loop region thought to be critically involved in translation due to its proximal location to the A site of the 30S subunit. While D88 mutants are lethal this residue has been found to be post-translationally modified to β-methylthioaspartic acid, a post-translational modification (PTM) identified in S12 orthologs from several phylogenetically distinct bacteria. In a previous report focused on characterizing this PTM, our results provided evidence that this conserved loop region might be involved in forming multiple proteins-protein interactions ( Strader , M. B. ; Costantino , N. ; Elkins , C. A. ; Chen , C. Y. ; Patel , I. ; Makusky , A. J. ; Choy , J. S. ; Court , D. L. ; Markey , S. P. ; Kowalak , J. A. A proteomic and transcriptomic approach reveals new insight into betamethylthiolation of Escherichia coli ribosomal protein S12. Mol. Cell. Proteomics 2011 , 10 , M110 005199 ). To follow-up on this study, the D88 containing loop was probed to identify candidate binders employing a two-step complementary affinity purification strategy. The first involved an endogenously expressed S12 protein containing a C-terminal tag for capturing S12 binding partners. The second strategy utilized a synthetic biotinylated peptide representing the D88 conserved loop region for capturing S12 loop interaction partners. Captured proteins from both approaches were detected by utilizing SDS-PAGE and one-dimensional liquid chromatography-tandem mass spectrometry. The results presented in this report revealed proteins that form direct interactions with the 30S subunit and elucidated which are likely to interact with S12. In addition, we provide evidence that two proteins involved in regulating ribosome and/or mRNA transcript levels under stress conditions, RNase R and Hfq, form direct interactions with the S12 conserved loop, suggesting that it is likely part of a protein binding interface.
JF  - Journal of proteome research
AU  - Strader, Michael Brad
AU  - Hervey, William Judson
AU  - Costantino, Nina
AU  - Fujigaki, Suwako
AU  - Chen, Cai Yun
AU  - Akal-Strader, Ayca
AU  - Ihunnah, Chibueze A
AU  - Makusky, Anthony J
AU  - Court, Donald L
AU  - Markey, Sanford P
AU  - Kowalak, Jeffrey A
AD  - Laboratory of Neurotoxicology, National Institute of Mental Health , Bethesda, Maryland 20892, United States.
Y1  - 2013/03/01/
PY  - 2013
DA  - 2013 Mar 01
SP  - 1289
EP  - 1299
VL  - 12
IS  - 3
KW  - Escherichia coli Proteins
KW  - 0
KW  - Ribosomal Proteins
KW  - ribosomal protein S12
KW  - Index Medicus
KW  - Electrophoresis, Polyacrylamide Gel
KW  - Molecular Sequence Data
KW  - Chromatography, Liquid
KW  - Amino Acid Sequence
KW  - Tandem Mass Spectrometry
KW  - Protein Binding
KW  - Escherichia coli Proteins -- chemistry
KW  - Escherichia coli Proteins -- metabolism
KW  - Ribosomal Proteins -- metabolism
KW  - Ribosomal Proteins -- chemistry
KW  - Proteomics
KW  - Escherichia coli Proteins -- isolation & purification
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314338052?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+proteome+research&rft.atitle=A+coordinated+proteomic+approach+for+identifying+proteins+that+interact+with+the+E.+coli+ribosomal+protein+S12.&rft.au=Strader%2C+Michael+Brad%3BHervey%2C+William+Judson%3BCostantino%2C+Nina%3BFujigaki%2C+Suwako%3BChen%2C+Cai+Yun%3BAkal-Strader%2C+Ayca%3BIhunnah%2C+Chibueze+A%3BMakusky%2C+Anthony+J%3BCourt%2C+Donald+L%3BMarkey%2C+Sanford+P%3BKowalak%2C+Jeffrey+A&rft.aulast=Strader&rft.aufirst=Michael&rft.date=2013-03-01&rft.volume=12&rft.issue=3&rft.spage=1289&rft.isbn=&rft.btitle=&rft.title=Journal+of+proteome+research&rft.issn=1535-3907&rft_id=info:doi/10.1021%2Fpr3009435
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-29
N1  - Date created - 2013-03-01
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1021/pr3009435
ER  - 



TY  - JOUR
T1  - Mrp1 is essential for sphingolipid signaling to p-glycoprotein in mouse blood-brain and blood-spinal cord barriers.
AN  - 1314338032; 23168528
AB  - At the blood-brain and blood-spinal cord barriers, P-glycoprotein, an ATP-driven drug efflux pump, is a major obstacle to central nervous system (CNS) pharmacotherapy. Recently, we showed that signaling through tumor necrosis factor-α (TNF-α), sphingolipids, and sphingosine-1-phosphate receptor 1 (S1PR1) rapidly and reversibly reduced basal P-glycoprotein transport activity in the rat blood-brain barrier. The present study extends those findings to the mouse blood-brain and blood-spinal cord barriers and, importantly, identifies multidrug resistance-associated protein 1 (Mrp1, Abcc1) as the transporter that mediates S1P efflux from brain and spinal cord endothelial cells. In brain and spinal cord capillaries isolated from wild-type mice, TNF-α, sphingosine, S1P, the S1PR agonist fingolimod (FTY720), and its active, phosphorylated metabolite, FTY720P, reduced P-glycoprotein transport activity; these effects were abolished by a specific S1PR1 antagonist. In brain and spinal cord capillaries isolated from Mrp1-null mice, neither TNF-α nor sphingosine nor FTY720 reduced P-glycoprotein transport activity. However, S1P and FTY720P had the same S1PR1-dependent effects on transport activity as in capillaries from wild-type mice. Thus, deletion of Mrp1 alone terminated endogenous signaling to S1PR1. These results identify Mrp1 as the transporter essential for S1P efflux from the endothelial cells and thus for inside-out S1P signaling to P-glycoprotein at the blood-brain and blood-spinal cord barriers.
JF  - Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
AU  - Cartwright, Tara A
AU  - Campos, Christopher R
AU  - Cannon, Ronald E
AU  - Miller, David S
AD  - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 381
EP  - 388
VL  - 33
IS  - 3
KW  - Immunosuppressive Agents
KW  - 0
KW  - Lysophospholipids
KW  - Multidrug Resistance-Associated Proteins
KW  - Nerve Tissue Proteins
KW  - P-Glycoprotein
KW  - Propylene Glycols
KW  - Receptors, Lysosphingolipid
KW  - S1pr1 protein, mouse
KW  - Sphingolipids
KW  - Tumor Necrosis Factor-alpha
KW  - sphingosine 1-phosphate
KW  - 26993-30-6
KW  - Fingolimod Hydrochloride
KW  - G926EC510T
KW  - Sphingosine
KW  - NGZ37HRE42
KW  - multidrug resistance-associated protein 1
KW  - Y49M64GZ4Q
KW  - Index Medicus
KW  - Propylene Glycols -- pharmacology
KW  - Receptors, Lysosphingolipid -- genetics
KW  - Animals
KW  - Biological Transport, Active -- physiology
KW  - Receptors, Lysosphingolipid -- metabolism
KW  - Mice
KW  - Tumor Necrosis Factor-alpha -- genetics
KW  - Immunosuppressive Agents -- pharmacology
KW  - Mice, Knockout
KW  - Biological Transport, Active -- drug effects
KW  - Tumor Necrosis Factor-alpha -- metabolism
KW  - Capillaries -- metabolism
KW  - Endothelial Cells -- metabolism
KW  - Receptors, Lysosphingolipid -- antagonists & inhibitors
KW  - Spinal Cord -- metabolism
KW  - Sphingosine -- metabolism
KW  - Blood-Brain Barrier -- metabolism
KW  - Nerve Tissue Proteins -- genetics
KW  - Sphingolipids -- genetics
KW  - Sphingosine -- genetics
KW  - Lysophospholipids -- genetics
KW  - Signal Transduction -- physiology
KW  - P-Glycoprotein -- genetics
KW  - P-Glycoprotein -- metabolism
KW  - Multidrug Resistance-Associated Proteins -- genetics
KW  - Multidrug Resistance-Associated Proteins -- metabolism
KW  - Signal Transduction -- drug effects
KW  - Lysophospholipids -- metabolism
KW  - Nerve Tissue Proteins -- metabolism
KW  - Sphingosine -- pharmacology
KW  - Sphingosine -- analogs & derivatives
KW  - Sphingolipids -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314338032?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cerebral+blood+flow+and+metabolism+%3A+official+journal+of+the+International+Society+of+Cerebral+Blood+Flow+and+Metabolism&rft.atitle=Mrp1+is+essential+for+sphingolipid+signaling+to+p-glycoprotein+in+mouse+blood-brain+and+blood-spinal+cord+barriers.&rft.au=Cartwright%2C+Tara+A%3BCampos%2C+Christopher+R%3BCannon%2C+Ronald+E%3BMiller%2C+David+S&rft.aulast=Cartwright&rft.aufirst=Tara&rft.date=2013-03-01&rft.volume=33&rft.issue=3&rft.spage=381&rft.isbn=&rft.btitle=&rft.title=Journal+of+cerebral+blood+flow+and+metabolism+%3A+official+journal+of+the+International+Society+of+Cerebral+Blood+Flow+and+Metabolism&rft.issn=1559-7016&rft_id=info:doi/10.1038%2Fjcbfm.2012.174
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-19
N1  - Date created - 2013-03-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Science. 2009 Sep 4;325(5945):1254-7 [19729656]
Science. 2009 Jan 23;323(5913):524-7 [19074308]
J Cereb Blood Flow Metab. 2010 Jul;30(7):1373-83 [20197783]
J Pharmacol Exp Ther. 2010 Aug;334(2):467-76 [20460386]
J Cereb Blood Flow Metab. 2010 Sep;30(9):1593-7 [20628400]
J Biol Chem. 2011 Jan 21;286(3):1758-66 [21084291]
Nat Rev Neurosci. 2011 Mar;12(3):169-82 [21331083]
Nat Rev Immunol. 2011 Jun;11(6):403-15 [21546914]
Acta Neuropathol. 2011 Jul;122(1):1-9 [21656168]
Essays Biochem. 2011 Sep 7;50(1):179-207 [21967058]
Lancet Neurol. 2011 Nov;10(11):1026-34 [22014437]
Arterioscler Thromb Vasc Biol. 2011 Dec;31(12):e107-15 [21940944]
J Clin Invest. 2012 Apr;122(4):1416-26 [22406534]
J Cereb Blood Flow Metab. 2012 Aug;32(8):1559-66 [22472606]
J Neurochem. 2012 Sep;122(5):962-75 [22716933]
Proc Natl Acad Sci U S A. 2012 Sep 25;109(39):15930-5 [22949658]
Biochim Biophys Acta. 2009 Jul;1791(7):692-6 [19268560]
Nat Rev Mol Cell Biol. 2003 May;4(5):397-407 [12728273]
FEBS Lett. 2003 Nov 20;554(3):443-9 [14623109]
Brain Res. 2004 Aug 20;1018(1):1-9 [15262198]
Mol Pharmacol. 2004 Sep;66(3):387-94 [15322229]
Am J Physiol. 1995 Jan;268(1 Pt 2):F46-52 [7840247]
Nat Med. 1997 Nov;3(11):1275-9 [9359705]
J Biol Chem. 2005 Oct 28;280(43):36318-25 [16103110]
Mol Pharmacol. 2006 Feb;69(2):462-70 [16278373]
Pharmacol Rev. 2006 Jun;58(2):140-61 [16714484]
Physiol Rev. 2006 Jul;86(3):849-99 [16816140]
Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16394-9 [17050692]
Brain. 2008 Oct;131(Pt 10):2679-89 [18796513]
Trends Pharmacol Sci. 2010 Jun;31(6):246-54 [20417575]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/jcbfm.2012.174
ER  - 



TY  - JOUR
T1  - Safety and feasibility of targeted agent combinations in solid tumours.
AN  - 1314332454; 23358316
AB  - The plethora of novel molecular-targeted agents (MTAs) has provided an opportunity to selectively target pathways involved in carcinogenesis and tumour progression. Combination strategies of MTAs are being used to inhibit multiple aberrant pathways in the hope of optimizing antitumour efficacy and to prevent development of resistance. While the selection of specific agents in a given combination has been based on biological considerations (including the role of the putative targets in cancer) and the interactions of the agents used in combination, there has been little exploration of the possible enhanced toxicity of combinations resulting from alterations in multiple signalling pathways in normal cell biology. Owing to the complex networks and crosstalk that govern normal and tumour cell proliferation, inhibiting multiple pathways with MTA combinations can result in unpredictable disturbances in normal physiology. This Review focuses on the main toxicities and the lack of tolerability of some common MTA combinations, particularly where evidence of enhanced toxicity compared to either agent alone is documented or there is development of unexpected toxicity. Toxicities caused by MTA combinations highlight the need to introduce new preclinical testing paradigms early in the drug development process for the assessment of chronic toxicities resulting from such combinations.
JF  - Nature reviews. Clinical oncology
AU  - Park, Sook Ryun
AU  - Davis, Myrtle
AU  - Doroshow, James H
AU  - Kummar, Shivaani
AD  - Division of Cancer Treatment and Diagnosis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 31, Room 3A44, 31 Center Drive, Bethesda, MD 20892, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 154
EP  - 168
VL  - 10
IS  - 3
KW  - Angiogenesis Inhibitors
KW  - 0
KW  - Biomarkers
KW  - Neoplasm Proteins
KW  - Protein Kinase Inhibitors
KW  - VEGFA protein, human
KW  - Vascular Endothelial Growth Factor A
KW  - MTOR protein, human
KW  - EC 2.7.1.1
KW  - TOR Serine-Threonine Kinases
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  - Animals
KW  - Drug Interactions
KW  - Receptor, Epidermal Growth Factor -- antagonists & inhibitors
KW  - Neoplasm Proteins -- antagonists & inhibitors
KW  - Receptor, ErbB-2 -- antagonists & inhibitors
KW  - Humans
KW  - Cardiovascular Diseases -- chemically induced
KW  - Angiogenesis Inhibitors -- pharmacology
KW  - Feasibility Studies
KW  - Neoplasm Proteins -- physiology
KW  - Drug Monitoring
KW  - Angiogenesis Inhibitors -- adverse effects
KW  - Forecasting
KW  - Drug Synergism
KW  - Drug Screening Assays, Antitumor
KW  - TOR Serine-Threonine Kinases -- antagonists & inhibitors
KW  - Protein Kinase Inhibitors -- pharmacology
KW  - Protein Kinase Inhibitors -- administration & dosage
KW  - Gastrointestinal Diseases -- chemically induced
KW  - Angiogenesis Inhibitors -- administration & dosage
KW  - Vascular Endothelial Growth Factor A -- antagonists & inhibitors
KW  - Hematologic Diseases -- chemically induced
KW  - Protein Kinase Inhibitors -- adverse effects
KW  - Clinical Trials, Phase I as Topic
KW  - Signal Transduction -- drug effects
KW  - Neoplasms -- drug therapy
KW  - Molecular Targeted Therapy
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/1314332454?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IDEAS+Working+Paper+Series+from+RePEc&rft.atitle=Economic+Integration+and+Openness+in+Europe+and+East+Asia&rft.au=Barrell%2C+Ray%3BChoy%2C+Amanda&rft.aulast=Barrell&rft.aufirst=Ray&rft.date=2003-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=IDEAS+Working+Paper+Series+from+RePEc&rft.issn=&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-12
N1  - Date created - 2013-02-28
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1038/nrclinonc.2012.245
ER  - 



TY  - JOUR
T1  - Stable isotope- and mass spectrometry-based metabolomics as tools in drug metabolism: a study expanding tempol pharmacology.
AN  - 1314322302; 23301521
AB  - The application of mass spectrometry-based metabolomics in the field of drug metabolism has yielded important insights not only into the metabolic routes of drugs but has provided unbiased, global perspectives of the endogenous metabolome that can be useful for identifying biomarkers associated with mechanism of action, efficacy, and toxicity. In this report, a stable isotope- and mass spectrometry-based metabolomics approach that captures both drug metabolism and changes in the endogenous metabolome in a single experiment is described. Here the antioxidant drug tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) was chosen because its mechanism of action is not completely understood and its metabolic fate has not been studied extensively. Furthermore, its small size (MW = 172.2) and chemical composition (C(9)H(18)NO(2)) make it challenging to distinguish from endogenous metabolites. In this study, mice were dosed with tempol or deuterated tempol (C(9)D(17)HNO(2)) and their urine was profiled using ultraperformance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry. Principal component analysis of the urinary metabolomics data generated a Y-shaped scatter plot containing drug metabolites (protonated and deuterated) that were clearly distinct from the endogenous metabolites. Ten tempol drug metabolites, including eight novel metabolites, were identified. Phase II metabolism was the major metabolic pathway of tempol in vivo, including glucuronidation and glucosidation. Urinary endogenous metabolites significantly elevated by tempol treatment included 2,8-dihydroxyquinoline (8.0-fold, P < 0.05) and 2,8-dihydroxyquinoline-β-d-glucuronide (6.8-fold, P < 0.05). Urinary endogenous metabolites significantly attenuated by tempol treatment including pantothenic acid (1.3-fold, P < 0.05) and isobutrylcarnitine (5.3-fold, P < 0.01). This study underscores the power of a stable isotope- and mass spectrometry-based metabolomics in expanding the view of drug pharmacology.
JF  - Journal of proteome research
AU  - Li, Fei
AU  - Pang, Xiaoyan
AU  - Krausz, Kristopher W
AU  - Jiang, Changtao
AU  - Chen, Chi
AU  - Cook, John A
AU  - Krishna, Murali C
AU  - Mitchell, James B
AU  - Gonzalez, Frank J
AU  - Patterson, Andrew D
AD  - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, United States.
Y1  - 2013/03/01/
PY  - 2013
DA  - 2013 Mar 01
SP  - 1369
EP  - 1376
VL  - 12
IS  - 3
KW  - Cyclic N-Oxides
KW  - 0
KW  - Isotopes
KW  - Spin Labels
KW  - tempol
KW  - U78ZX2F65X
KW  - Index Medicus
KW  - Animals
KW  - Principal Component Analysis
KW  - Mice, Inbred C57BL
KW  - Mice
KW  - Male
KW  - Cyclic N-Oxides -- urine
KW  - Cyclic N-Oxides -- pharmacology
KW  - Metabolomics
KW  - Cyclic N-Oxides -- pharmacokinetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1314322302?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+proteome+research&rft.atitle=Stable+isotope-+and+mass+spectrometry-based+metabolomics+as+tools+in+drug+metabolism%3A+a+study+expanding+tempol+pharmacology.&rft.au=Li%2C+Fei%3BPang%2C+Xiaoyan%3BKrausz%2C+Kristopher+W%3BJiang%2C+Changtao%3BChen%2C+Chi%3BCook%2C+John+A%3BKrishna%2C+Murali+C%3BMitchell%2C+James+B%3BGonzalez%2C+Frank+J%3BPatterson%2C+Andrew+D&rft.aulast=Li&rft.aufirst=Fei&rft.date=2013-03-01&rft.volume=12&rft.issue=3&rft.spage=1369&rft.isbn=&rft.btitle=&rft.title=Journal+of+proteome+research&rft.issn=1535-3907&rft_id=info:doi/10.1021%2Fpr301023x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-29
N1  - Date created - 2013-03-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Expert Opin Drug Metab Toxicol. 2005 Aug;1(2):303-24 [16922645]
Ther Drug Monit. 2005 Dec;27(6):747-51 [16404815]
Rapid Commun Mass Spectrom. 2007;21(7):1093-9 [17318924]
BMC Bioinformatics. 2007;8:105 [17389044]
Free Radic Biol Med. 2007 Jun 1;42(11):1632-50 [17462532]
Am J Physiol Heart Circ Physiol. 2007 May;292(5):H2073-82 [17237245]
Mol Endocrinol. 2007 Sep;21(9):2136-51 [17550978]
Drug Metab Rev. 2007;39(2-3):581-97 [17786640]
J Biol Chem. 2008 Feb 22;283(8):4543-59 [18093979]
J Proteome Res. 2008 Jun;7(6):2388-98 [18484765]
Anal Chem. 2008 Sep 15;80(18):6835-44 [18700783]
Rapid Commun Mass Spectrom. 2008 Nov;22(22):3693-9 [18951414]
Pharmacol Rev. 2008 Dec;60(4):418-69 [19112152]
Anal Bioanal Chem. 2009 Mar;393(6-7):1607-17 [19183967]
Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3354-9 [19208810]
Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3698-703 [19234110]
Br J Clin Pharmacol. 2009 Apr;67(4):445-54 [19371318]
Chem Res Toxicol. 2009 Apr;22(4):699-707 [19256530]
J Proteome Res. 2009 Sep;8(9):4293-300 [19569716]
Obesity (Silver Spring). 2009 Nov;17(11):1994-2002 [19424163]
J Clin Invest. 2010 Jan;120(1):142-56 [20038799]
Pharmacol Ther. 2010 May;126(2):119-45 [20153367]
Mass Spectrom Rev. 2010 May-Jun;29(3):503-21 [19890938]
Chem Res Toxicol. 2010 May 17;23(5):851-60 [20232918]
Biochem Pharmacol. 2010 Oct 1;80(7):1063-74 [20541539]
Biochem Pharmacol. 2011 Apr 15;81(8):1043-53 [21300029]
Drug Metab Dispos. 2012 Mar;40(3):625-34 [22190693]
J Biol Chem. 2012 Feb 24;287(9):6336-49 [22228769]
Biochem Pharmacol. 2012 May 15;83(10):1435-44 [22387617]
J Biol Chem. 2012 Jul 13;287(29):24784-94 [22619174]
J Lipid Res. 2012 Aug;53(8):1625-35 [22665165]
Free Radic Biol Med. 2003 Jan 1;34(1):93-102 [12498984]
Curr Mol Med. 2003 Sep;3(6):561-72 [14527087]
Curr Pharm Des. 2004;10(13):1439-55 [15134568]
Hum Mol Genet. 2004 Aug 15;13(16):1793-802 [15213104]
Proc Nutr Soc. 2004 May;63(2):323-30 [15294050]
Appl Environ Microbiol. 1986 Jun;51(6):1332-42 [3089153]
Hepatology. 1988 Jan-Feb;8(1):116-24 [3338698]
Biochem Pharmacol. 1989 Aug 15;38(16):2581-6 [2764982]
Microbios. 1989;59(238):47-63 [2770558]
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5537-41 [1319064]
J Med Chem. 1998 Aug 27;41(18):3477-92 [9719601]
Free Radic Biol Med. 1999 Apr;26(7-8):850-7 [10232828]
Prostate Cancer Prostatic Dis. 2006;9(3):230-4 [16683009]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1021/pr301023x
ER  - 



TY  - JOUR
T1  - The adoptive transfer of cultured T cells for patients with metastatic melanoma.
AN  - 1312838229; 23438384
AB  - T cells have been shown to be capable of rejecting a patient's tumor. Weak responses to current vaccines and the toxicity of exogenously administered cytokines limit the intensity of the T-cell response that can be actively generated in vivo. Adoptive T-cell transfer enhances an intrinsically weak immune response to cancer by activating and expanding tumor reactive T cells in vitro and manipulating the environment of the host at the time of transfer. One can frequently find tumor-reactive T cells in metastatic lesions in patients with melanoma, and expand them in vitro for readministration. When successful, this adoptive cellular immunotherapy has resulted in sustainable curative outcomes. Subsequently, the applicability of adoptive T-cell transfer has been greatly expanded by the development of methods to genetically engineer open-repertoire human T-cells to confer tumor reactivity. This re-direction of T-cell specificity can be achieved by introducing a variety of receptors that ligate tumor-associated antigens and then trigger the normal activation mechanism of T cells. Future T-cell engineering will add a new dimension by reprogramming T-cell functions for optimal tumor rejection. The antigens recognized by T cells, the techniques to procure and grow tumor reactive T cells, the conditioning of the recipient to optimize efficacy, and the results of clinical protocols are reviewed herein.
          Published by Elsevier Inc.
JF  - Clinics in dermatology
AU  - Yang, James C
AD  - Surgery Branch, Center for Clinical Research, National Cancer Institute, Building 10A, Rm 3-5952, Bethesda, MD 20892, USA. james_yang@nih.gov
PY  - 2013
SP  - 209
EP  - 219
VL  - 31
IS  - 2
KW  - Antigens, Neoplasm
KW  - 0
KW  - Index Medicus
KW  - Animals
KW  - Lymphocytes, Tumor-Infiltrating -- immunology
KW  - Humans
KW  - Clinical Trials as Topic
KW  - Cells, Cultured -- immunology
KW  - Mice
KW  - Skin Neoplasms -- immunology
KW  - Immunotherapy, Adoptive
KW  - Skin Neoplasms -- therapy
KW  - Melanoma -- therapy
KW  - Melanoma -- immunology
KW  - Antigens, Neoplasm -- immunology
KW  - T-Lymphocytes -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312838229?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinics+in+dermatology&rft.atitle=The+adoptive+transfer+of+cultured+T+cells+for+patients+with+metastatic+melanoma.&rft.au=Yang%2C+James+C&rft.aulast=Yang&rft.aufirst=James&rft.date=2013-03-01&rft.volume=31&rft.issue=2&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Clinics+in+dermatology&rft.issn=1879-1131&rft_id=info:doi/10.1016%2Fj.clindermatol.2012.08.019
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-08
N1  - Date created - 2013-02-26
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.clindermatol.2012.08.019
ER  - 



TY  - JOUR
T1  - The feline calicivirus leader of the capsid protein is associated with cytopathic effect.
AN  - 1312660816; 23269802
AB  - Open reading frame 2 (ORF2) of the feline calicivirus (FCV) genome encodes a capsid precursor that is posttranslationally processed to release the mature capsid protein (VP1) and a small protein of 124 amino acids, designated the leader of the capsid (LC). To investigate the role of the LC protein in the virus life cycle, mutations and deletions were introduced into the LC coding region of an infectious FCV cDNA clone. Three cysteine residues that are conserved among all vesivirus LC sequences were found to be critical for the recovery of FCV with a characteristic cytopathic effect in feline kidney cells. A cell-rounding phenotype associated with the transient expression of wild-type and mutagenized forms of the LC correlated with the cytopathic and growth properties of the corresponding engineered viruses. The host cellular protein annexin A2 was identified as a binding partner of the LC protein, consistent with a role for the LC in mediating host cell interactions that alter the integrity of the cell and enable virus spread.
JF  - Journal of virology
AU  - Abente, Eugenio J
AU  - Sosnovtsev, Stanislav V
AU  - Sandoval-Jaime, Carlos
AU  - Parra, Gabriel I
AU  - Bok, Karin
AU  - Green, Kim Y
AD  - Laboratory of Infectious Diseases, NIAID, NIH, Bethesda, MD, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 3003
EP  - 3017
VL  - 87
IS  - 6
KW  - Annexin A2
KW  - 0
KW  - Capsid Proteins
KW  - Virulence Factors
KW  - Index Medicus
KW  - Animals
KW  - Protein Processing, Post-Translational
KW  - Cats
KW  - Point Mutation
KW  - Annexin A2 -- metabolism
KW  - Protein Binding
KW  - Cell Line
KW  - Sequence Deletion
KW  - Host-Pathogen Interactions
KW  - Capsid Proteins -- metabolism
KW  - Virulence Factors -- metabolism
KW  - Calicivirus, Feline -- pathogenicity
KW  - Virulence Factors -- genetics
KW  - Cytopathogenic Effect, Viral
KW  - Capsid Proteins -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312660816?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+feline+calicivirus+leader+of+the+capsid+protein+is+associated+with+cytopathic+effect.&rft.au=Abente%2C+Eugenio+J%3BSosnovtsev%2C+Stanislav+V%3BSandoval-Jaime%2C+Carlos%3BParra%2C+Gabriel+I%3BBok%2C+Karin%3BGreen%2C+Kim+Y&rft.aulast=Abente&rft.aufirst=Eugenio&rft.date=2013-03-01&rft.volume=87&rft.issue=6&rft.spage=3003&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.02480-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-17
N1  - Date created - 2013-02-25
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Virol. 2010 Oct;84(19):9783-92 [20631122]
J Virol. 1996 Feb;70(2):1182-90 [8551579]
PLoS Pathog. 2011 Dec;7(12):e1002413 [22174679]
J Virol. 2012 Apr;86(8):4139-50 [22301157]
Syst Biol. 2012 May;61(3):539-42 [22357727]
J Virol. 2012 Jul;86(13):7414-26 [22532688]
J Gen Virol. 1997 May;78 ( Pt 5):1033-40 [9152420]
J Virol. 1998 Apr;72(4):3051-9 [9525628]
J Infect Dis. 1998 Dec;178(6):1571-8 [9815206]
J Virol. 1999 Aug;73(8):6626-33 [10400760]
Science. 1999 Oct 8;286(5438):287-90 [10514371]
J Virol. 2005 Apr;79(7):4012-24 [15767403]
J Gen Virol. 2006 Feb;87(Pt 2):357-61 [16432022]
J Virol. 2006 Mar;80(6):2694-704 [16501079]
Proc Natl Acad Sci U S A. 2006 May 23;103(21):8048-53 [16702551]
J Virol. 2006 Sep;80(18):9039-52 [16940516]
Bioinformatics. 2007 Nov 1;23(21):2947-8 [17846036]
Nucleic Acids Res. 2008 May;36(8):2530-46 [18319285]
J Cell Sci. 2008 Jul 1;121(Pt 13):2177-85 [18565825]
Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W70-4 [18424795]
J Virol. 2008 Sep;82(17):8838-48 [18562541]
J Virol. 2008 Oct;82(19):9306-17 [18632864]
J Biol Chem. 2009 Jan 16;284(3):1604-11 [18990701]
J Virol. 2009 Sep;83(17):8587-95 [19515767]
Virology. 2010 Apr 25;400(1):18-31 [20137802]
J Virol. 2010 Jun;84(11):5775-89 [20335258]
J Vet Med Sci. 1999 Sep;61(9):1043-7 [10535511]
FASEB J. 2000 Feb;14(2):231-41 [10657980]
J Infect Dis. 2000 May;181 Suppl 2:S387-91 [10804153]
Virology. 2000 Nov 10;277(1):193-203 [11062050]
Physiol Rev. 2002 Apr;82(2):331-71 [11917092]
J Virol. 2002 Jul;76(14):7060-72 [12072506]
Virus Res. 2002 Jul;87(1):89-93 [12135793]
J Struct Biol. 2003 Feb;141(2):143-8 [12615540]
Virus Res. 2003 Jul;94(1):1-10 [12837551]
J Gen Virol. 2003 Oct;84(Pt 10):2837-45 [13679618]
Ann N Y Acad Sci. 2003 Dec;1010:587-90 [15033797]
J Virol. 2004 May;78(9):4931-5 [15078978]
J Biol Chem. 2004 Apr 23;279(17):17013-8 [14744857]
Mol Cell Biol. 2004 Jun;24(11):4955-67 [15143187]
Arch Gesamte Virusforsch. 1970;32(2):249-60 [4100519]
Virology. 1978 Aug;89(1):318-21 [687392]
J Gen Virol. 1980 Mar;47(1):215-20 [7365464]
Arch Virol. 1983;76(3):257-61 [6307228]
Virus Res. 1988 Aug;11(1):59-72 [3176687]
Arch Virol. 1989;108(1-2):69-79 [2596975]
J Virol. 1991 Oct;65(10):5440-7 [1716692]
Arch Virol. 1992;122(3-4):223-35 [1731695]
J Mol Biol. 1994 Jul 15;240(3):256-64 [8028008]
J Virol. 1994 Dec;68(12):8111-7 [7966601]
Virology. 1995 Jul 10;210(2):383-90 [7618275]
Cell Signal. 2012 Feb;24(2):388-92 [22024281]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1128/JVI.02480-12
ER  - 



TY  - JOUR
T1  - Nuclear receptor CAR specifically activates the two-pore K+ channel Kcnk1 gene in male mouse livers, which attenuates phenobarbital-induced hepatic hyperplasia.
AN  - 1291602315; 23291559
AB  - KCNK1, a member of the family of two-pore K(+) ion channels, is specifically induced in the livers of male mice after phenobarbital treatment. Here, we have determined the molecular mechanism of this male-specific activation of the Kcnk1 gene and characterized KCNK1 as a phenobarbital-inducible antihyperplasia factor. Upon activation by phenobarbital, nuclear receptor CAR binds the 97-bp response element (-2441/-2345) within the Kcnk1 promoter. This binding is observed in the livers of male mice, but not in the livers of female mice and requires the pituitary gland, because hypophysectomy abrogates it. Hyperplasia further progressed in the livers of Kcnk1  (  -/-  ) male mice compared with those of Kcnk1  (  +/+  ) males after phenobarbital treatment. Thus, KCNK1 suppresses phenobarbital-induced hyperplasia. These results indicate that phenobarbital treatment induces KCNK1 to elicit a male-specific and growth-suppressing signal. Thus, KCNK1 and Kcnk1  (  -/-  ) mice provide an experimental tool for further investigation into the molecular mechanism of CAR-mediated promotion of the development of hepatocellular carcinoma in mice.
JF  - Toxicological sciences : an official journal of the Society of Toxicology
AU  - Saito, Kosuke
AU  - Moore, Rick
AU  - Negishi, Masahiko
AD  - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 151
EP  - 161
VL  - 132
IS  - 1
KW  - DNA Primers
KW  - 0
KW  - Kcnk1 protein, mouse
KW  - Potassium Channels, Tandem Pore Domain
KW  - Receptors, Cytoplasmic and Nuclear
KW  - constitutive androstane receptor
KW  - Phenobarbital
KW  - YQE403BP4D
KW  - Index Medicus
KW  - Real-Time Polymerase Chain Reaction
KW  - Animals
KW  - Promoter Regions, Genetic
KW  - Base Sequence
KW  - Molecular Sequence Data
KW  - Mice, Inbred C57BL
KW  - Mice, Inbred C3H
KW  - Chromatin Immunoprecipitation
KW  - Mice
KW  - Amino Acid Sequence
KW  - Male
KW  - Female
KW  - Receptors, Cytoplasmic and Nuclear -- physiology
KW  - Hyperplasia -- chemically induced
KW  - Liver -- drug effects
KW  - Hyperplasia -- genetics
KW  - Liver -- metabolism
KW  - Phenobarbital -- toxicity
KW  - Potassium Channels, Tandem Pore Domain -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291602315?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nuclear+receptor+CAR+specifically+activates+the+two-pore+K%2B+channel+Kcnk1+gene+in+male+mouse+livers%2C+which+attenuates+phenobarbital-induced+hepatic+hyperplasia.&rft.au=Saito%2C+Kosuke%3BMoore%2C+Rick%3BNegishi%2C+Masahiko&rft.aulast=Saito&rft.aufirst=Kosuke&rft.date=2013-03-01&rft.volume=132&rft.issue=1&rft.spage=151&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%2Fkfs338
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-29
N1  - Date created - 2013-02-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biochem Biophys Res Commun. 2000 Oct 14;277(1):1-6 [11027630]
Lab Invest. 2011 Nov;91(11):1624-33 [21826054]
Carcinogenesis. 2003 Jun;24(6):1059-65 [12807759]
Mol Endocrinol. 2004 Mar;18(3):747-60 [14684848]
Genes Dev. 2004 Apr 1;18(7):830-50 [15082532]
Cancer Res. 2004 Oct 15;64(20):7197-200 [15492232]
Cancer Res. 1984 Jul;44(7):2936-41 [6327029]
Carcinogenesis. 1986 Feb;7(2):215-20 [3948311]
Carcinogenesis. 1986 Jun;7(6):1025-8 [2871946]
Carcinogenesis. 1986 Jun;7(6):981-5 [3708759]
Cancer Lett. 1989 Nov 15;48(1):43-51 [2819695]
Eur J Biochem. 1991 Feb 14;195(3):585-91 [1999182]
J Biol Chem. 1992 Feb 25;267(6):3915-21 [1740439]
Carcinogenesis. 1996 Feb;17(2):191-6 [8625437]
EMBO J. 1996 Dec 2;15(23):6400-7 [8978667]
Mol Cell Biol. 1998 Oct;18(10):5652-8 [9742082]
Mol Cell Biol. 1999 Sep;19(9):6318-22 [10454578]
Mol Endocrinol. 2005 Jun;19(6):1646-53 [15831521]
J Thorac Cardiovasc Surg. 2005 Jun;129(6):1383-90 [15942582]
Pflugers Arch. 2005 Dec;451(3):479-88 [16025300]
Drug Metab Rev. 2006;38(1-2):75-87 [16684649]
Drug Metab Dispos. 2007 Jan;35(1):36-42 [17020958]
Endocrinology. 2007 May;148(5):1977-86 [17317776]
Gastroenterology. 2007 Jun;132(7):2557-76 [17570226]
Cell Biochem Biophys. 2007;47(2):209-56 [17652773]
J Pharmacol Exp Ther. 2008 Feb;324(2):612-21 [17993606]
EMBO J. 2008 Mar 5;27(5):792-803 [18239687]
Hepatology. 2008 Oct;48(4):1302-11 [18798339]
Toxicology. 2009 Feb 4;256(1-2):53-64 [19041682]
Exp Toxicol Pathol. 2009 Mar;61(2):101-11 [18809303]
FEBS Lett. 2009 Jun 18;583(12):2126-30 [19467232]
Gastroenterology. 2009 Aug;137(2):660-72 [19454287]
Trends Endocrinol Metab. 2009 Aug;20(6):273-9 [19595610]
J Biol Chem. 2009 Dec 11;284(50):34785-92 [19858220]
Pharmacogenet Genomics. 2010 Jan;20(1):9-17 [19898264]
Biol Chem. 2010 Feb-Mar;391(2-3):139-48 [20030591]
PLoS One. 2010;5(4):e10121 [20404936]
Biochem Pharmacol. 2010 Jul 1;80(1):129-35 [20211151]
Trends Pharmacol Sci. 2010 Dec;31(12):587-95 [20951446]
Int J Biochem Cell Biol. 2011 Feb;43(2):271-8 [19914393]
Mol Endocrinol. 2011 Aug;25(8):1326-36 [21680658]
Trends Endocrinol Metab. 2001 Aug;12(6):252-7 [11445442]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/toxsci/kfs338
ER  - 



TY  - JOUR
T1  - Development of immunoblotting techniques for DNA radical detection.
AN  - 1289485581; 23142572
AB  - Radical damage to DNA has been implicated in cell death, cellular dysfunction, and cancer. A recently developed method for detecting DNA radicals uses the nitrone spin trap DMPO (5,5-dimethyl-1-pyrroline N-oxide) to trap radicals. The trapped radicals then decay into stable nitrone adducts detectable with anti-DMPO antibodies and quantifiable by ELISA or dot-blot assay. However, the sequences of DNA that are damaged are likely to be as important as the total level of damage. Therefore, we have developed immunoblotting methods for detection of DNA nitrone adducts on electrophoretically separated DNA, comparable to Western blotting for proteins. These new techniques not only allow the assessment of relative radical adduct levels, but can reveal specific DNA fragments, and ultimately nucleotides, as radical targets. Moreover, we have determined that denaturation of samples into single-stranded DNA enhances the detection of DNA-DMPO adducts in our new blotting methods and also in ELISA.
          Published by Elsevier Inc.
JF  - Free radical biology & medicine
AU  - Summers, Fiona A
AU  - Mason, Ronald P
AU  - Ehrenshaft, Marilyn
AD  - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. summersfa@niehs.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 64
EP  - 71
VL  - 56
KW  - Cyclic N-Oxides
KW  - 0
KW  - Free Radicals
KW  - 5,5-dimethyl-1-pyrroline-1-oxide
KW  - 7170JZ1QF3
KW  - DNA
KW  - 9007-49-2
KW  - Index Medicus
KW  - Molecular Structure
KW  - Free Radicals -- analysis
KW  - Electrophoresis, Agar Gel
KW  - Enzyme-Linked Immunosorbent Assay
KW  - Cyclic N-Oxides -- chemistry
KW  - Immunoblotting -- methods
KW  - DNA -- analysis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1289485581?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+of+immunoblotting+techniques+for+DNA+radical+detection.&rft.au=Summers%2C+Fiona+A%3BMason%2C+Ronald+P%3BEhrenshaft%2C+Marilyn&rft.aulast=Summers&rft.aufirst=Fiona&rft.date=2013-03-01&rft.volume=56&rft.issue=&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.10.550
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-10-23
N1  - Date created - 2013-02-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Free Radic Res. 2000 Apr;32(4):333-41 [10741854]
J Biol Chem. 2009 Feb 27;284(9):5546-56 [19106092]
Free Radic Biol Med. 2002 Aug 1;33(3):364-9 [12126758]
Free Radic Biol Med. 2003 Jun 1;34(11):1473-81 [12757857]
FASEB J. 2003 Jul;17(10):1195-214 [12832285]
Arch Biochem Biophys. 2004 Mar 1;423(1):57-65 [14989265]
Biochemistry. 1985 Jul 16;24(15):3991-9 [4052380]
Free Radic Biol Med. 1987;3(2):97-105 [2822548]
Chem Biol Interact. 1989;69(4):293-317 [2659197]
Free Radic Biol Med. 1988;5(1):27-37 [3075945]
Mutat Res. 1989 Sep;214(1):41-6 [2671700]
Biotechniques. 1990 Jan;8(1):14-5 [2182072]
Biochem Biophys Res Commun. 1990 Nov 15;172(3):1073-80 [2173913]
Biochem J. 1991 Feb 1;273 ( Pt 3):601-4 [1899997]
J Biol Chem. 1991 Oct 25;266(30):20175-84 [1939078]
J Biol Chem. 1991 Oct 25;266(30):20185-91 [1939079]
Arch Biochem Biophys. 1992 May 15;295(1):205-13 [1315504]
Arch Biochem Biophys. 1992 Aug 1;296(2):640-4 [1321591]
Arch Biochem Biophys. 1993 Jul;304(1):102-9 [8323275]
Nucleic Acids Res. 1993 Aug 25;21(17):4093-101 [8371984]
Mutat Res. 1995 Feb;326(2):235-43 [7529889]
Arch Biochem Biophys. 1995 Jan 10;316(1):515-22 [7840659]
Free Radic Biol Med. 1995 Jun;18(6):1023-32 [7628728]
Free Radic Biol Med. 1995 Jun;18(6):1033-77 [7628729]
Free Radic Res. 1998 Dec;29(6):511-24 [10098456]
Free Radic Res. 1998 Dec;29(6):601-8 [10098465]
Free Radic Biol Med. 1999 Mar;26(5-6):714-21 [10218661]
Science. 1999 Apr 30;284(5415):805-8 [10221913]
Anal Biochem. 2005 Jan 1;336(1):46-50 [15582557]
FASEB J. 2005 Jan;19(1):82-4 [15533950]
Nat Methods. 2006 Feb;3(2):123-7 [16432522]
Nat Protoc. 2007;2(3):512-22 [17406615]
Free Radic Biol Med. 2008 Feb 1;44(3):464-73 [17983606]
Annu Rev Biochem. 2008;77:755-76 [18173371]
Curr Opin Struct Biol. 2009 Feb;19(1):65-71 [19208466]
Biochemistry (Mosc). 2009 Feb;74(2):117-29 [19267666]
J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942]
J Biol Chem. 2010 Jun 25;285(26):20062-71 [20406811]
J Biol Chem. 2010 Jul 30;285(31):24195-205 [20501663]
Free Radic Biol Med. 2011 Jun 1;50(11):1536-45 [21382477]
Mutat Res. 2011 Jun 3;711(1-2):3-12 [21329709]
Free Radic Biol Med. 2011 Jul 15;51(2):257-81 [21554949]
Pharmacol Ther. 2012 Jan;133(1):26-39 [21839775]
Nucleic Acids Res. 2012 Jul;40(12):5477-86 [22387463]
Free Radic Biol Med. 2012 Aug 1;53(3):406-14 [22634144]
Mol Cell Biol. 2001 Feb;21(3):916-27 [11154278]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.freeradbiomed.2012.10.550
ER  - 



TY  - JOUR
T1  - From targets to targeted therapies and molecular profiling in non-small cell lung carcinoma.
AN  - 1288995746; 23131389
AB  - Although tumor molecular-profile-directed therapy appears promising in early clinical studies, there are many practical challenges to its successful clinical application in non-small-cell lung cancer (NSCLC). These challenges may be broadly classified as those relating to tumor (heterogeneity), tissue (acquisition and processing), testing (assays for molecular profiling) and trials (clinical evaluation of molecular markers and drugs). Strategies to overcome these challenges include (i) understanding the biological basis of tumor heterogeneity and of carcinogenesis in the large subset of patients with no currently evident driver events; (ii) technological advances in minimally invasive acquisition of tumor and next-generation sequencing (NGS) which would enable single-platform analysis of molecular alterations in limited tissue at a reasonable turnaround time (TAT); (iii) deliberation in early stages of drug development as well as clinical trial design to identify, validate and assess the clinical utility of biomarkers in conjunction with drugs and (iv) collaboration to improve understanding of and accrual to trials enrolling patients with rare molecular alterations.
JF  - Annals of oncology : official journal of the European Society for Medical Oncology
AU  - Thomas, A
AU  - Rajan, A
AU  - Lopez-Chavez, A
AU  - Wang, Y
AU  - Giaccone, G
AD  - Medical Oncology Branch, National Cancer Institute, Bethesda, 20892, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 577
EP  - 585
VL  - 24
IS  - 3
KW  - Biomarkers, Tumor
KW  - 0
KW  - Proteome
KW  - Index Medicus
KW  - Proteome -- genetics
KW  - Biomarkers, Tumor -- metabolism
KW  - Gene Expression Profiling
KW  - Biomarkers, Tumor -- genetics
KW  - Tissue Array Analysis
KW  - Humans
KW  - DNA Mutational Analysis
KW  - Proteome -- metabolism
KW  - Molecular Targeted Therapy
KW  - Clinical Trials as Topic
KW  - Biopsy
KW  - Lung -- pathology
KW  - Carcinoma, Non-Small-Cell Lung -- metabolism
KW  - Carcinoma, Non-Small-Cell Lung -- genetics
KW  - Lung Neoplasms -- drug therapy
KW  - Lung Neoplasms -- genetics
KW  - Carcinoma, Non-Small-Cell Lung -- drug therapy
KW  - Lung Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1288995746?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=From+targets+to+targeted+therapies+and+molecular+profiling+in+non-small+cell+lung+carcinoma.&rft.au=Thomas%2C+A%3BRajan%2C+A%3BLopez-Chavez%2C+A%3BWang%2C+Y%3BGiaccone%2C+G&rft.aulast=Thomas&rft.aufirst=A&rft.date=2013-03-01&rft.volume=24&rft.issue=3&rft.spage=577&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%2Fmds478
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-30
N1  - Date created - 2013-02-18
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
N Engl J Med. 2008 Jul 24;359(4):366-77 [18596266]
Clin Trials. 2008;5(3):181-93 [18559407]
Ann Oncol. 2009 Apr;20(4):696-702 [19088172]
Cancer. 2009 Feb 25;117(1):67-72 [19347832]
J Thorac Oncol. 2009 Jul;4(7):809-15 [19487967]
Clin Cancer Res. 2009 Jul 15;15(14):4554-60 [19584155]
Nat Rev Genet. 2010 Jan;11(1):31-46 [19997069]
AJR Am J Roentgenol. 2010 Jan;194(1):266-9 [20028932]
Clin Cancer Res. 2010 Jan 15;16(2):691-8 [20068112]
Lung Cancer. 2010 Feb;67(2):166-9 [19450892]
Eur Respir J. 2010 Feb;35(2):391-5 [19643949]
Cancer Cell. 2010 Jan 19;17(1):77-88 [20129249]
Clin Cancer Res. 2010 Mar 1;16(5):1561-71 [20179225]
Sci Transl Med. 2010 Feb 24;2(20):20ra14 [20371490]
EMBO Mol Med. 2010 May;2(5):146-58 [20432502]
J Clin Oncol. 2010 May 20;28(15):2635-40 [20406927]
Cancer. 2010 Jun 1;116(11):2682-7 [20336783]
Nat Rev Cancer. 2010 Jul;10(7):514-23 [20535131]
Nat Rev Genet. 2010 Oct;11(10):685-96 [20847746]
N Engl J Med. 2010 Oct 28;363(18):1693-703 [20979469]
J Clin Oncol. 2010 Nov 20;28(33):4877-83 [20921468]
J Mol Diagn. 2011 Jan;13(1):74-84 [21227397]
N Engl J Med. 2011 Feb 3;364(5):476-80 [21288100]
J Thorac Oncol. 2011 Mar;6(3):466-72 [21258247]
J Thorac Oncol. 2011 Mar;6(3):451-8 [21266922]
J Thorac Oncol. 2011 Mar;6(3):459-65 [21278610]
Sci Transl Med. 2011 Mar 23;3(75):75ra26 [21430269]
J Exp Clin Cancer Res. 2011;30:30 [21414214]
Semin Respir Crit Care Med. 2011 Feb;32(1):22-31 [21500121]
J Clin Oncol. 2011 Aug 1;29(22):2972-7 [21730270]
J Clin Oncol. 2011 Aug 20;29(24):3331-2; author reply 3332-3 [21768461]
Lung Cancer. 2011 Oct;74(1):1-6 [21658788]
Ann Oncol. 2011 Dec;22(12):2616-24 [22071650]
J Natl Compr Canc Netw. 2011 Dec;9(12):1335-41 [22157554]
J Clin Oncol. 2012 Feb 1;30(4):433-40 [22215752]
J Clin Oncol. 2012 Mar 10;30(8):863-70 [22215748]
Clin Cancer Res. 2012 Mar 15;18(6):1531-9 [22422405]
Nat Rev Clin Oncol. 2012 Apr;9(4):208-14 [22143142]
Cancer Discov. 2011 Jun;1(1):44-53 [22586319]
Cancer Discov. 2011 Sep;1(4):297-311 [21935500]
Cancer Discov. 2012 Jan;2(1):82-93 [22585170]
Oncologist. 2012;17(7):978-85 [22673630]
Am J Pathol. 1999 Nov;155(5):1467-71 [10550302]
J Clin Oncol. 2004 Mar 1;22(5):777-84 [14990632]
J Clin Oncol. 2004 Mar 1;22(5):785-94 [14990633]
Control Clin Trials. 1989 Mar;10(1):1-10 [2702835]
J Clin Oncol. 2005 Sep 1;23(25):5892-9 [16043829]
Lancet. 2005 Oct 29-Nov 4;366(9496):1527-37 [16257339]
Clin Cancer Res. 2005 Nov 1;11(21):7872-8 [16278411]
Nat Genet. 2007 Mar;39(3):347-51 [17293865]
J Clin Oncol. 2007 Apr 20;25(12):1545-52 [17442998]
Ann Oncol. 2007 Jun;18(6):1043-50 [17355950]
Cancer Sci. 2008 May;99(5):929-35 [18325048]
Br J Cancer. 2008 Sep 16;99(6):923-9 [19238633]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1093/annonc/mds478
ER  - 



TY  - JOUR
T1  - Pilot study of topical acetyl hexapeptide-8 in the treatment for blepharospasm in patients receiving botulinum toxin therapy.
AN  - 1288312993; 23146065
AB  - Injectable botulinum neurotoxin (BoNT) is the principal effective treatment for blepharospasm (BSP). This trial explores the safety and efficacy of topical acetyl hexapeptide-8 (AH8), a competitive SNAP25 inhibitor, as a potential new therapy in BSP.
          Double-blind, placebo-controlled, randomized trial of daily topical application of AH8 in 24 patients with BSP. The primary outcome was time to return to baseline Jankovic Blepharospasm Rating Scale (JBRS) after a BoNT injection simultaneously with the initiation of AH8. Patients displaying a strictly regular pattern of response to 3-monthly injections of BoNT were included. There were no significant adverse events. There was a trend for longer time until return to baseline JBRS after injection in the active group compared to placebo (3.7 months vs. 3.0 months), and for better scores in the active group. One-third (4/12) of the patients in the active group had a considerable extension of symptom control after BoNT (range: 3.3-7.1 months).
          Topical AH8 is safe and promising for extending the duration of action of BoNT therapy for BSP. Published 2012. This article is a U.S. Government work and is in the public domain in the USA. European Journal of Neurology © 2012 EFNS.
JF  - European journal of neurology
AU  - Lungu, C
AU  - Considine, E
AU  - Zahir, S
AU  - Ponsati, B
AU  - Arrastia, S
AU  - Hallett, M
AD  - Office of the Clinical Director, NINDS, NIH, Bethesda, MD 20892, USA. lunguci@ninds.nih.gov
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 515
EP  - 518
VL  - 20
IS  - 3
KW  - Neuromuscular Agents
KW  - 0
KW  - Oligopeptides
KW  - SNAP25 protein, human
KW  - Synaptosomal-Associated Protein 25
KW  - acetyl-glutamyl-glutamyl-methionyl-glutaminyl-arginyl-argininamide
KW  - onabotulinumtoxinA
KW  - Botulinum Toxins, Type A
KW  - EC 3.4.24.69
KW  - Index Medicus
KW  - Drug Therapy, Combination
KW  - Double-Blind Method
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Pilot Projects
KW  - Middle Aged
KW  - Administration, Topical
KW  - Synaptosomal-Associated Protein 25 -- antagonists & inhibitors
KW  - Botulinum Toxins, Type A -- administration & dosage
KW  - Oligopeptides -- administration & dosage
KW  - Neuromuscular Agents -- administration & dosage
KW  - Blepharospasm -- drug therapy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1288312993?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neurology&rft.atitle=Pilot+study+of+topical+acetyl+hexapeptide-8+in+the+treatment+for+blepharospasm+in+patients+receiving+botulinum+toxin+therapy.&rft.au=Lungu%2C+C%3BConsidine%2C+E%3BZahir%2C+S%3BPonsati%2C+B%3BArrastia%2C+S%3BHallett%2C+M&rft.aulast=Lungu&rft.aufirst=C&rft.date=2013-03-01&rft.volume=20&rft.issue=3&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=European+journal+of+neurology&rft.issn=1468-1331&rft_id=info:doi/10.1111%2Fene.12009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-15
N1  - Date created - 2013-02-14
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Cosmet Sci. 2007 Mar-Apr;58(2):157-71 [17520155]
Neurology. 2008 May 6;70(19):1699-706 [18458230]
Angew Chem Int Ed Engl. 2008;47(44):8360-79 [18844202]
Mov Disord. 2009 Feb 15;24(3):407-13 [19053054]
Neurotoxicology. 2005 Oct;26(5):761-7 [15925409]
JAMA. 1982 Dec 17;248(23):3160-4 [7143695]
Mov Disord. 1995 Jul;10(4):444-9 [7565824]
J Neurol. 2011 Nov;258(11):2069-74 [21553081]
Insight. 2011 Jan-Mar;36(1):24 [21337984]
Neurology. 2002 Nov 12;59(9):1306-12 [12434791]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/ene.12009
ER  - 



TY  - JOUR
T1  - The diverse roles of nonsteroidal anti-inflammatory drug activated gene (NAG-1/GDF15) in cancer.
AN  - 1285086422; 23220538
AB  - Nonsteroidal anti-inflammatory drug (NSAID) activated gene-1, NAG-1, is a divergent member of the transforming growth factor-beta (TGF-β) superfamily that plays a complex but poorly understood role in several human diseases including cancer. NAG-1 expression is substantially increased during cancer development and progression especially in gastrointestinal, prostate, pancreatic, colorectal, breast, melanoma, and glioblastoma brain tumors. Aberrant increases in the serum levels of secreted NAG-1 correlate with poor prognosis and patient survival rates in some cancers. In contrast, the expression of NAG-1 is up-regulated by several tumor suppressor pathways including p53, GSK-3β, and EGR-1. NAG-1 expression is also induced by many drugs and dietary compounds which are documented to prevent the development and progression of cancer in mouse models. Studies with transgenic mice expressing human NAG-1 demonstrated that the expression of NAG-1 inhibits the development of intestinal tumors and prostate tumors in animal models. Laboratory and clinical evidence suggest that NAG-1, like other TGF-β family members, may have different or pleiotropic functions in the early and late stages of carcinogenesis. Upon understanding the molecular mechanism and function of NAG-1 during carcinogenesis, NAG-1 may serve as a potential biomarker for the diagnosis and prognosis of cancer and a therapeutic target for the inhibition and treatment of cancer development and progression.
          Published by Elsevier Inc.
JF  - Biochemical pharmacology
AU  - Wang, Xingya
AU  - Baek, Seung Joon
AU  - Eling, Thomas E
AD  - Eicosanoid Biochemistry Group, Laboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC 27709, USA.
Y1  - 2013/03/01/
PY  - 2013
DA  - 2013 Mar 01
SP  - 597
EP  - 606
VL  - 85
IS  - 5
KW  - Anti-Inflammatory Agents, Non-Steroidal
KW  - 0
KW  - Growth Differentiation Factor 15
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Epigenesis, Genetic
KW  - Growth Differentiation Factor 15 -- metabolism
KW  - Growth Differentiation Factor 15 -- genetics
KW  - Gene Expression Regulation, Neoplastic -- drug effects
KW  - Neoplasms -- genetics
KW  - Neoplasms -- metabolism
KW  - Anti-Inflammatory Agents, Non-Steroidal -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285086422?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=The+diverse+roles+of+nonsteroidal+anti-inflammatory+drug+activated+gene+%28NAG-1%2FGDF15%29+in+cancer.&rft.au=Wang%2C+Xingya%3BBaek%2C+Seung+Joon%3BEling%2C+Thomas+E&rft.aulast=Wang&rft.aufirst=Xingya&rft.date=2013-03-01&rft.volume=85&rft.issue=5&rft.spage=597&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=1873-2968&rft_id=info:doi/10.1016%2Fj.bcp.2012.11.025
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-29
N1  - Date created - 2013-02-06
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Cancer Res. 2004 Apr 1;10(7):2386-92 [15073115]
BMC Cancer. 2003 Oct 31;3:28 [14588079]
J Natl Cancer Inst. 2004 Aug 18;96(16):1248-54 [15316060]
BMC Cancer. 2011;11:146 [21504622]
J Cell Physiol. 2012 Jan;227(1):213-22 [21391217]
Carcinogenesis. 2004 Oct;25(10):1853-8 [15180942]
Cancer Epidemiol Biomarkers Prev. 2012 Feb;21(2):337-46 [22144502]
Prostate. 2012 May 1;72(6):677-89 [21809352]
J Nutr Biochem. 2012 Jun;23(6):646-55 [21764279]
Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11514-9 [9326641]
Biochim Biophys Acta. 1997 Oct 9;1354(1):40-4 [9375789]
Gene. 1997 Dec 5;203(1):17-26 [9426002]
J Biol Chem. 1998 May 29;273(22):13760-7 [9593718]
Gene. 1999 Sep 3;237(1):105-11 [10524241]
Toxicol Sci. 2004 Dec;82(2):429-35 [15342960]
Carcinogenesis. 2004 Dec;25(12):2425-32 [15308587]
Mol Pharmacol. 2005 Feb;67(2):356-64 [15509713]
Biochem Biophys Res Commun. 2005 Mar 4;328(1):63-9 [15670751]
Mol Cancer Ther. 2005 Mar;4(3):487-93 [15767558]
Cancer Res. 2005 Mar 15;65(6):2330-6 [15781647]
Mol Pharmacol. 2005 Dec;68(6):1782-92 [16155208]
Clin Cancer Res. 2006 Jan 1;12(1):89-96 [16397029]
Carcinogenesis. 2006 May;27(5):972-81 [16286461]
Genes Dev. 2006 May 15;20(10):1218-49 [16702400]
Mol Cancer Ther. 2006 May;5(5):1352-61 [16731769]
Cancer Biol Ther. 2006 May;5(5):518-22 [16582595]
Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1223-5 [16775185]
J Pharmacol Exp Ther. 2006 Aug;318(2):899-906 [16714403]
Clin Cancer Res. 2006 Jul 15;12(14 Pt 2):4396s-4402s [16857817]
J Cell Physiol. 2006 Sep;208(3):566-74 [16741990]
Gastroenterology. 2006 Nov;131(5):1553-60 [17101328]
Ann Oncol. 2012 Jun;23(6):1403-15 [22517822]
Mol Nutr Food Res. 2012 May;56(5):761-74 [22648623]
J Biol Chem. 2012 Jun 8;287(24):19841-55 [22511768]
J Nutr Biochem. 2012 Aug;23(8):915-23 [21852088]
Toxicol Appl Pharmacol. 2012 Sep 1;263(2):225-32 [22750490]
PLoS One. 2012;7(8):e43833 [22952779]
Curr Pharm Des. 2013;19(1):48-66 [22950499]
J Nutr Biochem. 2013 Jun;24(6):986-99 [23017582]
Int J Cancer. 2012 Jan 15;130(2):267-77 [21437897]
J Biochem Mol Biol. 2006 Nov 30;39(6):649-55 [17129398]
Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):532-7 [17372249]
Prostate. 2007 Apr 1;67(5):557-71 [17221842]
Cancer Lett. 2007 Jun 28;251(2):268-77 [17257745]
Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1309-11 [17548705]
J Pharmacol Exp Ther. 2007 Nov;323(2):746-56 [17715378]
Acta Pharmacol Sin. 2007 Nov;28(11):1842-50 [17959037]
Carcinogenesis. 2007 Nov;28(11):2337-46 [17724373]
Vet J. 2008 Jan;175(1):89-95 [17275371]
Int J Cancer. 2008 Apr 15;122(8):1765-73 [18076062]
Carcinogenesis. 2008 Apr;29(4):704-12 [18258606]
Biochem Pharmacol. 2008 May 1;75(9):1751-60 [18358453]
Breast Cancer Res Treat. 2008 May;109(2):273-83 [17624585]
Int J Stroke. 2006 Feb;1(1):4-8 [18706062]
J Biol Chem. 2008 Nov 28;283(48):33129-37 [18801729]
J Invest Dermatol. 2009 Feb;129(2):383-91 [18754039]
Clin Chim Acta. 2009 Mar;401(1-2):128-33 [19133249]
Nat Rev Gastroenterol Hepatol. 2009 May;6(5):297-305 [19404270]
Cancer Prev Res (Phila). 2009 May;2(5):450-8 [19401523]
Cancer Lett. 2009 Sep 18;282(2):152-8 [19375854]
Mol Carcinog. 2009 Aug;48(8):692-702 [19125423]
Clin Cancer Res. 2009 Nov 1;15(21):6658-64 [19843661]
Sichuan Da Xue Xue Bao Yi Xue Ban. 2009 Nov;40(6):1029-32 [20067113]
J Cancer Res Clin Oncol. 2010 Apr;136(4):571-6 [19784846]
BMB Rep. 2010 Feb;43(2):91-6 [20193126]
Oncogene. 2010 Mar 4;29(9):1293-302 [19946339]
Carcinogenesis. 2010 Apr;31(4):719-28 [20110283]
Biochem Pharmacol. 2010 Jul 1;80(1):62-71 [20230799]
J Cell Physiol. 2010 Sep;224(3):626-35 [20578239]
Eur J Cancer. 2010 Dec;46(18):3365-74 [20709524]
Eur J Pharmacol. 2011 Jan 10;650(1):170-7 [20969859]
Mol Cancer Res. 2010 Dec;8(12):1656-64 [21097678]
Cancer Prev Res (Phila). 2011 Jan;4(1):150-60 [21205743]
Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):109-14 [10618379]
Am J Pathol. 2000 Jan;156(1):175-82 [10623665]
Mol Cell Biol. 2000 May;20(10):3742-51 [10779363]
EMBO J. 2000 May 15;19(10):2212-20 [10811612]
J Biol Chem. 2000 Jun 30;275(26):20127-35 [10777512]
Biochemistry. 2001 Jan 9;40(1):65-73 [11141057]
Mol Pharmacol. 2001 Apr;59(4):901-8 [11259636]
J Biol Chem. 2001 Sep 7;276(36):33384-92 [11445565]
Carcinogenesis. 2002 Mar;23(3):425-34 [11895857]
J Nutr. 2002 Apr;132(4):773-8 [11925476]
Gastroenterology. 2002 May;122(5):1388-98 [11984525]
J Pharmacol Exp Ther. 2002 Jun;301(3):1126-31 [12023546]
Oncogene. 2002 Jun 20;21(27):4212-9 [12082608]
Nat Rev Cancer. 2002 Dec;2(12):897-909 [12459728]
J Biol Chem. 2003 Feb 21;278(8):5845-53 [12475986]
Mol Pharmacol. 2003 Mar;63(3):557-64 [12606762]
Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3410-5 [12624183]
Biochem Biophys Res Commun. 2003 Jun 6;305(3):598-604 [12763036]
Int J Cancer. 2003 Jul 20;105(6):747-53 [12767058]
Clin Cancer Res. 2003 Jul;9(7):2642-50 [12855642]
Cancer Res. 2003 Aug 1;63(15):4648-55 [12907645]
Cancer Res. 2003 Aug 15;63(16):5034-40 [12941831]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.bcp.2012.11.025
ER  - 



TY  - JOUR
T1  - Evolving therapeutic paradigms for multiple myeloma: back to the future.
AN  - 1284621991; 22880935
AB  - Multiple myeloma (MM) is an ancient disease, but until the alkylating agent melphalan was found to have anti-myeloma properties in the 1950s there was virtually no effective therapy. By the late 1960s, extended dosing with melphalan and prednisone tripled survival from diagnosis and became the standard of care for newly diagnosed MM. "Maintenance therapy" to prolong survival through sustained disease control following induction chemotherapy was sought by 1970, but early strategies were ineffective and toxic. Subsequent applications of high-dose therapy (HDT)/autologous stem cell transplant (ASCT) changed the treatment paradigm for MM from extended dosing to an intensive strategy designed to eradicate the malignant cells in a single course of treatment. Although HDT-ASCT resulted in prolonged duration of remission and improved survival, the vast majority of patients still relapsed. Interferon (IFN) and glucocorticoid maintenance therapies demonstrated marginal improvements in outcomes but significant adverse effects. Novel agents introduced over the last decade have prolonged survival when given for maintenance following HDT-ASCT, but have also challenged the HDT-ASCT paradigm by achieving comparable remission rates when used alone as extended frontline therapy. This article reviews the evolution of therapeutic strategies for MM and discusses future questions facing MM investigators.
JF  - Leukemia & lymphoma
AU  - Cherry, Benjamin M
AU  - Korde, Neha
AU  - Kwok, Mary
AU  - Roschewski, Mark
AU  - Landgren, Ola
AD  - Multiple Myeloma Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 451
EP  - 463
VL  - 54
IS  - 3
KW  - Glucocorticoids
KW  - 0
KW  - Interferons
KW  - 9008-11-1
KW  - Melphalan
KW  - Q41OR9510P
KW  - Prednisone
KW  - VB0R961HZT
KW  - Index Medicus
KW  - Combined Modality Therapy -- methods
KW  - Melphalan -- administration & dosage
KW  - Humans
KW  - Glucocorticoids -- administration & dosage
KW  - Interferons -- administration & dosage
KW  - Combined Modality Therapy -- trends
KW  - Transplantation, Autologous
KW  - Prednisone -- administration & dosage
KW  - Stem Cell Transplantation -- methods
KW  - Multiple Myeloma -- therapy
KW  - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1284621991?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evolving+therapeutic+paradigms+for+multiple+myeloma%3A+back+to+the+future.&rft.au=Cherry%2C+Benjamin+M%3BKorde%2C+Neha%3BKwok%2C+Mary%3BRoschewski%2C+Mark%3BLandgren%2C+Ola&rft.aulast=Cherry&rft.aufirst=Benjamin&rft.date=2013-03-01&rft.volume=54&rft.issue=3&rft.spage=451&rft.isbn=&rft.btitle=&rft.title=Leukemia+%26+lymphoma&rft.issn=1029-2403&rft_id=info:doi/10.3109%2F10428194.2012.717277
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-22
N1  - Date created - 2013-02-05
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.3109/10428194.2012.717277
ER  - 



TY  - JOUR
T1  - Molecular detection and targeting of EWSR1 fusion transcripts in soft tissue tumors.
AN  - 1273660641; 23329308
AB  - Soft tissue tumors are a heterogeneous group of tumors, traditionally classified according to morphology and histogenesis. Molecular classification divides sarcomas into two main categories: (a) sarcomas with specific genetic alterations and (b) sarcomas showing multiple complex karyotypic abnormalities without any specific pattern. Most chromosomal alterations are represented by translocations which are increasingly detected. The identification of fusion transcripts, in fact, not only support the diagnosis but also provides the basis for the development of new therapeutic strategies aimed at blocking aberrant activity of the chimeric proteins. One of the genes most susceptible to breakage/translocation in soft tissue tumors is represented by Ewing sarcoma breakpoint region 1 (EWSR1). This gene has a large number of fusion partners, mainly associated with the pathogenesis of Ewing's sarcoma but with other soft tissue tumors too. In this review, we illustrate the characteristics of this gene/protein, both in normal cellular physiology and in carcinogenesis. We describe the different fusion partners of EWSR1, the molecular pathways in which is involved and the main molecular biology techniques for the identification of fusion transcripts and for their inhibition.
JF  - Medical oncology (Northwood, London, England)
AU  - Cantile, Monica
AU  - Marra, Laura
AU  - Franco, Renato
AU  - Ascierto, Paolo
AU  - Liguori, Giuseppina
AU  - De Chiara, Annarosaria
AU  - Botti, Gerardo
AD  - Pathology Unit, National Cancer Institute "Fondazione G. Pascale", Via Mariano Semmola, 80131 Naples, Italy.
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 412
VL  - 30
IS  - 1
KW  - Calmodulin-Binding Proteins
KW  - 0
KW  - EWSR1 protein, human
KW  - Oncogene Proteins, Fusion
KW  - RNA-Binding Proteins
KW  - Index Medicus
KW  - Humans
KW  - RNA-Binding Proteins -- genetics
KW  - Oncogene Proteins, Fusion -- genetics
KW  - Calmodulin-Binding Proteins -- genetics
KW  - Soft Tissue Neoplasms -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273660641?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+oncology+%28Northwood%2C+London%2C+England%29&rft.atitle=Molecular+detection+and+targeting+of+EWSR1+fusion+transcripts+in+soft+tissue+tumors.&rft.au=Cantile%2C+Monica%3BMarra%2C+Laura%3BFranco%2C+Renato%3BAscierto%2C+Paolo%3BLiguori%2C+Giuseppina%3BDe+Chiara%2C+Annarosaria%3BBotti%2C+Gerardo&rft.aulast=Cantile&rft.aufirst=Monica&rft.date=2013-03-01&rft.volume=30&rft.issue=1&rft.spage=412&rft.isbn=&rft.btitle=&rft.title=Medical+oncology+%28Northwood%2C+London%2C+England%29&rft.issn=1559-131X&rft_id=info:doi/10.1007%2Fs12032-012-0412-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-25
N1  - Date created - 2013-01-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Acta Biochim Biophys Sin (Shanghai). 2008 Apr;40(4):289-96 [18401526]
Genes Chromosomes Cancer. 2008 Jul;47(7):558-64 [18383210]
BMC Cell Biol. 2008;9:37 [18620564]
Eur J Cancer Prev. 2008 Oct;17(5):392-8 [18714179]
J Mol Biol. 2009 Feb 13;386(1):1-13 [19133275]
Clin Cancer Res. 2009 Apr 1;15(7):2259-68 [19318479]
Nat Med. 2009 Jul;15(7):750-6 [19584866]
Clin Chem. 2009 Sep;55(9):1719-27 [19617290]
Mod Pathol. 2009 Sep;22(9):1201-9 [19561568]
Cancer Genet Cytogenet. 2009 Nov;195(1):12-8 [19837262]
PLoS One. 2009;4(10):e7608 [19859563]
Cancer Res. 2010 Jan 15;70(2):639-45 [20068147]
Lancet Oncol. 2010 Feb;11(2):129-35 [20036194]
Int J Oncol. 2010 Apr;36(4):823-31 [20198325]
Am J Clin Pathol. 2010 Apr;133(4):633-45 [20231617]
Am J Pathol. 2010 Apr;176(4):1973-82 [20203285]
Genes Dev. 2010 May;24(9):916-32 [20382729]
Cancer Lett. 2010 Aug 1;294(1):57-65 [20153576]
Genes Chromosomes Cancer. 2010 Dec;49(12):1114-24 [20815032]
J Cell Biochem. 2010 Nov 1;111(4):933-43 [20665663]
Int J Cancer. 2011 Jan 1;128(1):216-26 [20648560]
Anticancer Res. 2010 Nov;30(11):4679-83 [21115923]
Cancer Invest. 2011 Feb;29(2):162-6 [21261476]
Mod Pathol. 2011 Mar;24(3):333-42 [21113140]
Genes Chromosomes Cancer. 2011 Jul;50(7):559-70 [21484932]
PLoS One. 2011;6(8):e23592 [21853155]
Cancer Genet. 2011 Jul;204(7):351-65 [21872822]
Genes Chromosomes Cancer. 2011 Dec;50(12):1054-62 [21987447]
Cell Cycle. 2011 Oct 1;10(19):3397-408 [21926473]
Genes Chromosomes Cancer. 2012 Mar;51(3):207-18 [22072439]
Gastroenterology. 2012 Feb;142(2):388-98.e1-7 [22079596]
Cancer Genet. 2012 Jan-Feb;205(1-2):55-60 [22429598]
Hum Pathol. 2012 May;43(5):764-8 [22154050]
Am J Surg Pathol. 2012 Jun;36(6):883-8 [22588066]
Br J Cancer. 2012 Jun 5;106(12):1976-9 [22588557]
Cancer Res. 2012 Sep 1;72(17):4340-50 [22738913]
Cancer Res. 2012 Sep 1;72(17):4494-503 [22930730]
J Invest Dermatol. 2012 Nov;132(11):2652-60 [22718120]
J Transl Med. 2012;10:204 [23031272]
Nat Immunol. 2008 Jul;9(7):810-9 [18500345]
Dev Biol. 1996 Mar 15;174(2):288-97 [8631501]
Oncogene. 1996 Feb 1;12(3):489-94 [8637704]
Am J Pathol. 1997 Mar;150(3):1049-58 [9060841]
Oncogene. 1997 Mar 13;14(10):1159-64 [9121764]
Eur J Cancer. 1997 Feb;33(2):239-43 [9135495]
Hum Pathol. 1997 Jul;28(7):767-71 [9224742]
Virchows Arch. 1997 Jul;431(1):45-51 [9247632]
J Pathol. 1997 Aug;182(4):437-41 [9306965]
Nat Genet. 1997 Nov;17(3):309-13 [9354795]
Virchows Arch. 1998 Feb;432(2):131-4 [9504857]
Diagn Mol Pathol. 1998 Feb;7(1):29-35 [9646032]
Am J Surg Pathol. 1998 Aug;22(8):1026-32 [9706984]
Cancer Genet Cytogenet. 1998 Oct 15;106(2):156-8 [9797782]
Am J Surg Pathol. 1998 Nov;22(11):1417-22 [9808135]
Lab Invest. 1999 Dec;79(12):1535-43 [10616204]
Leukemia. 2000 Feb;14(2):329-35 [10673753]
Cancer Res. 2000 Mar 15;60(6):1536-40 [10749119]
Int J Cancer. 2000 Aug 1;87(3):328-35 [10897036]
Oncogene. 2000 Aug 3;19(33):3799-804 [10949935]
Diagn Mol Pathol. 2000 Sep;9(3):137-44 [10976720]
Cancer. 2000 Nov 1;89(9):1992-8 [11064357]
Curr Opin Struct Biol. 2001 Feb;11(1):39-46 [11179890]
Cancer Res. 2001 Mar 15;61(6):2690-5 [11289149]
Oncogene. 2001 May 31;20(25):3258-65 [11423975]
J Mol Diagn. 2002 Feb;4(1):44-52 [11826187]
J Mol Diagn. 2002 Feb;4(1):59-64 [11826189]
Diagn Mol Pathol. 2002 Mar;11(1):16-21 [11854597]
J Gastroenterol. 2002;37(7):543-9 [12162413]
J Mol Diagn. 2002 Aug;4(3):164-71 [12169678]
Cancer Res. 2002 Oct 1;62(19):5408-12 [12359745]
Leukemia. 2002 Dec;16(12):2447-53 [12454751]
Ann Hum Genet. 2002 Nov;66(Pt 5-6):331-42 [12485467]
J Biol Chem. 2003 Feb 14;278(7):5427-32 [12459554]
J Biol Chem. 2003 Mar 28;278(13):11369-75 [12554743]
Oncogene. 2003 Jul 17;22(29):4586-93 [12881716]
Exp Cell Res. 2003 Aug 15;288(2):374-81 [12915128]
Oncogene. 2004 May 6;23(21):3830-40 [15021903]
J Orthop Res. 2004 Jul;22(4):910-7 [15183454]
Mol Cell Biol. 2004 Aug;24(16):7275-83 [15282325]
J Virol. 1991 Jan;65(1):7-15 [1845910]
Nat Genet. 1993 Aug;4(4):341-5 [8401579]
Genomics. 1993 Dec;18(3):609-15 [8307570]
Mol Cell Biol. 1994 May;14(5):3230-41 [8164678]
Br J Cancer. 1994 Nov;70(5):908-13 [7524604]
Genomics. 1994 Sep 1;23(1):278-81 [7829090]
Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1028-32 [7862627]
Am J Pathol. 1995 Mar;146(3):626-34 [7887445]
Oncogene. 1995 Mar 16;10(6):1229-34 [7700648]
Ann Hematol. 1995 Apr;70(4):195-201 [7748964]
EMBO J. 1995 Oct 2;14(19):4654-61 [7588595]
Oncogene. 1996 Jan 18;12(2):229-35 [8570200]
Genes Chromosomes Cancer. 1998 Dec;23(4):358-60 [9824209]
Cytogenet Cell Genet. 1998;82(3-4):278-83 [9858836]
J Pathol. 1998 Dec;186(4):434-7 [10209495]
APMIS. 1999 Jun;107(6):577-84 [10379685]
Klin Padiatr. 2004 Nov-Dec;216(6):315-22 [15565546]
Hum Pathol. 2005 Jan;36(1):74-81 [15712185]
Diagn Mol Pathol. 2005 Mar;14(1):23-8 [15714060]
Genes Chromosomes Cancer. 2005 Jun;43(2):217-22 [15729702]
Int J Cancer. 2005 Jul 1;115(4):556-60 [15688424]
Stem Cells. 2005 Jun-Jul;23(6):738-51 [15917470]
Pediatr Dev Pathol. 2005 Mar-Apr;8(2):162-7 [15747098]
Genes Chromosomes Cancer. 2005 Sep;44(1):97-102 [15884099]
Cancer Biol Ther. 2005 Apr;4(4):449-55 [15846078]
Cancer Res. 2005 Oct 1;65(19):8984-92 [16204072]
Oligonucleotides. 2006 Summer;16(2):158-68 [16764539]
Biochem Biophys Res Commun. 2006 Sep 22;348(2):437-40 [16884691]
Pathol Int. 2006 Sep;56(9):543-8 [16930335]
Clin Cancer Res. 2006 Sep 15;12(18):5356-62 [17000668]
Cancer Lett. 2007 Mar 8;247(1):84-90 [16730884]
Mod Pathol. 2007 Mar;20(3):397-404 [17334332]
Cancer Lett. 2007 Jun 18;251(1):158-63 [17188428]
J Mol Diagn. 2007 Sep;9(4):498-509 [17690209]
PLoS One. 2007;2(10):e979 [17912356]
Genes Chromosomes Cancer. 2007 Dec;46(12):1051-60 [17724745]
Clin Cancer Res. 2007 Dec 15;13(24):7322-8 [18094413]
J Cutan Pathol. 2008 Apr;35(4):411-7 [18333903]
J Pathol. 2008 May;215(1):39-47 [18241078]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/s12032-012-0412-8
ER  - 



TY  - JOUR
T1  - Phase I trial and pharmacokinetic study of sorafenib in children with neurofibromatosis type I and plexiform neurofibromas.
AN  - 1273584449; 22961690
AB  - Sorafenib targets multiple pathways thought to be crucial in growth of plexiform neurofibroma (PN) in children with neurofibromatosis type 1 (NF1). Sorafenib has been tolerated with manageable toxicities in adults and children with refractory cancer. We conducted a separate study in this population. Monitoring long-term toxicities such as effects on growth and obtaining additional pharmacokinetic data were of importance due to the young age and long duration of therapy seen in previous phase I trials in children with NF1.
          Children ≥3 and ≤18-year-old with NF1 and inoperable PN were eligible. Sorafenib was administered orally twice daily for consecutive 28-day cycles. Maximum tolerated dose (MTD) was determined from toxicities observed during the first three cycles. Nine children enrolled, median age 8 (6-12) years. At the starting 115 mg/m(2) /dose (n = 5), two experienced dose-limiting grade 3 pain in their PN. At the de-escalated 80 mg/m(2) /dose (n = 4), approximately 40% of the pediatric solid tumor MTD, two had dose-limiting toxicity (grade 3 rash and grade 4 mood alteration), exceeding the MTD. At 80 mg/m(2) /dose, the median AUC(0-12 hours) at steady-state was 39.5 µg hours/ml. Toxicities appeared to correspond with decreases in quality of life (QOL). No tumor shrinkage was observed.
          Children with NF1 and PN did not tolerate sorafenib at doses substantially lower than the MTD in children and adults with malignant solid tumors. Future trials with targeted agents for children with NF1 may require a more conservative starting dose and separate definitions of dose limiting toxicities (DLT) than children with cancer. Copyright © 2012 Wiley Periodicals, Inc.
JF  - Pediatric blood & cancer
AU  - Kim, AeRang
AU  - Dombi, Eva
AU  - Tepas, Kathleen
AU  - Fox, Elizabeth
AU  - Martin, Staci
AU  - Wolters, Pamela
AU  - Balis, Frank M
AU  - Jayaprakash, Nalini
AU  - Turkbey, Baris
AU  - Muradyan, Naira
AU  - Choyke, Peter L
AU  - Reddy, Alyssa
AU  - Korf, Bruce
AU  - Widemann, Brigitte C
AD  - Pediatric Oncology Branch, NCI, CCR, Bethesda, Maryland, USA. aekim@childrensnational.org
Y1  - 2013/03//
PY  - 2013
DA  - March 2013
SP  - 396
EP  - 401
VL  - 60
IS  - 3
KW  - Antineoplastic Agents
KW  - 0
KW  - Phenylurea Compounds
KW  - Niacinamide
KW  - 25X51I8RD4
KW  - sorafenib
KW  - 9ZOQ3TZI87
KW  - Index Medicus
KW  - Humans
KW  - Child
KW  - Maximum Tolerated Dose
KW  - Adolescent
KW  - Male
KW  - Female
KW  - Child, Preschool
KW  - Neurofibromatosis 1 -- drug therapy
KW  - Niacinamide -- administration & dosage
KW  - Antineoplastic Agents -- administration & dosage
KW  - Neurofibroma, Plexiform -- etiology
KW  - Neurofibroma, Plexiform -- drug therapy
KW  - Niacinamide -- pharmacokinetics
KW  - Antineoplastic Agents -- pharmacokinetics
KW  - Niacinamide -- analogs & derivatives
KW  - Neurofibromatosis 1 -- complications
KW  - Phenylurea Compounds -- administration & dosage
KW  - Antineoplastic Agents -- adverse effects
KW  - Niacinamide -- adverse effects
KW  - Phenylurea Compounds -- pharmacokinetics
KW  - Phenylurea Compounds -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273584449?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+blood+%26+cancer&rft.atitle=Phase+I+trial+and+pharmacokinetic+study+of+sorafenib+in+children+with+neurofibromatosis+type+I+and+plexiform+neurofibromas.&rft.au=Kim%2C+AeRang%3BDombi%2C+Eva%3BTepas%2C+Kathleen%3BFox%2C+Elizabeth%3BMartin%2C+Staci%3BWolters%2C+Pamela%3BBalis%2C+Frank+M%3BJayaprakash%2C+Nalini%3BTurkbey%2C+Baris%3BMuradyan%2C+Naira%3BChoyke%2C+Peter+L%3BReddy%2C+Alyssa%3BKorf%2C+Bruce%3BWidemann%2C+Brigitte+C&rft.aulast=Kim&rft.aufirst=AeRang&rft.date=2013-03-01&rft.volume=60&rft.issue=3&rft.spage=396&rft.isbn=&rft.btitle=&rft.title=Pediatric+blood+%26+cancer&rft.issn=1545-5017&rft_id=info:doi/10.1002%2Fpbc.24281
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-08
N1  - Date created - 2013-01-16
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/pbc.24281
ER  - 



TY  - JOUR
T1  - Site-specific interaction between α-synuclein and membranes probed by NMR-observed methionine oxidation rates.
AN  - 1313411129; 23398174
AB  - α-Synuclein (αS) is an intrinsically disordered protein that is water-soluble but also can bind negatively charged lipid membranes while adopting an α-helical conformation. Membrane affinity is increased by post-translational N-terminal acetylation, a common modification in all eukaryotic cells. In the presence of lipid vesicles containing a small fraction of peroxidized lipids, the N-terminal Met residues in αS (Met1 and Met5) rapidly oxidize while reducing the toxic lipid hydroperoxide to a nonreactive lipid hydroxide, whereas C-terminal Met residues remain unaffected. Met oxidation can be probed conveniently and quantitatively by NMR spectroscopy. The results show that oxidation of Met1 reduces the rate of oxidation of Met5 and vice versa as a result of decreased membrane affinity of the partially oxidized protein. The effect of Met oxidation on the αS-membrane affinity extends over large distances, as in the V49M mutant, oxidation of Met1 and Met5 strongly impacts the oxidation rate of Met49 and vice versa. When not bound to membrane, oxidized Met1 and Met5 of αS are excellent substrates for methionine sulfoxide reductase (Msr), thereby providing an efficient vehicle for water-soluble Msr enzymes to protect the membrane against oxidative damage.
JF  - Journal of the American Chemical Society
AU  - Maltsev, Alexander S
AU  - Chen, Jue
AU  - Levine, Rodney L
AU  - Bax, Ad
AD  - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/02/27/
PY  - 2013
DA  - 2013 Feb 27
SP  - 2943
EP  - 2946
VL  - 135
IS  - 8
KW  - alpha-Synuclein
KW  - 0
KW  - Methionine
KW  - AE28F7PNPL
KW  - Index Medicus
KW  - Oxidation-Reduction
KW  - Magnetic Resonance Spectroscopy -- methods
KW  - alpha-Synuclein -- chemistry
KW  - Methionine -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313411129?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Chemical+Society&rft.atitle=Site-specific+interaction+between+%CE%B1-synuclein+and+membranes+probed+by+NMR-observed+methionine+oxidation+rates.&rft.au=Maltsev%2C+Alexander+S%3BChen%2C+Jue%3BLevine%2C+Rodney+L%3BBax%2C+Ad&rft.aulast=Maltsev&rft.aufirst=Alexander&rft.date=2013-02-27&rft.volume=135&rft.issue=8&rft.spage=2943&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=1520-5126&rft_id=info:doi/10.1021%2Fja312415q
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-12
N1  - Date created - 2013-02-27
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Mol Biol. 2001 Apr 6;307(4):1061-73 [11286556]
Science. 2012 Nov 16;338(6109):949-53 [23161999]
Free Radic Biol Med. 2003 Jan 15;34(2):145-69 [12521597]
J Mol Biol. 2003 Jun 13;329(4):763-78 [12787676]
Science. 2003 Oct 31;302(5646):841 [14593171]
Ann Neurol. 2004 Feb;55(2):164-73 [14755719]
Nat Rev Drug Discov. 2004 Mar;3(3):205-14 [15031734]
J Neurochem. 1989 Feb;52(2):381-9 [2911023]
Neuron. 1995 Feb;14(2):467-75 [7857654]
J Neuropathol Exp Neurol. 1996 Aug;55(8):889-95 [8759778]
Biochemistry. 1996 Oct 29;35(43):13709-15 [8901511]
Science. 1997 Jun 27;276(5321):2045-7 [9197268]
J Biol Chem. 1998 Mar 13;273(11):6088-95 [9497326]
J Biol Chem. 1998 Apr 17;273(16):9443-9 [9545270]
Proc Natl Acad Sci U S A. 1998 May 26;95(11):6469-73 [9600990]
J Lipid Res. 1998 Aug;39(8):1529-42 [9717713]
Exp Eye Res. 2006 May;82(5):816-27 [16364291]
Biochemistry. 2006 Jul 4;45(26):8135-42 [16800638]
Biochemistry. 2006 Oct 3;45(39):12117-24 [17002311]
Nature. 2006 Oct 19;443(7113):787-95 [17051205]
Neurodegener Dis. 2008;5(2):55-9 [18182779]
Proc Natl Acad Sci U S A. 2008 May 13;105(19):7088-93 [18458334]
J Am Chem Soc. 2008 Oct 1;130(39):12856-7 [18774805]
Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19666-71 [19066219]
Proc Natl Acad Sci U S A. 2009 Apr 7;106(14):5645-50 [19293380]
J Mol Biol. 2009 Jul 24;390(4):775-90 [19481095]
Annu Rev Cell Dev Biol. 2010;26:211-33 [20500090]
Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19573-8 [20974939]
J Biol Chem. 2011 Jun 24;286(25):22262-74 [21527634]
Nature. 2011 Sep 1;477(7362):107-10 [21841800]
J Am Soc Mass Spectrom. 2012 May;23(5):889-98 [22410873]
Biochem J. 2012 Mar 15;442(3):713-21 [22150111]
J Biol Chem. 2012 May 4;287(19):15345-64 [22315227]
Biochemistry. 2012 Jun 26;51(25):5004-13 [22694188]
Biochem Soc Trans. 2012 Oct;40(5):950-4 [22988846]
J Biol Chem. 2002 Jan 4;277(1):671-8 [11679584]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1021/ja312415q
ER  - 



TY  - JOUR
T1  - Macrophage migration inhibitory factor induces epithelial to mesenchymal transition, enhances tumor aggressiveness and predicts clinical outcome in resected pancreatic ductal adenocarcinoma.
AN  - 1702654622; 22821831
AB  - MIF is a proinflammatory cytokine and is implicated in cancer. A higher MIF level is found in many human cancer and cancer-prone inflammatory diseases, including chronic pancreatitis and pancreatic cancer. We tested the hypothesis that MIF contributes to pancreatic cancer aggressiveness and predicts disease outcome in resected cases. Consistent with our hypothesis we found that an elevated MIF mRNA expression in tumors was significantly associated with poor outcome in resected cases. Multivariate Cox-regression analysis further showed that MIF is independently associated with patients' survival (HR = 2.26, 95% CI = 1.17-4.37, p = 0.015). Mechanistic analyses revealed that MIF overexpression decreased E-cadherin and increased vimentin mRNA and protein levels in pancreatic cancer cell lines, consistent with the features of epithelial-to-mesenchymal transition (EMT). Furthermore, MIF-overexpression significantly increased ZEB1/2 and decreased miR-200b expression, while shRNA-mediated inhibition of MIF increased E-cadherin and miR-200b expression, and reduced the expression of ZEB1/2 in Panc1 cells. Re-expression of miR-200b in MIF overexpressing cells restored the epithelial characteristics, as indicated by an increase in E-cadherin and decrease in ZEB1/2 and vimentin expression. A reduced sensitivity to the chemotherapeutic drug, gemcitabine, occurred in MIF-overexpressing cells. Indicative of an increased malignant potential, MIF over-expressing cells showed significant increase in their invasion ability in vitro, and tumor growth and metastasis in an orthotopic xenograft mouse model. These results support a role of MIF in disease aggressiveness, indicating its potential usefulness as a candidate target for designing improved treatment in pancreatic cancer. 
          Copyright © 2012 UICC.
JF  - International journal of cancer
AU  - Funamizu, Naotake
AU  - Hu, Chaoxin
AU  - Lacy, Curtis
AU  - Schetter, Aaron
AU  - Zhang, Geng
AU  - He, Peijun
AU  - Gaedcke, Jochen
AU  - Ghadimi, Michael B
AU  - Ried, Thomas
AU  - Yfantis, Harris G
AU  - Lee, Dong H
AU  - Subleski, Jeffrey
AU  - Chan, Tim
AU  - Weiss, Jonathan M
AU  - Back, Timothy C
AU  - Yanaga, Katsuhiko
AU  - Hanna, Nader
AU  - Alexander, H Richard
AU  - Maitra, Anirban
AU  - Hussain, S Perwez
AD  - Laboratory of Human Carcinogenesis, Center for Cancer Research, NCI, NIH, Bethesda, MD.
Y1  - 2013/02/15/
PY  - 2013
DA  - 2013 Feb 15
SP  - 785
EP  - 794
VL  - 132
IS  - 4
KW  - Antimetabolites, Antineoplastic
KW  - 0
KW  - MIRN200 microRNA, human
KW  - Macrophage Migration-Inhibitory Factors
KW  - MicroRNAs
KW  - Deoxycytidine
KW  - 0W860991D6
KW  - gemcitabine
KW  - B76N6SBZ8R
KW  - Index Medicus
KW  - Cell Proliferation -- drug effects
KW  - Neoplasm Invasiveness
KW  - Animals
KW  - MicroRNAs -- genetics
KW  - Humans
KW  - Deoxycytidine -- analogs & derivatives
KW  - Prognosis
KW  - Aged
KW  - Mice, Nude
KW  - Cell Line, Tumor
KW  - Antimetabolites, Antineoplastic -- pharmacology
KW  - Kaplan-Meier Estimate
KW  - Gene Expression Regulation, Neoplastic
KW  - Apoptosis -- genetics
KW  - Aged, 80 and over
KW  - Adult
KW  - Apoptosis -- drug effects
KW  - Transplantation, Heterologous
KW  - Cell Proliferation -- genetics
KW  - Middle Aged
KW  - RNA Interference
KW  - Deoxycytidine -- pharmacology
KW  - Male
KW  - Female
KW  - Pancreatic Neoplasms -- pathology
KW  - Macrophage Migration-Inhibitory Factors -- metabolism
KW  - Pancreatic Neoplasms -- metabolism
KW  - Carcinoma, Pancreatic Ductal -- metabolism
KW  - Macrophage Migration-Inhibitory Factors -- genetics
KW  - Epithelial-Mesenchymal Transition -- genetics
KW  - Carcinoma, Pancreatic Ductal -- pathology
KW  - Carcinoma, Pancreatic Ductal -- genetics
KW  - Pancreatic Neoplasms -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1702654622?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Macrophage+migration+inhibitory+factor+induces+epithelial+to+mesenchymal+transition%2C+enhances+tumor+aggressiveness+and+predicts+clinical+outcome+in+resected+pancreatic+ductal+adenocarcinoma.&rft.au=Funamizu%2C+Naotake%3BHu%2C+Chaoxin%3BLacy%2C+Curtis%3BSchetter%2C+Aaron%3BZhang%2C+Geng%3BHe%2C+Peijun%3BGaedcke%2C+Jochen%3BGhadimi%2C+Michael+B%3BRied%2C+Thomas%3BYfantis%2C+Harris+G%3BLee%2C+Dong+H%3BSubleski%2C+Jeffrey%3BChan%2C+Tim%3BWeiss%2C+Jonathan+M%3BBack%2C+Timothy+C%3BYanaga%2C+Katsuhiko%3BHanna%2C+Nader%3BAlexander%2C+H+Richard%3BMaitra%2C+Anirban%3BHussain%2C+S+Perwez&rft.aulast=Funamizu&rft.aufirst=Naotake&rft.date=2013-02-15&rft.volume=132&rft.issue=4&rft.spage=785&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27736
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-11-17
N1  - Date created - 2015-08-06
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Immunity. 2007 Mar;26(3):281-5 [17376392]
J Clin Invest. 2010 Nov;120(11):3843-54 [20978357]
EMBO Rep. 2010 Sep;11(9):670-7 [20706219]
Oncogene. 2010 Aug 26;29(34):4741-51 [20531305]
JOP. 2010;11(3):199-202 [20442512]
N Engl J Med. 2010 Apr 29;362(17):1605-17 [20427809]
J Surg Res. 2010 May 1;160(1):29-34 [19726058]
Carcinogenesis. 2010 Jan;31(1):37-49 [19955394]
EMBO Mol Med. 2009 Sep;1(6-7):303-14 [20049734]
Nat Cell Biol. 2009 Dec;11(12):1487-95 [19935649]
Cell. 2009 Nov 25;139(5):871-90 [19945376]
Oncogene. 2012 Dec 13;31(50):5162-71 [22286770]
Oncogene. 2013 Jan 17;32(3):296-306 [22370643]
PLoS One. 2012;7(2):e31507 [22363658]
J Exp Med. 1999 Nov 15;190(10):1375-82 [10562313]
Cancer. 2000 Jul 15;89(2):334-41 [10918163]
Cancer Res. 2008 Jan 15;68(2):537-44 [18199550]
Cancer Lett. 2008 Mar 18;261(2):147-57 [18171602]
EMBO Rep. 2008 Jun;9(6):582-9 [18483486]
Cancer Res. 2008 Oct 1;68(19):7846-54 [18829540]
J Proteome Res. 2009 Jan;8(1):35-47 [19118450]
Future Oncol. 2009 Apr;5(3):313-21 [19374539]
J Clin Invest. 2009 Jun;119(6):1420-8 [19487818]
Cancer Res. 2009 Aug 15;69(16):6704-12 [19654291]
Clin Cancer Res. 2009 Nov 1;15(21):6519-28 [19861455]
Lancet. 2011 Aug 13;378(9791):607-20 [21620466]
Gastroenterology. 2011 Dec;141(6):2140-53 [21878201]
Oncogene. 2007 Feb 1;26(5):711-24 [16862183]
Cancer Res. 2007 Mar 1;67(5):2187-96 [17332349]
Nat Rev Gastroenterol Hepatol. 2011 Jan;8(1):27-33 [21102532]
CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781]
Cell. 2012 Jan 20;148(1-2):349-61 [22265420]
PLoS One. 2012;7(2):e30771 [22363487]
Cancer Res. 2007 Jan 1;67(1):186-93 [17210698]
J Cell Biochem. 2007 Jul 1;101(4):887-907 [17266048]
Genes Immun. 2007 Dec;8(8):646-52 [17728788]
Cancer Invest. 2006 Nov;24(7):696-703 [17118780]
Gut. 2006 Jun;55(6):797-802 [16488898]
Pancreatology. 2005;5(6):514-29 [16110250]
Ann N Y Acad Sci. 1999 Jun 30;880:201-9 [10415865]
N Engl J Med. 1993 May 20;328(20):1433-7 [8479461]
Nat Rev Immunol. 2003 Oct;3(10):791-800 [14502271]
Nat Rev Cancer. 2003 Apr;3(4):276-85 [12671666]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ijc.27736
ER  - 



TY  - JOUR
T1  - Data exploration, quality control and testing in single-cell qPCR-based gene expression experiments
AN  - 1323248708; 17788530
AB  - Motivation: Cell populations are never truly homogeneous; individual cells exist in biochemical states that define functional differences between them. New technology based on microfluidic arrays combined with multiplexed quantitative polymerase chain reactions now enables high-throughput single-cell gene expression measurement, allowing assessment of cellular heterogeneity. However, few analytic tools have been developed specifically for the statistical and analytical challenges of single-cell quantitative polymerase chain reactions data.Results: We present a statistical framework for the exploration, quality control and analysis of single-cell gene expression data from microfluidic arrays. We assess accuracy and within-sample heterogeneity of single-cell expression and develop quality control criteria to filter unreliable cell measurements. We propose a statistical model accounting for the fact that genes at the single-cell level can be on (and a continuous expression measure is recorded) or dichotomously off (and the recorded expression is zero). Based on this model, we derive a combined likelihood ratio test for differential expression that incorporates both the discrete and continuous components. Using an experiment that examines treatment-specific changes in expression, we show that this combined test is more powerful than either the continuous or dichotomous component in isolation, or a t-test on the zero-inflated data. Although developed for measurements from a specific platform (Fluidigm), these tools are generalizable to other multi-parametric measures over large numbers of events.Availability: All results presented here were obtained using the SingleCellAssay R package available on GitHub (http://github.com/RGLab/SingleCellAssay).Contact: rgottard[at]fhcrc.orgSupplementary information: Supplementary data are available at Bioinformatics online.
JF  - Bioinformatics
AU  - McDavid, Andrew
AU  - Finak, Greg
AU  - Chattopadyay, Pratip K
AU  - Dominguez, Maria
AU  - Lamoreaux, Laurie
AU  - Ma, Steven S
AU  - Roederer, Mario
AU  - Gottardo, Raphael
AD  - super(1)Department of Statistics, University of Washington, Seattle, WA 98195, USA, super(2)Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, super(3)ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH, Bethesda, MD 20892, USA and super(4)Immunology Laboratory, Vaccine Research Center, NIAID, NIH, Bethesda, MD 20892, USA
Y1  - 2013/02/15/
PY  - 2013
DA  - 2013 Feb 15
SP  - 461
EP  - 467
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 29
IS  - 4
SN  - 1367-4803, 1367-4803
KW  - Biotechnology and Bioengineering Abstracts
KW  - Gene expression
KW  - Filters
KW  - Microfluidics
KW  - Data processing
KW  - Statistics
KW  - Mathematical models
KW  - Quality control
KW  - Statistical analysis
KW  - Polymerase chain reaction
KW  - Bioinformatics
KW  - Internet
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323248708?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Data+exploration%2C+quality+control+and+testing+in+single-cell+qPCR-based+gene+expression+experiments&rft.au=McDavid%2C+Andrew%3BFinak%2C+Greg%3BChattopadyay%2C+Pratip+K%3BDominguez%2C+Maria%3BLamoreaux%2C+Laurie%3BMa%2C+Steven+S%3BRoederer%2C+Mario%3BGottardo%2C+Raphael&rft.aulast=McDavid&rft.aufirst=Andrew&rft.date=2013-02-15&rft.volume=29&rft.issue=4&rft.spage=461&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbts714
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Filters; Gene expression; Microfluidics; Mathematical models; Statistics; Data processing; Quality control; Statistical analysis; Polymerase chain reaction; Bioinformatics; Internet
DO  - http://dx.doi.org/10.1093/bioinformatics/bts714
ER  - 



TY  - JOUR
T1  - Combination antiretroviral use and preterm birth.
AN  - 1285464962; 23204173
AB  - Use of antiretroviral drugs (ARVs) during pregnancy has been associated with higher risk of preterm birth.
          The Pediatric HIV/AIDS Cohort Study network's Surveillance Monitoring for ART Toxicities study is a US-based cohort of human immunodeficiency virus (HIV)-exposed uninfected children. We evaluated maternal ARV use during pregnancy and the risk of any type of preterm birth (ie, birth before 37 completed weeks of gestation), the risk of spontaneous preterm birth (ie, preterm birth that occurred after preterm labor or membrane rupture, without other complications), and the risk of small for gestational age (SGA; ie, a birth weight of <10th percentile for gestational age). Multivariable logistic regression models were used to evaluate the association of ARVs and timing of exposure, while adjusting for maternal characteristics.
          Among 1869 singleton births, 18.6% were preterm, 10.2% were spontaneous preterm, and 7.3% were SGA. A total of 89% used 3-drug combination ARV regimens during pregnancy. In adjusted models, the odds of preterm birth and spontaneous preterm birth were significantly greater among mothers who used protease inhibitors during the first trimester (adjusted odds ratios, 1.55 and 1.59, respectively) but not among mothers who used nonnucleoside reverse-transcriptase inhibitor or triple-nucleoside regimens during the first trimester. Combination ARV exposure starting later in pregnancy was not associated with increased risk. No associations were observed between SGA and exposure to combination ARV regimens. Protease inhibitor use early in pregnancy may be associated with increased risk for prematurity.
JF  - The Journal of infectious diseases
AU  - Watts, D Heather
AU  - Williams, Paige L
AU  - Kacanek, Deborah
AU  - Griner, Raymond
AU  - Rich, Kenneth
AU  - Hazra, Rohan
AU  - Mofenson, Lynne M
AU  - Mendez, Hermann A
AU  - Pediatric HIV/AIDS Cohort Study
AD  - Pediatric, Adolescent, and Maternal AIDS Branch, Eunice Kennedy Shriver National Institute for Child Health and Human Development, Bethesda, Maryland, USA. hw59i@nih.gov ; Pediatric HIV/AIDS Cohort Study
Y1  - 2013/02/15/
PY  - 2013
DA  - 2013 Feb 15
SP  - 612
EP  - 621
VL  - 207
IS  - 4
KW  - Anti-HIV Agents
KW  - 0
KW  - HIV Protease Inhibitors
KW  - Reverse Transcriptase Inhibitors
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Drug Therapy, Combination
KW  - Young Adult
KW  - Infant, Low Birth Weight
KW  - Risk Factors
KW  - Humans
KW  - Gestational Age
KW  - Cohort Studies
KW  - Adult
KW  - Infant, Newborn
KW  - Infant, Premature
KW  - Female
KW  - Pregnancy
KW  - Reverse Transcriptase Inhibitors -- adverse effects
KW  - Anti-HIV Agents -- therapeutic use
KW  - HIV Infections -- drug therapy
KW  - Anti-HIV Agents -- adverse effects
KW  - HIV Protease Inhibitors -- therapeutic use
KW  - Reverse Transcriptase Inhibitors -- therapeutic use
KW  - HIV Protease Inhibitors -- adverse effects
KW  - Pregnancy Complications, Infectious -- drug therapy
KW  - Premature Birth -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285464962?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Combination+antiretroviral+use+and+preterm+birth.&rft.au=Watts%2C+D+Heather%3BWilliams%2C+Paige+L%3BKacanek%2C+Deborah%3BGriner%2C+Raymond%3BRich%2C+Kenneth%3BHazra%2C+Rohan%3BMofenson%2C+Lynne+M%3BMendez%2C+Hermann+A%3BPediatric+HIV%2FAIDS+Cohort+Study&rft.aulast=Watts&rft.aufirst=D&rft.date=2013-02-15&rft.volume=207&rft.issue=4&rft.spage=612&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjis728
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-15
N1  - Date created - 2013-01-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
AIDS. 2008 Sep 12;22(14):1815-20 [18753864]
Sex Transm Infect. 2009 Apr;85(2):82-7 [18987014]
AIDS. 2009 Jun 19;23(10):1235-43 [19424054]
Pharmacotherapy. 2009 Nov;29(11):1289-96 [19857146]
AIDS. 2000 Dec 22;14(18):2913-20 [11398741]
N Engl J Med. 2002 Jun 13;346(24):1863-70 [12063370]
BMC Pediatr. 2003 Dec 16;3:13 [14678563]
J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Feb 1;20(2):179-86 [10048906]
AIDS. 2004 Nov 19;18(17):2337-9 [15577551]
Am J Reprod Immunol. 2006 Jan;55(1):19-27 [16364008]
J Reprod Immunol. 2006 Jun;70(1-2):143-50 [16423410]
Aust N Z J Obstet Gynaecol. 2006 Jun;46(3):189-92 [16704470]
J Infect Dis. 2007 Mar 15;195(6):913-4; author reply 916-7 [17299723]
J Infect Dis. 2007 Mar 15;195(6):914-6; author reply 916-7 [17299724]
AIDS. 2007 Mar 12;21(5):607-15 [17314523]
Pediatrics. 2007 Apr;119(4):e900-6 [17353299]
AIDS. 2007 May 11;21(8):1019-26 [17457096]
Lancet. 2008 Jan 5;371(9606):75-84 [18177778]
HIV Med. 2008 Jan;9(1):6-13 [18199167]
AIDS. 2008 May 11;22(8):973-81 [18453857]
J Infect Dis. 2010 Apr 1;201(7):1035-44 [20196654]
BJOG. 2010 Oct;117(11):1399-410 [20716250]
AIDS Behav. 2010 Dec;14(6):1269-78 [20532607]
HIV Med. 2011 Apr;12(4):228-35 [20726902]
AIDS. 2011 Jun 1;25(9):1207-17 [21505304]
J Infect Dis. 2011 Aug 15;204(4):506-14 [21791651]
AIDS Patient Care STDS. 2011 Jul;25(7):385-94 [21992592]
AIDS. 2012 Jan 2;26(1):37-43 [22008651]
Clin Infect Dis. 2012 May;54(9):1348-60 [22460969]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/infdis/jis728
ER  - 



TY  - JOUR
T1  - Combination treatments with ABT-263 and an immunotoxin produce synergistic killing of ABT-263-resistant small cell lung cancer cell lines.
AN  - 1273263295; 22821746
AB  - Synergistic killing was achieved when Small Cell Lung Cancer (SCLC) cell lines were incubated with ABT-263 and an immunotoxin directed to the transferrin receptor. SCLC lines are variably sensitive to the BH-3 only peptide mimetic, ABT-263. To determine their sensitivity to toxin-based reagents, we incubated four representative SCLC lines with a model Pseudomonas exotoxin-based immunotoxin directed to the transferrin receptor. Remarkably in 4-of-4 lines, there was little evidence of immunotoxin-mediated cytotoxicity despite near complete inhibition of protein synthesis. However, when combinations of ABT-263 and immunotoxin were added to the ABT-263-resistant cell lines (H196 and H69AR), there was synergistic killing as evidenced by increased activation of caspase 3/7, annexin V staining, and loss of cell integrity. Synergistic killing was evident at 6 hr and correlated with loss of Mcl-1. This synergy was also noted when the closely related compound ABT-737 was combined with the same immunotoxin. To establish that the synergy seen in tissue culture could be achieved in vivo, H69AR cells were grown as tumors in nude mice and shown to be susceptible to the killing action of an immunotoxin-ABT-737 combination but not to either agent alone. When immunotoxin-ABT combinations were added to ABT-263-sensitive lines (H146 and H1417), killing was additive. Our data support combination approaches for treating ABT-263-resistant SCLC with ABT-263 and a second agent that provides synergistic killing action.
          Published 2012 UICC.
JF  - International journal of cancer
AU  - Mattoo, Abid R
AU  - FitzGerald, David J
AD  - Biotherapy Section, Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, HHS, Bethesda, MD 20819, USA.
Y1  - 2013/02/15/
PY  - 2013
DA  - 2013 Feb 15
SP  - 978
EP  - 987
VL  - 132
IS  - 4
KW  - ABT-737
KW  - 0
KW  - Aniline Compounds
KW  - Biphenyl Compounds
KW  - Immunotoxins
KW  - Mcl1 protein, mouse
KW  - Myeloid Cell Leukemia Sequence 1 Protein
KW  - Nitrophenols
KW  - Piperazines
KW  - Proto-Oncogene Proteins c-bcl-2
KW  - Receptors, Transferrin
KW  - Sulfonamides
KW  - Caspase 3
KW  - EC 3.4.22.-
KW  - Caspase 7
KW  - navitoclax
KW  - XKJ5VVK2WD
KW  - Index Medicus
KW  - Proto-Oncogene Proteins c-bcl-2 -- biosynthesis
KW  - Animals
KW  - Caspase 7 -- metabolism
KW  - Humans
KW  - Cell Line, Tumor
KW  - Mice
KW  - Mice, Nude
KW  - Mice, Inbred BALB C
KW  - Piperazines -- pharmacology
KW  - Proto-Oncogene Proteins c-bcl-2 -- antagonists & inhibitors
KW  - Receptors, Transferrin -- immunology
KW  - Drug Synergism
KW  - Caspase 3 -- metabolism
KW  - Drug Resistance, Neoplasm -- drug effects
KW  - Aniline Compounds -- pharmacology
KW  - Sulfonamides -- pharmacology
KW  - Small Cell Lung Carcinoma -- drug therapy
KW  - Nitrophenols -- pharmacology
KW  - Aniline Compounds -- therapeutic use
KW  - Immunotoxins -- therapeutic use
KW  - Biphenyl Compounds -- pharmacology
KW  - Immunotoxins -- pharmacology
KW  - Sulfonamides -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273263295?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Combination+treatments+with+ABT-263+and+an+immunotoxin+produce+synergistic+killing+of+ABT-263-resistant+small+cell+lung+cancer+cell+lines.&rft.au=Mattoo%2C+Abid+R%3BFitzGerald%2C+David+J&rft.aulast=Mattoo&rft.aufirst=Abid&rft.date=2013-02-15&rft.volume=132&rft.issue=4&rft.spage=978&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27732
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-02-20
N1  - Date created - 2012-12-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010]
FEBS J. 2011 Dec;278(23):4683-700 [21585657]
J Clin Oncol. 2011 Dec 20;29(36):4828-36 [22042955]
Mol Oncol. 2012 Apr;6(2):242-50 [22248437]
Clin Cancer Res. 2012 Jun 1;18(11):3163-9 [22496272]
J Gene Med. 2012 Jun;14(6):405-15 [22262649]
Cancer Res. 2007 Feb 1;67(3):1176-83 [17283153]
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17099-104 [17940013]
Cancer Res. 2008 Apr 1;68(7):2321-8 [18381439]
Cancer Res. 2008 May 1;68(9):3421-8 [18451170]
Clin Cancer Res. 2008 Jun 1;14(11):3268-77 [18519752]
J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673]
Br J Haematol. 2010 Jan;148(1):99-109 [19821820]
Mol Cancer Ther. 2010 Mar;9(3):545-57 [20179162]
Nat Rev Immunol. 2010 May;10(5):317-27 [20414205]
Clin Cancer Res. 2006 Aug 1;12(15):4695-701 [16899620]
Nature. 2005 Jun 2;435(7042):677-81 [15902208]
Biochemistry. 1998 Dec 1;37(48):16934-42 [9836586]
J Clin Oncol. 1997 Feb;15(2):723-34 [9053498]
J Cell Biochem. 1995 Jun;58(2):160-74 [7673324]
Mol Cell Biol. 1991 Apr;11(4):2200-5 [2005905]
Int J Cancer. 2004 Nov 10;112(3):475-83 [15382075]
Toxicon. 2004 Sep 15;44(4):361-70 [15302520]
Clin Cancer Res. 2002 Mar;8(3):893-903 [11895924]
Cancer Res. 2000 Nov 1;60(21):6101-10 [11085534]
Clin Cancer Res. 2000 Feb;6(2):326-34 [10690507]
PLoS One. 2011;6(9):e24012 [21915275]
Br J Haematol. 2011 Aug;154(4):471-6 [21732928]
Leuk Lymphoma. 2011 Jun;52 Suppl 2:82-6 [21599609]
Mol Cancer Ther. 2010 Jul;9(7):2007-15 [20587662]
J Clin Oncol. 2011 Mar 1;29(7):909-16 [21282543]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ijc.27732
ER  - 



TY  - JOUR
T1  - Daily treadmill exercise attenuates cocaine cue-induced reinstatement and cocaine induced locomotor response but increases cocaine-primed reinstatement
AN  - 1268653618; 17491863
AB  - Exercise affects neuroplasticity and neurotransmission including dopamine (DA), which modulates drug-taking behavior. Previous research in rodents has shown that exercise may attenuate the rewarding effects of drugs of abuse. The present study examined the effects of high and low exercise on cocaine responses in male Wistar rats that had been trained to self-administer and were compared to a group of sedentary rats. High exercise rats (HE) ran daily on a treadmill for 2h and low exercise (LE) ran daily for 1h. After 6 weeks of this exercise regimen, rats were tested over 2 days for reinstatement (day 1: cue-induced reinstatement; day 2: cocaine-primed reinstatement). During cue-induced reinstatement, the sedentary rats showed the expected increase in active lever responses when compared to maintenance, whereas these increased responses were inhibited in the exercised rats (HE and LE). During cocaine-primed reinstatement, however, there was a significant increase in active lever presses when compared to maintenance only in the HE group. This data suggests that chronic exercise during abstinence attenuates the cue-induced reinstatement seen in the sedentary rats by 26% (LE) and 21% (HE). In contrast, only the high exercise rats exhibited sensitized cocaine-seeking behavior (active lever presses) following cocaine-primed reinstatement. Finally, while sedentary rats increased locomotor activity during cocaine-primed reinstatement over that seen with cocaine during maintenance, this was not observed in the exercised rats, suggesting that exercise may interfere with the sensitized locomotor response during cocaine reinstatement.
JF  - Behavioural Brain Research
AU  - Thanos, Panayotis K
AU  - Stamos, Joshua
AU  - Robison, Lisa S
AU  - Heyman, Gary
AU  - Tucci, Andrew
AU  - Wang, Gene-Jack
AU  - Robinson, John K
AU  - Anderson, Brenda J
AU  - Volkow, Nora D
AD  - Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892, USA, thanos@bnl.gov
Y1  - 2013/02/15/
PY  - 2013
DA  - 2013 Feb 15
SP  - 8
EP  - 14
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 239
SN  - 0166-4328, 0166-4328
KW  - Physical Education Index; Animal Behavior Abstracts; CSA Neurosciences Abstracts
KW  - Data processing
KW  - Animal subjects
KW  - Brain
KW  - Exercise
KW  - Plasticity
KW  - Drug abuse
KW  - Reinstatement
KW  - Maintenance
KW  - Physical training
KW  - Dopamine
KW  - Neurotransmission
KW  - Behavior
KW  - Locomotor activity
KW  - Reinforcement
KW  - Cocaine
KW  - Drugs
KW  - Treadmill ergometry
KW  - N3 11001:Behavioral and Cognitive Neuroscience
KW  - Y 25110:Biochemical & Neurophysiological Correlates, Lesions and Stimuli
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1268653618?accountid=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=Behavioural+Brain+Research&rft.atitle=Daily+treadmill+exercise+attenuates+cocaine+cue-induced+reinstatement+and+cocaine+induced+locomotor+response+but+increases+cocaine-primed+reinstatement&rft.au=Thanos%2C+Panayotis+K%3BStamos%2C+Joshua%3BRobison%2C+Lisa+S%3BHeyman%2C+Gary%3BTucci%2C+Andrew%3BWang%2C+Gene-Jack%3BRobinson%2C+John+K%3BAnderson%2C+Brenda+J%3BVolkow%2C+Nora+D&rft.aulast=Thanos&rft.aufirst=Panayotis&rft.date=2013-02-15&rft.volume=239&rft.issue=&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Behavioural+Brain+Research&rft.issn=01664328&rft_id=info:doi/10.1016%2Fj.bbr.2012.10.035
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2013-01-01
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Behavior; Animal subjects; Brain; Exercise; Drugs; Treadmill ergometry; Maintenance; Data processing; Dopamine; Neurotransmission; Locomotor activity; Reinforcement; Drug abuse; Plasticity; Cocaine; Reinstatement; Physical training
DO  - http://dx.doi.org/10.1016/j.bbr.2012.10.035
ER  - 



TY  - CPAPER
T1  - Personal Genomics and Science Policy
T2  - 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS 2013)
AN  - 1369227485; 6213320
JF  - 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS 2013)
AU  - Gitlin, Jonathan
Y1  - 2013/02/14/
PY  - 2013
DA  - 2013 Feb 14
KW  - Policies
KW  - genomics
KW  - Science policy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369227485?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2013%29&rft.atitle=Personal+Genomics+and+Science+Policy&rft.au=Gitlin%2C+Jonathan&rft.aulast=Gitlin&rft.aufirst=Jonathan&rft.date=2013-02-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://aaas.confex.com/aaas/2013/webprogram/start.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Navigating the Dynamic Cell
T2  - 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS 2013)
AN  - 1369227146; 6213422
JF  - 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS 2013)
AU  - Lippincott-Schwartz, Jennifer
Y1  - 2013/02/14/
PY  - 2013
DA  - 2013 Feb 14
KW  - Economics
KW  - Social aspects
KW  - Science
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369227146?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2013%29&rft.atitle=Navigating+the+Dynamic+Cell&rft.au=Lippincott-Schwartz%2C+Jennifer&rft.aulast=Lippincott-Schwartz&rft.aufirst=Jennifer&rft.date=2013-02-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://aaas.confex.com/aaas/2013/webprogram/start.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - CPAPER
T1  - Nuclear Architecture and Disease
T2  - 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS 2013)
AN  - 1369226758; 6213153
JF  - 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS 2013)
AU  - Misteli, Thomas
Y1  - 2013/02/14/
PY  - 2013
DA  - 2013 Feb 14
KW  - Economics
KW  - Social aspects
KW  - Science
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369226758?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2013+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2013%29&rft.atitle=Nuclear+Architecture+and+Disease&rft.au=Misteli%2C+Thomas&rft.aulast=Misteli&rft.aufirst=Thomas&rft.date=2013-02-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2013+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2013%29&rft.issn=&rft_id=info:doi/
L2  - http://aaas.confex.com/aaas/2013/webprogram/start.html
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - JOUR
T1  - ONE Nano: NIEHS's Strategic Initiative on the Health and Safety Effects of Engineered Nanomaterials
AN  - 1352290648; 17970879
AB  - Background: The past decade has seen tremendous expansion in the production and application of engineered nanomaterials (ENMs). The unique properties that make ENMs useful in the marketplace also make their interactions with biological systems difficult to anticipate and critically important to explore. Currently, little is known about the health effects of human exposure to these materials. Objectives: As part of its role in supporting the National Nanotechnology Initiative, the National Institute of Environmental Health Sciences (NIEHS) has developed an integrated, strategic research program-"ONE Nano"-to increase our fundamental understanding of how ENMs interact with living systems, to develop predictive models for quantifying ENM exposure and assessing ENM health impacts, and to guide the design of second-generation ENMs to minimize adverse health effects. Discussion: The NIEHS's research investments in ENM health and safety include extramural grants and grantee consortia, intramural research activities, and toxicological studies being conducted by the National Toxicology Program (NTP). These efforts have enhanced collaboration within the nanotechnology research community and produced toxicological profiles for selected ENMs, as well as improved methods and protocols for conducting in vitro and in vivo studies to assess ENM health effects. Conclusion: By drawing upon the strengths of the NIEHS's intramural, extramural, and NTP programs and establishing productive partnerships with other institutes and agencies across the federal government, the NIEHS's strategic ONE Nano program is working toward new advances to improve our understanding of the health impacts of engineered nanomaterials and support the goals of the National Nanotechnology Initiative.
JF  - Environmental Health Perspectives
AU  - Schug, Thaddeus T
AU  - Johnson, Anne F
AU  - Balshaw, David M
AU  - Garantziotis, Stavros
AU  - Walker, Nigel J
AU  - Weis, Christopher
AU  - Nadadur, Srikanth S
AU  - Birnbaum, Linda S
AD  - Cellular, Organs and Systems Pathobiology Branch, 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  - 2013/02/12/
PY  - 2013
DA  - 2013 Feb 12
SP  - 410
EP  - 414
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 4
SN  - 0091-6765, 0091-6765
KW  - Environment Abstracts; Health & Safety Science Abstracts; Water Resources Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; Aqualine Abstracts
KW  - consortium-based research
KW  - health effects
KW  - nanoparticles
KW  - nanotechnology
KW  - Prediction
KW  - Environmental health
KW  - Expansion
KW  - Environmental factors
KW  - Nanotechnology
KW  - Public health
KW  - Public Health
KW  - Safety engineering
KW  - Exposure
KW  - Prediction models
KW  - Investment
KW  - Toxicology
KW  - Safety
KW  - Grants
KW  - Model Studies
KW  - Strength
KW  - Profiles
KW  - Health and safety
KW  - Governments
KW  - SW 5010:Network design
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW  - Q5 08504:Effects on organisms
KW  - AQ 00008:Effects of Pollution
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352290648?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=ONE+Nano%3A+NIEHS%27s+Strategic+Initiative+on+the+Health+and+Safety+Effects+of+Engineered+Nanomaterials&rft.au=Schug%2C+Thaddeus+T%3BJohnson%2C+Anne+F%3BBalshaw%2C+David+M%3BGarantziotis%2C+Stavros%3BWalker%2C+Nigel+J%3BWeis%2C+Christopher%3BNadadur%2C+Srikanth+S%3BBirnbaum%2C+Linda+S&rft.aulast=Schug&rft.aufirst=Thaddeus&rft.date=2013-02-12&rft.volume=121&rft.issue=4&rft.spage=410&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1206091
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2015-05-13
N1  - SubjectsTermNotLitGenreText - Prediction; Health and safety; Governments; Environmental factors; Toxicology; Public health; Safety engineering; Grants; Prediction models; Environmental health; Nanotechnology; Strength; Public Health; Profiles; Exposure; Safety; Expansion; Investment; Model Studies
DO  - http://dx.doi.org/10.1289/ehp.1206091
ER  - 



TY  - JOUR
T1  - Identification of functionally conserved regions in the structure of the chaperone/CenH3/H4 complex.
AN  - 1282513004; 23178171
AB  - In eukaryotes, a variant of conventional histone H3 termed CenH3 epigenetically marks the centromere. The conserved CenH3 chaperone specifically recognizes CenH3 and is required for CenH3 deposition at the centromere. Recently, the structures of the chaperone/CenH3/H4 complexes have been determined for Homo sapiens (Hs) and the budding yeasts Saccharomyces cerevisiae (Sc) and Kluyveromyces lactis (Kl). Surprisingly, the three structures are very different, leading to different proposed structural bases for chaperone function. The question of which structural region of CenH3 provides the specificity determinant for the chaperone recognition is not fully answered. Here, we investigated these issues using solution NMR and site-directed mutagenesis. We discovered that, in contrast to previous findings, the structures of the Kl and Sc chaperone/CenH3/H4 complexes are actually very similar. This new finding reveals that both budding yeast and human chaperones use a similar structural region to block DNA from binding to the histones. Our mutational analyses further indicate that the N-terminal region of the CenH3 α2 helix is sufficient for specific recognition by the chaperone for both budding yeast and human. Thus, our studies have identified conserved structural bases of how the chaperones recognize CenH3 and perform the chaperone function.
          Published by Elsevier Ltd.
JF  - Journal of molecular biology
AU  - Hong, Jingjun
AU  - Feng, Hanqiao
AU  - Zhou, Zheng
AU  - Ghirlando, Rodolfo
AU  - Bai, Yawen
AD  - Laboratory of Biochemistry and Molecular Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Y1  - 2013/02/08/
PY  - 2013
DA  - 2013 Feb 08
SP  - 536
EP  - 545
VL  - 425
IS  - 3
KW  - Histone Chaperones
KW  - 0
KW  - Histones
KW  - Index Medicus
KW  - Mutagenesis, Site-Directed
KW  - Models, Molecular
KW  - Humans
KW  - DNA Mutational Analysis
KW  - Saccharomyces cerevisiae -- chemistry
KW  - Kluyveromyces -- chemistry
KW  - Protein Binding
KW  - Magnetic Resonance Spectroscopy
KW  - Histone Chaperones -- metabolism
KW  - Protein Interaction Mapping
KW  - Histones -- metabolism
KW  - Histones -- chemistry
KW  - Histone Chaperones -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282513004?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=Identification+of+functionally+conserved+regions+in+the+structure+of+the+chaperone%2FCenH3%2FH4+complex.&rft.au=Hong%2C+Jingjun%3BFeng%2C+Hanqiao%3BZhou%2C+Zheng%3BGhirlando%2C+Rodolfo%3BBai%2C+Yawen&rft.aulast=Hong&rft.aufirst=Jingjun&rft.date=2013-02-08&rft.volume=425&rft.issue=3&rft.spage=536&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=1089-8638&rft_id=info:doi/10.1016%2Fj.jmb.2012.11.021
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-22
N1  - Date created - 2013-01-28
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Mol Cell. 2012 Jan 27;45(2):263-9 [22209075]
Proc Natl Acad Sci U S A. 2012 Jan 3;109(1):243-8 [22184235]
Dev Cell. 2012 Apr 17;22(4):749-62 [22406139]
Cell. 2012 Jul 20;150(2):304-16 [22817893]
Cell. 2009 Jun 26;137(7):1173-4 [19563746]
J Am Chem Soc. 2001 Apr 4;123(13):2970-8 [11457007]
Science. 2001 Aug 10;293(5532):1098-102 [11498581]
Cell. 2003 Feb 21;112(4):407-21 [12600307]
Anal Biochem. 2003 Sep 1;320(1):104-24 [12895474]
Nature. 2004 Jul 29;430(6999):578-82 [15282608]
J Biomol NMR. 1994 Mar;4(2):171-80 [8019132]
J Biomol NMR. 1995 Nov;6(3):277-93 [8520220]
J Biomol NMR. 1996 Dec;8(4):477-86 [9008363]
Nature. 1997 Sep 18;389(6648):251-60 [9305837]
Cell. 2007 Jun 15;129(6):1153-64 [17574026]
Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10571-6 [17548816]
Mol Cell. 2007 Jun 22;26(6):853-65 [17569568]
Methods Cell Biol. 2008;84:143-79 [17964931]
Mol Cell. 2009 Feb 13;33(3):287-98 [19217403]
Mol Cell. 2009 Feb 13;33(3):299-311 [19217404]
Cell. 2009 May 1;137(3):472-84 [19410544]
Cell. 2009 May 1;137(3):485-97 [19410545]
Mol Cell. 2010 Nov 12;40(3):444-54 [21070970]
Mol Cell. 2010 Nov 12;40(3):455-64 [21070971]
Nature. 2011 Apr 14;472(7342):234-7 [21412236]
Genes Dev. 2011 May 1;25(9):901-6 [21478274]
Proc Natl Acad Sci U S A. 2011 Jun 7;108(23):9367-71 [21606327]
Proc Natl Acad Sci U S A. 2011 Aug 30;108(35):E596; author reply E597 [21844330]
Cell Cycle. 2011 Oct 1;10(19):3217-8 [21926476]
Genetics. 2012 Apr;190(4):1575-7 [22234856]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.jmb.2012.11.021
ER  - 



TY  - JOUR
T1  - Postpartum Remodeling, Lactation, and Breast Cancer Risk: Summary of a National Cancer Institute-Sponsored Workshop
AN  - 1315622940; 17682450
AB  - The pregnancy-lactation cycle (PLC) is a period in which the breast is transformed from a less-developed, nonfunctional organ into a mature, milk-producing gland that has evolved to meet the nutritional, developmental, and immune protection needs of the newborn. Cessation of lactation initiates a process whereby the breast reverts to a resting state until the next pregnancy. Changes during this period permanently alter the morphology and molecular characteristics of the breast (molecular histology) and produce important, yet poorly understood, effects on breast cancer risk. To provide a state-of-the-science summary of this topic, the National Cancer Institute invited a multidisciplinary group of experts to participate in a workshop in Rockville, Maryland, on March 2, 2012. Topics discussed included: 1) the epidemiology of the PLC in relation to breast cancer risk, 2) breast milk as a biospecimen for molecular epidemiological and translational research, and 3) use of animal models to gain mechanistic insights into the effects of the PLC on breast carcinogenesis. This report summarizes conclusions of the workshop, proposes avenues for future research on the PLC and its relationship with breast cancer risk, and identifies opportunities to translate this knowledge to improve breast cancer outcomes.
JF  - Journal of the National Cancer Institute
AU  - Faupel-Badger, Jessica M
AU  - Arcaro, Kathleen F
AU  - Balkam, Jane J
AU  - Eliassen, AHeather
AU  - Hassiotou, Foteini
AU  - Lebrilla, Carlito B
AU  - Michels, Karin B
AU  - Palmer, Julie R
AU  - Schedin, Pepper
AU  - Stuebe, Alison M
AU  - Watson, Christine J
AU  - Sherman, Mark E
AD  - Affiliations of authors:Cancer Prevention Fellowship Program and Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (JMF-B); Department of Veterinary and Animal Sciences, University of Massachusetts-Amherst, Amherst, MA (KFA); School of Nursing, Notre Dame of Maryland University, Baltimore, MD (JJB); Channing Laboratory, Brigham and Women's Hospital, Harvard School of Public Health, Boston, MA (AHE); School of Chemistry and Biochemistry and School of Anatomy, Physiology and Human Biology, University of Western Australia, Crawley, Australia (FH); Department of Chemistry and Department of Biochemistry, University of California, Davis, CA (CBL); Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (KBM); Department of Epidemiology, Harvard School of Public Health, Boston, MA (KBM); Slone Epidemiology Center at Boston University, Boston, MA (JRP); Division of Medical Oncology,, shermanm@mail.nih.gov
Y1  - 2013/02/06/
PY  - 2013
DA  - 2013 Feb 06
SP  - 166
EP  - 174
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 3
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Animal models
KW  - Breast cancer
KW  - Breast milk
KW  - Cancer
KW  - Carcinogenesis
KW  - Histology
KW  - Nutrition
KW  - Organs
KW  - Pregnancy
KW  - USA, Maryland, Rockville
KW  - USA, Maryland
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315622940?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Postpartum+Remodeling%2C+Lactation%2C+and+Breast+Cancer+Risk%3A+Summary+of+a+National+Cancer+Institute-Sponsored+Workshop&rft.au=Faupel-Badger%2C+Jessica+M%3BArcaro%2C+Kathleen+F%3BBalkam%2C+Jane+J%3BEliassen%2C+AHeather%3BHassiotou%2C+Foteini%3BLebrilla%2C+Carlito+B%3BMichels%2C+Karin+B%3BPalmer%2C+Julie+R%3BSchedin%2C+Pepper%3BStuebe%2C+Alison+M%3BWatson%2C+Christine+J%3BSherman%2C+Mark+E&rft.aulast=Faupel-Badger&rft.aufirst=Jessica&rft.date=2013-02-06&rft.volume=105&rft.issue=3&rft.spage=166&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs505
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2013-03-22
N1  - SubjectsTermNotLitGenreText - Histology; Carcinogenesis; Animal models; Breast milk; Breast cancer; Nutrition; Organs; Cancer; Pregnancy; USA, Maryland, Rockville; USA, Maryland
DO  - http://dx.doi.org/10.1093/jnci/djs505
ER  - 



TY  - JOUR
T1  - Endocrine-Disrupting Chemicals (EDCs): In Vitro Mechanism of Estrogenic Activation and Differential Effects on ER Target Genes
AN  - 1660053126; 17970894
AB  - Background: Endocrine-disrupting chemicals (EDCs) influence the activity of estrogen receptors (ERs) and alter the function of the endocrine system. However, the diversity of EDC effects and mechanisms of action are poorly understood. Objectives: We examined the agonistic activity of EDCs through ER alpha and ER beta . We also investigated the effects of EDCs on ER-mediated target genes. Methods: HepG2 and HeLa cells were used to determine the agonistic activity of EDCs on ER alpha and ER beta via the luciferase reporter assay. Ishikawa cells stably expressing ER alpha were used to determine changes in endogenous ER target gene expression by EDCs. Results: Twelve EDCs were categorized into three groups on the basis of product class and similarity of chemical structure. As shown by luciferase reporter analysis, the EDCs act as ER agonists in a cell type- and promoter-specific manner. Bisphenol A, bisphenol AF, and 2-2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane (group 1) strongly activated ER alpha estrogen responsive element (ERE)-mediated responses. Daidzein, genistein, kaempferol, and coumestrol (group 2) activated both ER alpha and ER beta ERE-mediated activities. Endosulfan and kepone (group 3) weakly activated ER alpha . Only a few EDCs significantly activated the "tethered" mechanism via ER alpha or ER beta . Results of real-time polymerase chain reaction indicated that bisphenol A and bisphenol AF consistently activated endogenous ER target genes, but the activities of other EDCs on changes of ER target gene expression were compound specific. Conclusion: Although EDCs with similar chemical structures (in the same group) tended to have comparable ER alpha and ER beta ERE-mediated activities, similar chemical structure did not correlate with previously reported ligand binding affinities of the EDCs. Using ER alpha -stable cells, we observed that EDCs differentially induced activity of endogenous ER target genes.
JF  - Environmental Health Perspectives
AU  - Li, Yin
AU  - Luh, Colin J
AU  - Burns, Katherine A
AU  - Arao, Yukitomo
AU  - Jiang, Zhongliang
AU  - Teng, Christina T
AU  - Tice, Raymond R
AU  - Korach, Kenneth S
AD  - Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, Division of Intramural Research, 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  - 2013/02/05/
PY  - 2013
DA  - 2013 Feb 05
SP  - 459
EP  - 466
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 4
SN  - 0091-6765, 0091-6765
KW  - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - E2
KW  - EDCs
KW  - ER alpha
KW  - ER beta
KW  - ERE
KW  - ER target genes. Environ Health Perspect 121:459-466 (2013)
KW  - Bisphenol A
KW  - Activation
KW  - Estrogens
KW  - Genes
KW  - Bisphenols
KW  - Endocrine systems
KW  - Activated
KW  - Similarity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660053126?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Endocrine-Disrupting+Chemicals+%28EDCs%29%3A+In+Vitro+Mechanism+of+Estrogenic+Activation+and+Differential+Effects+on+ER+Target+Genes&rft.au=Li%2C+Yin%3BLuh%2C+Colin+J%3BBurns%2C+Katherine+A%3BArao%2C+Yukitomo%3BJiang%2C+Zhongliang%3BTeng%2C+Christina+T%3BTice%2C+Raymond+R%3BKorach%2C+Kenneth+S&rft.aulast=Li&rft.aufirst=Yin&rft.date=2013-02-05&rft.volume=121&rft.issue=4&rft.spage=459&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205951
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2015-05-04
DO  - http://dx.doi.org/10.1289/ehp.1205951
ER  - 



TY  - JOUR
T1  - Meat-Related Compounds and Colorectal Cancer Risk by Anatomical Subsite
AN  - 1842507894; 17848775
AB  - Since meat may be involved in the etiology of colorectal cancer, associations between meat-related compounds were examined to elucidate underlying mechanisms in a population-based case-control study. Participants (989 cases/1,033 healthy controls) completed a food frequency questionnaire with a meat-specific module. Multivariable logistic regression was used to examine associations between meat variables and colorectal cancer; polytomous logistic regression was used for subsite-specific analyses. The following significant positive associations were observed for meat-related compounds: 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) and colorectal, distal colon, and rectal tumors; 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and colorectal and colon cancer tumors; nitrites/nitrates and proximal colon cancer; 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and rectal cancer; and benzo[a]pyrene and rectal cancer (P-trends < 0.05). For analyses by meat type, cooking method, and doneness preference, positive associations between red processed meat and proximal colon cancer and pan-fried red meat and colorectal cancer were found (P-trends < 0.05). Inverse associations were observed between unprocessed poultry and colorectal, colon, proximal colon, and rectal tumors; grilled/barbequed poultry and proximal colon cancer; and well-done/charred poultry and colorectal, colon, and proximal colon tumors (P-trends < 0.05). HCAs, PAHs, nitrites, and nitrates may be involved in colorectal cancer etiology. Further examination into the unexpected inverse associations between poultry and colorectal cancer is warranted.
JF  - Nutrition and Cancer
AU  - Miller, Paige E
AU  - Lazarus, Philip
AU  - Lesko, Samuel M
AU  - Cross, Amanda J
AU  - Sinha, Rashmi
AU  - Laio, Jason
AU  - Zhu, Jay
AU  - Harper, Gregory
AU  - Muscat, Joshua E
AU  - Hartman, Terryl J
AD  - Cancer Prevention Fellowship Program, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA, pmiller@exponent.com
Y1  - 2013/02/01/
PY  - 2013
DA  - 2013 Feb 01
SP  - 202
EP  - 226
PB  - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL  - 65
IS  - 2
SN  - 0163-5581, 0163-5581
KW  - Toxicology Abstracts
KW  - Inventories
KW  - Nitrate
KW  - Etiology
KW  - Poultry
KW  - Rectum
KW  - Food
KW  - Colorectal cancer
KW  - Colon cancer
KW  - Tumors
KW  - Meat
KW  - Cooking
KW  - Benzo(a)pyrene
KW  - Nitrite
KW  - X 24320:Food Additives & Contaminants
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842507894?accountid=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=Nutrition+and+Cancer&rft.atitle=Meat-Related+Compounds+and+Colorectal+Cancer+Risk+by+Anatomical+Subsite&rft.au=Miller%2C+Paige+E%3BLazarus%2C+Philip%3BLesko%2C+Samuel+M%3BCross%2C+Amanda+J%3BSinha%2C+Rashmi%3BLaio%2C+Jason%3BZhu%2C+Jay%3BHarper%2C+Gregory%3BMuscat%2C+Joshua+E%3BHartman%2C+Terryl+J&rft.aulast=Miller&rft.aufirst=Paige&rft.date=2013-02-01&rft.volume=65&rft.issue=2&rft.spage=202&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+Cancer&rft.issn=01635581&rft_id=info:doi/10.1080%2F01635581.2013.756534
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Nitrate; Inventories; Poultry; Etiology; Rectum; Food; Colorectal cancer; Tumors; Colon cancer; Meat; Cooking; Benzo(a)pyrene; Nitrite
DO  - http://dx.doi.org/10.1080/01635581.2013.756534
ER  - 



TY  - JOUR
T1  - New and Evolving Rare Diseases Research Programs at the National Institutes of Health
AN  - 1773843875; PQ0002708138
AB  - Research emphasis on rare diseases and orphan products remains a major focus of the research Institutes and Centers of National Institutes of Health (NIH). NIH provides more than USD 31 billion annually in biomedical research and research support. This research is the basis of many of the health advances in rare and common diseases. Numerous efforts and a major emphasis by the public and private sector initiatives have resulted in an increase of interventions and diagnostics for rare diseases. Newer translational research programs provide a more systematic and coordinated approach to rare diseases research and orphan products development. The approach that is offered requires extensive public-private partnerships with the pharmaceutical industry, contract research organizations, philanthropic foundations, medical and scientific advisory boards, patient advocacy groups, the academic research community, research and regulatory scientists, government funding agencies, and the public. Each program is unique and requires lengthy planning and collaborative efforts to reach programmatic goals. copyright 2013 S. Karger AG, Basel
JF  - Public Health Genomics
AU  - Groft, S C
AU  - Rubinstein, Y R
AD  - Office of Rare Diseases Research, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Md., USA
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 259
EP  - 267
PB  - S. Karger AG, P.O. Box Basel CH-4009 Switzerland
VL  - 16
IS  - 6
SN  - 1662-4246, 1662-4246
KW  - Genetics Abstracts; Health & Safety Science Abstracts
KW  - Biospecimens
KW  - Common data elements
KW  - Orphan drugs
KW  - Patient advocacy groups
KW  - Patient registries
KW  - Rare and genetic diseases research
KW  - Research network
KW  - Undiagnosed diseases
KW  - Translation
KW  - Contracts
KW  - Intervention
KW  - Pharmaceuticals
KW  - Pharmaceutical industry
KW  - Advisory committees
KW  - Private sector
KW  - Research programs
KW  - Public health
KW  - G 07730:Development & Cell Cycle
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773843875?accountid=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+Genomics&rft.atitle=New+and+Evolving+Rare+Diseases+Research+Programs+at+the+National+Institutes+of+Health&rft.au=Groft%2C+S+C%3BRubinstein%2C+Y+R&rft.aulast=Groft&rft.aufirst=S&rft.date=2013-02-01&rft.volume=16&rft.issue=6&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Public+Health+Genomics&rft.issn=16624246&rft_id=info:doi/10.1159%2F000355929
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-03-01
N1  - Last updated - 2016-09-14
N1  - SubjectsTermNotLitGenreText - Translation; Pharmaceuticals; Research programs; Public health; Contracts; Intervention; Advisory committees; Pharmaceutical industry; Private sector
DO  - http://dx.doi.org/10.1159/000355929
ER  - 



TY  - JOUR
T1  - Quality Controls in Cellular Immunotherapies: Rapid Assessment of Clinical Grade Dendritic Cells by Gene Expression Profiling
AN  - 1668269008; PQ0001244712
AB  - Cell-based immunotherapies are among the most promising approaches for developing effective and targeted immune response. However, their clinical usefulness and the evaluation of their efficacy rely heavily on complex quality control assessment. Therefore, rapid systematic methods are urgently needed for the in-depth characterization of relevant factors affecting newly developed cell product consistency and the identification of reliable markers for quality control. Using dendritic cells (DCs) as a model, we present a strategy to comprehensively characterize manufactured cellular products in order to define factors affecting their variability, quality and function. After generating clinical grade human monocyte-derived mature DCs (mDCs), we tested by gene expression profiling the degrees of product consistency related to the manufacturing process and variability due to intra- and interdonor factors, and how each factor affects single gene variation. Then, by calculating for each gene an index of variation we selected candidate markers for identity testing, and defined a set of genes that may be useful comparability and potency markers. Subsequently, we confirmed the observed gene index of variation in a larger clinical data set. In conclusion, using high-throughput technology we developed a method for the characterization of cellular therapies and the discovery of novel candidate quality assurance markers.
JF  - Molecular Therapy
AU  - Castiello, Luciano
AU  - Sabatino, Marianna
AU  - Zhao, Yingdong
AU  - Tumaini, Barbara
AU  - Ren, Jiaqiang
AU  - Ping, Jin
AU  - Wang, Ena
AU  - Wood, Lauren V
AU  - Marincola, Francesco M
AU  - Puri, Raj K
AU  - Stroncek, David F
AD  - Cell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA, DStroncek@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 476
EP  - 484
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 2
SN  - 1525-0016, 1525-0016
KW  - Genetics Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Gene expression
KW  - Dendritic cells
KW  - Data processing
KW  - Quality control
KW  - Immunotherapy
KW  - Monocytes
KW  - F 06960:Molecular Immunology
KW  - G 07730:Development & Cell Cycle
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668269008?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quality+Controls+in+Cellular+Immunotherapies%3A+Rapid+Assessment+of+Clinical+Grade+Dendritic+Cells+by+Gene+Expression+Profiling&rft.au=Castiello%2C+Luciano%3BSabatino%2C+Marianna%3BZhao%2C+Yingdong%3BTumaini%2C+Barbara%3BRen%2C+Jiaqiang%3BPing%2C+Jin%3BWang%2C+Ena%3BWood%2C+Lauren+V%3BMarincola%2C+Francesco+M%3BPuri%2C+Raj+K%3BStroncek%2C+David+F&rft.aulast=Castiello&rft.aufirst=Luciano&rft.date=2013-02-01&rft.volume=21&rft.issue=2&rft.spage=476&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.89
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Gene expression; Dendritic cells; Data processing; Immunotherapy; Quality control; Monocytes
DO  - http://dx.doi.org/10.1038/mt.2012.89
ER  - 



TY  - JOUR
T1  - Assessing the Risks of Genotoxicity in the Therapeutic Development of Induced Pluripotent Stem Cells
AN  - 1668266907; PQ0001244692
AB  - Induced pluripotent stem cells (iPSCs) have great potential for regenerative medicine as well as for basic and translational research. However, following the initial excitement over the enormous prospects of this technology, several reports uncovered serious concerns regarding its safety for clinical applications and reproducibility for laboratory applications such as disease modeling or drug screening. In particular, the genomic integrity of iPSCs is the focus of extensive research. Epigenetic remodeling, aberrant expression of reprogramming factors, clonal selection, and prolonged in vitro culture are potential pathways for acquiring genomic alterations. In this review, we will critically discuss current reprogramming technologies particularly in the context of genotoxicity, and the consequences of these alternations for the potential applications of reprogrammed cells. In addition, current strategies of genetic modification of iPSCs, as well as applicable suicide strategies to control the risk of iPSC-based therapies will be introduced.
JF  - Molecular Therapy
AU  - Hong, So Gun
AU  - Dunbar, Cynthia E
AU  - Winkler, Thomas
AD  - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA, dunbarc@nhlbi.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 272
EP  - 281
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 2
SN  - 1525-0016, 1525-0016
KW  - Biotechnology and Bioengineering Abstracts
KW  - Translation
KW  - Clonal selection
KW  - Inhibitory postsynaptic potentials
KW  - Genotoxicity
KW  - Suicide
KW  - Therapeutic applications
KW  - Cell culture
KW  - Drug screening
KW  - Stem cells
KW  - epigenetics
KW  - Regeneration
KW  - genomics
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668266907?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Assessing+the+Risks+of+Genotoxicity+in+the+Therapeutic+Development+of+Induced+Pluripotent+Stem+Cells&rft.au=Hong%2C+So+Gun%3BDunbar%2C+Cynthia+E%3BWinkler%2C+Thomas&rft.aulast=Hong&rft.aufirst=So&rft.date=2013-02-01&rft.volume=21&rft.issue=2&rft.spage=272&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.255
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-03-01
N1  - Last updated - 2015-11-16
N1  - SubjectsTermNotLitGenreText - Translation; Clonal selection; Stem cells; epigenetics; Regeneration; Genotoxicity; Inhibitory postsynaptic potentials; Therapeutic applications; Suicide; Cell culture; genomics; Drug screening
DO  - http://dx.doi.org/10.1038/mt.2012.255
ER  - 



TY  - JOUR
T1  - Competitive Removal of Two Contaminants in a Goethite-Catalyzed Fenton Process at Neutral pH
AN  - 1560130100; 20435846
AB  - Plumes containing more than one contaminant can be found in sites polluted by gasoline or chlorinated solvents. This study evaluated Fenton-like removal efficiencies when two contaminants were coexistent. Perchloroethylene, trichloroethylene, cis-1,2-dichloroethylene, methyl-t-butyl-ether, benzene, and toluene were mixed in pairs and degraded by the goethite-catalyzed Fenton-like reaction at neutral pH and low H sub(2)O sub(2) doses. Results revealed that the amount of each compound removed in two-contaminant systems was less than that in one-contaminant systems. This decline in removal was related to the reactivity constant (k sub(HO).), initial concentration (C sub(0)), and number of double bonds of the compounds. In a solution that contained two compounds with similar k sub(HO). values, the amount of each compound removed was related primarily to the C sub(0) ratio of two compounds. When the k sub(HO). values of two compounds differed considerably, the one with the larger k sub(HO). value or the higher C sub(0) reduced or inhibited the Fenton-like reaction of the pollutant with the smaller k sub(HO). or lower C sub(0). Compounds with few double bonds tended to be less competitive for Fenton-like removal. By adding H sub(2)O sub(2) repeatedly, the removal of a compound that is less competitive for the Fenton-like reaction can be recovered.
JF  - Environmental Engineering Science
AU  - Yeh, Kuei-Jyum
AU  - Chen, Ting-Chien
AU  - Young, Wei-Lun
AD  - Department of Environmental Science and Engineering, Emerging Compounds Research Center, National Pingtung University of Science and Technology, 1 Hseuh Fu Rd, Nei Pu, Pingtung 91207, Taiwan, kjyeh@mail.npust.edu.tw
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 47
EP  - 52
PB  - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States
VL  - 30
IS  - 2
SN  - 1092-8758, 1092-8758
KW  - Pollution Abstracts; Environment Abstracts
KW  - Gasoline
KW  - Toluene
KW  - Solvents
KW  - Trichloroethylene
KW  - Contaminants
KW  - Plumes
KW  - pH
KW  - Benzene
KW  - Perchloroethylene
KW  - P 9999:GENERAL POLLUTION
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560130100?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Engineering+Science&rft.atitle=Competitive+Removal+of+Two+Contaminants+in+a+Goethite-Catalyzed+Fenton+Process+at+Neutral+pH&rft.au=Yeh%2C+Kuei-Jyum%3BChen%2C+Ting-Chien%3BYoung%2C+Wei-Lun&rft.aulast=Yeh&rft.aufirst=Kuei-Jyum&rft.date=2013-02-01&rft.volume=30&rft.issue=2&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Environmental+Engineering+Science&rft.issn=10928758&rft_id=info:doi/10.1089%2Fees.2012.0001.
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Number of references - 6
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Gasoline; Toluene; Solvents; Trichloroethylene; Contaminants; Plumes; Benzene; pH; Perchloroethylene
DO  - http://dx.doi.org/10.1089/ees.2012.0001.
ER  - 



TY  - JOUR
T1  - A universal nanoparticle cell secretion capture assay
AN  - 1492614060; 18967098
AB  - Secreted proteins play an important role in intercellular interactions, especially between cells of the immune system. Currently, there is no universal assay that allows a simple noninvasive identification and isolation of cells based on their secretion of various products. We have developed such a method. Our method is based on the targeting, to the cell surface, of heterofunctional nanoparticles coupled to a cell surface-specific antibody and to a secreted protein-specific antibody, which captures the secreted protein on the surface of the producing cell. Importantly, this method does not compromise cellviability and is compatible with further culture and expansion of the secreting cells. Published 2012 Wiley-Periodicals, Inc.
JF  - Cytometry Part A
AU  - Fitzgerald, Wendy
AU  - Grivel, Jean-Charles
AD  - Center for Human Immunology, National Institutes of Health, Bethesda, Maryland 20892., grivelj@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 205
EP  - 211
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 83A
IS  - 2
SN  - 1552-4922, 1552-4922
KW  - Biotechnology and Bioengineering Abstracts
KW  - Antibodies
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492614060?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+universal+nanoparticle+cell+secretion+capture+assay&rft.au=Fitzgerald%2C+Wendy%3BGrivel%2C+Jean-Charles&rft.aulast=Fitzgerald&rft.aufirst=Wendy&rft.date=2013-02-01&rft.volume=83A&rft.issue=2&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22199
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Antibodies
DO  - http://dx.doi.org/10.1002/cyto.a.22199
ER  - 



TY  - JOUR
T1  - Thyroid cancer risk and dietary nitrate and nitrite intake in the Shanghai women's health study
AN  - 1443369983; 18602504
AB  - Nitrate and nitrite are precursors in the endogenous formation of N-nitroso compounds and nitrate can disrupt thyroid homeostasis by inhibiting iodide uptake. We evaluated nitrate and nitrite intake and risk of thyroid cancer in the Shanghai Women's Health Study that included 73,317 women, aged 40-70 years enrolled in 1996-2000. Dietary intake was assessed at baseline using a food frequency questionnaire. During approximately 11 years of follow-up, 164 incident thyroid cancer cases with complete dietary information were identified. We used Cox proportional hazards regression to estimate relative risks (RRs). We determined the nitrate and nitrite contents of foods using values from the published literature and focusing on regional values for Chinese foods. Nitrate intake was not associated with thyroid cancer risk [RR sub(Q4) = 0.93; 95% confidence interval (CI): 0.42-2.07; p for trend = 0.40]. Compared to the lowest quartile, women with the highest dietary nitrite intake had about a twofold risk of thyroid cancer (RR sub(Q4) = 2.05; 95%CI: 1.20-3.51), but there was not a monotonic trend with increasing intake (p for trend = 0.36). The trend with increasing nitrite intake from animal sources was significant (p for trend = 0.02) and was stronger for nitrite from processed meats (RR sub(Q4) = 1.96; 95%CI: 1.28-2.99; p for trend < 0.01). Although we did not observe an association for nitrate as hypothesized, our results suggest that women consuming higher levels of nitrite from animal sources, particularly from processed meat, may have an increased risk of thyroid cancer.
JF  - International Journal of Cancer
AU  - Aschebrook-Kilfoy, Briseis
AU  - Shu, Xiao-Ou
AU  - Gao, Yu-Tang
AU  - Ji, Bu-Tian
AU  - Yang, Gong
AU  - Li, Hong Lan
AU  - Rothman, Nathaniel
AU  - Chow, Wong-Ho
AU  - Zheng, Wei
AU  - Ward, Mary H
AD  - Department of Medicine, Center for Health Services Research, Vanderbilt University, Nashville, TN., wardm@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 897
EP  - 904
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 4
SN  - 0020-7136, 0020-7136
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Diets
KW  - Risk assessment
KW  - Meat
KW  - Health risks
KW  - Iodides
KW  - Nitrites
KW  - Nitrates
KW  - Thyroid
KW  - China, People's Rep., Shanghai
KW  - Females
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/1443369983?accountid=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=Thyroid+cancer+risk+and+dietary+nitrate+and+nitrite+intake+in+the+Shanghai+women%27s+health+study&rft.au=Aschebrook-Kilfoy%2C+Briseis%3BShu%2C+Xiao-Ou%3BGao%2C+Yu-Tang%3BJi%2C+Bu-Tian%3BYang%2C+Gong%3BLi%2C+Hong+Lan%3BRothman%2C+Nathaniel%3BChow%2C+Wong-Ho%3BZheng%2C+Wei%3BWard%2C+Mary+H&rft.aulast=Aschebrook-Kilfoy&rft.aufirst=Briseis&rft.date=2013-02-01&rft.volume=132&rft.issue=4&rft.spage=897&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27659
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Meat; Risk assessment; Diets; Iodides; Health risks; Nitrates; Nitrites; Thyroid; Females; Cancer; China, People's Rep., Shanghai
DO  - http://dx.doi.org/10.1002/ijc.27659
ER  - 



TY  - JOUR
T1  - The analysis of risk perception with fuzzy means-end approach
AN  - 1438551193; 201339691
AB  - Visitors' risk perceptions have been found to influence the on-site behavior of tourists and their intention to return to a destination or to recommend it to others. This study discusses how the uses of a means-end approach with fuzzy conceptualization in eliciting the perception of tourism risks in a better understanding of the visitors' perceptual orientation toward the tourism values. We provide a hierarchy value map that fuses the attribute-consequence-value (A-C-V) and fuzzy linguistics to effectively and efficiently understand vacation risks and risk characteristics. Fuzzy logic is also adopted to deal with the ill-defined nature of the tourist linguistic judgments required in the proposed means-end chain. This research findings suggest that additionally to managing the most likely risks, tourist resorts should be prepared to cope with worst case scenarios such as "Thunderstorm", "Bus accident", "Food poisoning" and "Cable car accident". From an overall risk perceptive, tourists are most concerned with dominant perceptual orientation of risk delivers being "Bus accident" --> "Decrease of trust in the safety management as a result of the event of damage" --> "Anger". Adapted from the source document.
JF  - Quality and Quantity
AU  - Lin, Ling-Zhong
AU  - Hsu, Tsuen-Ho
AD  - Department of Marketing Management, Shih Chien University, Kaohsiung Campus, 200 University Road, Nei-Men Hsiang, Kaohsiung Hsien, 845, Taiwan ling@mail.kh.usc.edu.tw
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 713
EP  - 734
PB  - Springer, Dordrecht The Netherlands
VL  - 47
IS  - 2
SN  - 0033-5177, 0033-5177
KW  - Values
KW  - Tourism
KW  - Risk
KW  - Accidents
KW  - Management
KW  - Trust
KW  - Poisoning
KW  - Linguistics
KW  - Anger
KW  - article
KW  - 0104: methodology and research technology; research methods/tools
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1438551193?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Quality+and+Quantity&rft.atitle=The+analysis+of+risk+perception+with+fuzzy+means-end+approach&rft.au=Lin%2C+Ling-Zhong%3BHsu%2C+Tsuen-Ho&rft.aulast=Lin&rft.aufirst=Ling-Zhong&rft.date=2013-02-01&rft.volume=47&rft.issue=2&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=Quality+and+Quantity&rft.issn=00335177&rft_id=info:doi/10.1007%2Fs11135-011-9540-z
LA  - English
DB  - Sociological Abstracts
N1  - Date revised - 2013-10-01
N1  - Last updated - 2016-09-28
N1  - CODEN - QQEJAV
N1  - SubjectsTermNotLitGenreText - Risk; Tourism; Accidents; Linguistics; Values; Trust; Poisoning; Management; Anger
DO  - http://dx.doi.org/10.1007/s11135-011-9540-z
ER  - 



TY  - JOUR
T1  - Intravoxel incoherent motion MR imaging for prostate cancer: An evaluation of perfusion fraction and diffusion coefficient derived from different b-value combinations
AN  - 1434033577; 18496012
AB  - There has been a resurgent interest in intravoxel incoherent motion (IVIM) MR imaging to obtain perfusion as well as diffusion information on lesions, in which the diffusion was modeled as Gaussian diffusion. However, it was observed that this diffusion deviated from expected monoexponential decay at high b-values and the reported perfusion in prostate is contrary to the findings in dynamic contrast-enhanced (DCE) MRI studies and angiogenesis. Thus, this work is to evaluate the effect of different b-values on IVIM perfusion fractions (f) and diffusion coefficients (D) for prostate cancer detection. The results show that both parameters depended heavily on the b-values, and those derived without the highest b-value correlated best with the results from DCE-MRI studies; specifically, f was significantly elevated (7.2% vs. 3.7%) in tumors when compared with normal tissues, in accordance with the volume transfer constant (K super(trans); 0.39 vs. 0.18 min super(-1)) and plasma fractional volume (v sub(p); 8.4% vs. 3.4%). In conclusion, it is critical to choose an appropriate range of b-values in studies or include the non-Gaussian diffusion contribution to obtain unbiased IVIM measurements. These measurements could eliminate the need for DCE-MRI, which is especially relevant in patients who cannot receive intravenous gadolinium-based contrast media. Magn Reson Med, 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Magnetic Resonance in Medicine
AU  - Pang, Yuxi
AU  - Turkbey, Baris
AU  - Bernardo, Marcelino
AU  - Kruecker, Jochen
AU  - Kadoury, Samuel
AU  - Merino, Maria J
AU  - Wood, Bradford J
AU  - Pinto, Peter A
AU  - Choyke, Peter L
AD  - Philips Healthcare, BU-MR, Cleveland, Ohio, USA., pchoyke@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 553
EP  - 562
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 2
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - Intravenous administration
KW  - Perfusion
KW  - Prostate cancer
KW  - Magnetic resonance imaging
KW  - Angiogenesis
KW  - Contrast media
KW  - N.M.R.
KW  - Diffusion coefficient
KW  - Tumors
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434033577?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intravoxel+incoherent+motion+MR+imaging+for+prostate+cancer%3A+An+evaluation+of+perfusion+fraction+and+diffusion+coefficient+derived+from+different+b-value+combinations&rft.au=Pang%2C+Yuxi%3BTurkbey%2C+Baris%3BBernardo%2C+Marcelino%3BKruecker%2C+Jochen%3BKadoury%2C+Samuel%3BMerino%2C+Maria+J%3BWood%2C+Bradford+J%3BPinto%2C+Peter+A%3BChoyke%2C+Peter+L&rft.aulast=Pang&rft.aufirst=Yuxi&rft.date=2013-02-01&rft.volume=69&rft.issue=2&rft.spage=553&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24277
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Intravenous administration; Prostate cancer; Perfusion; Magnetic resonance imaging; Contrast media; Angiogenesis; N.M.R.; Tumors; Diffusion coefficient
DO  - http://dx.doi.org/10.1002/mrm.24277
ER  - 



TY  - JOUR
T1  - Modified Look-Locker T sub(1) evaluation using Bloch simulations: Human and phantom validation
AN  - 1434033414; 18496007
AB  - Modified Look-Locker imaging is frequently used for T sub(1) mapping of the myocardium. However, the specific effect of various MRI parameters (e.g., encoding scheme, modifications of flip angle, heart rate, T sub(2), and inversion times) on the accuracy of T sub(1) measurement has not been studied through Bloch simulations. In this work, modified Look-Locker imaging was characterized through a numerical solution for Bloch equations. MRI sequence parameters that may affect T sub(1) accuracy were systematically varied in the simulation. For validation, phantoms were constructed with various T sub(2) and T sub(1) times and compared with Bloch equation simulations. Human volunteers were also evaluated with various pulse sequences parameters to assess the validity of the numerical simulations. There was close agreement between simulated T sub(1) times and T sub(1) times measured in phantoms and volunteers. Lower T sub(2) times (i.e., <30 ms) resulted in errors greater than 5% for T sub(1) determination. Increasing maximum inversion time value improved T sub(1) accuracy particularly for precontrast myocardial T sub(1). Balanced steady-state free precession k space centric encoding improved accuracy for short T sub(1) times (post gadolinium), but linear encoding provided improved accuracy for precontrast T sub(1) values. Lower flip angles are preferred if the signal-to-noise ratio is sufficiently high. Bloch simulations for modified Look-Locker imaging provide an accurate method to comprehensively quantify the effect of pulse sequence parameters on T sub(1) accuracy. As an alternative to otherwise lengthy phantom studies or human studies, such simulations may be useful to optimize the modified Look-Locker imaging sequence and compare differences in T sub(1)-derived measurements from different scanners or institutions. Magn Reson Med, 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Magnetic Resonance in Medicine
AU  - Gai, Neville D
AU  - Stehning, Christian
AU  - Nacif, Marcelo
AU  - Bluemke, David A
AD  - Philips Research Europe, Hamburg, Germany., gaind@cc.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 329
EP  - 336
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 2
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - Mathematical models
KW  - Inversion
KW  - Magnetic resonance imaging
KW  - Gadolinium
KW  - Heart rate
KW  - N.M.R.
KW  - Mapping
KW  - Myocardium
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434033414?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modified+Look-Locker+T+sub%281%29+evaluation+using+Bloch+simulations%3A+Human+and+phantom+validation&rft.au=Gai%2C+Neville+D%3BStehning%2C+Christian%3BNacif%2C+Marcelo%3BBluemke%2C+David+A&rft.aulast=Gai&rft.aufirst=Neville&rft.date=2013-02-01&rft.volume=69&rft.issue=2&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24251
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Mathematical models; Inversion; Heart rate; Gadolinium; Magnetic resonance imaging; N.M.R.; Mapping; Myocardium
DO  - http://dx.doi.org/10.1002/mrm.24251
ER  - 



TY  - JOUR
T1  - Pseudo-continuous arterial spin labeling at 7 T for human brain: Estimation and correction for off-resonance effects using a Prescan
AN  - 1434033035; 18496011
AB  - Pseudo-continuous arterial spin labeling (ASL) can provide best signal-to-noise ratio efficiency with a sufficiently long tag at high fields such as 7 T, but it is very sensitive to off-resonance fields at the tagging location. Here, a robust Prescan procedure is demonstrated to estimate the pseudo-continuous ASL radiofrequency phase and gradients parameters required to compensate the off-resonance effects at each vessel location. The Prescan is completed in 1-2 min and is based on acquisition of label/control pair-wise ASL data as a function of the radiofrequency phase increment applied to the pseudo-continuous ASL train. It is shown that this approach can be used to acquire high quality whole-brain pseudo-continuous ASL perfusion data of the human brain at 7 T. Magn Reson Med, 2013. [copy 2012 Wiley Periodicals, Inc.
JF  - Magnetic Resonance in Medicine
AU  - Luh, Wen-Ming
AU  - Talagala, SLalith
AU  - Li, Tie-Qiang
AU  - Bandettini, Peter A
AD  - NIH MRI Research Facility, National Institute of Neurological Disorder and Stroke, National Institutes of Health, Bethesda, Maryland, USA., wmluh@nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 402
EP  - 410
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 2
SN  - 0740-3194, 0740-3194
KW  - Biotechnology and Bioengineering Abstracts
KW  - Data processing
KW  - Perfusion
KW  - Brain
KW  - N.M.R.
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434033035?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pseudo-continuous+arterial+spin+labeling+at+7+T+for+human+brain%3A+Estimation+and+correction+for+off-resonance+effects+using+a+Prescan&rft.au=Luh%2C+Wen-Ming%3BTalagala%2C+SLalith%3BLi%2C+Tie-Qiang%3BBandettini%2C+Peter+A&rft.aulast=Luh&rft.aufirst=Wen-Ming&rft.date=2013-02-01&rft.volume=69&rft.issue=2&rft.spage=402&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24266
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Perfusion; Data processing; Brain; N.M.R.
DO  - http://dx.doi.org/10.1002/mrm.24266
ER  - 



TY  - JOUR
T1  - Evaluation of cervical stiffness during pregnancy using semiquantitative ultrasound elastography
AN  - 1434025876; 18501928
AB  - Objective To evaluate cervical stiffness during pregnancy using ultrasound-derived elastography, a method used to estimate the average tissue displacement (strain) within a defined region of interest when oscillatory compression is applied. Methods Strain was calculated in two regions of interest, the endocervical canal and the entire cervix, from three anatomical planes of the cervix: mid-sagittal in the plane used for cervical length measurement and in cross-sectional planes located at the internal and external cervical os. Associations between strain values, method of ascertainment and patient characteristics were assessed using linear mixed models to account for within-subject correlation. Inter-rater agreement in defining the degree of cervical stiffness was evaluated in 120 regions of interest acquired by two operators in 20 patients. Results A total of 1557 strain estimations were performed in 262 patients at 8-40weeks of gestation. Adjusting for other sources of variation, (1) cervical tissue strain estimates obtained in the endocervical canal were on average 33% greater than those obtained in the entire cervix; (2) measurements obtained in the cross-sectional plane of the external cervical os and sagittal plane were 45% and 13% greater than those measured in the cross-sectional plane of the internal cervical os, respectively; (3) mean strain rates were 14% and 5% greater among parous women with and without a history of preterm delivery compared with those of nulliparous women, respectively, and were on average 13% greater among women with a cervical length of between 25 and 30mm compared to those with a cervical length of>30mm; and (4) cervical tissue strain was more strongly associated with cervical length than with gestational age. Conclusion Semiquantitative elastography can be employed to evaluate changes in cervical stiffness during pregnancy.
JF  - Ultrasound in Obstetrics and Gynecology
AU  - Hernandez-Andrade, E
AU  - Hassan, S S
AU  - Ahn, H
AU  - Korzeniewski, S J
AU  - Yeo, L
AU  - Chaiworapongsa, T
AU  - Romero, R
AD  - Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD and Detroit, MI, USA.
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 152
EP  - 161
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 41
IS  - 2
SN  - 0960-7692, 0960-7692
KW  - Biotechnology and Bioengineering Abstracts
KW  - Canals
KW  - Gestational age
KW  - Gynecology
KW  - Cervix
KW  - Ultrasound
KW  - Obstetrics
KW  - Pregnancy
KW  - Models
KW  - Compression
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434025876?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluation+of+cervical+stiffness+during+pregnancy+using+semiquantitative+ultrasound+elastography&rft.au=Hernandez-Andrade%2C+E%3BHassan%2C+S+S%3BAhn%2C+H%3BKorzeniewski%2C+S+J%3BYeo%2C+L%3BChaiworapongsa%2C+T%3BRomero%2C+R&rft.aulast=Hernandez-Andrade&rft.aufirst=E&rft.date=2013-02-01&rft.volume=41&rft.issue=2&rft.spage=152&rft.isbn=&rft.btitle=&rft.title=Ultrasound+in+Obstetrics+and+Gynecology&rft.issn=09607692&rft_id=info:doi/10.1002%2Fuog.12344
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Canals; Gestational age; Gynecology; Cervix; Obstetrics; Ultrasound; Compression; Models; Pregnancy
DO  - http://dx.doi.org/10.1002/uog.12344
ER  - 



TY  - JOUR
T1  - Health-related quality of life among survivors of aggressive non-Hodgkin lymphoma
AN  - 1434016662; 18486852
AB  - BACKGROUND: Non-Hodgkin lymphoma (NHL) is the fifth most common cancer among men and women. Patients with aggressive NHL receive intense medical treatments that can significantly compromise health-related quality of life (HRQOL). However, knowledge of HRQOL and its correlates among survivors of aggressive NHL is limited. METHODS: Self-reported data on HRQOL (physical and mental function, anxiety, depression, and fatigue) were analyzed for 319 survivors of aggressive NHL. Survivors 2 to 5 years postdiagnosis were selected from the Los Angeles County Cancer Registry. Bivariate and multivariable methods were used to assess the influence of sociodemographic, clinical, and cognitive health-appraisal factors on survivors' HRQOL. RESULTS: After accounting for other covariates, marital status was associated with all HRQOL outcomes (P < .05). Younger survivors reported worse mental function and higher levels of depression, anxiety, and fatigue (P < .01). Survivors who had more comorbid conditions or lacked private health insurance reported worse physical and mental function and higher levels of depression and fatigue (P < .05). Survivors who experienced a recurrence reported worse physical function and higher levels of depression and fatigue (P < .05). With the exception of a nonsignificant association between perceived control and physical function, greater perceptions of personal control and health competence were associated significantly with more positive HRQOL outcomes (P < .01). CONCLUSIONS: The current results indicated that survivors of aggressive NHL who are younger, are unmarried, lack private insurance, or experience greater illness burden may be at risk for poorer HRQOL. Cognitive health-appraisal factors were strongly related to HRQOL, suggesting potential benefits of interventions focused on these mutable factors for this population. Cancer 2013. [copy 2012 American Cancer Society. This community-based sample of survivors of aggressive non-Hodgkin lymphoma 2 to 5 years after diagnosis demonstrates that survivors who are younger, not married, lack private insurance, or experience a greater illness burden may be at risk for experiencing poorer health-related quality of life. Cognitive health appraisal factors are strongly related to health-related quality of life, suggesting the potential benefits of interventions focused on these mutable factors for this population.
JF  - Cancer
AU  - Jensen, Roxanne E
AU  - Arora, Neeraj K
AU  - Bellizzi, Keith M
AU  - Rowland, Julia H
AU  - Hamilton, Ann S
AU  - Aziz, Noreen M
AU  - Potosky, Arnold L
AD  - Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland., rj222@georgetown.edu
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 672
EP  - 680
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 3
SN  - 0008-543X, 0008-543X
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - USA, California, Los Angeles Cty.
KW  - Health risks
KW  - Non-Hodgkin's lymphoma
KW  - Fatigue
KW  - Depression
KW  - Perception
KW  - Intervention
KW  - Insurance
KW  - Cancer
KW  - Quality of life
KW  - H 11000:Diseases/Injuries/Trauma
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434016662?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Health-related+quality+of+life+among+survivors+of+aggressive+non-Hodgkin+lymphoma&rft.au=Jensen%2C+Roxanne+E%3BArora%2C+Neeraj+K%3BBellizzi%2C+Keith+M%3BRowland%2C+Julia+H%3BHamilton%2C+Ann+S%3BAziz%2C+Noreen+M%3BPotosky%2C+Arnold+L&rft.aulast=Jensen&rft.aufirst=Roxanne&rft.date=2013-02-01&rft.volume=119&rft.issue=3&rft.spage=672&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27781
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Non-Hodgkin's lymphoma; Health risks; Depression; Fatigue; Perception; Intervention; Insurance; Cancer; Quality of life; USA, California, Los Angeles Cty.
DO  - http://dx.doi.org/10.1002/cncr.27781
ER  - 



TY  - JOUR
T1  - Projecting prostate cancer mortality in the PCPT and REDUCE chemoprevention trials
AN  - 1434016032; 18486853
AB  - BACKGROUND. Two recent chemoprevention trials demonstrated significant reductions in overall prostate cancer incidence. However, a possible increase in high-grade disease has raised concerns that the harms of the drugs, including mortality because of high-grade disease, may outweigh the benefits. The authors attempted to estimate the effect of these drugs on prostate cancer mortality to be able to better evaluate the cost-benefit tradeoff. METHODS. The authors analyzed prostate cancer incidence in the Prostate Cancer Prevention Trial (PCPT) and Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, which evaluated finasteride and the related compound dutasteride, respectively (both vs placebo). They used 13-year prostate cancer survival data from the Prostate, Lung, Colorectal and Ovarian (PLCO) trial to project prostate cancer mortality from incidence patterns; survival rates were applied to incident cancers according to prognostic strata, which were defined by Gleason score, prostate-specific antigen level, and clinical stage. For PCPT, the analysis was performed using both original trial results and previously published adjusted analyses that attempted to account for artifacts related to the drugs' effect on prostate volume. RESULTS. For the PCPT trial, the estimated relative risk (RR) for prostate cancer mortality was 1.02 (95% confidence interval [95% CI], 0.85-1.23) using the original trial results and 0.87 (95% CI, 0.72-1.06) and 0.91 (95% CI, 0.76-1.09) based on the adjusted PCPT analyses. For the REDUCE trial, the RR for prostate cancer mortality was 0.93 (95% CI, 0.80-1.08). CONCLUSIONS. Projecting a mortality outcome of the PCPT and REDUCE trials as an approach to weighing benefits versus harms suggests at most a small increase in prostate cancer mortality in the treatment arms, and possibly a modest decrease. Cancer 2013. [copy 2012 American Cancer Society. The Prostate Cancer Prevention Trial (PCPT) and Reduction by Dutasteride of Prostate Cancer Events (REDUCE) chemoprevention trials demonstrated substantial overall reductions in prostate cancer incidence but hints of an increased rate of high-grade disease. A projection of the mortality outcomes of these trials suggests a possibly modest mortality benefit for these agents and, at worst, a small mortality excess.
JF  - Cancer
AU  - Pinsky, Paul F
AU  - Black, Amanda
AU  - Grubb, Robert
AU  - Crawford, EDavid
AU  - Andriole, Gerald
AU  - Thompson, Ian
AU  - Parnes, Howard
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland., pp4f@nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 593
EP  - 601
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 3
SN  - 0008-543X, 0008-543X
KW  - Risk Abstracts
KW  - Mortality
KW  - Health risks
KW  - Prevention
KW  - Prostate cancer
KW  - Artifacts
KW  - Chemotherapy
KW  - Survival
KW  - Drugs
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434016032?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Projecting+prostate+cancer+mortality+in+the+PCPT+and+REDUCE+chemoprevention+trials&rft.au=Pinsky%2C+Paul+F%3BBlack%2C+Amanda%3BGrubb%2C+Robert%3BCrawford%2C+EDavid%3BAndriole%2C+Gerald%3BThompson%2C+Ian%3BParnes%2C+Howard&rft.aulast=Pinsky&rft.aufirst=Paul&rft.date=2013-02-01&rft.volume=119&rft.issue=3&rft.spage=593&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27774
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Health risks; Mortality; Prevention; Artifacts; Prostate cancer; Chemotherapy; Survival; Drugs; Cancer
DO  - http://dx.doi.org/10.1002/cncr.27774
ER  - 



TY  - JOUR
T1  - Added cancer yield of breast magnetic resonance imaging screening in women with a prior history of chest radiation therapy
AN  - 1434015756; 18486844
AB  - BACKGROUND: Recommendation for breast magnetic resonance imaging (MRI) screening for women with a prior history of chest radiation is currently based on expert opinion, because existing data are very scant. The objective of this study was to evaluate added cancer yield of screening breast MRI in this population. METHODS: A retrospective review identified 98 women with a prior history of chest radiation therapy who had screening mammography and screening MRI performed at the authors' institution between January 2004 and July 2010. Medical records of these patients and results of 558 screening studies (296 mammograms and 262 MRI) were reviewed. Sensitivity, specificity, positive predictive value, negative predictive value, and added cancer yield were calculated. RESULTS: Malignancy was diagnosed in 13 patients, invasive cancer was diagnosed in 10 patients, and ductal carcinomas in situ was diagnosed in 3 patients. The median latency from completion of radiation to detection of the breast cancer was 18 years (range, 8-37 years). Of the 13 cancers, 12 (92%) were detected by MRI, and 9 (69%) by mammography. For mammography, the sensitivity, specificity, positive predictive value, and negative predictive value were 69%, 98%, 82%, and 95%, respectively; and, for MRI, these values were 92%, 94%, 71%, and 99%, respectively. In 4 of 98 patients, cancer was diagnosed on MRI only, resulting in an incremental cancer detection rate of 4.1% (95% confidence interval, 1.6%-10%). CONCLUSIONS: The current results indicated that MRI is a useful adjunct modality for screening high-risk women who have a prior history of chest radiation therapy, resulting in a 4.1% (4 of 98 women) added cancer detection rate. The authors concluded that both MRI and mammography should be used to screen women in this high-risk group. Cancer 2013. [copy 2012 American Cancer Society. Magnetic resonance imaging (MRI) is a useful adjunct modality to screen high-risk women with a previous history of chest radiation therapy, resulting in a 4.1% (4 of 98 women) added cancer detection rate. The results of this study support American Cancer Society recommendations that advise annual breast MRI screening in patients with a prior history of chest radiation therapy.
JF  - Cancer
AU  - Freitas, Vivianne
AU  - Scaranelo, Anabel
AU  - Menezes, Ravi
AU  - Kulkarni, Supriya
AU  - Hodgson, David
AU  - Crystal, Pavel
AD  - Breast Imaging Department, Brazilian National Cancer Institute, Rio De Janeiro, Brazil., pavel.crystal@utoronto.ca
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 495
EP  - 503
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 119
IS  - 3
SN  - 0008-543X, 0008-543X
KW  - Risk Abstracts
KW  - Radiation therapy
KW  - Historical account
KW  - Sensitivity
KW  - Reviews
KW  - Females
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434015756?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Added+cancer+yield+of+breast+magnetic+resonance+imaging+screening+in+women+with+a+prior+history+of+chest+radiation+therapy&rft.au=Freitas%2C+Vivianne%3BScaranelo%2C+Anabel%3BMenezes%2C+Ravi%3BKulkarni%2C+Supriya%3BHodgson%2C+David%3BCrystal%2C+Pavel&rft.aulast=Freitas&rft.aufirst=Vivianne&rft.date=2013-02-01&rft.volume=119&rft.issue=3&rft.spage=495&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27771
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2013-10-04
N1  - SubjectsTermNotLitGenreText - Radiation therapy; Sensitivity; Historical account; Reviews; Females
DO  - http://dx.doi.org/10.1002/cncr.27771
ER  - 



TY  - JOUR
T1  - Health Behavior in Ecological Context
AN  - 1430188137; 201319625
AB  - Health is best understood within an ecological context. Accordingly, health promotion involves processes that foster supportive environments and healthful behavior. Thus, effective health promotion programs are typically multilevel, focusing not only on the population at risk but also on the environmental conditions that contribute so importantly to health and health behavior. Health behavior is important at each societal level. Arguably, accomplishment of health promotion goals at each societal level requires changes in the behavior of those who control or influence the health outcomes of interest. Recognition of three distinct types of health behavior can guide multilevel health promotion program planning. Personal-health behavior affects the health of the person who engages in that behavior. Health-related behavior includes actions taken by proximal others that directly affect the health of others, although usually not purposefully. Health-protective behavior is undertaken purposefully to foster the health of others. Regardless of the outcome of interest or societal level, similar health promotion processes can be employed to alter health behavior. [Reprinted by permission of Sage Publications Inc., copyright, the Society for Public Health Education.]
JF  - Health Education & Behavior
AU  - Simons-Morton, Bruce
AD  - National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 6
EP  - 10
PB  - Sage Publications, Thousand Oaks CA
VL  - 40
IS  - 1
SN  - 1090-1981, 1090-1981
KW  - definitions health education health promotion health-related behavior multilevel planning personal health behavior protective health behavior social ecology
KW  - Goals
KW  - Health status
KW  - Health
KW  - At risk
KW  - Health promotion
KW  - Health behaviour
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430188137?accountid=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+Education+%26+Behavior&rft.atitle=Health+Behavior+in+Ecological+Context&rft.au=Simons-Morton%2C+Bruce&rft.aulast=Simons-Morton&rft.aufirst=Bruce&rft.date=2013-02-01&rft.volume=40&rft.issue=1&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=Health+Education+%26+Behavior&rft.issn=10901981&rft_id=info:doi/10.1177%2F1090198112464494
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - HEDBFS
N1  - SubjectsTermNotLitGenreText - Health behaviour; Health promotion; Health; Goals; At risk; Health status
DO  - http://dx.doi.org/10.1177/1090198112464494
ER  - 



TY  - JOUR
T1  - A Multi-Case Report of the Pathways To and Through Genetic Testing and Cancer Risk Management for BRCA Mutation-Positive Women Aged 18-25
AN  - 1430187990; 201318135
AB  - Much of the extant literature addressing the psychosocial aspects of BRCA1/2 mutation testing and risk management aggregates mutation carriers of all ages in study recruitment, data analysis, and interpretation. This analytic strategy does not adequately address the needs of the youngest genetic testing consumers, i.e., women aged 18-25. Despite low absolute cancer risk estimates before age 30, BRCA1/2 mutation-positive women aged 18-25 feel vulnerable to a cancer diagnosis but find themselves in a management quandary because the clinical utility of screening and prevention options are not yet well defined for such young carriers. We present three cases, selected from a larger study of 32 BRCA1/2 mutation-positive women who completed or considered genetic testing before age 25, to demonstrate the unique developmental, relational and temporal influences, as well as the challenges, experienced by very young BRCA mutation-positive women as they complete genetic testing and initiate cancer risk management. The first case describes the maturation of a young woman whose family participated in a national cancer registry. The second addresses the experiences and expectations of a young woman who completed genetic testing after learning that her unaffected father was a mutation carrier. The third case highlights the experiences of a young woman parentally bereaved in childhood, who presented for genetic counseling and testing due to intense family pressure. Together, these cases suggest that BRCA1/2-positive women aged 18-25 are challenged to reconcile their burgeoning independence from their families with risk-related support needs. Loved ones acting in ways meant to care for these young women may inadvertently apply pressure, convoluting family support dynamics and autonomous decision-making. Ongoing support from competent healthcare professionals will enable these young women to remain informed and receive objective counsel about their risk-management decisions. Adapted from the source document.
JF  - Journal of Genetic Counseling
AU  - Hoskins, Lindsey M
AU  - Werner-Lin, Allison
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA hoskinsl@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 27
EP  - 38
PB  - Springer Science+Business Media, New York NY
VL  - 22
IS  - 1
SN  - 1059-7700, 1059-7700
KW  - Risk management
KW  - Ovarian cancer
KW  - Women
KW  - Genetic screening
KW  - Breast cancer
KW  - Cancer
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430187990?accountid=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=A+Multi-Case+Report+of+the+Pathways+To+and+Through+Genetic+Testing+and+Cancer+Risk+Management+for+BRCA+Mutation-Positive+Women+Aged+18-25&rft.au=Hoskins%2C+Lindsey+M%3BWerner-Lin%2C+Allison&rft.aulast=Hoskins&rft.aufirst=Lindsey&rft.date=2013-02-01&rft.volume=22&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Journal+of+Genetic+Counseling&rft.issn=10597700&rft_id=info:doi/10.1007%2Fs10897-012-9521-y
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JGCOET
N1  - SubjectsTermNotLitGenreText - Ovarian cancer; Women; Breast cancer; Genetic screening; Cancer; Risk management
DO  - http://dx.doi.org/10.1007/s10897-012-9521-y
ER  - 



TY  - JOUR
T1  - Worry as a Predictor of Nutrition Behaviors: Results From a Nationally Representative Survey
AN  - 1430186592; 201317710
AB  - Worry has been shown to predict a variety of health behaviors, such as cancer screening, yet there are few studies linking worry and nutrition. This study used nationally representative data from National Cancer Institute's Food Attitudes and Behavior Survey (n = 3,397) to examine the association between health-related worry and a variety of nutrition behaviors. Greater worry was associated with higher fruit and vegetable consumption (B = 0.19, p < .01), but also more meals eaten when watching television (B = 0.34, p < .01) and fewer with family (B = -0.13, p = .02). Importantly, and counterintuitively, greater worry appeared to reverse the conventional relationship between self-efficacy and dietary restriction; those who were self-efficacious and worried were less likely to restrict unhealthy foods. Similarly, worry attenuated the relationship between perceived benefits and special effort to buy produce. A complex relationship between worry and nutrition emerged, with potentially important clinical implications. [Reprinted by permission of Sage Publications Inc., copyright, the Society for Public Health Education.]
JF  - Health Education & Behavior
AU  - Ferrer, Rebecca A
AU  - Bergman, Hannah E
AU  - Klein, William M P
AD  - Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 88
EP  - 96
PB  - Sage Publications, Thousand Oaks CA
VL  - 40
IS  - 1
SN  - 1090-1981, 1090-1981
KW  - emotions fruit vegetables worry
KW  - Attitudes
KW  - Healthy food
KW  - Worry
KW  - Television viewing
KW  - Nutrition
KW  - Cancer
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430186592?accountid=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+Education+%26+Behavior&rft.atitle=Worry+as+a+Predictor+of+Nutrition+Behaviors%3A+Results+From+a+Nationally+Representative+Survey&rft.au=Ferrer%2C+Rebecca+A%3BBergman%2C+Hannah+E%3BKlein%2C+William+M+P&rft.aulast=Ferrer&rft.aufirst=Rebecca&rft.date=2013-02-01&rft.volume=40&rft.issue=1&rft.spage=88&rft.isbn=&rft.btitle=&rft.title=Health+Education+%26+Behavior&rft.issn=10901981&rft_id=info:doi/10.1177%2F1090198112439410
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-09-27
N1  - CODEN - HEDBFS
N1  - SubjectsTermNotLitGenreText - Worry; Healthy food; Nutrition; Cancer; Attitudes; Television viewing
DO  - http://dx.doi.org/10.1177/1090198112439410
ER  - 



TY  - JOUR
T1  - Stability of human mesenchymal stem cells during in vitro culture: considerations for cell therapy
AN  - 1399904901; 17564326
AB  - Ex vivo expansion and manipulation of human mesenchymal stem cells are important approaches to immunoregulatory and regenerative cell therapies. Although these cells show great potential for use, issues relating to their overall nature emerge as problems in the field. The need for extensive cell quantity amplification in vitro to obtain sufficient cell numbers for use, poses a risk of accumulating genetic and epigenetic abnormalities that could lead to sporadic malignant cell transformation. In this study, we have examined human mesenchymal stem cells derived from bone marrow, over extended culture time, using cytogenetic analyses, mixed lymphocyte reactions, proteomics and gene expression assays to determine whether the cultures would retain their potential for use in subsequent passages. Results indicate that in vitro cultures of these cells demonstrated chromosome variability after passage 4, but their immunomodulatory functions and differentiation capacity were maintained. At the molecular level, changes were observed from passage 5 on, indicating initiation of differentiation. Together, these results lead to the hypothesis that human mesenchymal stem cells cultures can be used successfully in cell therapy up to passage 4. However, use of cells from higher passages would have to be analysed case by case.
JF  - Cell Proliferation
AU  - Binato, R
AU  - de Souza Fernandez, T
AU  - Lazzarotto-Silva, C
AU  - Du Rocher, B
AU  - Mencalha, A
AU  - Pizzatti, L
AU  - Bouzas, L F
AU  - Abdelhay, E
AD  - Bone Marrow Transplantation Unit. National Cancer Institute (INCA)
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 10
EP  - 22
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 46
IS  - 1
SN  - 0960-7722, 0960-7722
KW  - Biotechnology and Bioengineering Abstracts
KW  - Mixed leukocyte reaction
KW  - Transformation
KW  - Immunoregulation
KW  - Cell number
KW  - Bone marrow
KW  - Cell culture
KW  - Immunomodulation
KW  - Gene expression
KW  - Differentiation
KW  - Chromosomes
KW  - Stem cells
KW  - epigenetics
KW  - proteomics
KW  - Mesenchyme
KW  - Cell proliferation
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399904901?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+Proliferation&rft.atitle=Stability+of+human+mesenchymal+stem+cells+during+in+vitro+culture%3A+considerations+for+cell+therapy&rft.au=Binato%2C+R%3Bde+Souza+Fernandez%2C+T%3BLazzarotto-Silva%2C+C%3BDu+Rocher%2C+B%3BMencalha%2C+A%3BPizzatti%2C+L%3BBouzas%2C+L+F%3BAbdelhay%2C+E&rft.aulast=Binato&rft.aufirst=R&rft.date=2013-02-01&rft.volume=46&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Cell+Proliferation&rft.issn=09607722&rft_id=info:doi/10.1111%2Fcpr.12002
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Transformation; Mixed leukocyte reaction; Immunoregulation; Cell number; Bone marrow; Cell culture; Immunomodulation; Gene expression; Differentiation; Stem cells; Chromosomes; epigenetics; proteomics; Cell proliferation; Mesenchyme
DO  - http://dx.doi.org/10.1111/cpr.12002
ER  - 



TY  - JOUR
T1  - Modulation of quaternary structure and enhancement of ligand binding by the K-turn of tandem glycine riboswitches
AN  - 1372059771; 18159485
AB  - Most known glycine riboswitches have two homologous aptamer domains arranged in tandem and separated by a short linker. The two aptamers associate through reciprocal "quaternary" interactions that have been proposed to result in cooperative glycine binding. Recently, the interaptamer linker was found to form helix P0 with a previously unrecognized segment 5' to the first aptamer domain. P0 was shown to increase glycine affinity, abolish cooperativity, and conform to the K-turn motif consensus. We examine the global thermodynamic and structural role of P0 using isothermal titration calorimetry (ITC) and small-angle X-ray scattering (SAXS), respectively. To evaluate the generality of P0 function, we prepared glycine riboswitch constructs lacking and including P0 from Bacillus subtilis, Fusobacterium nucleatum, and Vibrio cholerae. We find that P0 indeed folds into a K-turn, supports partial pre-folding of all three glycine-free RNAs, and is required for ITC observation of glycine binding under physiologic Mg super(2+) concentrations. Except for the unusually small riboswitch from F. nucleatum, the K-turn is needed for maximally compacting the glycine-bound states of the RNAs. Formation of a ribonucleoprotein complex between the B. subtilis or the F. nucleatum RNA constructs and the bacterial K-turn binding protein YbxF promotes additional folding of the free riboswitch, and enhances glycine binding. Consistent with the previously reported loss of cooperativity, P0-containing B. subtilis and V. cholerae tandem aptamers bound no more than one glycine molecule per riboswitch. Our results indicate that the P0 K-turn helps organize the quaternary structure of tandem glycine riboswitches, thereby facilitating ligand binding under physiologic conditions.
JF  - RNA
AU  - Baird, N J
AU  - Ferre-D'Amare, A R
AD  - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-8012, USA, adrian.ferre@nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 167
EP  - 176
VL  - 19
IS  - 2
SN  - 1355-8382, 1355-8382
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Biochemistry Abstracts 2: Nucleic Acids
KW  - Aptamers
KW  - Palaeo studies
KW  - Riboswitches
KW  - Quaternary structure
KW  - Fusobacterium nucleatum
KW  - Protein structure
KW  - Protein folding
KW  - Titration
KW  - X-ray scattering
KW  - Bacillus subtilis
KW  - Thermodynamics
KW  - Quaternary
KW  - Glycine
KW  - Vibrio cholerae
KW  - RNA
KW  - Ribonucleoproteins
KW  - Calorimetry
KW  - Magnesium
KW  - Ligands
KW  - Cooperativity
KW  - N 14830:RNA
KW  - Q5 08524:Public health, medicines, dangerous organisms
KW  - Q1 08187:Palaeontology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1372059771?accountid=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=RNA&rft.atitle=Modulation+of+quaternary+structure+and+enhancement+of+ligand+binding+by+the+K-turn+of+tandem+glycine+riboswitches&rft.au=Baird%2C+N+J%3BFerre-D%27Amare%2C+A+R&rft.aulast=Baird&rft.aufirst=N&rft.date=2013-02-01&rft.volume=19&rft.issue=2&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=RNA&rft.issn=13558382&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Quaternary; Thermodynamics; Glycine; Palaeo studies; Titration; Calorimetry; Ligands; Aptamers; Riboswitches; Quaternary structure; Protein structure; RNA; Protein folding; Ribonucleoproteins; X-ray scattering; Magnesium; Cooperativity; Vibrio cholerae; Bacillus subtilis; Fusobacterium nucleatum
ER  - 



TY  - JOUR
T1  - Effects of Parental Alcoholism, Sense of Belonging, and Resilience on Depressive Symptoms: A Path Model
AN  - 1364767219; 201310145
AB  - This paper explored the relationships between parental alcoholism, sense of belonging, resilience, and depressive symptoms among Koreans in the U.S. Data from 206 Koreans (Mean age = 28.4 years; 59.8% females) living in a Midwestern state were collected in 2009, using a web-based survey, which included Children of Alcoholic Screening Test, Sense of Belonging Instrument, Connor-Davidson Resilience Scale, and Beck Depression Inventory-II. Path analysis results revealed sense of belonging as the most powerful, and resilience as the second important factor, resisting depressive symptoms associated with parental alcoholism. Implications for practice and research and study limitations are discussed. The study's limitations are noted. Adapted from the source document.
JF  - Substance Use & Misuse
AU  - Lee, Hyunhwa
AU  - Williams, Reg A
AD  - Intramural Research Program, NIH NINR, Bethesda, Maryland, USA leeh9@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 265
EP  - 273
PB  - Informa Healthcare, New York NY
VL  - 48
IS  - 3
SN  - 1082-6084, 1082-6084
KW  - adult children of alcoholics, sense of belonging, resilience, depressive symptoms, Koreans
KW  - Resilience
KW  - Depression
KW  - Sense of belonging
KW  - Alcoholism
KW  - Computer based
KW  - Parents
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364767219?accountid=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=Substance+Use+%26+Misuse&rft.atitle=Effects+of+Parental+Alcoholism%2C+Sense+of+Belonging%2C+and+Resilience+on+Depressive+Symptoms%3A+A+Path+Model&rft.au=Lee%2C+Hyunhwa%3BWilliams%2C+Reg+A&rft.aulast=Lee&rft.aufirst=Hyunhwa&rft.date=2013-02-01&rft.volume=48&rft.issue=3&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Substance+Use+%26+Misuse&rft.issn=10826084&rft_id=info:doi/10.3109%2F10826084.2012.754899
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - CODEN - SUMIFL
N1  - SubjectsTermNotLitGenreText - Sense of belonging; Resilience; Depression; Parents; Alcoholism; Computer based
DO  - http://dx.doi.org/10.3109/10826084.2012.754899
ER  - 



TY  - JOUR
T1  - Do Researchers Have an Obligation to Actively Look for Genetic Incidental Findings
AN  - 1364726659; 2011-410606
AB  - The rapid growth of next-generation genetic sequencing has prompted debate about the responsibilities of researchers toward genetic incidental findings. Assuming there is a duty to disclose significant incidental findings, might there be an obligation for researchers to actively look for these findings? We present an ethical framework for analyzing whether there is a positive duty to look for genetic incidental findings. Using the ancillary care framework as a guide, we identify three main criteria that must be present to give rise to an obligation to look: high benefit to participants, lack of alternative access for participants, and reasonable burden on researchers. Our analysis indicates that there is no obligation to look for incidental findings today, but during the ongoing translation of genomic analysis from research to clinical care, this obligation may arise. Adapted from the source document.
JF  - The American Journal of Bioethics
AU  - Gliwa, Catherine
AU  - Berkman, Benjamin E
AD  - National Institutes of Health
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 32
EP  - 42
PB  - Taylor & Francis, Philadelphia PA
VL  - 13
IS  - 2
SN  - 1526-5161, 1526-5161
KW  - Science and technology policy - Biology and biotechnology
KW  - Genetics
KW  - Benefits
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364726659?accountid=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=The+American+Journal+of+Bioethics&rft.atitle=Do+Researchers+Have+an+Obligation+to+Actively+Look+for+Genetic+Incidental+Findings&rft.au=Gliwa%2C+Catherine%3BBerkman%2C+Benjamin+E&rft.aulast=Gliwa&rft.aufirst=Catherine&rft.date=2013-02-01&rft.volume=13&rft.issue=2&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2012.754062
LA  - English
DB  - PAIS Index
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Genetics; Benefits
DO  - http://dx.doi.org/10.1080/15265161.2012.754062
ER  - 



TY  - JOUR
T1  - Attention to the Neglected: Prospects for Research on Child Neglect for the Next Decade
AN  - 1364705325; 201304597
AB  - In 1997, the National Institutes of Health within the United States Department of Health and Human Services reviewed the state of its research on child abuse and neglect (US Department of Health and Human Services, National Institutes of Health, 1997). The findings suggested that although neglect was the most frequent type of Child Maltreatment, research studies were lacking. Through an unprecedented partnership across federal funding agencies for research on child neglect, research was encouraged in several areas. Over the past fifteen years, consortia of researchers have continued to increase our knowledge of child neglect and to shape the field. Nonetheless, challenges for research on child neglect remain, including the changing demographics of the nation and health disparities. Evidenced-based early interventions and treatments may be an opportunity for prevention of child neglect and improving child welfare services, particularly in an era of health care reform. Developmental researchers across the translational pipeline are encouraged to integrate child neglect research in future studies to inform prevention, treatment and policy efforts for the improved health and well-being of children, families and communities. [Reprinted by permission of Sage Publications Inc., copyright holder.]
JF  - Child Maltreatment
AU  - Boyce, Cheryl Anne
AU  - Maholmes, Valerie
AD  - Department of Health and Human Services, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, USA cboyce@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 65
EP  - 68
PB  - Sage Publications, Thousand Oaks CA
VL  - 18
IS  - 1
SN  - 1077-5595, 1077-5595
KW  - child neglect child health children families
KW  - Human Services
KW  - Prevention
KW  - Child Neglect
KW  - United States of America
KW  - Health
KW  - Child Abuse
KW  - Knowledge
KW  - Treatment Methods
KW  - Health Care Services
KW  - article
KW  - 6143: child & family welfare
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364705325?accountid=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=Child+Maltreatment&rft.atitle=Attention+to+the+Neglected%3A+Prospects+for+Research+on+Child+Neglect+for+the+Next+Decade&rft.au=Boyce%2C+Cheryl+Anne%3BMaholmes%2C+Valerie&rft.aulast=Boyce&rft.aufirst=Cheryl&rft.date=2013-02-01&rft.volume=18&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Child+Maltreatment&rft.issn=10775595&rft_id=info:doi/10.1177%2F1077559513480426
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-28
N1  - CODEN - CMALFA
N1  - SubjectsTermNotLitGenreText - Child Neglect; Health Care Services; Prevention; Human Services; Health; Treatment Methods; United States of America; Child Abuse; Knowledge
DO  - http://dx.doi.org/10.1177/1077559513480426
ER  - 



TY  - JOUR
T1  - Systematic comparison between ecological momentary assessment and day reconstruction method for fatigue and mood states in healthy adults
AN  - 1347817864; 201306580
AB  - Objectives: While both ecological momentary assessment (EMA) and the day reconstruction method (DRM) have been used to overcome recall bias, a full systematic comparison of these methods has not been conducted. This study was aimed to investigate the differences and correlations between momentary fatigue and mood states recorded by EMA and reconstructed ones recorded by simultaneous DRM in healthy adults. Design: Each of two different designs (time-based and episode-based) of EMA and DRM were simultaneously conducted. Methods: Twenty-five healthy adults recorded momentary fatigue and mood states with EMA, and then, reconstructed them with DRM. Differences between the mean and the variability of momentary and reconstructed recordings, and the correlations between them, are analysed for different EMA designs. Results: No significant differences are found between the mean or the variability of EMA and DRM estimated over the monitoring period. However, correlations between EMA and DRM are low, albeit statistically significant. Conclusions: Although the overall mean and variability of EMA recordings may be accessible with DRM, detailed changes over time of momentary fatigue and mood states are not retrieved by DRM. Adapted from the source document.
JF  - British Journal of Health Psychology
AU  - Kim, Jinhyuk
AU  - Kikuchi, Hiroe
AU  - Yamamoto, Yoshiharu
AD  - National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8553, Japan
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 155
EP  - 167
PB  - John Wiley & Sons, Inc.
VL  - 18
IS  - 1
SN  - 1359-107X, 1359-107X
KW  - Assessment
KW  - Variability
KW  - Fatigue
KW  - Reconstruction
KW  - Moods
KW  - Recording
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347817864?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Health+Psychology&rft.atitle=Systematic+comparison+between+ecological+momentary+assessment+and+day+reconstruction+method+for+fatigue+and+mood+states+in+healthy+adults&rft.au=Kim%2C+Jinhyuk%3BKikuchi%2C+Hiroe%3BYamamoto%2C+Yoshiharu&rft.aulast=Kim&rft.aufirst=Jinhyuk&rft.date=2013-02-01&rft.volume=18&rft.issue=1&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Health+Psychology&rft.issn=1359107X&rft_id=info:doi/10.1111%2Fbjhp.12000
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-05-01
N1  - Last updated - 2016-09-27
N1  - CODEN - BJHPFP
N1  - SubjectsTermNotLitGenreText - Moods; Fatigue; Variability; Reconstruction; Assessment; Recording
DO  - http://dx.doi.org/10.1111/bjhp.12000
ER  - 



TY  - JOUR
T1  - Case-sibling studies that acknowledge unstudied parents and permit the inclusion of unmatched individuals
AN  - 1328511704; 17826858
AB  - Background Family-based designs enable assessment of genetic associations without bias from population stratification. When parents are not readily available - especially for diseases with onset later in life - the case-sibling design, where each case is matched with one or more unaffected siblings, is useful. Analysis typically accounts for within-family dependencies by using conditional logistic regression (CLR).Methods We consider an alternative to CLR that treats each case-sibling set as a nuclear family with both parents missing by design. One can carry out maximum likelihood analysis by using the Expectation-Maximization (EM) algorithm to account for missing parental genotypes. We compare conditional logistic regression and the missing-parents approach under several risk scenarios.Results We show that the missing-parents approach improves power when some families have more than one unaffected sibling and that under weak assumptions the approach permits the incorporation of supplemental cases who have no sibling available and supplemental controls whose case sibling is unavailable (e.g., due to disability or death).Conclusion The missing-parents approach offers both improved statistical efficiency and asymptotically unbiased estimation for genotype relative risks and genotype-by-exposure interaction parameters.
JF  - International Journal of Epidemiology
AU  - Shi, Min
AU  - Umbach, David M
AU  - Weinberg, Clarice R
AD  - Biostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA, shi2@niehs.nih.gov
PY  - 2013
SP  - 298
EP  - 307
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 42
IS  - 1
SN  - 0300-5771, 0300-5771
KW  - Risk Abstracts
KW  - Genetic association
KW  - case-sibling
KW  - missing parents
KW  - expectation-maximization algorithm
KW  - conditional logistic regression
KW  - Disabilities
KW  - Siblings
KW  - Genotypes
KW  - Stratification
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328511704?accountid=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+Epidemiology&rft.atitle=Case-sibling+studies+that+acknowledge+unstudied+parents+and+permit+the+inclusion+of+unmatched+individuals&rft.au=Shi%2C+Min%3BUmbach%2C+David+M%3BWeinberg%2C+Clarice+R&rft.aulast=Shi&rft.aufirst=Min&rft.date=2013-02-01&rft.volume=42&rft.issue=1&rft.spage=298&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Epidemiology&rft.issn=03005771&rft_id=info:doi/10.1093%2Fije%2Fdys212
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Disabilities; Siblings; Stratification; Genotypes
DO  - http://dx.doi.org/10.1093/ije/dys212
ER  - 



TY  - JOUR
T1  - Contribution of phage-derived genomic islands to the virulence of facultative bacterial pathogens
AN  - 1323819899; 17734669
AB  - Facultative pathogens have extremely dynamic pan-genomes, to a large extent derived from bacteriophages and other mobile elements. We developed a simple approach to identify phage-derived genomic islands and apply it to show that pathogens from diverse bacterial genera are significantly enriched in clustered phage-derived genes compared with related benign strains. These findings show that genome expansion by integration of prophages containing virulence factors is a major route of evolution of facultative bacterial pathogens.
JF  - Environmental Microbiology
AU  - Busby, Ben
AU  - Kristensen, David M
AU  - Koonin, Eugene V
AD  - National Center for Biotechnology Information National Library of Medicine. National Institutes of Health
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 307
EP  - 312
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 15
IS  - 2
SN  - 1462-2912, 1462-2912
KW  - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology
KW  - Benign
KW  - Bacteria
KW  - Pathogens
KW  - A 01450:Environmental Pollution & Waste Treatment
KW  - J 02430:Symbiosis, Antibiosis & Phages
KW  - G 07760:Viruses & Phages
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323819899?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Microbiology&rft.atitle=Contribution+of+phage-derived+genomic+islands+to+the+virulence+of+facultative+bacterial+pathogens&rft.au=Busby%2C+Ben%3BKristensen%2C+David+M%3BKoonin%2C+Eugene+V&rft.aulast=Busby&rft.aufirst=Ben&rft.date=2013-02-01&rft.volume=15&rft.issue=2&rft.spage=307&rft.isbn=&rft.btitle=&rft.title=Environmental+Microbiology&rft.issn=14622912&rft_id=info:doi/10.1111%2Fj.1462-2920.2012.02886.x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Pathogens; Bacteria
DO  - http://dx.doi.org/10.1111/j.1462-2920.2012.02886.x
ER  - 



TY  - JOUR
T1  - Sunlight, Polymorphisms of Vitamin D-related Genes and Risk of Breast Cancer
AN  - 1323808578; 17806561
AB  - Background/Aim: Geographic gradients in breast cancer incidence and mortality suggest that vitamin D may reduce risk. The enzyme 25-hydroxyvitamin D 24-hydroxylase (CYP24A1), which degrades the active form of vitamin D, and the vitamin D receptor (VDR) are both found in breast tissue. We investigated six polymorphisms in CYP24A1 and two in the VDR gene in association with breast cancer risk. Materials and Methods: We conducted a case-control study within the nationwide U.S. Radiologic Technologists cohort, including 845 controls and 484 incident breast cancer cases. Associations of polymorphic variants and ecologic and personal measures of sun exposure with breast cancer risk were assessed using unconditional logistic regression. Results: Two polymorphisms in CYP24A1 were associated with increased breast cancer risk (rs34043203, P sub(trend)=0.03; rs2762934, P sub(trend)=0,005) and one with reduced breast cancer risk (rs1570669, P sub(trend)=0.048). Risk was inversely associated with minor alleles for the VDR Bsm1 polymorphism (rs1544410, P sub(trend)=0.05) but not Fok1 (rs2228570). Sunlight measures were not associated with breast cancer risk, however significant interactions between time outdoors in the teen years and three unlinked genotypes were found for VDR (rs1544410, rs2228570) and CYP24A1 (rs1570669). Conclusion: In this nation-wide breast cancer case-control study, we found that the vitamin D pathway was involved in disease etiology and our results further suggest that reduced cancer risk, in association with sunlight, may depend on timing of exposure and genetic background. These findings merit further investigation.
JF  - Anticancer Research
AU  - Fuhrman, B J
AU  - Freedman, D M
AU  - Bhatti, P
AU  - Doody, M M
AU  - Fu, Y-P
AU  - Chang, S-C
AU  - Linet
AU  - Sigurdson, A J
AD  - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Blvd MSC 7238, Bethesda, MD 20892-7238, USA, sigurdsa@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 543
EP  - 551
VL  - 33
IS  - 2
SN  - 0250-7005, 0250-7005
KW  - Risk Abstracts; Genetics Abstracts
KW  - Mortality
KW  - Etiology
KW  - Gene polymorphism
KW  - 25-Hydroxyvitamin D
KW  - Enzymes
KW  - Risk reduction
KW  - Cancer
KW  - USA
KW  - Vitamin D
KW  - Vitamins
KW  - Sun
KW  - Breast cancer
KW  - Vitamin D receptors
KW  - Sunlight
KW  - G 07880:Human Genetics
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323808578?accountid=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=Anticancer+Research&rft.atitle=Sunlight%2C+Polymorphisms+of+Vitamin+D-related+Genes+and+Risk+of+Breast+Cancer&rft.au=Fuhrman%2C+B+J%3BFreedman%2C+D+M%3BBhatti%2C+P%3BDoody%2C+M+M%3BFu%2C+Y-P%3BChang%2C+S-C%3BLinet%3BSigurdson%2C+A+J&rft.aulast=Fuhrman&rft.aufirst=B&rft.date=2013-02-01&rft.volume=33&rft.issue=2&rft.spage=543&rft.isbn=&rft.btitle=&rft.title=Anticancer+Research&rft.issn=02507005&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Mortality; Etiology; Gene polymorphism; Sun; 25-Hydroxyvitamin D; Enzymes; Sunlight; Vitamin D receptors; Breast cancer; Vitamin D; Vitamins; Risk reduction; Cancer; USA
ER  - 



TY  - JOUR
T1  - The Toxicity and Pathology of Selected Dietary Herbal Medicines
AN  - 1323802569; 17782850
AB  - Toxicity studies were conducted by the National Toxicology Program (NTP) to provide information on the potential for toxicity from long-term use of commonly used herbal medicines. Here, we review the findings from these NTP toxicology/carcinogenesis 2-year rodent studies of 7 commonly used herbs. In these studies, the individual herb or herbal product was administered to F344/N rats and B6C3F1 mice by oral administration for up to 2 years. The spectrum of carcinogenic responses ranged from no or equivocal evidence for carcinogenic activity (ginseng, milk thistle, and turmeric oleoresin) to a liver tumor response (ginkgo, goldenseal, kava), thyroid tumor response (ginkgo), or an intestinal tumor response (Aloe vera whole leaf nondecolorized extract). Different mechanisms may be involved in the occurrence of liver (ginkgo, goldenseal, and kava kava) and gastrointestinal toxicity (turmeric oleoresin and Aloe vera whole leaf nondecolorized extract), while the toxic lesion is the same. The results from these hazard identification toxicity/carcinogenesis studies along with those from ongoing National Institute of Health clinical trials of herbal medicines provide more complete information on the risks and benefits from herbal medicine use in the general population.
JF  - Toxicologic Pathology
AU  - Dunnick, June K
AU  - Nyska, Abraham
AD  - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, dunnickj@niehs.nih.gov
PY  - 2013
SP  - 374
EP  - 386
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 41
IS  - 2
SN  - 0192-6233, 0192-6233
KW  - Toxicology Abstracts
KW  - Aloe vera whole leaf nondecolorized extract
KW  - ginkgo
KW  - ginseng
KW  - goldenseal
KW  - kava kava
KW  - milk thistle
KW  - turmeric oleoresin.
KW  - Milk
KW  - Thyroid
KW  - Leaves
KW  - Oral administration
KW  - Ginseng
KW  - Tumors
KW  - Toxicity
KW  - Clinical trials
KW  - Ginkgo
KW  - Cost-benefit analysis
KW  - Aloe vera
KW  - oleoresins
KW  - Curcuma longa
KW  - Reviews
KW  - Carcinogenesis
KW  - Liver
KW  - Herbal medicines
KW  - Intestine
KW  - X 24320:Food Additives & Contaminants
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323802569?accountid=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=The+Toxicity+and+Pathology+of+Selected+Dietary+Herbal+Medicines&rft.au=Dunnick%2C+June+K%3BNyska%2C+Abraham&rft.aulast=Dunnick&rft.aufirst=June&rft.date=2013-02-01&rft.volume=41&rft.issue=2&rft.spage=374&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623312466451
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Number of references - 60
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Milk; Oral administration; Leaves; Thyroid; Ginseng; Toxicity; Tumors; Clinical trials; Cost-benefit analysis; oleoresins; Reviews; Carcinogenesis; Intestine; Herbal medicines; Liver; Aloe vera; Curcuma longa; Ginkgo
DO  - http://dx.doi.org/10.1177/0192623312466451
ER  - 



TY  - JOUR
T1  - Commentary: Disregard for others: empathic dysfunction or emotional volatility? The relationship with future antisocial behavior -- reflections on Rhee et al. (2013)
AN  - 1323338652; 201303422
AB  - Comments on an article in the same journal issue by Soo Hyun Rhee, Naomi P. Friedman, Debra L. Boeldt, Robin P. Corley, John. K. Hewitt, Ariel Knafo, Benjamin B. Lahey, JoAnn Robinson, Carol A. Van Hulle, Irwin D. Waldman, Susan E. Young, and Carolyn Zahn-Waxler, 'Early concern and disregard for others as predictors of antisocial behavior' (p 157-166). Adapted from the source document.
JF  - The Journal of Child Psychology and Psychiatry
AU  - Blair, R J R
AD  - Unit of Affective Cognitive Neuroscience, National Institute of Mental Health, NIH, Department of Health and Human Services, Bethesda, MD, USA
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 167
EP  - 168
PB  - Blackwell Publishing, Oxford UK
VL  - 54
IS  - 2
SN  - 0021-9630, 0021-9630
KW  - Antisocial behaviour
KW  - Dysfunction
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323338652?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Child+Psychology+and+Psychiatry&rft.atitle=Commentary%3A+Disregard+for+others%3A+empathic+dysfunction+or+emotional+volatility%3F+The+relationship+with+future+antisocial+behavior+--+reflections+on+Rhee+et+al.+%282013%29&rft.au=Blair%2C+R+J+R&rft.aulast=Blair&rft.aufirst=R+J&rft.date=2013-02-01&rft.volume=54&rft.issue=2&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fjcpp.12026
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-06-01
N1  - Last updated - 2016-09-27
N1  - CODEN - JPPDAI
N1  - SubjectsTermNotLitGenreText - Antisocial behaviour; Dysfunction
DO  - http://dx.doi.org/10.1111/jcpp.12026
ER  - 



TY  - JOUR
T1  - Effects of organoselenium compound 2-(5-selenocyanato-pentyl)-benzo[de]isoquinoline 1,3-dione on cisplatin induced nephrotoxicity and genotoxicity: an investigation of the influence of the compound on oxidative stress and antioxidant enzyme system
AN  - 1323218139; 17683481
AB  - Cisplatin is one of the most active cytotoxic agents used in the treatment of cancer. However, cisplatin therapy is also associated with severe side effects like nephrotoxicity and genotoxicity. Free oxygen radicals are known to play a major role in cisplatin induced toxicities. Selenium is believed to be an important trace element and dietary antioxidant because of its ability to scavenge free oxygen radicals, thereby preventing cells from oxidative stress. The purpose of this study is to evaluate the protective role of a novel naphthalimide based organoselenium compound 2-(5-selenocyanato-pentyl)-benzo[de]isoquinoline 1,3-dione against cisplatin induced toxicities in Swiss albino mice. Cisplatin was administered intraperitoneally (5 mg/kg b.w.) and the organoselenium compound was given by oral gavages (3 mg/kg b.w.) in concomitant and pretreatment schedule. The results showed that the test compound substantially reduced cisplatin induced reactive oxygen species generation and lipid peroxidation in kidney as well as blood urea nitrogen and creatinine levels in serum. Treatment with organoselenium compound was also able to restore the renal antioxidant system by modulating the cisplatin induced depleted activities of glutathione S-transferase, thioredoxin reductase, superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione level. In addition, the organoselenium compound could efficiently minimize cisplatin induced chromosomal aberrations in bone marrow cells and extent of DNA damage in lymphocytes. Furthermore, the chemoprotective efficacy of the compound against cisplatin induced toxicity was confirmed by histopathological evaluation. The results suggest that the organoselenium compound has the potential to protect against cisplatin induced nephrotoxicity and genotoxicity in part by scavenging reactive oxygen species and by up regulating the antioxidant enzyme system.
JF  - BioMetals
AU  - Ghosh, Prosenjit
AU  - Roy, Somnath Singha
AU  - Chakraborty, Pramita
AU  - Ghosh, Sulekha
AU  - Bhattacharya, Sudin
AD  - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata, 700026, West Bengal, India, sudinb19572004@yahoo.co.in
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 61
EP  - 73
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 26
IS  - 1
SN  - 0966-0844, 0966-0844
KW  - Toxicology Abstracts
KW  - Antioxidants
KW  - Genotoxicity
KW  - Bone marrow
KW  - Enzymes
KW  - Thioredoxin-disulfide reductase
KW  - Cytotoxic agents
KW  - Urea
KW  - Glutathione transferase
KW  - Catalase
KW  - Cancer
KW  - Trace elements
KW  - DNA damage
KW  - Selenium compounds
KW  - Selenium
KW  - Reactive oxygen species
KW  - Cisplatin
KW  - Oxidative stress
KW  - Kidney
KW  - Chromosome aberrations
KW  - X 24360:Metals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323218139?accountid=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=BioMetals&rft.atitle=Effects+of+organoselenium+compound+2-%285-selenocyanato-pentyl%29-benzo%5Bde%5Disoquinoline+1%2C3-dione+on+cisplatin+induced+nephrotoxicity+and+genotoxicity%3A+an+investigation+of+the+influence+of+the+compound+on+oxidative+stress+and+antioxidant+enzyme+system&rft.au=Ghosh%2C+Prosenjit%3BRoy%2C+Somnath+Singha%3BChakraborty%2C+Pramita%3BGhosh%2C+Sulekha%3BBhattacharya%2C+Sudin&rft.aulast=Ghosh&rft.aufirst=Prosenjit&rft.date=2013-02-01&rft.volume=26&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=BioMetals&rft.issn=09660844&rft_id=info:doi/10.1007%2Fs10534-012-9594-y
LA  - Dutch
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 51
N1  - Last updated - 2015-03-19
N1  - SubjectsTermNotLitGenreText - Antioxidants; Genotoxicity; Bone marrow; Thioredoxin-disulfide reductase; Enzymes; Urea; Cytotoxic agents; Glutathione transferase; Cancer; Catalase; Trace elements; Selenium; Selenium compounds; DNA damage; Cisplatin; Reactive oxygen species; Oxidative stress; Kidney; Chromosome aberrations
DO  - http://dx.doi.org/10.1007/s10534-012-9594-y
ER  - 



TY  - JOUR
T1  - Obesity-related hormones and endometrial cancer among postmenopausal women: a nested case-control study within the B~FIT cohort.
AN  - 1321795457; 23222000
AB  - Endometrial cancer risk is strongly influenced by obesity, but the mechanisms of action remain unclear. Leptin and adiponectin, secreted from adipose tissue, reportedly play a role in such carcinogenic processes as cell proliferation, angiogenesis, and insulin regulation. In this case-control study, nested within the Breast and Bone Follow-up of the Fracture Intervention Trial (n=15,595), we assessed pre-diagnostic serum leptin, total adiponectin, and high-molecular-weight (HMW) adiponectin in relation to endometrial cancer among postmenopausal women. During the 10-year follow-up, 62 incident endometrial cases were identified and matched to 124 controls on age, geographical site, time of fasting blood draw at baseline (1992-1993), and trial participation status. Adipokines and C-peptide were measured by ELISA. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated via conditional logistic regression, with exposures categorized in tertiles (T). Multivariable models considered C-peptide, BMI (kg/m(2)), and estradiol (E2) as potential confounders. Endometrial cancer risk was significantly associated with higher leptin levels, adjusted for E2 and C-peptide (OR(T3 vs T1)=2.96; 95% CI, 1.21-7.25; P trend <0.01). After further adjustment for BMI, the estimates were attenuated and the positive trend was no longer statistically significant (OR(T3 vs T1)=2.11; 95% CI, 0.69-6.44; P trend=0.18). No significant associations were observed with adiponectin or HMW adiponectin and endometrial cancer. Our findings with leptin suggest that the leptin-BMI axis might increase endometrial cancer risk through mechanisms other than estrogen-driven proliferation. Continued exploration of these pathways in larger prospective studies may help elucidate mechanisms underlying observed obesity-endometrial cancer associations.
JF  - Endocrine-related cancer
AU  - Dallal, Cher M
AU  - Brinton, Louise A
AU  - Bauer, Douglas C
AU  - Buist, Diana S M
AU  - Cauley, Jane A
AU  - Hue, Trisha F
AU  - Lacroix, Andrea
AU  - Tice, Jeffrey A
AU  - Chia, Victoria M
AU  - Falk, Roni
AU  - Pfeiffer, Ruth
AU  - Pollak, Michael
AU  - Veenstra, Timothy D
AU  - Xu, Xia
AU  - Lacey, James V
AU  - B~FIT Research Group
AD  - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, Bethesda, Maryland 20852, USA. cher.dalla@nih.gov ; B~FIT Research Group
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 151
EP  - 160
VL  - 20
IS  - 1
KW  - Adipokines
KW  - 0
KW  - Adiponectin
KW  - C-Peptide
KW  - Estrogens
KW  - Leptin
KW  - Index Medicus
KW  - C-Peptide -- blood
KW  - Aged, 80 and over
KW  - Risk Factors
KW  - Humans
KW  - Prognosis
KW  - Case-Control Studies
KW  - Aged
KW  - Middle Aged
KW  - Body Mass Index
KW  - Longitudinal Studies
KW  - Female
KW  - Estrogens -- blood
KW  - Postmenopause -- blood
KW  - Endometrial Neoplasms -- pathology
KW  - Adipokines -- blood
KW  - Endometrial Neoplasms -- blood
KW  - Endometrial Neoplasms -- etiology
KW  - Adiponectin -- blood
KW  - Obesity -- complications
KW  - Obesity -- blood
KW  - Leptin -- blood
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1321795457?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-related+cancer&rft.atitle=Obesity-related+hormones+and+endometrial+cancer+among+postmenopausal+women%3A+a+nested+case-control+study+within+the+B%7EFIT+cohort.&rft.au=Dallal%2C+Cher+M%3BBrinton%2C+Louise+A%3BBauer%2C+Douglas+C%3BBuist%2C+Diana+S+M%3BCauley%2C+Jane+A%3BHue%2C+Trisha+F%3BLacroix%2C+Andrea%3BTice%2C+Jeffrey+A%3BChia%2C+Victoria+M%3BFalk%2C+Roni%3BPfeiffer%2C+Ruth%3BPollak%2C+Michael%3BVeenstra%2C+Timothy+D%3BXu%2C+Xia%3BLacey%2C+James+V%3BB%7EFIT+Research+Group&rft.aulast=Dallal&rft.aufirst=Cher&rft.date=2013-02-01&rft.volume=20&rft.issue=1&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Endocrine-related+cancer&rft.issn=1479-6821&rft_id=info:doi/10.1530%2FERC-12-0229
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-02
N1  - Date created - 2013-02-19
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Int J Cancer. 2004 Jan 20;108(3):425-32 [14648710]
J Surg Res. 2003 Jul;113(1):50-5 [12943810]
J Biol Chem. 2004 Mar 26;279(13):12152-62 [14699128]
Nat Rev Cancer. 2004 Aug;4(8):579-91 [15286738]
Osteoporos Int. 1993;3 Suppl 3:S29-39 [8298200]
J Natl Cancer Inst. 1996 Aug 21;88(16):1127-35 [8757192]
Lancet. 1996 Dec 7;348(9041):1535-41 [8950879]
Am J Epidemiol. 1997 Sep 15;146(6):476-82 [9290508]
Nature. 1998 Oct 22;395(6704):763-70 [9796811]
JAMA. 1998 Dec 23-30;280(24):2077-82 [9875874]
Biochem Biophys Res Commun. 1999 Apr 2;257(1):79-83 [10092513]
Obes Rev. 2005 Feb;6(1):13-21 [15655035]
Metabolism. 2005 Mar;54(3):281-6 [15736103]
J Allergy Clin Immunol. 2005 May;115(5):911-9; quiz 920 [15867843]
Am J Epidemiol. 2005 Jul 15;162(2):101-14 [15972940]
J Cell Physiol. 2006 Apr;207(1):12-22 [16110483]
Cancer. 2006 Jun 1;106(11):2376-81 [16639730]
JAMA. 2006 Dec 27;296(24):2927-38 [17190893]
J Clin Endocrinol Metab. 2007 Jan;92(1):255-63 [17062769]
Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1291-3 [17548700]
Anal Chem. 2007 Oct 15;79(20):7813-21 [17848096]
Eur J Obstet Gynecol Reprod Biol. 2008 Jan;136(1):74-7 [17007993]
Arch Physiol Biochem. 2008 Feb;114(1):71-83 [18465361]
Front Biosci (Schol Ed). 2009;1:329-57 [19482706]
Cancer Epidemiol Biomarkers Prev. 2009 Oct;18(10):2569-78 [19755644]
Annu Rev Med. 2010;61:301-16 [19824817]
Gynecol Oncol. 2010 Oct;119(1):65-9 [20674961]
Am J Obstet Gynecol. 2011 Feb;204(2):167.e1-5 [21047616]
Int J Cancer. 2004 Jan 10;108(2):262-8 [14639613]
Ann Nutr Metab. 2002;46(3-4):147-51 [12169858]
Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1531-43 [12496040]
J Clin Endocrinol Metab. 2003 Mar;88(3):993-7 [12629074]
J Clin Endocrinol Metab. 2004 Mar;89(3):1160-3 [15001602]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1530/ERC-12-0229
ER  - 



TY  - JOUR
T1  - Menopause and lead body burden among US women aged 45-55, NHANES 1999-2010
AN  - 1318689606; 17700253
AB  - Environmental factors in menopause have received limited attention. Lead is a known reproductive toxicant associated with delayed puberty in girls that may also affect menopause. The odds of menopause among US women aged 45-55 were estimated in the National Health and Nutrition Examination Survey, 1999-2010, in relation to quartiles of blood lead. Women still menstruating (n=2158) were compared to women with natural menopause (n=1063). Logistic regression models included age, race/ethnicity, current hormone use, poverty, smoking and where available, bone density or bone alkaline phosphatase. Lead levels (ug/dL) were higher in menopausal women, geometric mean (standard error)=1.71 (0.04) vs. 1.23 (0.02). Adjusted odds of menopause and 95% confidence intervals for lead quartiles (lowest quartile referent) were 1.7 (1.0-2.8), 2.1 (1.2-3.6), and 4.2 (2.5-7.0) respectively. Results adjusting for bone markers were generally similar but had less precision. Blood lead was associated with natural menopause in US women even after adjustment for bone turnover. This raises concern that lead exposure, even at low levels, may shorten women's reproductive lifespan.
JF  - Environmental Research
AU  - Mendola, Pauline
AU  - Brett, Kate
AU  - DiBari, Jessica N
AU  - Pollack, Anna Z
AU  - Tandon, Rashmi
AU  - Shenassa, Edmond D
AD  - Epidemiology Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Blvd, Rockville, MD 20852, USA, pauline.mendola@nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 110
EP  - 113
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 121
SN  - 0013-9351, 0013-9351
KW  - Toxicology Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - Lead
KW  - Menopause
KW  - Women's health
KW  - Epidemiology
KW  - Environment
KW  - Age
KW  - Toxicants
KW  - Bone density
KW  - Hormones
KW  - Nutrition
KW  - Environmental factors
KW  - Models
KW  - Smoking
KW  - Regression analysis
KW  - Ethnic groups
KW  - Races
KW  - Body burden
KW  - Life span
KW  - Blood levels
KW  - Bone
KW  - Blood
KW  - USA
KW  - Alkaline phosphatase
KW  - Bone turnover
KW  - Puberty
KW  - X 24380:Social Poisons & Drug Abuse
KW  - H 12000:Epidemiology and Public Health
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318689606?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Menopause+and+lead+body+burden+among+US+women+aged+45-55%2C+NHANES+1999-2010&rft.au=Mendola%2C+Pauline%3BBrett%2C+Kate%3BDiBari%2C+Jessica+N%3BPollack%2C+Anna+Z%3BTandon%2C+Rashmi%3BShenassa%2C+Edmond+D&rft.aulast=Mendola&rft.aufirst=Pauline&rft.date=2013-02-01&rft.volume=121&rft.issue=&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2012.12.009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2015-03-19
N1  - SubjectsTermNotLitGenreText - Age; Toxicants; Life span; Bone density; Environmental factors; Nutrition; Hormones; Lead; Models; Smoking; Blood; Alkaline phosphatase; Regression analysis; Bone turnover; Races; Menopause; Ethnic groups; Puberty; Bone; Body burden; Blood levels; USA
DO  - http://dx.doi.org/10.1016/j.envres.2012.12.009
ER  - 



TY  - JOUR
T1  - Mechanistic insights from the NTP studies of chromium.
AN  - 1315633731; 23334696
AB  - Hexavalent chromium (Cr(VI)) is a contaminant of water and soil and is a human lung carcinogen. Trivalent chromium (Cr(III)), a proposed essential element, is ingested by humans in the diet and in dietary supplements such as chromium picolinate (CP). The National Toxicology Program (NTP) demonstrated that Cr(VI) is also carcinogenic in rodents when administered in drinking water as sodium dichromate dihydrate (SDD), inducing neoplasms of the oral cavity and small intestine in rats and mice, respectively. In contrast, there was no definitive evidence of toxicity or carcinogenicity following exposure to Cr(III) administered in feed as CP monohydrate (CPM). Cr(VI) readily enters cells via nonspecific anion channels, in contrast to Cr(III), which cannot easily pass through the cell membrane. Extracellular reduction of Cr(VI) to Cr(III), which occurs primarily in the stomach, is considered a mechanism of detoxification, while intracellular reduction is thought to be a mechanism of genotoxicity and carcinogenicity. Tissue distribution studies in additional groups of male rats and female mice demonstrated higher Cr concentrations in tissues following exposure to Cr(VI) compared to controls and Cr(III) exposure at a similar external dose, indicating that some of the Cr(VI) escaped gastric reduction and was distributed systemically. The multiple potential pathways of Cr-induced genotoxicity will be discussed.
JF  - Toxicologic pathology
AU  - Witt, Kristine L
AU  - Stout, Matthew D
AU  - Herbert, Ronald A
AU  - Travlos, Gregory S
AU  - Kissling, Grace E
AU  - Collins, Bradley J
AU  - Hooth, Michelle J
AD  - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 326
EP  - 342
VL  - 41
IS  - 2
KW  - Water Pollutants, Chemical
KW  - 0
KW  - Chromium
KW  - 0R0008Q3JB
KW  - chromium hexavalent ion
KW  - 18540-29-9
KW  - Index Medicus
KW  - Animals
KW  - Water Pollutants, Chemical -- chemistry
KW  - Liver -- pathology
KW  - Mouth Mucosa -- pathology
KW  - Water Pollutants, Chemical -- toxicity
KW  - Tongue -- pathology
KW  - Lymph Nodes -- pathology
KW  - Water Pollutants, Chemical -- pharmacokinetics
KW  - Mice
KW  - Tissue Distribution
KW  - Mouth Mucosa -- drug effects
KW  - Rats
KW  - Mutagenicity Tests
KW  - Duodenum -- drug effects
KW  - Hyperplasia -- chemically induced
KW  - Liver -- drug effects
KW  - Neoplasms -- chemically induced
KW  - Carcinogenicity Tests
KW  - Histiocytes
KW  - Tongue -- drug effects
KW  - Lymph Nodes -- drug effects
KW  - Duodenum -- pathology
KW  - Female
KW  - Male
KW  - Chromium -- chemistry
KW  - Chromium -- pharmacokinetics
KW  - Chromium -- toxicity
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315633731?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanistic+insights+from+the+NTP+studies+of+chromium.&rft.au=Witt%2C+Kristine+L%3BStout%2C+Matthew+D%3BHerbert%2C+Ronald+A%3BTravlos%2C+Gregory+S%3BKissling%2C+Grace+E%3BCollins%2C+Bradley+J%3BHooth%2C+Michelle+J&rft.aulast=Witt&rft.aufirst=Kristine&rft.date=2013-02-01&rft.volume=41&rft.issue=2&rft.spage=326&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623312469856
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-30
N1  - Date created - 2013-03-08
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1177/0192623312469856
ER  - 



TY  - CONF
T1  - Proceedings of the 2012 National Toxicology Program Satellite Symposium.
AN  - 1315633714; 23262640
AB  - The 2012 annual National Toxicology Program (NTP) Satellite Symposium, entitled "Pathology Potpourri," was held in Boston in advance of the Society of Toxicologic Pathology's 31st annual meeting. The goal of the NTP Symposium is to present current diagnostic pathology or nomenclature issues to the toxicologic pathology community. This article presents summaries of the speakers' presentations, including diagnostic or nomenclature issues that were presented, along with select images that were used for audience voting or discussion. Some lesions and topics covered during the symposium include eosinophilic crystalline pneumonia in a transgenic mouse model; differentiating adrenal cortical cystic degeneration from adenoma; atypical eosinophilic foci of altered hepatocytes; differentiating cardiac schwannoma from cardiomyopathy; diagnosis of cardiac papillary muscle lesions; intrahepatocytic erythrocytes and venous subendothelial hepatocytes; lesions in Rathke's cleft and pars distalis; pernicious anemia and megaloblastic disorders; embryonic neuroepithelial dysplasia, holoprosencephaly and exencephaly; and INHAND nomenclature for select cardiovascular lesions.
JF  - Toxicologic pathology
AU  - Elmore, Susan A
AU  - Berridge, Brian R
AU  - Boyle, Michael C
AU  - Cora, Michelle C
AU  - Hoenerhoff, Mark J
AU  - Kooistra, Linda
AU  - Laast, Victoria A
AU  - Morrison, James P
AU  - Rao, Deepa
AU  - Rinke, Matthias
AU  - Yoshizawa, Katsuhiko
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 151
EP  - 180
VL  - 41
IS  - 2
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Diagnostic Techniques and Procedures
KW  - Terminology as Topic
KW  - Pathology
KW  - Toxicology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315633714?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Toxicologic+pathology&rft.atitle=Proceedings+of+the+2012+National+Toxicology+Program+Satellite+Symposium.&rft.au=Elmore%2C+Susan+A%3BBerridge%2C+Brian+R%3BBoyle%2C+Michael+C%3BCora%2C+Michelle+C%3BHoenerhoff%2C+Mark+J%3BKooistra%2C+Linda%3BLaast%2C+Victoria+A%3BMorrison%2C+James+P%3BRao%2C+Deepa%3BRinke%2C+Matthias%3BYoshizawa%2C+Katsuhiko&rft.aulast=Elmore&rft.aufirst=Susan&rft.date=2013-02-01&rft.volume=41&rft.issue=2&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623312467102
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-30
N1  - Date created - 2013-03-08
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Biol Chem. 2000 Mar 17;275(11):8032-7 [10713123]
Vet Pathol. 2012 May;49(3):569-73 [21997565]
Am J Pathol. 2001 Jan;158(1):323-32 [11141507]
Infect Immun. 2001 Apr;69(4):2723-7 [11254641]
J Biol Chem. 2001 May 18;276(20):17497-506 [11297523]
J Biol Chem. 2001 Nov 9;276(45):41969-76 [11553626]
J Biol Chem. 2002 Feb 15;277(7):5468-75 [11733538]
J Leukoc Biol. 2002 Jul;72(1):72-82 [12101265]
J Vet Med A Physiol Pathol Clin Med. 2003 Mar;50(2):103-7 [12667201]
Surgery. 2004 Mar;135(3):297-306 [14976480]
Histochem Cell Biol. 2004 Jun;121(6):473-82 [15148607]
Ann N Y Acad Sci. 1965 Sep 8;127(1):517-40 [5217278]
Am J Pathol. 1964 Apr;44(4):645-62 [5877511]
Toxicol Appl Pharmacol. 1969 Jul;15(1):189-205 [4185489]
J Comp Pathol. 1971 Jan;81(1):141-4 [5104544]
Toxicol Appl Pharmacol. 1971 Nov;20(3):442-5 [5132784]
Cancer Res. 1975 Aug;35(8):2269-77 [1149036]
Vet Pathol. 1978 Mar;15(2):170-8 [664185]
J Cell Sci. 1980 Apr;42:23-32 [7400234]
Lab Invest. 1983 Jul;49(1):78-81 [6865333]
Environ Health Perspect. 1983 Apr;50:149-61 [6873010]
Am J Pathol. 1984 Aug;116(2):179-92 [6380298]
Toxicol Appl Pharmacol. 1986 Mar 30;83(1):95-100 [3952753]
Toxicol Appl Pharmacol. 1986 Sep 30;85(3):450-5 [3020740]
Nihon Juigaku Zasshi. 1988 Feb;50(1):299-302 [3361733]
Appl Pathol. 1988;6(2):73-81 [2455530]
Vet Pathol. 1987 Nov;24(6):488-94 [3455078]
J Neurocytol. 1988 Aug;17(4):521-9 [3193129]
Vet Pathol. 1990 Jul;27(4):274-81 [2169666]
Int J Pancreatol. 1991 Feb;8(2):119-31 [2033323]
Vet Pathol. 1991 Mar;28(2):156-65 [2063516]
Differentiation. 1991 Sep;48(1):33-42 [1683842]
Arch Histol Cytol. 1991 Dec;54(5):511-8 [1665339]
Pancreas. 1992;7(2):153-8 [1553365]
Blood. 1992 May 1;79(9):2273-80 [1571542]
Toxicol Pathol. 1992;20(2):212-25 [1475582]
Exp Anim. 1995 Jul;44(3):245-9 [7556427]
Immunology. 1997 Apr;90(4):511-7 [9176103]
Q J Exp Physiol Cogn Med Sci. 1956 Jul;41(3):215-29 [13485337]
Toxicol Pathol. 2005;33(4):477-83 [16036865]
Proteomics. 2005 Jul;5(11):2799-807 [15996009]
J Vet Med A Physiol Pathol Clin Med. 2005 Oct;52(8):403-6 [16176570]
Development. 2005 Dec;132(23):5329-39 [16284123]
Vet Pathol. 2006 Sep;43(5):682-8 [16966445]
Blood Rev. 2006 Nov;20(6):299-318 [16716475]
Am J Pathol. 2009 Jan;174(1):153-63 [19095958]
Nephron Physiol. 2009;111(3):p39-53 [19276629]
J Clin Invest. 2009 Jun;119(6):1403-13 [19487816]
Trends Pharmacol Sci. 2009 Jun;30(6):303-12 [19443052]
Am Heart J. 2009 Jul;158(1):21-9 [19540388]
J Pathol. 2010 Jan;220(2):217-30 [19918803]
Am J Surg Pathol. 2009 Oct;33(10):1554-61 [19623031]
Curr Opin Neurobiol. 2010 Feb;20(1):58-67 [20080044]
Toxicol Pathol. 2010 Jan;38(1):9-36 [20008954]
Mol Immunol. 2010 Apr;47(7-8):1467-75 [20226534]
Birth Defects Res A Clin Mol Teratol. 2010 Aug;88(8):653-69 [20740593]
Toxicol Pathol. 2010 Aug;38(5):703-14 [20585145]
Toxicol Pathol. 2010 Dec;38(7 Suppl):5S-81S [21191096]
Toxicol Pathol. 2011 Jan;39(1):240-66 [21177527]
Neuron. 2011 Mar 24;69(6):1046-60 [21435552]
Curr Drug Targets. 2011 Jun;12(6):827-49 [21269267]
J Comp Pathol. 2000 Aug-Oct;123(2-3):190-4 [11032674]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1177/0192623312467102
ER  - 



TY  - JOUR
T1  - Quantitative Screening for Anticestode Drugs Based on Changes in Baseline Enzyme Secretion by Taenia crassiceps
AN  - 1315622767; 17709749
AB  - Neurocysticercosis (NCC), an infection of the brain with the larval stage of the Taenia solium tapeworm, is responsible for an estimated one-third of adult-onset epilepsy cases in regions of the world where it is endemic. Currently, anthelmintic drugs used for treatment of NCC are only partially effective, and there is, therefore, a pressing need for new therapeutic agents. Discovery of new anthelmintics with activity against T. solium has been limited by the lack of suitable sensitive assays that allow high-throughput screening. Using an in vitro culture system with Taenia crassiceps metacestodes, we demonstrate that changes in secretion of parasite-associated alkaline phosphatase (AP) and phosphoglucose isomerase (PGI) can be used to detect and quantify anthelmintic effects of praziquantel (PZQ), a drug with activity against T. solium. We applied two enzyme release assays to screen for anti-T. crassiceps activity in nonconventional antiparasitic drugs and demonstrate that nitazoxanide and artesunate induced release of both AP and PGI in differing time- and dose-related patterns. Furthermore, imatinib, a tyrosine kinase inhibitor previously reported to have parasiticidal activity against Schistosoma mansoni, also induced release of both AP and PGI in a dose-dependent manner, similar in pattern to that observed with the other anthelmintics. We also evaluated release of ATP into cyst supernatants as an indicator of drug effects but did not see any differences between treated and untreated cysts. These data provide the basis for rapid and quantitative screening assays for testing for anthelmintic activity in candidate anticestode agents.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Mahanty, Siddhartha
AU  - Madrid, Elise M
AU  - Nash, Theodore E
AD  - Helminth Immunology Section, SiddharthaMahanty,smahanty{at}niaid.nih.gov.
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 990
EP  - 995
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 2
SN  - 0066-4804, 0066-4804
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - ATP
KW  - Alkaline phosphatase
KW  - Brain
KW  - Cysticercosis
KW  - Cysts
KW  - Data processing
KW  - Drug screening
KW  - Drugs
KW  - Enzymes
KW  - Epilepsy
KW  - Imatinib
KW  - Infection
KW  - Praziquantel
KW  - Protein-tyrosine kinase
KW  - Secretion
KW  - artesunate
KW  - high-throughput screening
KW  - phosphoglucose isomerase
KW  - Schistosoma mansoni
KW  - Taenia crassiceps
KW  - Taenia solium
KW  - Taenia
KW  - A 01340:Antibiotics & Antimicrobials
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315622767?accountid=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=Quantitative+Screening+for+Anticestode+Drugs+Based+on+Changes+in+Baseline+Enzyme+Secretion+by+Taenia+crassiceps&rft.au=Mahanty%2C+Siddhartha%3BMadrid%2C+Elise+M%3BNash%2C+Theodore+E&rft.aulast=Mahanty&rft.aufirst=Siddhartha&rft.date=2013-02-01&rft.volume=57&rft.issue=2&rft.spage=990&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.01022-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 21
N1  - Last updated - 2013-04-05
N1  - SubjectsTermNotLitGenreText - Data processing; Secretion; Brain; ATP; Enzymes; Cysts; Infection; Drug screening; Imatinib; Alkaline phosphatase; Epilepsy; phosphoglucose isomerase; Protein-tyrosine kinase; Cysticercosis; high-throughput screening; Praziquantel; artesunate; Drugs; Schistosoma mansoni; Taenia crassiceps; Taenia solium; Taenia
DO  - http://dx.doi.org/10.1128/AAC.01022-12
ER  - 



TY  - JOUR
T1  - Malaria biology and disease pathogenesis: insights for new treatments
AN  - 1315621311; 17679670
AB  - Plasmodium falciparum malaria, an infectious disease caused by a parasitic protozoan, claims the lives of nearly a million children each year in Africa alone and is a top public health concern. Evidence is accumulating that resistance to artemisinin derivatives, the frontline therapy for the asexual blood stage of the infection, is developing in southeast Asia. Renewed initiatives to eliminate malaria will benefit from an expanded repertoire of antimalarials, including new drugs that kill circulating P. falciparum gametocytes, thereby preventing transmission. Our current understanding of the biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro lends optimism that high-throughput screenings of large chemical libraries will produce a new generation of antimalarial drugs. There is also a need for new therapies to reduce the high mortality of severe malaria. An understanding of the pathophysiology of severe disease may identify rational targets for drugs that improve survival.
JF  - Nature Medicine
AU  - Miller, Louis H
AU  - Ackerman, Hans C
AU  - Su, Xin-zhuan
AU  - Wellems, Thomas E
AD  - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, Rockville, Maryland, USA.
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 156
EP  - 167
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 19
IS  - 2
SN  - 1078-8956, 1078-8956
KW  - Health & Safety Science Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW  - Parasites
KW  - Human diseases
KW  - Survival
KW  - Malaria
KW  - Infection
KW  - Disease transmission
KW  - Public health
KW  - Infectious diseases
KW  - high-throughput screening
KW  - Southeast Asia
KW  - Drugs
KW  - Mortality
KW  - Gametocytes
KW  - Therapy
KW  - Plasmodium falciparum
KW  - Children
KW  - Blood
KW  - Africa
KW  - artemisinin
KW  - Mortality causes
KW  - K 03400:Human Diseases
KW  - Q1 08485:Species interactions: pests and control
KW  - Q5 08524:Public health, medicines, dangerous organisms
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315621311?accountid=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=Nature+Medicine&rft.atitle=Malaria+biology+and+disease+pathogenesis%3A+insights+for+new+treatments&rft.au=Miller%2C+Louis+H%3BAckerman%2C+Hans+C%3BSu%2C+Xin-zhuan%3BWellems%2C+Thomas+E&rft.aulast=Miller&rft.aufirst=Louis&rft.date=2013-02-01&rft.volume=19&rft.issue=2&rft.spage=156&rft.isbn=&rft.btitle=&rft.title=Nature+Medicine&rft.issn=10788956&rft_id=info:doi/10.1038%2Fnm.3073
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Therapy; Survival; Malaria; Drugs; Mortality causes; Public health; Mortality; Gametocytes; Children; Infection; Disease transmission; Blood; Infectious diseases; artemisinin; high-throughput screening; Plasmodium falciparum; Africa; Southeast Asia
DO  - http://dx.doi.org/10.1038/nm.3073
ER  - 



TY  - JOUR
T1  - Risk factors for gastric cancer in Latin America: a meta-analysis
AN  - 1315619547; 17681979
AB  - Background: Latin America has among the highest gastric cancer incidence rates in the world, for reasons that are still unknown. In order to identify region-specific risk factors for gastric cancer, we conducted a meta-analysis summarizing published literature. Methods: Searches of PubMed and regional databases for relevant studies published up to December 2011 yielded a total of 29 independent case-control studies. We calculated summary odds ratios (OR) for risk factors reported in at least five studies, including socioeconomic status (education), lifestyle habits (smoking and alcohol use), dietary factors (consumption of fruits, total vegetables, green vegetables, chili pepper, total meat, processed meat, red meat, fish, and salt), and host genetic variants (IL1B-511T, IL1B-31C, IL1RN*2, TNFA-308A, TP53 codon 72 Arg, and GSTM1 null). Study-specific ORs were extracted and summarized using random-effects models. Results: Chili pepper was the only region-specific factor reported in at least five studies. Consistent with multifactorial pathogenesis, smoking, alcohol use, high consumption of red meat or processed meat, excessive salt intake, and carriage of IL1RN*2 were each associated with a moderate increase in gastric cancer risk. Conversely, higher levels of education, fruit consumption, and total vegetable consumption were each associated with a moderately decreased risk. The other exposures were not significantly associated. No prospective study data were identified. Conclusion: Risk factor associations for gastric cancer in Latin America are based on case-control comparisons that have uncertain reliability, particularly with regard to diet; the specific factors identified and their magnitudes of association are largely similar to those globally recognized. Future studies should emphasize prospective data collection and focus on region-specific exposures that may explain high gastric cancer risk.
JF  - Cancer Causes & Control
AU  - Bonequi, Patricia
AU  - Meneses-Gonzalez, Fernando
AU  - Correa, Pelayo
AU  - Rabkin, Charles S
AU  - Camargo, MConstanza
AD  - Programa de Residencia en Epidemiologia, Direccion General Adjunta de Epidemiologia, Secretaria de Salud, Mexico City, Mexico, camargomc@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 217
EP  - 231
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 24
IS  - 2
SN  - 0957-5243, 0957-5243
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Alcohol
KW  - Cancer
KW  - Diets
KW  - Education
KW  - Fruits
KW  - Meat
KW  - Risk factors
KW  - Salts
KW  - Smoking
KW  - Latin America
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/1315619547?accountid=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+factors+for+gastric+cancer+in+Latin+America%3A+a+meta-analysis&rft.au=Bonequi%2C+Patricia%3BMeneses-Gonzalez%2C+Fernando%3BCorrea%2C+Pelayo%3BRabkin%2C+Charles+S%3BCamargo%2C+MConstanza&rft.aulast=Bonequi&rft.aufirst=Patricia&rft.date=2013-02-01&rft.volume=24&rft.issue=2&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0110-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 110
N1  - Last updated - 2013-05-06
N1  - SubjectsTermNotLitGenreText - Diets; Meat; Smoking; Salts; Fruits; Alcohol; Education; Risk factors; Cancer; Latin America
DO  - http://dx.doi.org/10.1007/s10552-012-0110-z
ER  - 



TY  - JOUR
T1  - In Vitro Analysis of Albendazole Sulfoxide Enantiomers Shows that (+)-(R)-Albendazole Sulfoxide Is the Active Enantiomer against Taenia solium
AN  - 1315617894; 17709763
AB  - Albendazole is an anthelmintic drug widely used in the treatment of neurocysticercosis (NCC), an infection of the brain with Taenia solium cysts. However, drug levels of its active metabolite, albendazole sulfoxide (ABZSO), are erratic, likely resulting in decreased efficacy and suboptimal cure rates in NCC. Racemic albendazole sulfoxide is composed of ABZSO (+)-(R)- and (-)-(S) enantiomers that have been shown to differ in pharmacokinetics and activity against other helminths. The antiparasitic activities of racemic ABZSO and its (+)-(R)- and (-)-(S) enantiomers against T. solium cysts were evaluated in vitro. Parasites were collected from naturally infected pigs, cultured, and exposed to the racemic mixture or to each enantiomer (range, 10 to 500 ng/ml) or to praziquantel as a reference drug. The activity of each compound against cysts was assayed by measuring the ability to evaginate and inhibition of alkaline phosphatase (AP) and parasite antigen release. (+)-(R)-ABZSO was significantly more active than (-)-(S)-ABZSO in suppressing the release of AP and antigen into the supernatant in a dose- and time-dependent manner, indicating that most of the activity of ABZSO resides in the (+)-(R) enantiomer. Use of this enantiomer alone may lead to increased efficacy and/or less toxicity compared to albendazole.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Paredes, Adriana
AU  - Campos Lourenco, Tiago de
AU  - Marzal, Miguel
AU  - Rivera, Andrea
AU  - Dorny, Pierre
AU  - Mahanty, Siddhartha
AU  - Guerra-Giraldez, Cristina
AU  - Garcia, Hector H
AU  - Nash, Theodore E
AU  - Cass, Quezia B
AD  - Laboratorio de Inmunopatologia en Neurocisticercosis, Facultad de Ciencias y Filosofia, Universidad Peruana Cayetano Heredia, Lima, Peru, TheodoreE.Nash,tnash{at}niaid.nih.gov.
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 944
EP  - 949
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 2
SN  - 0066-4804, 0066-4804
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - Albendazole
KW  - Alkaline phosphatase
KW  - Brain
KW  - Cysticercosis
KW  - Cysts
KW  - Drugs
KW  - Enantiomers
KW  - Infection
KW  - Metabolites
KW  - Parasites
KW  - Pharmacokinetics
KW  - Praziquantel
KW  - Toxicity
KW  - Taenia
KW  - Taenia solium
KW  - A 01340:Antibiotics & Antimicrobials
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315617894?accountid=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=In+Vitro+Analysis+of+Albendazole+Sulfoxide+Enantiomers+Shows+that+%28%2B%29-%28R%29-Albendazole+Sulfoxide+Is+the+Active+Enantiomer+against+Taenia+solium&rft.au=Paredes%2C+Adriana%3BCampos+Lourenco%2C+Tiago+de%3BMarzal%2C+Miguel%3BRivera%2C+Andrea%3BDorny%2C+Pierre%3BMahanty%2C+Siddhartha%3BGuerra-Giraldez%2C+Cristina%3BGarcia%2C+Hector+H%3BNash%2C+Theodore+E%3BCass%2C+Quezia+B&rft.aulast=Paredes&rft.aufirst=Adriana&rft.date=2013-02-01&rft.volume=57&rft.issue=2&rft.spage=944&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.01465-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 30
N1  - Last updated - 2013-04-05
N1  - SubjectsTermNotLitGenreText - Parasites; Brain; Metabolites; Toxicity; Cysts; Infection; Pharmacokinetics; Albendazole; Alkaline phosphatase; Enantiomers; Cysticercosis; Praziquantel; Drugs; Taenia solium; Taenia
DO  - http://dx.doi.org/10.1128/AAC.01465-12
ER  - 



TY  - JOUR
T1  - STB5 Is a Negative Regulator of Azole Resistance in Candida glabrata
AN  - 1315617358; 17709757
AB  - The opportunistic yeast pathogen Candida glabrata is recognized for its ability to acquire resistance during prolonged treatment with azole antifungals (J. E. Bennett, K. Izumikawa, and K. A. Marr. Antimicrob. Agents Chemother. 48:1773-1777, 2004). Resistance to azoles is largely mediated by the transcription factor PDR1, resulting in the upregulation of ATP-binding cassette (ABC) transporter proteins and drug efflux. Studies in the related yeast Saccharomyces cerevisiae have shown that Pdr1p forms a heterodimer with another transcription factor, Stb5p. In C. glabrata, the open reading frame (ORF) designated CAGL0I02552g has 38.8% amino acid identity with STB5 (YHR178w) and shares an N-terminal Zn2Cys6 binuclear cluster domain and a fungus-specific transcriptional factor domain, prompting us to test for homologous function and a possible role in azole resistance. Complementation of a Delta yhr178w ( Delta stb5) mutant with CAGL0I02552g resolved the increased sensitivity to cold, hydrogen peroxide, and caffeine of the mutant, for which reason we designated CAGl0I02552g CgSTB5. Overexpression of CgSTB5 in C. glabrata repressed azole resistance, whereas deletion of CgSTB5 caused a modest increase in resistance. Expression analysis found that CgSTB5 shares many transcriptional targets with CgPDR1 but, unlike the latter, is a negative regulator of pleiotropic drug resistance, including the ABC transporter genes CDR1, PDH1, and YOR1.
JF  - Antimicrobial Agents & Chemotherapy
AU  - Noble, Jason A
AU  - Tsai, Huei-Fung
AU  - Suffis, Sara D
AU  - Su, Qin
AU  - Myers, Timothy G
AU  - Bennett, John E
AD  - Clinical Mycology Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, jbennett@niaid.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 959
EP  - 967
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 57
IS  - 2
SN  - 0066-4804, 0066-4804
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW  - ABC transporter
KW  - Amino acids
KW  - Caffeine
KW  - Complementation
KW  - Drug resistance
KW  - Hydrogen peroxide
KW  - Open reading frames
KW  - Opportunist infection
KW  - Pathogens
KW  - Transcription factors
KW  - azoles
KW  - complementarity-determining region 1
KW  - Candida glabrata
KW  - Saccharomyces cerevisiae
KW  - A 01340:Antibiotics & Antimicrobials
KW  - K 03310:Genetics & Taxonomy
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315617358?accountid=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=STB5+Is+a+Negative+Regulator+of+Azole+Resistance+in+Candida+glabrata&rft.au=Noble%2C+Jason+A%3BTsai%2C+Huei-Fung%3BSuffis%2C+Sara+D%3BSu%2C+Qin%3BMyers%2C+Timothy+G%3BBennett%2C+John+E&rft.aulast=Noble&rft.aufirst=Jason&rft.date=2013-02-01&rft.volume=57&rft.issue=2&rft.spage=959&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.01278-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 23
N1  - Last updated - 2013-05-06
N1  - SubjectsTermNotLitGenreText - Complementation; Amino acids; Hydrogen peroxide; ABC transporter; Drug resistance; complementarity-determining region 1; Transcription factors; Caffeine; Pathogens; Open reading frames; azoles; Opportunist infection; Candida glabrata; Saccharomyces cerevisiae
DO  - http://dx.doi.org/10.1128/AAC.01278-12
ER  - 



TY  - JOUR
T1  - Multilaboratory Approach to Preclinical Evaluation of Vaccine Immunogens for Placental Malaria
AN  - 1315615740; 17709818
AB  - Pregnancy malaria is caused by Plasmodium falciparum-infected erythrocytes that adhere to the placental receptor chondroitin sulfate A (CSA) and sequester in the placenta; women become resistant to pregnancy malaria as they acquire antiadhesion antibodies that target surface proteins of placental parasites. VAR2CSA, a member of the P. falciparum EMP1 variant surface antigen family, is the leading candidate for a pregnancy malaria vaccine. Because VAR2CSA is a high-molecular-weight protein, a vaccine based on the full-length protein may not be feasible. An alternative approach has been to develop a vaccine targeting individual Duffy binding-like (DBL) domains. In this study, a consortium of laboratories under the Pregnancy Malaria Initiative compared the functional activity of antiadhesion antibodies elicited by different VAR2CSA domains and variants produced in prokaryotic and eukaryotic expression systems. Antisera were initially tested against laboratory lines of maternal parasites, and the most promising reagents were evaluated in the field against fresh placental parasite samples. Recombinant proteins expressed in Escherichia coli elicited antibody levels similar to those expressed in eukaryotic systems, as did the two allelic forms of the DBL4 and DBL5 domains. The procedures developed for this head-to-head comparison will be useful for future evaluation and down-selection of malaria vaccine immunogens.
JF  - Infection and Immunity
AU  - Fried, Michal
AU  - Avril, Marion
AU  - Chaturvedi, Richa
AU  - Fernandez, Pablo
AU  - Lograsso, Joseph
AU  - Narum, David
AU  - Nielsen, Morten A
AU  - Oleinikov, Andrew V
AU  - Resende, Mafalda
AU  - Salanti, Ali
AD  - Seattle Biomedical Research Institute, Seattle, Washington, USA ffa, MichalFried,michal.fried{at}nih.gov.
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 487
EP  - 495
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 81
IS  - 2
SN  - 0019-9567, 0019-9567
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Immunology Abstracts
KW  - Parasites
KW  - Human diseases
KW  - Chondroitin sulfate
KW  - Erythrocytes
KW  - Disease control
KW  - Malaria
KW  - Plasmodium falciparum
KW  - Public health
KW  - Pregnancy
KW  - Plasmodium
KW  - Antisera
KW  - Antibodies
KW  - Antigens
KW  - surface antigens
KW  - Placenta
KW  - Escherichia coli
KW  - Vaccines
KW  - K 03400:Human Diseases
KW  - Q1 08485:Species interactions: pests and control
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315615740?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Multilaboratory+Approach+to+Preclinical+Evaluation+of+Vaccine+Immunogens+for+Placental+Malaria&rft.au=Fried%2C+Michal%3BAvril%2C+Marion%3BChaturvedi%2C+Richa%3BFernandez%2C+Pablo%3BLograsso%2C+Joseph%3BNarum%2C+David%3BNielsen%2C+Morten+A%3BOleinikov%2C+Andrew+V%3BResende%2C+Mafalda%3BSalanti%2C+Ali&rft.aulast=Fried&rft.aufirst=Michal&rft.date=2013-02-01&rft.volume=81&rft.issue=2&rft.spage=487&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01106-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 39
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Antibodies; Human diseases; Antigens; Disease control; Malaria; Vaccines; Pregnancy; Public health; Antisera; Chondroitin sulfate; surface antigens; Placenta; Erythrocytes; Plasmodium; Escherichia coli; Plasmodium falciparum
DO  - http://dx.doi.org/10.1128/IAI.01106-12
ER  - 



TY  - JOUR
T1  - Pyocyanin effects on respiratory epithelium: relevance in Pseudomonas aeruginosa airway infections
AN  - 1315613996; 17643760
AB  - Pseudomonas aeruginosa (PA) uses several virulence factors to establish chronic respiratory infections in bronchiectasis, chronic obstructive pulmonary disease, and cystic fibrosis (CF) patients. One of its toxins, pyocyanin (PYO), is a redox-active pigment that is required for full virulence in animal models and has been detected in patients' airway secretions. PYO promotes virulence by interfering with several cellular functions in host cells including electron transport, cellular respiration, energy metabolism, gene expression, and innate immune mechanisms. This review summarizes recent advances in PYO biology with special attention to current views on its role in human airway infections and on its interactions with the first line of our airway defense, the respiratory epithelium.
JF  - Trends in Microbiology
AU  - Rada, Balazs
AU  - Leto, Thomas L
AD  - University of Georgia, College of Veterinary Medicine, Department of Infectious Diseases, 501 DW Brooks Drive, Athens, GA 30602, USA, tleto@niaid.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 73
EP  - 81
PB  - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL  - 21
IS  - 2
SN  - 0966-842X, 0966-842X
KW  - Microbiology Abstracts B: Bacteriology
KW  - virulence factors
KW  - Energy metabolism
KW  - Bronchiectasis
KW  - Respiration
KW  - Secretions
KW  - Animal models
KW  - Toxins
KW  - pyocyanin
KW  - Chronic obstructive pulmonary disease
KW  - Gene expression
KW  - Reviews
KW  - Pigments
KW  - Chronic infection
KW  - Pseudomonas aeruginosa
KW  - Electron transport
KW  - Cystic fibrosis
KW  - Respiratory tract
KW  - J 02350:Immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315613996?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Microbiology&rft.atitle=Pyocyanin+effects+on+respiratory+epithelium%3A+relevance+in+Pseudomonas+aeruginosa+airway+infections&rft.au=Rada%2C+Balazs%3BLeto%2C+Thomas+L&rft.aulast=Rada&rft.aufirst=Balazs&rft.date=2013-02-01&rft.volume=21&rft.issue=2&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=Trends+in+Microbiology&rft.issn=0966842X&rft_id=info:doi/10.1016%2Fj.tim.2012.10.004
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2013-09-20
N1  - SubjectsTermNotLitGenreText - Energy metabolism; virulence factors; Bronchiectasis; Respiration; Secretions; Animal models; Toxins; Chronic obstructive pulmonary disease; pyocyanin; Gene expression; Pigments; Reviews; Chronic infection; Electron transport; Cystic fibrosis; Respiratory tract; Pseudomonas aeruginosa
DO  - http://dx.doi.org/10.1016/j.tim.2012.10.004
ER  - 



TY  - JOUR
T1  - Holoendemic Malaria Exposure Is Associated with Altered Epstein-Barr Virus-Specific CD8+ T-Cell Differentiation
AN  - 1315611691; 17709708
AB  - Coinfection with Plasmodium falciparum malaria and Epstein-Barr virus (EBV) is a major risk factor for endemic Burkitt lymphoma (eBL), still one of the most prevalent pediatric cancers in equatorial Africa. Although malaria infection has been associated with immunosuppression, the precise mechanisms that contribute to EBV-associated lymphomagenesis remain unclear. In this study, we used polychromatic flow cytometry to characterize CD8+ T-cell subsets specific for EBV-derived lytic (BMFL1 and BRLF1) and latent (LMP1, LMP2, and EBNA3C) antigens in individuals with divergent malaria exposure. No malaria-associated differences in EBV-specific CD8+ T-cell frequencies were observed. However, based on a multidimensional analysis of CD45RO, CD27, CCR7, CD127, CD57, and PD-1 expression, we found that individuals living in regions with intense and perennial (holoendemic) malaria transmission harbored more differentiated EBV-specific CD8+ T-cell populations that contained fewer central memory cells than individuals living in regions with little or no (hypoendemic) malaria. This profile shift was most marked for EBV-specific CD8+ T-cell populations that targeted latent antigens. Importantly, malaria exposure did not skew the phenotypic properties of either cytomegalovirus (CMV)-specific CD8+ T cells or the global CD8+ memory T-cell pool. These observations define a malaria-associated aberration localized to the EBV-specific CD8+ T-cell compartment that illuminates the etiology of eBL.
JF  - Journal of Virology
AU  - Chattopadhyay, Pratip K
AU  - Chelimo, Kiprotich
AU  - Embury, Paula B
AU  - Mulama, David H
AU  - Sumba, Peter Odada
AU  - Gostick, Emma
AU  - Ladell, Kristin
AU  - Brodie, Tess M
AU  - Vulule, John
AU  - Roederer, Mario
AD  - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, AnnM.Moormann,ann.moormann{at}umassmed.edu.
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 1779
EP  - 1788
PB  - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL  - 87
IS  - 3
SN  - 0022-538X, 0022-538X
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Virology & AIDS Abstracts
KW  - Parasites
KW  - Human diseases
KW  - Immunological memory
KW  - Malaria
KW  - Infection
KW  - Cytomegalovirus
KW  - Phenotypes
KW  - Aetiology
KW  - Public health
KW  - Flow cytometry
KW  - Differentiation
KW  - Burkitt's lymphoma
KW  - Epstein-Barr virus
KW  - CC chemokine receptors
KW  - Endemic species
KW  - Antigens
KW  - CD27 antigen
KW  - Risk factors
KW  - Lymphocytes T
KW  - Etiology
KW  - Pediatrics
KW  - Memory cells
KW  - Plasmodium falciparum
KW  - CD8 antigen
KW  - Cancer
KW  - EBNA-3C protein
KW  - PD-1 protein
KW  - CD57 antigen
KW  - Africa
KW  - CCR7 protein
KW  - Immunosuppression
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
KW  - K 03320:Cell Biology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315611691?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Holoendemic+Malaria+Exposure+Is+Associated+with+Altered+Epstein-Barr+Virus-Specific+CD8%2B+T-Cell+Differentiation&rft.au=Chattopadhyay%2C+Pratip+K%3BChelimo%2C+Kiprotich%3BEmbury%2C+Paula+B%3BMulama%2C+David+H%3BSumba%2C+Peter+Odada%3BGostick%2C+Emma%3BLadell%2C+Kristin%3BBrodie%2C+Tess+M%3BVulule%2C+John%3BRoederer%2C+Mario&rft.aulast=Chattopadhyay&rft.aufirst=Pratip&rft.date=2013-02-01&rft.volume=87&rft.issue=3&rft.spage=1779&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.02158-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 54
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Flow cytometry; Parasites; Endemic species; Human diseases; Antigens; Malaria; Phenotypes; Aetiology; Public health; Etiology; Pediatrics; Immunological memory; Memory cells; CD8 antigen; Infection; Cancer; PD-1 protein; Burkitt's lymphoma; EBNA-3C protein; Differentiation; CC chemokine receptors; CD57 antigen; CD27 antigen; Risk factors; Lymphocytes T; CCR7 protein; Immunosuppression; Epstein-Barr virus; Plasmodium falciparum; Cytomegalovirus; Africa
DO  - http://dx.doi.org/10.1128/JVI.02158-12
ER  - 



TY  - JOUR
T1  - Differentiation of Reactive and Tumor Metastatic Lymph Nodes with Diffusion-weighted and SPIO-Enhanced MRI
AN  - 1291614342; 17680881
AB  - Objectives: Determination of lymphatic metastasis is of great importance for both treatment planning and patient prognosis. We aim to distinguish tumor metastatic lymph nodes (TLNs) and reactive lymph nodes (RLNs) with diffusion-weighted and superparamagnetic iron oxide (SPIO)-enhanced magnetic resonance imaging (MRI). Materials and Methods: Ipsilateral popliteal lymph node metastasis or lymphadenitis model was established by hock injection of either luciferase-expressing 4T1 murine breast cancer cells or complete Freund's adjuvant in male BALB/c mice. At different time points after inoculation, bioluminescence imaging and T sub(2)-weighted, diffusion-weighted, and SPIO-enhanced MRI were performed. Imaging findings were confirmed by histopathological staining. Results: Size enlargement was observed in both TLNs and RLNs. At day 28, TLNs showed strong bioluminescence signal and bigger size than RLNs (p<0.01). At early stages up to day 21, both TLNs and RLNs appeared homogeneous on diffusion-weighted imaging. At day 28, TLNs showed heterogeneous apparent diffusion coefficient (ADC) map with significantly higher average ADC value of 0.41 plus or minus 0.0310 super(-3)mm super(2)/s than that of RLNs (0.34 plus or minus 0.0210 super(-3)mm super(2)/s; p<0.05). On SPIO-enhanced MRI, both TLNs and RLNs showed distinct T sub(2) signal reduction at day 21 after inoculation. At day 28, TLNs demonstrated partial uptake of the iron oxide particles, which was confirmed by Prussian blue staining. Conclusions: Both diffusion-weighted and SPIO-enhanced MRI can distinguish tumor metastatic lymph nodes from reactive lymph nodes. However, neither method is able to detect tumor metastasis to the draining lymph nodes at early stages.
JF  - Molecular Imaging and Biology
AU  - Zhang, Fan
AU  - Zhu, Lei
AU  - Huang, Xinglu
AU  - Niu, Gang
AU  - Chen, Xiaoyuan
AD  - Center for Molecular Imaging and Translational Medicine, School of Public Health, Xiamen University, Xiamen, 361000, China, niug@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 40
EP  - 47
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 15
IS  - 1
SN  - 1536-1632, 1536-1632
KW  - Biotechnology and Bioengineering Abstracts
KW  - Animal models
KW  - Lymph nodes
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291614342?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Imaging+and+Biology&rft.atitle=Differentiation+of+Reactive+and+Tumor+Metastatic+Lymph+Nodes+with+Diffusion-weighted+and+SPIO-Enhanced+MRI&rft.au=Zhang%2C+Fan%3BZhu%2C+Lei%3BHuang%2C+Xinglu%3BNiu%2C+Gang%3BChen%2C+Xiaoyuan&rft.aulast=Zhang&rft.aufirst=Fan&rft.date=2013-02-01&rft.volume=15&rft.issue=1&rft.spage=40&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-012-0562-2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Lymph nodes
DO  - http://dx.doi.org/10.1007/s11307-012-0562-2
ER  - 



TY  - JOUR
T1  - A reporter system for replication-competent gammaretroviruses: the inGluc-MLV-DERSE assay
AN  - 1291613096; 17679573
AB  - Although novel retroviral vectors for use in gene-therapy products are reducing the potential for formation of replication-competent retrovirus (RCR), it remains crucial to screen products for RCR for both research and clinical purposes. For clinical-grade gammaretrovirus-based vectors, RCR screening is achieved by an extended S super(+)L super(-) or marker-rescue assay, whereas standard methods for replication-competent lentivirus detection are still in development. In this report, we describe a rapid and sensitive method for replication-competent gammaretrovirus detection. We used this assay to detect three members of the gammaretrovirus family and compared the sensitivity of our assay with well-established methods for retrovirus detection, including the extended S super(+)L super(-) assay. Results presented here demonstrate that this assay should be useful for gene-therapy product testing.
JF  - Gene Therapy
AU  - Aloia, A L
AU  - Duffy, L
AU  - Pak, V
AU  - Lee, K E
AU  - Sanchez-Martinez, S
AU  - Derse, D
AU  - Heidecker, G
AU  - Cornetta, K
AU  - Rein, A
AD  - HIV Drug Resistance Program, National Cancer Institute, Frederick, MD, USA
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 169
EP  - 176
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 20
IS  - 2
SN  - 0969-7128, 0969-7128
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Gene therapy
KW  - Retrovirus
KW  - Lentivirus
KW  - W 30905:Medical Applications
KW  - G 07730:Development & Cell Cycle
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291613096?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+reporter+system+for+replication-competent+gammaretroviruses%3A+the+inGluc-MLV-DERSE+assay&rft.au=Aloia%2C+A+L%3BDuffy%2C+L%3BPak%2C+V%3BLee%2C+K+E%3BSanchez-Martinez%2C+S%3BDerse%2C+D%3BHeidecker%2C+G%3BCornetta%2C+K%3BRein%2C+A&rft.aulast=Aloia&rft.aufirst=A&rft.date=2013-02-01&rft.volume=20&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2012.18
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2013-03-11
N1  - SubjectsTermNotLitGenreText - Retrovirus; Gene therapy; Lentivirus
DO  - http://dx.doi.org/10.1038/gt.2012.18
ER  - 



TY  - JOUR
T1  - Pesticide use and fatal injury among farmers in the Agricultural Health Study
AN  - 1291610988; 17681522
AB  - Purpose: To assess whether pesticide use practices were associated with injury mortality among 51,035 male farmers from NC and IA enrolled in the Agricultural Health Study. Methods: We used Cox proportional hazards models adjusted for age and state to estimate fatal injury risk associated with self-reported use of 49 specific pesticides, personal protective equipment, specific types of farm machinery, and other farm factors collected 1-15 years preceding death. Cause-specific mortality was obtained through linkage to mortality registries. Results: We observed 338 injury fatalities over 727,543 person-years of follow-up (1993-2008). Fatal injuries increased with days/year of pesticide application, with the highest risk among those with 60+ days of pesticide application annually [hazard ratio (HR) = 1.87; 95% confidence interval (CI) = 1.10, 3.18]. Chemical-resistant glove use was associated with decreased risk (HR = 0.73; 95% CI = 0.58, 0.93), but adjusting for glove use did not substantially change estimates for individual pesticides or pesticide use overall. Herbicides were associated with fatal injury, even after adjusting for operating farm equipment, which was independently associated with fatal injury. Ever use of five of 18 herbicides (2,4,5-T, paraquat, alachlor, metribuzin, and butylate) were associated with elevated risk. In addition, 2,4-D and cyanazine were associated with fatal injury in exposure-response analyses. There was no evidence of confounding of these results by other herbicides. Conclusion: The association between application of pesticides, particularly certain herbicides, and fatal injuries among farmers should be interpreted cautiously but deserves further evaluation, with particular focus on understanding timing of pesticide use and fatal injury.
JF  - International Archives of Occupational and Environmental Health
AU  - Waggoner, Jenna K
AU  - Henneberger, Paul K
AU  - Kullman, Greg J
AU  - Umbach, David M
AU  - Kamel, Freya
AU  - Beane Freeman, Laura E
AU  - Alavanja, Michael CR
AU  - Sandler, Dale P
AU  - Hoppin, Jane A
AD  - Division of Respiratory Disease Studies, NIOSH, CDC, DHHS, Morgantown, WV, USA, hoppin1@niehs.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 177
EP  - 187
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 86
IS  - 2
SN  - 0340-0131, 0340-0131
KW  - Pollution Abstracts; Risk Abstracts; Health & Safety Science Abstracts
KW  - Risk assessment
KW  - Mortality
KW  - 2,4,5-T
KW  - Farms
KW  - Injuries
KW  - Alachlor
KW  - Herbicides
KW  - Protective equipment
KW  - Machinery
KW  - Risk factors
KW  - Dose-response effects
KW  - Pesticides
KW  - 2,4-Dichlorophenoxyacetic acid
KW  - Gloves
KW  - R2 23060:Medical and environmental health
KW  - H 1000:Occupational Safety and Health
KW  - P 6000:TOXICOLOGY AND HEALTH
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291610988?accountid=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+Archives+of+Occupational+and+Environmental+Health&rft.atitle=Pesticide+use+and+fatal+injury+among+farmers+in+the+Agricultural+Health+Study&rft.au=Waggoner%2C+Jenna+K%3BHenneberger%2C+Paul+K%3BKullman%2C+Greg+J%3BUmbach%2C+David+M%3BKamel%2C+Freya%3BBeane+Freeman%2C+Laura+E%3BAlavanja%2C+Michael+CR%3BSandler%2C+Dale+P%3BHoppin%2C+Jane+A&rft.aulast=Waggoner&rft.aufirst=Jenna&rft.date=2013-02-01&rft.volume=86&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=International+Archives+of+Occupational+and+Environmental+Health&rft.issn=03400131&rft_id=info:doi/10.1007%2Fs00420-012-0752-x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 30
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Risk assessment; Mortality; 2,4,5-T; Farms; Injuries; Alachlor; Herbicides; Protective equipment; Dose-response effects; Risk factors; Machinery; Pesticides; Gloves; 2,4-Dichlorophenoxyacetic acid
DO  - http://dx.doi.org/10.1007/s00420-012-0752-x
ER  - 



TY  - JOUR
T1  - Metallothionein blocks oxidative DNA damage in vitro
AN  - 1291608268; 17680785
AB  - The role of metallothionein (MT) in mitigation of oxidative DNA damage (ODD) induced by either cadmium (Cd) or the direct oxidant hydrogen peroxide (H sub(2)O sub(2)) was systematically examined using MT-I/II double knockout (MT-null) or MT-competent wild-type (WT) cells. Both toxicants were much more lethal to MT-null cells (Cd LC sub(50) = 6.6 mu M; H sub(2)O sub(2) LC sub(50) = 550 mu M) than to WT cells (Cd LC sub(50) = 16.5 mu M; H sub(2)O sub(2) LC sub(50) = 930 mu M). Cd induced concentration-related MT increases in WT cells, while the basal levels were undetectable and not increased by Cd in MT-null cells. ODD, measured by the immuno-spin trapping method, was minimally induced by sub-toxic Cd levels (1 or 5 mu M; 24 h) in WT cells, but markedly increased in MT-null cells (>430 %). Similarly, ODD was induced to higher levels by lower concentrations of H sub(2)O sub(2) in MT-null cells than WT cells. Transfection of MT-I into MT-null cells reduced both Cd- and H sub(2)O sub(2)-induced cytolethality and ODD. Cd increased the expression of the oxidant defense genes, HO-1, and GSTa2 to a much greater extent in MT-null cells than in WT. Cd or H sub(2)O sub(2) exposure increased the expression of key transport genes, Mrp1 and Mrp2, in WT cells but not in MT-null cells. MT protects against Cd- and H sub(2)O sub(2)-induced ODD in MT-competent cells possibly by multiple mechanisms, potentially including direct metal ion sequestration and sequestration of oxidant radicals by MT. MT-deficient cells appear to adapt to Cd primarily by turning on oxidant response systems, while MT-competent cells activate MT and transport systems.
JF  - Archives of Toxicology
AU  - Qu, Wei
AU  - Pi, Jingbo
AU  - Waalkes, Michael P
AD  - Inorganic Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, PO Box 12233, Mail Drop E1-07, 111 Alexander Drive, Research Triangle Park, NC, 27709, USA, waalkes@niehs.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 311
EP  - 321
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 87
IS  - 2
SN  - 0340-5761, 0340-5761
KW  - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts
KW  - Cadmium
KW  - N:14820
KW  - X:24360
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291608268?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Toxicology&rft.atitle=Metallothionein+blocks+oxidative+DNA+damage+in+vitro&rft.au=Qu%2C+Wei%3BPi%2C+Jingbo%3BWaalkes%2C+Michael+P&rft.aulast=Qu&rft.aufirst=Wei&rft.date=2013-02-01&rft.volume=87&rft.issue=2&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-012-0927-y
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Cadmium
DO  - http://dx.doi.org/10.1007/s00204-012-0927-y
ER  - 



TY  - JOUR
T1  - Three-dimensional multipotent progenitor cell aggregates for expansion, osteogenic differentiation and 'in vivo' tracing with AAV vector serotype 6
AN  - 1291607834; 17679572
AB  - Multipotent adult progenitor cells (MAPCs) are bone marrow-derived stem cells with a high growth rate suitable for therapeutical applications as three-dimensional (3D) aggregates. Combined applications of osteogenically differentiated MAPC (OD-MAPC) aggregates and adeno-associated viral vectors (AAV) in bone bioengineering are still deferred until information with regard to expansion technologies, osteogenic potential, and AAV cytotoxicity and transduction efficiency is better understood. In this study, we tested whether self-complementary AAV (scAAV) can potentially be used as a gene delivery system in an OD-MAPC-based 'in vivo' bone formation model in the craniofacial region. Both expansion of rat MAPC (rMAPC) and osteogenic differentiation with dexamethasone were also tested in 3D aggregate culture systems 'in vitro' and 'vivo'. rMAPCs grew as undifferentiated aggregates for 4 days, with a population doubling time of 37 h. After expansion, constant levels of Oct4 transcripts, and Oct4 and CD31 surface markers were observed, which constitute a hallmark of undifferentiated stage of rMAPCs. Dexamethasone effectively mediated rMAPC osteogenic differentiation by inducing the formation of a mineralized collagen type I network, and facilitated the activation of the wnt/ beta -catenin, a crucial pathway in skeletal development. To investigate the genetic modification of rMAPCs grown as 3D aggregates before implantation, scAAV serotypes 2, 3 and 6 were evaluated. scAAV6 packaged with the enhanced green fluorescent protein expression cassette efficiently mediated long-term transduction (10 days) 'in vitro' and 'vivo'. The reporter transduction event allowed the tracing of OD-rMAPC (induced by dexamethasone) aggregates following OD-rMAPC transfer into a macro-porous hydroxyapatite scaffold implanted in a rat calvaria model. Furthermore, the scAAV6-transduced OD-rMAPCs generated a bone-like matrix with a collagenous matrix rich in bone-specific proteins (osteocalcin and osteopontin) in the scaffold macro-pores 10 days post-implantation. Newly formed bone was also observed in the interface between native bone and scaffold. The collective work supports future bone tissue engineering applications of 3D MAPC cultures for expansion, bone formation and the ability to alter genetically these cells using scAAV vectors.
JF  - Gene Therapy
AU  - Ferreira, J R
AU  - Hirsch, M L
AU  - Zhang, L
AU  - Park, Y
AU  - Samulski, R J
AU  - Hu, W-S
AU  - Ko, C-C
AD  - 1] School of Dentistry, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA [2] Matrix and Morphogenesis Section, National Institute of Dental and Craniofacial Research, Bethesda, MD, USA
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 158
EP  - 168
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 20
IS  - 2
SN  - 0969-7128, 0969-7128
KW  - Virology & AIDS Abstracts; Calcium & Calcified Tissue Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Bone marrow
KW  - Dexamethasone
KW  - Adeno-associated virus
KW  - W 30905:Medical Applications
KW  - T:2050
KW  - G:07730
KW  - V:22320
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291607834?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Three-dimensional+multipotent+progenitor+cell+aggregates+for+expansion%2C+osteogenic+differentiation+and+%27in+vivo%27+tracing+with+AAV+vector+serotype+6&rft.au=Ferreira%2C+J+R%3BHirsch%2C+M+L%3BZhang%2C+L%3BPark%2C+Y%3BSamulski%2C+R+J%3BHu%2C+W-S%3BKo%2C+C-C&rft.aulast=Ferreira&rft.aufirst=J&rft.date=2013-02-01&rft.volume=20&rft.issue=2&rft.spage=158&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2012.16
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Dexamethasone; Adeno-associated virus
DO  - http://dx.doi.org/10.1038/gt.2012.16
ER  - 



TY  - JOUR
T1  - The risky reliance on small surrogate end point studies when planning a large prevention trial
AN  - 1285626610; 4403001
AB  - Summary. The definitive evaluation of treatment to prevent a chronic disease with low incidence in middle age, such as cancer or cardiovascular disease, requires a trial with a large sample size of perhaps 20000 or more. To help to decide whether to implement a large true end point trial, investigators first typically estimate the effect of treatment on a surrogate end point in a trial with a greatly reduced sample size of perhaps 200 subjects. If investigators reject the null hypothesis of no treatment effect in the surrogate end point trial they implicitly assume that they would probably correctly reject the null hypothesis of no treatment effect for the true end point. Surrogate end point trials are generally designed with adequate power to detect an effect of treatment on the surrogate end point. However, we show that a small surrogate end point trial is more likely than a large surrogate end point trial to give a misleading conclusion about the beneficial effect of treatment on the true end point, which can lead to a faulty (and costly) decision about implementing a large true end point prevention trial. If a small surrogate end point trial rejects the null hypothesis of no treatment effect, an intermediate-sized surrogate end point trial could be a useful next step in the decision-making process for launching a large true end point prevention trial. Reprinted by permission of Blackwell Publishers
JF  - Journal of the Royal Statistical Society
AU  - Kramer, Barnett S
AU  - Baker, Stuart G
AD  - US National Institutes of Health
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 603
EP  - 608
VL  - 176
IS  - 2
SN  - 0964-1998, 0964-1998
KW  - Economics
KW  - Decision making
KW  - Prevention
KW  - Medical treatment
KW  - Diseases
KW  - Heart disease
KW  - Cancer
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285626610?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=The+risky+reliance+on+small+surrogate+end+point+studies+when+planning+a+large+prevention+trial&rft.au=Kramer%2C+Barnett+S%3BBaker%2C+Stuart+G&rft.aulast=Kramer&rft.aufirst=Barnett&rft.date=2013-02-01&rft.volume=176&rft.issue=2&rft.spage=603&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=09641998&rft_id=info:doi/10.1111%2Fj.1467-985X.2012.01052.x
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 3617 6220; 10072; 1939 3617 6220; 5796 3617 6220; 7890 5792 10484; 3322 6071 1542 11325
DO  - http://dx.doi.org/10.1111/j.1467-985X.2012.01052.x
ER  - 



TY  - JOUR
T1  - Detection of anti-tat antibodies in CSF of individuals with HIV-associated neurocognitive disorders.
AN  - 1285461527; 23329164
AB  - Despite major advances in the development of antiretroviral therapies, currently available treatments have no effect on the production of HIV-Tat protein once the proviral DNA is formed. Tat is a highly neurotoxic and neuroinflammatory protein, but its effects may be modulated by antibody responses against it. We developed an indirect enzyme-linked immunosorbent assay and measured anti-Tat antibody titers in CSF of a well characterized cohort of 52 HIV-infected and 13 control individuals. We successfully measured anti-Tat antibodies in CSF of HIV-infected individuals with excellent sensitivity and specificity, spanning a broad range of detection from 10,000 to over 100,000 relative light units. We analyzed them for relationship to cognitive function, CD4 cell counts, and HIV viral load. Anti-Tat antibody levels were higher in those without neurocognitive dysfunction than in those with HIV-associated neurocognitive dysfunction (HAND) and in individuals with lower CD4 cell counts and higher viral loads. We provide details of an assay which may have diagnostic, prognostic, or therapeutic implications for patients with HAND. Active viral replication may be needed to drive the immune response against Tat protein, but this robust immune response against the protein may be neuroprotective.
JF  - Journal of neurovirology
AU  - Bachani, M
AU  - Sacktor, N
AU  - McArthur, J C
AU  - Nath, A
AU  - Rumbaugh, J
AD  - Section of Infections of the Nervous System, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 82
EP  - 88
VL  - 19
IS  - 1
KW  - HIV Antibodies
KW  - 0
KW  - tat Gene Products, Human Immunodeficiency Virus
KW  - Index Medicus
KW  - Sensitivity and Specificity
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - Male
KW  - Female
KW  - Enzyme-Linked Immunosorbent Assay -- methods
KW  - AIDS Dementia Complex -- cerebrospinal fluid
KW  - AIDS Dementia Complex -- immunology
KW  - HIV Antibodies -- cerebrospinal fluid
KW  - tat Gene Products, Human Immunodeficiency Virus -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285461527?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neurovirology&rft.atitle=Detection+of+anti-tat+antibodies+in+CSF+of+individuals+with+HIV-associated+neurocognitive+disorders.&rft.au=Bachani%2C+M%3BSacktor%2C+N%3BMcArthur%2C+J+C%3BNath%2C+A%3BRumbaugh%2C+J&rft.aulast=Bachani&rft.aufirst=M&rft.date=2013-02-01&rft.volume=19&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurovirology&rft.issn=1538-2443&rft_id=info:doi/10.1007%2Fs13365-012-0144-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-09
N1  - Date created - 2013-02-08
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Neurovirol. 2000 Apr;6(2):145-55 [10822328]
Neurobiol Dis. 2013 Jan;49:169-76 [22940423]
J Neurochem. 2001 Aug;78(3):457-67 [11483648]
Ann Neurol. 2001 Aug;50(2):157-62 [11506397]
J Neurovirol. 2002 Apr;8(2):136-42 [11935465]
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13795-800 [12374865]
J Acquir Immune Defic Syndr. 2002 Oct 1;31(2):171-7 [12394795]
Brain Res. 2002 Nov 8;954(2):300-7 [12414113]
J Infect Dis. 2002 Dec 1;186 Suppl 2:S199-208 [12424698]
J Neurovirol. 2002 Dec;8 Suppl 2:115-21 [12491162]
BMC Neurosci. 2001;2:3 [11252157]
Neurology. 2003 May 13;60(9):1508-14 [12743240]
AIDS. 2003 Jul 4;17(10):1539-45 [12824792]
Brain Res. 2004 Jan 2;995(1):39-45 [14644469]
Neurology. 1988 Jan;38(1):9-14 [3422110]
Neurology. 1992 Sep;42(9):1736-9 [1513462]
J Virol. 1994 Jan;68(1):93-102 [8254781]
Neurology. 1994 Mar;44(3 Pt 1):481-7 [8145919]
Nature. 1995 Jun 8;375(6531):497-500 [7539892]
J Acquir Immune Defic Syndr Hum Retrovirol. 1996 May 1;12(1):19-25 [8624756]
AIDS. 1996 Jul;10(8):843-7 [8828741]
J Virol. 1997 Mar;71(3):2495-9 [9032389]
Am J Pathol. 1999 Jul;155(1):39-46 [10393834]
Arch Neurol. 2004 Nov;61(11):1687-96 [15534180]
Curr Pharm Des. 2006;12(9):1023-44 [16515484]
Neurology. 2001 Jan 23;56(2):257-60 [11160967]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/s13365-012-0144-8
ER  - 



TY  - JOUR
T1  - Nanofiber scaffold gradients for interfacial tissue engineering*
AN  - 1285093545; 17593992
AB  - We have designed a 2-spinnerette device that can directly electrospin nanofiber scaffolds containing a gradient in composition that can be used to engineer interfacial tissues such as ligament and tendon. Two types of nanofibers are simultaneously electrospun in an overlapping pattern to create a nonwoven mat of nanofibers containing a composition gradient. The approach is an advance over previous methods due to its versatility - gradients can be formed from any materials that can be electrospun. A dye was used to characterize the 2-spinnerette approach and applicability to tissue engineering was demonstrated by fabricating nanofibers with gradients in amorphous calcium phosphate nanoparticles (nACP). Adhesion and proliferation of osteogenic cells (MC3T3-E1 murine pre-osteoblasts) on gradients was enhanced on the regions of the gradients that contained higher nACP content yielding a graded osteoblast response. Since increases in soluble calcium and phosphate ions stimulate osteoblast function, we measured their release and observed significant release from nanofibers containing nACP. The nanofiber-nACP gradients fabricated herein can be applied to generate tissues with osteoblast gradients such as ligaments or tendons. In conclusion, these results introduce a versatile approach for fabricating nanofiber gradients that can have application for engineering graded tissues.
JF  - Journal of Biomaterials Applications
AU  - Ramalingam, Murugan
AU  - Young, Marian F
AU  - Thomas, Vinoy
AU  - Sun, Limin
AU  - Chow, Laurence C
AU  - Tison, Christopher K
AU  - Chatterjee, Kaushik
AU  - Miles, William C
AU  - Simon, Carl G
AD  - Polymers Division, National Institute of Standards and Technology, 100 Bureau Drive, Gaithersburg, MD 20899, USA, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA, National Institute of Health and Medical Research, Faculty of Medicine, University of Strasbourg, 67085 Strasbourg Cedex, France, carl.simon@nist.gov
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 695
EP  - 705
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 27
IS  - 6
SN  - 0885-3282, 0885-3282
KW  - Biotechnology and Bioengineering Abstracts
KW  - Nanofibers
KW  - scaffolds
KW  - calcium phosphate
KW  - gradient
KW  - osteoblast
KW  - Osteoblasts
KW  - Ions
KW  - Ligaments
KW  - Phosphate
KW  - Tissue engineering
KW  - Cell proliferation
KW  - nanoparticles
KW  - Calcium phosphate
KW  - Tendons
KW  - W 30920:Tissue Engineering
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285093545?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Biomaterials+Applications&rft.atitle=Nanofiber+scaffold+gradients+for+interfacial+tissue+engineering*&rft.au=Ramalingam%2C+Murugan%3BYoung%2C+Marian+F%3BThomas%2C+Vinoy%3BSun%2C+Limin%3BChow%2C+Laurence+C%3BTison%2C+Christopher+K%3BChatterjee%2C+Kaushik%3BMiles%2C+William+C%3BSimon%2C+Carl+G&rft.aulast=Ramalingam&rft.aufirst=Murugan&rft.date=2013-02-01&rft.volume=27&rft.issue=6&rft.spage=695&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomaterials+Applications&rft.issn=08853282&rft_id=info:doi/10.1177%2F0885328211423783
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 48
N1  - Last updated - 2015-05-27
N1  - SubjectsTermNotLitGenreText - Ions; Osteoblasts; Ligaments; Phosphate; Cell proliferation; Tissue engineering; nanoparticles; scaffolds; Tendons; Calcium phosphate
DO  - http://dx.doi.org/10.1177/0885328211423783
ER  - 



TY  - JOUR
T1  - Delayed-Type Hypersensitivity to Sand Fly Saliva in Humans from a Leishmaniasis-Endemic Area of Mali Is T sub(H)1-Mediated and Persists to Midlife
AN  - 1285091114; 17565854
AB  - Immunity to sand fly saliva in rodents induces a T sub(H)1 delayed-type hypersensitivity (DTH) response conferring protection against leishmaniasis. The relevance of DTH to sand fly bites in humans living in a leishmaniasis-endemic area remains unknown. Here, we describe the duration and nature of DTH to sand fly saliva in humans from an endemic area of Mali. DTH was assessed at 24, 48, 72, and 96 hours post bite in volunteers exposed to colony-bred sand flies. Dermal biopsies were obtained 48 hours post bite; cytokines were quantified from peripheral blood mononuclear cells (PBMCs) stimulated with sand fly saliva in vitro. A DTH response to bites was observed in 75% of individuals aged 1-15 years, decreasing gradually to 48% by age 45, and dropping to 21% thereafter. Dermal biopsies were dominated by T lymphocytes and macrophages. Abundant expression of IFN- gamma and absence of T sub(H)2 cytokines establishes the T sub(H)1 nature of this DTH response. PBMCs from 98% of individuals responded to sand fly saliva. Of these, 23% were polarized to a T sub(H)1 and 25% to a T sub(H)2 response. We demonstrate the durability and T sub(H)1 nature of DTH to sand fly bites in humans living in a cutaneous leishmaniasis-endemic area. A systemic T sub(H)2 response may explain why some individuals remain susceptible to disease.
JF  - Journal of Investigative Dermatology
AU  - Oliveira, Fabiano
AU  - Traore, Bourama
AU  - Gomes, Regis
AU  - Faye, Ousmane
AU  - Gilmore, Dana C
AU  - Keita, Somita
AU  - Traore, Pierre
AU  - Teixeira, Clarissa
AU  - Coulibaly, Cheick A
AU  - Samake, Sibiry
AU  - Meneses, Claudio
AU  - Sissoko, Ibrahim
AU  - Fairhurst, Rick M
AU  - Fay, Michael P
AU  - Anderson, Jennifer M
AU  - Doumbia, Seydou
AU  - Kamhawi, Shaden
AU  - Valenzuela, Jesus G
AD  - Vector Molecular Biology Section, Laboratory of Malaria and Vector Research (LMVR), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Rockville, Maryland, USA
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 452
EP  - 459
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 133
IS  - 2
SN  - 0022-202X, 0022-202X
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts
KW  - Leishmaniasis
KW  - Macrophages
KW  - gamma -Interferon
KW  - Age
KW  - Mali
KW  - Skin
KW  - Bites
KW  - Helper cells
KW  - Biopsy
KW  - Immunity
KW  - Lymphocytes
KW  - Public health
KW  - Peripheral blood mononuclear cells
KW  - Endemic species
KW  - Hypersensitivity (delayed)
KW  - Lymphocytes T
KW  - Toughness
KW  - Cytokines
KW  - Saliva
KW  - F 06925:Hypersensitivity
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285091114?accountid=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+Investigative+Dermatology&rft.atitle=Delayed-Type+Hypersensitivity+to+Sand+Fly+Saliva+in+Humans+from+a+Leishmaniasis-Endemic+Area+of+Mali+Is+T+sub%28H%291-Mediated+and+Persists+to+Midlife&rft.au=Oliveira%2C+Fabiano%3BTraore%2C+Bourama%3BGomes%2C+Regis%3BFaye%2C+Ousmane%3BGilmore%2C+Dana+C%3BKeita%2C+Somita%3BTraore%2C+Pierre%3BTeixeira%2C+Clarissa%3BCoulibaly%2C+Cheick+A%3BSamake%2C+Sibiry%3BMeneses%2C+Claudio%3BSissoko%2C+Ibrahim%3BFairhurst%2C+Rick+M%3BFay%2C+Michael+P%3BAnderson%2C+Jennifer+M%3BDoumbia%2C+Seydou%3BKamhawi%2C+Shaden%3BValenzuela%2C+Jesus+G&rft.aulast=Oliveira&rft.aufirst=Fabiano&rft.date=2013-02-01&rft.volume=133&rft.issue=2&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=Journal+of+Investigative+Dermatology&rft.issn=0022202X&rft_id=info:doi/10.1038%2Fjid.2012.315
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Macrophages; Endemic species; Toughness; Lymphocytes; Immunity; Public health; Leishmaniasis; gamma -Interferon; Age; Skin; Bites; Helper cells; Biopsy; Peripheral blood mononuclear cells; Hypersensitivity (delayed); Lymphocytes T; Cytokines; Saliva; Mali
DO  - http://dx.doi.org/10.1038/jid.2012.315
ER  - 



TY  - JOUR
T1  - DNA polymerase minor groove interactions modulate mutagenic bypass of a templating 8-oxoguanine lesion.
AN  - 1284287485; 23267011
AB  - A major base lesion resulting from oxidative stress is 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxoG) that has ambiguous coding potential. Error-free DNA synthesis involves 8-oxoG adopting an anti-conformation to base pair with cytosine whereas mutagenic bypass involves 8-oxoG adopting a syn-conformation to base pair with adenine. Left unrepaired the syn-8-oxoG/dAMP base pair results in a G-C to T-A transversion. During base excision repair of this mispair, DNA polymerase (pol) β is confronted with gap filling opposite 8-oxoG. To determine how pol β discriminates between anti- and syn-8-oxoG, we introduced a point mutation (R283K) to alter insertion specificity. Kinetic studies demonstrate that this substitution results in an increased fidelity opposite 8-oxoG. Structural studies with R283K pol β show that the binary DNA complex has 8-oxoG in equilibrium between anti- and syn-forms. Ternary complexes with incoming dCTP resemble the wild-type enzyme, with templating anti-8-oxoG base pairing with incoming cytosine. In contrast to wild-type pol β, the ternary complex of the R283K mutant with an incoming dATP-analogue and templating 8-oxoG resembles a G-A mismatched structure with 8-oxoG adopting an anti-conformation. These results demonstrate that the incoming nucleotide is unable to induce a syn-8-oxoG conformation without minor groove DNA polymerase interactions that influence templating (anti-/syn-equilibrium) of 8-oxoG while modulating fidelity.
JF  - Nucleic acids research
AU  - Freudenthal, Bret D
AU  - Beard, William A
AU  - Wilson, Samuel H
AD  - Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, PO Box 12233, Research Triangle Park, NC 27709-2233, USA.
Y1  - 2013/02/01/
PY  - 2013
DA  - 2013 Feb 01
SP  - 1848
EP  - 1858
VL  - 41
IS  - 3
KW  - 8-hydroxyguanine
KW  - 5614-64-2
KW  - Guanine
KW  - 5Z93L87A1R
KW  - DNA
KW  - 9007-49-2
KW  - DNA Polymerase beta
KW  - EC 2.7.7.-
KW  - Index Medicus
KW  - Models, Molecular
KW  - DNA Damage
KW  - Humans
KW  - Templates, Genetic
KW  - Nucleic Acid Conformation
KW  - Amino Acid Substitution
KW  - DNA Polymerase beta -- genetics
KW  - Guanine -- chemistry
KW  - DNA Polymerase beta -- chemistry
KW  - DNA -- chemistry
KW  - Guanine -- analogs & derivatives
KW  - DNA Polymerase beta -- metabolism
KW  - Mutagenesis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1284287485?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+polymerase+minor+groove+interactions+modulate+mutagenic+bypass+of+a+templating+8-oxoguanine+lesion.&rft.au=Freudenthal%2C+Bret+D%3BBeard%2C+William+A%3BWilson%2C+Samuel+H&rft.aulast=Freudenthal&rft.aufirst=Bret&rft.date=2013-02-01&rft.volume=41&rft.issue=3&rft.spage=1848&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgks1276
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-17
N1  - Date created - 2013-02-04
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Chem Rev. 2006 Feb;106(2):361-82 [16464010]
J Biol Chem. 2006 Jan 27;281(4):2358-72 [16306039]
Structure. 2006 Apr;14(4):757-66 [16615916]
J Mol Biol. 2007 Apr 13;367(5):1258-69 [17321545]
Biophys J. 2007 May 1;92(9):3063-70 [17293403]
J Biol Chem. 2007 Jul 6;282(27):19831-43 [17468100]
Mol Cell. 2008 May 9;30(3):315-24 [18471977]
PLoS One. 2009;4(6):e5766 [19492058]
J Biol Chem. 2009 Aug 14;284(33):22467-80 [19542228]
J Biol Chem. 2009 Nov 13;284(46):31680-9 [19759017]
Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702]
Biochemistry. 2010 Mar 23;49(11):2317-25 [20166748]
Biochemistry. 2010 May 18;49(19):4116-25 [20411947]
Nat Struct Mol Biol. 2010 Jul;17(7):889-90 [20526335]
J Biol Chem. 2010 Aug 6;285(32):24457-65 [20519499]
Structure. 2010 Nov 10;18(11):1463-70 [21070945]
Mutat Res. 2010 Nov 28;703(1):18-23 [20696268]
Proc Natl Acad Sci U S A. 2011 Feb 22;108(8):3210-5 [21300901]
J Biol Chem. 2011 Jun 3;286(22):19758-67 [21454515]
Proc Natl Acad Sci U S A. 2012 Jan 3;109(1):113-8 [22178760]
Nucleic Acids Res. 2012 Apr;40(7):2974-83 [22169953]
Structure. 2012 Nov 7;20(11):1829-37 [22959623]
Biochemistry. 2000 Feb 8;39(5):1029-33 [10653647]
Nat Genet. 2000 Aug;25(4):458-61 [10932195]
J Biol Chem. 2001 Feb 9;276(6):3764-71 [11110788]
J Biol Chem. 2002 Dec 6;277(49):47393-8 [12370169]
Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16000-5 [12444249]
Structure. 2003 Jan;11(1):121-7 [12517346]
Mol Cell Biol. 2003 Feb;23(4):1453-9 [12556503]
EMBO J. 2004 Apr 7;23(7):1494-505 [15057282]
J Biol Chem. 2004 Jul 23;279(30):31921-9 [15145936]
EMBO J. 2004 Sep 1;23(17):3452-61 [15297882]
Nature. 2004 Sep 9;431(7005):217-21 [15322558]
J Am Chem Soc. 1977 May 11;99(10):3250-3 [853179]
Biochemistry. 1991 Feb 5;30(5):1403-12 [1991121]
Nature. 1991 Jan 31;349(6308):431-4 [1992344]
Nucleic Acids Res. 1991 Apr 11;19(7):1407-12 [2027747]
Mutat Res. 1991 Sep-Oct;250(1-2):3-16 [1944345]
Chem Res Toxicol. 1989 Nov-Dec;2(6):416-22 [2519731]
Trends Genet. 1993 Jul;9(7):246-9 [8379000]
Biochemistry. 1994 Aug 30;33(34):10266-70 [8068665]
Proc Natl Acad Sci U S A. 1995 Jan 31;92(3):719-23 [7846041]
Methods Enzymol. 1995;262:98-107 [8594388]
Biochemistry. 1997 May 27;36(21):6475-87 [9174365]
Biochemistry. 1997 Sep 16;36(37):11205-15 [9287163]
Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765]
Mol Cell Biol. 2005 Mar;25(6):2169-76 [15743815]
Structure. 2005 Nov;13(11):1653-9 [16271888]
PLoS Biol. 2006 Jan;4(1):e11 [16379496]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/nar/gks1276
ER  - 



TY  - JOUR
T1  - Sorafenib for the treatment of unresectable hepatocellular carcinoma in HIV-positive patients.
AN  - 1282838135; 23197082
AB  - Few data are available on the safety and efficacy of sorafenib in HIV-infected patients with unresectable hepatocellular carcinoma (HIV-u-HCC) and concomitant highly active antiretroviral therapy (HAART). Between July 2007 and October 2010, 27 consecutive HIV-u-HCC patients were treated with sorafenib and concomitant HAART within the Gruppo Italiano Cooperativo AIDS e Tumori (GICAT). Three patients achieved a partial response, 12 achieved a stable disease, and 12 showed progression. The median time to progression and overall survival was 5.1 (range 0.5-13.3) and 12.8 (range 1.1-23.5) months, respectively. Grades 3-4 toxicities included diarrhea (four patients, 14.8%), hypertension (three patients, 11%), and hand-and-foot skin reaction (four patients, 14.9%). Most drug-related side effects were low grade and manageable. This retrospective study shows favorable survival data among HIV-u-HCC patients treated with sorafenib together with a reasonable safety profile.
JF  - Anti-cancer drugs
AU  - Berretta, Massimiliano
AU  - Di Benedetto, Fabrizio
AU  - Dal Maso, Luigino
AU  - Cacopardo, Bruno
AU  - Nasti, Guglielmo
AU  - Facchini, Gaetano
AU  - Bearz, Alessandra
AU  - Spina, Michele
AU  - Garlassi, Elisa
AU  - De Re, Valli
AU  - Fiorica, Francesco
AU  - Lleshi, Arben
AU  - Tirelli, Umberto
AD  - Department of Medical Oncology, National Cancer Institute--IRCCS, Aviano (PN), Italy. mberretta@cro.it
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 212
EP  - 218
VL  - 24
IS  - 2
KW  - Antineoplastic Agents
KW  - 0
KW  - Phenylurea Compounds
KW  - Niacinamide
KW  - 25X51I8RD4
KW  - sorafenib
KW  - 9ZOQ3TZI87
KW  - Index Medicus
KW  - Humans
KW  - Adult
KW  - Treatment Outcome
KW  - Retrospective Studies
KW  - Disease Progression
KW  - Aged
KW  - Middle Aged
KW  - Antiretroviral Therapy, Highly Active -- methods
KW  - Male
KW  - Female
KW  - Carcinoma, Hepatocellular -- virology
KW  - Liver Neoplasms -- virology
KW  - Niacinamide -- analogs & derivatives
KW  - Antineoplastic Agents -- adverse effects
KW  - HIV Infections -- complications
KW  - Niacinamide -- therapeutic use
KW  - Carcinoma, Hepatocellular -- drug therapy
KW  - Liver Neoplasms -- drug therapy
KW  - HIV Infections -- drug therapy
KW  - Niacinamide -- adverse effects
KW  - Phenylurea Compounds -- therapeutic use
KW  - Phenylurea Compounds -- adverse effects
KW  - Antineoplastic Agents -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282838135?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+drugs&rft.atitle=Sorafenib+for+the+treatment+of+unresectable+hepatocellular+carcinoma+in+HIV-positive+patients.&rft.au=Berretta%2C+Massimiliano%3BDi+Benedetto%2C+Fabrizio%3BDal+Maso%2C+Luigino%3BCacopardo%2C+Bruno%3BNasti%2C+Guglielmo%3BFacchini%2C+Gaetano%3BBearz%2C+Alessandra%3BSpina%2C+Michele%3BGarlassi%2C+Elisa%3BDe+Re%2C+Valli%3BFiorica%2C+Francesco%3BLleshi%2C+Arben%3BTirelli%2C+Umberto&rft.aulast=Berretta&rft.aufirst=Massimiliano&rft.date=2013-02-01&rft.volume=24&rft.issue=2&rft.spage=212&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+drugs&rft.issn=1473-5741&rft_id=info:doi/10.1097%2FCAD.0b013e32835c032f
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-05-23
N1  - Date created - 2012-12-14
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1097/CAD.0b013e32835c032f
ER  - 



TY  - JOUR
T1  - The hidden side of drug action: brain temperature changes induced by neuroactive drugs.
AN  - 1282835410; 23274506
AB  - Most neuroactive drugs affect brain metabolism as well as systemic and cerebral blood flow, thus altering brain temperature. Although this aspect of drug action usually remains in the shadows, drug-induced alterations in brain temperature reflect their metabolic neural effects and affect neural activity and neural functions.
          Here, I review brain temperature changes induced by neuroactive drugs, which are used therapeutically (general anesthetics), as a research tool (dopamine agonists and antagonists), and self-administered to induce desired psychic effects (cocaine, methamphetamine, ecstasy). I consider the mechanisms underlying these temperature fluctuations and their influence on neural, physiological, and behavioral effects of these drugs. By interacting with neural mechanisms regulating metabolic activity and heat exchange between the brain and the rest of the body, neuroactive drugs either increase or decrease brain temperatures both within (35-39 °C) and exceeding the range of physiological fluctuations. These temperature effects differ drastically depending upon the environmental conditions and activity state during drug administration. This state-dependence is especially important for drugs of abuse that are usually taken by humans during psycho-physiological activation and in environments that prevent proper heat dissipation from the brain. Under these conditions, amphetamine-like stimulants induce pathological brain hyperthermia (>40 °C) associated with leakage of the blood-brain barrier and structural abnormalities of brain cells.
          The knowledge on brain temperature fluctuations induced by neuroactive drugs provides new information to understand how they influence metabolic neural activity, why their effects depend upon the behavioral context of administration, and the mechanisms underlying adverse drug effects including neurotoxicity.
JF  - Psychopharmacology
AU  - Kiyatkin, Eugene A
AD  - In-Vivo Electrophysiology Unit, Behavioral Neuroscience Branch, National Institute on Drug Abuse-Intramural Research Program, National Institutes of Health, DHHS, 333 Cassell Drive, Baltimore, MD 21224, USA. ekiyatki@intra.nida.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 765
EP  - 780
VL  - 225
IS  - 4
KW  - Anesthetics, General
KW  - 0
KW  - Central Nervous System Stimulants
KW  - Dopamine Agents
KW  - Street Drugs
KW  - Index Medicus
KW  - Blood-Brain Barrier -- drug effects
KW  - Animals
KW  - Humans
KW  - Dopamine Agents -- pharmacology
KW  - Blood-Brain Barrier -- physiology
KW  - Central Nervous System Stimulants -- pharmacology
KW  - Street Drugs -- pharmacology
KW  - Body Temperature -- drug effects
KW  - Brain -- drug effects
KW  - Anesthetics, General -- pharmacology
KW  - Body Temperature -- physiology
KW  - Brain -- physiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282835410?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=The+hidden+side+of+drug+action%3A+brain+temperature+changes+induced+by+neuroactive+drugs.&rft.au=Kiyatkin%2C+Eugene+A&rft.aulast=Kiyatkin&rft.aufirst=Eugene&rft.date=2013-02-01&rft.volume=225&rft.issue=4&rft.spage=765&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=1432-2072&rft_id=info:doi/10.1007%2Fs00213-012-2957-9
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-10-17
N1  - Date created - 2013-01-29
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Clin Invest. 1962 Aug;41:1664-71 [14486452]
Jpn J Pharmacol. 1963 Dec;13:230-9 [14097554]
Curr Opin Pharmacol. 2005 Feb;5(1):34-41 [15661623]
Physiol Behav. 2005 Mar 31;84(4):563-70 [15811391]
Am J Physiol Regul Integr Comp Physiol. 2005 Jun;288(6):R1689-94 [15650123]
Eur J Neurosci. 2005 Aug;22(4):930-8 [16115216]
Ann N Y Acad Sci. 2000 Sep;914:92-103 [11085312]
Psychopharmacology (Berl). 2005 Dec;183(2):248-56 [16163516]
Brain Res Brain Res Rev. 2005 Dec 1;50(1):27-56 [15890410]
Drug Alcohol Depend. 2006 May 20;82(3):276-81 [16289931]
Neuroreport. 2006 Jul 17;17(10):1071-5 [16791106]
AAPS J. 2006;8(2):E413-8 [16808044]
Anesthesiology. 2008 Aug;109(2):318-38 [18648241]
Pharmacol Biochem Behav. 2008 Dec;91(2):233-42 [18727935]
Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1415-24 [18799633]
J Chem Neuroanat. 2009 Jan;37(1):18-32 [18773954]
Front Biosci (Landmark Ed). 2010;15:73-92 [20036808]
Front Biosci (Schol Ed). 2010;2:1145-54 [20515846]
J Neurosci. 1999 Dec 1;19(23):10417-27 [10575039]
Neurol Neurochir Pol. 1999 Nov-Dec;33(6):1325-37 [10791035]
Neurol Neurochir Pol. 2000 May-Jun;34(3):509-22 [10979544]
Trends Neurosci. 2000 Oct;23(10 Suppl):S57-63 [11052221]
Eur J Pharmacol. 2000 Dec 15;409(3):265-71 [11108820]
Brain Res. 2001 Jan 5;888(1):117-127 [11146058]
Brain Res. 2001 Jun 29;905(1-2):21-5 [11423075]
Brain Res Brain Res Rev. 2001 Aug;36(1):1-22 [11516769]
CMAJ. 2001 Oct 2;165(7):917-28 [11599334]
J Neurosci. 2001 Nov 1;21(21):8648-54 [11606652]
Br J Pharmacol. 2002 Jan;135(1):170-80 [11786492]
Neuroreport. 2012 Feb 15;23(3):129-33 [22186803]
J Intensive Care Med. 2013 Jul-Aug;28(4):252-8 [22640978]
Life Sci. 1985 May 20;36(20):1983-94 [3990520]
Zh Nevropatol Psikhiatr Im S S Korsakova. 1985;85(7):1016-20 [4041105]
J Neurol Sci. 1986 Jan;72(1):61-76 [2936871]
Alcohol Drug Res. 1987;7(3):123-34 [2881551]
Psychol Rev. 1987 Oct;94(4):469-92 [3317472]
Brain Res. 1989 May 1;486(1):73-8 [2720435]
Neuropharmacology. 1989 Oct;28(10):1145-50 [2554183]
Br J Neurosurg. 1990;4(1):31-8 [2334525]
Physiol Behav. 1990 May;47(5):963-91 [2201986]
Physiol Rev. 1991 Jan;71(1):155-234 [1986388]
Pharmacol Biochem Behav. 1991 Feb;38(2):339-44 [1676171]
Trends Neurosci. 1991 Jul;14(7):299-302 [1719677]
Neuroscience. 1992 Jun;48(4):889-901 [1630627]
Naunyn Schmiedebergs Arch Pharmacol. 1992 Nov;346(5):504-10 [1470222]
Pharmacol Biochem Behav. 1993 Jan;44(1):87-98 [8094252]
Anaesthesia. 1993 Oct;48(10):892-5 [7902026]
Arch Int Pharmacodyn Ther. 1993 Jul-Aug;324:17-32 [7905255]
Pain. 2006 Sep;124(1-2):211-21 [16806707]
Mol Neurobiol. 2006 Aug;34(1):1-26 [17003519]
Ann N Y Acad Sci. 2006 Aug;1074:198-224 [17105918]
Neuropsychopharmacology. 2007 Mar;32(3):673-81 [16641942]
Neuroscience. 2007 Mar 2;145(1):335-43 [17196751]
Neurotox Res. 2007 Apr;11(3-4):183-202 [17449459]
Prog Brain Res. 2007;162:63-79 [17645915]
Eur J Neurosci. 2007 Sep;26(5):1242-53 [17767502]
Drug Metab Dispos. 2007 Oct;35(10):1840-5 [17640955]
Exp Neurol. 1973 Mar;38(3):502-19 [4633121]
Neuron. 2008 Jan 24;57(2):178-201 [18215617]
J Appl Physiol (1985). 2008 Mar;104(3):871-8 [17962572]
J Pharmacol Exp Ther. 1994 Aug;270(2):752-60 [8071868]
Synapse. 1994 Jul;17(3):203-9 [7974204]
Brain Res. 1994 Sep 26;658(1-2):33-8 [7530580]
J Pharmacol Exp Ther. 1995 Feb;272(2):868-75 [7853205]
Pharmacol Ther. 1994;64(2):291-370 [7878079]
Brain Res. 1995 Jan 30;670(2):205-14 [7743187]
J Pharmacol Exp Ther. 1995 Dec;275(3):1104-14 [8531070]
Physiol Behav. 1995 Nov;58(5):877-82 [8577883]
NIDA Res Monogr. 1996;163:251-76 [8809863]
Neurology. 1997 Mar;48(3):762-7 [9065562]
Hum Cell. 1996 Dec;9(4):353-66 [9183669]
Crit Care Med. 1998 Mar;26(3):562-7 [9504587]
J Neurosci. 2002 Feb 1;22(3):1072-80 [11826136]
J Appl Physiol (1985). 2002 Jun;92(6):2667-79 [12015388]
Behav Brain Res. 2002 Dec 2;137(1-2):27-46 [12445714]
J Physiol. 2002 Dec 1;545(Pt 2):697-704 [12456844]
Di Yi Jun Yi Da Xue Xue Bao. 2003 Jan;23(1):21-4 [12527507]
Neuroscience. 2003;116(2):525-38 [12559108]
Environ Res. 2003 May;92(1):48-53 [12706754]
J Neurosci. 2003 May 1;23(9):3924-9 [12736362]
Brain Res. 2003 Jun 6;974(1-2):127-33 [12742630]
Int J Hyperthermia. 2003 May-Jun;19(3):252-66 [12745971]
Int J Hyperthermia. 2003 May-Jun;19(3):325-54 [12745974]
Neurosci Biobehav Rev. 2003 May;27(3):199-217 [12788333]
Spinal Cord. 2003 Jul;41(7):369-78 [12815368]
Neurobiol Aging. 2003 May-Jun;24 Suppl 1:S123-7; discussion S131 [12829120]
Neuroscience. 2003;119(4):1169-83 [12831871]
Pharmacol Rev. 2003 Sep;55(3):463-508 [12869661]
Neuroscience. 2003;121(4):991-8 [14580949]
Neuroreport. 2003 Dec 19;14(18):2429-32 [14663205]
Brain Res. 2004 Apr 16;1005(1-2):101-16 [15044070]
Eur J Neurosci. 2004 Jul;20(1):51-8 [15245478]
Am J Physiol. 1966 Sep;211(3):755-69 [5927906]
J Pharmacol Exp Ther. 1968 May;161(1):122-9 [5648489]
Am J Physiol. 1968 Aug;215(2):389-403 [4969787]
Farmakol Toksikol. 1968 Sep-Oct;31(5):563-7 [5707725]
J Pharm Pharmacol. 1972 Sep;24(9):702-5 [4404073]
Can Med Assoc J. 1975 Feb 8;112(3):299-304 [1089034]
Br J Pharmacol. 1975 May;54(1):123-4 [1139073]
Stroke. 1978 Jan-Feb;9(1):12-8 [622738]
Can J Physiol Pharmacol. 1979 May;57(5):469-75 [466574]
Brain Res. 1980 Jul 7;193(1):153-63 [7378814]
J Physiol. 1980 Mar;300:7-17 [7381796]
Am J Physiol. 1982 May;242(5):R471-81 [7081473]
Circ Res. 1983 Apr;52(4):367-79 [6339107]
Am J Physiol. 1983 Aug;245(2):R293-7 [6881387]
J Neurosci. 1985 Feb;5(2):297-306 [2857776]
Prog Brain Res. 1998;115:241-74 [9632939]
Acta Neurochir (Wien). 1998;140(6):585-90 [9755326]
J Pharmacol Exp Ther. 1998 Oct;287(1):107-14 [9765328]
J Neurosci. 1999 May 1;19(9):3594-609 [10212318]
Brain Res. 1999 Jul 24;835(2):154-61 [10415370]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/s00213-012-2957-9
ER  - 



TY  - JOUR
T1  - Reproducibility of linear array for human papillomavirus genotyping.
AN  - 1282517858; 23196360
AB  - We conducted a Linear Array test/retest analysis using cytologic specimens from 198 women. A total of 67.2% of samples had the same human papillomavirus (HPV) types detected in both tests (type-specific positive agreement was 83.3% overall [Kappa = 0.9] and 86.8% for carcinogenic types [Kappa = 0.92]). Discordance was highest with a low hybridization signal strength. Overall, Linear Array was highly reproducible.
JF  - Journal of clinical microbiology
AU  - Koshiol, Jill
AU  - Dunn, S Terence
AU  - Walker, Joan L
AU  - Zuna, Rosemary E
AU  - Schiffman, Mark
AU  - Sherman, Mark E
AU  - Gold, Michael A
AU  - Allen, Richard A
AU  - Zhang, Roy
AU  - Wang, Sophia S
AU  - Wentzensen, Nicolas
AD  - Division of Cancer Epidemiology and Genetics, NCI/NIH/DHHS, Bethesda, Maryland, USA. koshiolj@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 625
EP  - 628
VL  - 51
IS  - 2
KW  - Index Medicus
KW  - Sensitivity and Specificity
KW  - Reproducibility of Results
KW  - Humans
KW  - Female
KW  - Genotyping Techniques
KW  - Genotype
KW  - Papillomaviridae -- classification
KW  - Papillomaviridae -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282517858?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+microbiology&rft.atitle=Reproducibility+of+linear+array+for+human+papillomavirus+genotyping.&rft.au=Koshiol%2C+Jill%3BDunn%2C+S+Terence%3BWalker%2C+Joan+L%3BZuna%2C+Rosemary+E%3BSchiffman%2C+Mark%3BSherman%2C+Mark+E%3BGold%2C+Michael+A%3BAllen%2C+Richard+A%3BZhang%2C+Roy%3BWang%2C+Sophia+S%3BWentzensen%2C+Nicolas&rft.aulast=Koshiol&rft.aufirst=Jill&rft.date=2013-02-01&rft.volume=51&rft.issue=2&rft.spage=625&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+microbiology&rft.issn=1098-660X&rft_id=info:doi/10.1128%2FJCM.03036-12
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-01
N1  - Date created - 2013-01-28
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Clin Microbiol. 2010 Nov;48(11):4147-55 [20844222]
Sex Health. 2010 Sep;7(3):376-82 [20719230]
Lancet Oncol. 2011 Jul;12(7):663-72 [21684207]
Lancet Oncol. 2011 Sep;12(9):880-90 [21865084]
Am J Clin Pathol. 2011 Oct;136(4):578-86 [21917680]
J Obstet Gynaecol Res. 2012 Feb;38(2):408-14 [22175246]
J Clin Microbiol. 2012 May;50(5):1564-70 [22337992]
Acta Cytol. 2000 Sep-Oct;44(5):726-42 [11015972]
Anticancer Res. 2006 Sep-Oct;26(5B):3939-41 [17094425]
J Virol Methods. 2007 Jul;143(1):45-54 [17399803]
J Clin Microbiol. 2008 Jan;46(1):109-17 [17989194]
Am J Epidemiol. 2008 Jul 15;168(2):123-37 [18483125]
J Clin Virol. 2008 Aug;42(4):412-4 [18424229]
J Clin Microbiol. 2008 Aug;46(8):2759-65 [18550741]
J Clin Microbiol. 2008 Oct;46(10):3437-45 [18716224]
Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):113-20 [19124488]
Lancet Oncol. 2009 Apr;10(4):321-2 [19350698]
Int J Gynecol Cancer. 2009 Feb;19(2):266-72 [19396007]
J Natl Cancer Inst. 2011 Mar 2;103(5):368-83 [21282563]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1128/JCM.03036-12
ER  - 



TY  - JOUR
T1  - In vitro exposure of precision-cut lung slices to 2-(4-amino-3-methylphenyl)-5-fluorobenzothiazole lysylamide dihydrochloride (NSC 710305, Phortress) increases inflammatory cytokine content and tissue damage.
AN  - 1273813953; 23143926
AB  - The anticancer drug (2-[4-amino-3-methylphenyl]-5-fluorobenzothiazole lysylamide dihydrochloride) (NSC 710305, Phortress) is a metabolically activated prodrug that causes DNA adduct formation and subsequent toxicity. Preclinically, it was found that hepatic, bone marrow, and pulmonary toxicity presented challenges to developing this drug. An ex vivo precision-cut lung slice (PCLS) model was used to search for concentration dependent effects of NSC 710305 (10, 25, 50, and 100 µM) on cytokine content, protein content, and immuno/histological endpoints. Preparation and culture of PCLS caused an initial spike in proinflammatory cytokine expression and therefore treatment with NSC 710305 was delayed until 48 h after initiating the slice cultures to avoid confounding the response to slicing with any drug response. PCLSs were evaluated after 24, 48, and 72 h exposures to NSC 710305. Reversibility of toxicity due to the 72-h treatment was evaluated after a 24-h recovery period. NSC 710305 caused a concentration-dependent cytokine response, and only the toxicity caused by a 72-h exposure to 25 µM reversed during the 24-h recovery period. Immuno/histological examination and quantitation of tissue protein levels indicated that tissue destruction, ED-1 (activated macrophage) staining, and protein levels were associated with the levels of proinflammatory cytokines in the tissue. In conclusion, the concentration- and time-dependent inflammatory response of PCLS to NSC 710305 preceded relevant tissue damage by a few days. The no-observable adverse effect level (NOAEL) for 24, 48, and 72 h exposures was established as 10 µM NSC 710305.
JF  - Toxicological sciences : an official journal of the Society of Toxicology
AU  - Behrsing, Holger P
AU  - Furniss, Michael J
AU  - Davis, Myrtle
AU  - Tomaszewski, Joseph E
AU  - Parchment, Ralph E
AD  - Laboratory of Investigative & Screening Toxicology, LHTP, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA. behrsingh@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 470
EP  - 479
VL  - 131
IS  - 2
KW  - 2,6-diaminohexanoic acid (4-(5-fluorobenzothiazol-2-yl)-2-methylphenyl)amide
KW  - 0
KW  - Cytokines
KW  - Inflammation Mediators
KW  - Thiazoles
KW  - Lysine
KW  - K3Z4F929H6
KW  - Index Medicus
KW  - Rats
KW  - Animals
KW  - Rats, Inbred F344
KW  - In Vitro Techniques
KW  - Male
KW  - Lysine -- toxicity
KW  - Thiazoles -- toxicity
KW  - Lung -- drug effects
KW  - Lysine -- analogs & derivatives
KW  - Cytokines -- metabolism
KW  - Lung -- pathology
KW  - Inflammation Mediators -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273813953?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vitro+exposure+of+precision-cut+lung+slices+to+2-%284-amino-3-methylphenyl%29-5-fluorobenzothiazole+lysylamide+dihydrochloride+%28NSC+710305%2C+Phortress%29+increases+inflammatory+cytokine+content+and+tissue+damage.&rft.au=Behrsing%2C+Holger+P%3BFurniss%2C+Michael+J%3BDavis%2C+Myrtle%3BTomaszewski%2C+Joseph+E%3BParchment%2C+Ralph+E&rft.aulast=Behrsing&rft.aufirst=Holger&rft.date=2013-02-01&rft.volume=131&rft.issue=2&rft.spage=470&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%2Fkfs319
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-12
N1  - Date created - 2013-01-23
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Mol Cancer Ther. 2002 Feb;1(4):239-46 [12467219]
Drug Metab Dispos. 2002 Nov;30(11):1206-13 [12386126]
Curr Pharm Des. 2003;9(1):39-49 [12570673]
Eur Respir J. 2003 Jun;21(6):1024-32 [12797499]
Curr Opin Infect Dis. 2003 Jun;16(3):193-8 [12821807]
Crit Care Med. 2003 Aug;31(8 Suppl):S524-31 [12907882]
Toxicol Sci. 2003 Sep;75(1):169-80 [12832656]
Eur Respir J Suppl. 2003 Aug;42:10s-14s [12945995]
Cytokine Growth Factor Rev. 2003 Dec;14(6):523-35 [14563354]
JAMA. 1980 Aug 15;244(7):687-8 [7392168]
Toxicology. 1996 Jun 17;110(1-3):95-101 [8658564]
Am J Respir Crit Care Med. 1996 Sep;154(3 Pt 1):602-11 [8810593]
Biochim Biophys Acta. 1996 Nov 14;1298(1):131-40 [8948497]
Drug Metab Dispos. 1998 May;26(5):396-400 [9571220]
Clin Sci (Lond). 1998 Jun;94(6):557-72 [9854452]
Toxicol In Vitro. 2006 Jun;20(4):426-38 [16198082]
Expert Opin Drug Metab Toxicol. 2006 Dec;2(6):875-94 [17125407]
J Invest Dermatol. 2007 Mar;127(3):514-25 [17299434]
Toxicol Appl Pharmacol. 2008 Aug 15;231(1):68-76 [18504053]
Pharmacology. 2009;83(2):99-109 [19088497]
Eur Respir J. 2009 Sep;34(3):559-67 [19696157]
Chest. 2009 Nov;136(5):1364-70 [19892675]
Am J Respir Cell Mol Biol. 2009 Dec;41(6):661-70 [19265174]
Biol Pharm Bull. 2010;33(5):780-3 [20460754]
Toxicol Lett. 2010 Jul 1;196(2):117-24 [20394810]
Am J Physiol Lung Cell Mol Physiol. 2010 Jun;298(6):L715-31 [20363851]
Drug Saf. 2010 Jul 1;33(7):539-58 [20553056]
Am J Physiol Lung Cell Mol Physiol. 2010 Oct;299(4):L442-52 [20562227]
Philos Trans R Soc Lond B Biol Sci. 2011 Jan 27;366(1562):286-90 [21149364]
Am J Physiol Lung Cell Mol Physiol. 2011 Jan;300(1):L112-20 [20952494]
Mol Med. 2011 Mar-Apr;17(3-4):293-307 [21046059]
PLoS One. 2011;6(3):e17644 [21464978]
Wound Repair Regen. 2011 May-Jun;19(3):337-47 [21371163]
J Biol Chem. 2011 May 20;286(20):17435-44 [21398522]
Drug Saf. 2000 Aug;23(2):143-64 [10945376]
Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1184-90 [11076808]
Arch Toxicol. 2000 Oct;74(8):460-6 [11097383]
Immunol Cell Biol. 2001 Aug;79(4):376-84 [11488985]
Am J Respir Crit Care Med. 2001 Nov 15;164(10 Pt 1):1896-903 [11734443]
Respir Res. 2002;3:5 [11806840]
Cancer Lett. 2002 Apr 8;178(1):25-36 [11849738]
Br J Cancer. 2002 Apr 22;86(8):1348-54 [11953897]
Br J Cancer. 2003 Feb 10;88(3):470-7 [12569393]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/toxsci/kfs319
ER  - 



TY  - CONF
T1  - PPTOX III: environmental stressors in the developmental origins of disease--evidence and mechanisms.
AN  - 1273808447; 22956631
AB  - Fetal and early postnatal development constitutes the most vulnerable time period of human life in regard to adverse effects of environmental hazards. Subtle effects during development can lead to functional deficits and increased disease risk later in life. The hypothesis stating that environmental exposures leads to altered programming and, thereby, to increased susceptibility to disease or dysfunction later in life has garnered much support from both experimental and epidemiological studies. Similar observations have been made on the long-term impact of nutritional unbalance during early development. In an effort to bridge the fields of nutritional and environmental developmental toxicity, the Society of Toxicology sponsored this work. This report summarizes novel findings in developmental toxicity as reported by select invited experts and meeting attendees. Recommendations for the application and improvement of current and future research efforts are also presented.
JF  - Toxicological sciences : an official journal of the Society of Toxicology
AU  - Schug, Thaddeus T
AU  - Barouki, Robert
AU  - Gluckman, Peter D
AU  - Grandjean, Philippe
AU  - Hanson, Mark
AU  - Heindel, Jerold J
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 343
EP  - 350
VL  - 131
IS  - 2
KW  - Index Medicus
KW  - Animals
KW  - Risk Factors
KW  - Humans
KW  - Gene Expression
KW  - Immune System -- physiology
KW  - Epigenesis, Genetic
KW  - Disease -- etiology
KW  - Environmental Exposure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273808447?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=PPTOX+III%3A+environmental+stressors+in+the+developmental+origins+of+disease--evidence+and+mechanisms.&rft.au=Schug%2C+Thaddeus+T%3BBarouki%2C+Robert%3BGluckman%2C+Peter+D%3BGrandjean%2C+Philippe%3BHanson%2C+Mark%3BHeindel%2C+Jerold+J&rft.aulast=Schug&rft.aufirst=Thaddeus&rft.date=2013-02-01&rft.volume=131&rft.issue=2&rft.spage=343&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%2Fkfs267
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-12
N1  - Date created - 2013-01-23
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Mol Endocrinol. 2006 Sep;20(9):2141-55 [16613991]
PLoS One. 2011;6(9):e25455 [21980463]
Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):90-3 [18226060]
Am J Respir Crit Care Med. 2008 May 15;177(10):1103-10 [18292469]
Front Neuroendocrinol. 2008 Jun;29(3):358-74 [18394690]
J Clin Invest. 2008 Oct;118(10):3462-9 [18802477]
BMC Genomics. 2008;9:598 [19077247]
Endocr Rev. 2009 Jun;30(4):293-342 [19502515]
Obstet Gynecol Clin North Am. 2009 Jun;36(2):227-44, xii [19501311]
Environ Health Perspect. 2009 Jul;117(7):1131-8 [19654924]
Biochim Biophys Acta. 2009 Sep;1790(9):878-85 [19364482]
Am J Respir Crit Care Med. 2009 Sep 1;180(5):462-7 [19498054]
J Nutr. 2010 Mar;140(3):662-6 [20107142]
Int J Androl. 2010 Apr;33(2):346-59 [20487042]
Annu Rev Nutr. 2010 Aug 21;30:315-39 [20415585]
Environ Health Perspect. 2010 Sep;118(9):1243-50 [20488778]
Environ Health Perspect. 2010 Oct;118(10):1429-33 [20562055]
Environ Mol Mutagen. 2010 Oct-Dec;51(8-9):851-70 [20872848]
Science. 2010 Oct 22;330(6003):460-1 [20966241]
Front Neuroendocrinol. 2010 Oct;31(4):400-19 [20347861]
APMIS. 2011 Jan;119(1):17-35 [21143523]
Int J Gynaecol Obstet. 2011 Nov;115 Suppl 1:S3-5 [22099437]
Environ Health Perspect. 2012 Jan;120(1):29-37 [21878421]
Endocrinology. 2012 Feb;153(2):712-20 [22166976]
JAMA. 2012 Jan 25;307(4):391-7 [22274686]
Cancer Res. 2012 Feb 1;72(3):707-15 [22139380]
Environ Health Perspect. 2012 Mar;120(3):451-7 [22027556]
Clin Genet. 2012 Apr;81(4):341-9 [22236068]
Curr Opin Endocrinol Diabetes Obes. 2012 Jun;19(3):197-203 [22499221]
Horm Res Paediatr. 2012;77(3):137-45 [22508036]
Proc Natl Acad Sci U S A. 2012 May 15;109(20):7871-6 [22547821]
Reprod Toxicol. 2012 Aug;34(1):22-30 [22429997]
Biol Psychiatry. 2012 Jul 1;72(1):41-8 [22444201]
Environ Health. 2012;11:42 [22715989]
Environ Health Perspect. 2012 Jul;120(7):984-9 [22763116]
Environ Health Perspect. 2001 Jul;109(7):675-80 [11485865]
Genes Dev. 2002 Jan 1;16(1):6-21 [11782440]
Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):13994-9 [14610279]
Lancet. 1989 Sep 9;2(8663):577-80 [2570282]
Chest. 2005 Apr;127(4):1232-41 [15821200]
Early Hum Dev. 2005 Dec;81(12):981-8 [16257499]
Endocrinology. 2006 Jun;147(6 Suppl):S50-5 [16690801]
Matern Child Nutr. 2005 Jul;1(3):130-41 [16881892]
Proc Natl Acad Sci U S A. 2006 Aug 8;103(32):12033-8 [16882715]
Birth Defects Res C Embryo Today. 2011 Mar;93(1):12-8 [21425438]
Birth Defects Res C Embryo Today. 2011 Mar;93(1):34-50 [21425440]
Reprod Toxicol. 2011 Apr;31(3):327-36 [20851760]
Reprod Toxicol. 2011 Apr;31(3):280-9 [20951797]
Prog Biophys Mol Biol. 2011 Jul;106(1):272-80 [21219925]
Am J Respir Crit Care Med. 2011 Jul 15;184(2):191-7 [21512169]
Endocrinology. 2011 Aug;152(8):3049-61 [21586551]
Environ Health Perspect. 2011 Aug;119(8):1196-201 [21507777]
Rev Endocr Metab Disord. 2007 Jun;8(2):143-59 [17674209]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/toxsci/kfs267
ER  - 



TY  - JOUR
T1  - Estrogen receptor and progesterone receptor expression in normal terminal duct lobular units surrounding invasive breast cancer.
AN  - 1273803835; 23271326
AB  - Molecular and morphological alterations related to carcinogenesis have been found in terminal duct lobular units (TDLUs), the microscopic structures from which most breast cancer precursors and cancers develop, and therefore, analysis of these structures may reveal early changes in breast carcinogenesis and etiologic heterogeneity. Accordingly, we evaluated relationships of breast cancer risk factors and tumor pathology to estrogen receptor (ER) and progesterone receptor (PR) expression in TDLUs surrounding breast cancers. We analyzed 270 breast cancer cases included in a population-based breast cancer case-control study conducted in Poland. TDLUs were mapped in relation to breast cancer: within the same block as the tumor (TDLU-T), proximal to tumor (TDLU-PT), or distant from (TDLU-DT). ER/PR was quantitated using image analysis of immunohistochemically stained TDLUs prepared as tissue microarrays. In surgical specimens containing ER-positive breast cancers, ER and PR levels were significantly higher in breast cancer cells than in normal TDLUs, and higher in TDLU-T than in TDLU-DT or TDLU-PT, which showed similar results. Analyses combining DT-/PT TDLUs within subjects demonstrated that ER levels were significantly lower in premenopausal women versus postmenopausal women (odds ratio [OR] = 0.38, 95 % confidence interval [CI] = 0.19, 0.76, P = 0.0064) and among recent or current menopausal hormone therapy users compared with never users (OR = 0.14, 95 % CI = 0.046-0.43, P                 (trend) = 0.0006). Compared with premenopausal women, TDLUs of postmenopausal women showed lower levels of PR (OR = 0.90, 95 % CI = 0.83-0.97, P                 (trend) = 0.007). ER and PR expression in TDLUs was associated with epidermal growth factor receptor (EGFR) expression in invasive tumors (P = 0.019 for ER and P = 0.03 for PR), but not with other tumor features. Our data suggest that TDLUs near breast cancers reflect field effects, whereas those at a distance demonstrate influences of breast cancer risk factors on at-risk breast tissue. Analyses of mapped TDLUs may provide information about the sequence of molecular changes occurring in breast carcinogenesis.
JF  - Breast cancer research and treatment
AU  - Yang, Xiaohong R
AU  - Figueroa, Jonine D
AU  - Hewitt, Stephen M
AU  - Falk, Roni T
AU  - Pfeiffer, Ruth M
AU  - Lissowska, Jolanta
AU  - Peplonska, Beata
AU  - Brinton, Louise A
AU  - Garcia-Closas, Montserrat
AU  - Sherman, Mark E
AD  - Genetic Epidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, NIH/DHHS, 6120 Executive Blvd., Bethesda, MD USA. royang@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 837
EP  - 847
VL  - 137
IS  - 3
KW  - Receptors, Estrogen
KW  - 0
KW  - Receptors, Progesterone
KW  - Index Medicus
KW  - Neoplasm Invasiveness
KW  - Risk Factors
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - Menopause
KW  - Female
KW  - Receptors, Progesterone -- metabolism
KW  - Breast Neoplasms -- pathology
KW  - Mammary Glands, Human -- metabolism
KW  - Breast Neoplasms -- metabolism
KW  - Receptors, Estrogen -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273803835?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Estrogen+receptor+and+progesterone+receptor+expression+in+normal+terminal+duct+lobular+units+surrounding+invasive+breast+cancer.&rft.au=Yang%2C+Xiaohong+R%3BFigueroa%2C+Jonine+D%3BHewitt%2C+Stephen+M%3BFalk%2C+Roni+T%3BPfeiffer%2C+Ruth+M%3BLissowska%2C+Jolanta%3BPeplonska%2C+Beata%3BBrinton%2C+Louise+A%3BGarcia-Closas%2C+Montserrat%3BSherman%2C+Mark+E&rft.aulast=Yang&rft.aufirst=Xiaohong&rft.date=2013-02-01&rft.volume=137&rft.issue=3&rft.spage=837&rft.isbn=&rft.btitle=&rft.title=Breast+cancer+research+and+treatment&rft.issn=1573-7217&rft_id=info:doi/10.1007%2Fs10549-012-2380-2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-27
N1  - Date created - 2013-01-23
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cancer Epidemiol Biomarkers Prev. 1999 Oct;8(10):867-72 [10548314]
Breast Cancer Res. 2012;14(2):R64 [22513288]
Breast Cancer Res Treat. 2001 Feb;65(3):241-7 [11336246]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 [12829800]
Endocrinology. 1978 Nov;103(5):1742-51 [748014]
Br Med J (Clin Res Ed). 1988 May 14;296(6633):1349-51 [3134982]
Mol Endocrinol. 1991 Dec;5(12):1955-63 [1791840]
Br J Cancer. 1992 Apr;65(4):601-7 [1562470]
Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):874-9 [8456895]
Cancer Res. 1994 Feb 15;54(4):993-7 [8313390]
Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182]
J Natl Cancer Inst. 1998 Jan 7;90(1):37-42 [9428781]
J Pathol. 1999 Jul;188(3):237-44 [10419589]
JAMA. 2006 Jun 7;295(21):2492-502 [16757721]
Br J Cancer. 2006 Jul 3;95(1):123-9 [16755295]
Diagn Mol Pathol. 2006 Sep;15(3):157-61 [16932071]
J Natl Cancer Inst. 2006 Nov 15;98(22):1600-7 [17105983]
Clin Cancer Res. 2006 Nov 15;12(22):6626-36 [17121881]
Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):439-43 [17372238]
Int J Cancer. 2007 Sep 1;121(5):1079-85 [17487843]
Int J Cancer. 2008 Apr 1;122(7):1557-66 [18058819]
Endocr Rev. 2008 Apr;29(2):217-33 [18216219]
Breast Cancer Res Treat. 2009 Nov;118(2):229-39 [19685287]
J Clin Oncol. 2009 Dec 10;27(35):5893-8 [19805686]
Br J Cancer. 2010 Apr 13;102(8):1284-93 [20197764]
Clin Cancer Res. 2011 Jan 15;17(2):236-46 [21059815]
Horm Cancer. 2010 Feb;1(1):2-10 [21761346]
Br J Cancer. 2011 Aug 23;105(5):709-22 [21772329]
Mol Cancer Res. 2011 Sep;9(9):1209-21 [21775421]
Breast Cancer Res Treat. 2012 Jan;131(1):159-67 [21830014]
Breast Cancer Res Treat. 2012 Feb;131(3):1067-76 [22101408]
Nature. 2012 Jun 21;486(7403):346-52 [22522925]
Nat Rev Clin Oncol. 2012 Aug;9(8):460-70 [22733233]
Nature. 2000 Aug 17;406(6797):747-52 [10963602]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/s10549-012-2380-2
ER  - 



TY  - JOUR
T1  - The role of co-factors in the progression from human papillomavirus infection to cervical cancer.
AN  - 1273781291; 23146688
AB  - Co-factors for cervical cancer, including oral contraceptive (OC) use, smoking and multiparity have been identified; however, the stage at which they act in cervical carcinogenesis is not clear. We compared established risk factors among women with CIN2 and CIN3 to evaluate the heterogeneity of these factors in precancer and also assessed their role during cervical carcinogenesis.
          The current analysis included 2783 women with various stages of cervical disease who were enrolled in the Study to Understand Cervical Cancer Early Endpoints and Determinants (SUCCEED) and the Biopsy Study. Associations of co-factors within cervical precancer and at different stages of cervical carcinogenesis were estimated using logistic regression. Long-term OC use (10+years vs. never: OR=2.42, 95% CI: [1.13-5.15]), multiparity (3+ births vs. nulliparous: OR=1.54 [1.04-2.28]), smoking (ever vs. never: OR=1.95 [1.48-2.58]), and no Pap test in the previous five years (2.05 [1.32-3.17]) were positively associated with CIN3 compared to CIN2. We observed that long-term OC use, parity and smoking were associated with an increased risk of CIN3 compared to <CIN2 (1.97 [1.12-3.46]; 2.23 [1.59-3.11]; 2.60 [2.04-3.30], respectively), whereas associations were not significantly different (OC use, parity) or showed decreased risk (smoking) when comparing cancer to CIN3. Differences in established risk factors suggest that CIN3 is a more specific definition of precancer than CIN2. Hormonally-related factors and smoking play a role in the transition from human papillomavirus infection to precancer.
          Published by Elsevier Inc.
JF  - Gynecologic oncology
AU  - Luhn, Patricia
AU  - Walker, Joan
AU  - Schiffman, Mark
AU  - Zuna, Rosemary E
AU  - Dunn, S Terence
AU  - Gold, Michael A
AU  - Smith, Katherine
AU  - Mathews, Cara
AU  - Allen, Richard A
AU  - Zhang, Roy
AU  - Wang, Sophia
AU  - Wentzensen, Nicolas
AD  - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20892, USA. luhnpa@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 265
EP  - 270
VL  - 128
IS  - 2
KW  - Contraceptives, Oral
KW  - 0
KW  - Index Medicus
KW  - Contraceptives, Oral -- adverse effects
KW  - Parity
KW  - Contraceptives, Oral -- administration & dosage
KW  - Cell Transformation, Neoplastic -- pathology
KW  - Humans
KW  - Uterine Cervical Diseases -- virology
KW  - Disease Progression
KW  - Smoking -- epidemiology
KW  - Adult
KW  - Uterine Cervical Diseases -- pathology
KW  - Uterine Cervical Diseases -- etiology
KW  - Surveys and Questionnaires
KW  - Middle Aged
KW  - Uterine Cervical Diseases -- epidemiology
KW  - Female
KW  - Oklahoma -- epidemiology
KW  - Uterine Cervical Neoplasms -- etiology
KW  - Papillomavirus Infections -- pathology
KW  - Papillomavirus Infections -- epidemiology
KW  - Cervical Intraepithelial Neoplasia -- pathology
KW  - Uterine Cervical Neoplasms -- epidemiology
KW  - Papillomavirus Infections -- complications
KW  - Cervical Intraepithelial Neoplasia -- virology
KW  - Uterine Cervical Neoplasms -- pathology
KW  - Uterine Cervical Neoplasms -- virology
KW  - Cervical Intraepithelial Neoplasia -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273781291?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+role+of+co-factors+in+the+progression+from+human+papillomavirus+infection+to+cervical+cancer.&rft.au=Luhn%2C+Patricia%3BWalker%2C+Joan%3BSchiffman%2C+Mark%3BZuna%2C+Rosemary+E%3BDunn%2C+S+Terence%3BGold%2C+Michael+A%3BSmith%2C+Katherine%3BMathews%2C+Cara%3BAllen%2C+Richard+A%3BZhang%2C+Roy%3BWang%2C+Sophia%3BWentzensen%2C+Nicolas&rft.aulast=Luhn&rft.aufirst=Patricia&rft.date=2013-02-01&rft.volume=128&rft.issue=2&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Gynecologic+oncology&rft.issn=1095-6859&rft_id=info:doi/10.1016%2Fj.ygyno.2012.11.003
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-25
N1  - Date created - 2013-01-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Int J Cancer. 2007 Oct 1;121(7):1417-23 [17546591]
Am J Clin Pathol. 2007 May;127(5):805-15 [17439841]
J Natl Cancer Inst. 2009 Apr 1;101(7):475-87 [19318628]
Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):113-20 [19124488]
Int J Gynecol Pathol. 2007 Oct;26(4):441-6 [17885496]
Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494]
Trends Endocrinol Metab. 2010 Aug;21(8):504-11 [20456973]
J Natl Cancer Inst. 2011 Mar 2;103(5):368-83 [21282563]
Int J STD AIDS. 2011 May;22(5):263-72 [21571974]
PLoS One. 2012;7(1):e29051 [22253702]
J Int Med Res. 2012;40(2):486-96 [22613409]
J Low Genit Tract Dis. 2012 Jul;16(3):205-42 [22820980]
Clin Cancer Res. 2012 Aug 1;18(15):4154-62 [22675168]
Int J Cancer. 2012 Nov 15;131(10):2349-59 [22323075]
Arch Pathol Lab Med. 2012 Oct;136(10):1266-97 [22742517]
Gynecol Oncol. 2012 Nov;127(2):278-82 [22858904]
Int J Cancer. 2013 Jan 1;132(1):148-54 [22488167]
Lancet. 2007 Nov 10;370(9599):1609-21 [17993361]
Lancet Oncol. 2008 May;9(5):425-34 [18407790]
Cancer Epidemiol Biomarkers Prev. 2008 Sep;17(9):2350-5 [18768503]
Obstet Gynecol. 2008 Dec;112(6):1335-42 [19037044]
Int J Cancer. 2009 Feb 15;124(4):964-9 [19030188]
Obstet Gynecol. 2009 Jan;113(1):18-25 [19104355]
JAMA. 2001 Mar 21;285(11):1500-5 [11255427]
Am J Obstet Gynecol. 2003 Jun;188(6):1406-12 [12824970]
Int J Gynecol Pathol. 1993 Apr;12(2):186-92 [8463044]
Int J Cancer. 2006 Mar 15;118(6):1481-95 [16206285]
Int J Cancer. 2006 Sep 1;119(5):1108-24 [16570271]
Lancet. 2007 Sep 8;370(9590):890-907 [17826171]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.ygyno.2012.11.003
ER  - 



TY  - JOUR
T1  - RBCK1, an E3 ubiquitin ligase, interacts with and ubiquinates the human pregnane X receptor.
AN  - 1273664656; 23160820
AB  - The pregnane X receptor (PXR, NR1I2) plays a pivotal role in the disposition and detoxification of numerous foreign and endogenous chemicals by increasing transcription of numerous target genes, including phase I and II drug-metabolizing enzymes and transporters. In the present study, yeast two-hybrid screening identified an E3 ubiquitin ligase, RBCK1 (Ring-B-box-coiled-coil protein interacting with protein kinase C-1), as a human pregnane X receptor (hPXR)-interacting protein. Coimmunoprecipitation studies confirmed the interaction between RBCK1 and hPXR when both were ectopically expressed in AD-293 cells. Domain mapping studies showed that the interaction between RBCK1 and hPXR involves all RBCK1 domains. We further demonstrate that RBCK1 ubiquitinates hPXR, and this may target hPXR for degradation by the ubiquitin-proteasome pathway. Simultaneous ectopic overexpression of RBCK1 and PXR decreased PXR levels in AD-293 cells, and this decrease was inhibited by the proteasomal inhibitor MG-132 (carbobenzoxy-Leu-Leu-leucinal). Furthermore, overexpression of RBCK1 decreased endogenous levels of PXR in HepG2 cells. Of importance, ectopic overexpression and silencing of endogenous RBCK1 in primary human hepatocytes resulted in a decrease and increase, respectively, in endogenous PXR protein levels and in the induction of PXR target genes by rifampicin. These results suggest that RBCK1 is important for the ubiquitination of PXR and may play a role in its proteasomal degradation.
JF  - Drug metabolism and disposition: the biological fate of chemicals
AU  - Rana, Ritu
AU  - Coulter, Sherry
AU  - Kinyamu, Harriet
AU  - Goldstein, Joyce A
AD  - Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 398
EP  - 405
VL  - 41
IS  - 2
KW  - Leupeptins
KW  - 0
KW  - Proteasome Inhibitors
KW  - Receptors, Steroid
KW  - Transcription Factors
KW  - pregnane X receptor
KW  - RBCK1 protein, human
KW  - EC 2.3.2.27
KW  - Ubiquitin-Protein Ligases
KW  - Proteasome Endopeptidase Complex
KW  - EC 3.4.25.1
KW  - benzyloxycarbonylleucyl-leucyl-leucine aldehyde
KW  - RF1P63GW3K
KW  - Index Medicus
KW  - Proteasome Inhibitors -- pharmacology
KW  - Humans
KW  - Two-Hybrid System Techniques
KW  - Immunoprecipitation
KW  - Primary Cell Culture
KW  - Protein Binding
KW  - Leupeptins -- pharmacology
KW  - Hep G2 Cells
KW  - Proteasome Endopeptidase Complex -- metabolism
KW  - Protein Interaction Mapping
KW  - Transfection
KW  - Ubiquitination
KW  - Gene Expression Regulation
KW  - RNA Interference
KW  - Protein Interaction Domains and Motifs
KW  - Hepatocytes -- drug effects
KW  - Transcription Factors -- metabolism
KW  - Receptors, Steroid -- metabolism
KW  - Receptors, Steroid -- genetics
KW  - Hepatocytes -- enzymology
KW  - Transcription Factors -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273664656?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=RBCK1%2C+an+E3+ubiquitin+ligase%2C+interacts+with+and+ubiquinates+the+human+pregnane+X+receptor.&rft.au=Rana%2C+Ritu%3BCoulter%2C+Sherry%3BKinyamu%2C+Harriet%3BGoldstein%2C+Joyce+A&rft.aulast=Rana&rft.aufirst=Ritu&rft.date=2013-02-01&rft.volume=41&rft.issue=2&rft.spage=398&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.112.048728
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-12
N1  - Date created - 2013-01-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3369-74 [11248085]
Mol Cell Endocrinol. 2001 Feb 14;172(1-2):47-56 [11165039]
Cell. 2001 Oct 5;107(1):55-65 [11595185]
Drug Metab Dispos. 2001 Nov;29(11):1467-72 [11602523]
Eur J Biochem. 2001 Dec;268(24):6346-58 [11737189]
Endocrinology. 2002 Jan;143(1):55-61 [11751591]
Physiol Rev. 2002 Apr;82(2):373-428 [11917093]
Mol Pharmacol. 2002 Sep;62(3):638-46 [12181440]
EMBO J. 2002 Nov 1;21(21):5645-52 [12411482]
Mol Biol Evol. 2002 Dec;19(12):2039-50 [12446796]
Nat Cell Biol. 2003 Apr;5(4):336-40 [12629548]
Mol Endocrinol. 2003 Jul;17(7):1268-82 [12663745]
Brain Res Mol Brain Res. 2003 Oct 7;117(2):179-89 [14559152]
J Biol Chem. 1997 Jun 27;272(26):16482-9 [9195957]
Cell. 1998 Jan 9;92(1):73-82 [9489701]
Biochem Biophys Res Commun. 1998 Mar 17;244(2):353-9 [9514928]
J Clin Invest. 1998 Sep 1;102(5):1016-23 [9727070]
Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12208-13 [9770465]
Genes Dev. 1998 Oct 15;12(20):3195-205 [9784494]
FEBS Lett. 1999 Jul 9;454(3):257-61 [10431818]
Clin Cancer Res. 1999 Aug;5(8):2103-7 [10473093]
Mol Cell Endocrinol. 2005 Feb 28;231(1-2):75-85 [15713537]
J Mol Endocrinol. 2005 Apr;34(2):281-97 [15821097]
Mol Endocrinol. 2005 May;19(5):1170-80 [15650019]
J Biol Chem. 2005 Jun 17;280(24):22937-44 [15833741]
J Pharmacol Exp Ther. 2005 Sep;314(3):1125-33 [15919766]
Mol Pharmacol. 2006 Jan;69(1):99-108 [16219912]
Drug Metab Dispos. 2006 May;34(5):756-64 [16455805]
Pharmacogenet Genomics. 2006 Aug;16(8):579-99 [16847427]
Drug Metab Rev. 2006;38(3):515-97 [16877263]
J Biol Chem. 2007 Jun 8;282(23):16776-82 [17449468]
Pharmacogenet Genomics. 2008 Apr;18(4):325-37 [18334917]
Mol Pharmacol. 2008 Sep;74(3):913-23 [18552123]
Cell Res. 2008 Nov;18(11):1096-104 [18711448]
AAPS J. 2009 Sep;11(3):590-601 [19688601]
Drug Metab Dispos. 2010 Apr;38(4):591-9 [20086032]
Adv Drug Deliv Rev. 2010 Oct 30;62(13):1238-49 [20727377]
Pharmacol Res. 2011 Jul;64(1):4-10 [21397695]
J Clin Invest. 2011 Aug;121(8):3220-32 [21747170]
J Lipid Res. 2011 Sep;52(9):1652-9 [21685500]
Biochem Biophys Res Commun. 2000 Sep 16;276(1):144-50 [11006097]
J Biol Chem. 2001 May 4;276(18):14581-7 [11297522]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1124/dmd.112.048728
ER  - 



TY  - JOUR
T1  - Occupational exposure to formaldehyde and alterations in lymphocyte subsets.
AN  - 1273580114; 22767408
AB  - Formaldehyde is used in many occupational settings, most notably in manufacturing, health care, and embalming. Formaldehyde has been classified as a human carcinogen, but its mechanism of action remains uncertain.
          We carried out a cross-sectional study of 43 formaldehyde-exposed workers and 51 unexposed age and sex-matched controls in Guangdong, China to study formaldehyde's early biologic effects. To follow up our previous report that the total lymphocyte count was decreased in formaldehyde-exposed workers compared with controls, we evaluated each major lymphocyte subset (i.e., CD4(+) T cells, CD8(+) T cells, natural killer [NK] cells, and B cells) and T cell lymphocyte subset (CD4(+) naïve and memory T cells, CD8(+) naïve and memory T cells, and regulatory T cells). Linear regression of each subset was used to test for differences between exposed workers and controls, adjusting for potential confounders.
          Total NK cell and T cell counts were about 24% (P = 0.037) and 16% (P = 0.0042) lower, respectively, among exposed workers. Among certain T cell subsets, decreased counts among exposed workers were observed for CD8(+) T cells (P = 0.026), CD8(+) effector memory T cells (P = 0.018), and regulatory T cells (CD4(+) FoxP3(+) : P = 0.04; CD25(+) FoxP3(+) : P = 0.008). Formaldehyde-exposed workers experienced decreased counts of NK cells, regulatory T cells, and CD8(+) effector memory T cells; however, due to the small sample size; these findings need to be confirmed in larger studies.
          Copyright © 2012 Wiley Periodicals, Inc.
JF  - American journal of industrial medicine
AU  - Hosgood, H Dean
AU  - Zhang, Luoping
AU  - Tang, Xiaojiang
AU  - Vermeulen, Roel
AU  - Hao, Zhenyue
AU  - Shen, Min
AU  - Qiu, Chuangyi
AU  - Ge, Yichen
AU  - Hua, Ming
AU  - Ji, Zhiying
AU  - Li, Senhua
AU  - Xiong, Jun
AU  - Reiss, Boris
AU  - Liu, Songwang
AU  - Xin, Kerry X
AU  - Azuma, Mariko
AU  - Xie, Yuxuan
AU  - Freeman, Laura Beane
AU  - Ruan, Xiaolin
AU  - Guo, Weihong
AU  - Galvan, Noe
AU  - Blair, Aaron
AU  - Li, Laiyu
AU  - Huang, Hanlin
AU  - Smith, Martyn T
AU  - Rothman, Nathaniel
AU  - Lan, Qing
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892-7240, USA. hosgoodd@mail.nih.gov
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 252
EP  - 257
VL  - 56
IS  - 2
KW  - Air Pollutants, Occupational
KW  - 0
KW  - Biomarkers
KW  - Formaldehyde
KW  - 1HG84L3525
KW  - Index Medicus
KW  - CD8-Positive T-Lymphocytes -- metabolism
KW  - Humans
KW  - Linear Models
KW  - B-Lymphocytes -- metabolism
KW  - T-Lymphocytes, Regulatory -- metabolism
KW  - Matched-Pair Analysis
KW  - Cross-Sectional Studies
KW  - Lymphocyte Count
KW  - Adult
KW  - Biomarkers -- blood
KW  - Killer Cells, Natural -- metabolism
KW  - Female
KW  - Male
KW  - Air Pollutants, Occupational -- analysis
KW  - Air Pollutants, Occupational -- adverse effects
KW  - Occupational Exposure -- adverse effects
KW  - Formaldehyde -- adverse effects
KW  - Lymphocyte Subsets -- metabolism
KW  - Formaldehyde -- analysis
KW  - Occupational Exposure -- analysis
KW  - Chemical Industry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273580114?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Occupational+exposure+to+formaldehyde+and+alterations+in+lymphocyte+subsets.&rft.au=Hosgood%2C+H+Dean%3BZhang%2C+Luoping%3BTang%2C+Xiaojiang%3BVermeulen%2C+Roel%3BHao%2C+Zhenyue%3BShen%2C+Min%3BQiu%2C+Chuangyi%3BGe%2C+Yichen%3BHua%2C+Ming%3BJi%2C+Zhiying%3BLi%2C+Senhua%3BXiong%2C+Jun%3BReiss%2C+Boris%3BLiu%2C+Songwang%3BXin%2C+Kerry+X%3BAzuma%2C+Mariko%3BXie%2C+Yuxuan%3BFreeman%2C+Laura+Beane%3BRuan%2C+Xiaolin%3BGuo%2C+Weihong%3BGalvan%2C+Noe%3BBlair%2C+Aaron%3BLi%2C+Laiyu%3BHuang%2C+Hanlin%3BSmith%2C+Martyn+T%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Hosgood&rft.aufirst=H&rft.date=2013-02-01&rft.volume=56&rft.issue=2&rft.spage=252&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=1097-0274&rft_id=info:doi/10.1002%2Fajim.22088
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-25
N1  - Date created - 2013-01-16
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nature. 1999 Oct 14;401(6754):708-12 [10537110]
Immunol Res. 2007;38(1-3):112-21 [17917016]
Immunol Rev. 2000 Oct;177:134-40 [11138771]
Cancer Epidemiol Biomarkers Prev. 2001 Nov;10(11):1145-53 [11700262]
Immunol Lett. 2002 Apr 22;81(2):133-40 [11852118]
Nat Rev Cancer. 2002 May;2(5):373-82 [12044013]
Arthritis Res. 2002;4(4):241-6 [12106494]
J Med Genet. 2002 Aug;39(8):537-45 [12161590]
Curr Opin Immunol. 2003 Dec;15(6):627-33 [14630195]
Annu Rev Immunol. 2004;22:329-60 [15032581]
Annu Rev Immunol. 2004;22:765-87 [15032596]
Semin Immunol. 2004 Oct;16(5):295-303 [15528074]
Leukemia. 2008 May;22(5):1007-17 [18323802]
Front Biosci. 2008;13:3986-4001 [18508492]
Int Immunopharmacol. 2009 May;9(5):590-2 [19539572]
Lancet Oncol. 2009 Dec;10(12):1143-4 [19998521]
Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):80-8 [20056626]
Nat Rev Immunol. 2010 Dec;10(12):849-59 [21107346]
Mutat Res. 2005 Dec 7;588(1):22-7 [16257574]
Expert Opin Biol Ther. 2006 Nov;6(11):1193-205 [17049016]
Eur J Immunol. 2006 Nov;36(11):2832-6 [17051620]
Nat Rev Microbiol. 2007 Jun;5(6):405-17 [17487145]
Nat Genet. 2001 Jan;27(1):68-73 [11138001]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ajim.22088
ER  - 



TY  - JOUR
T1  - Human papillomavirus genotype attribution and estimation of preventable fraction of anal intraepithelial neoplasia cases among HIV-infected men who have sex with men.
AN  - 1273262351; 23162133
AB  - The prevention of human papillomavirus (HPV)-induced anal cancer in high-risk populations such as human immunodeficiency virus (HIV)-infected men who have sex with men (MSM) remains an urgent priority, given rising incidence rates despite widespread antiretroviral therapy use.
          HPV genotypes and anal disease prevalence, by cytology and histopathologic findings, were evaluated among 363 HIV-infected MSM. We modeled fractions of high-grade anal intraepithelial neoplasia (HGAIN) attributable to individual carcinogenic HPV genotypes and estimated the range of the proportion of HGAIN cases potentially preventable by prophylactic HPV vaccines. HPV16 was the most common genotype overall (26.4% of cases) and among HGAIN cases (55%). Prevalence of multiple (≥ 2) carcinogenic HPV genotypes increased from 30.9% in cases of AIN grade <1 to 76.3% in cases of AIN grade 3 (P(trend) < .001). The fractions of HGAIN cases attributable to carcinogenic HPV16/18 targeted by currently licensed bivalent and quadrivalent HPV vaccines ranged from 12% to 61.5%, and the fractions attributable to carcinogenic HPV16/18/31/33/45/52/58 targeted by an investigational nonavalent HPV vaccine ranged from 39% to 89.4%.
          Our analytical framework allows estimation of HGAIN cases attributable to individual HPV genotypes in the context of multiple concurrent HPV infections, which are very common among HIV-infected MSM. Our results suggest that licensed and investigational HPV prophylactic vaccines have the potential to prevent a substantial proportion of HGAIN cases in this population.
JF  - The Journal of infectious diseases
AU  - Sahasrabuddhe, Vikrant V
AU  - Castle, Philip E
AU  - Follansbee, Stephen
AU  - Borgonovo, Sylvia
AU  - Tokugawa, Diane
AU  - Schwartz, Lauren M
AU  - Lorey, Thomas S
AU  - LaMere, Brandon J
AU  - Gage, Julia C
AU  - Fetterman, Barbara
AU  - Boyle, Sean
AU  - Sadorra, Mark
AU  - Tang, Scott Dahai
AU  - Darragh, Teresa M
AU  - Wentzensen, Nicolas
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland 20852, USA. vikrant.sahasrabuddhe@nih.gov
Y1  - 2013/02/01/
PY  - 2013
DA  - 2013 Feb 01
SP  - 392
EP  - 401
VL  - 207
IS  - 3
KW  - Papillomavirus Vaccines
KW  - 0
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Cross-Sectional Studies
KW  - Humans
KW  - Adult
KW  - Neoplasm Grading
KW  - Aged
KW  - Middle Aged
KW  - Male
KW  - Prevalence
KW  - Coinfection
KW  - Genotype
KW  - Sexual Behavior
KW  - Papillomavirus Infections -- epidemiology
KW  - Anus Neoplasms -- prevention & control
KW  - HIV Infections -- complications
KW  - Papillomavirus Infections -- complications
KW  - Carcinoma in Situ -- epidemiology
KW  - Papillomaviridae -- genetics
KW  - Anus Neoplasms -- epidemiology
KW  - Carcinoma in Situ -- virology
KW  - Carcinoma in Situ -- prevention & control
KW  - Anus Neoplasms -- virology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273262351?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+papillomavirus+genotype+attribution+and+estimation+of+preventable+fraction+of+anal+intraepithelial+neoplasia+cases+among+HIV-infected+men+who+have+sex+with+men.&rft.au=Sahasrabuddhe%2C+Vikrant+V%3BCastle%2C+Philip+E%3BFollansbee%2C+Stephen%3BBorgonovo%2C+Sylvia%3BTokugawa%2C+Diane%3BSchwartz%2C+Lauren+M%3BLorey%2C+Thomas+S%3BLaMere%2C+Brandon+J%3BGage%2C+Julia+C%3BFetterman%2C+Barbara%3BBoyle%2C+Sean%3BSadorra%2C+Mark%3BTang%2C+Scott+Dahai%3BDarragh%2C+Teresa+M%3BWentzensen%2C+Nicolas&rft.aulast=Sahasrabuddhe&rft.aufirst=Vikrant&rft.date=2013-02-01&rft.volume=207&rft.issue=3&rft.spage=392&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjis694
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-14
N1  - Date created - 2013-01-07
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
JAMA. 2002 Apr 24;287(16):2114-9 [11966386]
Int J Cancer. 2012 Sep 15;131(6):E946-53 [22419273]
AIDS. 2005 Sep 2;19(13):1407-14 [16103772]
AIDS. 2006 Nov 28;20(18):2337-44 [17117020]
Br J Cancer. 2007 May 7;96(9):1480-3 [17437020]
Curr HIV/AIDS Rep. 2008 May;5(2):78-85 [18510893]
Cancer Epidemiol Biomarkers Prev. 2008 Jul;17(7):1611-22 [18628412]
Int J Cancer. 2009 Apr 1;124(7):1626-36 [19115209]
Dis Colon Rectum. 2009 Feb;52(2):239-47 [19279418]
Lancet Oncol. 2009 Apr;10(4):321-2 [19350698]
Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494]
Cancer Res. 2010 Nov 1;70(21):8578-86 [20959485]
Health Technol Assess. 2010 Nov;14(53):iii-iv, ix-x, 1-101 [21083999]
Lancet Infect Dis. 2010 Dec;10(12):845-52 [21051295]
Cancer Cytopathol. 2011 Feb 25;119(1):5-19 [21319310]
AIDS. 2011 Mar 13;25(5):635-42 [21139488]
Dis Colon Rectum. 2011 Aug;54(8):1003-7 [21730790]
Acta Cytol. 2011;55(4):364-7 [21791907]
J Assoc Nurses AIDS Care. 2011 Nov-Dec;22(6):454-64 [22035525]
MMWR Morb Mortal Wkly Rep. 2011 Dec 23;60(50):1705-8 [22189893]
Clin Infect Dis. 2012 Apr;54(7):1026-34 [22291097]
Lancet Oncol. 2012 May;13(5):438-40 [22445258]
Lancet Oncol. 2012 May;13(5):487-500 [22445259]
J Clin Microbiol. 2003 Mar;41(3):1080-6 [12624033]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/infdis/jis694
ER  - 



TY  - JOUR
T1  - Chlorpromazine-induced hepatotoxicity during inflammation is mediated by TIRAP-dependent signaling pathway in mice
AN  - 1272739648; 17565198
AB  - Inflammation is a major component of idiosyncratic adverse drug reactions (IADRs). To understand the molecular mechanism of inflammation-mediated IADRs, we determined the role of the Toll-like receptor (TLR) signaling pathway in idiosyncratic hepatotoxicity of the anti-psychotic drug, chlorpromazine (CPZ). Activation of TLRs recruits the first adaptor protein, Toll-interleukin 1 receptor domain containing adaptor protein (TIRAP) to the TIR domain of TLRs leading to the activation of the downstream kinase, c-Jun-N-terminal kinase (JNK). Prolonged activation of JNK leads to cell-death. We hypothesized that activation of TLR2 by lipoteichoic acid (LTA) or TLR4 by lipopolysaccharide (LPS) will augment the hepatotoxicity of CPZ by TIRAP-dependent mechanism involving prolonged activation of JNK. Adult male C57BL/6, TIRAP+/+ and TIRAP-/- mice were pretreated with saline, LPS (2mg/kg) or LTA (6mg/kg) for 30min or 16h followed by CPZ (5mg/kg) or saline (vehicle) up to 24h. We found that treatment of mice with CPZ in presence of LPS or LTA leads to ~3-4 fold increase in serum ALT levels, a marked reduction in hepatic glycogen content, significant induction of serum tumor necrosis factor (TNF) alpha and prolonged JNK activation, compared to LPS or LTA alone. Similar results were observed in TIRAP+/+ mice, whereas the effects of LPS or LTA on CPZ-induced hepatotoxicity were attenuated in TIRAP-/- mice. For the first time, we show that inflammation-mediated hepatotoxicity of CPZ is dependent on TIRAP, and involves prolonged JNK activation in vivo. Thus, TIRAP-dependent pathways may be targeted to predict and prevent inflammation-mediated IADRs.
JF  - Toxicology and Applied Pharmacology
AU  - Gandhi, Adarsh
AU  - Guo, Tao
AU  - Shah, Pranav
AU  - Moorthy, Bhagavatula
AU  - Ghose, Romi
AD  - University of Houston, Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, 1441 Moursund Street, Room 517, Houston, TX 77030, USA, adarsh.gandhi@nih.gov
Y1  - 2013/02/01/
PY  - 2013
DA  - 2013 Feb 01
SP  - 430
EP  - 438
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 266
IS  - 3
SN  - 0041-008X, 0041-008X
KW  - Toxicology Abstracts
KW  - Chlorpromazine
KW  - Drugs
KW  - Glycogen
KW  - Inflammation
KW  - Lipopolysaccharides
KW  - Lipoteichoic acid
KW  - Liver
KW  - Molecular modelling
KW  - Signal transduction
KW  - TIRAP protein
KW  - TLR2 protein
KW  - TLR4 protein
KW  - Toll-like receptors
KW  - Tumor necrosis factor
KW  - adaptor proteins
KW  - c-Jun amino-terminal kinase
KW  - hepatotoxicity
KW  - X 24370:Natural Toxins
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272739648?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=Chlorpromazine-induced+hepatotoxicity+during+inflammation+is+mediated+by+TIRAP-dependent+signaling+pathway+in+mice&rft.au=Gandhi%2C+Adarsh%3BGuo%2C+Tao%3BShah%2C+Pranav%3BMoorthy%2C+Bhagavatula%3BGhose%2C+Romi&rft.aulast=Gandhi&rft.aufirst=Adarsh&rft.date=2013-02-01&rft.volume=266&rft.issue=3&rft.spage=430&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/10.1016%2Fj.taap.2012.11.030
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2013-02-08
N1  - SubjectsTermNotLitGenreText - Molecular modelling; c-Jun amino-terminal kinase; Tumor necrosis factor; TLR2 protein; Chlorpromazine; Glycogen; hepatotoxicity; Inflammation; Lipoteichoic acid; adaptor proteins; TIRAP protein; Liver; Lipopolysaccharides; TLR4 protein; Drugs; Toll-like receptors; Signal transduction
DO  - http://dx.doi.org/10.1016/j.taap.2012.11.030
ER  - 



TY  - JOUR
T1  - Chronic clozapine reduces rat brain arachidonic acid metabolism by reducing plasma arachidonic acid availability
AN  - 1272737318; 17563670
AB  - Chronic administration of mood stabilizers to rats down-regulates the brain arachidonic acid (AA) cascade. This down-regulation may explain their efficacy against bipolar disorder (BD), in which brain AA cascade markers are elevated. The atypical antipsychotics, olanzapine (OLZ) and clozapine (CLZ), also act against BD. When given to rats, both reduce brain cyclooxygenase activity and prostaglandin E2 concentration; OLZ also reduces rat plasma unesterified and esterified AA concentrations, and AA incorporation and turnover in brain phospholipid. To test whether CLZ produces similar changes, we used our in vivo fatty acid method in rats given 10 mg/kg/day i.p. CLZ, or vehicle, for 30 days; or 1 day after CLZ washout. [1-14C]AA was infused intravenously for 5 min, arterial plasma was collected and high-energy microwaved brain was analyzed. CLZ increased incorporation coefficients ki* and rates Jin,i of plasma unesterified AA into brain phospholipids i, while decreasing plasma unesterified but not esterified AA. These effects disappeared after washout. Thus, CLZ and OLZ similarly down-regulated kinetics and cyclooxygenase expression of the brain AA cascade, likely by reducing plasma unesterified AA availability. Atypical antipsychotics and mood stabilizers may be therapeutic in BD by down-regulating, indirectly or directly respectively, the elevated brain AA cascade of that disease. The atypical antipsychotic clozapine, like olanzapine, downregulates rat brain arachidonic acid (AA) metabolism (cyclooxygenase activity and PGE2 concentration) by reducing plasma unesterified AA concentration and AA incorporation rate Jin into brain phospholipids. Brain AA incorporation coefficient k* (uptake affinity) is increased. Thus two atypical antipsychotics, like mood stabilizers, may act in bipolar disorder by dampening its upregulated brain AA metabolism.
JF  - Journal of Neurochemistry
AU  - Modi, Hiren R
AU  - Taha, Ameer Y
AU  - Kim, Hyung-Wook
AU  - Chang, Lisa
AU  - Rapoport, Stanley I
AU  - Cheon, Yewon
AD  - Brain Physiology and Metabolism Section. National Institute on AgingLaboratory of Neurosciences, National Institutes of Health
Y1  - 2013/02//
PY  - 2013
DA  - February 2013
SP  - 376
EP  - 387
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 124
IS  - 3
SN  - 0022-3042, 0022-3042
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - olanzapine
KW  - Brain
KW  - Arachidonic acid
KW  - Prostaglandin E2
KW  - Mood
KW  - Bipolar disorder
KW  - Kinetics
KW  - Neuroleptics
KW  - Clozapine
KW  - Fatty acids
KW  - Prostaglandin-endoperoxide synthase
KW  - Metabolism
KW  - Phospholipids
KW  - X 24310:Pharmaceuticals
KW  - N3 11001:Behavioral and Cognitive Neuroscience
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272737318?accountid=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+Neurochemistry&rft.atitle=Chronic+clozapine+reduces+rat+brain+arachidonic+acid+metabolism+by+reducing+plasma+arachidonic+acid+availability&rft.au=Modi%2C+Hiren+R%3BTaha%2C+Ameer+Y%3BKim%2C+Hyung-Wook%3BChang%2C+Lisa%3BRapoport%2C+Stanley+I%3BCheon%2C+Yewon&rft.aulast=Modi&rft.aufirst=Hiren&rft.date=2013-02-01&rft.volume=124&rft.issue=3&rft.spage=376&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurochemistry&rft.issn=00223042&rft_id=info:doi/10.1111%2Fjnc.12078
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - olanzapine; Brain; Arachidonic acid; Prostaglandin E2; Mood; Bipolar disorder; Neuroleptics; Kinetics; Clozapine; Prostaglandin-endoperoxide synthase; Fatty acids; Metabolism; Phospholipids
DO  - http://dx.doi.org/10.1111/jnc.12078
ER  - 



TY  - JOUR
T1  - Endoglin in Amniotic Fluid as a Risk Factor for the Subsequent Development of Bronchopulmonary Dysplasia
AN  - 1272728831; 17563869
AB  - Cross-talk between inflammation and angiogenesis pathways has been recently reported. The objectives of this study were to: (i) examine whether amniotic fluid (AF) concentrations of soluble endoglin (sEng), a protein with anti-angiogenic properties, change during pregnancy, parturition, or intra-amniotic infection and/or inflammation (IAI); (ii) determine whether an increase in sEng in the AF of patients with preterm labor (PTL) and preterm prelabor rupture of membranes (PROM) is associated with adverse neonatal outcomes; and (iii) investigate potential sources of sEng in AF. A cross-sectional study was conducted to include patients in the following groups: (i) mid-trimester (n = 20); (ii) PTL with term delivery (n = 95); (iii) PTL leading to preterm delivery with (n = 40) and without IAI (n = 46); (iv) preterm PROM with (n = 37) and without IAI (n = 37); (v) term in labor (n = 48) and not in labor (n = 44). AF concentrations of sEng were determined by enzyme-linked immunosorbent assay. Chorioamniotic membranes, umbilical cord blood, and AF macrophages were examined for the expression of endoglin. (i) Patients with IAI had a higher median AF concentration of sEng than those without IAI (P = 0.02 for PTL and 0.06 for preterm PROM); (ii) AF concentrations of sEng in the 3rd and 4th quartiles were associated with IAI (OR 2.5 and 7.9, respectively); (iii) an AF sEng concentration greater than or equal to 779.5 pg/mL was associated with bronchopulmonary dysplasia (BPD) (OR 7.9); (iv) endoglin was co-localized with CD14+ macrophages in AF pellets of patients with IAI by immunofluorescence and flow cytometry; and (v) the concentration of sEng in the supernatant was significantly increased after the treatment of macrophages with endotoxin or TNF- alpha . Soluble endoglin participates in the host response against IAI. Activated macrophages may be a source of sEng concentrations in the AF of patients with IAI. An increase of sEng in the AF is associated with BPD and adverse neonatal outcomes.
JF  - American Journal of Reproductive Immunology
AU  - Kim, Sun K
AU  - Romero, Roberto
AU  - Savasan, Zeynep A
AU  - Xu, Yi
AU  - Dong, Zhong
AU  - Lee, Deug-Chan
AU  - Yeo, Lami
AU  - Hassan, Sonia S
AU  - Chaiworapongsa, Tinnakorn
AD  - Perinatology Research Branch. NICHD/NIH/DHHS
Y1  - 2013/02//
PY  - 2013
DA  - Feb 2013
SP  - 105
EP  - 123
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 2
SN  - 1046-7408, 1046-7408
KW  - Risk Abstracts; Immunology Abstracts
KW  - Amniotic fluid
KW  - Angiogenesis
KW  - Dysplasia
KW  - Endoglin
KW  - Endotoxins
KW  - Enzyme-linked immunosorbent assay
KW  - Flow cytometry
KW  - Immunoassays
KW  - Immunofluorescence
KW  - Immunology
KW  - Infection
KW  - Inflammation
KW  - Macrophages
KW  - Membranes
KW  - Neonates
KW  - Parturition
KW  - Pregnancy
KW  - Proteins
KW  - Risk factors
KW  - Rupture
KW  - Tumor necrosis factor- alpha
KW  - Umbilical cord
KW  - R2 23060:Medical and environmental health
KW  - F 06935:Development, Aging & Organ Systems
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272728831?accountid=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+Reproductive+Immunology&rft.atitle=Endoglin+in+Amniotic+Fluid+as+a+Risk+Factor+for+the+Subsequent+Development+of+Bronchopulmonary+Dysplasia&rft.au=Kim%2C+Sun+K%3BRomero%2C+Roberto%3BSavasan%2C+Zeynep+A%3BXu%2C+Yi%3BDong%2C+Zhong%3BLee%2C+Deug-Chan%3BYeo%2C+Lami%3BHassan%2C+Sonia+S%3BChaiworapongsa%2C+Tinnakorn&rft.aulast=Kim&rft.aufirst=Sun&rft.date=2013-02-01&rft.volume=69&rft.issue=2&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Reproductive+Immunology&rft.issn=10467408&rft_id=info:doi/10.1111%2Faji.12046
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2013-02-22
N1  - SubjectsTermNotLitGenreText - Endotoxins; Macrophages; Amniotic fluid; Enzyme-linked immunosorbent assay; Dysplasia; Angiogenesis; Parturition; Rupture; Immunofluorescence; Infection; Umbilical cord; Inflammation; Pregnancy; Flow cytometry; Risk factors; Neonates; Tumor necrosis factor- alpha; Endoglin; Membranes; Immunology; Proteins; Immunoassays
DO  - http://dx.doi.org/10.1111/aji.12046
ER  - 



TY  - JOUR
T1  - Determination of protein concentration for protein-protein conjugates using ultraviolet absorption
AN  - 1268655172; 17491750
AB  - The present study reports a method to determine the total protein concentration or concentration of a protein of interest in a protein-protein conjugate using ultraviolet absorption, after determining the molar ratio of proteins in the conjugates, from which an extinction coefficient can be calculated. A Microsoft Excel solver-based template using amino acid analysis data was developed for determining the molar ratio. The percent mass of each protein in the conjugate is calculated from the amino acid composition data using the least squares method in the Microsoft Excel solver function, and the percent mass is converted to molar portion of each protein using corresponding molecular weight. A molar ratio is obtained by dividing the molar portion of protein 1 by the molar portion of protein 2. A weighted extinction coefficient is calculated using the molar ratio, and the total protein concentration is determined using ultraviolet absorption at 280nm. The accuracy of the method was verified using mixtures of known proteins. The present study provides a rapid, simple and accurate method for determining protein concentration in protein-protein conjugates.
JF  - Journal of Immunological Methods
AU  - Zhu, Daming
AU  - Qian, Feng
AU  - Wu, Yimin
AU  - Jones, David S
AU  - Rowe, Christopher
AU  - Narum, David L
AU  - Duffy, Patrick
AU  - Miller, Louis H
AU  - Saul, Allan
AD  - Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA, dzhu@niaid.nih.gov
Y1  - 2013/01/31/
PY  - 2013
DA  - 2013 Jan 31
SP  - 317
EP  - 321
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 387
IS  - 1-2
SN  - 0022-1759, 0022-1759
KW  - Toxicology Abstracts; Immunology Abstracts
KW  - Concentration of protein-protein conjugate
KW  - Molar ratio
KW  - Microsoft Excel solver
KW  - Amino acid analysis
KW  - Least squares analysis
KW  - U.V. radiation
KW  - Data processing
KW  - Extinction
KW  - Molecular weight
KW  - Amino acid composition
KW  - F 06900:Methods
KW  - X 24300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1268655172?accountid=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+Immunological+Methods&rft.atitle=Determination+of+protein+concentration+for+protein-protein+conjugates+using+ultraviolet+absorption&rft.au=Zhu%2C+Daming%3BQian%2C+Feng%3BWu%2C+Yimin%3BJones%2C+David+S%3BRowe%2C+Christopher%3BNarum%2C+David+L%3BDuffy%2C+Patrick%3BMiller%2C+Louis+H%3BSaul%2C+Allan&rft.aulast=Zhu&rft.aufirst=Daming&rft.date=2013-01-31&rft.volume=387&rft.issue=1-2&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunological+Methods&rft.issn=00221759&rft_id=info:doi/10.1016%2Fj.jim.2012.10.011
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2014-10-02
N1  - SubjectsTermNotLitGenreText - Data processing; U.V. radiation; Extinction; Molecular weight; Amino acid composition
DO  - http://dx.doi.org/10.1016/j.jim.2012.10.011
ER  - 



TY  - JOUR
T1  - Incidental genetic findings in randomized clinical trials: recommendations from the Genomics and Randomized Trials Network (GARNET)
AN  - 1492610114; 18970874
AB  - Recommendations and guidance on how to handle the return of genetic results to patients have offered limited insight into how to approach incidental genetic findings in the context of clinical trials. This paper provides the Genomics and Randomized Trials Network (GARNET) recommendations on incidental genetic findings in the context of clinical trials, and discusses the ethical and practical issues considered in formulating our recommendations. There are arguments in support of as well as against returning incidental genetic findings in clinical trials. For instance, reporting incidental findings in clinical trials may improve the investigator-participant relationship and the satisfaction of participation, but it may also blur the line between clinical care and research. The issues of whether and how to return incidental genetic findings, including the costs of doing so, should be considered when developing clinical trial protocols. Once decided, plans related to sharing individual results from the aim(s) of the trial, as well as incidental findings, should be discussed explicitly in the consent form. Institutional Review Boards (IRBs) and other study-specific governing bodies should be part of the decision as to if, when, and how to return incidental findings, including when plans in this regard are being reconsidered.
JF  - Genome Medicine
AU  - Bookman, Ebony B
AU  - Din-Lovinescu, Corina
AU  - Worrall, Bradford B
AU  - Manolio, Teri A
AU  - Bennett, Siiri N
AU  - Laurie, Cathy
AU  - Mirel, Daniel B
AU  - Doheny, Kimberly F
AU  - Anderson, Garnet L
AU  - Wehr, Kate
AU  - Weinshilboum, Richard
AU  - Chen, Donna T
AD  - National Human Genome Research Institute, 5635 Fishers Lane, Bethesda, MD 20892, USA, ebony.bookman@nih.gov
Y1  - 2013/01/30/
PY  - 2013
DA  - 2013 Jan 30
SP  - 7
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 5
IS  - 1
KW  - Biotechnology and Bioengineering Abstracts; Genetics Abstracts
KW  - Clinical trials
KW  - G 07880:Human Genetics
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492610114?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+Medicine&rft.atitle=Incidental+genetic+findings+in+randomized+clinical+trials%3A+recommendations+from+the+Genomics+and+Randomized+Trials+Network+%28GARNET%29&rft.au=Bookman%2C+Ebony+B%3BDin-Lovinescu%2C+Corina%3BWorrall%2C+Bradford+B%3BManolio%2C+Teri+A%3BBennett%2C+Siiri+N%3BLaurie%2C+Cathy%3BMirel%2C+Daniel+B%3BDoheny%2C+Kimberly+F%3BAnderson%2C+Garnet+L%3BWehr%2C+Kate%3BWeinshilboum%2C+Richard%3BChen%2C+Donna+T&rft.aulast=Bookman&rft.aufirst=Ebony&rft.date=2013-01-30&rft.volume=5&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Genome+Medicine&rft.issn=1756-994X&rft_id=info:doi/10.1186%2Fgm411
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Clinical trials
DO  - http://dx.doi.org/10.1186/gm411
ER  - 



TY  - JOUR
T1  - The study of the core part and non-repeating elements of the O-antigen of Brucella lipopolysaccharide.
AN  - 1273302246; 23261780
AB  - Brucella is an animal and human pathogen that expresses several virulence factors required for host cell invasion and intracellular survival. It produces LPS with unusually low toxicity, which hampers the detection of bacteria by the host immune system and thus provides resistance against intracellular antimicrobial mechanisms of the host. By chemical and spectroscopic methods we determined the structure of the LPS core and of a non-repetitive oligosaccharide fragment at the reducing end of the O-specific polysaccharide. These data should be useful for understanding the biological role of the Brucella LPS.
          Crown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.
JF  - Carbohydrate research
AU  - Kubler-Kielb, Joanna
AU  - Vinogradov, Evgeny
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/01/25/
PY  - 2013
DA  - 2013 Jan 25
SP  - 33
EP  - 37
VL  - 366
KW  - O Antigens
KW  - 0
KW  - Index Medicus
KW  - Brucella -- chemistry
KW  - O Antigens -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273302246?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carbohydrate+research&rft.atitle=The+study+of+the+core+part+and+non-repeating+elements+of+the+O-antigen+of+Brucella+lipopolysaccharide.&rft.au=Kubler-Kielb%2C+Joanna%3BVinogradov%2C+Evgeny&rft.aulast=Kubler-Kielb&rft.aufirst=Joanna&rft.date=2013-01-25&rft.volume=366&rft.issue=&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Carbohydrate+research&rft.issn=1873-426X&rft_id=info:doi/10.1016%2Fj.carres.2012.11.004
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-01-23
N1  - Date created - 2013-01-08
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
FEBS Lett. 1987 Jun 1;216(2):261-4 [3582676]
Biochemistry. 1987 Dec 29;26(26):8717-26 [3442684]
Can J Microbiol. 1987 Nov;33(11):979-81 [3129169]
Infect Immun. 1989 Sep;57(9):2820-8 [2474504]
PLoS Pathog. 2012;8(5):e1002675 [22589715]
Curr Opin Microbiol. 2005 Feb;8(1):60-6 [15694858]
J Biol Chem. 2006 Jun 30;281(26):18135-44 [16632471]
Lancet Infect Dis. 2007 Dec;7(12):775-86 [18045560]
Carbohydr Res. 1998 Jan;306(1-2):283-90 [9691452]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.carres.2012.11.004
ER  - 



TY  - JOUR
T1  - Markedly enhanced permeability and retention effects induced by photo-immunotherapy of tumors.
AN  - 1273771344; 23214407
AB  - A major barrier to cancer treatment is the inability to deliver sufficient concentrations of drug to the tumor without incurring systemic toxicities. Nanomaterials are appealing because they can carry a large drug payload; however, tumor delivery is limited by modest leakage and retention in most tumors. We observed that after photoimmunotherapy (PIT), which is a light-mediated treatment based on an antibody-photosensitizer conjugate, there was surprisingly high leakage of nanosized (10-200 nm) agents into the tumor bed. PIT rapidly induced death in perivascular cancer cells, leading to immediate and dramatic increases in vascular permeability, resulting in up to 24-fold greater accumulation of nanomaterials within the PIT-treated tumor compared with controls, an effect termed "super-enhanced permeability and retention". In a treatment study, PIT followed by liposome-containing daunorubicin, DaunoXome (diameter 50 nm), resulted in greater survival in tumor-bearing mice than either PIT or DaunoXome alone. Thus, PIT greatly enhances delivery of nanosized reagents and thus holds promise to improve therapeutic responses.
JF  - ACS nano
AU  - Sano, Kohei
AU  - Nakajima, Takahito
AU  - Choyke, Peter L
AU  - Kobayashi, Hisataka
AD  - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-1088, USA.
Y1  - 2013/01/22/
PY  - 2013
DA  - 2013 Jan 22
SP  - 717
EP  - 724
VL  - 7
IS  - 1
KW  - Antibiotics, Antineoplastic
KW  - 0
KW  - Nanocapsules
KW  - Photosensitizing Agents
KW  - Daunorubicin
KW  - ZS7284E0ZP
KW  - Index Medicus
KW  - Permeability -- drug effects
KW  - Animals
KW  - Antibiotics, Antineoplastic -- administration & dosage
KW  - Combined Modality Therapy
KW  - Immunotherapy
KW  - Treatment Outcome
KW  - Mice, Nude
KW  - Mice
KW  - Light
KW  - Cell Line, Tumor
KW  - Female
KW  - Daunorubicin -- administration & dosage
KW  - Photosensitizing Agents -- chemistry
KW  - Nanocapsules -- therapeutic use
KW  - Neoplasms, Experimental -- therapy
KW  - Neoplasms, Experimental -- chemistry
KW  - Photosensitizing Agents -- therapeutic use
KW  - Photochemotherapy -- methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273771344?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+nano&rft.atitle=Markedly+enhanced+permeability+and+retention+effects+induced+by+photo-immunotherapy+of+tumors.&rft.au=Sano%2C+Kohei%3BNakajima%2C+Takahito%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Sano&rft.aufirst=Kohei&rft.date=2013-01-22&rft.volume=7&rft.issue=1&rft.spage=717&rft.isbn=&rft.btitle=&rft.title=ACS+nano&rft.issn=1936-086X&rft_id=info:doi/10.1021%2Fnn305011p
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-27
N1  - Date created - 2013-01-22
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Trends Biotechnol. 2006 Jan;24(1):39-47 [16307811]
Adv Drug Deliv Rev. 2005 Dec 14;57(15):2271-86 [16290152]
Nat Rev Cancer. 2006 Aug;6(8):583-92 [16862189]
Clin Cancer Res. 2008 Mar 1;14(5):1296-302 [18316547]
Nat Nanotechnol. 2007 Dec;2(12):751-60 [18654426]
Cancer Res. 2009 Feb 15;69(4):1259-62 [19208831]
Cancer Sci. 2009 Dec;100(12):2426-30 [19793083]
J Control Release. 2010 Mar 19;142(3):296-8 [20074683]
Bioconjug Chem. 2010 May 19;21(5):797-802 [20397686]
Adv Drug Deliv Rev. 2011 Mar 18;63(3):129-30 [20457195]
Nat Med. 2011 Dec;17(12):1685-91 [22057348]
J Control Release. 2012 Dec 10;164(2):138-44 [22595146]
Radiology. 2000 Mar;214(3):787-94 [10715047]
Nat Med. 2003 Mar;9(3):269-77 [12612576]
J Natl Cancer Inst. 1981 Sep;67(3):663-9 [6944536]
J Surg Oncol. 1986 Apr;31(4):229-34 [3724177]
Ann N Y Acad Sci. 1987;507:199-210 [3327413]
AJR Am J Roentgenol. 1989 Jan;152(1):167-73 [2783272]
Cancer Res. 1992 May 1;52(9 Suppl):2747s-2751s [1563006]
Cancer Res. 1992 Jun 15;52(12):3255-61 [1596882]
Lancet. 1993 May 15;341(8855):1242-3 [8098393]
Cancer. 1993 Dec 15;72(12):3671-5 [8252484]
Nat Med. 1998 Jun;4(6):655-7 [9623964]
Nat Biotechnol. 2005 Sep;23(9):1073-8 [16151394]
Cancer Lett. 2006 Jul 28;239(1):129-35 [16198049]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1021/nn305011p
ER  - 



TY  - JOUR
T1  - The Natural Estrogenic Compound Diarylheptanoid (D3): In Vitro Mechanisms of Action and in Vivo Uterine Responses via Estrogen Receptor alpha
AN  - 1660052834; 17970887
AB  - Background: Diarylheptanoid (D3) isolated from the medicinal plant, Curcuma comosa, has estrogenic activity. Objective: We aimed to elucidate the mechanism(s) of D3 action and compare it with that of 17 beta -estradiol (E2) using both in vitro and in vivo uterine models. Methods: We used human uterine (Ishikawa) cells to determine the estrogenic action of D3 on the activation and nuclear translocation of estrogen receptor alpha (ER alpha ). In addition, we further characterized the uterine response to D3 treatment in vivo. Results: D3 activated an estrogen responsive element (ERE) luciferase reporter through ER alpha , and molecular modeling suggested that D3 could be accommodated in the ER alpha binding pocket. Using modified ER alpha to assay ligand-dependent nuclear translocation, we observed D3-dependent ER alpha interaction and translocation. In mouse uteri, early- and late-phase estrogen-regulated gene responses were increased in D3-treated ovariectomized wild-type animals, in a manner similar to that of E2; no response was seen in ER alpha knockout animals. We observed a divergence in estrogen responses after D3 treatment: D3 induced robust DNA synthesis in uterine epithelial cells, linked to an increase in cell-cycle-related genes; however, no increase in uterine weight was observed 24 hr after treatment. D3 also affected uterine progesterone receptor expression patterns similar to E2. When D3 and E2 were administered together, we observed no additive or antagonistic effects of D3 on E2. Our findings suggest that D3 is a weak estrogenic agonist compound. Conclusion: D3 is a weakly acting phytoestrogen that mimics the mitogenic responses produced by E2 in an ER alpha -dependent manner, but it is unable to increase uterine weight or enhance or antagonize the effects of estrogen.
JF  - Environmental Health Perspectives
AU  - Winuthayanon, Wipawee
AU  - Piyachaturawat, Pawinee
AU  - Suksamrarn, Apichart
AU  - Burns, Katherine A
AU  - Arao, Yukitomo
AU  - Hewitt, Sylvia C
AU  - Pedersen, Lars C
AU  - Korach, Kenneth S
AD  - Laboratory of Reproductive and Developmental Toxicology, 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  - 2013/01/18/
PY  - 2013
DA  - 2013 Jan 18
SP  - 433
EP  - 439
PB  - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL  - 121
IS  - 4
SN  - 0091-6765, 0091-6765
KW  - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW  - diarylheptanoid
KW  - ER-dependent
KW  - nuclear translocation
KW  - phytoestrogen
KW  - uterus
KW  - Biomedical materials
KW  - Estrogens
KW  - Biocompatibility
KW  - In vitro testing
KW  - Surgical implants
KW  - In vivo testing
KW  - Receptors
KW  - In vivo tests
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660052834?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=The+Natural+Estrogenic+Compound+Diarylheptanoid+%28D3%29%3A+In+Vitro+Mechanisms+of+Action+and+in+Vivo+Uterine+Responses+via+Estrogen+Receptor+alpha&rft.au=Winuthayanon%2C+Wipawee%3BPiyachaturawat%2C+Pawinee%3BSuksamrarn%2C+Apichart%3BBurns%2C+Katherine+A%3BArao%2C+Yukitomo%3BHewitt%2C+Sylvia+C%3BPedersen%2C+Lars+C%3BKorach%2C+Kenneth+S&rft.aulast=Winuthayanon&rft.aufirst=Wipawee&rft.date=2013-01-18&rft.volume=121&rft.issue=4&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1206122
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Last updated - 2015-05-04
DO  - http://dx.doi.org/10.1289/ehp.1206122
ER  - 



TY  - JOUR
T1  - Drugging topoisomerases: lessons and challenges.
AN  - 1273658702; 23259582
AB  - Topoisomerases are ubiquitous enzymes that control DNA supercoiling and entanglements. They are essential during transcription and replication, and topoisomerase inhibitors are among the most effective and most commonly used anticancer and antibacterial drugs. This review consists of two parts. In the first part ("Lessons"), it gives background information on the catalytic mechanisms of the different enzyme families (6 different genes in humans and 4 in most bacteria), describes the "interfacial inhibition" by which topoisomerase-targeted drugs act as topoisomerase poisons, and describes clinically relevant topoisomerase inhibitors. It generalizes the interfacial inhibition principle, which was discovered from the mechanism of action of topoisomerase inhibitors, and discusses how topoisomerase inhibitors kill cells by trapping topoisomerases on DNA rather than by classical enzymatic inhibition. Trapping protein-DNA complexes extends to a novel mechanism of action of PARP inhibitors and could be applied to the targeting of transcription factors. The second part of the review focuses on the challenges for discovery and precise use of topoisomerase inhibitors, including targeting topoisomerase inhibitors using chemical coupling and encapsulation for selective tumor delivery, use of pharmacodynamic biomarkers to follow drug activity, complexity of the response determinants for anticancer activity and patient selection, prospects of rational combinations with DNA repair inhibitors targeting tyrosyl-DNA-phosphodiesterases 1 and 2 (TDP1 and TDP2) and PARP, and the unmet need to develop inhibitors for type IA enzymes.
JF  - ACS chemical biology
AU  - Pommier, Yves
AD  - Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States. pommier@nih.gov
Y1  - 2013/01/18/
PY  - 2013
DA  - 2013 Jan 18
SP  - 82
EP  - 95
VL  - 8
IS  - 1
KW  - Anti-Bacterial Agents
KW  - 0
KW  - Antineoplastic Agents
KW  - Topoisomerase Inhibitors
KW  - Index Medicus
KW  - Molecular Structure
KW  - Humans
KW  - Drug Delivery Systems
KW  - Topoisomerase Inhibitors -- classification
KW  - Anti-Bacterial Agents -- chemistry
KW  - Anti-Bacterial Agents -- pharmacology
KW  - Topoisomerase Inhibitors -- chemistry
KW  - Antineoplastic Agents -- chemistry
KW  - Antineoplastic Agents -- pharmacology
KW  - Topoisomerase Inhibitors -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273658702?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+chemical+biology&rft.atitle=Drugging+topoisomerases%3A+lessons+and+challenges.&rft.au=Pommier%2C+Yves&rft.aulast=Pommier&rft.aufirst=Yves&rft.date=2013-01-18&rft.volume=8&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=ACS+chemical+biology&rft.issn=1554-8937&rft_id=info:doi/10.1021%2Fcb300648v
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-02
N1  - Date created - 2013-01-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):11014-9 [17578914]
Nature. 2007 Jul 12;448(7150):213-7 [17589503]
Cancer Res. 2007 Sep 15;67(18):8752-61 [17875716]
Cancer Res. 2007 Nov 1;67(21):10397-405 [17974983]
Biochem Pharmacol. 2008 Mar 15;75(6):1262-71 [18061144]
Cancer Res. 2012 Jul 15;72(14):3499-511 [22802077]
J Biol Chem. 2012 Aug 31;287(36):30842-52 [22822062]
Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14634-9 [22908287]
Proc Natl Acad Sci U S A. 2012 Sep 11;109(37):15030-5 [22927417]
Nucleic Acids Res. 2012 Sep 1;40(17):8371-80 [22740648]
Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):16125-30 [22991469]
Cell. 2012 Oct 12;151(2):344-55 [23063124]
Cancer Res. 2012 Nov 1;72(21):5588-99 [23118055]
Nat Struct Mol Biol. 2012 Nov;19(11):1147-54 [23022727]
Nat Med. 2012 Nov;18(11):1639-42 [23104132]
Nat Struct Mol Biol. 2012 Dec;19(12):1363-71 [23104055]
Nat Struct Mol Biol. 2012 Dec;19(12):1372-7 [23104058]
PLoS One. 2012;7(12):e50494 [23284638]
Nat Protoc. 2008;3(11):1736-50 [18927559]
Nat Struct Mol Biol. 2009 Jun;16(6):667-9 [19448616]
Curr Top Med Chem. 2009;9(11):981-98 [19747119]
PLoS One. 2010;5(4):e10186 [20419121]
Chem Biol. 2010 May 28;17(5):421-33 [20534341]
PLoS One. 2010;5(6):e11338 [20596531]
Nat Genet. 2010 Aug;42(8):668-75 [20601956]
Nature. 2010 Aug 19;466(7309):935-40 [20686482]
Nat Rev Drug Discov. 2010 Sep;9(9):665-7 [20811367]
Clin Cancer Res. 2010 Nov 15;16(22):5447-57 [20924131]
Biochem Pharmacol. 2011 Feb 1;81(3):345-54 [20959117]
Invest New Drugs. 2011 Feb;29(1):9-21 [19777159]
Mol Cancer Ther. 2009 May;8(5):1008-14 [19383846]
Proc Natl Acad Sci U S A. 2011 Apr 26;108(17):6939-44 [21482796]
Nucleic Acids Res. 2011 May;39(9):3607-20 [21227924]
Science. 2011 Jul 22;333(6041):459-62 [21778401]
Mol Cancer Ther. 2011 Aug;10(8):1490-9 [21636699]
Expert Opin Ther Pat. 2011 Sep;21(9):1285-92 [21843105]
Eur J Nucl Med Mol Imaging. 2011 Oct;38(10):1832-41 [21660624]
J Cell Biol. 2011 Nov 28;195(5):739-49 [22123861]
Nat Rev Drug Discov. 2012 Jan;11(1):25-36 [22173432]
Curr Cancer Drug Targets. 2011 Oct;11(8):976-86 [21834757]
Nature. 2012 Mar 29;483(7391):570-5 [22460902]
Nature. 2012 Mar 29;483(7391):603-7 [22460905]
J Virol. 2012 May;86(9):5134-50 [22379076]
J Biol Chem. 2012 Apr 13;287(16):12848-57 [22375014]
Proc Natl Acad Sci U S A. 2012 Jun 5;109(23):8989-94 [22615413]
Chem Rev. 2012 Jul 11;112(7):3611-40 [22397403]
Genes Cells. 2001 Aug;6(8):677-87 [11532027]
Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12009-14 [11572945]
Annu Rev Biochem. 2001;70:369-413 [11395412]
Structure. 2002 Feb;10(2):237-48 [11839309]
Nucleic Acids Res. 2002 Mar 1;30(5):1198-204 [11861912]
Biochem Pharmacol. 2002 May 15;63(10):1807-15 [12034365]
Nat Genet. 2002 Oct;32(2):267-72 [12244316]
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13669-74 [12368472]
Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15387-92 [12426403]
J Mol Biol. 2002 Dec 13;324(5):917-32 [12470949]
Chem Biol. 2003 Feb;10(2):139-47 [12618186]
Eur J Biochem. 2003 Oct;270(20):4173-86 [14519130]
Oncogene. 2003 Oct 20;22(47):7296-304 [14576839]
Structure. 2003 Nov;11(11):1349-58 [14604525]
Nature. 2003 Dec 18;426(6968):870-4 [14685245]
Cancer Res. 2004 Feb 1;64(3):1114-21 [14871846]
Proc Natl Acad Sci U S A. 1976 Nov;73(11):3872-6 [186775]
Biochim Biophys Acta. 1978 Jun 22;519(1):23-30 [566561]
Annu Rev Biochem. 1981;50:879-910 [6267993]
Biochemistry. 1981 Nov 10;20(23):6553-63 [6895473]
J Biol Chem. 1982 Aug 10;257(15):8957-63 [7096345]
J Med Chem. 2005 Jul 28;48(15):4803-14 [16033260]
Curr Med Chem Anticancer Agents. 2005 Jul;5(4):421-9 [16101492]
Biochem Soc Trans. 2005 Dec;33(Pt 6):1465-70 [16246147]
J Biol Chem. 2005 Nov 18;280(46):38489-95 [16159875]
Mol Cancer Ther. 2006 Feb;5(2):287-95 [16505102]
Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):8953-8 [16751265]
Science. 2006 Jun 23;312(5781):1798-802 [16794079]
Prog Nucleic Acid Res Mol Biol. 2006;81:179-229 [16891172]
DNA Repair (Amst). 2006 Sep 8;5(9-10):1093-108 [16857431]
Curr Cancer Drug Targets. 2006 Nov;6(7):579-602 [17100565]
J Biol Chem. 2006 Nov 24;281(47):35997-6003 [16973621]
Curr Med Chem. 2006;13(27):3291-305 [17168852]
J Mol Biol. 2007 Apr 20;368(1):105-18 [17331537]
Biochimie. 2007 Apr;89(4):456-67 [17141394]
Biochimie. 2007 Apr;89(4):427-46 [17293019]
J Clin Pathol. 2007 Jul;60(7):768-72 [16882699]
Cancer Res. 1999 Dec 1;59(23):5938-46 [10606239]
Biochem Pharmacol. 2000 Mar 15;59(6):629-38 [10677579]
Prog Nucleic Acid Res Mol Biol. 2000;64:221-53 [10697411]
Br J Cancer. 2001 Jan 5;84(1):106-12 [11139322]
Cancer Res. 2001 May 1;61(9):3535-40 [11325813]
Biochemistry. 1984 Mar 13;23(6):1183-8 [6712942]
J Biol Chem. 1984 Jul 25;259(14):9182-7 [6086625]
Biochemistry. 1984 Jul 3;23(14):3194-201 [6087890]
J Biol Chem. 1984 Nov 10;259(21):13560-6 [6092381]
Science. 1984 Oct 26;226(4673):466-8 [6093249]
Cancer Res. 1985 Jul;45(7):3106-12 [3839166]
J Biol Chem. 1985 Nov 25;260(27):14873-8 [2997227]
Cancer Res. 1987 Jul 15;47(14):3752-6 [3474061]
NCI Monogr. 1987;(4):117-21 [3041238]
Proc Natl Acad Sci U S A. 1988 Oct;85(20):7501-5 [2845409]
Mol Pharmacol. 1988 Dec;34(6):755-60 [2849043]
Cancer Res. 1989 Sep 15;49(18):5016-22 [2548707]
Biochemistry. 1989 Jul 25;28(15):6229-36 [2551367]
Science. 1989 Nov 24;246(4933):1046-8 [2555920]
Nucleic Acids Res. 1990 Nov 25;18(22):6611-9 [2174543]
J Biol Chem. 1991 Oct 25;266(30):20418-23 [1657924]
Nucleic Acids Res. 1991 Nov 11;19(21):5973-80 [1658748]
J Mol Biol. 1991 Dec 20;222(4):909-24 [1662289]
Cancer Res. 1992 Jun 1;52(11):3125-30 [1317259]
J Natl Cancer Inst. 1994 Jun 1;86(11):836-42 [8182764]
Cancer Res. 1995 Feb 15;55(4):753-60 [7850785]
Cancer Res. 1995 May 15;55(10):2097-103 [7743509]
Mol Pharmacol. 1995 May;47(5):907-14 [7538195]
Annu Rev Biochem. 1996;65:635-92 [8811192]
Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11534-9 [8876170]
Mol Pharmacol. 1996 Dec;50(6):1463-71 [8967966]
Cancer Res. 1996 Dec 15;56(24):5533-46 [8971150]
Science. 1998 Mar 6;279(5356):1534-41 [9488652]
Biochimie. 1998 Mar;80(3):235-46 [9615863]
Mol Pharmacol. 1998 Jul;54(1):50-8 [9658189]
Mol Pharmacol. 1998 Jul;54(1):78-85 [9658192]
Biochim Biophys Acta. 1998 Oct 1;1400(1-3):139-54 [9748545]
Biochim Biophys Acta. 1998 Oct 1;1400(1-3):185-94 [9748568]
Biochem Soc Trans. 1999 Feb;27(2):48-53 [10093705]
J Mol Biol. 1999 Sep 24;292(3):685-96 [10497031]
Proc Natl Acad Sci U S A. 1999 Oct 12;96(21):12168-73 [10518594]
Science. 1999 Oct 15;286(5439):552-5 [10521354]
J Med Pharm Chem. 1962 Sep;91:1063-5 [14056431]
Chem Rev. 2005 Feb;105(2):559-92 [15700957]
Trends Pharmacol Sci. 2005 Mar;26(3):138-45 [15749159]
Nature. 2005 Mar 31;434(7033):671-4 [15800630]
J Med Chem. 2005 Apr 7;48(7):2336-45 [15801827]
EMBO J. 2005 Jun 15;24(12):2224-33 [15920477]
Anticancer Agents Med Chem. 2008 May;8(4):381-9 [18473723]
Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9053-8 [18574145]
J Biol Chem. 2008 Jul 25;283(30):21074-83 [18515798]
Q Rev Biophys. 2008 Feb;41(1):41-101 [18755053]
Clin Cancer Res. 2008 Nov 1;14(21):6877-85 [18980982]
Nucleic Acids Res. 2009 Feb;37(3):738-48 [19042970]
Nucleic Acids Res. 2009 Feb;37(3):731-7 [19042977]
Nat Rev Cancer. 2009 May;9(5):327-37 [19377505]
Nat Rev Cancer. 2009 May;9(5):338-50 [19377506]
J Natl Cancer Inst. 2009 May 6;101(9):644-50 [19401546]
Chem Rev. 2009 Jul;109(7):2894-902 [19476377]
Mol Cancer Ther. 2009 Jul;8(7):1878-84 [19584232]
Biochem Biophys Res Commun. 2009 Sep 18;387(2):256-60 [19580783]
Cancer Chemother Pharmacol. 2009 Oct;64(5):1039-46 [19274461]
Nature. 2009 Oct 1;461(7264):674-8 [19794497]
J Biol Chem. 2009 Oct 9;284(41):28084-92 [19666469]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1021/cb300648v
ER  - 



TY  - JOUR
T1  - Roles of alcohol and tobacco exposure in the development of hepatocellular carcinoma.
AN  - 1273751752; 23123447
AB  - The purpose of this report is to summarize the roles of alcohol and tobacco exposure in the development of hepatocellular carcinoma (HCC). Chronic heavy alcohol exposure is a major risk factor for HCC, which is the most frequent type of liver cancer. Alcohol ingestion may initiate and or promote the development of HCC by: 1) acetaldehyde-DNA adduct formation; 2) cytochrome P4502E1-associated reactive oxygen species (ROS) generation , lipid peroxidation, p53 mutation, and conversion of pro-carcinogens to carcinogens; 3) iron accumulation that leads to ROS generation, lipid peroxidation, p53 mutation, and initiation of inflammatory cascade via nuclear factor-KappaB (NF-kB) activation; 4) glutathione depletion leading to oxidative stress; 5) s-adenosylmethionine (SAM) depletion and associated DNA hypomethylation of oncogenes ; 6) retinoic acid depletion and resultant hepatocyte proliferation via up-regulation of activator protein-1 (AP-1); 7) initiating an inflammatory cascade through increased transfer of endotoxin from intestine to liver, Kupffer cell activation via CD14/toll-like receptor-4 (TLR-4), oxidative stress, NF-kB or early growth response-1(Egr-1) activation, and generation of inflammatory cytokines and chemokines; 8) induction of liver fibrosis; and 9) decreasing the number and/or function of natural killer cells. Tobacco exposure is also a risk factor for HCC. It may contribute to the initiation and promotion of HCC due the presence of mutagenic and carcinogenic compounds as well as by causing oxidative stress due to generation of ROS and depletion of endogenous antioxidants. Simultaneous exposure to alcohol and tobacco is expected to promote the development of HCC in an additive and/or synergistic manner.
          Published by Elsevier Inc.
JF  - Life sciences
AU  - Purohit, Vishnudutt
AU  - Rapaka, Rao
AU  - Kwon, Oh Sang
AU  - Song, B J
AD  - Chemistry and Physiological Systems Research Branch, Division of Basic Neuroscience & Behavioral Research, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD 20892, USA. vpurohit@nida.nih.gov
Y1  - 2013/01/17/
PY  - 2013
DA  - 2013 Jan 17
SP  - 3
EP  - 9
VL  - 92
IS  - 1
KW  - Antioxidants
KW  - 0
KW  - Inflammation Mediators
KW  - Reactive Oxygen Species
KW  - Ethanol
KW  - 3K9958V90M
KW  - Index Medicus
KW  - Reactive Oxygen Species -- metabolism
KW  - Ethanol -- adverse effects
KW  - Animals
KW  - Antioxidants -- metabolism
KW  - Risk Factors
KW  - Humans
KW  - Oxidative Stress -- drug effects
KW  - Ethanol -- administration & dosage
KW  - Inflammation Mediators -- metabolism
KW  - Liver Neoplasms -- pathology
KW  - Carcinoma, Hepatocellular -- etiology
KW  - Carcinoma, Hepatocellular -- pathology
KW  - Alcohol Drinking -- adverse effects
KW  - Smoking -- adverse effects
KW  - Liver Neoplasms -- epidemiology
KW  - Liver Neoplasms -- etiology
KW  - Alcohol Drinking -- epidemiology
KW  - Smoking -- epidemiology
KW  - Carcinoma, Hepatocellular -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273751752?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Roles+of+alcohol+and+tobacco+exposure+in+the+development+of+hepatocellular+carcinoma.&rft.au=Purohit%2C+Vishnudutt%3BRapaka%2C+Rao%3BKwon%2C+Oh+Sang%3BSong%2C+B+J&rft.aulast=Purohit&rft.aufirst=Vishnudutt&rft.date=2013-01-17&rft.volume=92&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=1879-0631&rft_id=info:doi/10.1016%2Fj.lfs.2012.10.009
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-02-21
N1  - Date created - 2013-01-01
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Int J Cancer. 1999 May 31;81(5):695-9 [10328218]
J Hepatol. 1999 Sep;31(3):508-13 [10488711]
Biochem Biophys Res Commun. 2004 Dec 3;325(1):97-100 [15522206]
Cancer Res. 1963 Jun;23:667-70 [14032175]
Hepatology. 2005 Feb;41(2):336-44 [15660387]
Alcohol. 2005 Apr;35(3):155-60 [16054976]
Alcohol. 2005 Apr;35(3):187-93 [16054980]
Alcohol. 2005 Apr;35(3):243-9 [16054986]
Alcohol. 2005 Apr;35(3):251-8 [16054987]
Alcohol Clin Exp Res. 2005 Nov;29(11):1959-64 [16340452]
Toxicol Sci. 2006 Feb;89(2):547-53 [16280382]
Int J Cancer. 2006 Mar 15;118(6):1501-7 [16187278]
Int J Cancer. 2006 Apr 15;118(8):1998-2002 [16287084]
Liver Int. 2007 Aug;27(6):735-41 [17617115]
J Biol Chem. 2007 Oct 19;282(42):30452-65 [17724027]
Cancer Sci. 2008 Jan;99(1):93-7 [17956590]
Gastroenterology. 2008 Jan;134(1):248-58 [18166357]
Alcohol. 2008 Aug;42(5):349-61 [18504085]
Nature. 2008 Jul 24;454(7203):436-44 [18650914]
Cancer Lett. 2008 Nov 18;271(1):98-104 [18603357]
J Clin Invest. 2000 Oct;106(7):867-72 [11018074]
Gastroenterology. 2001 Jan;120(1):179-89 [11208727]
Proc Natl Acad Sci U S A. 2001 May 8;98(10):5560-5 [11320206]
Biol Signals Recept. 2001 May-Aug;10(3-4):189-99 [11351128]
Hepatology. 2001 Jul;34(1):101-8 [11431739]
Carcinogenesis. 2001 Aug;22(8):1213-9 [11470752]
J Pharmacol Exp Ther. 2001 Nov;299(2):442-8 [11602653]
Hepatology. 2001 Nov;34(5):935-42 [11679964]
Free Radic Biol Med. 2001 Dec 15;31(12):1544-9 [11744328]
FASEB J. 2002 Jan;16(1):15-26 [11772932]
Gastroenterology. 2002 Feb;122(2):281-9 [11832443]
Chem Res Toxicol. 2002 Mar;15(3):367-72 [11896684]
Int J Cancer. 2002 May 1;99(1):14-21 [11948486]
Virchows Arch. 2002 Apr;440(4):345-52 [11956813]
Alcohol. 2002 May;27(1):3-6 [12062629]
Hepatology. 2002 Jul;36(1):122-34 [12085356]
FASEB J. 2002 Aug;16(10):1292-4 [12060674]
Alcohol. 2002 Jul;27(3):151-4 [12163142]
Alcohol. 2002 Jul;27(3):179-83 [12163147]
Alcohol Clin Exp Res. 2002 Aug;26(8 Suppl):26S-31S [12198371]
Hepatology. 2002 Nov;36(5):1206-13 [12395331]
Carcinogenesis. 2002 Nov;23(11):1781-9 [12419825]
Biochem J. 2002 Dec 1;368(Pt 2):545-53 [12180906]
Nature. 2002 Dec 19-26;420(6917):860-7 [12490959]
J Cancer Res Clin Oncol. 2003 Jun;129(6):355-60 [12759747]
J Pharmacol Exp Ther. 2003 Sep;306(3):941-7 [12750430]
Alcohol. 2003 Jun;30(2):93-7 [12957291]
Alcohol. 2003 Jun;30(2):145-50 [12957299]
Mutat Res. 2003 Dec 10;533(1-2):153-71 [14643418]
Annu Rev Pharmacol Toxicol. 2004;44:239-67 [14744246]
Alcohol Clin Exp Res. 2004 Mar;28(3):385-93 [15084895]
Carcinogenesis. 2004 Jun;25(6):1027-31 [14742317]
Gastroenterology. 2004 Nov;127(5 Suppl 1):S35-50 [15508101]
Gastroenterology. 2004 Nov;127(5 Suppl 1):S79-86 [15508107]
Gastroenterology. 2004 Nov;127(5 Suppl 1):S87-96 [15508108]
N Engl J Med. 1982 Sep 2;307(10):597-601 [7202119]
IARC Monogr Eval Carcinog Risks Hum Suppl. 1987;7:1-440 [3482203]
Carcinogenesis. 1988 May;9(5):761-6 [3365837]
Gastroenterology. 1989 Jul;97(1):140-6 [2542116]
Cancer Res. 1989 Aug 1;49(15):4094-7 [2743304]
Hepatology. 1990 Feb;11(2):165-72 [2307395]
Drug Metab Rev. 1990;22(2-3):147-59 [2272285]
J Clin Immunol. 1991 Sep;11(5):246-53 [1839029]
Cancer Res. 1992 Apr 1;52(7 Suppl):2071s-2077s [1544143]
Cancer Lett. 1992 Mar 15;62(3):205-9 [1596864]
Cancer Res. 1992 Sep 15;52(18):4979-86 [1516054]
Ann N Y Acad Sci. 1993 May 28;686:140-60 [8512245]
Gastroenterology. 1994 Apr;106(4):1085-105 [8143977]
Proc Soc Exp Biol Med. 1994 Mar;205(3):243-7 [8171045]
J Pharmacol Exp Ther. 1994 Nov;271(2):722-9 [7965788]
Gastroenterology. 1995 Jan;108(1):218-24 [7806045]
Carcinogenesis. 1995 Feb;16(2):427-30 [7859377]
Environ Health Perspect. 1994 Nov;102 Suppl 9:49-53 [7698084]
Cancer Res. 1995 May 1;55(9):1894-901 [7794383]
J Clin Invest. 1995 Jul;96(1):620-30 [7615836]
Nat Med. 1996 Apr;2(4):457-60 [8597957]
Alcohol Clin Exp Res. 1996 Nov;20(8):1352-61 [8947310]
Drug Metab Dispos. 1997 Feb;25(2):154-62 [9029045]
Carcinogenesis. 1997 Apr;18(4):627-32 [9111191]
Hepatology. 1997 May;25(5):1096-100 [9141423]
Alcohol Clin Exp Res. 1997 Sep;21(6):974-80 [9309304]
Alcohol Clin Exp Res. 1998 Feb;22(1):192-6 [9514306]
Cancer Res. 1998 Apr 1;58(7):1444-50 [9537246]
J Hepatol. 1998 Apr;28(4):564-71 [9566824]
Hepatology. 1998 Sep;28(3):744-50 [9731567]
J Gastroenterol Hepatol. 1998 Sep;13 Suppl:S39-50 [9792033]
Hepatogastroenterology. 1998 Sep-Oct;45(23):1753-9 [9840141]
Semin Liver Dis. 1998;18(4):389-401 [9875556]
Hepatology. 1999 Mar;29(3):703-9 [10051471]
IUBMB Life. 2001 Sep-Nov;52(3-5):159-64 [11798028]
Environ Res. 2008 Oct;108(2):199-204 [18721919]
Alcohol Clin Exp Res. 2009 Feb;33(2):191-205 [19032584]
Ann N Y Acad Sci. 2009 Feb;1155:206-21 [19250206]
J Clin Oncol. 2009 Mar 20;27(9):1485-91 [19224838]
Semin Liver Dis. 2009 May;29(2):222-32 [19387921]
Hepatology. 2009 Aug;50(2):453-61 [19489076]
J Leukoc Biol. 2009 Sep;86(3):513-28 [19542050]
Int J Epidemiol. 2009 Dec;38(6):1497-511 [19720726]
J Biol Chem. 2010 Aug 6;285(32):24609-19 [20529841]
Cardiovasc Res. 2011 Jun 1;90(3):475-83 [21285293]
J Ethnopharmacol. 2011 Jun 14;136(1):168-77 [21540101]
Br J Cancer. 2011 Oct 25;105(9):1430-5 [21915129]
Gastroenterology. 2011 Nov;141(5):1572-85 [21920463]
Am J Pathol. 2011 Dec;179(6):2866-75 [22093263]
Alcohol Clin Exp Res. 2011 Dec;35(12):2216-25 [21790668]
Alcohol Clin Exp Res. 2012 Apr;36(4):641-53 [22017344]
Food Chem Toxicol. 2012 May;50(5):1194-200 [22365892]
Alcohol Clin Exp Res. 2012 May;36(5):835-46 [22150547]
Med Clin (Barc). 2012 Jun 16;139(2):47-53 [22401725]
Annu Rev Nutr. 2012 Aug 21;32:343-68 [22524187]
Hepatology. 2012 Aug;56(2):769-75 [22378017]
Arch Toxicol. 2012 Sep;86(9):1337-48 [22367091]
Exp Toxicol Pathol. 2013 Jan;65(1-2):165-71 [21924598]
J Gastroenterol Hepatol. 1999 Mar;14(3):202-14 [10197487]
Am J Physiol. 1999 Dec;277(6 Pt 1):G1240-50 [10600822]
Int J Cancer. 2000 Feb 15;85(4):498-502 [10699921]
Am J Physiol Gastrointest Liver Physiol. 2000 Jul;279(1):G178-85 [10898761]
Annu Rev Nutr. 2000;20:395-430 [10940340]
Proc Soc Exp Biol Med. 2000 Sep;224(4):302-8 [10964266]
Neuropharmacology. 2006 Apr;50(5):568-75 [16368115]
Hepatology. 2006 Apr;43(4):872-8 [16502397]
Biol Chem. 2006 Apr;387(4):349-60 [16606331]
Nature. 2006 May 25;441(7092):431-6 [16724054]
Alcohol Clin Exp Res. 2006 Sep;30(9):1615-23 [16930225]
J Gastroenterol Hepatol. 2006 Oct;21 Suppl 3:S3-6 [16958667]
Chem Biol Interact. 2006 Oct 27;163(1-2):54-67 [16600197]
J Gastroenterol Hepatol. 2007 Jun;22 Suppl 1:S1-6 [17567455]
J Gastroenterol Hepatol. 2007 Jun;22 Suppl 1:S53-6 [17567466]
Gastroenterology. 2007 Jun;132(7):2557-76 [17570226]
Toxicol Lett. 2007 Jun 15;171(1-2):78-86 [17543481]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1016/j.lfs.2012.10.009
ER  - 



TY  - JOUR
T1  - Phase 1 trial of IL-15 trans presentation blockade using humanized Mikβ1 mAb in patients with T-cell large granular lymphocytic leukemia.
AN  - 1273661908; 23212516
AB  - In the present study, Hu-Mikβ1, a humanized mAb directed at the shared IL-2/IL-15Rβ subunit (CD122) was evaluated in patients with T-cell large granular lymphocytic (T-LGL) leukemia. Hu-Mikβ1 blocked the trans presentation of IL-15 to T cells expressing IL-2/IL-15Rβ and the common γ-chain (CD132), but did not block IL-15 action in cells that expressed the heterotrimeric IL-15 receptor in cis. There was no significant toxicity associated with Hu-Mikβ1 administration in patients with T-LGL leukemia, but no major clinical responses were observed. One patient who had previously received murine Mikβ1 developed a measurable Ab response to the infused Ab. Nevertheless, the safety profile of this first in-human study of the humanized mAb to IL-2/IL-15Rβ (CD122) supports its evaluation in disorders such as refractory celiac disease, in which IL-15 and its receptor have been proposed to play a critical role in the pathogenesis and maintenance of disease activity.
JF  - Blood
AU  - Waldmann, Thomas A
AU  - Conlon, Kevin C
AU  - Stewart, Donn M
AU  - Worthy, TatYana A
AU  - Janik, John E
AU  - Fleisher, Thomas A
AU  - Albert, Paul S
AU  - Figg, William D
AU  - Spencer, Shawn D
AU  - Raffeld, Mark
AU  - Decker, Jean R
AU  - Goldman, Carolyn K
AU  - Bryant, Bonita R
AU  - Petrus, Michael N
AU  - Creekmore, Stephen P
AU  - Morris, John C
AD  - Metabolism Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20892, USA. tawald@helix.nih.gov
Y1  - 2013/01/17/
PY  - 2013
DA  - 2013 Jan 17
SP  - 476
EP  - 484
VL  - 121
IS  - 3
KW  - Antibodies, Monoclonal
KW  - 0
KW  - Antibodies, Monoclonal, Humanized
KW  - IL2RG protein, human
KW  - Interleukin Receptor Common gamma Subunit
KW  - Interleukin-15
KW  - Interleukin-2 Receptor beta Subunit
KW  - RNA, Messenger
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Animals
KW  - Macaca fascicularis
KW  - Injections, Intravenous
KW  - Humans
KW  - Interleukin-15 -- genetics
KW  - Aged
KW  - Mice
KW  - Cell Line, Tumor
KW  - Interleukin Receptor Common gamma Subunit -- immunology
KW  - RNA, Messenger -- metabolism
KW  - Aged, 80 and over
KW  - Cell Division -- immunology
KW  - Treatment Outcome
KW  - Middle Aged
KW  - Interleukin-15 -- immunology
KW  - Male
KW  - Female
KW  - Antibodies, Monoclonal, Humanized -- adverse effects
KW  - Leukemia, Large Granular Lymphocytic -- immunology
KW  - Leukemia, Large Granular Lymphocytic -- therapy
KW  - Interleukin-2 Receptor beta Subunit -- genetics
KW  - Antibodies, Monoclonal, Humanized -- immunology
KW  - Antibodies, Monoclonal -- adverse effects
KW  - Antibodies, Monoclonal, Humanized -- administration & dosage
KW  - Antibodies, Monoclonal -- administration & dosage
KW  - Interleukin-2 Receptor beta Subunit -- immunology
KW  - Antibodies, Monoclonal -- immunology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273661908?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+1+trial+of+IL-15+trans+presentation+blockade+using+humanized+Mik%CE%B21+mAb+in+patients+with+T-cell+large+granular+lymphocytic+leukemia.&rft.au=Waldmann%2C+Thomas+A%3BConlon%2C+Kevin+C%3BStewart%2C+Donn+M%3BWorthy%2C+TatYana+A%3BJanik%2C+John+E%3BFleisher%2C+Thomas+A%3BAlbert%2C+Paul+S%3BFigg%2C+William+D%3BSpencer%2C+Shawn+D%3BRaffeld%2C+Mark%3BDecker%2C+Jean+R%3BGoldman%2C+Carolyn+K%3BBryant%2C+Bonita+R%3BPetrus%2C+Michael+N%3BCreekmore%2C+Stephen+P%3BMorris%2C+John+C&rft.aulast=Waldmann&rft.aufirst=Thomas&rft.date=2013-01-17&rft.volume=121&rft.issue=3&rft.spage=476&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2012-08-450585
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-12
N1  - Date created - 2013-01-18
N1  - Date revised - 2017-01-14
N1  - Genetic sequence - NCT00076180; ClinicalTrials.gov
N1  - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11445-50 [11016962]
Blood. 2010 Dec 23;116(26):5948-56 [20858854]
J Immunol. 2001 Feb 15;166(4):2602-9 [11160322]
Immunity. 2001 Feb;14(2):105-10 [11239443]
Blood. 2001 Sep 1;98(5):1506-11 [11520801]
Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14559-64 [11717409]
J Immunol. 2002 Jul 1;169(1):460-8 [12077277]
J Neuroimmunol. 2002 Jul;128(1-2):90-4 [12098515]
Blood. 2002 Nov 15;100(10):3633-8 [12393617]
Immunity. 2002 Nov;17(5):537-47 [12433361]
Gastroenterology. 2003 Sep;125(3):730-45 [12949719]
J Immunol. 2004 Sep 15;173(6):3594-8 [15356102]
Immunity. 2004 Sep;21(3):357-66 [15357947]
Blood. 1987 Oct;70(4):1069-72 [3115332]
Neurology. 1988 Aug;38(8):1302-7 [2899862]
Proc Natl Acad Sci U S A. 1989 Mar;86(6):1982-6 [2467293]
Proc Natl Acad Sci U S A. 1989 Dec;86(24):10029-33 [2513570]
J Exp Med. 1993 Mar 1;177(3):741-50 [8094736]
Blood. 1993 Jul 1;82(1):1-14 [8324214]
J Immunol. 1993 Jul 15;151(2):1075-85 [8335891]
Science. 1994 May 13;264(5161):965-8 [8178155]
Proc Natl Acad Sci U S A. 1994 May 24;91(11):4940-4 [8197161]
J Immunol. 1994 Nov 1;153(9):4330-8 [7930631]
EMBO J. 1995 Aug 1;14(15):3654-63 [7641685]
Blood. 1997 Jan 1;89(1):201-11 [8978293]
Nat Med. 1997 Feb;3(2):189-95 [9018238]
Blood. 2001 Jan 1;97(1):14-32 [11133738]
Immunity. 1998 May;8(5):591-9 [9620680]
J Immunol. 1998 Jun 15;160(12):5742-8 [9637483]
Immunity. 1998 Nov;9(5):669-76 [9846488]
Annu Rev Immunol. 1999;17:19-49 [10358752]
Diabetes Res Clin Pract. 2005 Sep;69(3):231-6 [16098919]
Arthritis Rheum. 2005 Sep;52(9):2686-92 [16142748]
Proc Natl Acad Sci U S A. 2006 Jan 10;103(2):401-6 [16387851]
Toxicol Pathol. 2006;34(1):67-74 [16507546]
Gut. 2006 Apr;55(4):469-77 [16105889]
J Exp Med. 2006 May 15;203(5):1343-55 [16682498]
Nat Rev Immunol. 2006 Aug;6(8):595-601 [16868550]
Nat Clin Pract Gastroenterol Hepatol. 2006 Sep;3(9):516-25 [16951668]
Gastroenterology. 2007 Mar;132(3):994-1008 [17324400]
Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16308-13 [18852469]
Toxicol Pathol. 2009 Oct;37(6):814-8 [19706931]
Proc Natl Acad Sci U S A. 2009 Sep 15;106(37):15849-54 [19805228]
Toxicol Pathol. 2010 Feb;38(2):297-302 [20124493]
Toxicol Pathol. 2010 Jun;38(4):642-57 [20448082]
Blood. 2012 Jan 5;119(1):137-43 [22049515]
Am J Surg Pathol. 2012 May;36(5):716-25 [22367293]
N Engl J Med. 2012 May 17;366(20):1905-13 [22591296]
Comment In:
Expert Rev Clin Immunol. 2013 May;9(5):405-8 [23634735]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1182/blood-2012-08-450585
ER  - 



TY  - JOUR
T1  - Modulation of cancer traits by tumor suppressor microRNAs.
AN  - 1273625273; 23325049
AB  - MicroRNAs (miRNAs) are potent post-transcriptional regulators of gene expression. In mammalian cells, miRNAs typically suppress mRNA stability and/or translation through partial complementarity with target mRNAs. Each miRNA can regulate a wide range of mRNAs, and a single mRNA can be regulated by multiple miRNAs. Through these complex regulatory interactions, miRNAs participate in many cellular processes, including carcinogenesis. By altering gene expression patterns, cancer cells can develop specific phenotypes that allow them to proliferate, survive, secure oxygen and nutrients, evade immune recognition, invade other tissues and metastasize. At the same time, cancer cells acquire miRNA signature patterns distinct from those of normal cells; the differentially expressed miRNAs contribute to enabling the cancer traits. Over the past decade, several miRNAs have been identified, which functioned as oncogenic miRNAs (oncomiRs) or tumor-suppressive miRNAs (TS-miRNAs). In this review, we focus specifically on TS-miRNAs and their effects on well-established cancer traits. We also discuss the rising interest in TS-miRNAs in cancer therapy.
JF  - International journal of molecular sciences
AU  - Grammatikakis, Ioannis
AU  - Gorospe, Myriam
AU  - Abdelmohsen, Kotb
AD  - Laboratory of Genetics, National Institute on Aging-Intramural Research Program, National Institutes of Health, 251 Bayview Blvd, Baltimore, MD 21224, USA. abdelmohsenk@mail.nih.gov.
Y1  - 2013/01/16/
PY  - 2013
DA  - 2013 Jan 16
SP  - 1822
EP  - 1842
VL  - 14
IS  - 1
KW  - MicroRNAs
KW  - 0
KW  - RNA, Messenger
KW  - RNA, Neoplasm
KW  - Index Medicus
KW  - Animals
KW  - RNA, Messenger -- metabolism
KW  - Humans
KW  - RNA, Messenger -- genetics
KW  - MicroRNAs -- metabolism
KW  - MicroRNAs -- genetics
KW  - Genes, Tumor Suppressor
KW  - Quantitative Trait Loci
KW  - RNA, Neoplasm -- genetics
KW  - Neoplasms -- genetics
KW  - RNA, Neoplasm -- metabolism
KW  - Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273625273?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+cancer+traits+by+tumor+suppressor+microRNAs.&rft.au=Grammatikakis%2C+Ioannis%3BGorospe%2C+Myriam%3BAbdelmohsen%2C+Kotb&rft.aulast=Grammatikakis&rft.aufirst=Ioannis&rft.date=2013-01-16&rft.volume=14&rft.issue=1&rft.spage=1822&rft.isbn=&rft.btitle=&rft.title=International+journal+of+molecular+sciences&rft.issn=&rft_id=info:doi/10.3390%2Fijms14011822
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2015-09-16
N1  - Date created - 2013-01-17
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Exp Med. 2013 May;13(2):109-17 [22623155]
PLoS One. 2011;6(2):e16403 [21346806]
Cell. 2011 Mar 4;144(5):646-74 [21376230]
Clin Cancer Res. 2011 Mar 15;17(6):1297-305 [21138859]
Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21558-63 [21118985]
J Immunol. 2011 Apr 15;186(8):4716-24 [21383238]
Cancer Biol Ther. 2012 Mar;13(5):281-8 [22310976]
Gastroenterology. 2012 Apr;142(4):886-896.e9 [22240480]
Oncogene. 2012 Apr 12;31(15):1884-95 [21874051]
Nucleic Acids Res. 2012 Apr;40(8):3689-703 [22210864]
Carcinogenesis. 2012 May;33(5):976-85 [22382496]
J Hematol Oncol. 2012;5:13 [22453030]
Int J Cancer. 2000 Jan 15;85(2):176-81 [10629074]
Leukemia. 2000 Aug;14(8):1509-13 [10942251]
Cancer Res. 2000 Dec 15;60(24):6788-93 [11156366]
J Orthod. 2000 Sep;27(3):227-33 [11099555]
Nat Immunol. 2001 Mar;2(3):255-60 [11224526]
Oncogene. 2002 Mar 28;21(14):2161-70 [11948399]
Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853]
Nat Immunol. 2002 Nov;3(11):999-1005 [12407407]
Clin Cancer Res. 2003 Feb;9(2):551-4 [12576417]
Nat Med. 2003 Jun;9(6):677-84 [12778166]
Nat Med. 2003 Oct;9(10):1269-74 [14502282]
Oncogene. 2003 Nov 24;22(53):8568-80 [14634619]
Nat Med. 2004 Jan;10(1):48-54 [14702634]
Nat Rev Cancer. 2004 Feb;4(2):118-32 [14964308]
Tissue Antigens. 2004 Jul;64(1):1-12 [15191517]
Proc Natl Acad Sci U S A. 1996 May 14;93(10):4974-8 [8643514]
Science. 1997 Feb 21;275(5303):1129-32 [9027314]
Cell. 1997 Feb 7;88(3):323-31 [9039259]
Curr Opin Cell Biol. 1999 Apr;11(2):255-60 [10209153]
Mol Endocrinol. 2005 Mar;19(3):644-56 [15550471]
Cancer Res. 2005 Jul 1;65(13):5554-60 [15994927]
J Immunol. 2005 Oct 1;175(7):4583-92 [16177103]
Oncology. 2005;69 Suppl 3:4-10 [16301830]
Cancer Res. 2006 Jun 15;66(12):6288-95 [16778205]
Genes Dev. 2006 Aug 15;20(16):2202-7 [16882971]
Dev Cell. 2006 Oct;11(4):441-50 [17011485]
Mol Cell Biol. 2006 Nov;26(21):8191-201 [16940181]
Cancer Res. 2007 Jan 15;67(2):433-6 [17234748]
J Transl Med. 2010;8:61 [20569470]
Biochim Biophys Acta. 2010 Nov;1803(11):1231-43 [20619301]
Cancer Res. 2010 Sep 15;70(18):7027-30 [20807816]
Cancer Sci. 2010 Oct;101(10):2087-92 [20624164]
Nat Struct Mol Biol. 2010 Oct;17(10):1169-74 [20924405]
BMC Cancer. 2010;10:502 [20858276]
Brain Res. 2010 Nov 4;1359:14-21 [20816946]
Int J Cancer. 2011 Feb 1;128(3):608-16 [20473869]
Cancer. 2010 Dec 15;116(24):5637-49 [20737563]
Eur J Cancer. 2011 Jan;47(1):138-50 [20832293]
Cell Cycle. 2010 Apr 1;9(7):1354-9 [20305372]
Cell Cycle. 2010 Apr 1;9(7):1234 [20404521]
Eur J Cancer. 2011 Jan;47(2):163-74 [21145728]
Mol Cancer. 2011;10:1 [21205300]
PLoS One. 2011;6(5):e20509 [21637828]
Cancer. 2011 Jul 1;117(13):2842-52 [21692045]
PLoS One. 2011;6(6):e20769 [21698099]
Clin Cancer Res. 2011 Jul 15;17(14):4761-71 [21610143]
J Cell Sci. 2011 Sep 1;124(Pt 17):2997-3005 [21878506]
Cancer Res. 2011 Sep 1;71(17):5659-69 [21693658]
J Clin Endocrinol Metab. 2011 Sep;96(9):E1388-98 [21752897]
J Mol Med (Berl). 2011 Oct;89(10):1037-50 [21656380]
Wiley Interdiscip Rev RNA. 2010 Sep-Oct;1(2):214-29 [21935886]
Nat Nanotechnol. 2011 Oct;6(10):668-74 [21892163]
Hepatology. 2011 Nov;54(5):1729-40 [21793034]
Carcinogenesis. 2011 Dec;32(12):1832-9 [21983127]
J Pathol. 2012 Jan;226(1):61-72 [22131135]
Gene Ther. 2011 Dec;18(12):1121-6 [21633392]
Cancer Res. 2011 May 15;71(10):3552-62 [21444677]
Cell Cycle. 2010 Mar 15;9(6):1031-6 [20190569]
Nat Rev Mol Cell Biol. 2011 Jun;12(6):349-61 [21602905]
Cancer Res. 2007 Mar 1;67(5):2098-106 [17332339]
Immunology. 2007 May;121(1):1-14 [17386080]
Mol Cell. 2007 Jun 8;26(5):745-52 [17540599]
Mol Cell. 2007 Sep 21;27(6):992-1004 [17889671]
Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15472-7 [17875987]
Annu Rev Cell Dev Biol. 2007;23:175-205 [17506695]
Clin Cancer Res. 2007 Nov 1;13(21):6247-51 [17975134]
Mol Cell Biol. 2007 Dec;27(23):8284-95 [17908790]
Cancer Res. 2008 May 15;68(10):3697-706 [18483252]
Expert Rev Mol Med. 2008;10:e17 [18549522]
Cancer Res. 2008 Jul 1;68(13):5049-58 [18593903]
J Leukoc Biol. 2008 Oct;84(4):988-93 [18515327]
J Biol Chem. 2008 Nov 28;283(48):33394-405 [18818206]
Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20297-302 [19088191]
Oncogene. 2009 Jan 22;28(3):445-60 [18850005]
Cell. 2009 Jan 23;136(2):215-33 [19167326]
Nat Rev Cancer. 2009 Mar;9(3):153-66 [19238148]
Cancer Res. 2009 Mar 15;69(6):2623-9 [19258506]
Cancer Metastasis Rev. 2009 Jun;28(1-2):151-66 [19153669]
Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1559-65 [19029026]
Proc Natl Acad Sci U S A. 2009 Apr 7;106(14):5761-6 [19307576]
Blood. 2009 Apr 16;113(16):3801-8 [18941118]
Int J Oncol. 2009 Aug;35(2):393-400 [19578755]
Mol Cell. 2009 Sep 11;35(5):610-25 [19748357]
Semin Cancer Biol. 2009 Oct;19(5):329-37 [19482086]
RNA Biol. 2009 Nov-Dec;6(5):575-83 [19875930]
J Pathol. 2010 Feb;220(3):382-91 [19960504]
Genes Dev. 2010 Mar 1;24(5):478-90 [20194440]
Cancer Res. 2010 Apr 1;70(7):2675-85 [20233879]
Physiology (Bethesda). 2010 Apr;25(2):85-101 [20430953]
Cold Spring Harb Perspect Biol. 2009 Dec;1(6):a003129 [20457567]
Annu Rev Biochem. 2010;79:351-79 [20533884]
J Hepatol. 2010 Jul;53(1):57-66 [20447714]
J Mammary Gland Biol Neoplasia. 2010 Jun;15(2):117-34 [20490631]
Aging (Albany NY). 2010 Jun;2(6):333-43 [20606251]
Cancer Res. 2010 Jul 15;70(14):6015-25 [20610624]
Clin Cancer Res. 2011 Dec 15;17(24):7574-83 [21994419]
Nucleic Acids Res. 2012 Jan;40(1):37-52 [21911355]
Oncol Rep. 2012 Mar;27(3):807-12 [22139444]
Nucleic Acids Res. 2012 Jan;40(2):761-74 [21917858]
Br J Cancer. 2012 Jan 17;106(2):405-13 [22068816]
PLoS One. 2012;7(1):e30034 [22276142]
Int J Cancer. 2012 Apr 1;130(7):1620-8 [21557218]
Crit Rev Oncol Hematol. 2012 Feb;81(2):103-22 [21546262]
J Genet Genomics. 2012 Jan;39(1):29-35 [22293115]
Oncol Rep. 2012 Apr;27(4):1097-103 [22139384]
Oncol Rep. 2012 Apr;27(4):1200-6 [22159356]
Neuro Oncol. 2012 Mar;14(3):278-87 [22217655]
J Biochem Mol Toxicol. 2012 Feb;26(2):79-86 [22162084]
Biomarkers. 2012 Mar;17(2):104-10 [22263628]
J Cancer Res Clin Oncol. 2012 Apr;138(4):573-84 [22207524]
Exp Biol Med (Maywood). 2012 Mar;237(3):227-35 [22345301]
PLoS One. 2012;7(3):e32709 [22442669]
Biochem Biophys Res Commun. 2012 Mar 23;419(4):621-6 [22369946]
Expert Opin Ther Targets. 2012 Apr;16 Suppl 2:S103-9 [22443195]
Cancer Discov. 2012 Mar;2(3):270-87 [22585997]
Mol Cell Biol. 2012 Jul;32(13):2530-48 [22547681]
PLoS Genet. 2012;8(6):e1002751 [22685420]
Cell Cycle. 2012 Jun 1;11(11):2137-45 [22592534]
Mol Cancer Ther. 2012 Jul;11(7):1454-66 [22564723]
Stem Cells. 2012 Aug;30(8):1756-70 [22714950]
PLoS Genet. 2012;8(7):e1002797 [22844244]
Prostate. 2012 Sep 15;72(13):1443-52 [22298030]
Technol Cancer Res Treat. 2012 Oct;11(5):483-90 [22568628]
PLoS One. 2012;7(10):e46684 [23056401]
Clin Cancer Res. 2012 Nov 15;18(22):6260-70 [23035210]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.3390/ijms14011822
ER  - 



TY  - JOUR
T1  - Prespecified falsification end points: can they validate true observational associations?
AN  - 1273583027; 23321761
JF  - JAMA
AU  - Prasad, Vinay
AU  - Jena, Anupam B
AD  - Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Y1  - 2013/01/16/
PY  - 2013
DA  - 2013 Jan 16
SP  - 241
EP  - 242
VL  - 309
IS  - 3
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Product Surveillance, Postmarketing
KW  - Sample Size
KW  - Observer Variation
KW  - Research Design
KW  - Causality
KW  - Endpoint Determination
KW  - Fraud
KW  - Drug-Related Side Effects and Adverse Reactions
KW  - Observation
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273583027?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Prespecified+falsification+end+points%3A+can+they+validate+true+observational+associations%3F&rft.au=Prasad%2C+Vinay%3BJena%2C+Anupam+B&rft.aulast=Prasad&rft.aufirst=Vinay&rft.date=2013-01-16&rft.volume=309&rft.issue=3&rft.spage=241&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=1538-3598&rft_id=info:doi/10.1001%2Fjama.2012.96867
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-01-18
N1  - Date created - 2013-01-16
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Comment In:
JAMA. 2013 May 1;309(17):1769-70 [23632712]
JAMA. 2013 May 1;309(17):1770-1 [23632713]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1001/jama.2012.96867
ER  - 



TY  - JOUR
T1  - Sunlight and Other Determinants of Circulating 25-Hydroxyvitamin D Levels in Black and White Participants in a Nationwide US Study
AN  - 1318697817; 17767643
AB  - Circulating 25-hydroxyvitamin D (25(OH)D), a marker for vitamin D status, is associated with bone health and possibly cancers and other diseases; yet, the determinants of 25(OH)D status, particularly ultraviolet radiation (UVR) exposure, are poorly understood. Determinants of 25(OH)D were analyzed in a subcohort of 1,500 participants of the US Radiologic Technologists (USRT) Study that included whites (n = 842), blacks (n = 646), and people of other races/ethnicities (n = 12). Participants were recruited monthly (2008-2009) across age, sex, race, and ambient UVR level groups. Questionnaires addressing UVR and other exposures were generally completed within 9 days of blood collection. The relation between potential determinants and 25(OH)D levels was examined through regression analysis in a random two-thirds sample and validated in the remaining one third. In the regression model for the full study population, age, race, body mass index, some seasons, hours outdoors being physically active, and vitamin D supplement use were associated with 25(OH)D levels. In whites, generally, the same factors were explanatory. In blacks, only age and vitamin D supplement use predicted 25(OH)D concentrations. In the full population, determinants accounted for 25% of circulating 25(OH)D variability, with similar correlations for subgroups. Despite detailed data on UVR and other factors near the time of blood collection, the ability to explain 25(OH)D was modest.
JF  - American Journal of Epidemiology
AU  - Freedman, D Michal
AU  - Cahoon, Elizabeth K
AU  - Rajaraman, Preetha
AU  - Major, Jacqueline M
AU  - Doody, Michele M
AU  - Alexander, Bruce H
AU  - Hoffbeck, Richard W
AU  - Kimlin, Michael G
AU  - Graubard, Barry I
AU  - Linet, Martha S
AD  - Correspondence to Dr. D. Michal Freedman, National Cancer Institute, Division of Cancer Epidemiology and Genetics, NIH, DHHS, EPS Room 7036, 6120 Executive Blvd., Bethesda, MD 20892-7238., mf101e@nih.gov
Y1  - 2013/01/15/
PY  - 2013
DA  - 2013 Jan 15
SP  - 180
EP  - 192
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 2
SN  - 0002-9262, 0002-9262
KW  - Health & Safety Science Abstracts
KW  - Bone
KW  - USA
KW  - Age
KW  - Vitamin D
KW  - Body mass
KW  - Ultraviolet radiation
KW  - Sunlight
KW  - Cancer
KW  - Ethnic groups
KW  - H 8000:Radiation Safety/Electrical Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318697817?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Sunlight+and+Other+Determinants+of+Circulating+25-Hydroxyvitamin+D+Levels+in+Black+and+White+Participants+in+a+Nationwide+US+Study&rft.au=Freedman%2C+D+Michal%3BCahoon%2C+Elizabeth+K%3BRajaraman%2C+Preetha%3BMajor%2C+Jacqueline+M%3BDoody%2C+Michele+M%3BAlexander%2C+Bruce+H%3BHoffbeck%2C+Richard+W%3BKimlin%2C+Michael+G%3BGraubard%2C+Barry+I%3BLinet%2C+Martha+S&rft.aulast=Freedman&rft.aufirst=D&rft.date=2013-01-15&rft.volume=177&rft.issue=2&rft.spage=180&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws223
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2014-06-12
N1  - SubjectsTermNotLitGenreText - Bone; Age; Vitamin D; Body mass; Ultraviolet radiation; Sunlight; Ethnic groups; Cancer; USA
DO  - http://dx.doi.org/10.1093/aje/kws223
ER  - 



TY  - JOUR
T1  - Endometrial Cancer Risk Factors by 2 Main Histologic Subtypes
AN  - 1318697366; 17767642
AB  - On the basis of clinical and pathologic criteria, endometrial carcinoma has been distinguished as Types I (mainly endometrioid) and II (nonendometrioid). Limited data suggest that these subtypes have different risk factor profiles. The authors prospectively evaluated risk factors for Types I (n = 1,312) and II (n = 138) incident endometrial carcinoma among 114,409 women in the National Institutes of Health (NIH)-AARP Diet and Health Study (1995-2006). For individual risk factors, relative risks were estimated with Cox regression by subtype, and P sub(heterogeneity) was assessed in case-case comparisons with Type I as the referent. Stronger relations for Type I versus Type II tumors were seen for menopausal hormone therapy use (relative risk (RR) of 1.18 vs. 0.84; P sub(heterogeneity) = 0.01) and body mass index of greater than or equal to 30 vs. <30 kg/m super(2) (RR of 2.93 vs. 1.83; P sub(heterogeneity) = 0.001). Stronger relations for Type II versus Type I tumors were observed for being black versus white (RR of 2.18 vs. 0.66; P sub(heterogeneity) = 0.0004) and having a family history of breast cancer (RR of 1.93 vs. 0.80; P sub(heterogeneity) = 0.002). Other risk factor associations were similar by subtype. In conclusion, the authors noted different risk factor associations for Types I and II endometrial carcinomas, supporting the etiologic heterogeneity of these tumors. Because of the limited number of Type II cancers, additional evaluation of risk factors will benefit from consortial efforts.
JF  - American Journal of Epidemiology
AU  - Yang, Hannah P
AU  - Wentzensen, Nicolas
AU  - Trabert, Britton
AU  - Gierach, Gretchen L
AU  - Felix, Ashley S
AU  - Gunter, Marc J
AU  - Hollenbeck, Albert
AU  - Park, Yikyung
AU  - Sherman, Mark E
AU  - Brinton, Louise A
AD  - Correspondence to Dr. Hannah P. Yang, National Cancer Institute, 6120 Executive Boulevard, EPS/5030, Rockville, MD 20852., yanghan@mail.nih.gov
Y1  - 2013/01/15/
PY  - 2013
DA  - 2013 Jan 15
SP  - 142
EP  - 151
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 2
SN  - 0002-9262, 0002-9262
KW  - Risk Abstracts
KW  - Diets
KW  - Genetics
KW  - Risk factors
KW  - Body mass
KW  - Breast cancer
KW  - Tumors
KW  - Hormones
KW  - Cancer
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318697366?accountid=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=Endometrial+Cancer+Risk+Factors+by+2+Main+Histologic+Subtypes&rft.au=Yang%2C+Hannah+P%3BWentzensen%2C+Nicolas%3BTrabert%2C+Britton%3BGierach%2C+Gretchen+L%3BFelix%2C+Ashley+S%3BGunter%2C+Marc+J%3BHollenbeck%2C+Albert%3BPark%2C+Yikyung%3BSherman%2C+Mark+E%3BBrinton%2C+Louise+A&rft.aulast=Yang&rft.aufirst=Hannah&rft.date=2013-01-15&rft.volume=177&rft.issue=2&rft.spage=142&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws200
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Diets; Genetics; Body mass; Risk factors; Breast cancer; Tumors; Hormones; Cancer
DO  - http://dx.doi.org/10.1093/aje/kws200
ER  - 



TY  - JOUR
T1  - Structural basis for the specific recognition of dual receptors by the homopolymeric pH 6 antigen (Psa) fimbriae of Yersinia pestis.
AN  - 1273588866; 23277582
AB  - The pH 6 antigen (Psa) of Yersinia pestis consists of fimbriae that bind to two receptors: β1-linked galactosyl residues in glycosphingolipids and the phosphocholine group in phospholipids. Despite the ubiquitous presence of either moiety on the surface of many mammalian cells, Y. pestis appears to prefer interacting with certain types of human cells, such as macrophages and alveolar epithelial cells of the lung. The molecular mechanism of this apparent selectivity is not clear. Site-directed mutagenesis of the consensus choline-binding motif in the sequence of PsaA, the subunit of the Psa fimbrial homopolymer, identified residues that abolish galactosylceramide binding, phosphatidylcholine binding, or both. The crystal structure of PsaA in complex with both galactose and phosphocholine reveals separate receptor binding sites that share a common structural motif, thus suggesting a potential interaction between the two sites. Mutagenesis of this shared structural motif identified Tyr126, which is part of the choline-binding consensus sequence but is found in direct contact with the galactose in the structure of PsaA, important for both receptor binding. Thus, this structure depicts a fimbrial subunit that forms a polymeric adhesin with a unique arrangement of dual receptor binding sites. These findings move the field forward by providing insights into unique types of multiple receptor-ligand interactions and should steer research into the synthesis of dual receptor inhibitor molecules to slow down the rapid progression of plague.
JF  - Proceedings of the National Academy of Sciences of the United States of America
AU  - Bao, Rui
AU  - Nair, Manoj K M
AU  - Tang, Wai-kwan
AU  - Esser, Lothar
AU  - Sadhukhan, Annapurna
AU  - Holland, Robin L
AU  - Xia, Di
AU  - Schifferli, Dieter M
AD  - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Y1  - 2013/01/15/
PY  - 2013
DA  - 2013 Jan 15
SP  - 1065
EP  - 1070
VL  - 110
IS  - 3
KW  - Antigens, Bacterial
KW  - 0
KW  - Bacterial Proteins
KW  - DNA, Bacterial
KW  - Receptors, Cell Surface
KW  - pH 6 antigen, Yersinia
KW  - Phosphorylcholine
KW  - 107-73-3
KW  - Galactose
KW  - X2RN3Q8DNE
KW  - Index Medicus
KW  - Animals
KW  - Models, Molecular
KW  - Humans
KW  - Amino Acid Sequence
KW  - Mice
KW  - Host-Pathogen Interactions
KW  - Virulence
KW  - Static Electricity
KW  - Receptors, Cell Surface -- metabolism
KW  - Mutagenesis, Site-Directed
KW  - Base Sequence
KW  - Plague -- microbiology
KW  - DNA, Bacterial -- genetics
KW  - Galactose -- chemistry
KW  - Molecular Sequence Data
KW  - Crystallography, X-Ray
KW  - Binding Sites -- genetics
KW  - Sequence Homology, Amino Acid
KW  - Phosphorylcholine -- chemistry
KW  - Cell Line
KW  - Bacterial Proteins -- genetics
KW  - Antigens, Bacterial -- metabolism
KW  - Bacterial Proteins -- chemistry
KW  - Fimbriae, Bacterial -- chemistry
KW  - Yersinia pestis -- physiology
KW  - Yersinia pestis -- genetics
KW  - Bacterial Proteins -- metabolism
KW  - Yersinia pestis -- pathogenicity
KW  - Fimbriae, Bacterial -- metabolism
KW  - Antigens, Bacterial -- genetics
KW  - Antigens, Bacterial -- chemistry
KW  - Fimbriae, Bacterial -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273588866?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Structural+basis+for+the+specific+recognition+of+dual+receptors+by+the+homopolymeric+pH+6+antigen+%28Psa%29+fimbriae+of+Yersinia+pestis.&rft.au=Bao%2C+Rui%3BNair%2C+Manoj+K+M%3BTang%2C+Wai-kwan%3BEsser%2C+Lothar%3BSadhukhan%2C+Annapurna%3BHolland%2C+Robin+L%3BXia%2C+Di%3BSchifferli%2C+Dieter+M&rft.aulast=Bao&rft.aufirst=Rui&rft.date=2013-01-15&rft.volume=110&rft.issue=3&rft.spage=1065&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.1212431110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-14
N1  - Date created - 2013-01-16
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - 4F8L; PDB; 4F8O; 4F8N; 4F8P
N1  - SuppNotes - Cited By:
Infect Immun. 2002 Mar;70(3):1453-60 [11854232]
Infect Immun. 2010 Oct;78(10):4134-50 [20679446]
Cell. 2003 May 30;113(5):587-96 [12787500]
Biochem J. 2004 Sep 15;382(Pt 3):769-81 [15214846]
Immunochemistry. 1976 Nov;13(11):945-9 [827496]
Annu Rev Biochem. 1989;58:309-50 [2673013]
Infect Immun. 1990 Aug;58(8):2569-77 [2164509]
Science. 1990 Dec 14;250(4987):1558-60 [2274786]
Mol Microbiol. 1993 Apr;8(2):311-24 [8100346]
J Biol Chem. 1993 Jul 25;268(21):16002-8 [8340421]
Mol Microbiol. 1993 Aug;9(3):507-20 [8105362]
Infect Immun. 1996 Jul;64(7):2483-9 [8698470]
Infect Immun. 1998 Sep;66(9):4545-8 [9712817]
Infect Immun. 2004 Dec;72(12):7212-9 [15557646]
Nat Struct Mol Biol. 2005 Jun;12(6):533-8 [15895092]
Annu Rev Microbiol. 2005;59:69-89 [15847602]
Proc Natl Acad Sci U S A. 2006 Sep 5;103(36):13514-9 [16938880]
Infect Immun. 2006 Oct;74(10):5636-44 [16988239]
Mol Microbiol. 2007 Mar;63(5):1372-84 [17302815]
Infect Immun. 2007 Mar;75(3):1272-9 [17178780]
J Mol Biol. 2007 May 4;368(3):791-9 [17368480]
FEMS Microbiol Rev. 2007 Jul;31(4):478-514 [17576202]
PLoS Med. 2008 Jan 15;5(1):e3 [18198939]
J Bacteriol. 2008 May;190(9):3381-5 [18310330]
J Mol Biol. 2008 May 23;379(1):174-87 [18448124]
J Am Chem Soc. 2008 Nov 5;130(44):14625-33 [18844354]
FEMS Microbiol Rev. 2009 May;33(3):572-86 [19396958]
Proc Natl Acad Sci U S A. 2009 Jun 30;106(26):10793-8 [19515814]
Infect Immun. 2010 Aug;78(8):3443-53 [20498260]
Structure. 2002 Apr;10(4):505-14 [11937055]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1073/pnas.1212431110
ER  - 



TY  - JOUR
T1  - Dietary intake of nitrate and nitrite and risk of renal cell carcinoma in the NIH-AARP Diet and Health Study.
AN  - 1273585434; 23169285
AB  - Nitrate and nitrite are present in many foods and are precursors of N-nitroso compounds, known animal carcinogens and potential human carcinogens. We prospectively investigated the association between nitrate and nitrite intake from dietary sources and risk of renal cell carcinoma (RCC) overall and clear cell and papillary histological subtypes in the NIH-AARP Diet and Health Study.
          Nitrate and nitrite intakes were estimated from a 124-item food frequency questionnaire. Over a mean follow-up of 9 years, we identified 1816 RCC cases (n=498, clear cell; n=115, papillary cell) among 491 841 participants. Cox proportional hazard regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Individuals in the highest quintile of nitrite intake from animal sources compared with those in the lowest quintile, had an increased risk of total RCC and clear cell subtype (HR=1.28, 95% CI, 1.10-1.49 and HR=1.68, 95% CI, 1.25-2.27, respectively). Nitrite from processed meats and other animal sources were associated with increased clear cell adenocarcinoma risk (HR=1.33, 95% CI, 1.01-1.76 and HR=1.78, 95% CI, 1.34-2.36, respectively). We found no association for nitrite intake from plant sources or nitrate intake overall.
          Our findings suggest that nitrite from animal sources may increase the risk of RCC, particularly clear cell adenocarcinomas.
JF  - British journal of cancer
AU  - Dellavalle, C T
AU  - Daniel, C R
AU  - Aschebrook-Kilfoy, B
AU  - Hollenbeck, A R
AU  - Cross, A J
AU  - Sinha, R
AU  - Ward, M H
AD  - Department of Health and Human Services, Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, NIH/DHHS, 6120 Executive Boulevard, EPS 8011, Bethesda, Rockville, MD 20892, USA. dellavallec@mail.nih.gov
Y1  - 2013/01/15/
PY  - 2013
DA  - 2013 Jan 15
SP  - 205
EP  - 212
VL  - 108
IS  - 1
KW  - Nitrates
KW  - 0
KW  - Nitrites
KW  - Index Medicus
KW  - Risk
KW  - Humans
KW  - Adenocarcinoma, Clear Cell -- epidemiology
KW  - Aged
KW  - Middle Aged
KW  - United States -- epidemiology
KW  - Male
KW  - Female
KW  - Meat
KW  - Nitrites -- adverse effects
KW  - Food
KW  - Kidney Neoplasms -- epidemiology
KW  - Nitrates -- adverse effects
KW  - Carcinoma, Renal Cell -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273585434?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dietary+intake+of+nitrate+and+nitrite+and+risk+of+renal+cell+carcinoma+in+the+NIH-AARP+Diet+and+Health+Study.&rft.au=Dellavalle%2C+C+T%3BDaniel%2C+C+R%3BAschebrook-Kilfoy%2C+B%3BHollenbeck%2C+A+R%3BCross%2C+A+J%3BSinha%2C+R%3BWard%2C+M+H&rft.aulast=Dellavalle&rft.aufirst=C&rft.date=2013-01-15&rft.volume=108&rft.issue=1&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2012.522
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-07
N1  - Date created - 2013-01-16
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Epidemiology. 2003 Mar;14(2):183-90 [12606884]
Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517]
Cancer Causes Control. 2003 Oct;14(8):705-14 [14674734]
Int J Cancer. 1981;27(4):471-4 [7275353]
Int J Epidemiol. 1984 Sep;13(3):324-31 [6490303]
Mutat Res. 1988 Dec;202(2):307-24 [3057363]
Cancer Res. 1989 Jun 1;49(11):3117-21 [2720669]
Cancer Res. 1994 Apr 1;54(7 Suppl):1948s-1951s [8137317]
J Natl Cancer Inst. 1994 Aug 3;86(15):1131-9 [8028035]
Eur J Pharmacol. 1994 Nov 1;292(1):1-38 [7867685]
Int J Cancer. 1996 Jan 3;65(1):67-73 [8543399]
Eur J Cancer Prev. 1997 Jun;6(3):226-68 [9306073]
Toxicol Pathol. 1998 Jan-Feb;26(1):104-12 [9502392]
Int J Cancer. 1998 Jul 17;77(2):211-6 [9650554]
JAMA. 1999 May 5;281(17):1628-31 [10235157]
Int J Cancer. 2005 Jan 20;113(3):451-5 [15455348]
Cancer Invest. 2005;23(3):240-55 [15945510]
Mol Nutr Food Res. 2005 Jul;49(7):648-55 [15986387]
Environ Health Perspect. 2005 Nov;113(11):1607-14 [16263519]
Epidemiology. 2006 Jul;17(4):375-82 [16699473]
Cancer Causes Control. 2007 Dec;18(10):1141-51 [17717631]
Public Health Nutr. 2008 Feb;11(2):183-95 [17610761]
Hum Pathol. 2009 Jan;40(1):10-29 [19027455]
J Am Diet Assoc. 2009 Apr;109(4):656-67 [19328261]
Br J Nutr. 2009 Apr;101(8):1228-38 [18786276]
Cancer Detect Prev. 2009;32(5-6):340-51 [19303221]
Nat Rev Urol. 2010 May;7(5):245-57 [20448658]
Int J Cancer. 2011 Jul 1;129(1):160-72 [20824705]
Am J Clin Nutr. 2012 Jan;95(1):155-62 [22170360]
Br J Nutr. 1999 May;81(5):349-58 [10615207]
Epidemiology. 2001 May;12(3):327-38 [11338313]
Cancer Detect Prev. 2003;27(2):116-21 [12670522]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/bjc.2012.522
ER  - 



TY  - JOUR
T1  - CYP2E1-dependent elevation of serum cholesterol, triglycerides, and hepatic bile acids by isoniazid
AN  - 1268651532; 17497664
AB  - Isoniazid is the first-line medication in the prevention and treatment of tuberculosis. Isoniazid is known to have a biphasic effect on the inhibition-induction of CYP2E1 and is also considered to be involved in isoniazid-induced hepatotoxicity. However, the full extent and mechanism of involvement of CYP2E1 in isoniazid-induced hepatotoxicity remain to be thoroughly investigated. In the current study, isoniazid was administered to wild-type and Cyp2e1-null mice to investigate the potential toxicity of isoniazid in vivo. The results revealed that isoniazid caused no hepatotoxicity in wild-type and Cyp2e1-null mice, but produced elevated serum cholesterol and triglycerides, and hepatic bile acids in wild-type mice, as well as decreased abundance of free fatty acids in wild-type mice and not in Cyp2e1-null mice. Metabolomic analysis demonstrated that production of isoniazid metabolites was elevated in wild-type mice along with a higher abundance of bile acids, bile acid metabolites, carnitine and carnitine derivatives; these were not observed in Cyp2e1-null mice. In addition, the enzymes responsible for bile acid synthesis were decreased and proteins involved in bile acid transport were significantly increased in wild-type mice. Lastly, treatment of targeted isoniazid metabolites to wild-type mice led to similar changes in cholesterol, triglycerides and free fatty acids. These findings suggest that while CYP2E1 is not involved in isoniazid-induced hepatotoxicity, while an isoniazid metabolite might play a role in isoniazid-induced cholestasis through enhancement of bile acid accumulation and mitochondria beta -oxidation.
JF  - Toxicology and Applied Pharmacology
AU  - Cheng, Jie
AU  - Krausz, Kristopher W
AU  - Li, Feng
AU  - Ma, Xiaochao
AU  - Gonzalez, Frank J
AD  - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, fjgonz@helix.nih.gov
Y1  - 2013/01/15/
PY  - 2013
DA  - 2013 Jan 15
SP  - 245
EP  - 253
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 266
IS  - 2
SN  - 0041-008X, 0041-008X
KW  - Toxicology Abstracts
KW  - Abundance
KW  - Bile acids
KW  - Carnitine
KW  - Cholestasis
KW  - Cholesterol
KW  - Enzymes
KW  - Fatty acids
KW  - Isoniazid
KW  - Liver
KW  - Metabolites
KW  - Mitochondria
KW  - Toxicity
KW  - Triglycerides
KW  - Tuberculosis
KW  - hepatotoxicity
KW  - metabolomics
KW  - Mycobacterium
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1268651532?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=CYP2E1-dependent+elevation+of+serum+cholesterol%2C+triglycerides%2C+and+hepatic+bile+acids+by+isoniazid&rft.au=Cheng%2C+Jie%3BKrausz%2C+Kristopher+W%3BLi%2C+Feng%3BMa%2C+Xiaochao%3BGonzalez%2C+Frank+J&rft.aulast=Cheng&rft.aufirst=Jie&rft.date=2013-01-15&rft.volume=266&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/10.1016%2Fj.taap.2012.10.024
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2013-02-08
N1  - SubjectsTermNotLitGenreText - Cholestasis; Abundance; Mitochondria; Enzymes; Metabolites; Cholesterol; Toxicity; hepatotoxicity; Triglycerides; Bile acids; Fatty acids; Liver; Tuberculosis; metabolomics; Carnitine; Isoniazid; Mycobacterium
DO  - http://dx.doi.org/10.1016/j.taap.2012.10.024
ER  - 



TY  - JOUR
T1  - RNA polymerase III mutants in TFIIFα-like C37 that cause terminator readthrough with no decrease in transcription output.
AN  - 1273708249; 23093604
AB  - How eukaryotic RNA polymerases switch from elongation to termination is unknown. Pol III subunits Rpc53 and Rpc37 (C53/37) form a heterodimer homologous to TFIIFβ/α. C53/37 promotes efficient termination and together with C11 also mediates pol III recycling in vitro. We previously developed Schizosaccharomyces pombe strains that report on two pol III termination activities: RNA oligo(U) 3'-end cleavage, and terminator readthrough. We randomly mutagenized C53 and C37 and isolated many C37 mutants with terminator readthrough but no comparable C53 mutants. The majority of C37 mutants have strong phenotypes with up to 40% readthrough and map to a C-terminal tract previously localized near Rpc2p in the pol III active center while a minority represent a distinct class with weaker phenotype, less readthrough and 3'-oligo(U) lengthening. Nascent pre-tRNAs released from a terminator by C37 mutants have shorter 3'-oligo(U) tracts than in cleavage-deficient C11 double mutants indicating RNA 3'-end cleavage during termination. We asked whether termination deficiency affects transcription output in the mutants in vivo both by monitoring intron-containing nascent transcript levels and (14)C-uridine incorporation. Surprisingly, multiple termination mutants have no decrease in transcript output relative to controls. These data are discussed in context of current models of pol III transcription.
JF  - Nucleic acids research
AU  - Rijal, Keshab
AU  - Maraia, Richard J
AD  - Intramural Research Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Y1  - 2013/01/07/
PY  - 2013
DA  - 2013 Jan 07
SP  - 139
EP  - 155
VL  - 41
IS  - 1
KW  - Oligonucleotides
KW  - 0
KW  - Protein Subunits
KW  - Schizosaccharomyces pombe Proteins
KW  - RNA, Transfer
KW  - 9014-25-9
KW  - RNA Polymerase III
KW  - EC 2.7.7.6
KW  - Index Medicus
KW  - Protein Subunits -- genetics
KW  - Sequence Alignment
KW  - RNA, Transfer -- genetics
KW  - RNA, Transfer -- biosynthesis
KW  - Molecular Sequence Data
KW  - Catalytic Domain
KW  - RNA Cleavage
KW  - Transcription, Genetic
KW  - Amino Acid Sequence
KW  - Oligonucleotides -- metabolism
KW  - Mutation
KW  - Genes, Suppressor
KW  - Schizosaccharomyces -- genetics
KW  - Transcription Termination, Genetic
KW  - Schizosaccharomyces pombe Proteins -- genetics
KW  - Schizosaccharomyces -- enzymology
KW  - RNA Polymerase III -- metabolism
KW  - RNA Polymerase III -- genetics
KW  - RNA Polymerase III -- chemistry
KW  - Schizosaccharomyces pombe Proteins -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273708249?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=RNA+polymerase+III+mutants+in+TFIIF%CE%B1-like+C37+that+cause+terminator+readthrough+with+no+decrease+in+transcription+output.&rft.au=Rijal%2C+Keshab%3BMaraia%2C+Richard+J&rft.aulast=Rijal&rft.aufirst=Keshab&rft.date=2013-01-07&rft.volume=41&rft.issue=1&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgks985
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-22
N1  - Date created - 2012-12-28
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Biol Chem. 2000 Sep 15;275(37):29076-81 [10843998]
J Biol Chem. 1994 Sep 16;269(37):23374-81 [8083243]
EMBO J. 2000 Dec 15;19(24):6823-32 [11118217]
Mol Cell. 2002 May;9(5):1113-23 [12049746]
Genes Dev. 2002 Oct 15;16(20):2593-620 [12381659]
Mol Cell. 2002 Dec;10(6):1489-94 [12504022]
Nucleic Acids Res. 2003 Apr 15;31(8):2108-16 [12682361]
Proc Natl Acad Sci U S A. 1995 May 23;92(11):4738-42 [7761393]
Cell. 1996 Jan 26;84(2):245-52 [8565070]
J Mol Biol. 1996 Feb 2;255(4):589-603 [8568899]
Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3383-7 [8622944]
Cell. 1997 Mar 7;88(5):707-15 [9054510]
RNA. 1997 Dec;3(12):1434-43 [9404894]
J Mol Biol. 1998 May 1;278(2):307-16 [9571053]
Mol Cell. 1998 Apr;1(5):749-57 [9660958]
Genes Dev. 1998 Dec 15;12(24):3857-71 [9869639]
Cold Spring Harb Symp Quant Biol. 1998;63:381-9 [10384303]
J Biol Chem. 1999 Jul 23;274(30):21342-8 [10409694]
Mol Cell Biol. 2005 Jan;25(2):621-36 [15632064]
Nat Rev Mol Cell Biol. 2005 Jan;6(1):69-78 [15688068]
EMBO J. 2006 Jan 11;25(1):118-28 [16362040]
Nat Struct Mol Biol. 2006 Jul;13(7):611-8 [16799560]
Curr Biol. 2006 Oct 10;16(19):R849-51 [17027482]
PLoS One. 2006;1:e134 [17205138]
Trends Biochem Sci. 2007 Feb;32(2):51-3 [17174096]
Mol Cell. 2007 Mar 23;25(6):813-23 [17386259]
Mol Cell Biol. 2007 May;27(9):3303-12 [17308035] J Biol Chem. 2008 Dec 26;283(52):36108-17 [18974046]
Nat Struct Mol Biol. 2009 Apr;16(4):430-7 [19287396]
Genes Dev. 2009 Jun 1;23(11):1247-69 [19487567]
Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14265-70 [19706510]
J Biol Chem. 2010 Jan 22;285(4):2695-706 [19940126]
RNA. 2010 Apr;16(4):673-95 [20181738]
Mol Biol Evol. 2010 May;27(5):1035-43 [20026480]
Mol Cell. 2010 Aug 27;39(4):583-94 [20797630]
Cell. 2010 Oct 1;143(1):59-70 [20887893]
EMBO J. 2010 Nov 17;29(22):3762-72 [20967027]
Mol Cell Biol. 2011 Jul;31(13):2715-28 [21536656]
Nucleic Acids Res. 2011 Jun;39(11):4728-42 [21317186]
Nat Rev Mol Cell Biol. 2011 Aug;12(8):483-92 [21779025]
Nucleic Acids Res. 2011 Jul;39(13):5499-512 [21421562]
Nucleic Acids Res. 2011 Aug;39(14):6100-13 [21450810]
J Biol Chem. 2011 Nov 11;286(45):39478-88 [21940626]
Mol Biol Cell. 2012 Feb;23(3):480-91 [22160596]
Wiley Interdiscip Rev RNA. 2011 May-Jun;2(3):362-75 [21572561]
Genome Res. 2012 Apr;22(4):666-80 [22287103]
RNA. 2012 Jul;18(7):1358-72 [22586155]
Cell. 2012 Jun 22;149(7):1438-45 [22726433]
Nature. 1969 Oct 18;224(5216):234-7 [5344598]
Proc Natl Acad Sci U S A. 2004 Sep 14;101(37):13442-7 [15347814]
Cell. 1980 Sep;21(2):509-16 [7407924]
Nature. 1980 Oct 23;287(5784):750-2 [6253814]
Nucleic Acids Res. 1984 Jan 25;12(2):1101-15 [6320115]
EMBO J. 1985 Oct;4(10):2657-64 [3902472]
EMBO J. 1989 Mar;8(3):841-50 [2498086]
EMBO J. 1989 Mar;8(3):851-61 [2470590]
Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1453-7 [1741399]
Mol Cell Biol. 1992 May;12(5):2260-72 [1314952]
Cell. 1992 May 15;69(4):685-96 [1586947]
Gene. 1993 Jan 15;123(1):127-30 [8422996]
Mol Cell Biol. 1994 Mar;14(3):2147-58 [8114745]
J Biol Chem. 1994 Apr 1;269(13):10050-60 [8144504]
Mol Cell. 2000 Aug;6(2):339-48 [10983981]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/nar/gks985
ER  - 



TY  - CPAPER
T1  - The Metadata Access Tool for Climate and Health: a new resource for assessing health impacts of climate change
T2  - 93rd American Meteorological Society Annual Meeting (AMS 2013)
AN  - 1369230223; 6216076
JF  - 93rd American Meteorological Society Annual Meeting (AMS 2013)
AU  - Balbus, John
AU  - Trtanj, J
Y1  - 2013/01/06/
PY  - 2013
DA  - 2013 Jan 06
KW  - Climatic changes
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1369230223?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=93rd+American+Meteorological+Society+Annual+Meeting+%28AMS+2013%29&rft.atitle=The+Metadata+Access+Tool+for+Climate+and+Health%3A+a+new+resource+for+assessing+health+impacts+of+climate+change&rft.au=Balbus%2C+John%3BTrtanj%2C+J&rft.aulast=Balbus&rft.aufirst=John&rft.date=2013-01-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=93rd+American+Meteorological+Society+Annual+Meeting+%28AMS+2013%29&rft.issn=&rft_id=info:doi/
L2  - https://ams.confex.com/ams/93Annual/webprogram/meeting.html#
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-31
N1  - Last updated - 2013-06-19
ER  - 



TY  - JOUR
T1  - Psychoactive "bath salts": not so soothing.
AN  - 1273294995; 23178799
AB  - Recently there has been a dramatic rise in the abuse of so-called "bath salts" products that are purchased as legal alternatives to illicit drugs like cocaine and 3,4-methylenedioxymethamphetamine (MDMA). Baths salts contain one or more synthetic derivatives of the naturally-occurring stimulant cathinone. Low doses of bath salts produce euphoria and increase alertness, but high doses or chronic use can cause serious adverse effects such as hallucinations, delirium, hyperthermia and tachycardia. Owing to the risks posed by bath salts, the governments of many countries have made certain cathinones illegal, namely: 4-methylmethcathinone (mephedrone), 3,4-methylenedioxymethcathinone (methylone) and 3,4-methylenedioxypyrovalerone (MDPV). Similar to other psychomotor stimulants, synthetic cathinones target plasma membrane transporters for dopamine (i.e., DAT), norepinephrine (i.e., NET) and serotonin (i.e, SERT). Mephedrone and methylone act as non-selective transporter substrates, thereby stimulating non-exocytotic release of dopamine, norepinephrine and serotonin. By contrast, MDPV acts as a potent blocker at DAT and NET, with little effect at SERT. Administration of mephedrone or methylone to rats increases extracellular concentrations of dopamine and serotonin in the brain, analogous to the effects of MDMA. Not surprisingly, synthetic cathinones elicit locomotor activation in rodents. Stimulation of dopamine transmission by synthetic cathinones predicts a high potential for addiction and may underlie clinical adverse effects. As popular synthetic cathinones are rendered illegal, new replacement cathinones are appearing in the marketplace. More research on the pharmacology and toxicology of abused cathinones is needed to inform public health policy and develop strategies for treating medical consequence of bath salts abuse. Published by Elsevier B.V.
JF  - European journal of pharmacology
AU  - Baumann, Michael H
AU  - Partilla, John S
AU  - Lehner, Kurt R
AD  - Medicinal Chemistry Section, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Suite 4500, Baltimore, MD 21224, USA. mbaumann@mail.nih.gov
Y1  - 2013/01/05/
PY  - 2013
DA  - 2013 Jan 05
SP  - 1
EP  - 5
VL  - 698
IS  - 1-3
KW  - Alkaloids
KW  - 0
KW  - Catecholamine Plasma Membrane Transport Proteins
KW  - Central Nervous System Stimulants
KW  - Psychotropic Drugs
KW  - cathinone
KW  - 540EI4406J
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Catecholamine Plasma Membrane Transport Proteins -- metabolism
KW  - Central Nervous System Stimulants -- pharmacology
KW  - Psychotropic Drugs -- toxicity
KW  - Baths
KW  - Central Nervous System Stimulants -- toxicity
KW  - Alkaloids -- adverse effects
KW  - Psychotropic Drugs -- pharmacology
KW  - Alkaloids -- toxicity
KW  - Alkaloids -- pharmacology
KW  - Psychotropic Drugs -- adverse effects
KW  - Central Nervous System Stimulants -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273294995?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Psychoactive+%22bath+salts%22%3A+not+so+soothing.&rft.au=Baumann%2C+Michael+H%3BPartilla%2C+John+S%3BLehner%2C+Kurt+R&rft.aulast=Baumann&rft.aufirst=Michael&rft.date=2013-01-05&rft.volume=698&rft.issue=1-3&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=1879-0712&rft_id=info:doi/10.1016%2Fj.ejphar.2012.11.020
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-10
N1  - Date created - 2013-01-01
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Pharmacol Exp Ther. 2003 Oct;307(1):138-45 [12954796]
J Med Toxicol. 2012 Mar;8(1):33-42 [22108839]
J Med Toxicol. 2012 Mar;8(1):69-75 [22271565]
J Med Toxicol. 2012 Mar;8(1):15-32 [22271566]
J Neurochem. 2012 Mar;120(6):1097-107 [22191803]
Neuropsychopharmacology. 2012 Apr;37(5):1192-203 [22169943]
Toxicol Lett. 2012 Jun 1;211(2):144-9 [22459606]
J Anal Toxicol. 2012 Jul;36(6):360-71 [22586208]
Ann Emerg Med. 2012 Jul;60(1):103-5 [22387085]
Br J Pharmacol. 2012 Sep;167(2):407-20 [22509960]
PLoS One. 2012;7(8):e44652 [22952999]
Am J Drug Alcohol Abuse. 2012 Nov;38(6):616-7 [22783894]
Neurotoxicology. 2012 Oct;33(5):1305-13 [22922498]
Drug Alcohol Depend. 2012 Nov 1;126(1-2):257-62 [22652295]
Drug Alcohol Depend. 2012 Nov 1;126(1-2):168-75 [22664136]
Br J Pharmacol. 2013 Jan;168(2):458-70 [22897747]
Neuropsychopharmacology. 2013 Mar;38(4):552-62 [23072836]
Drug Test  Anal. 2013 Feb;5(2):130-2 [22611039]
Addict Biol. 2014 Mar;19(2):165-74 [22784198]
Synapse. 2001 Jan;39(1):32-41 [11071707]
Pharmacol Biochem Behav. 1987 Mar;26(3):547-51 [3575369]
Pharmacol Toxicol. 1992 Feb;70(2):77-86 [1508843]
Eur J Pharmacol. 1994 Nov 3;264(3):391-8 [7698180]
J Forensic Sci. 1997 Jan;42(1):25-31 [8988571]
Eur J Pharmacol. 1999 Sep 17;381(1):63-9 [10528135]
J Med Chem. 2006 Feb 23;49(4):1420-32 [16480278]
Xenobiotica. 2006 Aug;36(8):709-23 [16891251]
Psychopharmacology (Berl). 2007 Jan;189(4):407-24 [16541247]
Annu Rev Pharmacol Toxicol. 2007;47:681-98 [17209801]
Eur J Pharmacol. 2007 Mar 22;559(2-3):132-7 [17223101]
Biochem Pharmacol. 2008 Jan 1;75(1):196-217 [17825265]
Neurotox Res. 2008 Oct;14(2-3):169-83 [19073424]
Forensic Sci Int. 2009 Sep 10;190(1-3):e13-9 [19541436]
J Neurochem. 2010 Jan;112(2):340-55 [19891736]
Drug Test  Anal. 2010 Aug;2(8):377-82 [20687197]
J Mass Spectrom. 2010 Dec;45(12):1426-42 [21053377]
Psychopharmacology (Berl). 2011 Apr;214(3):593-602 [21072502]
Forensic Sci Int. 2011 Mar 20;206(1-3):e93-5 [21227604]
J Anal Toxicol. 2011 Apr;35(3):188-91 [21439157]
MMWR Morb Mortal Wkly Rep. 2011 May 20;60(19):624-7 [21597456]
Emerg Med J. 2011 Aug;28(8):686-9 [20798084]
Clin Toxicol (Phila). 2011 Jul;49(6):499-505 [21824061]
N Engl J Med. 2011 Sep 8;365(10):967-8 [21899474]
J Pharmacol Exp Ther. 2011 Nov;339(2):530-6 [21810934]
Fed Regist. 2011 Oct 21;76(204):65371-5 [22016903]
Gen Hosp Psychiatry. 2011 Nov-Dec;33(6):640.e5-6 [21749840]
Br J Pharmacol. 2011 Dec;164(8):1949-58 [21615721]
Eur Neuropsychopharmacol. 2012 Mar;22(3):231-6 [21824752]
J Miss State Med Assoc. 2011 Dec;52(12):375-7 [22329114]
Addict Biol. 2012 Mar;17(2):409-22 [21995495]
Am J Drug Alcohol Abuse. 2012 Mar;38(2):176-80 [22221190]
Eur J Pharmacol. 2003 Oct 31;479(1-3):23-40 [14612135]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.ejphar.2012.11.020
ER  - 



TY  - JOUR
T1  - Early-life prevention of non-communicable diseases.
AN  - 1273257655; 23290956
JF  - Lancet (London, England)
AU  - Balbus, John M
AU  - Barouki, Robert
AU  - Birnbaum, Linda S
AU  - Etzel, Ruth A
AU  - Gluckman, Peter D
AU  - Grandjean, Philippe
AU  - Hancock, Christine
AU  - Hanson, Mark A
AU  - Heindel, Jerrold J
AU  - Hoffman, Kate
AU  - Jensen, Génon K
AU  - Keeling, Ann
AU  - Neira, Maria
AU  - Rabadán-Diehl, Cristina
AU  - Ralston, Johanna
AU  - Tang, Kwok-Cho
AD  - National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD 20892, USA. john.balbus@nih.gov
Y1  - 2013/01/05/
PY  - 2013
DA  - 2013 Jan 05
SP  - 3
EP  - 4
VL  - 381
IS  - 9860
KW  - Environmental Pollutants
KW  - 0
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Humans
KW  - Epigenesis, Genetic
KW  - Female
KW  - Environmental Pollutants -- adverse effects
KW  - Pregnancy
KW  - Diabetes Mellitus -- prevention & control
KW  - Pulmonary Disease, Chronic Obstructive -- prevention & control
KW  - Prenatal Care
KW  - Neoplasms -- prevention & control
KW  - Cardiovascular Diseases -- prevention & control
KW  - Prenatal Exposure Delayed Effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273257655?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+%28London%2C+England%29&rft.atitle=Early-life+prevention+of+non-communicable+diseases.&rft.au=Balbus%2C+John+M%3BBarouki%2C+Robert%3BBirnbaum%2C+Linda+S%3BEtzel%2C+Ruth+A%3BGluckman%2C+Peter+D%3BGrandjean%2C+Philippe%3BHancock%2C+Christine%3BHanson%2C+Mark+A%3BHeindel%2C+Jerrold+J%3BHoffman%2C+Kate%3BJensen%2C+G%C3%A9non+K%3BKeeling%2C+Ann%3BNeira%2C+Maria%3BRabad%C3%A1n-Diehl%2C+Cristina%3BRalston%2C+Johanna%3BTang%2C+Kwok-Cho&rft.aulast=Balbus&rft.aufirst=John&rft.date=2013-01-05&rft.volume=381&rft.issue=9860&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Lancet+%28London%2C+England%29&rft.issn=1474-547X&rft_id=info:doi/10.1016%2FS0140-6736%2812%2961609-2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-01-24
N1  - Date created - 2013-01-07
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Eur J Obstet Gynecol Reprod Biol. 1998 Jun;78(2):141-50 [9622311]
Pediatrics. 2005 Mar;115(3):e290-6 [15741354]
Arterioscler Thromb Vasc Biol. 2006 Aug;26(8):1877-82 [16728657]
Environ Health. 2012;11:42 [22715989]
Reprod Toxicol. 2011 Apr;31(3):337-43 [21055462]
Reprod Toxicol. 2011 Apr;31(3):363-73 [21256208]
Int J Epidemiol. 2012 Feb;41(1):79-105 [22253299]
PLoS One. 2009;4(2):e4488 [19221603]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/S0140-6736(12)61609-2
ER  - 



TY  - JOUR
T1  - CYLD, a deubiquitinase specific for lysine63-linked polyubiquitins, accumulates at the postsynaptic density in an activity-dependent manner
AN  - 1419360540; 17565452
AB  - Polyubiquitin chains on proteins flag them for distinct fates depending on the type of polyubiquitin linkage. While lysine48-linked polyubiquitination directs proteins to proteasomal degradation, lysine63-linked polyubiquitination promotes different protein trafficking and is involved in autophagy. Here we show that postsynaptic density (PSD) fractions from adult rat brain contain deubiquitinase activity that targets both lysine48 and lysine63-linked polyubiquitins. Comparison of PSD fractions with parent subcellular fractions by Western immunoblotting reveals that CYLD, a deubiquitinase specific for lysine63-linked polyubiquitins, is highly enriched in the PSD fraction. Electron microscopic examination of hippocampal neurons in culture under basal conditions shows immunogold label for CYLD at the PSD complex in approximately one in four synapses. Following depolarization by exposure to high K+, the proportion of CYLD-labeled PSDs as well as the labeling intensity of CYLD at the PSD increased by more than eighty percent, indicating that neuronal activity promotes accumulation of CYLD at the PSD. An increase in postsynaptic CYLD following activity would promote removal of lysine63-polyubiquitins from PSD proteins and thus could regulate their trafficking and prevent their autophagic degradation.
JF  - Biochemical and Biophysical Research Communications
AU  - Dosemeci, Ayse
AU  - Thein, Soe
AU  - Yang, Yijung
AU  - Reese, Thomas S
AU  - Tao-Cheng, Jung-Hwa
AD  - Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA, dosemeca@mail.nih.gov
Y1  - 2013/01/04/
PY  - 2013
DA  - 2013 Jan 04
SP  - 245
EP  - 249
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 430
IS  - 1
SN  - 0006-291X, 0006-291X
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - Immunoblotting
KW  - Protein transport
KW  - Synapses
KW  - Hippocampus
KW  - Neurons
KW  - postsynaptic density
KW  - Brain
KW  - proteasomes
KW  - Potassium
KW  - Cell culture
KW  - Phagocytosis
KW  - N3 11008:Neurochemistry
KW  - X 24490:Other
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419360540?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=CYLD%2C+a+deubiquitinase+specific+for+lysine63-linked+polyubiquitins%2C+accumulates+at+the+postsynaptic+density+in+an+activity-dependent+manner&rft.au=Dosemeci%2C+Ayse%3BThein%2C+Soe%3BYang%2C+Yijung%3BReese%2C+Thomas+S%3BTao-Cheng%2C+Jung-Hwa&rft.aulast=Dosemeci&rft.aufirst=Ayse&rft.date=2013-01-04&rft.volume=430&rft.issue=1&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/10.1016%2Fj.bbrc.2012.10.131
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Protein transport; Immunoblotting; Synapses; Hippocampus; Neurons; proteasomes; Brain; postsynaptic density; Potassium; Cell culture; Phagocytosis
DO  - http://dx.doi.org/10.1016/j.bbrc.2012.10.131
ER  - 



TY  - JOUR
T1  - Recombinant expression and purification of a tumor-targeted toxin in Bacillus anthracis
AN  - 1315606449; 17565470
AB  - Many recombinant therapeutic proteins are purified from Escherichia coli. While expression in E. coli is easily achieved, some disadvantages such as protein aggregation, formation of inclusion bodies, and contamination of purified proteins with the lipopolysaccharides arise. Lipopolysaccharides have to be removed to prevent inflammatory responses in patients. Use of the Gram-positive Bacillus anthracis as an expression host offers a solution to circumvent these problems. Using the multiple protease-deficient strain BH460, we expressed a fusion of the N-terminal 254 amino acids of anthrax lethal factor (LFn), the N-terminal 389 amino acids of diphtheria toxin (DT389) and human transforming growth factor alpha (TGF alpha ). The resulting fusion protein was constitutively expressed and successfully secreted by B. anthracis into the culture supernatant. Purification was achieved by anion exchange chromatography and proteolytic cleavage removed LFn from the desired fusion protein (DT389 fused to TGF alpha ). The fusion protein showed the intended specific cytotoxicity to epidermal growth factor receptor-expressing human head and neck cancer cells. Final analyses showed low levels of lipopolysaccharides, originating most likely from contamination during the purification process. Thus, the fusion to LFn for protein secretion and expression in B. anthracis BH460 provides an elegant tool to obtain high levels of lipopolysaccharide-free recombinant protein.
JF  - Biochemical and Biophysical Research Communications
AU  - Bachran, Christopher
AU  - Abdelazim, Suzanne
AU  - Fattah, Rasem J
AU  - Liu, Shihui
AU  - Leppla, Stephen H
AD  - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA, sleppla@niaid.nih.gov
Y1  - 2013/01/04/
PY  - 2013
DA  - 2013 Jan 04
SP  - 150
EP  - 155
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 430
IS  - 1
SN  - 0006-291X, 0006-291X
KW  - Toxicology Abstracts; Genetics Abstracts
KW  - Proteolysis
KW  - Anions
KW  - Amino acids
KW  - Contamination
KW  - Chromatography
KW  - Secretion
KW  - Lethal factor
KW  - Cell culture
KW  - protein purification
KW  - Bacillus anthracis
KW  - Diphtheria toxin
KW  - Toxins
KW  - Cytotoxicity
KW  - Escherichia coli
KW  - Anthrax
KW  - Inclusion bodies
KW  - Lipopolysaccharides
KW  - Head and neck cancer
KW  - Fusion protein
KW  - Transforming growth factor- alpha
KW  - Epidermal growth factor
KW  - X 24370:Natural Toxins
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315606449?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Recombinant+expression+and+purification+of+a+tumor-targeted+toxin+in+Bacillus+anthracis&rft.au=Bachran%2C+Christopher%3BAbdelazim%2C+Suzanne%3BFattah%2C+Rasem+J%3BLiu%2C+Shihui%3BLeppla%2C+Stephen+H&rft.aulast=Bachran&rft.aufirst=Christopher&rft.date=2013-01-04&rft.volume=430&rft.issue=1&rft.spage=150&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/10.1016%2Fj.bbrc.2012.11.055
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Last updated - 2013-08-23
N1  - SubjectsTermNotLitGenreText - Proteolysis; Amino acids; Anions; Contamination; Chromatography; Lethal factor; Secretion; Cell culture; protein purification; Toxins; Diphtheria toxin; Cytotoxicity; Head and neck cancer; Lipopolysaccharides; Inclusion bodies; Anthrax; Fusion protein; Epidermal growth factor; Transforming growth factor- alpha; Escherichia coli; Bacillus anthracis
DO  - http://dx.doi.org/10.1016/j.bbrc.2012.11.055
ER  - 



TY  - JOUR
T1  - NCI-RTOG Translational Program Strategic Guidelines for the Early-Stage Development of Radiosensitizers
AN  - 1285091934; 17577537
AB  - The addition of chemotherapeutic agents to ionizing radiation has improved survival in many malignancies. Cure rates may be further improved by adding novel targeted agents to current radiotherapy or radiochemotherapy regimens. Despite promising laboratory data, progress in the clinical development of new drugs with radiation has been limited. To define and address the problems involved, a collaborative effort between individuals within the translational research program of the Radiation Oncology Therapy Group and the National Cancer Institute was established. We discerned challenges to drug development with radiation including: 1) the limited relevance of preclinical work, 2) the pharmaceutical industry's diminished interest, and 3) the important individual skills and institutional commitments required to ensure a successful program. The differences between early-phase trial designs with and without radiation are noted as substantial. The traditional endpoints for early-phase clinical trials-acute toxicity and maximum-tolerated dose-are of limited value when combining targeted agents with radiation. Furthermore, response rate is not a useful surrogate marker of activity in radiation combination trials.Consequently, a risk-stratified model for drug-dose escalation with radiation is proposed, based upon the known and estimated adverse effects. The guidelines discuss new clinical trial designs, such as the time-to-event continual reassessment method design for phase I trials, randomized phase II "screening" trials, and the use of surrogate endpoints, such as pathological response. It is hoped that by providing a clear pathway, this article will accelerate the rate of drug development with radiation.
JF  - Journal of the National Cancer Institute
AU  - Lawrence, Yaacov Richard
AU  - Vikram, Bhadrasain
AU  - Dignam, James J
AU  - Chakravarti, Arnab
AU  - Machtay, Mitchell
AU  - Freidlin, Boris
AU  - Takebe, Naoko
AU  - Curran, Walter J
AU  - Bentzen, Soren M
AU  - Okunieff, Paul
AU  - Coleman, CNorman
AU  - Dicker, Adam P
AD  - Affiliations of authors: Department Radiation Oncology, Sheba Medical Center, Tel HaShomer, Israel (YRL); Department of Radiation Oncology, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA (YRL, APD); Division of Cancer Treatment and Diagnosis (BV) and Biometric Research Branch (BF), National Cancer Institute, National Institutes of Health, Bethesda, MD (BV); Department of Health Studies, University of Chicago, Chicago, IL (JJD); Department of Radiation Oncology, Ohio State University College of Medicine, Columbus, OH (AC); Department of Radiation Oncology, Seidman Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH (MM); Division of Cancer Treatment and Diagnosis, Cancer Therapy Evaluation Program, Investigational Drug Branch, National Cancer Institute, National Institutes of Health, Rockville, MD (NT); Department of Radiation Oncology, Winship Cancer Institute of Emory University, Atlanta, GA (WC); Departmen, yaacovla@gmail.com
Y1  - 2013/01/02/
PY  - 2013
DA  - 2013 Jan 02
SP  - 11
EP  - 24
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 105
IS  - 1
SN  - 0027-8874, 0027-8874
KW  - Risk Abstracts
KW  - Cancer
KW  - Clinical trials
KW  - Drugs
KW  - Guidelines
KW  - Ionizing radiation
KW  - Side effects
KW  - Survival
KW  - Toxicity
KW  - radiotherapy
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285091934?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=NCI-RTOG+Translational+Program+Strategic+Guidelines+for+the+Early-Stage+Development+of+Radiosensitizers&rft.au=Lawrence%2C+Yaacov+Richard%3BVikram%2C+Bhadrasain%3BDignam%2C+James+J%3BChakravarti%2C+Arnab%3BMachtay%2C+Mitchell%3BFreidlin%2C+Boris%3BTakebe%2C+Naoko%3BCurran%2C+Walter+J%3BBentzen%2C+Soren+M%3BOkunieff%2C+Paul%3BColeman%2C+CNorman%3BDicker%2C+Adam+P&rft.aulast=Lawrence&rft.aufirst=Yaacov&rft.date=2013-01-02&rft.volume=105&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs472
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2013-02-22
N1  - SubjectsTermNotLitGenreText - Ionizing radiation; Guidelines; Survival; Toxicity; Clinical trials; radiotherapy; Drugs; Side effects; Cancer
DO  - http://dx.doi.org/10.1093/jnci/djs472
ER  - 



TY  - JOUR
T1  - Pharmacotherapy for childhood obesity: present and future prospects
AN  - 1837293901; 17531787
AB  - Pediatric obesity is a serious medical condition associated with significant comorbidities during childhood and adulthood. Lifestyle modifications are essential for treating children with obesity, yet many have insufficient response to improve health with behavioral approaches alone. This review summarizes the relatively sparse data on pharmacotherapy for pediatric obesity and presents information on obesity medications in development. Most previously studied medications demonstrated, at best, modest effects on body weight and obesity-related conditions. It is to be hoped that the future will bring new drugs targeting specific obesity phenotypes that will allow clinicians to use etiology-specific, and therefore more effective, anti-obesity therapies.
JF  - International Journal of Obesity
AU  - Sherafat-Kazemzadeh, R
AU  - Yanovski, S Z
AU  - Yanovski, J A
AD  - Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 1
EP  - 15
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 37
IS  - 1
SN  - 0307-0565, 0307-0565
KW  - Physical Education Index
KW  - Obesity
KW  - Growth and development
KW  - Weight
KW  - Pediatrics
KW  - Medications
KW  - Therapy
KW  - Health
KW  - Children
KW  - Lifestyle
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837293901?accountid=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=Pharmacotherapy+for+childhood+obesity%3A+present+and+future+prospects&rft.au=Sherafat-Kazemzadeh%2C+R%3BYanovski%2C+S+Z%3BYanovski%2C+J+A&rft.aulast=Sherafat-Kazemzadeh&rft.aufirst=R&rft.date=2013-01-01&rft.volume=37&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2012.144
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2016-11-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Obesity; Growth and development; Weight; Pediatrics; Therapy; Medications; Health; Children; Lifestyle
DO  - http://dx.doi.org/10.1038/ijo.2012.144
ER  - 



TY  - JOUR
T1  - SIRT1 and energy metabolism
AN  - 1823946381; 20378040
AB  - Sirtuin 1 (SIRT1) is the most conserved mammalian NAD+-dependent protein deacetylase that has emerged as a key metabolic sensor in various metabolic tissues. In response to different environmental stimuli, SIRT1 directly links the cellular metabolic status to the chromatin structure and the regulation of gene expression, thereby modulating a variety of cellular processes such as energy metabolism and stress response. Recent studies have shown that SIRT1 controls both glucose and lipid metabolism in the liver, promotes fat mobilization and stimulates brown remodeling of the white fat in white adipose tissue, controls insulin secretion in the pancreas, senses nutrient availability in the hypothalamus, influences obesity-induced inflammation in macrophages, and modulates the activity of circadian clock in metabolic tissues. This review focuses on the role of SIRT1 in regulating energy metabolism at different metabolic tissues.
JF  - Acta Biochimica et Biophysica Sinica
AU  - Li, Xiaoling
AD  - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA, Lix3@niehs.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 51
EP  - 60
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 45
IS  - 1
SN  - 1672-9145, 1672-9145
KW  - Biotechnology and Bioengineering Abstracts
KW  - SIRT1
KW  - energy metabolism
KW  - aging
KW  - nutrients
KW  - metabolic sensor
KW  - Macrophages
KW  - SIRT1 protein
KW  - Chromatin
KW  - Energy metabolism
KW  - Secretion
KW  - Pancreas
KW  - Nutrient availability
KW  - Sirtuins
KW  - Stress
KW  - Glucose metabolism
KW  - Insulin
KW  - Inflammation
KW  - Lipid metabolism
KW  - Gene expression
KW  - Circadian rhythms
KW  - Liver
KW  - Environmental effects
KW  - Adipose tissue
KW  - W 30955:Biosensors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1823946381?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+Biochimica+et+Biophysica+Sinica&rft.atitle=SIRT1+and+energy+metabolism&rft.au=Li%2C+Xiaoling&rft.aulast=Li&rft.aufirst=Xiaoling&rft.date=2013-01-01&rft.volume=45&rft.issue=1&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Acta+Biochimica+et+Biophysica+Sinica&rft.issn=16729145&rft_id=info:doi/10.1093%2Fabbs%2Fgms108
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2016-09-01
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Macrophages; SIRT1 protein; Energy metabolism; Chromatin; Pancreas; Secretion; Nutrient availability; Sirtuins; Stress; Glucose metabolism; Insulin; Lipid metabolism; Inflammation; Gene expression; Environmental effects; Liver; Circadian rhythms; Adipose tissue
DO  - http://dx.doi.org/10.1093/abbs/gms108
ER  - 



TY  - JOUR
T1  - Ortak Calisma ve Ekip Bilimi: Teoriden Pratige (Joint Working Team and Science: From Theory to Practice)
TT  - Collaboration and Team Science: From Theory to Practice
AN  - 1676061109
AB  - Turkish:Disiplinler arasi calismalar, bilimsel buluslar ve donusumsel arastirma calismalari icin giderek daha onemli hale gelmektedir. Yuksek katilimli ve aralarinda etkilesim halinde olan arastirma ekipleri birtakim ortak ozellikleri paylasirlar. Bu ozellikler calismalarinin gelistirilmesi ve zamanla surdurulebilirligine iliskin basarilarina katkida bulunur. Cok basarili arastirma ekipleri ile hedeflerine ulasamayan veya aralarindaki uyusmazliklar nedeniyle dagilan ekiplerin uyeleriyle etraflica yaptigimiz gorusmelerle, ekip basarisi ve etkinligi icin gerekli anahtar unsurlari belirledik. Hic kuskusuz bilimsel hedefortak calismanin merkezinde yer almaktadir. Buna karsin ekibin raydan cikmasini onlemek icin destekleyici ogelere de ihtiyac vardir. Bunlarin icinde en onemlisi guvendir; guven olmadan ekip dinamikleri zamanla bozulma riskiyle karsi karsiya kalir. Hem liderler hem de diger katilimcilar icin farkinda olunmasi gereken diger kritik faktorler; ortak bir vizyon gelistirmek, ekip uyelerini stratejik olarak belirlemek ve ekibin kurulmasinda kararli davranmak, uyusmazlik ciktiginda ihtilaflari ortaya koymak ve kredi (itibar, destek vb.)ile yazarligi paylasirken beklentileri acikca ortaya koymaktir. Ozfarkindalik ve guclu iletisim becerilerine sahip olmak, etkin birliderlige ve bilim ekiplerinin yonetim stratejilerine onemli katki saglar. Tum basarili ekipler bu aktiviteleri etkin olarak gerceklestirme ozelligini paylasirken, farkli guclu ve zayif ozelliklere sahip her liderle basariya ulasmak icin tek bir formul yoktur. Basarili bilimsel ortakliklar, kendisini bilen, dusunceli, isin merkezinde bilimin olmasini destekleyen kritik unsurlari onemseyen guclu liderlere sahiptir.English:Interdisciplinary efforts are becoming more critical for scientific discovery and translational research efforts. Highly integrated and interactive research teams share a number of features that contribute to their success in developing and sustaining their efforts over time. Through analysis of in-depth interviews with members of highly successful research teams and others who did not meet their goals or ended because of conflicts, we identified key elements that are critical for team success and effectiveness. There is no debate that the scientific goal sits at the center of the collaborative effort. However, supporting features need to be in place to avoid the derailment of the team. Among the most important of these is trust: without trust, the team dynamic runs the risk of deteriorating over time. Other critical factors of which both leaders and participants need to be aware include developing a shared vision, strategically identifying team members and purposefully building the team, promoting disagreement while containing conflict, and setting clear expectations for sharing credit and authorship. Self-awareness and strong communication skills contribute greatly to effective leadership and management strategies of scientific teams. While all successful teams share the characteristic of effectively carrying out these activities, there is no single formula for execution with every leader exemplifying different strengths and weaknesses. Successful scientific collaborations have strong leaders who are self-aware and are mindful of the many elements critical for supporting the science at the center of the effort.
JF  - Bilgi Dunyasi = Information World
AU  - BENNETT, Michelle L
AU  - GADLIN, Howard
AD  - BENNETT, L Michelle; Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, MD., Amerika Birlesik Devletleri; GADLIN, Howard; Center for Cooperative Resolution, Office of the Director, National Institutes of Health, Bethesda, MD., Amerika Birlesik Devletleri
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 420
EP  - 439
CY  - Ankara
PB  - Iletisim Bilgileri
VL  - 14
IS  - 2
SN  - 1302-3217
KW  - Library And Information Sciences
KW  - Collaboration
KW  - Trust
KW  - Translational research
KW  - Managing conflict
KW  - Promoting disagreement
KW  - Sharing credit
KW  - Leadership
KW  - Research
KW  - Science
KW  - Teamwork
KW  - 17.1:RESEARCH
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676061109?accountid=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=Bilgi+Dunyasi+%3D+Information+World&rft.atitle=Ortak+Calisma+ve+Ekip+Bilimi%3A+Teoriden+Pratige+%28Joint+Working+Team+and+Science%3A+From+Theory+to+Practice%29&rft.au=BENNETT%2C+Michelle+L%3BGADLIN%2C+Howard%3BBENNETT%2C+L+Michelle&rft.aulast=BENNETT&rft.aufirst=Michelle&rft.date=2013-01-01&rft.volume=14&rft.issue=2&rft.spage=420&rft.isbn=&rft.btitle=&rft.title=Bilgi+Dunyasi+%3D+Information+World&rft.issn=13023217&rft_id=info:doi/
LA  - Turkish
DB  - Library & Information Science Abstracts (LISA)
N1  - Date revised - 2015-04-27
N1  - Last updated - 2016-05-25
ER  - 



TY  - JOUR
T1  - Relationship of sense of coherence to stressful events, coping strategies, health status, and quality of life in women with breast cancer
AN  - 1665154293
AB  - Objective To test the hypothesis that Antonovskyʼs concept of sense of coherence (SOC) predicts stressful events, coping strategies, health status, and quality of life (QoL) in a cohort of postmenopausal women ( n=131) with newly diagnosed primary or recurrent breast cancer. Methods Regression analyses of longitudinal data at baseline through 6months following breast cancer diagnosis examined the relationships between SOC (13-item version), daily assessment of coping with stressful events, health status, and QoL (EORTC QLQ-30). Results The findings support Antonovskyʼs concept of SOC. Women with strong SOC reported fewer stressful events and more days without stressful events. They used more coping strategies and more frequently used distraction, situation redefinition, direct action, and relaxation, but seldom religion, to cope with stressful events, and reported better health status and QoL. Women with weak SOC experienced more distress and used fewer coping strategies, and they more frequently used coping strategies such as catharsis and seeking social and spiritual support, but seldom acceptance of the situation. They reported worse health status and QoL, regardless of disease stage or treatment. The relationships between SOC and health status and QoL were linear. Conclusions Sense of coherence significantly predicts distress, number and type of coping strategies such as direct action and relaxation, health status, and QoL in women with breast cancer. Our data suggest that the SOC scale may be a useful screening tool to identify individuals particularly vulnerable to distress and unable to cope adequately. Assessing SOC strength may assist health care providers to provide individualized patient interventions. Copyright © 2011 John Wiley & Sons, Ltd.
JF  - Psycho-Oncology
AU  - Sarenmalm, Elisabeth Kenne
AU  - Browall, Maria
AU  - Persson, L-O
AU  - Fall-Dickson, J
AU  - Gaston-Johansson, Fanny
AD  - Research and Development Centre, Skaraborg Hospital, Skövde, Sweden., Institute of Health and Caring Sciences, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden., Johns Hopkins School of Nursing, Baltimore, MD, USA. ; Johns Hopkins School of Nursing, Baltimore, MD, USA., Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden., School of Life Sciences, University of Skövde, Skövde, Sweden. ; Institute of Health and Caring Sciences, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden. ; National Institute of Nursing Research, National Institutes of Health, Bethesda, MD, USA. ; Johns Hopkins School of Nursing, Baltimore, MD, USA. ; Research and Development Centre, Skaraborg Hospital, Skövde, Sweden.; Institute of Health and Caring Sciences, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden.; Johns Hopkins School of Nursing, Baltimore, MD, USA.
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 20
EP  - 27
CY  - Chichester
PB  - Wiley Subscription Services, Inc.
VL  - 22
IS  - 1
SN  - 1057-9249
KW  - Medical Sciences--Psychiatry And Neurology
KW  - Acceptance
KW  - Interventions
KW  - Newly diagnosed
KW  - Postmenopausal women
KW  - Psychological distress
KW  - Quality of life
KW  - Recurrent
KW  - Redefinition
KW  - Relaxation
KW  - Screening
KW  - Sense of coherence
KW  - Stressful events
KW  - Women's issues
KW  - Breast cancer
KW  - Cancer
KW  - Catharsis
KW  - Clinical assessment
KW  - Coherence
KW  - Coping
KW  - Coping strategies
KW  - Diagnosis
KW  - Distraction
KW  - Health
KW  - Health care
KW  - Health professionals
KW  - Health status
KW  - Individualized
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665154293?accountid=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=Relationship+of+sense+of+coherence+to+stressful+events%2C+coping+strategies%2C+health+status%2C+and+quality+of+life+in+women+with+breast+cancer&rft.au=Sarenmalm%2C+Elisabeth+Kenne%3BBrowall%2C+Maria%3BPersson%2C+L-O%3BFall-Dickson%2C+J%3BGaston-Johansson%2C+Fanny&rft.aulast=Sarenmalm&rft.aufirst=Elisabeth&rft.date=2013-01-01&rft.volume=22&rft.issue=1&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.2053
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.2053
ER  - 



TY  - JOUR
T1  - Coagulase-negative staphylococci as reservoirs of genes facilitating MRSA infection
AN  - 1560105413; 20427277
AB  - Recent research has suggested that Staphylococcus epidermidis is a reservoir of genes that, after horizontal transfer, facilitate the potential of Staphylococcus aureus to colonize, survive during infection, or resist antibiotic treatment, traits that are notably manifest in methicillin-resistant S. aureus (MRSA). S. aureus is a dangerous human pathogen and notorious for acquiring antibiotic resistance. MRSA in particular is one of the most frequent causes of morbidity and death in hospitalized patients. S. aureus is an extremely versatile pathogen with a multitude of mechanisms to cause disease and circumvent immune defenses. In contrast, most other staphylococci, such as S. epidermidis, are commonly benign commensals and only occasionally cause disease. Recent findings highlight the key importance of efforts to better understand how genes of staphylococci other than S. aureus contribute to survival in the human host, how they are transferred to S. aureus, and why this exchange appears to be uni-directional. Staphylococcus epidermidis is a source for factors that - after horizontal gene transfer - enable Staphylococcus aureus to survive in the human host and cause disease: colonization factors, antibiotic resistance genes, and rarely toxins. The transfer of genes from S. aureus to S. epidermidis is unusual and possibly blocked by CRISPR-mediated interference.
JF  - Bioessays
AU  - Otto, Michael
AD  - Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases (NIAID), The National Institutes of Health (NIH), Bethesda, MD, USA., motto@niaid.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 4
EP  - 11
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 35
IS  - 1
SN  - 0265-9247, 0265-9247
KW  - Genetics Abstracts; Microbiology Abstracts B: Bacteriology
KW  - Drug resistance
KW  - Commensals
KW  - Survival
KW  - Antibiotics
KW  - Pathogens
KW  - Infection
KW  - Morbidity
KW  - Toxins
KW  - Horizontal transfer
KW  - Staphylococcus aureus
KW  - Staphylococcus epidermidis
KW  - Antibiotic resistance
KW  - Colonization factor
KW  - Benign
KW  - J 02400:Human Diseases
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560105413?accountid=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=Bioessays&rft.atitle=Coagulase-negative+staphylococci+as+reservoirs+of+genes+facilitating+MRSA+infection&rft.au=Otto%2C+Michael&rft.aulast=Otto&rft.aufirst=Michael&rft.date=2013-01-01&rft.volume=35&rft.issue=1&rft.spage=4&rft.isbn=&rft.btitle=&rft.title=Bioessays&rft.issn=02659247&rft_id=info:doi/10.1002%2Fbies.201200112
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Last updated - 2014-10-15
N1  - SubjectsTermNotLitGenreText - Drug resistance; Commensals; Survival; Antibiotics; Pathogens; Infection; Horizontal transfer; Toxins; Colonization factor; Morbidity; Antibiotic resistance; Benign; Staphylococcus aureus; Staphylococcus epidermidis
DO  - http://dx.doi.org/10.1002/bies.201200112
ER  - 



TY  - JOUR
T1  - Ninja Kitchen to the rescue. Evaluation of a food safety education game for middle school youth
AN  - 1559650577; 18465388
AB  - Purpose - The purpose of this paper is to assess the effect of Ninja Kitchen, a food safety educational video game, on middle school students' food safety knowledge, psychographic characteristics, and usual and intended behaviors. Design/methodology/approach - The experimental group (n=903) completed the following activities about one week apart from each other: pretest, played the game, posttest, and follow-up test. The control group (n=365) completed the same activities at similar intervals but did not have access to the game until after the follow-up test. Findings - Linear mixed-effects models, controlling for gender, grade, and geographic location revealed significant time by group effects for knowledge of safe cooking temperatures for animal proteins and danger zone hazard prevention, and usual produce washing behaviors. Pairwise comparisons, adjusted for multiple comparisons, indicated that after playing the game, the experimental group felt more susceptible to foodborne illness, had stronger attitudes toward the importance of handling food safely and handwashing, had greater confidence in their ability to practice safe food handling, and had greater intentions to practice handwashing and safe food handling. Teachers and students found the game highly acceptable. Originality/value - The game has the potential to promote positive food safety behaviors among youth, in a fun and educational format.
JF  - British Food Journal
AU  - Quick, Virginia
AU  - Corda, Kirsten W
AU  - Chamberlin, Barbara
AU  - Schaffner, Donald W
AU  - Byrd-Bredbenner, Carol
AD  - Prevention Research Branch, Eunice Kennedy Shriver National Institute of Child Health & Human Development/National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 686
EP  - 699
PB  - Emerald Group Publishing Limited, 60-62 Toller Lane Bradford West Yorkshire BD8 9BY United Kingdom
VL  - 115
IS  - 5
SN  - 0007-070X, 0007-070X
KW  - Health & Safety Science Abstracts
KW  - Video games
KW  - Food safety
KW  - Hygiene
KW  - Individual behaviour
KW  - Middle schools
KW  - Attitudes
KW  - Self-efficacy
KW  - Intentions
KW  - Serious games
KW  - Kitchen
KW  - Cooking
KW  - Education
KW  - Prevention
KW  - Gender
KW  - Temperature
KW  - Group effects
KW  - Proteins
KW  - Food contamination
KW  - Food-borne diseases
KW  - H 4000:Food and Drugs
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1559650577?accountid=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=British+Food+Journal&rft.atitle=Ninja+Kitchen+to+the+rescue.+Evaluation+of+a+food+safety+education+game+for+middle+school+youth&rft.au=Quick%2C+Virginia%3BCorda%2C+Kirsten+W%3BChamberlin%2C+Barbara%3BSchaffner%2C+Donald+W%3BByrd-Bredbenner%2C+Carol&rft.aulast=Quick&rft.aufirst=Virginia&rft.date=2013-01-01&rft.volume=115&rft.issue=5&rft.spage=686&rft.isbn=&rft.btitle=&rft.title=British+Food+Journal&rft.issn=0007070X&rft_id=info:doi/10.1108%2F00070701311331481
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-09-01
N1  - Number of references - 43
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Prevention; Education; Attitudes; Cooking; Gender; Temperature; Proteins; Group effects; Food contamination; Food-borne diseases
DO  - http://dx.doi.org/10.1108/00070701311331481
ER  - 



TY  - JOUR
T1  - SRAdb: query and use public next-generation sequencing data from within R
AN  - 1554954542; 17636066
AB  - Background: The Sequence Read Archive (SRA) is the largest public repository of sequencing data from the next generation of sequencing platforms including Illumina (Genome Analyzer, HiSeq, MiSeq, .etc), Roche 454 GS System, Applied Biosystems SOLiD System, Helicos Heliscope, PacBio RS, and others. Results: SRAdb is an attempt to make queries of the metadata associated with SRA submission, study, sample, experiment and run more robust and precise, and make access to sequencing data in the SRA easier. We have parsed all the SRA metadata into a SQLite database that is routinely updated and can be easily distributed. The SRAdb R/Bioconductor package then utilizes this SQLite database for querying and accessing metadata. Full text search functionality makes querying metadata very flexible and powerful. Fastq files associated with query results can be downloaded easily for local analysis. The package also includes an interface from R to a popular genome browser, the Integrated Genomics Viewer. Conclusions: SRAdb Bioconductor package provides a convenient and integrated framework to query and access SRA metadata quickly and powerfully from within R.
JF  - BMC Bioinformatics
AU  - Zhu, Yuelin
AU  - Stephens, Robert M
AU  - Meltzer, Paul S
AU  - Davis, Sean R
AD  - Genetics Branch, National Cancer Institute, National Institutes of HealthBethesda, MD 20892, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 19
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2105, 1471-2105
KW  - Biotechnology and Bioengineering Abstracts
KW  - Databases
KW  - Data processing
KW  - Nucleotide sequence
KW  - genomics
KW  - Bioinformatics
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554954542?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=SRAdb%3A+query+and+use+public+next-generation+sequencing+data+from+within+R&rft.au=Zhu%2C+Yuelin%3BStephens%2C+Robert+M%3BMeltzer%2C+Paul+S%3BDavis%2C+Sean+R&rft.aulast=Zhu&rft.aufirst=Yuelin&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-14-19
L2  - http://www.biomedcentral.com/1471-2105/14/19
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Number of references - 4
N1  - Last updated - 2015-08-05
N1  - SubjectsTermNotLitGenreText - Databases; Data processing; Nucleotide sequence; Bioinformatics; genomics
DO  - http://dx.doi.org/10.1186/1471-2105-14-19
ER  - 



TY  - JOUR
T1  - PD-1 promotes immune exhaustion by inducing antiviral T cell motility paralysis
AN  - 1551644081; 20352555
AB  - PD-L1 decreases anti-viral CD8+ T cell motility and PD-1 blockade restores motility in the presence of high viral loads.
JF  - Journal of Experimental Medicine
AU  - Zinselmeyer, Bernd H
AU  - Heydari, Sara
AU  - Sacristan, Catarina
AU  - Nayak, Debasis
AU  - Cammer, Michael
AU  - Herz, Jasmin
AU  - Cheng, Xiaoxiao
AU  - Davis, Simon J
AU  - Dustin, Michael L
AU  - McGavern, Dorian B
AD  - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 757
EP  - 774
PB  - Rockefeller University Press, 1114 First Avenue New York NY 10021-8325 United States
VL  - 210
IS  - 4
SN  - 0022-1007, 0022-1007
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Immunology Abstracts
KW  - Paralysis
KW  - PD-1 protein
KW  - Antiviral agents
KW  - Lymphocytes T
KW  - PD-L1 protein
KW  - Cell migration
KW  - CD8 antigen
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22340:Antiviral Agents
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551644081?accountid=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+Experimental+Medicine&rft.atitle=PD-1+promotes+immune+exhaustion+by+inducing+antiviral+T+cell+motility+paralysis&rft.au=Zinselmeyer%2C+Bernd+H%3BHeydari%2C+Sara%3BSacristan%2C+Catarina%3BNayak%2C+Debasis%3BCammer%2C+Michael%3BHerz%2C+Jasmin%3BCheng%2C+Xiaoxiao%3BDavis%2C+Simon+J%3BDustin%2C+Michael+L%3BMcGavern%2C+Dorian+B&rft.aulast=Zinselmeyer&rft.aufirst=Bernd&rft.date=2013-01-01&rft.volume=210&rft.issue=4&rft.spage=757&rft.isbn=&rft.btitle=&rft.title=Journal+of+Experimental+Medicine&rft.issn=00221007&rft_id=info:doi/10.1084%2Fjem.20121416
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - Paralysis; PD-1 protein; Antiviral agents; PD-L1 protein; Lymphocytes T; CD8 antigen; Cell migration
DO  - http://dx.doi.org/10.1084/jem.20121416
ER  - 



TY  - JOUR
T1  - p53 integrates host defense and cell fate during bacterial pneumonia
AN  - 1551640697; 20352564
AB  - p53 deletion augments neutrophil-mediated bacterial clearance in the lung at the expense of tissue homeostasis, leading to increased mortality.
JF  - Journal of Experimental Medicine
AU  - Madenspacher, Jennifer H
AU  - Azzam, Kathleen M
AU  - Gowdy, Kymberly M
AU  - Malcolm, Kenneth C
AU  - Nick, Jerry A
AU  - Dixon, Darlene
AU  - Aloor, Jim J
AU  - Draper, David W
AU  - Guardiola, John J
AU  - Shatz, Maria
AU  - Menendez, Daniel
AU  - Lowe, Julie
AU  - Lu, Jun
AU  - Bushel, Pierre
AU  - Li, Leping
AU  - Merrick, BAlex
AU  - Resnick, Michael A
AU  - Fessler, Michael B
AD  - Laboratory of Respiratory Biology; Cellular and Molecular Pathology Branch, National Toxicology Program; Laboratory of Molecular Genetics; and Biostatistics Branch; National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 891
EP  - 904
PB  - Rockefeller University Press, 1114 First Avenue New York NY 10021-8325 United States
VL  - 210
IS  - 5
SN  - 0022-1007, 0022-1007
KW  - Oncogenes & Growth Factors Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW  - Bacteria
KW  - Mortality
KW  - Lung
KW  - Homeostasis
KW  - Cell fate
KW  - Pneumonia
KW  - p53 protein
KW  - B 26670:Tumor Suppressors
KW  - J 02350:Immunology
KW  - F 06910:Microorganisms & Parasites
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551640697?accountid=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+Experimental+Medicine&rft.atitle=p53+integrates+host+defense+and+cell+fate+during+bacterial+pneumonia&rft.au=Madenspacher%2C+Jennifer+H%3BAzzam%2C+Kathleen+M%3BGowdy%2C+Kymberly+M%3BMalcolm%2C+Kenneth+C%3BNick%2C+Jerry+A%3BDixon%2C+Darlene%3BAloor%2C+Jim+J%3BDraper%2C+David+W%3BGuardiola%2C+John+J%3BShatz%2C+Maria%3BMenendez%2C+Daniel%3BLowe%2C+Julie%3BLu%2C+Jun%3BBushel%2C+Pierre%3BLi%2C+Leping%3BMerrick%2C+BAlex%3BResnick%2C+Michael+A%3BFessler%2C+Michael+B&rft.aulast=Madenspacher&rft.aufirst=Jennifer&rft.date=2013-01-01&rft.volume=210&rft.issue=5&rft.spage=891&rft.isbn=&rft.btitle=&rft.title=Journal+of+Experimental+Medicine&rft.issn=00221007&rft_id=info:doi/10.1084%2Fjem.20121674
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-08-01
N1  - Last updated - 2014-11-12
N1  - SubjectsTermNotLitGenreText - Mortality; Lung; Cell fate; Homeostasis; Pneumonia; p53 protein; Bacteria
DO  - http://dx.doi.org/10.1084/jem.20121674
ER  - 



TY  - JOUR
T1  - EVALUATION OF THE USE OF SURROGATE TISSUES FOR CALCULATING RADIATION DOSE TO LYMPHATIC NODES FROM EXTERNAL PHOTON BEAMS
AN  - 1534820308; 19796929
AB  - Lymphatic node chains of the human body are particularly difficult to realistically model in computational human phantoms. In the absence of a lymphatic node model, researchers have used the following surrogate tissues to calculate the radiation dose to the lymphatic nodes: blood vessels, muscle and the combination of the muscle and adipose tissues. In the present work, the authors investigated whether and in which extent the use of different surrogate tissues is appropriate to assess the lymph node dose, using a realistic model of lymphatic nodes that the authors recently reported. To validate the results of this study, the lymph node dose calculated here was compared with the dose published by the International Commission on Radiological Protection for the adult male reference phantom. The lymph node dose conversion coefficients with the values calculated for the blood vessels, muscle, adipose tissue and the combination of muscle and adipose tissues were then compared.
JF  - Radiation Protection Dosimetry
AU  - Lamart, Stephanie
AU  - Moroz, Brian E
AU  - Lee, Choonsik
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA, leechoonsik@mail.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 600
EP  - 609
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 157
IS  - 4
SN  - 0144-8420, 0144-8420
KW  - Environment Abstracts
KW  - Tissues
KW  - Radiation
KW  - Adipose tissues
KW  - Dosimetry
KW  - Commissions
KW  - Muscles
KW  - Lymph nodes
KW  - ENA 08:International
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534820308?accountid=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=Radiation+Protection+Dosimetry&rft.atitle=EVALUATION+OF+THE+USE+OF+SURROGATE+TISSUES+FOR+CALCULATING+RADIATION+DOSE+TO+LYMPHATIC+NODES+FROM+EXTERNAL+PHOTON+BEAMS&rft.au=Lamart%2C+Stephanie%3BMoroz%2C+Brian+E%3BLee%2C+Choonsik&rft.aulast=Lamart&rft.aufirst=Stephanie&rft.date=2013-01-01&rft.volume=157&rft.issue=4&rft.spage=600&rft.isbn=&rft.btitle=&rft.title=Radiation+Protection+Dosimetry&rft.issn=01448420&rft_id=info:doi/10.1093%2Frpd%2Fnct164
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-06-01
N1  - Last updated - 2014-07-24
N1  - SubjectsTermNotLitGenreText - Tissues; Radiation; Adipose tissues; Commissions; Dosimetry; Muscles; Lymph nodes
DO  - http://dx.doi.org/10.1093/rpd/nct164
ER  - 



TY  - JOUR
T1  - Simultaneous quantification of 28 synthetic cathinones and metabolites in urine by liquid chromatography-high resolution mass spectrometry
AN  - 1520934749; 19317162
AB  - Synthetic cathinones are novel stimulants derived from cathinone, with amphetamines or cocaine-like effects, often labeled "not for human consumption" and considered "legal highs". Emergence of these new designer drugs complicate interpretation of forensic and clinical cases, with introduction of many new analogs designed to circumvent legislation and vary effects and potencies. We developed a method for the simultaneous quantification of 28 synthetic cathinones, including four metabolites, in urine by liquid chromatography coupled to high resolution mass spectrometry (LC-HRMS). These cathinones include cathinone, methcathinone, and synthetic cathinones position-3'-substituted, N-alkyl-substituted, ring-substituted, methylenedioxy-substituted, and pyrrolidinyl-substituted. We employed a Q Exactive high resolution mass spectrometer, with compounds identified and quantified by target-MSMS experiments. The method was applied to authentic urine specimens from synthetic cathinone users. This method provides a comprehensive confirmation method for 28 synthetic cathinones in urine, with good selectivity and specificity.
JF  - Analytical and Bioanalytical Chemistry
AU  - Concheiro, Marta
AU  - Anizan, Sebastien
AU  - Ellefsen, Kayla
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 05A721, Baltimore, MD 21224, USA, mhuestis@intra.nida.nih.gov
PY  - 2013
SP  - 9437
EP  - 9448
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 405
IS  - 29
SN  - 1618-2642, 1618-2642
KW  - Aqualine Abstracts; Water Resources Abstracts
KW  - Synthetic cathinones
KW  - Urine
KW  - LC-HRMS
KW  - Stability
KW  - Mass Spectrometry
KW  - Metabolites
KW  - Liquid Chromatography
KW  - Selectivity
KW  - Drugs
KW  - Legislation
KW  - Spectrometers
KW  - AQ 00001:Water Resources and Supplies
KW  - SW 0810:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520934749?accountid=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=Simultaneous+quantification+of+28+synthetic+cathinones+and+metabolites+in+urine+by+liquid+chromatography-high+resolution+mass+spectrometry&rft.au=Concheiro%2C+Marta%3BAnizan%2C+Sebastien%3BEllefsen%2C+Kayla%3BHuestis%2C+Marilyn+A&rft.aulast=Concheiro&rft.aufirst=Marta&rft.date=2013-01-01&rft.volume=405&rft.issue=29&rft.spage=9437&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-013-7386-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2015-12-01
N1  - Number of references - 34
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Mass Spectrometry; Urine; Liquid Chromatography; Metabolites; Drugs; Selectivity; Legislation; Spectrometers
DO  - http://dx.doi.org/10.1007/s00216-013-7386-z
ER  - 



TY  - JOUR
T1  - Burkitt Lymphoma: beyond discoveries
AN  - 1520375618; 18713868
AB  - First described in 1958 in Uganda, Burkitt lymphoma (BL) attracted interest worldwide following reports of its uneven geographic distribution and rapidly fatal clinical course. Both suggested infectious etiology and curability. Seminal discoveries followed in quick succession. Viral etiology - due to Epstein-Barr virus (EBV) - was confirmed. Chromosomal translocations, involving cellular MYC, a protooncogene, were discovered, shown to be a hallmark of BL, and central to the genetic basis of cancer. Cure of BL using combination chemotherapy was demonstrated. Unfortunately, civil disturbance in Africa disrupted BL research and blunted its impact on education and oncology care in Africa. Important questions went unanswered. The risk of BL due to malaria or EBV was not quantified. Efforts to answer whether BL could be prevented - by preventing malaria or early EBV infection - were abandoned. The mechanism of malaria in BL is unknown. In Africa, BL remains mostly fatal and diagnosis is still made clinically. Unprecedented advances in molecular, genomics and proteomic technologies, promising to unlock mysteries of cancers, have re-awakened interest in BL. With return of stability to Africa, the unanswered questions about BL are re-attracting global interest. This interest now includes exploiting the knowledge gained about genetics, proteomics, and bioinformatics to enable the development of targeted less toxic treatment for BL; and simpler methods to diagnose BL with high accuracy and sensitivity. The articles in the Burkitt Lymphoma (BL): Beyond Discoveries in Infectious Agents and Cancer highlight BL as priority. Authors explore etiology, pathology, pathogenesis of BL, and whether knowledge gained in the studies of BL can catalyze sustainable cancer services in one of the world's poorest served regions.
JF  - Infectious Agents and Cancer
AU  - Mbulaiteye, Sam M
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Infections and Immunoepidemiology Branch, 9609 Medical Center Dr, Rm. 6E118 MSC 9704, Bethesda, MD 20892-9704, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 35
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 8
IS  - 1
SN  - 1750-9378, 1750-9378
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW  - Human diseases
KW  - Geographical distribution
KW  - Pathology
KW  - Uganda
KW  - Malaria
KW  - Aetiology
KW  - Ecosystem disturbance
KW  - Epstein-Barr virus
KW  - Education
KW  - Chromosomes
KW  - Viral diseases
KW  - Africa
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/1520375618?accountid=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=Infectious+Agents+and+Cancer&rft.atitle=Burkitt+Lymphoma%3A+beyond+discoveries&rft.au=Mbulaiteye%2C+Sam+M&rft.aulast=Mbulaiteye&rft.aufirst=Sam&rft.date=2013-01-01&rft.volume=8&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Infectious+Agents+and+Cancer&rft.issn=17509378&rft_id=info:doi/10.1186%2F1750-9378-8-35
L2  - http://www.infectagentscancer.com/content/8/1/35
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Number of references - 37
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Chromosomes; Geographical distribution; Education; Human diseases; Pathology; Viral diseases; Malaria; Ecosystem disturbance; Aetiology; Epstein-Barr virus; Africa; Uganda
DO  - http://dx.doi.org/10.1186/1750-9378-8-35
ER  - 



TY  - JOUR
T1  - Dose escalation using ultra-high dose IMRT in intermediate risk prostate cancer without androgen deprivation therapy: preliminary results of toxicity and biochemical control
AN  - 1512333576; 18961057
AB  - Background: To investigate the feasibility of dose escalation (86 Gy at 2 Gy/fraction) with intensity modulated radiation therapy (IMRT) in intermediate-risk prostate cancer without androgen deprivation therapy. Methods: Patients with histologically proven adenocarcinoma of the prostate, intermediate prognostic category, were enrolled in this study. Early and late toxicity were scored according to the Cancer Therapy Evaluation Program, Common Terminology Criteria for Adverse Events, Version 3.0. Treatment outcome was stated in terms of biochemical failure, biopsy result and clinical failure. Results: 39 patients with a median follow-up of 71 months were analyzed. No patient experienced G3 or G4 acute gastrointestinal (GI) or genitourinary (GU) toxicity. G2 acute GI and GU toxicity were observed in 17 (44%) and 20 (51%) patients, respectively. Fourteen patients (36%) did not experience acute GI toxicity and 4 patients (10%) did not experience acute GU toxicity. G2 late GI bleeding occurred in 7 of 39 patients (18%). Both G3 and G4 late GI toxicity were seen only in one patient (2.5%). Two patients (5%) experienced G2 late GU toxicity, while G3 late GU toxicity occurred in 3 patients (8%). The 5-year actuarial freedom from biochemical failure (FFBF) was 87%. Thirty-four patients (87%) did not show biochemical relapse. Seventeen patients (44%) underwent biopsy two year after radiotherapy; of these only two were non-negative and both did not show evidence of biochemical disease. Conclusions: IMRT treatment of patients with localized intermediate-risk prostate cancer at high dose levels without using androgen deprivation therapy (ADT) seems to give good disease control. Nevertheless, future trials should aim at further decreasing toxicity by exploiting image guidance techniques and by reducing the dose delivered at the interface between organs at risk and prostate.
JF  - Journal of Experimental and Clinical Cancer Research
AU  - Petrongari, Maria Grazia
AU  - Landoni, Valeria
AU  - Saracino, Biancamaria
AU  - Gomellini, Sara
AU  - Arcangeli, Stefano
AU  - Iaccarino, Giuseppe
AU  - Pinnaro, Paola
AU  - Arcangeli, Giorgio
AU  - Strigari, Lidia
AD  - Department of Radiation Oncology, Regina Elena National Cancer Institute, Rome, Italy
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 103
PB  - Regina Elena Institute for Cancer Research
VL  - 32
IS  - 1
SN  - 1756-9966, 1756-9966
KW  - Toxicology Abstracts
KW  - Prostate cancer
KW  - Radiation
KW  - Disease control
KW  - Bleeding
KW  - Radiotherapy
KW  - Biopsy
KW  - Toxicity
KW  - Adenocarcinoma
KW  - Clinical trials
KW  - Androgens
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512333576?accountid=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+Experimental+and+Clinical+Cancer+Research&rft.atitle=Dose+escalation+using+ultra-high+dose+IMRT+in+intermediate+risk+prostate+cancer+without+androgen+deprivation+therapy%3A+preliminary+results+of+toxicity+and+biochemical+control&rft.au=Petrongari%2C+Maria+Grazia%3BLandoni%2C+Valeria%3BSaracino%2C+Biancamaria%3BGomellini%2C+Sara%3BArcangeli%2C+Stefano%3BIaccarino%2C+Giuseppe%3BPinnaro%2C+Paola%3BArcangeli%2C+Giorgio%3BStrigari%2C+Lidia&rft.aulast=Petrongari&rft.aufirst=Maria&rft.date=2013-01-01&rft.volume=32&rft.issue=1&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Journal+of+Experimental+and+Clinical+Cancer+Research&rft.issn=17569966&rft_id=info:doi/10.1186%2F1756-9966-32-103
L2  - http://www.jeccr.com/content/32/1/103
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Number of references - 35
N1  - Last updated - 2014-05-02
N1  - SubjectsTermNotLitGenreText - Prostate cancer; Radiation; Bleeding; Disease control; Radiotherapy; Biopsy; Toxicity; Adenocarcinoma; Clinical trials; Androgens
DO  - http://dx.doi.org/10.1186/1756-9966-32-103
ER  - 



TY  - JOUR
T1  - Evidence from a breast cancer hypofractionated schedule: late skin toxicity assessed by ultrasound
AN  - 1512330160; 18746516
AB  - Background: Feasibility of whole breast hypofractionated radiotherapy schedules in breast conserving therapy is recognized however concerns remain about the role of the boost dose on the overall treatment's potential toxicity. In this study we report on the possibility to quantitatively evaluate radiation induced toxicity in patients treated with an abbreviated course with major concern in the irradiated boost region. Methods: Eighty-nine patients who underwent conservative surgery for early-stage breast cancer followed by adjuvant accelerated hypofractionated whole breast radiotherapy were included in this study to assess skin and subcutaneous tissue late toxicity by means of ultrasonographic quantitative examination. For each patient the skin thickness was measured at four positions: on the irradiated breast, in the boost region and in the corresponding positions in the contra-lateral not treated breast. All patients were scanned by the same radiologist to reduce potential inter-operator variability, the operator was blind to the scoring of the patient CTCv3 late toxicity as well as patient treatment characteristics. Ultrasound assessment and clinical evaluation were compared. Results: The median time between the end of adjuvant radiotherapy and ultrasound examination was 20.5 months. The measured mean skin thickness in the irradiated breast was 2.13 plus or minus 0.72 mm while in the mirror region of the contra-lateral healthy breast was 1.61 plus or minus 0.29 mm. The measured mean skin thickness in the irradiated boost region was 2.25 plus or minus 0.79 mm versus 1.63 plus or minus 0.33 mm in the corresponding region of contra-lateral healthy breast. The mean increment in skin thickness respect to the counterpart in the healthy breast was 0.52 plus or minus 0.67 mm and 0.62 plus or minus 0.74 mm for the breast and the boost region respectively. A significant direct correlation was found between the increment in skin thickness in the irradiated breast and in the boost region with fibrosis (G > or = 1). Conclusions: In this study results from a breast cancer hypofractionated schedule in terms of late skin toxicity are reported. In particular our study confirms that late cutaneous reactions can be reliably assed by ultrasonographic examination, also discriminating between regions irradiated at different doses, and that this instrumental evaluation is in agreement with clinical stated toxicity.
JF  - Journal of Experimental and Clinical Cancer Research
AU  - Landoni, Valeria
AU  - Giordano, Carolina
AU  - Marsella, Annelisa
AU  - Saracino, Biancamaria
AU  - Petrongari, Maria Grazia
AU  - Ferraro, Anna Maria
AU  - Strigari, Lidia
AU  - Pinnaro, Paola
AD  - Laboratory of Medical Physics and Expert Systems, Regina Elena National Cancer Institute, Rome, Italy
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 80
PB  - Regina Elena Institute for Cancer Research
VL  - 32
IS  - 1
SN  - 1756-9966, 1756-9966
KW  - Toxicology Abstracts
KW  - Skin
KW  - Radiation
KW  - Fibrosis
KW  - Surgery
KW  - Breast cancer
KW  - Radiotherapy
KW  - Toxicity
KW  - Adjuvants
KW  - Ultrasound
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512330160?accountid=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+Experimental+and+Clinical+Cancer+Research&rft.atitle=Evidence+from+a+breast+cancer+hypofractionated+schedule%3A+late+skin+toxicity+assessed+by+ultrasound&rft.au=Landoni%2C+Valeria%3BGiordano%2C+Carolina%3BMarsella%2C+Annelisa%3BSaracino%2C+Biancamaria%3BPetrongari%2C+Maria+Grazia%3BFerraro%2C+Anna+Maria%3BStrigari%2C+Lidia%3BPinnaro%2C+Paola&rft.aulast=Landoni&rft.aufirst=Valeria&rft.date=2013-01-01&rft.volume=32&rft.issue=1&rft.spage=80&rft.isbn=&rft.btitle=&rft.title=Journal+of+Experimental+and+Clinical+Cancer+Research&rft.issn=17569966&rft_id=info:doi/10.1186%2F1756-9966-32-80
L2  - http://www.jeccr.com/content/32/1/80
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-04-01
N1  - Number of references - 18
N1  - Last updated - 2014-05-02
N1  - SubjectsTermNotLitGenreText - Skin; Radiation; Fibrosis; Surgery; Radiotherapy; Breast cancer; Adjuvants; Toxicity; Ultrasound
DO  - http://dx.doi.org/10.1186/1756-9966-32-80
ER  - 



TY  - JOUR
T1  - An Alternative Approach to Water Regulations for Public Health Protection at Bathing Beaches
AN  - 1508757975; 19389010
AB  - New approaches should be considered as the US Environmental Protection Agency (EPA) moves rapidly to develop new beach monitoring guidelines by the end of 2012, as these guidelines serve as the basis by which states and territories with coasts along the oceans and Great Lakes can then develop and implement monitoring programs for recreational waters. We describe and illustrate one possible approach to beach regulation termed as the "Comprehensive Toolbox within an Approval Process (CTBAP)." The CTBAP consists of three components. The first is a "toolbox" consisting of an inventory of guidelines on monitoring targets, a series of measurement techniques, and guidance to improve water quality through source identification and prevention methods. The second two components are principles of implementation. These include first, "flexibility" to encourage and develop an individualized beach management plan tailored to local conditions and second, "consistency" of this management plan to ensure a consistent national level of public health protection. The results of this approach are illustrated through a case study at a well-studied South Florida recreational marine beach. This case study explores different monitoring targets based on two different health endpoints (skin versus gastrointestinal illness) and recommends a beach regulation program for the study beach that focuses predominately on source prevention.
JF  - Journal of Environmental and Public Health
AU  - Abdelzaher, Amir M
AU  - Solo-Gabriele, Helena M
AU  - Phillips, Matthew C
AU  - Elmir, Samir M
AU  - Fleming, Lora E
AD  - NSF NIEHS Oceans and Human Health Center, University of Miami, Miami, FL 33149, USA, hmsolo@miami.edu
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2013
SN  - 1687-9805, 1687-9805
KW  - Pollution Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; Oceanic Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW  - Pollution monitoring
KW  - Bathing
KW  - Management plans
KW  - Territory
KW  - Water quality
KW  - Public health
KW  - Lakes
KW  - Case studies
KW  - Coastal morphology
KW  - Recreational waters
KW  - ASW, USA, Florida
KW  - Beaches
KW  - Skin
KW  - Guidelines
KW  - Illustrations
KW  - Identification
KW  - Coastal zone management
KW  - EPA
KW  - Coastal zone
KW  - Prevention
KW  - Recreation areas
KW  - Oceans
KW  - North America, Great Lakes
KW  - Environment management
KW  - O 4090:Conservation and Environmental Protection
KW  - P 1000:MARINE POLLUTION
KW  - Q5 08502:Methods and instruments
KW  - ENA 12:Oceans & Estuaries
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508757975?accountid=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+Environmental+and+Public+Health&rft.atitle=An+Alternative+Approach+to+Water+Regulations+for+Public+Health+Protection+at+Bathing+Beaches&rft.au=Abdelzaher%2C+Amir+M%3BSolo-Gabriele%2C+Helena+M%3BPhillips%2C+Matthew+C%3BElmir%2C+Samir+M%3BFleming%2C+Lora+E&rft.aulast=Abdelzaher&rft.aufirst=Amir&rft.date=2013-01-01&rft.volume=2013&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+Environmental+and+Public+Health&rft.issn=16879805&rft_id=info:doi/10.1155%2F2013%2F138521
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-03-01
N1  - Last updated - 2014-12-11
N1  - SubjectsTermNotLitGenreText - Pollution monitoring; Coastal morphology; Illustrations; Bathing; Recreational waters; Identification; Environment management; Coastal zone management; Public health; Beaches; Skin; Guidelines; Management plans; Territory; Water quality; EPA; Prevention; Lakes; Coastal zone; Case studies; Recreation areas; Oceans; ASW, USA, Florida; North America, Great Lakes
DO  - http://dx.doi.org/10.1155/2013/138521
ER  - 



TY  - JOUR
T1  - Auditory analysis of xeroderma pigmentosum 1971-2012: hearing function, sun sensitivity and DNA repair predict neurological degeneration
AN  - 1504416521; 201403893
AB  - To assess the role of DNA repair in maintenance of hearing function and neurological integrity, we examined hearing status, neurological function, DNA repair complementation group and history of acute burning on minimal sun exposure in all patients with xeroderma pigmentosum, who had at least one complete audiogram, examined at the National Institutes of Health from 1971 to 2012. Seventy-nine patients, aged 1-61 years, were diagnosed with xeroderma pigmentosum (n = 77) or xeroderma pigmentosum/Cockayne syndrome (n = 2). A total of 178 audiograms were included. Clinically significant hearing loss (>20 dB) was present in 23 (29%) of 79 patients. Of the 17 patients with xeroderma pigmentosum-type neurological degeneration, 13 (76%) developed hearing loss, and all 17 were in complementation groups xeroderma pigmentosum type A or type D and reported acute burning on minimal sun exposure. Acute burning on minimal sun exposure without xeroderma pigmentosum-type neurological degeneration was present in 18% of the patients (10/55). Temporal bone histology in a patient with severe xeroderma pigmentosum-type neurological degeneration revealed marked atrophy of the cochlear sensory epithelium and neurons. The 19-year mean age of detection of clinically significant hearing loss in the patients with xeroderma pigmentosum with xeroderma pigmentosum-type neurological degeneration was 54 years younger than that predicted by international norms. The four frequency (0.5/1/2/4 kHz) pure-tone average correlated with degree of neurodegeneration (P =10 dB hearing loss was associated with a 39-fold increased risk (P = 0.002) of having xeroderma pigmentosum-type neurological degeneration. Severity of hearing loss parallels neurological decline in patients with xeroderma pigmentosum-type neurological degeneration. Audiometric findings, complementation group, acute burning on minimal sun exposure and age were important predictors of xeroderma pigmentosum-type neurological degeneration. These results provide evidence that DNA repair is critical in maintaining neurological integrity of the auditory system. Adapted from the source document
JF  - Brain
AU  - Totonchy, Mariam B
AU  - Tamura, Deborah
AU  - Pantell, Matthew S
AU  - Zalewski, Christopher
AU  - Bradford, Porcia T
AU  - Merchant, Saumil N
AU  - Nadol, Joseph
AU  - Khan, Sikandar G
AU  - Schiffmann, Raphael
AU  - Pierson, Tyler Mark
AU  - Wiggs, Edythe
AU  - Griffith, Andrew J
AU  - DiGiovanna, John J
AU  - Kraemer, Kenneth H
AU  - Brewer, Carmen C
AD  - Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USA Kraemerk@nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 194
EP  - 208
VL  - 136
IS  - 1
SN  - 0006-8950, 0006-8950
KW  - Hearing (31150)
KW  - Auditory System (06100)
KW  - Genetics (27600)
KW  - Cochlea (12639)
KW  - Sensorineural Hearing Loss (77290)
KW  - article
KW  - 6310: hearing-pathological and normal; hearing-pathological and normal
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504416521?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain&rft.atitle=Auditory+analysis+of+xeroderma+pigmentosum+1971-2012%3A+hearing+function%2C+sun+sensitivity+and+DNA+repair+predict+neurological+degeneration&rft.au=Totonchy%2C+Mariam+B%3BTamura%2C+Deborah%3BPantell%2C+Matthew+S%3BZalewski%2C+Christopher%3BBradford%2C+Porcia+T%3BMerchant%2C+Saumil+N%3BNadol%2C+Joseph%3BKhan%2C+Sikandar+G%3BSchiffmann%2C+Raphael%3BPierson%2C+Tyler+Mark%3BWiggs%2C+Edythe%3BGriffith%2C+Andrew+J%3BDiGiovanna%2C+John+J%3BKraemer%2C+Kenneth+H%3BBrewer%2C+Carmen+C&rft.aulast=Totonchy&rft.aufirst=Mariam&rft.date=2013-01-01&rft.volume=136&rft.issue=1&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/
LA  - English
DB  - Linguistics and Language Behavior Abstracts (LLBA)
N1  - Date revised - 2014-03-01
N1  - Last updated - 2016-09-27
N1  - CODEN - BRAIAK
N1  - SubjectsTermNotLitGenreText - Sensorineural Hearing Loss (77290); Hearing (31150); Auditory System (06100); Genetics (27600); Cochlea (12639)
ER  - 



TY  - JOUR
T1  - Using passenger mutations to estimate the timing of driver mutations and identify mutator alterations
AN  - 1500767603; 19157752
AB  - Background: Recent developments in high-throughput genomic technologies make it possible to have a comprehensive view of genomic alterations in tumors on a whole genome scale. Only a small number of somatic alterations detected in tumor genomes are driver alterations which drive tumorigenesis. Most of the somatic alterations are passengers that are neutral to tumor cell selection. Although most research efforts are focused on analyzing driver alterations, the passenger alterations also provide valuable information about the history of tumor development. Results: In this paper, we develop a method for estimating the age of the tumor lineage and the timing of the driver alterations based on the number of passenger alterations. This method also identifies mutator genes which increase genomic instability when they are altered and provides estimates of the increased rate of alterations caused by each mutator gene. We applied this method to copy number data and DNA sequencing data for ovarian and lung tumors. We identified well known mutators such as TP53, PRKDC, BRCA1/2 as well as new mutator candidates PPP2R2A and the chromosomal region 22q13.33. We found that most mutator genes alter early during tumorigenesis and were able to estimate the age of individual tumor lineage in cell generations. Conclusions: This is the first computational method to identify mutator genes and to take into account the increase of the alteration rate by mutator genes, providing more accurate estimates of the tumor age and the timing of driver alterations.
JF  - BMC Bioinformatics
AU  - Youn, Ahrim
AU  - Simon, Richard
AD  - Biometric Research Branch, National Cancer Institute, Bethesda, Maryland, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 363
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2105, 1471-2105
KW  - Biotechnology and Bioengineering Abstracts
KW  - Age
KW  - Tumorigenesis
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500767603?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=Using+passenger+mutations+to+estimate+the+timing+of+driver+mutations+and+identify+mutator+alterations&rft.au=Youn%2C+Ahrim%3BSimon%2C+Richard&rft.aulast=Youn&rft.aufirst=Ahrim&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=363&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-14-363
L2  - http://www.biomedcentral.com/1471-2105/14/363
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Number of references - 1
N1  - Last updated - 2014-03-20
N1  - SubjectsTermNotLitGenreText - Tumorigenesis
DO  - http://dx.doi.org/10.1186/1471-2105-14-363
ER  - 



TY  - JOUR
T1  - Anticancer Activity of beta -Elemene and its Synthetic Analogs in Human Malignant Brain Tumor Cells
AN  - 1496891979; 17573579
AB  - Malignant brain tumors are aggressive in both children and adults. Despite recent improvements in diagnostic techniques, therapeutic approaches remain disappointing and unsuccessful. There is an urgent need for promising anticancer agents to improve overall survival of patients with brain cancer. beta -Elemene has been shown to have antiproliferative effects on many types of carcinomas. In this study, we compared the cytotoxic efficacy of beta -elemene and its synthetic analogs in the brain tumor cell lines A172, CCF-STTG1, and U-87MG. beta -Elemene exhibited cytotoxicity towards the tumor lines, effectively suppressing tumor cell survival. The inhibitory effect of beta -elemene was mediated by the induction of apoptosis, as demonstrated by three assays. The annexin V assay showed that beta -elemene increased the percentage of early- and late-apoptotic cells. Apoptotic nuclei were detected in cancer cells in situ by the terminal deoxynucleotidyltransferase-mediated deoxy- UTP-fluorescein nick end labeling (TUNEL) staining, and the number of TUNEL-positive cells was significantly increased at 24-72 h following drug treatment of the cell lines. Cell death enzyme-linked immunosorbent assay (ELISA) gave similar results. Furthermore, beta -elemene increased caspase-3/7/10 activity, up-regulated protein expression of BAX, and down-regulated the one of BCL-2, BCL-XL, and of X-linked inhibitor of apoptosis (XIAP) in the cells, suggesting that apoptotic signaling pathways are involved in the responses triggered by beta -elemene. Compared with beta -elemene, only three of the 10 synthetic beta -elemene analogs studied here, exerted comparable cytotoxic efficacy towards the three brain tumor lines: the analogs Lr-1 and Lr-2 had the same antitumor efficacy, while Lr-3 was less potent than beta -elemene. Thus, some synthetic analogs of beta -elemene may inhibit brain cancer cell growth and proliferation, and the synthetic analogs Lr-1 and Lr-2 may have great potential as alternatives to beta -elemene for anticancer therapy. Overall, this study provides, to our knowledge, the first evidence showing that synthetic analogs of beta -elemene hold promise for patients with brain tumors.
JF  - Anticancer Research
AU  - Li, Q Q
AU  - Lee, R X
AU  - Liang, H
AU  - Zhong, Y
AD  - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, liquenti@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 65
EP  - 76
VL  - 33
IS  - 1
SN  - 0250-7005, 0250-7005
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Annexin V
KW  - Brain tumors
KW  - N3 11001:Behavioral and Cognitive Neuroscience
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496891979?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anticancer+Research&rft.atitle=Anticancer+Activity+of+beta+-Elemene+and+its+Synthetic+Analogs+in+Human+Malignant+Brain+Tumor+Cells&rft.au=Li%2C+Q+Q%3BLee%2C+R+X%3BLiang%2C+H%3BZhong%2C+Y&rft.aulast=Li&rft.aufirst=Q&rft.date=2013-01-01&rft.volume=33&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Anticancer+Research&rft.issn=02507005&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Brain tumors
ER  - 



TY  - JOUR
T1  - Oral fluid cannabinoid concentrations following controlled smoked cannabis in chronic frequent and occasional smokers
AN  - 1492654887; 18900782
AB  - Oral fluid (OF) is an alternative biological matrix for monitoring cannabis intake in drug testing, and drugged driving (DUID) programs, but OF cannabinoid test interpretation is challenging. Controlled cannabinoid administration studies provide a scientific database for interpreting cannabinoid OF tests. We compared differences in OF cannabinoid concentrations from 19 h before to 30 h after smoking a 6.8% THC cigarette in chronic frequent and occasional cannabis smokers. OF was collected with the Statsure Saliva Sampler(trademark sign) OF device. 2D-GC-MS was used to quantify cannabinoids in 357 OF specimens; 65 had inadequate OF volume within 3 h after smoking. All OF specimens were THC-positive for up to 13.5 h after smoking, without significant differences between frequent and occasional smokers over 30 h. Cannabidiol (CBD) and cannabinol (CBN) had short median last detection times (2.5-4 h for CBD and 6-8 h for CBN) in both groups. THCCOOH was detected in 25 and 212 occasional and frequent smokers' OF samples, respectively. THCCOOH provided longer detection windows than THC in all frequent smokers. As THCCOOH is not present in cannabis smoke, its presence in OF minimizes the potential for false positive results from passive environmental smoke exposure, and can identify oral THC ingestion, while OF THC cannot. THC(greater-than or equal to)1 (mu)g/L, in addition to CBD(greater-than or equal to)1 (mu)g/L or CBN(greater-than or equal to)1 (mu)g/L suggested recent cannabis intake ((less-than or equal to)13.5 h), important for DUID cases, whereas THC(greater-than or equal to)1 (mu)g/L or THC(greater-than or equal to)2 (mu)g/L cutoffs had longer detection windows ((greater-than or equal to)30 h), important for workplace testing. THCCOOH windows of detection for chronic, frequent cannabis smokers extended beyond 30 h, while they were shorter (0-24 h) for occasional cannabis smokers.
JF  - Analytical and Bioanalytical Chemistry
AU  - Anizan, Sebastien
AU  - Milman, Garry
AU  - Desrosiers, Nathalie
AU  - Barnes, Allan J
AU  - Gorelick, David A
AU  - Huestis, Marilyn A
AD  - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, 251 Bayview Boulevard, Baltimore, MD 21224, USA, mhuestis@intra.nida.nih.gov
PY  - 2013
SP  - 8451
EP  - 8461
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 405
IS  - 26
SN  - 1618-2642, 1618-2642
KW  - Aqualine Abstracts; Water Resources Abstracts; Toxicology Abstracts
KW  - Cigarettes
KW  - Drug abuse
KW  - Smoking
KW  - Computer programs
KW  - Cannabinoids
KW  - Administration
KW  - Exposure
KW  - Cannabis
KW  - Drugs
KW  - oral fluids
KW  - Testing Procedures
KW  - Cutoffs
KW  - Detection Times
KW  - Tetrahydrocannabinol
KW  - Smoke
KW  - Databases
KW  - Saliva
KW  - Monitoring
KW  - AQ 00001:Water Resources and Supplies
KW  - X 24380:Social Poisons & Drug Abuse
KW  - SW 0810:General
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492654887?accountid=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=Oral+fluid+cannabinoid+concentrations+following+controlled+smoked+cannabis+in+chronic+frequent+and+occasional+smokers&rft.au=Anizan%2C+Sebastien%3BMilman%2C+Garry%3BDesrosiers%2C+Nathalie%3BBarnes%2C+Allan+J%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Anizan&rft.aufirst=Sebastien&rft.date=2013-01-01&rft.volume=405&rft.issue=26&rft.spage=8451&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-013-7291-5
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 49
N1  - Last updated - 2016-01-21
N1  - SubjectsTermNotLitGenreText - Smoke; Tetrahydrocannabinol; Databases; Computer programs; Smoking; Cigarettes; Cannabinoids; Cannabis; Saliva; Drug abuse; oral fluids; Testing Procedures; Cutoffs; Exposure; Administration; Monitoring; Drugs; Detection Times
DO  - http://dx.doi.org/10.1007/s00216-013-7291-5
ER  - 



TY  - JOUR
T1  - Viral and Cellular Biomarkers in the Diagnosis of Cervical Intraepithelial Neoplasia and Cancer
AN  - 1492654803; 18962160
AB  - Cervical cancer arises from cells localized in the ectoendocervical squamocolumnar junction of the cervix persistently infected with one of about 13 human papillomavirus (HPV) genotypes. The majority of HPV infections induces low grade squamous epithelial lesions that in more than 90% of cases spontaneously regress and in about 10% eventually progress to high grade lesions and even less frequently evolve to invasive cancer. Tumor progression is characterized by (1) increased expression of E6 and E7 genes of high risk HPVs, known to bind to and inactivate p53 and pRb oncosuppressors, respectively; (2) integration of viral DNA into host genome, with disruption of E2 viral genes and host chromosomal loci; and (3) molecular alterations of key regulators of cell cycle. Molecular markers with high sensitivity and specificity in differentiating viral infections associated with cellular abnormalities with high risk of progression are strongly needed for cervical cancer screening and triage. This review will focus on the analysis of clinical validated or candidate biomarkers, such as HPV DNA, HPV E6/E7 mRNA, HPV proteins, p16(INK4a) and Ki67, TOP2A and MCM2 cellular factors, and DNA methylation profiles, which will likely improve the identification of premalignant lesions that have a high risk to evolve into invasive cervical cancer.
JF  - BioMed Research International
AU  - Tornesello, Maria Lina
AU  - Buonaguro, Luigi
AU  - Giorgi-Rossi, Paolo
AU  - Buonaguro, Franco M
AD  - Molecular Biology and Viral Oncology, National Cancer Institute "Fondazione Pascale", Cappella Cangiani, 80131 Naples, Italy, ml.tornesello@istitutotumori.na.it
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2013
SN  - 2314-6133, 2314-6133
KW  - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Cell cycle
KW  - Risk factors
KW  - Human papillomavirus
KW  - V:22370
KW  - W 30900:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492654803?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Viral+and+Cellular+Biomarkers+in+the+Diagnosis+of+Cervical+Intraepithelial+Neoplasia+and+Cancer&rft.au=Tornesello%2C+Maria+Lina%3BBuonaguro%2C+Luigi%3BGiorgi-Rossi%2C+Paolo%3BBuonaguro%2C+Franco+M&rft.aulast=Tornesello&rft.aufirst=Maria&rft.date=2013-01-01&rft.volume=2013&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2013%2F519619
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Risk factors; Human papillomavirus
DO  - http://dx.doi.org/10.1155/2013/519619
ER  - 



TY  - JOUR
T1  - A deep insight into the sialotranscriptome of the mosquito, Psorophora albipes
AN  - 1492644986; 18961078
AB  - Background: Psorophora mosquitoes are exclusively found in the Americas and have been associated with transmission of encephalitis and West Nile fever viruses, among other arboviruses. Mosquito salivary glands represent the final route of differentiation and transmission of many parasites. They also secrete molecules with powerful pharmacologic actions that modulate host hemostasis, inflammation, and immune response. Here, we employed next generation sequencing and proteome approaches to investigate for the first time the salivary composition of a mosquito member of the Psorophora genus. We additionally discuss the evolutionary position of this mosquito genus into the Culicidae family by comparing the identity of its secreted salivary compounds to other mosquito salivary proteins identified so far. Results: Illumina sequencing resulted in 13,535,229 sequence reads, which were assembled into 3,247 contigs. All families were classified according to their in silico-predicted function/ activity. Annotation of these sequences allowed classification of their products into 83 salivary protein families, twenty (24.39%) of which were confirmed by our subsequent proteome analysis. Two protein families were deorphanized from Aedes and one from Ochlerotatus, while four protein families were described as novel to Psorophora genus because they had no match with any other known mosquito salivary sequence. Several protein families described as exclusive to Culicines were present in Psorophora mosquitoes, while we did not identify any member of the protein families already known as unique to Anophelines. Also, the Psorophora salivary proteins had better identity to homologs in Aedes (69.23%), followed by Ochlerotatus (8.15%), Culex (6.52%), and Anopheles (4.66%), respectively. Conclusions: This is the first sialome (from the Greek sialo = saliva) catalog of salivary proteins from a Psorophora mosquito, which may be useful for better understanding the lifecycle of this mosquito and the role of its salivary secretion in arboviral transmission.
JF  - BMC Genomics
AU  - Chagas, Andrezza C
AU  - Calvo, Eric
AU  - Rios-Velasquez, Claudia M
AU  - Pessoa, Felipe AC
AU  - Medeiros, Jansen F
AU  - Ribeiro, Jose MC
AD  - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 875
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2164, 1471-2164
KW  - Genetics Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Entomology Abstracts
KW  - Parasites
KW  - Catalogs
KW  - Anopheles
KW  - Viruses
KW  - Catalogues
KW  - Salivary gland
KW  - Defence mechanisms
KW  - Public health
KW  - Fever
KW  - Differentiation
KW  - Classification
KW  - Glands
KW  - Ochlerotatus
KW  - Aquatic insects
KW  - Aedes
KW  - Psorophora
KW  - protein families
KW  - Culicidae
KW  - Encephalitis
KW  - Inflammation
KW  - Culex
KW  - hemostasis
KW  - Saliva
KW  - Immune response
KW  - Evolution
KW  - G 07810:Insects
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Z 05360:Genetics and Evolution
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492644986?accountid=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=BMC+Genomics&rft.atitle=A+deep+insight+into+the+sialotranscriptome+of+the+mosquito%2C+Psorophora+albipes&rft.au=Chagas%2C+Andrezza+C%3BCalvo%2C+Eric%3BRios-Velasquez%2C+Claudia+M%3BPessoa%2C+Felipe+AC%3BMedeiros%2C+Jansen+F%3BRibeiro%2C+Jose+MC&rft.aulast=Chagas&rft.aufirst=Andrezza&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=875&rft.isbn=&rft.btitle=&rft.title=BMC+Genomics&rft.issn=14712164&rft_id=info:doi/10.1186%2F1471-2164-14-875
L2  - http://www.biomedcentral.com/1471-2164/14/875
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Number of references - 72
N1  - Last updated - 2016-02-18
N1  - SubjectsTermNotLitGenreText - Classification; Glands; Viruses; Catalogues; Defence mechanisms; Aquatic insects; Evolution; Public health; Fever; Differentiation; Parasites; Catalogs; hemostasis; protein families; Immune response; Saliva; Salivary gland; Encephalitis; Inflammation; Culex; Aedes; Psorophora; Anopheles; Culicidae; Ochlerotatus
DO  - http://dx.doi.org/10.1186/1471-2164-14-875
ER  - 



TY  - JOUR
T1  - The neurological principle: how traditional Chinese medicine unifies body and mind
AN  - 1492643110; 18954981
AB  - The unity of body and mind is an important concept in Chinese philosophy. Traditionally, the concept is informal and fuzzy, with no well defined meaning in the mathematical sense. This paper proposes a formal information-theoretical model for neural signal processing, arguing that physical principles are neural phenomena. For example, using the proposed model, the paper shows that time-dilation in Einstein's theory of relativity and Heisenberg's uncertainty principle can both be observed in neural signal processing. The paper therefore proposes a new concept, the neurological principle, which subsumes different natural principles. In particular, the paper shows that Yin and Yang, the two forces that according to Chinese philosophy pervade the universe and every entity therein, can be explained with the proposed model. These results provide Chinese medicine with a stronger mathematical foundation.
JF  - International Journal of Function Informatics and Personalised Medicine
AU  - Jaeger, Stefan
AD  - National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 84
EP  - 102
PB  - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom
VL  - 4
IS  - 2
SN  - 1756-2104, 1756-2104
KW  - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW  - HEALTHCARE AND BIOSCIENCES
KW  - Biosciences and Bioinformatics
KW  - Healthcare and Medical Engineering
KW  - Mathematical models
KW  - Data processing
KW  - Informatics
KW  - Philosophy
KW  - Traditional Chinese Medicine
KW  - N3 11027:Neurology & neuropathology
KW  - W 30965:Miscellaneous, Reviews
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492643110?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Function+Informatics+and+Personalised+Medicine&rft.atitle=The+neurological+principle%3A+how+traditional+Chinese+medicine+unifies+body+and+mind&rft.au=Jaeger%2C+Stefan&rft.aulast=Jaeger&rft.aufirst=Stefan&rft.date=2013-01-01&rft.volume=4&rft.issue=2&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Function+Informatics+and+Personalised+Medicine&rft.issn=17562104&rft_id=info:doi/10.1504%2FIJFIPM.2013.057391
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-01-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Data processing; Mathematical models; Informatics; Philosophy; Traditional Chinese Medicine
DO  - http://dx.doi.org/10.1504/IJFIPM.2013.057391
ER  - 



TY  - JOUR
T1  - Obesity and addiction: neurobiological overlaps
AN  - 1492631275; 17513844
AB  - Drug addiction and obesity appear to share several properties. Both can be defined as disorders in which the saliency of a specific type of reward (food or drug) becomes exaggerated relative to, and at the expense of others rewards. Both drugs and food have powerful reinforcing effects, which are in part mediated by abrupt dopamine increases in the brain reward centres. The abrupt dopamine increases, in vulnerable individuals, can override the brain's homeostatic control mechanisms. These parallels have generated interest in understanding the shared vulnerabilities between addiction and obesity. Predictably, they also engendered a heated debate. Specifically, brain imaging studies are beginning to uncover common features between these two conditions and delineate some of the overlapping brain circuits whose dysfunctions may underlie the observed deficits. The combined results suggest that both obese and drug-addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning, self-control, stress reactivity and interoceptive awareness. In parallel, studies are also delineating differences between them that centre on the key role that peripheral signals involved with homeostatic control exert on food intake. Here, we focus on the shared neurobiological substrates of obesity and addiction.
JF  - Obesity Reviews
AU  - Volkow, N D
AU  - Wang, G-J
AU  - Tomasi, D
AU  - Baler, R D
AD  - National Institute on Drug Abuse. National Institutes of Health
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 2
EP  - 18
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 14
IS  - 1
SN  - 1467-7881, 1467-7881
KW  - CSA Neurosciences Abstracts; Physical Education Index
KW  - Addiction
KW  - Obesity
KW  - N3 11001:Behavioral and Cognitive Neuroscience
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492631275?accountid=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=Obesity+Reviews&rft.atitle=Obesity+and+addiction%3A+neurobiological+overlaps&rft.au=Volkow%2C+N+D%3BWang%2C+G-J%3BTomasi%2C+D%3BBaler%2C+R+D&rft.aulast=Volkow&rft.aufirst=N&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Obesity+Reviews&rft.issn=14677881&rft_id=info:doi/10.1111%2Fj.1467-789X.2012.01031.x
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2014-01-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Obesity
DO  - http://dx.doi.org/10.1111/j.1467-789X.2012.01031.x
ER  - 



TY  - JOUR
T1  - Sexual selection acting on a speciation trait in darters (Percidae: Etheostoma)
AN  - 1492629268; 18890922
AB  - Lay summary: Species in which males are colorful and females are less colorful are often assumed to exhibit female mate choice based on male coloration. We show that female darter fish prefer the population mean male color (orange) over an extreme color (red). Evidence of color-driven mate choice within a species may relate to previous studies on mate choice between species of two distinct colors (orange-red vs. green) and the role of color in darter speciation. Lay summary: Species in which males are colorful and females are less colorful are often assumed to exhibit female mate choice based on male coloration. We show that female darter fish prefer the population mean male color (orange) over an extreme color (red). Evidence of color-driven mate choice within a species may relate to previous studies on mate choice between species of two distinct colors (orange-red vs. green) and the role of color in darter speciation.
JF  - Behavioral Ecology
AU  - Williams, Tory H
AU  - Gumm, Jennifer M
AU  - Mendelson, Tamra C
AD  - super(a)Section on Model Synaptic Systems, Laboratory of Molecular Physiology, NIAAA, NIH, 5625 Fishers Lane, Rockville, MD, 20852, USA,, tory.williams@nih.gov
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 1407
EP  - 1414
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 24
IS  - 6
SN  - 1045-2249, 1045-2249
KW  - ASFA 1: Biological Sciences & Living Resources; Animal Behavior Abstracts; Ecology Abstracts
KW  - association preference
KW  - behavioral isolation
KW  - female choice
KW  - male nuptial color
KW  - model.
KW  - Speciation
KW  - Sexual selection
KW  - Coloration
KW  - Mate selection
KW  - Etheostoma
KW  - Reproductive behaviour
KW  - Percidae
KW  - Color
KW  - D 04040:Ecosystem and Ecology Studies
KW  - Q1 08423:Behaviour
KW  - Y 25050:Genetics and Evolution
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492629268?accountid=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=Behavioral+Ecology&rft.atitle=Sexual+selection+acting+on+a+speciation+trait+in+darters+%28Percidae%3A+Etheostoma%29&rft.au=Williams%2C+Tory+H%3BGumm%2C+Jennifer+M%3BMendelson%2C+Tamra+C&rft.aulast=Williams&rft.aufirst=Tory&rft.date=2013-01-01&rft.volume=24&rft.issue=6&rft.spage=1407&rft.isbn=&rft.btitle=&rft.title=Behavioral+Ecology&rft.issn=10452249&rft_id=info:doi/10.1093%2Fbeheco%2Fart080
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-12-22
N1  - SubjectsTermNotLitGenreText - Sexual selection; Reproductive behaviour; Speciation; Coloration; Mate selection; Color; Etheostoma; Percidae
DO  - http://dx.doi.org/10.1093/beheco/art080
ER  - 



TY  - JOUR
T1  - Patterns of Population Structure for Inshore Bottlenose Dolphins along the Eastern United States
AN  - 1492614203; 18892508
AB  - Globally distributed, the bottlenose dolphin (Tursiops truncatus) is found in a range of offshore and coastal habitats. Using 15 microsatellite loci and mtDNA control region sequences, we investigated patterns of genetic differentiation among putative populations along the eastern US shoreline (the Indian River Lagoon, Florida, and Charleston Harbor, South Carolina) (microsatellite analyses: n = 125, mtDNA analyses: n = 132). We further utilized the mtDNA to compare these populations with those from the Northwest Atlantic, Gulf of Mexico, and Caribbean. Results showed strong differentiation among inshore, alongshore, and offshore habitats ( Phi sub(ST) = 0.744). In addition, Bayesian clustering analyses revealed the presence of 2 genetic clusters (populations) within the 250 km Indian River Lagoon. Habitat heterogeneity is likely an important force diversifying bottlenose dolphin populations through its influence on social behavior and foraging strategy. We propose that the spatial pattern of genetic variation within the lagoon reflects both its steep longitudinal transition of climate and also its historical discontinuity and recent connection as part of Intracoastal Waterway development. These findings have important management implications as they emphasize the role of habitat and the consequence of its modification in shaping bottlenose dolphin population structure and highlight the possibility of multiple management units existing in discrete inshore habitats along the entire eastern US shoreline.
JF  - Journal of Heredity
AU  - Richards, Vincent P
AU  - Greig, Thomas W
AU  - Fair, Patricia A
AU  - McCulloch, Stephen D
AU  - Politz, Christine
AU  - Natoli, Ada
AU  - Driscoll, Carlos A
AU  - Hoelzel, A Rus
AU  - David, Victor
AU  - Bossart, Gregory D
AU  - Lopez, Jose V
AD  - From the Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853 (Richards); the Marine Mammal Research and Conservation Program, Harbor Branch Oceanographic Institute at Florida Atlantic University, Ft. Pierce, FL (Greig and Fair); the National Oceanic and Atmospheric Administration, Center for Coastal Environmental Health and Biomolecular Research, Charleston, SC (McCulloch, Politz, Driscoll, Bossart, and Lopez); the School of Biological and Biomedical Sciences, University of Durham, South Road Durham, UK (Natoli and Hoelzel); the Basic Research Laboratory of Genomic Diversity, National Cancer Institute, Frederick, MD (David); the Georgia Aquarium, NW Atlanta, GA (Bossart); and the Nova Southeastern University Oceanographic Center, Dania Beach, FL (Lopez). Ada Natoli is now at the Biology Department, United Arab Emirates University, Al-Ain, Abu Dhabi, United Arab Emirates., vpr3@cornell.edu
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 765
EP  - 778
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 104
IS  - 6
SN  - 0022-1503, 0022-1503
KW  - Ecology Abstracts; ASFA 1: Biological Sciences & Living Resources; Oceanic Abstracts; Genetics Abstracts
KW  - Indian River Lagoon
KW  - microsatellite
KW  - mtDNA
KW  - Tursiops truncatus
KW  - ASW, USA, Florida, Indian River Lagoon
KW  - Bayesian analysis
KW  - Nucleotide sequence
KW  - Ecological distribution
KW  - Genetic diversity
KW  - Genotypes
KW  - Lagoons
KW  - Differentiation
KW  - Population genetics
KW  - Genetics
KW  - ASW, Caribbean Sea
KW  - Rivers
KW  - Marine
KW  - Foraging behavior
KW  - Climate
KW  - ANW, USA, South Carolina, Charleston, Charleston Harbor
KW  - Microsatellites
KW  - Habitat
KW  - ASW, Mexico Gulf
KW  - Mitochondrial DNA
KW  - Marine mammals
KW  - Social behavior
KW  - DNA
KW  - Population structure
KW  - Coastal lagoons
KW  - O 1070:Ecology/Community Studies
KW  - D 04040:Ecosystem and Ecology Studies
KW  - G 07750:Ecological & Population Genetics
KW  - Q1 08372:Geographical distribution
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492614203?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Heredity&rft.atitle=Patterns+of+Population+Structure+for+Inshore+Bottlenose+Dolphins+along+the+Eastern+United+States&rft.au=Richards%2C+Vincent+P%3BGreig%2C+Thomas+W%3BFair%2C+Patricia+A%3BMcCulloch%2C+Stephen+D%3BPolitz%2C+Christine%3BNatoli%2C+Ada%3BDriscoll%2C+Carlos+A%3BHoelzel%2C+A+Rus%3BDavid%2C+Victor%3BBossart%2C+Gregory+D%3BLopez%2C+Jose+V&rft.aulast=Richards&rft.aufirst=Vincent&rft.date=2013-01-01&rft.volume=104&rft.issue=6&rft.spage=765&rft.isbn=&rft.btitle=&rft.title=Journal+of+Heredity&rft.issn=00221503&rft_id=info:doi/10.1093%2Fjhered%2Fest070
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2014-12-11
N1  - SubjectsTermNotLitGenreText - Genetics; Population genetics; Ecological distribution; Nucleotide sequence; Marine mammals; DNA; Population structure; Genotypes; Coastal lagoons; Rivers; Foraging behavior; Bayesian analysis; Climate; Microsatellites; Genetic diversity; Habitat; Lagoons; Differentiation; Mitochondrial DNA; Social behavior; Tursiops truncatus; ASW, USA, Florida, Indian River Lagoon; ASW, Mexico Gulf; ASW, Caribbean Sea; ANW, USA, South Carolina, Charleston, Charleston Harbor; Marine
DO  - http://dx.doi.org/10.1093/jhered/est070
ER  - 



TY  - JOUR
T1  - Nonsteroidal anti-inflammatory drugs and other analgesic use and bladder cancer in northern New England
AN  - 1468370422; 18602412
AB  - A few epidemiologic studies have found that use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with reduced risk of bladder cancer. However, the effects of specific NSAID use and individual variability in risk have not been well studied. We examined the association between NSAIDs use and bladder cancer risk, and its modification by 39 candidate genes related to NSAID metabolism. A population-based case-control study was conducted in northern New England, enrolling 1,171 newly diagnosed cases and 1,418 controls. Regular use of nonaspirin, nonselective NSAIDs was associated with reduced bladder cancer risk, with a statistically significant inverse trend in risk with duration of use (ORs of 1.0, 0.8, 0.6 and 0.6 for <5, 5-9, 10-19 and 20+ years, respectively; p sub(trend) = 0.015). This association was driven mainly by ibuprofen; significant inverse trends in risk with increasing duration and dose of ibuprofen were observed (p sub(trend) = 0.009 and 0.054, respectively). The reduced risk from ibuprofen use was limited to individuals carrying the T allele of a single nucleotide polymorphism (rs4646450) compared to those who did not use ibuprofen and did not carry the T allele in the CYP3A locus, providing new evidence that this association might be modified by polymorphisms in genes that metabolize ibuprofen. Significant positive trends in risk with increasing duration and cumulative dose of selective cyclooxygenase (COX-2) inhibitors were observed. Our results are consistent with those from previous studies linking use of NSAIDs, particularly ibuprofen, with reduced risk. We observed a previously unrecognized risk associated with use of COX-2 inhibitors, which merits further evaluation.
JF  - International Journal of Cancer
AU  - Baris, Dalsu
AU  - Karagas, Margaret R
AU  - Koutros, Stella
AU  - Colt, Joanne S
AU  - Johnson, Alison
AU  - Schwenn, Molly
AU  - Fischer, Alexander H
AU  - Figueroa, Jonine D
AU  - Berndt, Sonja I
AU  - Han, Summer
AU  - Beane Freeman, Laura E
AU  - Lubin, Jay H
AU  - Cherala, Sai
AU  - Cantor, Kenneth P
AU  - Jacobs, Kevin
AU  - Chanock, Stephen
AU  - Chatterjee, Nilanjan
AU  - Rothman, Nathaniel
AU  - Silverman, Debra T
AD  - Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Dartmouth Medical School, Hanover, NH., barisd@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 162
EP  - 173
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 1
SN  - 0020-7136, 0020-7136
KW  - Biotechnology and Bioengineering Abstracts
KW  - Cyclooxygenase-2
KW  - Ibuprofen
KW  - Urinary bladder
KW  - Single-nucleotide polymorphism
KW  - Gene polymorphism
KW  - Statistical analysis
KW  - Analgesics
KW  - Cancer
KW  - Metabolism
KW  - Nonsteroidal antiinflammatory drugs
KW  - W 30915:Pharmaceuticals & Vaccines
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468370422?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Cancer&rft.atitle=Nonsteroidal+anti-inflammatory+drugs+and+other+analgesic+use+and+bladder+cancer+in+northern+New+England&rft.au=Baris%2C+Dalsu%3BKaragas%2C+Margaret+R%3BKoutros%2C+Stella%3BColt%2C+Joanne+S%3BJohnson%2C+Alison%3BSchwenn%2C+Molly%3BFischer%2C+Alexander+H%3BFigueroa%2C+Jonine+D%3BBerndt%2C+Sonja+I%3BHan%2C+Summer%3BBeane+Freeman%2C+Laura+E%3BLubin%2C+Jay+H%3BCherala%2C+Sai%3BCantor%2C+Kenneth+P%3BJacobs%2C+Kevin%3BChanock%2C+Stephen%3BChatterjee%2C+Nilanjan%3BRothman%2C+Nathaniel%3BSilverman%2C+Debra+T&rft.aulast=Baris&rft.aufirst=Dalsu&rft.date=2013-01-01&rft.volume=132&rft.issue=1&rft.spage=162&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27590
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-12-01
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Cyclooxygenase-2; Ibuprofen; Single-nucleotide polymorphism; Urinary bladder; Gene polymorphism; Statistical analysis; Analgesics; Metabolism; Cancer; Nonsteroidal antiinflammatory drugs
DO  - http://dx.doi.org/10.1002/ijc.27590
ER  - 



TY  - JOUR
T1  - Design of RNA splicing analysis null models for post hoc filtering of Drosophila head RNA-Seq data with the splicing analysis kit (Spanki)
AN  - 1464513231; 18811416
AB  - Background: The production of multiple transcript isoforms from one gene is a major source of transcriptome complexity. RNA-Seq experiments, in which transcripts are converted to cDNA and sequenced, allow the resolution and quantification of alternative transcript isoforms. However, methods to analyze splicing are underdeveloped and errors resulting in incorrect splicing calls occur in every experiment. Results: We used RNA-Seq data to develop sequencing and aligner error models. By applying these error models to known input from simulations, we found that errors result from false alignment to minor splice motifs and antisense stands, shifted junction positions, paralog joining, and repeat induced gaps. By using a series of quantitative and qualitative filters, we eliminated diagnosed errors in the simulation, and applied this to RNA-Seq data from Drosophila melanogaster heads. We used high-confidence junction detections to specifically interrogate local splicing differences between transcripts. This method out-performed commonly used RNA-seq methods to identify known alternative splicing events in the Drosophila sex determination pathway. We describe a flexible software package to perform these tasks called Splicing Analysis Kit (Spanki), available at http://www.cbcb.umd.edu/software/spanki . Conclusions: Splice-junction centric analysis of RNA-Seq data provides advantages in specificity for detection of alternative splicing. Our software provides tools to better understand error profiles in RNA-Seq data and improve inference from this new technology. The splice-junction centric approach that this software enables will provide more accurate estimates of differentially regulated splicing than current tools.
JF  - BMC Bioinformatics
AU  - Sturgill, David
AU  - Malone, John H
AU  - Sun, Xia
AU  - Smith, Harold E
AU  - Rabinow, Leonard
AU  - Samson, Marie-Laure
AU  - Oliver, Brian
AD  - National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 320
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2105, 1471-2105
KW  - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW  - Alternative splicing
KW  - Data processing
KW  - Drosophila melanogaster
KW  - N 14810:Methods
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464513231?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=Design+of+RNA+splicing+analysis+null+models+for+post+hoc+filtering+of+Drosophila+head+RNA-Seq+data+with+the+splicing+analysis+kit+%28Spanki%29&rft.au=Sturgill%2C+David%3BMalone%2C+John+H%3BSun%2C+Xia%3BSmith%2C+Harold+E%3BRabinow%2C+Leonard%3BSamson%2C+Marie-Laure%3BOliver%2C+Brian&rft.aulast=Sturgill&rft.aufirst=David&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=320&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-14-320
L2  - http://www.biomedcentral.com/1471-2105/14/320
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 1
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Data processing; Drosophila melanogaster
DO  - http://dx.doi.org/10.1186/1471-2105-14-320
ER  - 



TY  - JOUR
T1  - Human Induced Pluripotent Stem Cells from Basic Research to Potential Clinical Applications in Cancer
AN  - 1464512081; 18812225
AB  - The human induced pluripotent stem cells (hiPSCs) are derived from a direct reprogramming of human somatic cells to a pluripotent stage through ectopic expression of specific transcription factors. These cells have two important properties, which are the self-renewal capacity and the ability to differentiate into any cell type of the human body. So, the discovery of hiPSCs opens new opportunities in biomedical sciences, since these cells may be useful for understanding the mechanisms of diseases in the production of new diseases models, in drug development/drug toxicity tests, gene therapies, and cell replacement therapies. However, the hiPSCs technology has limitations including the potential for the development of genetic and epigenetic abnormalities leading to tumorigenicity. Nowadays, basic research in the hiPSCs field has made progress in the application of new strategies with the aim to enable an efficient production of high-quality of hiPSCs for safety and efficacy, necessary to the future application for clinical practice. In this review, we show the recent advances in hiPSCs' basic research and some potential clinical applications focusing on cancer. We also present the importance of the use of statistical methods to evaluate the possible validation for the hiPSCs for future therapeutic use toward personalized cell therapies.
JF  - BioMed Research International
AU  - de Souza Fernandez, Teresa
AU  - de Souza Fernandez, Cecilia
AU  - Mencalha, Andre Luiz
AD  - National Cancer Institute (INCA), Bone Marrow Transplantation Center (CEMO), Laboratory Division, 20230-130 Rio de Janeiro, RJ, Brazil, teresafernandez@inca.gov.br
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2013
SN  - 2314-6133, 2314-6133
KW  - Biotechnology and Bioengineering Abstracts
KW  - Cancer
KW  - Stem cells
KW  - W 30905:Medical Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464512081?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+Induced+Pluripotent+Stem+Cells+from+Basic+Research+to+Potential+Clinical+Applications+in+Cancer&rft.au=de+Souza+Fernandez%2C+Teresa%3Bde+Souza+Fernandez%2C+Cecilia%3BMencalha%2C+Andre+Luiz&rft.aulast=de+Souza+Fernandez&rft.aufirst=Teresa&rft.date=2013-01-01&rft.volume=2013&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2013%2F430290
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Stem cells
DO  - http://dx.doi.org/10.1155/2013/430290
ER  - 



TY  - JOUR
T1  - Relationships among parent and youth healthful eating attitudes and youth dietary intake in a cross-sectional study of youth with type 1 diabetes
AN  - 1464505699; 18811675
AB  - Background: Constructs based on Social Cognitive Theory have shown utility in understanding dietary behavior; however, little research has examined these relations in youth and parents concurrently. Unique demands of dietary management among families of youth with type 1 diabetes (T1D) suggest the importance of investigation in this population. The purpose of this study was to develop and evaluate youth and parent measures of self-efficacy, outcome expectations, and barriers for healthful eating, and parent modeling of healthful eating, in a sample of youth with type 1 diabetes and their parents. Methods: Youth (n=252) ages 8-18 years with diabetes duration > or =1 year and parents completed self-report measures of healthful eating attitudes including self-efficacy, perceived barriers, positive and negative outcome expectations; youth reported parent modeling of healthful eating. Youth dietary intake from 3-day diet records was used to calculate the Healthy Eating Index 2005 and the Nutrient Rich Foods 9.3 index, measures of overall diet quality. The relations among parent and youth healthful eating attitudes, parent modeling, and youth diet quality were examined using structural equation modeling. Results: Internal consistency and test-retest reliability of the measures were acceptable. The structural equation model demonstrated acceptable fit (CFI/TLI=0.94/0.94; RMSEA=0.03), and items loaded the hypothesized factors.
JF  - International Journal of Behavioral Nutrition and Physical Activity
AU  - Nansel, Tonja R
AU  - Haynie, Denise L
AU  - Lipsky, Leah M
AU  - Wang, Jing
AU  - Mehta, Sanjeev N
AU  - Laffel, Lori MB
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development, Health Behavior Branch, Division of Intramural Population Health Research, NIH, DHHS, 6100 Executive Blvd., Rm. 7B13, MSC 7510, Bethesda, MD 20892-7510, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 125
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 10
IS  - 1
SN  - 1479-5868, 1479-5868
KW  - Physical Education Index
KW  - Attitudes
KW  - Diet (effects)
KW  - Barriers
KW  - Health (attitudes)
KW  - Youth
KW  - Modeling
KW  - Diabetes
KW  - Public health
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1464505699?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.atitle=Relationships+among+parent+and+youth+healthful+eating+attitudes+and+youth+dietary+intake+in+a+cross-sectional+study+of+youth+with+type+1+diabetes&rft.au=Nansel%2C+Tonja+R%3BHaynie%2C+Denise+L%3BLipsky%2C+Leah+M%3BWang%2C+Jing%3BMehta%2C+Sanjeev+N%3BLaffel%2C+Lori+MB&rft.aulast=Nansel&rft.aufirst=Tonja&rft.date=2013-01-01&rft.volume=10&rft.issue=1&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.issn=14795868&rft_id=info:doi/10.1186%2F1479-5868-10-125
L2  - http://www.ijbnpa.org/content/10/1/125
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2013-11-01
N1  - Number of references - 65
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Diet (effects); Attitudes; Barriers; Health (attitudes); Modeling; Youth; Public health; Diabetes
DO  - http://dx.doi.org/10.1186/1479-5868-10-125
ER  - 



TY  - JOUR
T1  - Systems and Cascades in Cognitive Development and Academic Achievement
AN  - 1463067264; 201325561
AB  - A large-scale (N=552) controlled multivariate prospective 14-year longitudinal study of a developmental cascade embedded in a developmental system showed that information-processing efficiency in infancy (4 months), general mental development in toddlerhood (18 months), behavior difficulties in early childhood (36 months), psychometric intelligence in middle childhood (8 years), and maternal education either directly or indirectly (or both) contribute to academic achievement in adolescence (14 years). Adapted from the source document.
JF  - Child Development
AU  - Bornstein, Marc H
AU  - Hahn, Chun-Shin
AU  - Wolke, Dieter
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 154
EP  - 162
PB  - Wiley-Blackwell, Oxford UK
VL  - 84
IS  - 1
SN  - 0009-3920, 0009-3920
KW  - Infancy
KW  - Academic achievement
KW  - Childhood
KW  - Adolescence
KW  - Cognitive development
KW  - Psychometric intelligence
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463067264?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+Development&rft.atitle=Systems+and+Cascades+in+Cognitive+Development+and+Academic+Achievement&rft.au=Bornstein%2C+Marc+H%3BHahn%2C+Chun-Shin%3BWolke%2C+Dieter&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2013-01-01&rft.volume=84&rft.issue=1&rft.spage=154&rft.isbn=&rft.btitle=&rft.title=Child+Development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fj.1467-8624.2012.01849.x
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-09-27
N1  - CODEN - CHDEAW
N1  - SubjectsTermNotLitGenreText - Academic achievement; Psychometric intelligence; Infancy; Childhood; Cognitive development; Adolescence
DO  - http://dx.doi.org/10.1111/j.1467-8624.2012.01849.x
ER  - 



TY  - JOUR
T1  - War sick: Meaningful illness and military victimhood
AN  - 1463015073; 201346110
AB  - A review essay on books by 1) Erin Finley, Fields of combat: Understanding PTSD among veterans of Iraq and Afghanistan (2011); 2) Susie Kilshaw, Impotent warriors: Gulf War syndrome, vulnerability and masculinity (2009).
JF  - Focaal - European Journal of Anthropology
AU  - Wool, Zoe H
AD  - NIMH-funded postdoctoral fellow, Institute for Health Care Policy and Aging Research at Rutgers University zoe.h.wool@rutgers.edu
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 139
EP  - 147
PB  - Berghahn Journals, New York NY
IS  - 66
SN  - 0920-1297, 0920-1297
KW  - Masculinity
KW  - Veterans
KW  - War
KW  - Afghanistan
KW  - Vulnerability
KW  - Posttraumatic Stress Disorder
KW  - Illness
KW  - Victimization
KW  - Iraq
KW  - article
KW  - 0514: culture and social structure; social anthropology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463015073?accountid=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=Focaal+-+European+Journal+of+Anthropology&rft.atitle=War+sick%3A+Meaningful+illness+and+military+victimhood&rft.au=Wool%2C+Zoe+H&rft.aulast=Wool&rft.aufirst=Zoe&rft.date=2013-01-01&rft.volume=&rft.issue=66&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Focaal+-+European+Journal+of+Anthropology&rft.issn=09201297&rft_id=info:doi/10.3167%2Ffcl.2013.660112
LA  - English
DB  - Sociological Abstracts
N1  - Date revised - 2013-12-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - War; Iraq; Vulnerability; Veterans; Illness; Posttraumatic Stress Disorder; Afghanistan; Masculinity; Victimization
DO  - http://dx.doi.org/10.3167/fcl.2013.660112
ER  - 



TY  - JOUR
T1  - Comparative toxicogenomic responses of mercuric and methyl-mercury
AN  - 1458538004; 18777502
AB  - Background: Mercury is a ubiquitous environmental toxicant that exists in multiple chemical forms. A paucity of information exists regarding the differences or similarities by which different mercurials act at the molecular level. Results: Transcriptomes of mixed-stage C. elegans following equitoxic sub-, low- and high-toxicity exposures to inorganic mercuric chloride (HgCl sub(2)) and organic methylmercury chloride (MeHgCl) were analyzed. In C. elegans, the mercurials had highly different effects on transcription, with MeHgCl affecting the expression of significantly more genes than HgCl sub(2). Bioinformatics analysis indicated that inorganic and organic mercurials affected different biological processes. RNAi identified 18 genes that were important in C. elegans response to mercurial exposure, although only two of these genes responded to both mercurials. To determine if the responses observed in C. elegans were evolutionarily conserved, the two mercurials were investigated in human neuroblastoma (SK-N-SH), hepatocellular carcinoma (HepG2) and embryonic kidney (HEK293) cells. The human homologs of the affected C. elegans genes were then used to test the effects on gene expression and cell viability after using siRNA during HgCl sub(2) and MeHgCl exposure. As was observed with C. elegans, exposure to the HgCl sub(2) and MeHgCl had different effects on gene expression, and different genes were important in the cellular response to the two mercurials. Conclusions: These results suggest that, contrary to previous reports, inorganic and organic mercurials have different mechanisms of toxicity. The two mercurials induced disparate effects on gene expression, and different genes were important in protecting the organism from mercurial toxicity.
JF  - BMC Genomics
AU  - McElwee, Matthew K
AU  - Ho, Lindsey A
AU  - Chou, Jeff W
AU  - Smith, Marjolein V
AU  - Freedman, Jonathan H
AD  - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIH, 111 T.W Alexander Drive, Research Triangle Park, P.O. Box 12233, 27709 Durham, NC, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 698
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2164, 1471-2164
KW  - Genetics Abstracts; Toxicology Abstracts
KW  - Bioinformatics
KW  - Toxicity
KW  - G 07730:Development & Cell Cycle
KW  - X 24330:Agrochemicals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458538004?accountid=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=BMC+Genomics&rft.atitle=Comparative+toxicogenomic+responses+of+mercuric+and+methyl-mercury&rft.au=McElwee%2C+Matthew+K%3BHo%2C+Lindsey+A%3BChou%2C+Jeff+W%3BSmith%2C+Marjolein+V%3BFreedman%2C+Jonathan+H&rft.aulast=McElwee&rft.aufirst=Matthew&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=BMC+Genomics&rft.issn=14712164&rft_id=info:doi/10.1186%2F1471-2164-14-698
L2  - http://www.biomedcentral.com/1471-2164/14/698
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 1
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Toxicity
DO  - http://dx.doi.org/10.1186/1471-2164-14-698
ER  - 



TY  - JOUR
T1  - The dynamic sustainability framework: addressing the paradox of sustainment amid ongoing change
AN  - 1458532216; 18728020
AB  - Background: Despite growth in implementation research, limited scientific attention has focused on understanding and improving sustainability of health interventions. Models of sustainability have been evolving to reflect challenges in the fit between intervention and context. Discussion: We examine the development of concepts of sustainability, and respond to two frequent assumptions -'voltage drop,' whereby interventions are expected to yield lower benefits as they move from efficacy to effectiveness to implementation and sustainability, and 'program drift,' whereby deviation from manualized protocols is assumed to decrease benefit. We posit that these assumptions limit opportunities to improve care, and instead argue for understanding the changing context of healthcare to continuously refine and improve interventions as they are sustained. Sustainability has evolved from being considered as the endgame of a translational research process to a suggested 'adaptation phase' that integrates and institutionalizes interventions within local organizational and cultural contexts. These recent approaches locate sustainability in the implementation phase of knowledge transfer, but still do not address intervention improvement as a central theme. We propose a Dynamic Sustainability Framework that involves: continued learning and problem solving, ongoing adaptation of interventions with a primary focus on fit between interventions and multi-level contexts, and expectations for ongoing improvement as opposed to diminishing outcomes over time. Summary: A Dynamic Sustainability Framework provides a foundation for research, policy and practice that supports development and testing of falsifiable hypotheses and continued learning to advance the implementation, transportability and impact of health services research.
JF  - Implementation Science
AU  - Chambers, David A
AU  - Glasgow, Russell E
AU  - Stange, Kurt C
AD  - Division of Services and Intervention Research, National Institute of Mental Health, 6001 Executive Blvd, Rockville, MD, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 117
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 8
IS  - 1
SN  - 1748-5908, 1748-5908
KW  - Sustainability Science Abstracts
KW  - Sustainability
KW  - Maintenance
KW  - Adaptation
KW  - Dissemination
KW  - Implementation
KW  - Framework
KW  - Model
KW  - Adaptability
KW  - Culture
KW  - Health care
KW  - Intervention
KW  - Problem solving
KW  - Health promotion
KW  - M3 1010:Issues in Sustainable Development
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458532216?accountid=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=Implementation+Science&rft.atitle=The+dynamic+sustainability+framework%3A+addressing+the+paradox+of+sustainment+amid+ongoing+change&rft.au=Chambers%2C+David+A%3BGlasgow%2C+Russell+E%3BStange%2C+Kurt+C&rft.aulast=Chambers&rft.aufirst=David&rft.date=2013-01-01&rft.volume=8&rft.issue=1&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Implementation+Science&rft.issn=17485908&rft_id=info:doi/10.1186%2F1748-5908-8-117
L2  - http://www.implementationscience.com/content/8/1/117
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 59
N1  - Last updated - 2015-08-05
N1  - SubjectsTermNotLitGenreText - Culture; Adaptability; Health care; Problem solving; Intervention; Sustainability; Health promotion
DO  - http://dx.doi.org/10.1186/1748-5908-8-117
ER  - 



TY  - JOUR
T1  - Matrix Metalloproteinase-9 as a Potential Tumor Marker in Breast Cancer
AN  - 1458531449; 18750045
AB  - This study aimed to detect the comparative expression and activity of matrix metalloproteinase-9 (MMP-9) and its correlation with known pathological parameters such as estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2) in 81 malignant breast tumors and adjacent normal breast tissues and in blood sera of these patients from different clinical TNM stages (ductal carcinoma in situ to T4) of breast cancer. MMP-9 was highly expressed in node-positive tumors and the preoperative blood serum of patients, but MMP-9 activity was appreciably inhibited in blood serum samples collected after surgery. The mature form of MMP-9 (84 kD) was expressed only in clinical stage III tumors (T2 pound sterling ). Appreciable reduction of tissue inhibitor of metalloproteinase 1, phosphorylation of epidermal growth factor receptor, and translocation of nuclear factor-KB suggested their possible role in MMP-9 activation in HER2-positive breast cancer. Overexpression and activation of MMP-9 predicted a higher stage of hormone-sensitive ductal breast carcinoma. Downregulation of the endogenous inhibitor of MMP-9, tissue inhibitor of metalloproteinase 1, and translocation of the transcription factor nuclear factor-KB in tumors may have an appreciable role in the overexpression of MMP-9. However, MMP-9 activation was not correlated with expression of estrogen and progesterone receptors. Evaluation of MMP-9 expression may provide valuable information about breast cancer treatment.
JF  - Journal of Environmental Pathology, Toxicology and Oncology
AU  - Nanda, Durga Prasad
AU  - Sil, Hrishikesh
AU  - Moulik, Shuvojit
AU  - Biswas, Jaydip
AU  - Mandal, Shyam Sundar
AU  - Chatterjee, Amitava
AD  - Department of Receptor Biology & Tumor Metastasis, Chittaranjan National Cancer Institute, Kolkata, India, amitavacosmos@redifrmail.com
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 115
EP  - 129
PB  - Begell House Inc., 79 Madison Avenue, Suite 1201 New York NY 10016-7892 United States
VL  - 32
IS  - 2
SN  - 0731-8898, 0731-8898
KW  - Toxicology Abstracts
KW  - ErbB-2 protein
KW  - Tumor markers
KW  - Epidermal growth factor receptors
KW  - Tumors
KW  - NF- Kappa B protein
KW  - Metalloproteinase
KW  - Nuclear transport
KW  - Progesterone receptors
KW  - Blood
KW  - Phosphorylation
KW  - Transcription factors
KW  - Surgery
KW  - Breast carcinoma
KW  - Gelatinase B
KW  - Estrogen receptors
KW  - X 24360:Metals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458531449?accountid=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+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.atitle=Matrix+Metalloproteinase-9+as+a+Potential+Tumor+Marker+in+Breast+Cancer&rft.au=Nanda%2C+Durga+Prasad%3BSil%2C+Hrishikesh%3BMoulik%2C+Shuvojit%3BBiswas%2C+Jaydip%3BMandal%2C+Shyam+Sundar%3BChatterjee%2C+Amitava&rft.aulast=Nanda&rft.aufirst=Durga&rft.date=2013-01-01&rft.volume=32&rft.issue=2&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Journal+of+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.issn=07318898&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-11-01
N1  - Number of references - 61
N1  - Last updated - 2015-04-16
N1  - SubjectsTermNotLitGenreText - Tumor markers; ErbB-2 protein; Epidermal growth factor receptors; Tumors; NF- Kappa B protein; Metalloproteinase; Blood; Progesterone receptors; Nuclear transport; Phosphorylation; Surgery; Transcription factors; Breast carcinoma; Gelatinase B; Estrogen receptors
ER  - 



TY  - JOUR
T1  - Pain in long-term breast cancer survivors: the role of body mass index, physical activity, and sedentary behavior
AN  - 1458525278; 17668882
AB  - Although pain is common among post-treatment breast cancer survivors, studies that are longitudinal, identify a case definition of clinically meaningful pain, or examine factors contributing to pain in survivors are limited. This study describes longitudinal patterns of pain in long-term breast cancer survivors, evaluating associations of body mass index (BMI), physical activity, sedentary behavior with mean pain severity and above-average pain. Women newly diagnosed with stages 0-IIIA breast cancer (N = 1183) were assessed, on average, 6 months (demographic/clinical characteristics), 30 months (demographics), 40 months (demographics, pain), 5 years (BMI, physical activity, and sedentary behavior), and 10 years (demographics, pain, BMI, physical activity, and sedentary behavior) post-diagnosis. This analysis includes survivors who completed pain assessments 40 months post-diagnosis (N = 801), 10 years post-diagnosis (N = 563), or both (N = 522). Above-average pain was defined by SF-36 bodily pain scores greater than or equal to 1/2 standard deviation worse than age-specific population norms. We used multiple regression models to test unique associations of BMI, physical activity, and sedentary behavior with pain adjusting for demographic and clinical factors. The proportion of survivors reporting above-average pain was higher at 10 years than at 40 months (32.3 vs. 27.8 %, p 5 %) was positively associated, while meeting physical activity guidelines was inversely associated, with above-average pain (OR, 95 % CI = 1.76, 1.03-3.01 and 0.40, 0.20-0.84, respectively) (p < 0.05). Weight gain and lack of physical activity place breast cancer survivors at risk for pain long after treatment ends. Weight control and exercise interventions should be tested for effects on long-term pain in these women.
JF  - Breast Cancer Research and Treatment
AU  - Forsythe, Laura P
AU  - Alfano, Catherine M
AU  - George, Stephanie M
AU  - McTiernan, Anne
AU  - Baumgartner, Kathy B
AU  - Bernstein, Leslie
AU  - Ballard-Barbash, Rachel
AD  - Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA, lforsythe@pcori.org
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 617
EP  - 630
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 137
IS  - 2
SN  - 0167-6806, 0167-6806
KW  - Physical Education Index
KW  - Obesity
KW  - Behavior
KW  - Body mass
KW  - Women
KW  - Pain
KW  - Breasts
KW  - Exercise
KW  - Cancer
KW  - Demographics
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458525278?accountid=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=Breast+Cancer+Research+and+Treatment&rft.atitle=Pain+in+long-term+breast+cancer+survivors%3A+the+role+of+body+mass+index%2C+physical+activity%2C+and+sedentary+behavior&rft.au=Forsythe%2C+Laura+P%3BAlfano%2C+Catherine+M%3BGeorge%2C+Stephanie+M%3BMcTiernan%2C+Anne%3BBaumgartner%2C+Kathy+B%3BBernstein%2C+Leslie%3BBallard-Barbash%2C+Rachel&rft.aulast=Forsythe&rft.aufirst=Laura&rft.date=2013-01-01&rft.volume=137&rft.issue=2&rft.spage=617&rft.isbn=&rft.btitle=&rft.title=Breast+Cancer+Research+and+Treatment&rft.issn=01676806&rft_id=info:doi/10.1007%2Fs10549-012-2335-7
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2013-11-01
N1  - Number of references - 69
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Obesity; Behavior; Body mass; Women; Breasts; Pain; Exercise; Demographics; Cancer
DO  - http://dx.doi.org/10.1007/s10549-012-2335-7
ER  - 



TY  - JOUR
T1  - A Meta-Analysis of Adherence to Antiretroviral Therapy and Virologic Responses in HIV-Infected Children, Adolescents, and Young Adults
AN  - 1448999173; 201308813
AB  - The relationship between adherence to antiretroviral therapy (ART) and virologic outcomes in HIV+ children, adolescents, and young adults has been notably understudied, with much of the extant research focused on specific sub-literatures, such as resource-limited regions, specific clinical outcomes and time frames. The authors sought to better characterize the relationship between adherence to ART and virologic functioning along various sample and methodological factors. The authors conducted a meta-analysis of thirty-seven studies and utilized a random effects model to generate weighted mean effect sizes. In addition, the authors conducted meta-ANOVAs to examine potential factors influencing the relationship between adherence and three categories of clinical outcomes, specifically Viral Load (VL) <100, VL < 400, and continuously measured VL. The analyses included 5,344 HIV+ children, adolescents, and young adults. The relationship between adherence behaviors and virologic outcomes varied across different methods of measurement and analysis. The relationship between adherence and continuously measured VL was significantly larger than for dichotomously-coded VL < 400 at Qb (20.69(1), p < .0005). Caregiver self-report indices elicited very small to small magnitude effects across both VL < 100 and VL < 400 outcomes and combined informant reporting (youth/adolescent and parent) produced significantly larger effects than caregiver report alone with adherence and VL < 400 outcomes at Qb (9.28(1), p < .005). More recently published trials reported smaller relationships between adherence and categorical clinical outcomes, such that year of publication significantly negatively correlated with VL < 100 (r = -.71(14), p < .005) and VL < 400 (r = -.43(26), p < .02). The data suggest that the magnitude of the relationship between ART adherence and virologic outcomes among heterogeneous samples of HIV+ children, adolescents and young adults varies across virologic outcomes and may be affected by moderating sample and methodological factors. Methodological and research recommendations for the interpretation of the current findings as well as for future HIV adherence related research are presented. Adapted from the source document.
JF  - AIDS and Behavior
AU  - Kahana, Shoshana Y
AU  - Rohan, Jennifer
AU  - Allison, Susannah
AU  - Frazier, Thomas W
AU  - Drotar, Dennis
AD  - Services Research Branch, Division of Epidemiology, Services and Prevention Research, National Institute on Drug Abuse, 6001 Executive Blvd, Bethesda, MD, 20892, USA kahanas@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 41
EP  - 60
PB  - Springer, Dordrecht, The Netherlands
VL  - 17
IS  - 1
SN  - 1090-7165, 1090-7165
KW  - Treatment Outcomes
KW  - Methodology (Data Collection)
KW  - Acquired Immune Deficiency Syndrome
KW  - Medications
KW  - Young Adults
KW  - Parents
KW  - Children
KW  - Youth
KW  - Adolescents
KW  - article
KW  - 6126: acquired immune deficiency syndrome (AIDS)
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448999173?accountid=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=A+Meta-Analysis+of+Adherence+to+Antiretroviral+Therapy+and+Virologic+Responses+in+HIV-Infected+Children%2C+Adolescents%2C+and+Young+Adults&rft.au=Kahana%2C+Shoshana+Y%3BRohan%2C+Jennifer%3BAllison%2C+Susannah%3BFrazier%2C+Thomas+W%3BDrotar%2C+Dennis&rft.aulast=Kahana&rft.aufirst=Shoshana&rft.date=2013-01-01&rft.volume=17&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=AIDS+and+Behavior&rft.issn=10907165&rft_id=info:doi/10.1007%2Fs10461-012-0159-4
LA  - English
DB  - Social Services Abstracts
N1  - Date revised - 2013-11-01
N1  - Last updated - 2016-09-28
N1  - CODEN - AIBEFC
N1  - SubjectsTermNotLitGenreText - Adolescents; Acquired Immune Deficiency Syndrome; Children; Young Adults; Treatment Outcomes; Medications; Methodology (Data Collection); Parents; Youth
DO  - http://dx.doi.org/10.1007/s10461-012-0159-4
ER  - 



TY  - JOUR
T1  - Insights Gained from P. falciparum Cultivation in Modified Media
AN  - 1448220507; 18656475
AB  - In vitro cultivation of Plasmodium falciparum , the agent of severe human malaria, has enabled advances in basic research and accelerated the development of new therapies. Since the introduction of in vitro parasite culture nearly 40 years ago, most workers have used a medium consisting of RPMI 1640 medium supplemented with lipids and hypoxanthine. While these standardized conditions yield robust parasite growth and facilitate comparison of results from different studies, they may also lead to implicit assumptions that limit future advances. Here, I review recent studies that used modified culture conditions to challenge these assumptions and explore parasite physiology. The findings are relevant to understanding in vivo parasite phenotypes and the prioritization of antimalarial targets.
JF  - The Scientific World Journal
AU  - Desai, Sanjay A
AD  - The Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA, sdesai@niaid.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
PB  - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL  - 2013
KW  - Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW  - Parasites
KW  - Human diseases
KW  - Lipids
KW  - Therapy
KW  - Malaria
KW  - Plasmodium falciparum
KW  - Phenotypes
KW  - Public health
KW  - Workers
KW  - Growth
KW  - Reviews
KW  - Hypoxanthine
KW  - Media (culture)
KW  - K 03410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448220507?accountid=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=The+Scientific+World+Journal&rft.atitle=Insights+Gained+from+P.+falciparum+Cultivation+in+Modified+Media&rft.au=Desai%2C+Sanjay+A&rft.aulast=Desai&rft.aufirst=Sanjay&rft.date=2013-01-01&rft.volume=2013&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=The+Scientific+World+Journal&rft.issn=1537-744X&rft_id=info:doi/10.1155%2F2013%2F363505
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Growth; Human diseases; Therapy; Malaria; Phenotypes; Public health; Workers; Lipids; Reviews; Hypoxanthine; Media (culture); Plasmodium falciparum
DO  - http://dx.doi.org/10.1155/2013/363505
ER  - 



TY  - JOUR
T1  - Combination treatments with the PKC inhibitor, enzastaurin, enhance the cytotoxicity of the anti-mesothelin immunotoxin, SS1P.
AN  - 1443994222; 24130723
AB  - Activated protein kinase C (PKC) contributes to tumor survival and proliferation, provoking the development of inhibitory agents as potential cancer therapeutics. Immunotoxins are antibody-based recombinant proteins that employ antibody fragments for cancer targeting and bacterial toxins as the cytotoxic agent. Pseudomonas exotoxin-based immunotoxins act via the ADP-ribosylation of EF2 leading to the enzymatic inhibition of protein synthesis. Combining PKC inhibitors with the immunotoxin SS1P, targeted to surface mesothelin, was undertaken to explore possible therapeutic strategies. Enzastaurin but not two other PKC inhibitors combined with SS1P to produce synergistic cell death via apoptosis. Mechanistic insights of the synergistic killing centered on the complete loss of the prosurvival Bcl2 protein, Mcl-1, the loss of AKT and the activation of caspase 3/7. Synergy was most evident when cells exhibited resistance to the immunotoxin alone. Further, because PKC inhibition by itself was not sufficient to enhance SS1P action, enzastaurin must target other kinases that are involved in the immunotoxin pathway.
JF  - PloS one
AU  - Mattoo, Abid R
AU  - Pastan, Ira
AU  - Fitzgerald, David
AD  - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 1
VL  - 8
IS  - 10
KW  - Antibodies, Monoclonal
KW  - 0
KW  - GPI-Linked Proteins
KW  - Indoles
KW  - SS1(dsFv)PE38
KW  - mesothelin
KW  - Protein Kinase C beta
KW  - EC 2.7.11.13
KW  - enzastaurin
KW  - UC96G28EQF
KW  - Index Medicus
KW  - Blotting, Western
KW  - Combined Modality Therapy
KW  - Humans
KW  - Apoptosis -- drug effects
KW  - Cell Line, Tumor
KW  - Inhibitory Concentration 50
KW  - Drug Synergism
KW  - Indoles -- therapeutic use
KW  - GPI-Linked Proteins -- antagonists & inhibitors
KW  - Protein Kinase C beta -- antagonists & inhibitors
KW  - Antibodies, Monoclonal -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443994222?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Combination+treatments+with+the+PKC+inhibitor%2C+enzastaurin%2C+enhance+the+cytotoxicity+of+the+anti-mesothelin+immunotoxin%2C+SS1P.&rft.au=Mattoo%2C+Abid+R%3BPastan%2C+Ira%3BFitzgerald%2C+David&rft.aulast=Mattoo&rft.aufirst=Abid&rft.date=2013-01-01&rft.volume=8&rft.issue=10&rft.spage=e75576&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0075576
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-06-02
N1  - Date created - 2013-10-16
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Nat Rev Immunol. 2010 May;10(5):317-27 [20414205]
Mol Pharmacol. 2010 Mar;77(3):416-23 [19933775]
Mol Cancer Ther. 2010 Jul;9(7):2007-15 [20587662]
Mol Cancer Ther. 2010 Oct;9(10):2814-24 [20876745]
Cancer Res. 2011 Apr 1;71(7):2643-53 [21324920]
Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054]
Leuk Lymphoma. 2011 Jun;52 Suppl 2:87-90 [21504287]
Leuk Lymphoma. 2011 Jun;52 Suppl 2:79-81 [21599608]
Br J Haematol. 2011 Aug;154(4):471-6 [21732928]
Cancer Res. 2011 Aug 1;71(15):5204-13 [21670080]
Cancer Res. 2011 Sep 1;71(17):5915-22 [21775520]
PLoS One. 2011;6(9):e24012 [21915275]
Clin Cancer Res. 2011 Sep 15;17(18):5926-34 [21813632]
Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010]
FEBS J. 2011 Dec;278(23):4683-700 [21585657]
PLoS One. 2012;7(1):e29622 [22253748]
Nat Rev Drug Discov. 2012 Dec;11(12):937-57 [23197040]
Int J Cancer. 2013 Feb 15;132(4):978-87 [22821746]
Oncogene. 2013 Jan 24;32(4):453-61 [22391570]
Cancer Res. 2013 Apr 1;73(7):2281-8 [23348423]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10386-91 [11517301]
Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):3937-42 [15217923]
Int J Cancer. 2004 Nov 10;112(3):475-83 [15382075]
Somat Cell Mol Genet. 1985 Mar;11(2):117-26 [3856953]
Cell. 1987 Jan 16;48(1):129-36 [3098436]
Cancer Res. 2005 Aug 15;65(16):7462-9 [16103100]
Annu Rev Med. 2007;58:221-37 [17059365]
Clin Cancer Res. 2007 Mar 1;13(5):1571-5 [17332303]
Pharmacol Res. 2007 Jun;55(6):477-86 [17548205]
Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569]
Eur J Haematol. 2007 Oct;79(4):281-6 [17803679]
Expert Opin Investig Drugs. 2007 Oct;16(10):1693-707 [17922632]
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17099-104 [17940013]
Immunol Rev. 2008 Apr;222:9-27 [18363992]
Mol Cancer Ther. 2008 May;7(5):1156-63 [18483303]
Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11311-6 [18678888]
Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873]
J Pediatr Hematol Oncol. 2009 Dec;31(12):936-41 [19875969]
J Immunother. 2010 Apr;33(3):297-304 [20445350]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0075576
ER  - 



TY  - JOUR
T1  - Inhibition of mTOR reduces anal carcinogenesis in transgenic mouse model.
AN  - 1443426990; 24124460
AB  - The molecular mechanism of human anal squamous cell carcinoma (ASCC) is unclear, and the accumulating evidence indicate association of ASCC with the activation of the Akt/mTOR pathway. Here we describe a mouse model with spontaneous anal squamous cell cancer, wherein a combined deletion of Tgfbr1 and Pten in stratified squamous epithelia was induced using inducible K14-Cre. Histopathologic analyses confirmed that 33.3% of the mice showed increased susceptibility to ASCC and precancerous lesions. Biomarker analyses demonstrated that the activation of the Akt pathway in ASCC of the Tgfbr1 and Pten double knockout (2cKO) mouse was similar to that observed in human anal cancer. Chemopreventive experiments using mTOR inhibitor-rapamycin treatment significantly delayed the onset of the ASCC tumors and reduced the tumor burden in 2cKO mice by decreasing the phosphorylation of Akt and S6. This is the first conditional knockout mouse model used for investigating the contributions of viral and cellular factors in anal carcinogenesis without carcinogen-mediated induction, and it would provide a platform for assessing new therapeutic modalities for treating and/or preventing this type of cancer.
JF  - PloS one
AU  - Sun, Zhi-Jun
AU  - Zhang, Lu
AU  - Zhang, Wei
AU  - Hall, Bradford
AU  - Bian, Yansong
AU  - Kulkarni, Ashok B
AD  - The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China ; Functional Genomics Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 1
VL  - 8
IS  - 10
KW  - Anti-Bacterial Agents
KW  - 0
KW  - Receptors, Transforming Growth Factor beta
KW  - TOR Serine-Threonine Kinases
KW  - EC 2.7.1.1
KW  - TGF-beta type I receptor
KW  - EC 2.7.1.11
KW  - Protein-Serine-Threonine Kinases
KW  - EC 2.7.11.1
KW  - PTEN Phosphohydrolase
KW  - EC 3.1.3.67
KW  - Sirolimus
KW  - W36ZG6FT64
KW  - Index Medicus
KW  - Receptors, Transforming Growth Factor beta -- genetics
KW  - Animals
KW  - Anti-Bacterial Agents -- therapeutic use
KW  - Protein-Serine-Threonine Kinases -- deficiency
KW  - Protein-Serine-Threonine Kinases -- genetics
KW  - Mice
KW  - Sirolimus -- therapeutic use
KW  - Reverse Transcriptase Polymerase Chain Reaction
KW  - Mice, Transgenic
KW  - Receptors, Transforming Growth Factor beta -- deficiency
KW  - PTEN Phosphohydrolase -- genetics
KW  - Mice, Knockout
KW  - In Situ Nick-End Labeling
KW  - Blotting, Western
KW  - Phosphorylation
KW  - PTEN Phosphohydrolase -- deficiency
KW  - Immunohistochemistry
KW  - Female
KW  - Male
KW  - Anus Neoplasms -- metabolism
KW  - TOR Serine-Threonine Kinases -- metabolism
KW  - Anus Neoplasms -- genetics
KW  - TOR Serine-Threonine Kinases -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443426990?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+mTOR+reduces+anal+carcinogenesis+in+transgenic+mouse+model.&rft.au=Sun%2C+Zhi-Jun%3BZhang%2C+Lu%3BZhang%2C+Wei%3BHall%2C+Bradford%3BBian%2C+Yansong%3BKulkarni%2C+Ashok+B&rft.aulast=Sun&rft.aufirst=Zhi-Jun&rft.date=2013-01-01&rft.volume=8&rft.issue=10&rft.spage=e74888&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0074888
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-07-11
N1  - Date created - 2013-10-14
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Cell. 2000 Feb 18;100(4):387-90 [10693755]
Gut. 2001 Aug;49(2):190-8 [11454793]
Cancer Lett. 2001 Dec 28;174(2):189-94 [11689295]
Curr Opin Genet Dev. 2002 Feb;12(1):22-9 [11790550]
Prev Med. 2003 May;36(5):555-60 [12689800]
Cell. 2003 Jun 13;113(6):685-700 [12809600]
Cancer. 2004 Jul 15;101(2):281-8 [15241824]
Cancer Res. 2005 Nov 1;65(21):9953-61 [16267020]
Cell. 2006 Feb 10;124(3):471-84 [16469695]
Nat Rev Cancer. 2006 Sep;6(9):729-34 [16915295]
Cell Cycle. 2007 Jun 1;6(11):1360-6 [17534148]
Cancer Cell. 2007 Oct;12(4):313-27 [17936557]
Int J Cancer. 2007 Dec 15;121(12):2668-73 [17721920]
Mol Cancer. 2008;7:3 [18184435]
J Exp Med. 2008 Mar 17;205(3):565-74 [18283119]
Cell. 2008 Jul 25;134(2):215-30 [18662538]
J Clin Invest. 2008 Aug;118(8):2722-32 [18618014]
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18758-63 [19022904]
Trends Immunol. 2009 May;30(5):218-26 [19362054]
Cancer Res. 2009 Jul 15;69(14):5918-26 [19584284]
BMC Cancer. 2010;10:118 [20346172]
Cancer Prev Res (Phila). 2010 Dec;3(12):1534-41 [20947489]
Cancer Prev Res (Phila). 2010 Dec;3(12):1542-51 [21149330]
Virology. 2011 Dec 20;421(2):114-8 [21999991]
Cancer Lett. 2012 Jan 1;314(1):1-7 [22018778]
PLoS One. 2012;7(3):e33396 [22413021]
PLoS One. 2012;7(5):e36653 [22586484]
Oncogene. 2012 Jul 12;31(28):3322-32 [22037217]
Cancer Res. 2012 Oct 1;72(19):5004-13 [22991304]
Clin Cancer Res. 2012 Oct 1;18(19):5304-13 [22859719]
Eur J Immunol. 2012 Oct;42(10):2683-96 [22740122]
Sex Health. 2012 Dec;9(6):593-609 [22951027]
Cancer Lett. 2013 May 1;331(2):230-8 [23340180]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1371/journal.pone.0074888
ER  - 



TY  - JOUR
T1  - Sec-mediated secretion by Coxiella burnetii
AN  - 1443374289; 18681819
AB  - Background: Coxiella burnetii is a Gram-negative intracellular bacterial pathogen that replicates within a phagolysosome-like parasitophorous vacuole (PV) of macrophages. PV formation requires delivery of effector proteins directly into the host cell cytoplasm by a type IVB secretion system. However, additional secretion systems are likely responsible for modification of the PV lumen microenvironment that promote pathogen replication. Results: To assess the potential of C. burnetii to secrete proteins into the PV, we analyzed the protein content of modified acidified citrate cysteine medium for the presence of C. burnetii proteins following axenic (host cell-free) growth. Mass spectrometry generated a list of 105 C. burnetii proteins that could be secreted. Based on bioinformatic analysis, 55 proteins were selected for further study by expressing them in C. burnetii with a C-terminal 3xFLAG-tag. Secretion of 27 proteins by C. burnetii transformants was confirmed by immunoblotting culture supernatants. Tagged proteins expressed by C. burnetii transformants were also found in the soluble fraction of infected Vero cells, indicating secretion occurs ex vivo. All secreted proteins contained a signal sequence, and deletion of this sequence from selected proteins abolished secretion. These data indicate protein secretion initially requires translocation across the inner-membrane into the periplasm via the activity of the Sec translocase. Conclusions: C. burnetii secretes multiple proteins, in vitro and ex vivo, in a Sec-dependent manner. Possible roles for secreted proteins and secretion mechanisms are discussed.
JF  - BMC Microbiology
AU  - Stead, Christopher M
AU  - Omsland, Anders
AU  - Beare, Paul A
AU  - Sandoz, Kelsi M
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, MT 59840, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 222
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1471-2180, 1471-2180
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology
KW  - Macrophages
KW  - Immunoblotting
KW  - translocase
KW  - Protein transport
KW  - Data processing
KW  - Vero cells
KW  - Replication
KW  - Cell culture
KW  - Pathogens
KW  - Mass spectroscopy
KW  - parasitophorous vacuole
KW  - Coxiella burnetii
KW  - Cysteine
KW  - Cytoplasm
KW  - Microenvironments
KW  - Bioinformatics
KW  - periplasm
KW  - Citric acid
KW  - J 02320:Cell Biology
KW  - A 01300:Methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443374289?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Microbiology&rft.atitle=Sec-mediated+secretion+by+Coxiella+burnetii&rft.au=Stead%2C+Christopher+M%3BOmsland%2C+Anders%3BBeare%2C+Paul+A%3BSandoz%2C+Kelsi+M%3BHeinzen%2C+Robert+A&rft.aulast=Stead&rft.aufirst=Christopher&rft.date=2013-01-01&rft.volume=13&rft.issue=1&rft.spage=222&rft.isbn=&rft.btitle=&rft.title=BMC+Microbiology&rft.issn=14712180&rft_id=info:doi/10.1186%2F1471-2180-13-222
L2  - http://www.biomedcentral.com/1471-2180/13/222
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 64
N1  - Last updated - 2013-12-16
N1  - SubjectsTermNotLitGenreText - Macrophages; Protein transport; translocase; Immunoblotting; Data processing; Vero cells; Replication; Cell culture; Pathogens; Mass spectroscopy; parasitophorous vacuole; Cysteine; Cytoplasm; Microenvironments; Bioinformatics; periplasm; Citric acid; Coxiella burnetii
DO  - http://dx.doi.org/10.1186/1471-2180-13-222
ER  - 



TY  - JOUR
T1  - Is estrogen plus progestin menopausal hormone therapy safe with respect to endometrial cancer risk?
AN  - 1443370178; 18602429
AB  - Given the strong link between use of unopposed estrogens and development of endometrial cancers, estrogens are usually prescribed with a progestin, particularly for women with intact uteri. Some studies suggest that sequential use of progestins may increase risk; however, the moderating effects of usage patterns or patient characteristics, including body mass index (BMI), are unknown. We evaluated menopausal hormone use and incident endometrial cancer (n = 885) in 68,419 postmenopausal women with intact uteri enrolled in the National Institutes of Health-American Association of Retired Persons Diet and Health study. Participants completed a risk factor questionnaire in 1996-1997 and were followed up through 2006. Hazard rate ratios (RRs) and 95% confidence intervals (CIs) were estimated using Cox regression. Among 19,131 women reporting exclusive estrogen plus progestin use, 176 developed endometrial cancer (RR = 0.88; 95% CI = 0.74-1.06). Long-duration ( greater than or equal to 10 years) sequential (25 days progestin per month) estrogen plus progestin use was associated with a decreased risk (RR = 0.64; 95% CI = 0.49-0.83). Increased risk for sequential estrogen plus progestin was seen only among thin-to-normal weight women (BMI < 25 kg/m super(2); RR = 2.53). Our findings support that specific categories of estrogen plus progestin use increases endometrial cancer risk, specifically long durations of sequential progestins, whereas decreased endometrial cancer risk was observed for users of short-duration continuous progestins. Risks were highest among thin-to-normal weight women, presumably reflecting their lower endogenous estrogen levels, suggesting that menopausal hormones and obesity increase endometrial cancer through common etiologic pathways.
JF  - International Journal of Cancer
AU  - Trabert, Britton
AU  - Wentzensen, Nicolas
AU  - Yang, Hannah P
AU  - Sherman, Mark E
AU  - Hollenbeck, Albert R
AU  - Park, Yikyung
AU  - Brinton, Louise A
AD  - American Association of Retired Persons, Washington, DC., britton.trabert@nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 417
EP  - 426
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 132
IS  - 2
SN  - 0020-7136, 0020-7136
KW  - Health & Safety Science Abstracts; Risk Abstracts
KW  - Diets
KW  - Health risks
KW  - Obesity
KW  - Estrogens
KW  - Post-menopause
KW  - Risk factors
KW  - Body mass
KW  - Hormones
KW  - Cancer
KW  - H 11000:Diseases/Injuries/Trauma
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443370178?accountid=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=Is+estrogen+plus+progestin+menopausal+hormone+therapy+safe+with+respect+to+endometrial+cancer+risk%3F&rft.au=Trabert%2C+Britton%3BWentzensen%2C+Nicolas%3BYang%2C+Hannah+P%3BSherman%2C+Mark+E%3BHollenbeck%2C+Albert+R%3BPark%2C+Yikyung%3BBrinton%2C+Louise+A&rft.aulast=Trabert&rft.aufirst=Britton&rft.date=2013-01-01&rft.volume=132&rft.issue=2&rft.spage=417&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27623
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2013-11-15
N1  - SubjectsTermNotLitGenreText - Diets; Obesity; Health risks; Estrogens; Post-menopause; Body mass; Risk factors; Hormones; Cancer
DO  - http://dx.doi.org/10.1002/ijc.27623
ER  - 



TY  - JOUR
T1  - Is Bisphenol-A Exposure During Pregnancy Associated with Blood Glucose Levels or Diagnosis of Gestational Diabetes?
AN  - 1443369537; 18647791
AB  - Recent epidemiological studies indicate bisphenol A (BPA), an estrogenic chemical used in production of epoxy, polycarbonate, and plastic may increase risk of insulin resistance and type 2 diabetes. Exposure to BPA during pregnancy may contribute to development of gestational diabetes mellitus (GDM), a precursor to type 2 diabetes in women. This pilot study examined the association between BPA exposure, fasting blood glucose levels (FBG), and GDM diagnosis during pregnancy. Banked urine samples from 22 cases of GDM and 72 controls were analyzed for total (free BPA + conjugates) urinary BPA concentrations ( mu g/L). FBG levels (mg/dl) were obtained from 1-h 50-g glucose tolerance tests (GTT) that women underwent for routine GDM screening (mean gestational age = 26.6 weeks, SD = 3.8). Those with an initial screening value greater than or equal to 135 mg/dl underwent 3-h 100 g oral GTT. GDM diagnoses were made when the initial screening value was greater than or equal to 200 mg/dl or when values at greater than or equal to 2 time points exceeded 3-h oral GTT thresholds. Among controls, median FBG levels (mg/dL) did not differ across exposure tertiles, defined according to the distribution of total specific-gravity-adjusted urinary BPA concentrations. Logistic regression models controlling for race/ethnicity did not provide evidence of association between BPA exposure and case status across increasing tertiles of BPA exposure (number of GDM cases/controls in tertile1: 13/24; in tertile 2: 6/24; in tertile 3: 3/24). Findings do not support a relationship between total urinary BPA concentrations and altered glucose metabolism during pregnancy. However, due to study limitations, findings need to be interpreted with caution.
JF  - Journal of Toxicology and Environmental Health, Part A: Current Issues
AU  - Robledo, Candace
AU  - Peck, Jennifer D
AU  - Stoner, Julie A
AU  - Carabin, Helene
AU  - Cowan, Linda
AU  - Koch, Holger M
AU  - Goodman, Jean R
AD  - Department of Biostatistics & Epidemiology, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA, robledoc@mail.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 865
EP  - 873
PB  - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL  - 76
IS  - 14
SN  - 1528-7394, 1528-7394
KW  - Pollution Abstracts; Environment Abstracts; Toxicology Abstracts
KW  - Age
KW  - Glucose
KW  - Fasting
KW  - Glucose metabolism
KW  - Insulin
KW  - Models
KW  - Bisphenol A
KW  - Regression analysis
KW  - Plastics
KW  - polycarbonate
KW  - Ethnic groups
KW  - Races
KW  - Estrogens
KW  - Gestational age
KW  - Pregnancy
KW  - Diabetes mellitus
KW  - Blood
KW  - Urine
KW  - Glucose tolerance
KW  - Metabolism
KW  - X 24360:Metals
KW  - P 6000:TOXICOLOGY AND HEALTH
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443369537?accountid=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+Toxicology+and+Environmental+Health%2C+Part+A%3A+Current+Issues&rft.atitle=Is+Bisphenol-A+Exposure+During+Pregnancy+Associated+with+Blood+Glucose+Levels+or+Diagnosis+of+Gestational+Diabetes%3F&rft.au=Robledo%2C+Candace%3BPeck%2C+Jennifer+D%3BStoner%2C+Julie+A%3BCarabin%2C+Helene%3BCowan%2C+Linda%3BKoch%2C+Holger+M%3BGoodman%2C+Jean+R&rft.aulast=Robledo&rft.aufirst=Candace&rft.date=2013-01-01&rft.volume=76&rft.issue=14&rft.spage=865&rft.isbn=&rft.btitle=&rft.title=Journal+of+Toxicology+and+Environmental+Health%2C+Part+A%3A+Current+Issues&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2013.824395
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Gestational age; Glucose metabolism; Fasting; Insulin; Pregnancy; Models; Diabetes mellitus; Bisphenol A; Blood; Urine; Regression analysis; Glucose tolerance; Plastics; Races; Ethnic groups; polycarbonate; Age; Estrogens; Glucose; Metabolism
DO  - http://dx.doi.org/10.1080/15287394.2013.824395
ER  - 



TY  - JOUR
T1  - Association between Perfluoroalkyl substances and thyroid stimulating hormone among pregnant women: a cross-sectional study
AN  - 1439228740; 18602777
AB  - Background: Perfluoroalkyl substances (PFASs) are a group of highly persistent chemicals that are widespread contaminants in wildlife and humans. Exposure to PFAS affects thyroid homeostasis in experimental animals and possibly in humans. The objective of this study was to examine the association between plasma concentrations of PFASs and thyroid stimulating hormone (TSH) among pregnant women. Methods: A total of 903 pregnant women who enrolled in the Norwegian Mother and Child Cohort Study from 2003 to 2004 were studied. Concentrations of thirteen PFASs and TSH were measured in plasma samples collected around the 18 super(th) week of gestation. Linear regression models were used to evaluate associations between PFASs and TSH. Results: Among the thirteen PFASs, seven were detected in more than 60% of samples and perfluorooctane sulfonate (PFOS) had the highest concentrations (median, 12.8 ng/mL; inter-quartile range [IQR], 10.1 -16.5 ng/mL). The median TSH concentration was 3.5 (IQR, 2.4 - 4.8) [mu]IU/mL. Pregnant women with higher PFOS had higher TSH levels. After adjustment, with each 1 ng/mL increase in PFOS concentration, there was a 0.8% (95% confidence interval: 0.1%, 1.6%) rise in TSH. The odds ratio of having an abnormally high TSH, however, was not increased, and other PFASs were unrelated to TSH. Conclusions: Our results suggest an association between PFOS and TSH in pregnant women that is small and may be of no clinical significance.
JF  - Environmental Health (London)
AU  - Wang, Yan
AU  - Starling, Anne P
AU  - Haug, Line S
AU  - Eggesbo, Merete
AU  - Becher, Georg
AU  - Thomsen, Cathrine
AU  - Travlos, Gregory
AU  - King, Debra
AU  - Hoppin, Jane A
AU  - Rogan, Walter J
AU  - Longnecker, Matthew P
AD  - Department of Health and Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 76
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 12
IS  - 1
SN  - 1476-069X, 1476-069X
KW  - Health & Safety Science Abstracts
KW  - Chemicals
KW  - Sulfonates
KW  - Wildlife
KW  - Thyroid
KW  - Females
KW  - Norway
KW  - Hormones
KW  - Pregnancy
KW  - H 6000:Natural Disasters/Civil Defense/Emergency Management
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439228740?accountid=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+%28London%29&rft.atitle=Association+between+Perfluoroalkyl+substances+and+thyroid+stimulating+hormone+among+pregnant+women%3A+a+cross-sectional+study&rft.au=Wang%2C+Yan%3BStarling%2C+Anne+P%3BHaug%2C+Line+S%3BEggesbo%2C+Merete%3BBecher%2C+Georg%3BThomsen%2C+Cathrine%3BTravlos%2C+Gregory%3BKing%2C+Debra%3BHoppin%2C+Jane+A%3BRogan%2C+Walter+J%3BLongnecker%2C+Matthew+P&rft.aulast=Wang&rft.aufirst=Yan&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+%28London%29&rft.issn=1476069X&rft_id=info:doi/10.1186%2F1476-069X-12-76
L2  - http://www.ehjournal.net/content/12/1/76
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 48
N1  - Last updated - 2014-05-02
N1  - SubjectsTermNotLitGenreText - Chemicals; Sulfonates; Wildlife; Thyroid; Females; Hormones; Pregnancy; Norway
DO  - http://dx.doi.org/10.1186/1476-069X-12-76
ER  - 



TY  - JOUR
T1  - Agricultural Exposures and Stroke Mortality in the Agricultural Health Study
AN  - 1439228080; 18614287
AB  - Exposures associated with common agricultural activities may increase risk of stroke. The authors evaluated associations between self-reported agricultural activities including pesticide use and handling of crops and stroke mortality among 51,603 male pesticide applicators enrolled in the Agricultural Health Study (AHS). Vital status was obtained through 2008. Stroke mortality was defined by underlying or contributing cause of death (ICD-9 430-438, ICD-10 I60-I69). Information regarding lifetime pesticide use, working with crops or animals, engagement in other agricultural activities, and potential confounders was self-reported at enrollment. Cox proportional hazards models, with age as the time scale, were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) adjusted for state of residence, smoking status, and alcohol consumption. Median follow-up time was 13 yr, during which 308 stroke deaths occurred. No measure of overall or specific pesticide use was positively associated with mortality due to stroke. Stroke mortality was inversely associated with handling hay, grain, or silage at least once each year as reported at enrollment (HR: 0.75; 95% CI: 0.58, 0.98). There was no evidence of an association between pesticide use and stroke mortality. The inverse association between handling of hays and grains and stroke mortality may be due to (1) those engaging in such activities being healthier than those who did not or (2) exposure to some biological agent present in hays and grains. Further investigation of incident stroke, rather than stroke mortality, as well as stroke subtypes, is needed to determine the full role of agricultural exposures and stroke.
JF  - Journal of Toxicology and Environmental Health, Part A: Current Issues
AU  - Rinsky, Jessica L
AU  - Hoppin, Jane A
AU  - Blair, Aaron
AU  - He, Ka
AU  - Beane Freeman, Laura E
AU  - Chen, Honglei
AD  - Department of Epidemiology, University of North Carolina Gillings School of Global Public Health, Chapel Hill, North Carolina, USA, hoppin1@niehs.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 798
EP  - 814
PB  - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL  - 76
IS  - 13
SN  - 1528-7394, 1528-7394
KW  - Health & Safety Science Abstracts; Pollution Abstracts; Environment Abstracts; Toxicology Abstracts
KW  - Alcohol
KW  - Mortality
KW  - Age
KW  - Stroke
KW  - Hay
KW  - Crops
KW  - Models
KW  - Silage
KW  - Smoking
KW  - Pesticides
KW  - Grain
KW  - Grains
KW  - Ethanol
KW  - X 24380:Social Poisons & Drug Abuse
KW  - H 5000:Pesticides
KW  - P 6000:TOXICOLOGY AND HEALTH
KW  - ENA 02:Toxicology & Environmental Safety
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439228080?accountid=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+Toxicology+and+Environmental+Health%2C+Part+A%3A+Current+Issues&rft.atitle=Agricultural+Exposures+and+Stroke+Mortality+in+the+Agricultural+Health+Study&rft.au=Rinsky%2C+Jessica+L%3BHoppin%2C+Jane+A%3BBlair%2C+Aaron%3BHe%2C+Ka%3BBeane+Freeman%2C+Laura+E%3BChen%2C+Honglei&rft.aulast=Rinsky&rft.aufirst=Jessica&rft.date=2013-01-01&rft.volume=76&rft.issue=13&rft.spage=798&rft.isbn=&rft.btitle=&rft.title=Journal+of+Toxicology+and+Environmental+Health%2C+Part+A%3A+Current+Issues&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2013.819308
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Silage; Smoking; Mortality; Pesticides; Stroke; Grain; Hay; Crops; Ethanol; Models; Alcohol; Age; Grains
DO  - http://dx.doi.org/10.1080/15287394.2013.819308
ER  - 



TY  - JOUR
T1  - Novel autoproteolytic and DNA-damage sensing components in the bacterial SOS response and oxidized methylcytosine-induced eukaryotic DNA demethylation systems
AN  - 1439227145; 18541230
AB  - The bacterial SOS response is an elaborate program for DNA repair, cell cycle regulation and adaptive mutagenesis under stress conditions. Using sensitive sequence and structure analysis, combined with contextual information derived from comparative genomics and domain architectures, we identify two novel domain superfamilies in the SOS response system. We present evidence that one of these, the SOS response associated peptidase (SRAP; Pfam: DUF159) is a novel thiol autopeptidase. Given the involvement of other autopeptidases, such as LexA and UmuD, in the SOS response, this finding suggests that multiple structurally unrelated peptidases have been recruited to this process. The second of these, the ImuB-C superfamily, is linked to the Y-family DNA polymerase-related domain in ImuB, and also occurs as a standalone protein. We present evidence using gene neighborhood analysis that both these domains function with different mutagenic polymerases in bacteria, such as Pol IV (DinB), Pol V (UmuCD) and ImuA-ImuB-DnaE2 and also other repair systems, which either deploy Ku and an ATP-dependent ligase or a SplB-like radical SAM photolyase. We suggest that the SRAP superfamily domain functions as a DNA-associated autoproteolytic switch that recruits diverse repair enzymes upon DNA damage, whereas the ImuB-C domain performs a similar function albeit in a non-catalytic fashion. We propose that C3Orf37, the eukaryotic member of the SRAP superfamily, which has been recently shown to specifically bind DNA with 5-hydroxymethylcytosine, 5-formylcytosine and 5-carboxycytosine, is a sensor for these oxidized bases generated by the TET enzymes from methylcytosine. Hence, its autoproteolytic activity might help it act as a switch that recruits DNA repair enzymes to remove these oxidized methylcytosine species as part of the DNA demethylation pathway downstream of the TET enzymes. Reviewers: This article was reviewed by RDS, RF and GJ.
JF  - Biology Direct
AU  - Aravind, L
AU  - Anand, Swadha
AU  - Iyer, Lakshminarayan M
AD  - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 20
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 8
IS  - 1
SN  - 1745-6150, 1745-6150
KW  - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology
KW  - Bacteria
KW  - Cell cycle
KW  - Stress
KW  - Enzymes
KW  - DNA repair
KW  - peptidase
KW  - Mutagenesis
KW  - DNA damage
KW  - Demethylation
KW  - Reviews
KW  - Thiols
KW  - SOS response
KW  - Photolyase
KW  - genomics
KW  - Radicals
KW  - N 14820:DNA Metabolism & Structure
KW  - J 02320:Cell Biology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439227145?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+Direct&rft.atitle=Novel+autoproteolytic+and+DNA-damage+sensing+components+in+the+bacterial+SOS+response+and+oxidized+methylcytosine-induced+eukaryotic+DNA+demethylation+systems&rft.au=Aravind%2C+L%3BAnand%2C+Swadha%3BIyer%2C+Lakshminarayan+M&rft.aulast=Aravind&rft.aufirst=L&rft.date=2013-01-01&rft.volume=8&rft.issue=1&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-8-20
L2  - http://www.biologydirect.com/content/8/1/20
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 29
N1  - Last updated - 2016-08-17
N1  - SubjectsTermNotLitGenreText - Cell cycle; Enzymes; Stress; DNA repair; peptidase; Mutagenesis; DNA damage; Demethylation; Reviews; SOS response; Thiols; Photolyase; genomics; Radicals; Bacteria
DO  - http://dx.doi.org/10.1186/1745-6150-8-20
ER  - 



TY  - JOUR
T1  - Parabolic replicator dynamics and the principle of minimum Tsallis information gain
AN  - 1439220417; 18541229
AB  - Background: Non-linear, parabolic (sub-exponential) and hyperbolic (super-exponential) models of prebiological evolution of molecular replicators have been proposed and extensively studied. The parabolic models appear to be the most realistic approximations of real-life replicator systems due primarily to product inhibition. Unlike the more traditional exponential models, the distribution of individual frequencies in an evolving parabolic population is not described by the Maximum Entropy (MaxEnt) Principle in its traditional form, whereby the distribution with the maximum Shannon entropy is chosen among all the distributions that are possible under the given constraints. We sought to identify a more general form of the MaxEnt principle that would be applicable to parabolic growth. Results: We consider a model of a population that reproduces according to the parabolic growth law and show that the frequencies of individuals in the population minimize the Tsallis relative entropy (non-additive information gain) at each time moment. Next, we consider a model of a parabolically growing population that maintains a constant total size and provide an "implicit" solution for this system. We show that in this case, the frequencies of the individuals in the population also minimize the Tsallis information gain at each moment of the 'internal time" of the population. Conclusions: The results of this analysis show that the general MaxEnt principle is the underlying law for the evolution of a broad class of replicator systems including not only exponential but also parabolic and hyperbolic systems. The choice of the appropriate entropy (information) function depends on the growth dynamics of a particular class of systems. The Tsallis entropy is non-additive for independent subsystems, i.e. the information on the subsystems is insufficient to describe the system as a whole. In the context of prebiotic evolution, this "non-reductionist" nature of parabolic replicator systems might reflect the importance of group selection and competition between ensembles of cooperating replicators. Reviewers: This article was reviewed by Viswanadham Sridhara (nominated by Claus Wilke), Puushottam Dixit (nominated by Sergei Maslov), and Nick Grishin. For the complete reviews, see the Reviewers' Reports section.
JF  - Biology Direct
AU  - Karev, Georgy P
AU  - Koonin, Eugene V
AD  - National Center for Biotechnology Information, NLM, National Institutes of Health, Bethesda, Maryland 20894, USA
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 19
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 8
IS  - 1
SN  - 1745-6150, 1745-6150
KW  - Ecology Abstracts
KW  - Replicator equation
KW  - Parabolic growth
KW  - Tsallis entropy
KW  - Non-extensive statistical mechanics
KW  - MaxEnt principle
KW  - Molecular modelling
KW  - Reviews
KW  - Group selection
KW  - Competition
KW  - Entropy
KW  - Evolution
KW  - Models
KW  - D 04040:Ecosystem and Ecology Studies
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439220417?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+Direct&rft.atitle=Parabolic+replicator+dynamics+and+the+principle+of+minimum+Tsallis+information+gain&rft.au=Karev%2C+Georgy+P%3BKoonin%2C+Eugene+V&rft.aulast=Karev&rft.aufirst=Georgy&rft.date=2013-01-01&rft.volume=8&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-8-19
L2  - http://www.biologydirect.com/content/8/1/19
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-10-01
N1  - Number of references - 35
N1  - Last updated - 2016-08-17
N1  - SubjectsTermNotLitGenreText - Molecular modelling; Group selection; Reviews; Competition; Evolution; Entropy; Models
DO  - http://dx.doi.org/10.1186/1745-6150-8-19
ER  - 



TY  - JOUR
T1  - Surface plasmon resonance applied to G protein-coupled receptors
AN  - 1434032982; 18512136
AB  - G protein-coupled receptors (GPCR) are integral membrane proteins that transmit signals from external stimuli to the cell interior via activation of GTP-binding proteins (G proteins) thereby mediating key sensorial, hormonal, metabolic, immunological and neurotransmission processes. Elucidating their structure and mechanism of interaction with extracellular and intracellular binding partners is of fundamental importance and highly relevant to rational design of new effective drugs. Surface plasmon resonance (SPR) has become a method of choice for studying biomolecular interactions at interfaces because measurements take place in real-time and do not require labeling of any of the interactants. However, due to the particular challenges imposed by the high hydrophobicity of membrane proteins and the great diversity of receptor-stimulating ligands, the application of this technique to characterize interactions of GPCR is still in the developmental phase. Here we give an overview of the principle of SPR and analyze current approaches for the preparation of the sensor chip surface, capture and stabilization of GPCR, and experimental design to characterize their interaction with ligands, G proteins and specific antibodies.
JF  - Biomedical Spectroscopy and Imaging
AU  - Locatelli-Hoops, Silvia
AU  - Yeliseev, Alexei A
AU  - Gawrisch, Klaus
AU  - Gorshkova, Inna
AD  - National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 155
EP  - 181
PB  - IOS Press, Nieuwe Hemweg 6B Amsterdam 1013 BG Netherlands
VL  - 2
IS  - 3
SN  - 2212-8794, 2212-8794
KW  - Biotechnology and Bioengineering Abstracts
KW  - Guanine nucleotide-binding protein
KW  - Drug development
KW  - Hydrophobicity
KW  - Membrane proteins
KW  - Spectroscopy
KW  - External stimuli
KW  - Cell activation
KW  - Antibodies
KW  - surface plasmon resonance
KW  - Neurotransmission
KW  - G protein-coupled receptors
KW  - GTP-binding protein
KW  - Reviews
KW  - Drugs
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434032982?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+Spectroscopy+and+Imaging&rft.atitle=Surface+plasmon+resonance+applied+to+G+protein-coupled+receptors&rft.au=Locatelli-Hoops%2C+Silvia%3BYeliseev%2C+Alexei+A%3BGawrisch%2C+Klaus%3BGorshkova%2C+Inna&rft.aulast=Locatelli-Hoops&rft.aufirst=Silvia&rft.date=2013-01-01&rft.volume=2&rft.issue=3&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Biomedical+Spectroscopy+and+Imaging&rft.issn=22128794&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Guanine nucleotide-binding protein; Hydrophobicity; Drug development; Membrane proteins; Spectroscopy; External stimuli; Cell activation; Antibodies; surface plasmon resonance; GTP-binding protein; G protein-coupled receptors; Neurotransmission; Reviews; Drugs
ER  - 



TY  - JOUR
T1  - RCircos: an R package for Circos 2D track plots
AN  - 1434022037; 18541276
AB  - Background: Circos is a Perl language based software package for visualizing similarities and differences of genome structure and positional relationships between genomic intervals. Running Circos requires extra data processing procedures to prepare plot data files and configure files from datasets, which limits its capability of integrating directly with other software tools such as R. Recently published R Bioconductor package ggbio provides a function to display genomic data in circular layout based on multiple other packages, which increases its complexity of usage and decreased the flexibility in integrating with other R pipelines. Results: We implemented an R package, RCircos, using only R packages that come with R base installation. The package supports Circos 2D data track plots such as scatter, line, histogram, heatmap, tile, connectors, links, and text labels. Each plot is implemented with a specific function and input data for all functions are data frames which can be objects read from text files or generated with other R pipelines. Conclusion: RCircos package provides a simple and flexible way to make Circos 2D track plots with R and could be easily integrated into other R data processing and graphic manipulation pipelines for presenting large-scale multi-sample genomic research data. It can also serve as a base tool to generate complex Circos images.
JF  - BMC Bioinformatics
AU  - Zhang, Hongen
AU  - Meltzer, Paul
AU  - Davis, Sean
AD  - Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 6138, 37 Convent Drive, Bethesda, MD 20892-4265, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 244
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2105, 1471-2105
KW  - Biotechnology and Bioengineering Abstracts
KW  - Software
KW  - RCircos
KW  - R package
KW  - Circos
KW  - Genomic data visualization
KW  - Genomes
KW  - Computer programs
KW  - software
KW  - Data processing
KW  - Language
KW  - genomics
KW  - Bioinformatics
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434022037?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=RCircos%3A+an+R+package+for+Circos+2D+track+plots&rft.au=Zhang%2C+Hongen%3BMeltzer%2C+Paul%3BDavis%2C+Sean&rft.aulast=Zhang&rft.aufirst=Hongen&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-14-244
L2  - http://www.biomedcentral.com/1471-2105/14/244
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Number of references - 7
N1  - Last updated - 2015-04-09
N1  - SubjectsTermNotLitGenreText - Genomes; Computer programs; software; Data processing; Language; Bioinformatics; genomics
DO  - http://dx.doi.org/10.1186/1471-2105-14-244
ER  - 



TY  - JOUR
T1  - How Should We Think about Climate Justice?
AN  - 1430856746; 18439114
AB  - Climate change raises questions of justice. Some people are enjoying the benefits of energy use and other emissions-generating activities, but those activities are causing other people to suffer the burdens of climate change. Political philosophers have begun to pay more attention to the problem of "climate justice." However, contributors to the literature have made quite different methodological assumptions about how we should develop a theory of climate justice and defend principles of climate justice. So far. there has been little systematic or detailed discussion of these methodological issues. One way to approach these issues is by developing a methodological framework for thinking about climate justice, or more specifically, a five-stage framework, drawing on recent work on two issues: first, the distinction between "ideal" and "non-ideal" theory; and second, the distinction between "integrationist" and "isolationist" approaches to environmental and climate justice. This methodological framework can also be used to inform critical analysis of extant theories of climate justice, for example, through a critical discussion of two key features of the theory of climate justice developed by Simon Caney.
JF  - Environmental Ethics
AU  - Bell, D
AD  - Department of Politics, School of Geography, Politics, and Sociology, University of Newcastle. 40-12 Great North Road, Newcastle upon Tyne NEI 7RU, UK
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 189
EP  - 208
VL  - 35
IS  - 2
SN  - 0163-4275, 0163-4275
KW  - Meteorological & Geoastrophysical Abstracts; Environment Abstracts; Sustainability Science Abstracts
KW  - Politics
KW  - Climate change
KW  - Energy consumption
KW  - M2 551.583:Variations (551.583)
KW  - M3 1010:Issues in Sustainable Development
KW  - ENA 20:Weather Modification & Geophysical Change
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1430856746?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Ethics&rft.atitle=How+Should+We+Think+about+Climate+Justice%3F&rft.au=Bell%2C+D&rft.aulast=Bell&rft.aufirst=D&rft.date=2013-01-01&rft.volume=35&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Environmental+Ethics&rft.issn=01634275&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-09-01
N1  - Last updated - 2016-07-20
N1  - SubjectsTermNotLitGenreText - Climate change; Politics; Energy consumption
ER  - 



TY  - JOUR
T1  - Body mass index, occupational activity, and leisure-time physical activity: an exploration of risk factors and modifiers for knee osteoarthritis in the 1946 British birth cohort
AN  - 1427002562; 18312308
AB  - Background: Knee osteoarthritis (kOA) risk is increased by obesity and physical activities (PA) which mechanically stress the joint. We examined the associations of midlife kOA with body mass index (BMI) and activity exposure across adult life and their interaction. Methods: Data are from a UK birth cohort of 2597 participants with a clinical assessment for kOA at age 53. At ages 36, 43 and 53 BMI (kg/m super(2)), self-reported leisure-time PA, and occupational activity (kneeling/squatting; lifting; climbing; sitting; assigned using a job-exposure matrix) were ascertained. Associations were explored using the multiplicative logistic model. Results: BMI was strongly and positively associated with kOA in men and women. Men and women in manual occupations also had greater odds of kOA; there was a weak suggestion that kOA risk was higher among men exposed to lifting or kneeling at work. For men, the only evidence of a multiplicative interaction between BMI and activities was for lifting (p = 0.01) at age 43; BMI conferred higher kOA risk among those most-likely to lift at work (OR per increase in BMI z-score: 3.55, 95% CI: 1.72-7.33). For women, the only evidence of an interaction was between BMI and leisure-time PA (p = 0.005) at age 43; BMI conferred higher kOA risk among those at higher PA levels (OR per increase in BMI z-score: 1.59, 95% CI: 1.26-2.00 in inactive; 1.70, 95% CI: 1.14-2.55 (less-active); and 4.44; 95% CI: 2.26-8.36 (most-active). Conclusions: At the very least, our study suggests that more active individuals (at work and in leisure) may see a greater reduction in risk of kOA from avoiding a high BMI than those less active.
JF  - BMC Musculoskeletal Disorders
AU  - Martin, Kathryn R
AU  - Kuh, Diana
AU  - Harris, Tamara B
AU  - Guralnik, Jack M
AU  - Coggon, David
AU  - Wills, Andrew K
AD  - Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, 7201 Wisconsin Avenue, Room 3C309, Bethesda, Maryland 20814, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 219
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2474, 1471-2474
KW  - Physical Education Index; Calcium & Calcified Tissue Abstracts; Risk Abstracts; Health & Safety Science Abstracts
KW  - Age
KW  - Osteoarthritis
KW  - Physical activity
KW  - Body mass
KW  - Women
KW  - Knees
KW  - Work
KW  - Models
KW  - Evaluation
KW  - Climbing
KW  - Risk factors
KW  - Arthritis
KW  - British Isles
KW  - Obesity
KW  - Men
KW  - Stress
KW  - Exercise
KW  - Knee
KW  - Joints
KW  - Musculoskeletal system
KW  - Body mass index
KW  - Lifting
KW  - T 2030:Cartilage and Cartilage Diseases
KW  - R2 23060:Medical and environmental health
KW  - H 1000:Occupational Safety and Health
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1427002562?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Musculoskeletal+Disorders&rft.atitle=Body+mass+index%2C+occupational+activity%2C+and+leisure-time+physical+activity%3A+an+exploration+of+risk+factors+and+modifiers+for+knee+osteoarthritis+in+the+1946+British+birth+cohort&rft.au=Martin%2C+Kathryn+R%3BKuh%2C+Diana%3BHarris%2C+Tamara+B%3BGuralnik%2C+Jack+M%3BCoggon%2C+David%3BWills%2C+Andrew+K&rft.aulast=Martin&rft.aufirst=Kathryn&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=BMC+Musculoskeletal+Disorders&rft.issn=14712474&rft_id=info:doi/10.1186%2F1471-2474-14-219
L2  - http://www.biomedcentral.com/1471-2474/14/219
LA  - English
DB  - Physical Education Index; ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 42
N1  - Last updated - 2013-11-04
N1  - SubjectsTermNotLitGenreText - Evaluation; Men; Arthritis; Body mass; Women; Knees; Work; Exercise; Lifting; Obesity; Climbing; Age; Osteoarthritis; Physical activity; Risk factors; Stress; Body mass index; Knee; Models; Joints; Musculoskeletal system; British Isles
DO  - http://dx.doi.org/10.1186/1471-2474-14-219
ER  - 



TY  - JOUR
T1  - Rigorous science as the road to better public health
AN  - 1419366749; 18272607
AB  - In the current issue of Population Health Metrics, two reports paint a bleak picture of American public health. Both physical inactivity and obesity remain highly prevalent; yet, it is not clear that increased physical activity will reduce the burden of obesity. There continue to be widespread disparities in life expectancy across United States counties. These reports appear against a backdrop of debate regarding how we should allocate our scarce resources for improving health: should we focus more on improving access to high-quality medical care, or should we instead focus on more and better public health interventions? While optimal solutions remain obscure, a look at prior successes suggests that ultimately they will come from the conduct and implementation of rigorous science, and in particular event-driven trials.
JF  - Population Health Metrics
AU  - Lauer, Michael S
AD  - Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute (NHLBI), 6701 Rockledge Drive, Room 8128, Bethesda, MD 20892, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 10
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 11
IS  - 1
SN  - 1478-7954, 1478-7954
KW  - Health & Safety Science Abstracts
KW  - Obesity
KW  - USA
KW  - Physical activity
KW  - Life span
KW  - Intervention
KW  - Public health
KW  - Paints
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419366749?accountid=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=Population+Health+Metrics&rft.atitle=Rigorous+science+as+the+road+to+better+public+health&rft.au=Lauer%2C+Michael+S&rft.aulast=Lauer&rft.aufirst=Michael&rft.date=2013-01-01&rft.volume=11&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Population+Health+Metrics&rft.issn=14787954&rft_id=info:doi/10.1186%2F1478-7954-11-10
L2  - http://www.pophealthmetrics.com/content/11/1/10
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-08-01
N1  - Number of references - 17
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Obesity; Physical activity; Life span; Intervention; Paints; Public health; USA
DO  - http://dx.doi.org/10.1186/1478-7954-11-10
ER  - 



TY  - JOUR
T1  - Internet accelerator transformations in Russia
TT  - Internet, accelerator delle trasformazioni in Russia
AN  - 1417524252; 201332809
AB  - Abstract not available.
JF  - Aggiornamenti Sociali
AU  - Nocetti, Julien
AD  - Ricercatore del Centro Russia/NEI dell'Institut Francais des relations internationales, Parigi
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 407
EP  - 415
PB  - San Fedele Edizioni, Milan Italy
VL  - 64
IS  - 5
SN  - 0002-094X, 0002-094X
KW  - Russia
KW  - Internet
KW  - article
KW  - 0828: mass phenomena; communication
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1417524252?accountid=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=Aggiornamenti+Sociali&rft.atitle=Internet+accelerator+transformations+in+Russia&rft.au=Nocetti%2C+Julien&rft.aulast=Nocetti&rft.aufirst=Julien&rft.date=2013-01-01&rft.volume=64&rft.issue=5&rft.spage=407&rft.isbn=&rft.btitle=&rft.title=Aggiornamenti+Sociali&rft.issn=0002094X&rft_id=info:doi/
LA  - Italian
DB  - Sociological Abstracts
N1  - Date revised - 2013-08-01
N1  - Last updated - 2016-09-28
N1  - SubjectsTermNotLitGenreText - Internet; Russia
ER  - 



TY  - JOUR
T1  - Metformin improves healthspan and lifespan in mice.
AN  - 1416695856; 23900241
AB  - Metformin is a drug commonly prescribed to treat patients with type 2 diabetes. Here we show that long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice, while a higher dose (1% w/w) was toxic. Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced low-density lipoprotein and cholesterol levels without a decrease in caloric intake. At a molecular level, metformin increases AMP-activated protein kinase activity and increases antioxidant protection, resulting in reductions in both oxidative damage accumulation and chronic inflammation. Our results indicate that these actions may contribute to the beneficial effects of metformin on healthspan and lifespan. These findings are in agreement with current epidemiological data and raise the possibility of metformin-based interventions to promote healthy aging.
JF  - Nature communications
AU  - Martin-Montalvo, Alejandro
AU  - Mercken, Evi M
AU  - Mitchell, Sarah J
AU  - Palacios, Hector H
AU  - Mote, Patricia L
AU  - Scheibye-Knudsen, Morten
AU  - Gomes, Ana P
AU  - Ward, Theresa M
AU  - Minor, Robin K
AU  - Blouin, Marie-José
AU  - Schwab, Matthias
AU  - Pollak, Michael
AU  - Zhang, Yongqing
AU  - Yu, Yinbing
AU  - Becker, Kevin G
AU  - Bohr, Vilhelm A
AU  - Ingram, Donald K
AU  - Sinclair, David A
AU  - Wolf, Norman S
AU  - Spindler, Stephen R
AU  - Bernier, Michel
AU  - de Cabo, Rafael
AD  - Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, 251 Bayview Boulevard, Baltimore, Maryland 21224, USA.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 2192
VL  - 4
KW  - Antioxidants
KW  - 0
KW  - Biomarkers
KW  - Metformin
KW  - 9100L32L2N
KW  - AMP-Activated Protein Kinases
KW  - EC 2.7.11.1
KW  - Index Medicus
KW  - Animals
KW  - Inflammation -- blood
KW  - Caloric Restriction
KW  - Inflammation -- drug therapy
KW  - Mice
KW  - Electron Transport -- drug effects
KW  - Antioxidants -- pharmacology
KW  - Transcriptome -- genetics
KW  - Mitochondria -- drug effects
KW  - Mice, Inbred C57BL
KW  - Enzyme Activation -- drug effects
KW  - Mitochondria -- metabolism
KW  - Biomarkers -- blood
KW  - Male
KW  - Transcriptome -- drug effects
KW  - Survival Analysis
KW  - Inflammation -- pathology
KW  - Metformin -- therapeutic use
KW  - Metformin -- pharmacology
KW  - Longevity -- drug effects
KW  - Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1416695856?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Metformin+improves+healthspan+and+lifespan+in+mice.&rft.au=Martin-Montalvo%2C+Alejandro%3BMercken%2C+Evi+M%3BMitchell%2C+Sarah+J%3BPalacios%2C+Hector+H%3BMote%2C+Patricia+L%3BScheibye-Knudsen%2C+Morten%3BGomes%2C+Ana+P%3BWard%2C+Theresa+M%3BMinor%2C+Robin+K%3BBlouin%2C+Marie-Jos%C3%A9%3BSchwab%2C+Matthias%3BPollak%2C+Michael%3BZhang%2C+Yongqing%3BYu%2C+Yinbing%3BBecker%2C+Kevin+G%3BBohr%2C+Vilhelm+A%3BIngram%2C+Donald+K%3BSinclair%2C+David+A%3BWolf%2C+Norman+S%3BSpindler%2C+Stephen+R%3BBernier%2C+Michel%3Bde+Cabo%2C+Rafael&rft.aulast=Martin-Montalvo&rft.aufirst=Alejandro&rft.date=2013-01-01&rft.volume=4&rft.issue=&rft.spage=2192&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms3192
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2014-02-27
N1  - Date created - 2013-07-31
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - GSE40936; GEO
N1  - SuppNotes - Cited By:
J Gerontol A Biol Sci Med Sci. 2010 May;65(5):468-74 [20304770]
PLoS One. 2010;5(1):e8758 [20090912]
Biochem Biophys Res Commun. 2010 May 28;396(2):199-205 [20398632]
Diabetes Care. 2010 Jul;33(7):1674-85 [20587728]
Free Radic Biol Med. 2010 Sep 15;49(6):1082-7 [20600832]
Am J Epidemiol. 2010 Sep 1;172(5):558-65 [20682520]
Diabetologia. 2010 Nov;53(11):2406-16 [20652679]
Aging (Albany NY). 2010 Dec;2(12):945-58 [21164223]
Oncogene. 2011 Feb 3;30(5):505-20 [21057541]
Aging (Albany NY). 2011 Feb;3(2):148-57 [21386129]
J Biol Chem. 2011 Jun 3;286(22):19270-9 [21467030]
Cancer Res. 2011 Jul 1;71(13):4366-72 [21540236]
Aging (Albany NY). 2011 Oct;3(10):1028-38 [22067284]
Diabetologia. 2012 Feb;55(2):443-9 [22009334]
J Nutr. 2012 Feb;142(2):213-20 [22223580]
Sci Transl Med. 2012 Mar 7;4(124):124ra27 [22323820]
Nat Rev Mol Cell Biol. 2012 Apr;13(4):251-62 [22436748]
Cancer Prev Res (Phila). 2012 Apr;5(4):536-43 [22262811]
Proc Natl Acad Sci U S A. 2012 Jun 5;109(23):8977-82 [22611195]
Ugeskr Laeger. 2012 Jun 4;174(23):1598-602 [22673379]
Rev Esp Anestesiol Reanim. 2012 May;59(5):276-9 [22609263]
Biochim Biophys Acta. 2012 Oct;1817(10):1768-75 [22386881]
J Hepatol. 2012 Sep;57(3):642-54 [22634126]
Cancer Discov. 2012 Sep;2(9):778-90 [22926251]
PLoS One. 2012;7(10):e47699 [23077661]
Oncogene. 2013 Mar 21;32(12):1475-87 [22665053]
Antioxid Redox Signal. 2013 Jul 20;19(3):310-20 [22901095]
J Biol Chem. 2000 Jan 7;275(1):223-8 [10617608]
J Clin Invest. 2001 Oct;108(8):1167-74 [11602624]
J Mol Diagn. 2003 May;5(2):73-81 [12707371]
Curr Drug Targets Immune Endocr Metabol Disord. 2003 Jun;3(2):151-69 [12769787]
Diabetes. 2004 Apr;53(4):1052-9 [15047621]
J Biol Chem. 2004 Jun 18;279(25):25995-6004 [15078893]
Diabet Med. 1992 Jan-Feb;9(1):61-5 [1551312]
Toxicol Pathol. 1995 Jul-Aug;23(4):458-76 [7501958]
Brain Res Mol Brain Res. 2005 Mar 24;134(1):109-18 [15790535]
BMC Bioinformatics. 2005;6:144 [15941488]
Physiol Genomics. 2005 Nov 17;23(3):343-50 [16189280]
Aging Cell. 2006 Feb;5(1):39-50 [16441842]
Am J Physiol Endocrinol Metab. 2006 Jul;291(1):E182-9 [16478780]
Nature. 2006 Nov 16;444(7117):337-42 [17086191]
FEBS Lett. 2008 Jan 9;582(1):97-105 [18053812]
Diabetes. 2008 Feb;57(2):306-14 [17909097]
Am J Physiol Heart Circ Physiol. 2008 Jun;294(6):H2497-506 [18375721]
Cell Metab. 2008 Aug;8(2):157-68 [18599363]
Mini Rev Med Chem. 2008 Nov;8(13):1343-54 [18991752]
Toxicol Lett. 2009 Mar 10;185(2):132-41 [19136048]
Cell. 2009 May 15;137(4):635-46 [19450513]
Nature. 2009 Jul 16;460(7253):392-5 [19587680]
Diabetes Care. 2009 Sep;32(9):1620-5 [19564453]
Cardiovasc Res. 2010 May 1;86(2):211-8 [20202975]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1038/ncomms3192
ER  - 



TY  - JOUR
T1  - Two novel PIWI families: roles in inter-genomic conflicts in bacteria and Mediator-dependent modulation of transcription in eukaryotes
AN  - 1412516614; 18238758
AB  - Background: The PIWI module, found in the PIWI/AGO superfamily of proteins, is a critical component of several cellular pathways including germline maintenance, chromatin organization, regulation of splicing, RNA interference, and virus suppression. It binds a guide strand which helps it target complementary nucleic strands. Results: Here we report the discovery of two divergent, novel families of PIWI modules, the first such to be described since the initial discovery of the PIWI/AGO superfamily over a decade ago. Both families display conservation patterns consistent with the binding of oligonucleotide guide strands. The first family is bacterial in distribution and is typically encoded by a distinctive three-gene operon alongside genes for a restriction endonuclease fold enzyme and a helicase of the DinG family. The second family is found only in eukaryotes. It is the core conserved module of the Med13 protein, a subunit of the CDK8 subcomplex of the transcription regulatory Mediator complex. Conclusions: Based on the presence of the DinG family helicase, which specifically acts on R-loops, we infer that the first family of PIWI modules is part of a novel RNA-dependent restriction system which could target invasive DNA from phages, plasmids or conjugative transposons. It is predicted to facilitate restriction of actively transcribed invading DNA by utilizing RNA guides. The PIWI family found in the eukaryotic Med13 proteins throws new light on the regulatory switch through which the CDK8 subcomplex modulates transcription at Mediator-bound promoters of highly transcribed genes. We propose that this involves recognition of small RNAs by the PIWI module in Med13 resulting in a conformational switch that propagates through the Mediator complex. Reviewers: This article was reviewed by Sandor Pongor, Frank Eisenhaber and Balaji Santhanam.
JF  - Biology Direct
AU  - Burroughs, A Maxwell
AU  - Iyer, Lakshminarayan M
AU  - Aravind, L
AD  - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 13
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 8
IS  - 1
SN  - 1745-6150, 1745-6150
KW  - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology
KW  - Chromatin
KW  - Transcription
KW  - A 01490:Miscellaneous
KW  - J 02430:Symbiosis, Antibiosis & Phages
KW  - G 07760:Viruses & Phages
KW  - V 22310:Genetics, Taxonomy & Structure
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412516614?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+Direct&rft.atitle=Two+novel+PIWI+families%3A+roles+in+inter-genomic+conflicts+in+bacteria+and+Mediator-dependent+modulation+of+transcription+in+eukaryotes&rft.au=Burroughs%2C+A+Maxwell%3BIyer%2C+Lakshminarayan+M%3BAravind%2C+L&rft.aulast=Burroughs&rft.aufirst=A&rft.date=2013-01-01&rft.volume=8&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-8-13
L2  - http://www.biology-direct.com/content/8/1/13
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 1
N1  - Last updated - 2014-04-03
N1  - SubjectsTermNotLitGenreText - Transcription
DO  - http://dx.doi.org/10.1186/1745-6150-8-13
ER  - 



TY  - JOUR
T1  - Analysis of dimerization of BTB-IVR domains of Keap1 and its interaction with Cul3, by molecular modeling
AN  - 1399922822; 18229850
AB  - Oxidative damage has been associated with various neurodegenerative diseases including Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease, as well as non-neurodegenerative conditions such as cancer and heart disease. The Keap1-Nrf2 system plays a central role in the protection of cells against oxidative and xenobiotic stress. The Nrf2 transcription function and its degradation by the proteasomal pathway (Keap1-Nrf2-Cul3-Roc1 complex) are regulated by the cytoplasmic repressor protein, Keap1 which possesses BTB, BACK (IVR region) and Kelch domains. The BTB-BACK domains are important for Keap1 homo-dimerization as well as to interact with Cullin-3 for Nrf2 degradation. The crystal structure of the Keap1-Kelch domain is known; however, that of the BTB-BACK domains are not yet determined. We present here, through molecular modeling studies, the analysis of Keap1-BTB dimerization, and of BTB-BACK domains role in complex with Cul3. The electrostatic charge distribution at the BTB dimer interface of Keap1 is significantly different from other known BTB containing protein structures. Another intriguing feature is also observed that the non-conserved residues at the BTB-BACK-Cul3 interface region may play critical role for differentiating Cul3 recognition by Keap1 from other adaptor proteins for their specific substrates proteasomal degradation.
JF  - Bioinformation
AU  - Chauhan, N
AU  - Chaunsali, L
AU  - Deshmukh, P
AU  - Padmanabhan, B
AD  - Department of Biophysics, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore 560029, India, paddy@nimhans.kar.nic.in
A2  - Kangueane, P (ed)
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 450
EP  - 455
VL  - 9
IS  - 9
SN  - 0973-2063, 0973-2063
KW  - Biotechnology and Bioengineering Abstracts
KW  - Molecular modelling
KW  - Parkinson's disease
KW  - Alzheimer's disease
KW  - proteasomes
KW  - Stress
KW  - Transcription
KW  - Cancer
KW  - Protein structure
KW  - Neurodegenerative diseases
KW  - adaptor proteins
KW  - Movement disorders
KW  - Amyotrophic lateral sclerosis
KW  - Crystal structure
KW  - Repressors
KW  - Heart diseases
KW  - W 30940:Products
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399922822?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformation&rft.atitle=Analysis+of+dimerization+of+BTB-IVR+domains+of+Keap1+and+its+interaction+with+Cul3%2C+by+molecular+modeling&rft.au=Chauhan%2C+N%3BChaunsali%2C+L%3BDeshmukh%2C+P%3BPadmanabhan%2C+B&rft.aulast=Chauhan&rft.aufirst=N&rft.date=2013-01-01&rft.volume=9&rft.issue=9&rft.spage=450&rft.isbn=&rft.btitle=&rft.title=Bioinformation&rft.issn=09732063&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Last updated - 2013-08-12
N1  - SubjectsTermNotLitGenreText - Molecular modelling; Parkinson's disease; Alzheimer's disease; proteasomes; Transcription; Stress; Cancer; Protein structure; Neurodegenerative diseases; adaptor proteins; Amyotrophic lateral sclerosis; Movement disorders; Crystal structure; Repressors; Heart diseases
ER  - 



TY  - JOUR
T1  - Host immune constraints on malaria transmission: insights from population biology of within-host parasites
AN  - 1399918688; 18214802
AB  - Background: Plasmodium infections trigger complex immune reactions from their hosts against several life stages of the parasite, including gametocytes. These immune responses are highly variable, depending on age, genetics, and exposure history of the host as well as species and strain of parasite. Although the effects of host antibodies that act against gamete stages in the mosquito (due to uptake in the blood meal) are well documented, the effects of host immunity upon within-host gametocytes are not as well understood. This report consists of a theoretical population biology-based analysis to determine constraints that host immunity impose upon gametocyte population growth. The details of the mathematical models used for the analysis were guided by published reports of clinical and animal studies, incorporated plausible modalities of immune reactions to parasites, and were tailored to the life cycl es of the two most widespread human malaria pathogens, Plasmodium falciparum and Plasmodium vivax. Results: For the same ability to bind and clear a target, the model simulations suggest that an antibody attacking immature gametocytes would tend to lower the overall density of transmissible mature gametocytes more than an antibody attacking the mature forms directly. Transmission of P. falciparum would be especially vulnerable to complete blocking by antibodies to its immature forms since its gametocytes take much longer to reach maturity than those of P. vivax. On the other hand, antibodies attacking the mature gametocytes directly would reduce the time the mature forms can linger in the host. Simulation results also suggest that varying the standard deviation in the time necessary for individual asexual parasites to develop and produce schizonts can affect the efficiency of production of transmissible gametocytes. Conclusions: If mature gametocyte density determines the probability of transmission, both Plasmodium species, but especially P. falciparum, could bolster this probability through evasion or suppression of host immune responses against the immature gametocytes. However, if the long term lingering of mature gametocytes at low density in the host is also important to ensure transmission, then evasion or suppression of antibodies against the mature stages would bolster probability of transmission as well.
JF  - Malaria Journal
AU  - McQueen, Philip G
AU  - Williamson, Kim C
AU  - McKenzie, F Ellis
AD  - Mathematical and Statistical Computing Laboratory, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, Maryland, USA
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 206
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 12
IS  - 1
SN  - 1475-2875, 1475-2875
KW  - Immunology Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Parasites
KW  - Age
KW  - Human diseases
KW  - Population growth
KW  - Plasmodium vivax
KW  - Malaria
KW  - Blood meals
KW  - Hosts
KW  - Infection
KW  - Public health
KW  - Maturity
KW  - Vulnerability
KW  - Mathematical models
KW  - Gametes
KW  - Gametocytes
KW  - Developmental stages
KW  - Schizonts
KW  - Plasmodium falciparum
KW  - Pathogens
KW  - Immunity
KW  - Antibodies
KW  - Standard deviation
KW  - Immune response
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - F 06910:Microorganisms & Parasites
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399918688?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Malaria+Journal&rft.atitle=Host+immune+constraints+on+malaria+transmission%3A+insights+from+population+biology+of+within-host+parasites&rft.au=McQueen%2C+Philip+G%3BWilliamson%2C+Kim+C%3BMcKenzie%2C+F+Ellis&rft.aulast=McQueen&rft.aufirst=Philip&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=206&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-12-206
L2  - http://www.malariajournal.com/content/12/1/206
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 94
N1  - Last updated - 2016-02-04
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Antibodies; Malaria; Vulnerability; Immunity; Hosts; Public health; Age; Mathematical models; Gametocytes; Gametes; Population growth; Schizonts; Developmental stages; Blood meals; Pathogens; Infection; Standard deviation; Maturity; Immune response; Plasmodium vivax; Plasmodium falciparum
DO  - http://dx.doi.org/10.1186/1475-2875-12-206
ER  - 



TY  - JOUR
T1  - HASP server: a database and structural visualization platform for comparative models of influenza A hemagglutinin proteins
AN  - 1399918674; 18214774
AB  - Background: Influenza A viruses possess RNA genomes that mutate frequently in response to immune pressures. The mutations in the hemagglutinin genes are particularly significant, as the hemagglutinin proteins mediate attachment and fusion to host cells, thereby influencing viral pathogenicity and species specificity. Large-scale influenza A genome sequencing efforts have been ongoing to understand past epidemics and pandemics and anticipate future outbreaks. Sequencing efforts thus far have generated nearly 9,000 distinct hemagglutinin amino acid sequences. Description: Comparative models for all publicly available influenza A hemagglutinin protein sequences (8,769 to date) were generated using the Rosetta modeling suite. The C-alpha root mean square deviations between a randomly chosen test set of models and their crystallographic templates were less than 2 Aa, suggesting that the modeling protocols yielded high-quality results. The models were compiled into an online resource, the Hemagglutinin Structure Prediction (HASP) server. The HASP server was designed as a scientific tool for researchers to visualize hemagglutinin protein sequences of interest in a three-dimensional context. With a built-in molecular viewer, hemagglutinin models can be compared side-by-side and navigated by a corresponding sequence alignment. The models and alignments can be downloaded for offline use and further analysis. Conclusions: The modeling protocols used in the HASP server scale well for large amounts of sequences and will keep pace with expanded sequencing efforts. The conservative approach to modeling and the intuitive search and visualization interfaces allow researchers to quickly analyze hemagglutinin sequences of interest in the context of the most highly related experimental structures, and allow them to directly compare hemagglutinin sequences to each other simultaneously in their two- and three-dimensional contexts. The models and methodology have shown utility in current research efforts and the ongoing aim of the HASP server is to continue to accelerate influenza A research and have a positive impact on global public health.
JF  - BMC Bioinformatics
AU  - Ambroggio, Xavier I
AU  - Dommer, Jennifer
AU  - Gopalan, Vivek
AU  - Dunham, Eleca J
AU  - Taubenberger, Jeffery K
AU  - Hurt, Darrell E
AD  - Bioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 197
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 14
IS  - 1
SN  - 1471-2105, 1471-2105
KW  - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts
KW  - Influenza A
KW  - HASP
KW  - Hemagglutinin
KW  - Receptor binding
KW  - Membrane fusion
KW  - ROSETTA
KW  - Sialic acid
KW  - Flu
KW  - Homology modeling
KW  - Molecular visualization
KW  - Prediction
KW  - Genomes
KW  - Molecular modelling
KW  - Nucleotide sequence
KW  - Hemagglutinins
KW  - Viruses
KW  - RNA viruses
KW  - Public health
KW  - Influenza
KW  - pandemics
KW  - Pathogenicity
KW  - Pressure
KW  - Ethnic groups
KW  - Amino acids
KW  - Epidemics
KW  - Databases
KW  - RNA
KW  - Proteins
KW  - Outbreaks
KW  - Bioinformatics
KW  - Mutation
KW  - Internet
KW  - H 0500:General
KW  - V 22310:Genetics, Taxonomy & Structure
KW  - W 30960:Bioinformatics & Computer Applications
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399918674?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=HASP+server%3A+a+database+and+structural+visualization+platform+for+comparative+models+of+influenza+A+hemagglutinin+proteins&rft.au=Ambroggio%2C+Xavier+I%3BDommer%2C+Jennifer%3BGopalan%2C+Vivek%3BDunham%2C+Eleca+J%3BTaubenberger%2C+Jeffery+K%3BHurt%2C+Darrell+E&rft.aulast=Ambroggio&rft.aufirst=Xavier&rft.date=2013-01-01&rft.volume=14&rft.issue=1&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-14-197
L2  - http://www.biomedcentral.com/1471-2105/14/197
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 19
N1  - Last updated - 2015-03-20
N1  - SubjectsTermNotLitGenreText - Genomes; Molecular modelling; Epidemics; Hemagglutinins; Influenza A; Nucleotide sequence; RNA viruses; Public health; Databases; pandemics; Pathogenicity; RNA; Bioinformatics; Pressure; Mutation; Internet; Prediction; Influenza; Amino acids; Viruses; Proteins; Outbreaks; Ethnic groups
DO  - http://dx.doi.org/10.1186/1471-2105-14-197
ER  - 



TY  - JOUR
T1  - Hypervariable antigen genes in malaria have ancient roots
AN  - 1399910418; 18155134
AB  - Background: The var genes of the human malaria parasite Plasmodium falciparum are highly polymorphic loci coding for the erythrocyte membrane proteins 1 (PfEMP1), which are responsible for the cytoaherence of P. falciparum infected red blood cells to the human vasculature. Cytoadhesion, coupled with differential expression of var genes, contributes to virulence and allows the parasite to establish chronic infections by evading detection from the host's immune system. Although studying genetic diversity is a major focus of recent work on the var genes, little is known about the gene family's origin and evolutionary history. Results: Using a novel hidden Markov model-based approach and var sequences assembled from additional isolates and species, we are able to reveal elements of both the early evolution of the var genes as well as recent diversifying events. We compare sequences of the var gene DBL[alpha] domains from divergent isolates of P. falciparum (3D7 and HB3), and a closely-related species, Plasmodium reichenowi. We find that the gene family is equally large in P. reichenowi and P. falciparum -- with a minimum of 51 var genes in the P. reichenowi genome (compared to 61 in 3D7 and a minimum of 48 in HB3). In addition, we are able to define large, continuous blocks of homologous sequence among P. falciparum and P. reichenowi var gene DBL[alpha] domains. These results reveal that the contemporary structure of the var gene family was present before the divergence of P. falciparum and P. reichenowi, estimated to be between 2.5 to 6 million years ago. We also reveal that recombination has played an important and traceable role in both the establishment, and the maintenance, of diversity in the sequences. Conclusions: Despite the remarkable diversity and rapid evolution found in these loci within and among P. falciparum populations, the basic structure of these domains and the gene family is surprisingly old and stable. Revealing a common structure as well as conserved sequence among two species also has implications for developing new primate-parasite models for studying the pathology and immunology of falciparum malaria, and for studying the population genetics of var genes and associated virulence phenotypes.
JF  - BMC Evolutionary Biology
AU  - Zilversmit, Martine M
AU  - Chase, Ella K
AU  - Chen, Donald S
AU  - Awadalla, Philip
AU  - Day, Karen P
AU  - McVean, Gil
AD  - National Institute of Allergy of Infectious Disease, National Institutes of Health, 12735 Twinbrook Parkway, Rockville, MD 20852, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 110
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1471-2148, 1471-2148
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; Genetics Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources
KW  - Non-allelic homologous recombination
KW  - Hidden Markov-model
KW  - var genes
KW  - Malaria
KW  - PfEMP1
KW  - Gene family evolution
KW  - Balancing selection
KW  - Genomes
KW  - Parasites
KW  - Human diseases
KW  - var gene
KW  - Immune system
KW  - Erythrocytes
KW  - Roots
KW  - Genetic diversity
KW  - Public health
KW  - Virulence
KW  - Recombination
KW  - Population genetics
KW  - Conserved sequence
KW  - Evolutionary genetics
KW  - Plasmodium reichenowi
KW  - Phylogeny
KW  - Plasmodium falciparum
KW  - Chronic infection
KW  - erythrocyte membrane protein 1
KW  - Evolution
KW  - G 07740:Evolution
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
KW  - K 03320:Cell Biology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399910418?accountid=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=BMC+Evolutionary+Biology&rft.atitle=Hypervariable+antigen+genes+in+malaria+have+ancient+roots&rft.au=Zilversmit%2C+Martine+M%3BChase%2C+Ella+K%3BChen%2C+Donald+S%3BAwadalla%2C+Philip%3BDay%2C+Karen+P%3BMcVean%2C+Gil&rft.aulast=Zilversmit&rft.aufirst=Martine&rft.date=2013-01-01&rft.volume=13&rft.issue=1&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=BMC+Evolutionary+Biology&rft.issn=14712148&rft_id=info:doi/10.1186%2F1471-2148-13-110
L2  - http://www.biomedcentral.com/1471-2148/13/110
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-07-01
N1  - Number of references - 35
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Virulence; Phylogeny; Population genetics; Human diseases; Erythrocytes; Genetic diversity; Malaria; Evolution; Public health; Genomes; Parasites; var gene; Immune system; Roots; Recombination; Chronic infection; Conserved sequence; Evolutionary genetics; erythrocyte membrane protein 1; Plasmodium falciparum; Plasmodium reichenowi
DO  - http://dx.doi.org/10.1186/1471-2148-13-110
ER  - 



TY  - JOUR
T1  - Identification and optimization of small-molecule agonists of the human relaxin hormone receptor RXFP1.
AN  - 1367884455; 23764525
AB  - The anti-fibrotic, vasodilatory and pro-angiogenic therapeutic properties of recombinant relaxin peptide hormone have been investigated in several diseases, and recent clinical trial data has shown benefit in treating acute heart failure. However, the remodelling capacity of these peptide hormones is difficult to study in chronic settings because of their short half-life and the need for intravenous administration. Here we present the first small-molecule series of human relaxin/insulin-like family peptide receptor 1 agonists. These molecules display similar efficacy as the natural hormone in several functional assays. Mutagenesis studies indicate that the small molecules activate relaxin receptor through an allosteric site. These compounds have excellent physical and in vivo pharmacokinetic properties to support further investigation of relaxin biology and animal efficacy studies of the therapeutic benefits of relaxin/insulin-like family peptide receptor 1 activation.
JF  - Nature communications
AU  - Xiao, Jingbo
AU  - Huang, Zaohua
AU  - Chen, Catherine Z
AU  - Agoulnik, Irina U
AU  - Southall, Noel
AU  - Hu, Xin
AU  - Jones, Raisa E
AU  - Ferrer, Marc
AU  - Zheng, Wei
AU  - Agoulnik, Alexander I
AU  - Marugan, Juan J
AD  - NIH Chemical Genomics Center, Discovery Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, USA.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 1953
VL  - 4
KW  - RXFP1 protein, human
KW  - 0
KW  - Receptors, G-Protein-Coupled
KW  - Receptors, Peptide
KW  - Small Molecule Libraries
KW  - Vascular Endothelial Growth Factor A
KW  - Relaxin
KW  - 9002-69-1
KW  - Cyclic AMP
KW  - E0399OZS9N
KW  - Index Medicus
KW  - Animals
KW  - Drug Stability
KW  - HEK293 Cells
KW  - Humans
KW  - Relaxin -- pharmacology
KW  - Electric Impedance
KW  - Amino Acid Sequence
KW  - Mice
KW  - Structure-Activity Relationship
KW  - Transfection
KW  - Molecular Sequence Data
KW  - Cyclic AMP -- metabolism
KW  - Crystallography, X-Ray
KW  - Gene Expression Regulation -- drug effects
KW  - Molecular Conformation
KW  - Hydrogen Bonding
KW  - Vascular Endothelial Growth Factor A -- genetics
KW  - Vascular Endothelial Growth Factor A -- metabolism
KW  - Receptors, Peptide -- chemistry
KW  - Receptors, Peptide -- metabolism
KW  - Small Molecule Libraries -- pharmacology
KW  - Receptors, G-Protein-Coupled -- agonists
KW  - Receptors, G-Protein-Coupled -- chemistry
KW  - Receptors, G-Protein-Coupled -- metabolism
KW  - Receptors, Peptide -- agonists
KW  - Small Molecule Libraries -- pharmacokinetics
KW  - Drug Evaluation, Preclinical -- methods
KW  - Small Molecule Libraries -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367884455?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+and+optimization+of+small-molecule+agonists+of+the+human+relaxin+hormone+receptor+RXFP1.&rft.au=Xiao%2C+Jingbo%3BHuang%2C+Zaohua%3BChen%2C+Catherine+Z%3BAgoulnik%2C+Irina+U%3BSouthall%2C+Noel%3BHu%2C+Xin%3BJones%2C+Raisa+E%3BFerrer%2C+Marc%3BZheng%2C+Wei%3BAgoulnik%2C+Alexander+I%3BMarugan%2C+Juan+J&rft.aulast=Xiao&rft.aufirst=Jingbo&rft.date=2013-01-01&rft.volume=4&rft.issue=&rft.spage=1953&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms2953
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-12-30
N1  - Date created - 2013-06-14
N1  - Date revised - 2017-01-13
N1  - Genetic sequence - 162211061; PubChem-Substance; 162211062; 162211060; 162211056; 162211057; 162211063; 162211058; 162211059
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1038/ncomms2953
ER  - 



TY  - JOUR
T1  - The assessment of risk factors for the Central/East African Genotype of chikungunya virus infections in the state of Kelantan: a case control study in Malaysia
AN  - 1367487494; 18058645
AB  - Background: The aims of the study were to assess the risk factors in relation to cross border activities, exposure to mosquito bite and preventive measures taken. An outbreak of chikungunya virus (CHIKV) infection in Malaysia has been reported in Klang, Selangor (1998) and Bagan Panchor, Perak (2006). In 2009, CHIKV infection re-emerged in some states in Malaysia. It raises the possibilities that re-emergence is part of the epidemics in neighbouring countries or the disease is endemic in Malaysia. For this reason, A community-based case control study was carried out in the state of Kelantan. Methods: Prospective case finding was performed from June to December 2009. Those who presented with signs and symptoms of CHIKV infection were investigated. We designed a case control study to assess the risk factors. Assessment consisted of answering questions, undergoing a medical examination, and being tested for the presence of IgM antibodies to CHIKV. Descriptive epidemiological studies were conducted by reviewing both the national surveillance and laboratory data. Multivariable logistic regression analysis was performed to determine risk factors contributing to the illness. Cases were determined by positive to RT-PCR or serological for antibodies by IgM. CHIKV specificity was confirmed by DNA sequencing. Results: There were 129 suspected cases and 176 controls. Among suspected cases, 54.4% were diagnosed to have CHIKV infection. Among the controls, 30.1% were found to be positive to serology for antibodies [IgM, 14.2% and IgG, 15.9%]. For analytic study and based on laboratory case definition, 95 were considered as cases and 123 as controls. Those who were positive to IgG were excluded. CHIKV infection affected all ages and mostly between 50-59 years old. Staying together in the same house with infected patients and working as rubber tappers were at a higher risk of infection. The usage of Mosquito coil insecticide had shown to be a significant protective factor. Most cases were treated as outpatient, only 7.5% needed hospitalization. The CHIKV infection was attributable to central/east African genotype CHIKV. Conclusions: In this study, cross border activity was not a significant risk factor although Thailand and Malaysia shared the same CHIKV genotype during the episode of infections.
JF  - BMC Infectious Diseases
AU  - Yusoff, Ahmad Faudzi
AU  - Mustafa, Amal Nasir
AU  - Husaain, Hani Mat
AU  - Hamzah, Wan Mansor
AU  - Yusof, Apandi Mohd
AU  - Harun, Rozilawati
AU  - Abdullah, Faezah Noor
AD  - Institute for Medical Research, National Institutes of Health, Ministry of Health, Jalan Pahang, Kuala Lumpur 50588, Malaysia
Y1  - 2013///0,
PY  - 2013
DA  - 0, 2013
SP  - 211
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
KW  - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Risk Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW  - Chikungunya
KW  - Case-control study
KW  - Central/East African genotype
KW  - Risk factors
KW  - Age
KW  - Housing
KW  - Bites
KW  - Thailand
KW  - Community involvement
KW  - Malaysia, Malaya, Selangor
KW  - Genotypes
KW  - Infection
KW  - Serology
KW  - Risks
KW  - Public health
KW  - DNA sequencing
KW  - Endemic species
KW  - Serological studies
KW  - Insecticides
KW  - Malaysia
KW  - Malaysia, Malaya, Kelantan
KW  - Regression analysis
KW  - Polymerase chain reaction
KW  - Aquatic insects
KW  - Biological surveys
KW  - Houses
KW  - Chikungunya virus
KW  - Epidemics
KW  - Data processing
KW  - Rubber
KW  - Pest control
KW  - Antibodies
KW  - Residential areas
KW  - DNA
KW  - Immunoglobulin G
KW  - Africa
KW  - Outbreaks
KW  - Immunoglobulin M
KW  - V 22410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - R2 23060:Medical and environmental health
KW  - H 12000:Epidemiology and Public Health
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367487494?accountid=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=BMC+Infectious+Diseases&rft.atitle=The+assessment+of+risk+factors+for+the+Central%2FEast+African+Genotype+of+chikungunya+virus+infections+in+the+state+of+Kelantan%3A+a+case+control+study+in+Malaysia&rft.au=Yusoff%2C+Ahmad+Faudzi%3BMustafa%2C+Amal+Nasir%3BHusaain%2C+Hani+Mat%3BHamzah%2C+Wan+Mansor%3BYusof%2C+Apandi+Mohd%3BHarun%2C+Rozilawati%3BAbdullah%2C+Faezah+Noor&rft.aulast=Yusoff&rft.aufirst=Ahmad&rft.date=2013-01-01&rft.volume=13&rft.issue=1&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=BMC+Infectious+Diseases&rft.issn=1471-2334&rft_id=info:doi/10.1186%2F1471-2334-13-211
L2  - http://www.biomedcentral.com/1471-2334/13/211
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-06-01
N1  - Number of references - 17
N1  - Last updated - 2016-10-12
N1  - SubjectsTermNotLitGenreText - Biological surveys; Serological studies; Endemic species; Antibodies; Pest control; Genotypes; Aquatic insects; Risks; Public health; Age; Houses; Data processing; Epidemics; Bites; Rubber; Infection; Serology; DNA sequencing; Insecticides; Risk factors; Immunoglobulin G; Regression analysis; Polymerase chain reaction; Immunoglobulin M; Housing; Community involvement; DNA; Residential areas; Outbreaks; Chikungunya virus; Thailand; Malaysia; Malaysia, Malaya, Kelantan; Africa; Malaysia, Malaya, Selangor
DO  - http://dx.doi.org/10.1186/1471-2334-13-211
ER  - 



TY  - JOUR
T1  - Synthesis of the Alzheimer drug Posiphen into its primary metabolic products (+)-N1-norPosiphen, (+)-N8-norPosiphen and (+)-N1, N8-bisnorPosiphen, their inhibition of amyloid precursor protein, α-Synuclein synthesis, interleukin-1β release, and cholinergic action.
AN  - 1355479807; 23360256
AB  - A major pathological hallmark of Alzheimer disease (AD) is the appearance in the brain of senile plaques that are primarily composed of aggregated forms of β-amyloid peptide (Aβ) that derive from amyloid precursor protein (APP). Posiphen (1) tartrate is an experimental AD drug in current clinical trials that reduces Aβ levels by lowering the rate of APP synthesis without toxicity. To support the clinical development of Posiphen (1) and elucidate its efficacy, its three major metabolic products, (+)-N1-norPosiphen (15), (+)-N8-norPosiphen (17) and (+)-N1, N8-bisnorPosiphen (11), were required in high chemical and optical purity. The efficient transformation of Posiphen (1) into these metabolic products, 15, 17 and 11, is described. The biological activity of these metabolites together with Posiphen (1) and its enantiomer, the AD drug candidate (-)-phenserine (2), was assessed against APP,α-synuclein and classical cholinergic targets. All the compounds potently inhibited the generation of APP and α-synuclein in neuronal cultures. In contrast, metabolites 11 and 15, and (-)-phenserine (2) but not Posiphen (1) or 17, possessed acetyl cholinesterase inhibitory action and no compounds bound either nicotinic or muscarinic receptors. As Posiphen (1) lowered CSF markers of inflammation in a recent clinical trial, the actions of 1 and 2 on proinflammatory cytokine interleukin (IL)-1β release human peripheral blood mononuclear cells was evaluated, and found to be potently inhibited by both agents.
JF  - Anti-inflammatory & anti-allergy agents in medicinal chemistry
AU  - Yu, Qian-Sheng
AU  - Reale, Marcella
AU  - Kamal, Mohammad A
AU  - Holloway, Harold W
AU  - Luo, Weiming
AU  - Sambamurti, Kumar
AU  - Ray, Balmiki
AU  - Lahiri, Debomoy K
AU  - Rogers, Jack T
AU  - Greig, Nigel H
AD  - Drug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 117
EP  - 128
VL  - 12
IS  - 2
KW  - Amyloid beta-Protein Precursor
KW  - 0
KW  - Interleukin-1beta
KW  - Receptors, Muscarinic
KW  - Receptors, Nicotinic
KW  - alpha-Synuclein
KW  - phenserine
KW  - Physostigmine
KW  - 9U1VM840SP
KW  - Index Medicus
KW  - alpha-Synuclein -- biosynthesis
KW  - Stereoisomerism
KW  - Interleukin-1beta -- biosynthesis
KW  - Receptors, Nicotinic -- metabolism
KW  - Humans
KW  - Plaque, Amyloid -- metabolism
KW  - Amyloid beta-Protein Precursor -- biosynthesis
KW  - Receptors, Muscarinic -- metabolism
KW  - Physostigmine -- pharmacology
KW  - Alzheimer Disease -- physiopathology
KW  - Alzheimer Disease -- drug therapy
KW  - Physostigmine -- analogs & derivatives
KW  - Physostigmine -- chemistry
KW  - Physostigmine -- pharmacokinetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1355479807?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-inflammatory+%26+anti-allergy+agents+in+medicinal+chemistry&rft.atitle=Synthesis+of+the+Alzheimer+drug+Posiphen+into+its+primary+metabolic+products+%28%2B%29-N1-norPosiphen%2C+%28%2B%29-N8-norPosiphen+and+%28%2B%29-N1%2C+N8-bisnorPosiphen%2C+their+inhibition+of+amyloid+precursor+protein%2C+%CE%B1-Synuclein+synthesis%2C+interleukin-1%CE%B2+release%2C+and+cholinergic+action.&rft.au=Yu%2C+Qian-Sheng%3BReale%2C+Marcella%3BKamal%2C+Mohammad+A%3BHolloway%2C+Harold+W%3BLuo%2C+Weiming%3BSambamurti%2C+Kumar%3BRay%2C+Balmiki%3BLahiri%2C+Debomoy+K%3BRogers%2C+Jack+T%3BGreig%2C+Nigel+H&rft.aulast=Yu&rft.aufirst=Qian-Sheng&rft.date=2013-01-01&rft.volume=12&rft.issue=2&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Anti-inflammatory+%26+anti-allergy+agents+in+medicinal+chemistry&rft.issn=1875-614X&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-11-12
N1  - Date created - 2013-05-24
N1  - Date revised - 2017-01-14
N1  - Last updated - 2017-01-19
ER  - 



TY  - JOUR
T1  - Genetic analysis of putative familial relationships in a captive chimpanzee (pan troglodytes) population
AN  - 1353280170; 4440039
AB  - Twelve autosomal dinucleotide repeat loci were analyzed in chimpanzees genomes by DNA amplification using primers designed for analysis of human loci. The markers span the entire length of human chromosomes 21 and 22. Nine markers were polymorphic in chimpanzee as well, with a somewhat comparable level of polymorphism and allele size range. Even in the presence of very limited information and in spite of missing samples, it was possible to reconstruct a complex pedigree and to provide molecular data that corroborate family relationships that were deduced from cage history and behavioral data. The conclusions were further supported by mitochondrial DNA analysis. The data presented in this report show that the extremely abundant source of human markers may be exploited to validate, with molecular evidence, hypotheses on individual relationship or alleged pedigrees, based upon behavioral observations. Reprinted by permission of Croatian Anthropological Society and Institute for Anthropological Research, Zagreb, Croatia
JF  - Collegium antropologicum
AU  - Robledo, R
AU  - Lorenz, J
AU  - Beck, J
AU  - Else, J
AU  - Bender, P
AD  - Università di Cagliari ; Central Washington University ; Coriell Institute for Medical Research ; Emory University ; National Institute of Mental Health
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 245
EP  - 250
VL  - 37
IS  - 1
SN  - 0350-6134, 0350-6134
KW  - Anthropology
KW  - Chimpanzees
KW  - Genetics
KW  - Chromosomes
KW  - DNA
KW  - Data analysis
KW  - Evidence
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1353280170?accountid=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=Collegium+antropologicum&rft.atitle=Genetic+analysis+of+putative+familial+relationships+in+a+captive+chimpanzee+%28pan+troglodytes%29+population&rft.au=Robledo%2C+R%3BLorenz%2C+J%3BBeck%2C+J%3BElse%2C+J%3BBender%2C+P&rft.aulast=Robledo&rft.aufirst=R&rft.date=2013-01-01&rft.volume=37&rft.issue=1&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Collegium+antropologicum&rft.issn=03506134&rft_id=info:doi/
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 5460 1615 8573 11325; 2218 10148; 3254 5460 1615 8573 11325; 4560; 2257 5455 1678; 3279 971 3286
ER  - 



TY  - JOUR
T1  - Personal, behavioral and socio-environmental predictors of overweight incidence in young adults: 10-yr longitudinal findings
AN  - 1352284860; 17938751
AB  - Background: The objective of this study was to identify 10-year longitudinal predictors of overweight incidence during the transition from adolescence to young adulthood. Methods: Data were from Project EAT (Eating and Activity in Teens and Young Adults). A diverse, population-based cohort (N = 2,134) completed baseline surveys in 1998-1999 (mean age = 15.0 plus or minus 1.6, 'adolescence') and follow-up surveys in 2008-2009 (mean age = 25.4 plus or minus 1.7, 'young adulthood'). Surveys assessed personal, behavioral and socio-environmental factors hypothesized to be of relevance to obesity, in addition to height and weight. Multivariable logistic regression was used to estimate the adjusted odds for each personal, behavioral and socio-environmental factor at baseline, and 10-year changes for these factors, among non-overweight adolescents (n = 1,643) being predictive of the incidence of overweight (BMI greater than or equal to 25) at 10-year follow-up. Results: At 10-year follow-up, 51% of young adults were overweight (26% increase from baseline). Among females and males, higher levels of body dissatisfaction, weight concerns, unhealthy weight control behaviors (e.g., fasting, purging), dieting, binge eating, weight-related teasing, and parental weight-related concerns and behaviors during adolescence and/or increases in these factors over the study period predicted the incidence of overweight at 10-year follow-up. Females with higher levels of whole grain intake and breakfast and dinner consumption frequency during adolescence were protected against becoming overweight. Among males, increases in vegetable intake protected against the incidence of overweight 10 years later. Conclusions: Findings suggest that obesity prevention interventions for adolescents should address weight-specific factors from within the domains of personal, behavioral, and socio-environmental factors such as promoting positive body image, decreasing unhealthy weight control behaviors, and limiting negative weight talk.
JF  - International Journal of Behavioral Nutrition and Physical Activity
AU  - Quick, Virginia
AU  - Wall, Melanie
AU  - Larson, Nicole
AU  - Haines, Jess
AU  - Neumark-Sztainer, Dianne
AD  - Eunice Kennedy Shriver National Institute of Child Health and Human Development, Division of Epidemiology, Statistics and Prevention Research, NIH, DHHS, Bethesda, MD, 20892, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 37
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 10
IS  - 1
SN  - 1479-5868, 1479-5868
KW  - Physical Education Index
KW  - Obesity
KW  - Weight control
KW  - Eating disorders
KW  - Preventive health
KW  - Adolescence
KW  - Diet (weight control)
KW  - Surveys
KW  - Adults
KW  - Youth
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1352284860?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.atitle=Personal%2C+behavioral+and+socio-environmental+predictors+of+overweight+incidence+in+young+adults%3A+10-yr+longitudinal+findings&rft.au=Quick%2C+Virginia%3BWall%2C+Melanie%3BLarson%2C+Nicole%3BHaines%2C+Jess%3BNeumark-Sztainer%2C+Dianne&rft.aulast=Quick&rft.aufirst=Virginia&rft.date=2013-01-01&rft.volume=10&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.issn=14795868&rft_id=info:doi/10.1186%2F1479-5868-10-37
L2  - http://www.ijbnpa.org/content/10/1/37
LA  - English
DB  - Physical Education Index
N1  - Date revised - 2013-05-01
N1  - Number of references - 48
N1  - Last updated - 2013-06-14
N1  - SubjectsTermNotLitGenreText - Obesity; Weight control; Preventive health; Eating disorders; Adolescence; Diet (weight control); Surveys; Adults; Youth
DO  - http://dx.doi.org/10.1186/1479-5868-10-37
ER  - 



TY  - JOUR
T1  - Potential hazard drug-drug interaction between boosted protease inhibitors and vinblastine in HIV patients with Hodekin's lymphoma
AN  - 1348491690; 17958788
AB  - Highly active antiretroviral therapy (HAART) has significantly increased life expectancy in patients with HIV infection [1,2]. However, cancer is still a substantial problem in this population. The aging HIV patients are now at increased risk for a multitude of non-AIDS malignancies, including Hodgkin's lymphoma [3,4]. Management of drug-drug interactions remains a critical component of HIV and cancer care [5].
JF  - AIDS
AU  - Corona, G
AU  - Vaccher, E
AU  - Spina, M
AU  - Toffoli, G
AD  - Experimental and Clinical Pharmacology Unit - IRCCS - National Cancer Institute, 33081 Aviano (PN), Italy, giuseppe.corona@cro.it
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 1033
EP  - 1035
VL  - 27
IS  - 6
SN  - 0269-9370, 0269-9370
KW  - Risk Abstracts; Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW  - Drug interaction
KW  - Acquired immune deficiency syndrome
KW  - Hodgkin's disease
KW  - Life span
KW  - Aging
KW  - Proteinase inhibitors
KW  - Vinblastine
KW  - Infection
KW  - Antiretroviral agents
KW  - Cancer
KW  - Malignancy
KW  - Human immunodeficiency virus
KW  - highly active antiretroviral therapy
KW  - Lymphoma
KW  - V 22360:AIDS and HIV
KW  - H 11000:Diseases/Injuries/Trauma
KW  - F 06915:Cancer Immunology
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1348491690?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Potential+hazard+drug-drug+interaction+between+boosted+protease+inhibitors+and+vinblastine+in+HIV+patients+with+Hodekin%27s+lymphoma&rft.au=Corona%2C+G%3BVaccher%2C+E%3BSpina%2C+M%3BToffoli%2C+G&rft.aulast=Corona&rft.aufirst=G&rft.date=2013-01-01&rft.volume=27&rft.issue=6&rft.spage=1033&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0b013e32835e0777
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-05-01
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Malignancy; Hodgkin's disease; highly active antiretroviral therapy; Proteinase inhibitors; Aging; Life span; Vinblastine; Infection; Cancer; Drug interaction; Acquired immune deficiency syndrome; Human immunodeficiency virus; Antiretroviral agents; Lymphoma
DO  - http://dx.doi.org/10.1097/QAD.0b013e32835e0777
ER  - 



TY  - JOUR
T1  - "Effect of pranayama and meditation as an add-on therapy in rehabilitation of patients with Guillain-Barre syndrome -- a randomized control pilot study"
AN  - 1347817807; 201307486
AB  - Objective: To study the add-on effects of pranayama and meditation in rehabilitation of patients with Guillain-Barre syndrome (GBS). Patients and Method: This randomized control pilot study was conducted in neurological rehabilitation unit of university tertiary research hospital. Twenty-two GBS patients, who consented for the study and satisfied selection criteria, were randomly assigned to yoga and control groups. Ten patients in each group completed the study. The yoga group received 15 sessions in total over a period of 3 weeks (1 h/session), one session per day on 5 days per week that consisted of relaxation, Pranayama (breathing practices) and Guided meditation in addition to conventional rehabilitation therapeutics. The control group received usual rehabilitation care. All the patients were assessed using Pittsburgh Sleep Quality Index, Numeric pain rating scale, Hospital anxiety and Depression scale and Barthel index score. Mann-Whitney U test and Wilcoxon's signed rank test were used for statistical analysis. Results: Quality of sleep improved significantly with reduction of PSQI score in the yoga group (p = 0.04). There was reduction of pain scores, anxiety and depression in both the groups without statistical significance between groups (pain p > 0.05, anxiety p > 0.05 and depression p > 0.05). Overall functional status improved in both groups without significant difference (p > 0.05). Conclusions: Significant improvement was observed in quality of sleep with yogic relaxation, pranayama, and meditation in GBS patients. Adapted from the source document.
JF  - Disability and Rehabilitation
AU  - Sendhilkumar, Ragupathy
AU  - Gupta, Anupam
AU  - Nagarathna, Raghuram
AU  - Taly, Arun B
AD  - Neurological Rehabilitation Division, Department of Psychiatric and Neurological Rehabilitation, National Institute of Mental Health and Neuro-Sciences (NIMHANS), Bangalore, India
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 57
EP  - 62
PB  - Informa Healthcare, New York NY
VL  - 35
IS  - 1
SN  - 0963-8288, 0963-8288
KW  - Guillain-Barre syndrome, yoga
KW  - Yoga
KW  - Rehabilitation
KW  - Sleep problems
KW  - Pain
KW  - Meditation
KW  - Anxiety-Depression
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347817807?accountid=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=Disability+and+Rehabilitation&rft.atitle=%22Effect+of+pranayama+and+meditation+as+an+add-on+therapy+in+rehabilitation+of+patients+with+Guillain-Barre+syndrome+--+a+randomized+control+pilot+study%22&rft.au=Sendhilkumar%2C+Ragupathy%3BGupta%2C+Anupam%3BNagarathna%2C+Raghuram%3BTaly%2C+Arun+B&rft.aulast=Sendhilkumar&rft.aufirst=Ragupathy&rft.date=2013-01-01&rft.volume=35&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Disability+and+Rehabilitation&rft.issn=09638288&rft_id=info:doi/10.3109%2F09638288.2012.687031
LA  - English
DB  - Applied Social Sciences Index & Abstracts (ASSIA)
N1  - Date revised - 2013-05-01
N1  - Last updated - 2016-09-27
N1  - CODEN - DREHET
N1  - SubjectsTermNotLitGenreText - Anxiety-Depression; Rehabilitation; Meditation; Sleep problems; Yoga; Pain
DO  - http://dx.doi.org/10.3109/09638288.2012.687031
ER  - 



TY  - JOUR
T1  - Common data elements for substance use disorders in electronic health records: the NIDA Clinical Trials Network experience
AN  - 1347802811; 2011-392718
AB  - Aims Electronic health records (EHRs) are essential in improving quality and enhancing efficiency of health-care delivery. By 2015, medical care receiving service reimbursement from US Centers for Medicare and Medicaid Services (CMS) must show 'meaningful use' of EHRs. Substance use disorders (SUD) are grossly under-detected and under-treated in current US medical care settings. Hence, an urgent need exists for improved identification of and clinical intervention for SUD in medical settings. The National Institute on Drug Abuse Clinical Trials Network (NIDA CTN) has leveraged its infrastructure and expertise and brought relevant stakeholders together to develop consensus on brief screening and initial assessment tools for SUD in general medical settings, with the objective of incorporation into US EHRs. Methods Stakeholders were identified and queried for input and consensus on validated screening and assessment for SUD in general medical settings to develop common data elements to serve as shared resources for EHRs on screening, brief intervention and referral to treatment (SBIRT), with the intent of supporting interoperability and data exchange in a developing Nationwide Health Information Network. Results Through consensus of input from stakeholders, a validated screening and brief assessment instrument, supported by Clinical Decision Support tools, was chosen to be used at out-patient general medical settings. Conclusions The creation and adoption of a core set of validated common data elements and the inclusion of such consensus-based data elements for general medical settings will enable the integration of SUD treatment within mainstream health care, and support the adoption and 'meaningful use' of the US Office of the National Coordinator for Health Information Technology (ONC)-certified EHRs, as well as CMS reimbursement. Adapted from the source document.
JF  - Addiction
AU  - Ghitza, Udi E
AU  - Gore-Langton, Robert E
AU  - Lindblad, Robert
AU  - Shide, David
AU  - Subramaniam, Geetha
AU  - Tai, Betty
AD  - Center for the Clinical Trials Network, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 3
EP  - 8
PB  - Blackwell Publishing, Oxford UK
VL  - 108
IS  - 1
SN  - 0965-2140, 0965-2140
KW  - Health conditions and policy - Health and health policy
KW  - Health conditions and policy - Medicine and health care
KW  - Social conditions and policy - History
KW  - Science and technology policy - Computer science and information technology
KW  - Social conditions and policy - Public welfare and social services
KW  - Economic conditions and policy - Economic policy, planning, and development
KW  - Social conditions and policy - Drinking, smoking, and drug addiction
KW  - Infrastructure
KW  - United States
KW  - Records
KW  - Medicaid program
KW  - Medicare
KW  - Information technology
KW  - Health policy
KW  - Drug abuse
KW  - Medical service
KW  - Clinical trials
KW  - article
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347802811?accountid=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=Addiction&rft.atitle=Common+data+elements+for+substance+use+disorders+in+electronic+health+records%3A+the+NIDA+Clinical+Trials+Network+experience&rft.au=Ghitza%2C+Udi+E%3BGore-Langton%2C+Robert+E%3BLindblad%2C+Robert%3BShide%2C+David%3BSubramaniam%2C+Geetha%3BTai%2C+Betty&rft.aulast=Ghitza&rft.aufirst=Udi&rft.date=2013-01-01&rft.volume=108&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fj.1360-0443.2012.03876.x
LA  - English
DB  - PAIS Index
N1  - Date revised - 2013-05-01
N1  - Last updated - 2016-09-28
N1  - CODEN - ADICE5
N1  - SubjectsTermNotLitGenreText - Health policy; Medical service; United States; Clinical trials; Records; Information technology; Medicaid program; Medicare; Infrastructure; Drug abuse
DO  - http://dx.doi.org/10.1111/j.1360-0443.2012.03876.x
ER  - 



TY  - JOUR
T1  - Escherichia coli avoids high dissolved oxygen stress by activation of SoxRS and manganese-superoxide dismutase
AN  - 1328512502; 17841972
AB  - Background: High concentrations of reactive oxygen species (ROS) were reported to cause oxidative stress to E. coli cells associated with reduced or inhibited growth. The high ROS concentrations described in these reports were generated by exposing the bacteria to H sub(2)O sub(2) and superoxide-generating chemicals which are non-physiological growth conditions. However, the effect of molecular oxygen on oxidative stress response has not been evaluated. Since the use of oxygen-enriched air is a common strategy to support high density growth of E. coli, it was important to investigate the effect of high dissolved oxygen concentrations on the physiology and growth of E. coli and the way it responds to oxidative stress. Results: To determine the effect of elevated oxygen concentrations on the growth characteristics, specific gene expression and enzyme activity in E. coli, the parental and SOD-deficient strain were evaluated when the dissolved oxygen (dO sub(2)) level was increased from 30% to 300%. No significant differences in the growth parameters were observed in the parental strain except for a temporary decrease of the respiration and acetate accumulation profile. By performing transcriptional analysis, it was determined that the parental strain responded to the oxidative stress by activating the SoxRS regulon. However, following the dO sub(2) switch, the SOD-deficient strain activated both the SoxRS and OxyR regulons but it was unable to resume its initial growth rate. Conclusion: The transcriptional analysis and enzyme activity results indicated that when E. coli is exposed to dO sub(2) shift, the superoxide stress regulator SoxRS is activated and causes the stimulation of the superoxide dismutase system. This enables the E. coli to protect itself from the poisoning effects of oxygen. The OxyR protecting system was not activated, indicating that H sub(2)O sub(2) did not increase to stressing levels.
JF  - Microbial Cell Factories
AU  - Baez, Antonino
AU  - Shiloach, Joseph
AD  - Biotechnology Core Laboratory, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 23
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 12
IS  - 1
SN  - 1475-2859, 1475-2859
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts
KW  - Growth rate
KW  - Growth conditions
KW  - Respiration
KW  - Poisoning
KW  - Enzymes
KW  - Transcription
KW  - Acetic acid
KW  - Dissolved oxygen
KW  - Gene expression
KW  - Oxygen
KW  - Reactive oxygen species
KW  - Hydrogen peroxide
KW  - Oxidative stress
KW  - Superoxide dismutase
KW  - Escherichia coli
KW  - A 01450:Environmental Pollution & Waste Treatment
KW  - W 30940:Products
KW  - J 02320:Cell Biology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328512502?accountid=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=Microbial+Cell+Factories&rft.atitle=Escherichia+coli+avoids+high+dissolved+oxygen+stress+by+activation+of+SoxRS+and+manganese-superoxide+dismutase&rft.au=Baez%2C+Antonino%3BShiloach%2C+Joseph&rft.aulast=Baez&rft.aufirst=Antonino&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Microbial+Cell+Factories&rft.issn=14752859&rft_id=info:doi/10.1186%2F1475-2859-12-23
L2  - http://www.microbialcellfactories.com/content/12/1/23
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Number of references - 37
N1  - Last updated - 2013-05-31
N1  - SubjectsTermNotLitGenreText - Growth rate; Growth conditions; Respiration; Poisoning; Transcription; Enzymes; Acetic acid; Dissolved oxygen; Gene expression; Oxygen; Reactive oxygen species; Superoxide dismutase; Oxidative stress; Hydrogen peroxide; Escherichia coli
DO  - http://dx.doi.org/10.1186/1475-2859-12-23
ER  - 



TY  - JOUR
T1  - Elevations in D-dimer and C-reactive protein are associated with the development of osteonecrosis of the hip in HIV-infected adults
AN  - 1328511333; 17806508
AB  - Background: A high incidence of nontraumatic osteonecrosis has been reported in HIV-infected patients. We investigated the levels of D-dimer and C-reactive protein (CRP) in a cohort of HIV-infected adults with and without osteonecrosis of the femoral head. Methods: Forty-three HIV-infected patients with osteonecrosis of the femoral head and a comparison group of 50 HIV-infected patients with negative MRI of the hips and for whom serial plasma samples were available were included. D-dimer and CRP levels were measured prior to and at the time of diagnosis for osteonecrosis patients, at the time of negative MRI of the hips for controls, and at least 6 months later for both groups. Results: Biomarker levels were elevated at the time of diagnosis in the osteonecrosis cohort compared with controls. Median D-dimer value was 0.32 mu g/ml in the osteonecrosis group compared with less than 0.22 mu g/ml in the control group (P = 0.016). For CRP, the corresponding values were 2.52 mg/l and 1.23 mg/l (P = 0.003). Postdiagnosis, D-dimer and CRP levels were also elevated in the osteonecrosis patients compared with controls. Linear regression demonstrated a rise in D-dimer levels from prediagnosis to diagnosis in the osteonecrosis patients whereas CRP levels did not change significantly over time. Conclusion: Compared to controls, patients who developed osteonecrosis had elevated levels of D-dimer and CRP at diagnosis. D-dimer levels increased whereas CRP levels did not change significantly from prediagnosis to diagnosis. These data suggest that patients with higher levels of inflammation are at an increased risk of osteonecrosis.
JF  - AIDS
AU  - Morse, C G
AU  - Dodd, LE
AU  - Nghiem, K
AU  - Costello, R
AU  - Csako, G
AU  - Lane, H C
AU  - Lozier, J N
AU  - Kovacs, JA
AD  - Building 10, Room 5A06, MSC 1403, Bethesda, MD 20892-1403, USA, cmorse@mail.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 591
EP  - 595
VL  - 27
IS  - 4
SN  - 0269-9370, 0269-9370
KW  - Calcium & Calcified Tissue Abstracts; Risk Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW  - Acquired immune deficiency syndrome
KW  - Osteonecrosis
KW  - Human immunodeficiency virus
KW  - Proteins
KW  - V 22360:AIDS and HIV
KW  - F 06910:Microorganisms & Parasites
KW  - T 2025:Bone and Bone Diseases
KW  - R2 23010:General: Models, forecasting
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328511333?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Elevations+in+D-dimer+and+C-reactive+protein+are+associated+with+the+development+of+osteonecrosis+of+the+hip+in+HIV-infected+adults&rft.au=Morse%2C+C+G%3BDodd%2C+LE%3BNghiem%2C+K%3BCostello%2C+R%3BCsako%2C+G%3BLane%2C+H+C%3BLozier%2C+J+N%3BKovacs%2C+JA&rft.aulast=Morse&rft.aufirst=C&rft.date=2013-01-01&rft.volume=27&rft.issue=4&rft.spage=591&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0b013e32835c206a
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Osteonecrosis; Proteins; Human immunodeficiency virus
DO  - http://dx.doi.org/10.1097/QAD.0b013e32835c206a
ER  - 



TY  - JOUR
T1  - Risk of Kaposi sarcoma during the first months on combination antiretroviral therapy
AN  - 1323819964; 17806513
AB  - Objective: To determine whether incident AIDS-defining Kaposi sarcoma or Pneumocystis jiroveci pneumonia (PJP) is associated with combination antiretroviral therapy (cART) initiation. Design: Compare risk for Kaposi sarcoma and PJP by time on cART and CD4 reconstitution. Methods: In the FHDH-ANRS CO4 cohort (N = 66 369), Kaposi sarcoma (N = 1811) and PJP (N = 1718) incidence rates were computed by demographic and HIV strata. Crude and adjusted relative risk (RR) with 95% confidence intervals (CIs) following cART initiation were calculated by Poisson regression with untreated patients during 1996-2009 as reference. CD4 cell counts were compared by Wilcoxon rank sum tests. Results: The risk of Kaposi sarcoma was very high during months 1-3 on cART (N = 160, RR sub(Crude) 3.94, 95% CI 3.26-4.76), which was incompletely attenuated by adjustment for demographics and contemporaneous CD4 cell count (RR sub(Adj) 1.25, 95% CI 1.02-1.53). Corresponding PJP risk was minimally elevated (N = 84, RR sub(Crude) 1-80, 95% CI 1.42-2.30) and markedly reduced with adjustment on the same variables and PJP prophylaxis (RR sub(Adj) 0.52, CI 0.41-0.67). HIV load had no added effect. Median CD4 cell count at cART initiation was much lower in patients with incident Kaposi sarcoma (82 cells/ mu l) or PJP (61 cells/ mu l) within 3 months than in those who did not develop these conditions (>25O cells/ mu l). Notably, median CD4 cell count change was +44cells/ mu l per month with incident Kaposi sarcoma within 3 months of cART initiation versus o cells/ mu l per month with incident PJP (P = 0.0003). Conclusion: Failure of CD4 cell count reconstitution during months 1-3 on cART fully accounted for incident PJP. In contrast, there were 1.6 additional Kaposi sarcoma cases per 1000 person-years during months 1-3 on cART, suggesting that immune recon-stitution may contribute to the risk for AIDS-defining Kaposi sarcoma.
JF  - AIDS
AU  - Lacombe, J-M
AU  - Boue, F
AU  - Grabar, S
AU  - Viget, N
AU  - Gazaignes, S
AU  - Lascaux-Cametz, A-S
AU  - Pacanowski, J
AU  - Partisani, M
AU  - Launay, O
AU  - Matheron, S
AU  - Rosenthal, E
AU  - Rouveix, E
AU  - Tattevin, P
AU  - Goedert, J J
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, Room 7068, Rockville, MD 20852, USA, goedertj@mail.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 635
EP  - 643
VL  - 27
IS  - 4
SN  - 0269-9370, 0269-9370
KW  - Risk Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW  - Risk assessment
KW  - Acquired immune deficiency syndrome
KW  - antiretroviral therapy
KW  - Pneumocystis
KW  - Antiretroviral agents
KW  - Demography
KW  - CD4 antigen
KW  - Human immunodeficiency virus
KW  - Sarcoma
KW  - Prophylaxis
KW  - Pneumonia
KW  - V 22360:AIDS and HIV
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/1323819964?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Risk+of+Kaposi+sarcoma+during+the+first+months+on+combination+antiretroviral+therapy&rft.au=Lacombe%2C+J-M%3BBoue%2C+F%3BGrabar%2C+S%3BViget%2C+N%3BGazaignes%2C+S%3BLascaux-Cametz%2C+A-S%3BPacanowski%2C+J%3BPartisani%2C+M%3BLaunay%2C+O%3BMatheron%2C+S%3BRosenthal%2C+E%3BRouveix%2C+E%3BTattevin%2C+P%3BGoedert%2C+J+J&rft.aulast=Lacombe&rft.aufirst=J-M&rft.date=2013-01-01&rft.volume=27&rft.issue=4&rft.spage=635&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0b013e32835cba6c
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Risk assessment; Demography; CD4 antigen; antiretroviral therapy; Prophylaxis; Sarcoma; Pneumonia; Acquired immune deficiency syndrome; Human immunodeficiency virus; Antiretroviral agents; Pneumocystis
DO  - http://dx.doi.org/10.1097/QAD.0b013e32835cba6c
ER  - 



TY  - JOUR
T1  - Reproducibility of physical activity recall over fifteen years: longitudinal evidence from the CARDIA study
AN  - 1323818761; 17806982
AB  - Background: To examine the benefits of physical activity (PA) on diseases with a long developmental period, it is important to determine reliability of long-term PA recall. Methods: We investigated 15-year reproducibility of PA recall. Participants were 3605 White and African-American adults in the Coronary Artery Risk Development in Young Adults study, aged 33-45 at the time of recall assessment. Categorical questions assessed PA before and during high school (HS) and overall PA level at Baseline, with the same timeframes recalled 15 years later. Moderate- and vigorous-intensity scores were calculated from reported months of participation in specific activities. Results: HS PA recall had higher reproducibility than overall PA recall (weighted kappa = 0.43 vs. 0.21). Correlations between 15-year recall and Baseline reports of PA were r = 0.29 for moderate-intensity scores, and r = 0.50 for vigorous-intensity. Recall of vigorous activities had higher reproducibility than moderate-intensity activities. Regardless of number of months originally reported for specific activities, most participants recalled either no activity or activity during all 12 months. Conclusion: PA recall from the distant past is moderately reproducible, but poor at the individual level, among young and middle aged adults.
JF  - BMC Public Health
AU  - Smith, Ashley Wilder
AU  - Cronin, Kathleen A
AU  - Bowles, Heather
AU  - Willis, Gordon
AU  - Jacobs, David R
AU  - Ballard-Barbash, Rachel
AU  - Troiano, Richard P
AD  - Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 180
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 13
IS  - 1
SN  - 1471-2458, 1471-2458
KW  - Physical Education Index; Risk Abstracts; Health & Safety Science Abstracts
KW  - Physical activity
KW  - Reliability
KW  - Middle aged adults
KW  - Adults
KW  - Exercise
KW  - Public health
KW  - Evaluation
KW  - High schools
KW  - Young adults
KW  - Activities
KW  - Ethnic groups
KW  - Youth
KW  - Circulatory system
KW  - H 12000:Epidemiology and Public Health
KW  - R2 23060:Medical and environmental health
KW  - PE 030:Exercise, Health & Physical Fitness
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323818761?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+Public+Health&rft.atitle=Reproducibility+of+physical+activity+recall+over+fifteen+years%3A+longitudinal+evidence+from+the+CARDIA+study&rft.au=Smith%2C+Ashley+Wilder%3BCronin%2C+Kathleen+A%3BBowles%2C+Heather%3BWillis%2C+Gordon%3BJacobs%2C+David+R%3BBallard-Barbash%2C+Rachel%3BTroiano%2C+Richard+P&rft.aulast=Smith&rft.aufirst=Ashley&rft.date=2013-01-01&rft.volume=13&rft.issue=1&rft.spage=180&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-13-180
L2  - http://www.biomedcentral.com/1471-2458/13/180
LA  - English
DB  - Physical Education Index; ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Number of references - 23
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Evaluation; High schools; Reliability; Exercise; Adults; Activities; Youth; Circulatory system; Public health; Physical activity; Middle aged adults; Young adults; Ethnic groups
DO  - http://dx.doi.org/10.1186/1471-2458-13-180
ER  - 



TY  - JOUR
T1  - Residential proximity to industrial combustion facilities and risk of non-Hodgkin lymphoma: a case-control study
AN  - 1323806777; 17803408
AB  - Background: Residence near municipal solid waste incinerators, a major historical source of dioxin emissions, has been associated with increased risk of non-Hodgkin lymphoma (NHL) in European studies. The aim of our study was to evaluate residence near industrial combustion facilities and estimates of dioxin emissions in relation to NHL risk in the United States. Methods: We conducted a population-based case-control study of NHL (1998-2000) in four National Cancer Institute-Surveillance Epidemiology and End Results centers (Detroit, Iowa, Los Angeles, Seattle). Residential histories 15 years before diagnosis (similar date for controls) were linked to an Environmental Protection Agency database of dioxin-emitting facilities for 969 cases and 749 controls. We evaluated proximity (3 and 5 km) to 10 facility types that accounted for >85% of U.S. emissions and a distance-weighted average emission index (AEI [ng toxic equivalency quotient (TEQ)/year]). Results: Proximity to any dioxin-emitting facility was not associated with NHL risk (3 km OR = 1.0, 95% CI 0.8-1.3). Risk was elevated for residence near cement kilns (5 km OR = 1.7, 95% CI 0.8-3.3; 3 km OR = 3.8, 95% CI 1.1-14.0) and reduced for residence near municipal solid waste incinerators (5 km OR = 0.5, 95% CI 0.3-0.9; 3 km OR = 0.3, 95% CI 0.1-1.4). The AEI was not associated with risk of NHL overall. Risk for marginal zone lymphoma was increased for the highest versus lowest quartile (5 km OR = 2.6, 95% CI 1.0-6.8; 3 km OR = 3.0, 95% CI 1.1-8.3). Conclusions: Overall, we found no association with residential exposure to dioxins and NHL risk. However, findings for high emissions and marginal zone lymphoma and for specific facility types and all NHL provide some evidence of an association and deserve future study.
JF  - Environmental Health (London)
AU  - Pronk, Anjoeka
AU  - Nuckols, John R
AU  - De Roos, Anneclaire J
AU  - Airola, Matthew
AU  - Colt, Joanne S
AU  - Cerhan, James R
AU  - Morton, Lindsay
AU  - Cozen, Wendy
AU  - Severson, Richard
AU  - Blair, Aaron
AU  - Cleverly, David
AU  - Ward, Mary H
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services, Rockville, MD, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 20
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 12
IS  - 1
SN  - 1476-069X, 1476-069X
KW  - Toxicology Abstracts; Risk Abstracts; Pollution Abstracts; Health & Safety Science Abstracts
KW  - Cancer
KW  - Emissions
KW  - INE, USA, Washington, Seattle
KW  - Lymphoma
KW  - H 11000:Diseases/Injuries/Trauma
KW  - P 0000:AIR POLLUTION
KW  - X 24350:Industrial Chemicals
KW  - R2 23050:Environment
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323806777?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+%28London%29&rft.atitle=Residential+proximity+to+industrial+combustion+facilities+and+risk+of+non-Hodgkin+lymphoma%3A+a+case-control+study&rft.au=Pronk%2C+Anjoeka%3BNuckols%2C+John+R%3BDe+Roos%2C+Anneclaire+J%3BAirola%2C+Matthew%3BColt%2C+Joanne+S%3BCerhan%2C+James+R%3BMorton%2C+Lindsay%3BCozen%2C+Wendy%3BSeverson%2C+Richard%3BBlair%2C+Aaron%3BCleverly%2C+David%3BWard%2C+Mary+H&rft.aulast=Pronk&rft.aufirst=Anjoeka&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+%28London%29&rft.issn=1476069X&rft_id=info:doi/10.1186%2F1476-069X-12-20
L2  - http://www.ehjournal.net/content/12/1/20
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-11
N1  - SubjectsTermNotLitGenreText - Lymphoma; Emissions; INE, USA, Washington, Seattle
DO  - http://dx.doi.org/10.1186/1476-069X-12-20
ER  - 



TY  - JOUR
T1  - Is Sporadic Alzheimers Disease Associated with Diphtheria Toxin?
AN  - 1323800895; 17788340
AB  - The two major aspects of Alzheimers disease (AD) that must be considered in a search for causative agents are its association with aging and its widespread epidemiology. While a number of agents have been identified, additional factors may play a role. An association with diphtheria toxin was suggested by observations that vaccinations may provide protective effects, and the observation that decreased proteins synthesis in cortical regions from AD patients is associated with modification of elongation factor 2, the target of diphtheria toxin. While protection against diphtheria toxin is provided by vaccination, the known decline in the immune system associated with aging would result in a renewed sensitivity to the toxin. An association with diphtheria toxin would be consistent with the observations that the bacteria associated with the toxin, Corynebacterium diphtheria, is often found in the nasopharynx and an early symptom of AD is the loss of smell with a disease progression from the entorhinal cortex to the hippocampus and the neocortical areas. If diphtheria toxin is involved in sporadic AD, booster vaccinations given to elderly individuals might result in a decreased incidence of this disease. As booster DPT vaccinations are already recommended for individuals over 65, cognitive testing at the time of the booster and 5 years later, along with similar cognitive testing in age-matched individuals who decline vaccination, might provide an inexpensive method to investigate whether diphtheria toxin plays a role in AD and the efficacy of DPT booster vaccines for AD.
JF  - Journal of Alzheimer's Disease
AU  - Merril, Carl R
AD  - Retired Emeritus Scientist, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 595
EP  - 600
PB  - IOS Press, Nieuwe Hemweg 6B Amsterdam 1013 BG Netherlands
VL  - 34
IS  - 3
SN  - 1387-2877, 1387-2877
KW  - Toxicology Abstracts; CSA Neurosciences Abstracts
KW  - Cortex (entorhinal)
KW  - Protein biosynthesis
KW  - Hippocampus
KW  - Immune system
KW  - Aging
KW  - Alzheimer's disease
KW  - Nasopharynx
KW  - Diphtheria
KW  - Toxins
KW  - Diphtheria toxin
KW  - Corynebacterium
KW  - Elongation
KW  - Neurodegenerative diseases
KW  - Cortex
KW  - Epidemiology
KW  - Cognitive ability
KW  - Geriatrics
KW  - Vaccines
KW  - X 24370:Natural Toxins
KW  - N3 11027:Neurology & neuropathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323800895?accountid=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+Alzheimer%27s+Disease&rft.atitle=Is+Sporadic+Alzheimers+Disease+Associated+with+Diphtheria+Toxin%3F&rft.au=Merril%2C+Carl+R&rft.aulast=Merril&rft.aufirst=Carl&rft.date=2013-01-01&rft.volume=34&rft.issue=3&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Journal+of+Alzheimer%27s+Disease&rft.issn=13872877&rft_id=info:doi/
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-04-01
N1  - Last updated - 2013-08-23
N1  - SubjectsTermNotLitGenreText - Cortex (entorhinal); Protein biosynthesis; Hippocampus; Immune system; Alzheimer's disease; Aging; Nasopharynx; Diphtheria; Diphtheria toxin; Toxins; Neurodegenerative diseases; Elongation; Cortex; Epidemiology; Cognitive ability; Geriatrics; Vaccines; Corynebacterium
ER  - 



TY  - JOUR
T1  - Targeting heat shock proteins by phenethyl isothiocyanate results in cell-cycle arrest and apoptosis of human breast cancer cells.
AN  - 1321338748; 23530648
AB  - Heat shock proteins (HSPs) are chaperones for several client proteins involved in transcriptional regulation, signal transduction, and cell cycle control. HSPs (27, 70, and 90) are abundantly expressed in a wide range of cancers and are transcriptionally regulated by heat shock factor (HSF1). Most of the synthetic HSP inhibitors exhibit toxicity, therefore, searching for inhibitors with limited or no toxicity will be of help. The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53). PEITC significantly inhibited the expression of HSPs (particularly HSP 90) and HSF1. Molecular consequences due to HSP inhibition were downregulation of cell-cycle regulatory proteins like Cyclin B1, CDK1, Cdc25C, PLK-1, and upregulation of p21 irrespective of p53 status. These modulations were accompanied by cell-cycle arrest at G2/M phase and apoptosis by activation of caspases 3 and 9. PEITC therefore may be regarded as a potent HSP inhibitor and an antitumor agent in the treatment of breast cancer.
JF  - Nutrition and cancer
AU  - Sarkars, Ruma
AU  - Mukherjee, Sutapa
AU  - Roy, Madhumita
AD  - Department of Environmental Carcinogenesis & Toxicology, Chittaranjan National Cancer Institute, Kolkata, India.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 480
EP  - 493
VL  - 65
IS  - 3
KW  - Antineoplastic Agents
KW  - 0
KW  - CDKN1A protein, human
KW  - Cyclin-Dependent Kinase Inhibitor p21
KW  - Heat-Shock Proteins
KW  - Isothiocyanates
KW  - NF-kappa B
KW  - Proto-Oncogene Proteins c-bcl-2
KW  - Tumor Suppressor Protein p53
KW  - bcl-2-Associated X Protein
KW  - phenethyl isothiocyanate
KW  - 6U7TFK75KV
KW  - Cytochromes c
KW  - 9007-43-6
KW  - Index Medicus
KW  - Tumor Suppressor Protein p53 -- analysis
KW  - Cytochromes c -- metabolism
KW  - Cyclin-Dependent Kinase Inhibitor p21 -- analysis
KW  - Proto-Oncogene Proteins c-bcl-2 -- analysis
KW  - Humans
KW  - MCF-7 Cells
KW  - Cell Line, Tumor
KW  - DNA Fragmentation
KW  - bcl-2-Associated X Protein -- analysis
KW  - NF-kappa B -- metabolism
KW  - Isothiocyanates -- pharmacology
KW  - Heat-Shock Proteins -- analysis
KW  - Breast Neoplasms -- pathology
KW  - Apoptosis -- drug effects
KW  - Cell Cycle Checkpoints -- drug effects
KW  - Breast Neoplasms -- chemistry
KW  - Breast Neoplasms -- metabolism
KW  - Heat-Shock Proteins -- antagonists & inhibitors
KW  - Antineoplastic Agents -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1321338748?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+cancer&rft.atitle=Targeting+heat+shock+proteins+by+phenethyl+isothiocyanate+results+in+cell-cycle+arrest+and+apoptosis+of+human+breast+cancer+cells.&rft.au=Sarkars%2C+Ruma%3BMukherjee%2C+Sutapa%3BRoy%2C+Madhumita&rft.aulast=Sarkars&rft.aufirst=Ruma&rft.date=2013-01-01&rft.volume=65&rft.issue=3&rft.spage=480&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+cancer&rft.issn=1532-7914&rft_id=info:doi/10.1080%2F01635581.2013.767366
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-16
N1  - Date created - 2013-03-27
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1080/01635581.2013.767366
ER  - 



TY  - JOUR
T1  - The association between chronic renal failure and renal cell carcinoma may differ between black and white Americans
AN  - 1315619055; 17667330
AB  - Purpose: In the United States, renal cell carcinoma (RCC) incidence is higher among blacks than among whites. Risk of RCC is elevated among end-stage renal disease patients, although no studies have looked at differences by race in the relationship between chronic renal failure and RCC. Methods: We investigated RCC risk in relation to chronic renal failure in a population-based case-control study of blacks and whites in Chicago and Detroit. Data, including information on kidney disease, were collected from interviews with 1,217 RCC cases (361 blacks, 856 whites) and 1,235 controls (523 blacks, 712 whites). Odds ratios (OR) and 95 % confidence intervals (CI) were estimated using unconditional logistic regression. Results: Risk of RCC was increased in relation to chronic renal failure (OR 4.7, 95 % CI 2.2-10.1) and dialysis (OR 18.0, 95 % CI 3.6-91). The association remained after defining exposure as those who had chronic renal failure greater than or equal to 10 years prior to RCC diagnosis. Chronic renal failure was more strongly associated with RCC among blacks than among whites (OR 8.7, 95 % CI 3.3-22.9 and 2.0, 0.7-5.6, respectively; p sub(interaction) = 0.03) and among those without a history of diabetes relative to diabetic subjects (OR 8.3, 95 % CI 3.1-22.7 and 1.9, 0.6-5.9, respectively; p sub(interaction) = 0.03). Conclusions: These results suggest that chronic renal failure is a strong risk factor for RCC, particularly among black and non-diabetic subjects. Our findings of differences in risk estimates by race, to our knowledge the first such report, require replication.
JF  - Cancer Causes & Control
AU  - Hofmann, Jonathan N
AU  - Schwartz, Kendra
AU  - Chow, Wong-Ho
AU  - Ruterbusch, Julie J
AU  - Shuch, Brian M
AU  - Karami, Sara
AU  - Rothman, Nathaniel
AU  - Wacholder, Sholom
AU  - Graubard, Barry I
AU  - Colt, Joanne S
AU  - Purdue, Mark P
AD  - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, Bethesda, MD, 20892-7240, USA, hofmannjn@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 167
EP  - 174
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 24
IS  - 1
SN  - 0957-5243, 0957-5243
KW  - Risk Abstracts
KW  - Cancer
KW  - Diabetes mellitus
KW  - Dialysis
KW  - Historical account
KW  - Kidney
KW  - Risk factors
KW  - USA, Illinois, Chicago
KW  - USA
KW  - USA, Michigan, Detroit
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315619055?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=The+association+between+chronic+renal+failure+and+renal+cell+carcinoma+may+differ+between+black+and+white+Americans&rft.au=Hofmann%2C+Jonathan+N%3BSchwartz%2C+Kendra%3BChow%2C+Wong-Ho%3BRuterbusch%2C+Julie+J%3BShuch%2C+Brian+M%3BKarami%2C+Sara%3BRothman%2C+Nathaniel%3BWacholder%2C+Sholom%3BGraubard%2C+Barry+I%3BColt%2C+Joanne+S%3BPurdue%2C+Mark+P&rft.aulast=Hofmann&rft.aufirst=Jonathan&rft.date=2013-01-01&rft.volume=24&rft.issue=1&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0102-z
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 23
N1  - Last updated - 2013-03-22
N1  - SubjectsTermNotLitGenreText - Diabetes mellitus; Historical account; Dialysis; Risk factors; Kidney; Cancer; USA, Illinois, Chicago; USA; USA, Michigan, Detroit
DO  - http://dx.doi.org/10.1007/s10552-012-0102-z
ER  - 



TY  - JOUR
T1  - Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: a pooled analysis within the InterLymph consortium
AN  - 1315613411; 17667346
AB  - Purpose: Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2. Methods: We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case-control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models. Results: Current smoking was associated with a significant 30 % increased risk of follicular lymphoma (n = 1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95 % CI 1.07-1.75) and intermediate/rapid (OR 1.27; 95 % CI 0.95-1.69) acetylators (p sub(interaction) = 0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes. Conclusion: The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.
JF  - Cancer Causes & Control
AU  - Gibson, Todd M
AU  - Smedby, Karin E
AU  - Skibola, Christine F
AU  - Hein, David W
AU  - Slager, Susan L
AU  - Sanjose, Silvia
AU  - Vajdic, Claire M
AU  - Zhang, Yawei
AU  - Chiu, Brian C-H
AU  - Wang, Sophia S
AU  - Hjalgrim, Henrik
AU  - Nieters, Alexandra
AU  - Bracci, Paige M
AU  - Kricker, Anne
AU  - Zheng, Tongzhang
AU  - Kolar, Carol
AU  - Cerhan, James R
AU  - Darabi, Hatef
AU  - Becker, Nikolaus
AU  - Conde, Lucia
AU  - Holford, Theodore R
AU  - Weisenburger, Dennis D
AU  - Roos, Anneclaire J
AU  - Butterbach, Katja
AU  - Riby, Jacques
AU  - Cozen, Wendy
AU  - Benavente, Yolanda
AU  - Palmers, Casey
AU  - Holly, Elizabeth A
AU  - Sampson, Joshua N
AU  - Rothman, Nathaniel
AU  - Armstrong, Bruce K
AU  - Morton, Lindsay M
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., EPS 7090, Bethesda, MD, 20892, USA, gibsontm@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 125
EP  - 134
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 24
IS  - 1
SN  - 0957-5243, 0957-5243
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Cancer
KW  - Carcinogens
KW  - Enzymes
KW  - Genetic diversity
KW  - Lymphoma
KW  - Metabolism
KW  - Non-Hodgkin's lymphoma
KW  - Smoking
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/1315613411?accountid=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=Smoking%2C+variation+in+N-acetyltransferase+1+%28NAT1%29+and+2+%28NAT2%29%2C+and+risk+of+non-Hodgkin+lymphoma%3A+a+pooled+analysis+within+the+InterLymph+consortium&rft.au=Gibson%2C+Todd+M%3BSmedby%2C+Karin+E%3BSkibola%2C+Christine+F%3BHein%2C+David+W%3BSlager%2C+Susan+L%3BSanjose%2C+Silvia%3BVajdic%2C+Claire+M%3BZhang%2C+Yawei%3BChiu%2C+Brian+C-H%3BWang%2C+Sophia+S%3BHjalgrim%2C+Henrik%3BNieters%2C+Alexandra%3BBracci%2C+Paige+M%3BKricker%2C+Anne%3BZheng%2C+Tongzhang%3BKolar%2C+Carol%3BCerhan%2C+James+R%3BDarabi%2C+Hatef%3BBecker%2C+Nikolaus%3BConde%2C+Lucia%3BHolford%2C+Theodore+R%3BWeisenburger%2C+Dennis+D%3BRoos%2C+Anneclaire+J%3BButterbach%2C+Katja%3BRiby%2C+Jacques%3BCozen%2C+Wendy%3BBenavente%2C+Yolanda%3BPalmers%2C+Casey%3BHolly%2C+Elizabeth+A%3BSampson%2C+Joshua+N%3BRothman%2C+Nathaniel%3BArmstrong%2C+Bruce+K%3BMorton%2C+Lindsay+M&rft.aulast=Gibson&rft.aufirst=Todd&rft.date=2013-01-01&rft.volume=24&rft.issue=1&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0098-4
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 38
N1  - Last updated - 2013-03-22
N1  - SubjectsTermNotLitGenreText - Non-Hodgkin's lymphoma; Smoking; Genetic diversity; Enzymes; Carcinogens; Lymphoma; Metabolism; Cancer
DO  - http://dx.doi.org/10.1007/s10552-012-0098-4
ER  - 



TY  - JOUR
T1  - The association between cancer and amyotrophic lateral sclerosis
AN  - 1315613329; 17667339
AB  - Objective: Increasing evidence suggests that some neurodegenerative disorders, such as Parkinson's disease, are inversely related to cancer. Few epidemiologic studies have examined the relationship between cancer and amyotrophic lateral sclerosis (ALS), another major neurodegenerative disease. This study addresses that gap. Methods: Using data from 16 population-based cancer registries of the Surveillance, Epidemiology, and End Results (SEER) Program of the U.S. National Cancer Institute and death certificates, we followed 2.7 million cancer survivors who were diagnosed between 1973 and 2007, and who survived at least 1 year following cancer diagnosis. The standardized mortality ratio (SMR) of observed to expected ALS deaths in cancer survivors was calculated. Results: A total of 1,216 ALS deaths were reported among 1 year survivors of cancer over 16.6 million person-years of follow-up. ALS mortality was not significantly associated with the incidence of total cancers [SMR = 1.00 (95 % confidence interval (CI), 0.95-1.06)]. There was, however, a significantly elevated risk of ALS death among survivors of melanoma [SMR = 1.49 (95 % (CI), 1.17-1.85)] and of tongue cancer [SMR = 2.57 (95 % CI, 1.41-4.32)], and a significantly reduced ALS death risk among prostate cancer survivors [SMR = 0.86 (95 % CI, 0.76-0.96)]. Conclusions: Cancer at certain sites may be related to risk of ALS death. Possible biologic factors linking ALS to these cancers are discussed. Future studies should attempt to confirm these associations using incident ALS outcomes. Establishing relationships between cancer and neurodegenerative diseases, such as ALS, opens new opportunities for understanding related pathophysiologic and therapeutic possibilities for these diseases.
JF  - Cancer Causes & Control
AU  - Freedman, DMichal
AU  - Curtis, Rochelle E
AU  - Daugherty, Sarah E
AU  - Goedert, James J
AU  - Kuncl, Ralph W
AU  - Tucker, Margaret A
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, EPS Room 7036, 6120 Exec. Blvd., Bethesda, MD, 20892-7238, USA, freedmam@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 55
EP  - 60
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 24
IS  - 1
SN  - 0957-5243, 0957-5243
KW  - Risk Abstracts
KW  - Cancer
KW  - Melanoma
KW  - Mortality
KW  - Parkinson's disease
KW  - Prostate cancer
KW  - Standards
KW  - USA
KW  - R2 23060:Medical and environmental health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315613329?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=The+association+between+cancer+and+amyotrophic+lateral+sclerosis&rft.au=Freedman%2C+DMichal%3BCurtis%2C+Rochelle+E%3BDaugherty%2C+Sarah+E%3BGoedert%2C+James+J%3BKuncl%2C+Ralph+W%3BTucker%2C+Margaret+A&rft.aulast=Freedman&rft.aufirst=DMichal&rft.date=2013-01-01&rft.volume=24&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0089-5
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 44
N1  - Last updated - 2013-03-22
N1  - SubjectsTermNotLitGenreText - Mortality; Prostate cancer; Parkinson's disease; Standards; Cancer; Melanoma; USA
DO  - http://dx.doi.org/10.1007/s10552-012-0089-5
ER  - 



TY  - JOUR
T1  - Diabetes and risk of pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium
AN  - 1315611620; 17667336
AB  - Purpose: Diabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan). Methods: The pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (<2 years) of pancreatic cancer diagnosis were excluded from all analyses. All analyses were adjusted for age, race, gender, study, alcohol use, smoking, BMI, and family history of pancreatic cancer. Results: Self-reported diabetes was associated with a forty percent increased risk of pancreatic cancer (OR = 1.40, 95 % CI: 1.07, 1.84). The association differed by duration of diabetes; risk was highest for those with a duration of 2-8 years (OR = 1.79, 95 % CI: 1.25, 2.55); there was no association for those with 9+ years of diabetes (OR = 1.02, 95 % CI: 0.68, 1.52). Conclusions: These findings provide support for a relationship between diabetes and pancreatic cancer risk. The absence of association in those with the longest duration of diabetes may reflect hypoinsulinemia and warrants further investigation.
JF  - Cancer Causes & Control
AU  - Elena, Joanne W
AU  - Steplowski, Emily
AU  - Yu, Kai
AU  - Hartge, Patricia
AU  - Tobias, Geoffrey S
AU  - Brotzman, Michelle J
AU  - Chanock, Stephen J
AU  - Stolzenberg-Solomon, Rachael Z
AU  - Arslan, Alan A
AU  - Bueno-de-Mesquita, HBas
AU  - Helzlsouer, Kathy
AU  - Jacobs, Eric J
AU  - LaCroix, Andrea
AU  - Petersen, Gloria
AU  - Zheng, Wei
AU  - Albanes, Demetrius
AU  - Allen, Naomi E
AU  - Amundadottir, Laufey
AU  - Bao, Ying
AU  - Boeing, Heiner
AU  - Boutron-Ruault, Marie-Christine
AU  - Buring, Julie E
AU  - Gaziano, JMichael
AU  - Giovannucci, Edward L
AU  - Duell, Eric J
AU  - Hallmans, Goran
AU  - Howard, Barbara V
AU  - Hunter, David J
AU  - Hutchinson, Amy
AU  - Jacobs, Kevin B
AU  - Kooperberg, Charles
AU  - Kraft, Peter
AU  - Mendelsohn, Julie B
AU  - Michaud, Dominique S
AU  - Palli, Domenico
AU  - Phillips, Lawrence S
AU  - Overvad, Kim
AU  - Patel, Alpa V
AU  - Sansbury, Leah
AU  - Shu, Xiao-Ou
AU  - Simon, Michael S
AU  - Slimani, Nadia
AU  - Trichopoulos, Dimitrios
AU  - Visvanathan, Kala
AU  - Virtamo, Jarmo
AU  - Wolpin, Brian M
AU  - Zeleniuch-Jacquotte, Anne
AU  - Fuchs, Charles S
AU  - Hoover, Robert N
AU  - Gross, Myron
AD  - Division of Cancer Control and Population Science (DCCPS), National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA, elenajw@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 13
EP  - 25
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 24
IS  - 1
SN  - 0957-5243, 0957-5243
KW  - Risk Abstracts; Health & Safety Science Abstracts
KW  - Age
KW  - Alcohol
KW  - Body mass
KW  - Cancer
KW  - Diabetes mellitus
KW  - Gender
KW  - Genetics
KW  - Pancreatic cancer
KW  - Risk factors
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/1315611620?accountid=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=Diabetes+and+risk+of+pancreatic+cancer%3A+a+pooled+analysis+from+the+pancreatic+cancer+cohort+consortium&rft.au=Elena%2C+Joanne+W%3BSteplowski%2C+Emily%3BYu%2C+Kai%3BHartge%2C+Patricia%3BTobias%2C+Geoffrey+S%3BBrotzman%2C+Michelle+J%3BChanock%2C+Stephen+J%3BStolzenberg-Solomon%2C+Rachael+Z%3BArslan%2C+Alan+A%3BBueno-de-Mesquita%2C+HBas%3BHelzlsouer%2C+Kathy%3BJacobs%2C+Eric+J%3BLaCroix%2C+Andrea%3BPetersen%2C+Gloria%3BZheng%2C+Wei%3BAlbanes%2C+Demetrius%3BAllen%2C+Naomi+E%3BAmundadottir%2C+Laufey%3BBao%2C+Ying%3BBoeing%2C+Heiner%3BBoutron-Ruault%2C+Marie-Christine%3BBuring%2C+Julie+E%3BGaziano%2C+JMichael%3BGiovannucci%2C+Edward+L%3BDuell%2C+Eric+J%3BHallmans%2C+Goran%3BHoward%2C+Barbara+V%3BHunter%2C+David+J%3BHutchinson%2C+Amy%3BJacobs%2C+Kevin+B%3BKooperberg%2C+Charles%3BKraft%2C+Peter%3BMendelsohn%2C+Julie+B%3BMichaud%2C+Dominique+S%3BPalli%2C+Domenico%3BPhillips%2C+Lawrence+S%3BOvervad%2C+Kim%3BPatel%2C+Alpa+V%3BSansbury%2C+Leah%3BShu%2C+Xiao-Ou%3BSimon%2C+Michael+S%3BSlimani%2C+Nadia%3BTrichopoulos%2C+Dimitrios%3BVisvanathan%2C+Kala%3BVirtamo%2C+Jarmo%3BWolpin%2C+Brian+M%3BZeleniuch-Jacquotte%2C+Anne%3BFuchs%2C+Charles+S%3BHoover%2C+Robert+N%3BGross%2C+Myron&rft.aulast=Elena&rft.aufirst=Joanne&rft.date=2013-01-01&rft.volume=24&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0078-8
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-03-01
N1  - Number of references - 50
N1  - Last updated - 2013-05-06
N1  - SubjectsTermNotLitGenreText - Diabetes mellitus; Alcohol; Genetics; Age; Body mass; Risk factors; Gender; Pancreatic cancer; Cancer
DO  - http://dx.doi.org/10.1007/s10552-012-0078-8
ER  - 



TY  - JOUR
T1  - Prenatal methamphetamine exposure, home environment, and primary caregiver risk factors predict child behavioral problems at 5 years
AN  - 1312416360; 4407741
AB  - This study investigated the prospective association between prenatal methamphetamine (MA) exposure and child behavioral problems at 5 years while also examining the home environment at 30 months and several primary caregiver (PC) risk factors. Participants were 97 MA-exposed and 117 comparison children and their PCs enrolled in the Infant Development, Environment and Lifestyle Study. Hypotheses were that child behaviors would be adversely impacted by (a) prenatal MA exposure, (b) home environments that provided less developmental stimulation and emotional responsiveness to the child, and (c) the presence of PC psychological symptoms and other risk factors. Prenatal MA exposure was associated with child externalizing behavioral problems at 5 years. Home environments that were more conducive to meeting children's developmental and emotional needs were associated with fewer internalizing and externalizing behavioral problems. Independent of prenatal MA exposure, PC parenting stress and psychological symptoms were associated with increased child behavioral problems. Findings suggest prenatal MA exposure may contribute to externalizing behavioral problems in early childhood and the importance of considering possible vulnerabilities related to prenatal MA exposure in the context of the child's caregiving environment.
JF  - American journal of orthopsychiatry
AU  - Dellagrotta, Sheri
AU  - Roberts, Mary
AU  - Dansereau, Lynne
AU  - Neal, Charles
AU  - Lester, Barry
AU  - Twomey, Jean
AU  - Lagasse, Linda
AU  - Derauf, Chris
AU  - Newman, Elana
AU  - Shah, Rizwan
AU  - Smith, Lynne
AU  - Arria, Amelia
AU  - Huestis, Marilyn
AD  - Brown University ; Mayo Clinic ; University of Tulsa ; University of California, Los Angeles ; University of Maryland ; National Institute on Drug Abuse ; University of Hawaii
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 64
EP  - 72
VL  - 83
IS  - 1
SN  - 0002-9432, 0002-9432
KW  - Sociology
KW  - Drug users
KW  - Parent-child relations
KW  - Drug abuse
KW  - Children
KW  - Developmental psychology
KW  - Child care
KW  - Child development
KW  - Child rearing practices
KW  - Behavioural disorders
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312416360?accountid=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=American+journal+of+orthopsychiatry&rft.atitle=Prenatal+methamphetamine+exposure%2C+home+environment%2C+and+primary+caregiver+risk+factors+predict+child+behavioral+problems+at+5+years&rft.au=Dellagrotta%2C+Sheri%3BRoberts%2C+Mary%3BDansereau%2C+Lynne%3BNeal%2C+Charles%3BLester%2C+Barry%3BTwomey%2C+Jean%3BLagasse%2C+Linda%3BDerauf%2C+Chris%3BNewman%2C+Elana%3BShah%2C+Rizwan%3BSmith%2C+Lynne%3BArria%2C+Amelia%3BHuestis%2C+Marilyn&rft.aulast=Dellagrotta&rft.aufirst=Sheri&rft.date=2013-01-01&rft.volume=83&rft.issue=1&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=American+journal+of+orthopsychiatry&rft.issn=00029432&rft_id=info:doi/10.1111%2Fajop.12007
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 2212; 2207 2206 2212; 2197 2212 6075 3483; 9178 4777 6093 6823; 3742 1121 11776 3753 3755; 3754 3755; 2192; 1538 6071 1542 11325; 3518 10404
DO  - http://dx.doi.org/10.1111/ajop.12007
ER  - 



TY  - JOUR
T1  - Purification of clinical-grade disulfide stabilized antibody fragment variable-Pseudomonas exotoxin conjugate (dsFv-PE38) expressed in Escherichia coli
AN  - 1291613788; 17670461
AB  - Immunotoxins are rationally designed cancer targeting and killing agents. Disulfide stabilized antibody Fv portion-toxin conjugates (dsFv-toxin) are third generation immunotoxins containing only the antibody fragment variable portions and a toxin fused to the V sub(H) or V sub(L). Pseudomonas exotoxin fragment (PE-38) is a commonly used toxin in immunotoxin clinical trials. dsFv-toxin purification was previously published, but the recovery was not satisfactory. This report describes the development of a cGMP production process of the dsFv-toxin that incorporated a novel purification method. The method has been successfully applied to the clinical manufacturing of two dsFv-PE38 immunotoxins, MR1-1 targeting EGFRvIII and HA22 targeting CD22. The two subunits, V sub(L) and V sub(H) PE-38 were expressed separately in Escherichia coli using recombinant technology. Following cell lysis, inclusion bodies were isolated from the biomass harvested from fermentation in animal source component-free media. The dsFv-toxin was formed after denaturation and refolding, and subsequently purified to homogeneity through ammonium sulfate precipitation, hydrophobic interaction and ion-exchange chromatography steps. It was shown, in a direct comparison experiment using MR1-1 as model protein, that the recovery from the new purification method was improved three times over that from previously published method. The improved recovery was also demonstrated during the clinical production of two dsFv-PE38 immunotoxins-MR1-1 and HA22.
JF  - Applied Microbiology and Biotechnology
AU  - Jiang, Hua
AU  - Xie, Yueqing
AU  - Burnette, Andrew
AU  - Roach, John
AU  - Giardina, Steven L
AU  - Hecht, Toby T
AU  - Creekmore, Stephen P
AU  - Mitra, Gautam
AU  - Zhu, Jianwei
AD  - Biopharmaceutical Development Program, Frederick National Laboratory for Cancer Research, SAIC-Frederick Inc., Frederick, MD, 21702, USA, zhujianwei@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 621
EP  - 632
PB  - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL  - 97
IS  - 2
SN  - 0175-7598, 0175-7598
KW  - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts
KW  - Ammonium sulfate
KW  - Escherichia coli
KW  - Immunotoxins
KW  - A:01310
KW  - J:02350
KW  - W 30945:Fermentation & Cell Culture
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291613788?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+Microbiology+and+Biotechnology&rft.atitle=Purification+of+clinical-grade+disulfide+stabilized+antibody+fragment+variable-Pseudomonas+exotoxin+conjugate+%28dsFv-PE38%29+expressed+in+Escherichia+coli&rft.au=Jiang%2C+Hua%3BXie%2C+Yueqing%3BBurnette%2C+Andrew%3BRoach%2C+John%3BGiardina%2C+Steven+L%3BHecht%2C+Toby+T%3BCreekmore%2C+Stephen+P%3BMitra%2C+Gautam%3BZhu%2C+Jianwei&rft.aulast=Jiang&rft.aufirst=Hua&rft.date=2013-01-01&rft.volume=97&rft.issue=2&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Applied+Microbiology+and+Biotechnology&rft.issn=01757598&rft_id=info:doi/10.1007%2Fs00253-012-4319-2
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Immunotoxins; Escherichia coli
DO  - http://dx.doi.org/10.1007/s00253-012-4319-2
ER  - 



TY  - JOUR
T1  - Markers of microbial translocation and risk of AIDS-related lymphoma
AN  - 1291612944; 17671902
AB  - Background: Depletion of gut-associated lymphocytes by HIV infection facilitates microbial translocation, which may contribute to non-Hodgkin lymphoma (NHL) risk via chronic immune activation and B-cell hyperstimulation. Method: We therefore examined associations of four microbial translocation markers with subsequent NHL risk in a case-control study nested within four prospective cohort studies of HIV-infected individuals. Prediagnostic blood specimens for 56 NHL cases and 190 controls matched for age, sex, race, specimen type, cohort, and CD4 super(+) T-cell count were tested for the endotoxin lipopolysaccharide (LPS), anti-endotoxin core antibody (EndoCab), LPS-binding protein (LBP), and soluble CD14 (sCD14). Results: Elevated levels of sCD14 were associated with significantly increased NHL risk [odds ratio (OR) 2.72 (95% confidence interval [95% CI] 1.29-5.76)]. In subgroup analyses, elevated LPS levels were also associated with significantly increased NHL risk [OR 3.24 (95% CI 1.10-9.53)]. EndoCab and LBP levels were not associated with NHL risk. Conclusion: The association of sCD14 and LPS with NHL risk supports an etiologic role for gut microbial translocation in lymphomagenesis among HIV-infected individuals. Additional studies with larger sample sizes are needed to confirm these observations.
JF  - AIDS
AU  - Marks, MA
AU  - Rabkin, C S
AU  - Engels, E A
AU  - Busch, E
AU  - Kopp, W
AU  - Rager, H
AU  - Goederf, J J
AU  - Chaturvedi, A K
AD  - 6120 Executive Blvd, EPS/7055 Rockville, MD, USA, morgan.marks@nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 469
EP  - 474
VL  - 27
IS  - 3
SN  - 0269-9370, 0269-9370
KW  - Microbiology Abstracts A: Industrial & Applied Microbiology; Risk Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW  - Endotoxins
KW  - Acquired immune deficiency syndrome
KW  - Age
KW  - Lymphocytes
KW  - Infection
KW  - CD14 antigen
KW  - Non-Hodgkin's lymphoma
KW  - CD4 antigen
KW  - Lymphocytes T
KW  - Lipopolysaccharides
KW  - Lymphoma
KW  - Translocation
KW  - Races
KW  - Sex
KW  - Lymphocytes B
KW  - Blood
KW  - Antibodies
KW  - Digestive tract
KW  - Human immunodeficiency virus
KW  - Chronic infection
KW  - LPS-binding protein
KW  - Proteins
KW  - Immune response
KW  - A 01340:Antibiotics & Antimicrobials
KW  - V 22360:AIDS and HIV
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/1291612944?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Markers+of+microbial+translocation+and+risk+of+AIDS-related+lymphoma&rft.au=Marks%2C+MA%3BRabkin%2C+C+S%3BEngels%2C+E+A%3BBusch%2C+E%3BKopp%2C+W%3BRager%2C+H%3BGoederf%2C+J+J%3BChaturvedi%2C+A+K&rft.aulast=Marks&rft.aufirst=MA&rft.date=2013-01-01&rft.volume=27&rft.issue=3&rft.spage=469&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0b013e32835c1333
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2013-09-09
N1  - SubjectsTermNotLitGenreText - Endotoxins; Lymphocytes B; Lymphocytes; CD14 antigen; Blood; Antibodies; CD4 antigen; Digestive tract; Chronic infection; Lymphocytes T; LPS-binding protein; Lipopolysaccharides; Immune response; Translocation; Lymphoma; Races; Sex; Non-Hodgkin's lymphoma; Age; Acquired immune deficiency syndrome; Human immunodeficiency virus; Proteins; Infection
DO  - http://dx.doi.org/10.1097/QAD.0b013e32835c1333
ER  - 



TY  - JOUR
T1  - Cytoplasmic free Ca super(2+) is essential for multiple steps in malaria parasite egress from infected erythrocytes
AN  - 1291611952; 17659283
AB  - Background: Egress of Plasmodium falciparum, from erythrocytes at the end of its asexual cycle and subsequent parasite invasion into new host cells, is responsible for parasite dissemination in the human body. The egress pathway is emerging as a coordinated multistep programme that extends in time for tens of minutes, ending with rapid parasite extrusion from erythrocytes. While the Ca super(2+) regulation of the invasion of P. falciparum in erythrocytes is well established, the role of Ca super(2+) in parasite egress is poorly understood. This study analysed the involvement of cytoplasmic free Ca super(2+) in infected erythrocytes during the multistep egress programme of malaria parasites. Methods: Live-cell fluorescence microscopy was used to image parasite egress from infected erythrocytes, assessing the effect of drugs modulating Ca super(2+) homeostasis on the egress programme. Results: A steady increase in cytoplasmic free Ca super(2+) is found to precede parasite egress. This increase is independent of extracellular Ca super(2+) for at least the last two hours of the cycle, but is dependent upon Ca super(2+) release from internal stores. Intracellular BAPTA chelation of Ca super(2+) within the last 45 minutes of the cycle inhibits egress prior to parasitophorous vacuole swelling and erythrocyte membrane poration, two characteristic morphological transformations preceding parasite egress. Inhibitors of the parasite endoplasmic reticulum (ER) Ca super(2+)-ATPase accelerate parasite egress, indicating that Ca super(2+) stores within the ER are sufficient in supporting egress. Markedly accelerated egress of apparently viable parasites was achieved in mature schizonts using Ca super(2+) ionophore A23187. Ionophore treatment overcomes the BAPTA-induced block of parasite egress, confirming that free Ca super(2+) is essential in egress initiation. Ionophore treatment of immature schizonts had an adverse effect inducing parasitophorous vacuole swelling and killing the parasites within the host cell. Conclusions: The parasite egress programme requires intracellular free Ca super(2+) for egress initiation, vacuole swelling, and host cell cytoskeleton digestion. The evidence that parasitophorous vacuole swelling, a stage of unaffected egress, is dependent upon a rise in intracellular Ca super(2+) suggests a mechanism for ionophore-inducible egress and a new target for Ca super(2+) in the programme liberating parasites from the host cell. A regulatory pathway for egress that depends upon increases in intracellular free Ca super(2+) is proposed.
JF  - Malaria Journal
AU  - Glushakova, Svetlana
AU  - Lizunov, Vladimir
AU  - Blank, Paul S
AU  - Melikov, Kamran
AU  - Humphrey, Glen
AU  - Zimmerberg, Joshua
AD  - Program in Physical Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, 20892, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 41
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 12
IS  - 1
SN  - 1475-2875, 1475-2875
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Plasmodium falciparum
KW  - Asexual cycle of replication
KW  - Parasite egress
KW  - Free calcium
KW  - Swelling of parasitophorous vacuole
KW  - Transformation
KW  - Parasites
KW  - Human diseases
KW  - Calcium
KW  - Chelation
KW  - Calcimycin
KW  - Erythrocytes
KW  - Disease control
KW  - Malaria
KW  - Hosts
KW  - Public health
KW  - Digestion
KW  - Cytoskeleton
KW  - Endoplasmic reticulum
KW  - Ca super(2+)-transporting ATPase
KW  - Inhibitors
KW  - Drugs
KW  - Ionophores
KW  - Calcium homeostasis
KW  - Schizonts
KW  - Calcium (extracellular)
KW  - Calcium (intracellular)
KW  - parasitophorous vacuole
KW  - Vacuoles
KW  - Side effects
KW  - Fluorescence microscopy
KW  - K 03400:Human Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291611952?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Malaria+Journal&rft.atitle=Cytoplasmic+free+Ca+super%282%2B%29+is+essential+for+multiple+steps+in+malaria+parasite+egress+from+infected+erythrocytes&rft.au=Glushakova%2C+Svetlana%3BLizunov%2C+Vladimir%3BBlank%2C+Paul+S%3BMelikov%2C+Kamran%3BHumphrey%2C+Glen%3BZimmerberg%2C+Joshua&rft.aulast=Glushakova&rft.aufirst=Svetlana&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-12-41
L2  - http://www.malariajournal.com/content/12/1/41
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 55
N1  - Last updated - 2015-10-28
N1  - SubjectsTermNotLitGenreText - Parasites; Human diseases; Erythrocytes; Disease control; Inhibitors; Malaria; Hosts; Fluorescence microscopy; Public health; Transformation; Calcium homeostasis; Calcium; Calcimycin; Chelation; Schizonts; Calcium (extracellular); Calcium (intracellular); Cytoskeleton; parasitophorous vacuole; Digestion; Ca super(2+)-transporting ATPase; Endoplasmic reticulum; Vacuoles; Ionophores; Drugs; Side effects; Plasmodium falciparum
DO  - http://dx.doi.org/10.1186/1475-2875-12-41
ER  - 



TY  - JOUR
T1  - Pulmonary Function Impairment May Be an Early Risk Factor for Late-Life Cognitive Impairment
AN  - 1291602803; 17628457
AB  - To determine the association between change in pulmonary function (PF) and mid- and late-life cognitive function. Prospective population-based cohort study that included measures of pulmonary function in midlife and brain magnetic resonance imaging data acquired in late life. The Age, Gene/Environment Susceptibility-Reykjavik Study. Three thousand six hundred sixty-five subjects who had at least one measure of forced expiratory volume in 1 second (FEV1) and were cognitively tested on average 23 years later. A subset of 1,281 subjects had two or three measures of FEV1 acquired over a 7.8-year period. Pulmonary function was estimated as FEV1/height2. Rate of PF decline was estimated as the slope of decline over time. Cognitive status was measured with continuous scores of memory, speed of processing, and executive function and as the outcome of mild cognitive impairment (MCI) and dementia. Lower PF measured in midlife predicted poorer memory, slower speed of processing, poorer executive function, and greater likelihood of MCI and dementia 23 years later. Decrease in PF over a 7.8-year period in midlife was not associated with MCI or dementia. Low PF measured in midlife may be an early marker of later cognitive problems. Additional studies characterizing early and late PF changes are needed.
JF  - Journal of the American Geriatrics Society
AU  - Vidal, Jean-Sebastien
AU  - Aspelund, Thor
AU  - Jonsdottir, Maria K
AU  - Jonsson, Palmi V
AU  - Harris, Tamara B
AU  - Lopez, Oscar L
AU  - Gudnason, Vilmundur
AU  - Launer, Lenore J
AD  - Laboratory of Epidemiology, Demography, and Biometry. National Institute on Aging National Institutes of Health
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 79
EP  - 83
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 61
IS  - 1
SN  - 0002-8614, 0002-8614
KW  - CSA Neurosciences Abstracts; Risk Abstracts
KW  - Age
KW  - Cognitive ability
KW  - Respiratory function
KW  - N3 11001:Behavioral and Cognitive Neuroscience
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291602803?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Geriatrics+Society&rft.atitle=Pulmonary+Function+Impairment+May+Be+an+Early+Risk+Factor+for+Late-Life+Cognitive+Impairment&rft.au=Vidal%2C+Jean-Sebastien%3BAspelund%2C+Thor%3BJonsdottir%2C+Maria+K%3BJonsson%2C+Palmi+V%3BHarris%2C+Tamara+B%3BLopez%2C+Oscar+L%3BGudnason%2C+Vilmundur%3BLauner%2C+Lenore+J&rft.aulast=Vidal&rft.aufirst=Jean-Sebastien&rft.date=2013-01-01&rft.volume=61&rft.issue=1&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Geriatrics+Society&rft.issn=00028614&rft_id=info:doi/10.1111%2Fjgs.12069
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2014-03-10
N1  - SubjectsTermNotLitGenreText - Cognitive ability; Respiratory function
DO  - http://dx.doi.org/10.1111/jgs.12069
ER  - 



TY  - JOUR
T1  - Modification of pharmacokinetic and abuse-related effects of cocaine by human-derived cocaine hydrolase in monkeys.
AN  - 1286946241; 22264200
AB  - Although substantial research effort has focused on developing pharmacological treatments for cocaine abuse, no effective medications have been developed. Recent studies show that enzymes that metabolize cocaine in the periphery, forestalling its entry into the brain, can prevent cocaine toxicity and its behavioral effects in rodents. Here we report on effects of one such enzyme (Albu-CocH) on the pharmacokinetic and behavioral effects of cocaine in squirrel monkeys. Albu-CocH was developed from successive mutations of human butyrylcholinesterase (BChE) and has 1000-fold greater catalytic activity against cocaine than naturally occurring BChE. Pharmacokinetic studies showed that Albu-CocH (5 mg/kg) had a half-life of 56.6 hours in squirrel monkeys. In these studies, plasma levels of cocaine following i.v. 1 mg/kg cocaine were reduced 2 hours after administration of Albu-CocH, whereas plasma levels of the cocaine metabolite ecgonine methyl ester were increased. These effects were still evident 72 hours following Albu-CocH administration. In behavioral experiments in monkeys, pre-treatment with 5 mg/kg Albu-CocH dramatically decreased self-administration of a reinforcing dose of i.v. cocaine (30 µg/kg/injection) for over 24 hours. Pre-treatment with 5 mg/kg Albu-CocH also attenuated the reinstatement of extinguished cocaine self-administration by an i.v. priming injection of cocaine (0.1 or 0.3 mg/kg) and, in separate studies, attenuated the discriminative-stimulus effects of cocaine. The ability of Albu-CocH to attenuate the abuse-related effects of cocaine in squirrel monkeys indicates that further investigation of BChE mutants as potential treatment for cocaine abuse and toxicity is warranted.
          Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
JF  - Addiction biology
AU  - Schindler, Charles W
AU  - Justinova, Zuzana
AU  - Lafleur, David
AU  - Woods, Doug
AU  - Roschke, Viktor
AU  - Hallak, Hussein
AU  - Sklair-Tavron, Liora
AU  - Redhi, Godfrey H
AU  - Yasar, Sevil
AU  - Bergman, Jack
AU  - Goldberg, Steven R
AD  - Preclinical Pharmacology Section, Behavioral Neuroscience Research Branch, DHHS/NIH/NIDA Intramural Research Program, Baltimore, MD, USA. cschindl@helix.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 30
EP  - 39
VL  - 18
IS  - 1
KW  - Albumins
KW  - 0
KW  - Dopamine Uptake Inhibitors
KW  - Butyrylcholinesterase
KW  - EC 3.1.1.-
KW  - Cocaine
KW  - I5Y540LHVR
KW  - Index Medicus
KW  - Discrimination Learning -- drug effects
KW  - Animals
KW  - Analysis of Variance
KW  - Dose-Response Relationship, Drug
KW  - Humans
KW  - Reinforcement (Psychology)
KW  - Biocatalysis
KW  - Drug-Seeking Behavior -- drug effects
KW  - Saimiri
KW  - Self Administration
KW  - Half-Life
KW  - Drug-Related Side Effects and Adverse Reactions -- prevention & control
KW  - Antibody Formation -- drug effects
KW  - Male
KW  - Butyrylcholinesterase -- pharmacokinetics
KW  - Albumins -- pharmacology
KW  - Dopamine Uptake Inhibitors -- antagonists & inhibitors
KW  - Dopamine Uptake Inhibitors -- administration & dosage
KW  - Butyrylcholinesterase -- pharmacology
KW  - Albumins -- pharmacokinetics
KW  - Cocaine-Related Disorders -- drug therapy
KW  - Cocaine -- pharmacokinetics
KW  - Dopamine Uptake Inhibitors -- pharmacokinetics
KW  - Cocaine -- administration & dosage
KW  - Cocaine -- antagonists & inhibitors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1286946241?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+biology&rft.atitle=Modification+of+pharmacokinetic+and+abuse-related+effects+of+cocaine+by+human-derived+cocaine+hydrolase+in+monkeys.&rft.au=Schindler%2C+Charles+W%3BJustinova%2C+Zuzana%3BLafleur%2C+David%3BWoods%2C+Doug%3BRoschke%2C+Viktor%3BHallak%2C+Hussein%3BSklair-Tavron%2C+Liora%3BRedhi%2C+Godfrey+H%3BYasar%2C+Sevil%3BBergman%2C+Jack%3BGoldberg%2C+Steven+R&rft.aulast=Schindler&rft.aufirst=Charles&rft.date=2013-01-01&rft.volume=18&rft.issue=1&rft.spage=30&rft.isbn=&rft.btitle=&rft.title=Addiction+biology&rft.issn=1369-1600&rft_id=info:doi/10.1111%2Fj.1369-1600.2011.00424.x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-17
N1  - Date created - 2013-01-02
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Drug Metab Dispos. 2000 Mar;28(3):367-71 [10681384]
Psychopharmacology (Berl). 2011 Feb;213(4):817-29 [20972552]
NIDA Res Monogr. 1984;50:34-53 [6440024]
Nat Med. 1996 Oct;2(10):1129-32 [8837612]
Toxicol Appl Pharmacol. 1997 Aug;145(2):363-71 [9266810]
Toxicol Appl Pharmacol. 1997 Aug;145(2):372-80 [9266811]
Drug Alcohol Depend. 1997 Dec 15;48(3):159-65 [9449014]
Exp Clin Psychopharmacol. 1998 Aug;6(3):274-9 [9725111]
Diabetes. 2005 Jan;54(1):251-8 [15616036]
Eur J Pharmacol. 2005 Jul 11;517(3):186-90 [15967428]
Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16656-61 [16275916]
Mol Pharmacol. 2006 Dec;70(6):1885-91 [16968810]
Int J Neuropsychopharmacol. 2008 May;11(3):425-38 [17927843]
Chem Biol Interact. 2008 Sep 25;175(1-3):83-7 [18514640]
Neuropsychopharmacology. 2008 Oct;33(11):2715-25 [18199998]
J Pharmacol Exp Ther. 2009 Aug;330(2):449-57 [19478136]
J Pharmacol Exp Ther. 2009 Nov;331(2):445-55 [19710369]
Biol Psychiatry. 2010 Jan 1;67(1):59-65 [19846066]
Drug Alcohol Depend. 2010 Jan 15;106(2-3):219-29 [19800183]
Mol Pharmacol. 2010 Apr;77(4):593-600 [20086035]
Chem Biol Interact. 2010 Sep 6;187(1-3):421-4 [20219449]
Psychopharmacology (Berl). 2003 Sep;169(2):135-40 [12827345]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1111/j.1369-1600.2011.00424.x
ER  - 



TY  - JOUR
T1  - Rethinking intractability: a new framework for conflict
AN  - 1285627818; 4402975
AB  - For scholars, intractable conicts are the most challenging puzzle, daring researchers to penetrate their shield of daunting complexity and uncover their essence. Intractable conicts challenge our theories and methodologies and, ultimately, our intelligence. For mediators and other dispute resolution practitioners, the intractable conict is the ultimate test: it is the mountain nobody has ever been able to scale, the wild animal nobody has ever been able to tame. Some of the best dispute resolution scholars and practitioners have tried to intervene in and to explain intractable conicts, although the terminologies they use and which aspects they choose to focus on will vary. What unites these efforts is the recognition of these conicts tremendous complexity and their profound resistance to resolution especially by traditional modes of conict intervention. For example, Daniel Bar-Tal (2000: 353), citing several other researchers, has written,Intractable conicts are characterized as being protracted, irreconcilable, violent, of a zero-sum nature, total and central, with the parties involved having an interest in their continuation. . . . They are demanding, stressful, painful, exhausting, and costly both in human and material terms. He goes on to discuss a conceptual framework of eight societal beliefs that constitute what he calls a conictive ethos of a society. He does not, however, concentrate on the essence of these conicts but rather on the process of reconciliation he considers essential to their resolution. Reprinted by permission of Blackwell Publishing
JF  - Negotiation journal
AU  - Gadlin, Howard
AD  - National Institutes of Health
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 99
EP  - 117
VL  - 29
IS  - 1
SN  - 0748-4526, 0748-4526
KW  - Political Science
KW  - Society
KW  - Intelligence
KW  - Reconciliation
KW  - Conflict resolution
KW  - Interventionism
KW  - Recognition of states
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285627818?accountid=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=Negotiation+journal&rft.atitle=Rethinking+intractability%3A+a+new+framework+for+conflict&rft.au=Gadlin%2C+Howard&rft.aulast=Gadlin&rft.aufirst=Howard&rft.date=2013-01-01&rft.volume=29&rft.issue=1&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=Negotiation+journal&rft.issn=07484526&rft_id=info:doi/10.1111%2Fnejo.12007
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 11979; 10657; 2703 2698; 6828 7869 2703 2698 5200 5574 10472; 10656 12168 9008 12092 9720 6590; 6608 6085
DO  - http://dx.doi.org/10.1111/nejo.12007
ER  - 



TY  - JOUR
T1  - Structure and ligand-binding properties of the biogenic amine-binding protein from the saliva of a blood-feeding insect vector of Trypanosoma cruzi
AN  - 1285101966; 17562489
AB  - Proteins that bind small-molecule mediators of inflammation and hemostasis are essential for blood-feeding by arthropod vectors of infectious disease. In ticks and triatomine insects, the lipocalin protein family is greatly expanded and members have been shown to bind biogenic amines, eicosanoids and ADP. These compounds are potent mediators of platelet activation, inflammation and vascular tone. In this paper, the structure of the amine-binding protein (ABP) from Rhodnius prolixus, a vector of the trypanosome that causes Chagas disease, is described. ABP binds the biogenic amines serotonin and norepinephrine with high affinity. A complex with tryptamine shows the presence of a binding site for a single ligand molecule in the central cavity of the beta -barrel structure. The cavity contains significant additional volume, suggesting that this protein may have evolved from the related nitrophorin proteins, which bind a much larger heme ligand in the central cavity.
JF  - Acta Crystallographica Section D
AU  - Xu, Xueqing
AU  - Chang, Bianca W
AU  - Mans, Ben J
AU  - Ribeiro, Jose MC
AU  - Andersen, John F
AD  - Laboratory of Malaria and Vector Research, NIH/NIAID, 12735 Twinbrook Parkway, Rockville, MD 20852, USA
Y1  - 2013/01/01/
PY  - 2013
DA  - 2013 Jan 01
SP  - 105
EP  - 113
PB  - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL  - 69
IS  - 1
SN  - 0907-4449, 0907-4449
KW  - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology
KW  - Heme
KW  - eicosanoids
KW  - Hosts
KW  - Rhodnius prolixus
KW  - Disease transmission
KW  - Public health
KW  - Infectious diseases
KW  - Lipocalin
KW  - Aquatic insects
KW  - Biogenic amines
KW  - Trypanosoma cruzi
KW  - Ixodidae
KW  - tryptamine
KW  - protein families
KW  - Vectors
KW  - Amines
KW  - Serotonin
KW  - Inflammation
KW  - Arthropoda
KW  - ADP
KW  - hemostasis
KW  - Norepinephrine
KW  - Platelets
KW  - Proteins
KW  - Saliva
KW  - Ligands
KW  - Chagas' disease
KW  - K 03410:Animal Diseases
KW  - Q1 08484:Species interactions: parasites and diseases
KW  - Q5 08524:Public health, medicines, dangerous organisms
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285101966?accountid=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=Acta+Crystallographica+Section+D&rft.atitle=Structure+and+ligand-binding+properties+of+the+biogenic+amine-binding+protein+from+the+saliva+of+a+blood-feeding+insect+vector+of+Trypanosoma+cruzi&rft.au=Xu%2C+Xueqing%3BChang%2C+Bianca+W%3BMans%2C+Ben+J%3BRibeiro%2C+Jose+MC%3BAndersen%2C+John+F&rft.aulast=Xu&rft.aufirst=Xueqing&rft.date=2013-01-01&rft.volume=69&rft.issue=1&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=Acta+Crystallographica+Section+D&rft.issn=09074449&rft_id=info:doi/10.1107%2FS0907444912043326
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Document feature - figure 0
N1  - Last updated - 2016-03-17
N1  - SubjectsTermNotLitGenreText - ADP; Infectious diseases; Proteins; Hosts; Amines; Aquatic insects; Ligands; Public health; Disease transmission; Biogenic amines; eicosanoids; Heme; tryptamine; Vectors; protein families; Serotonin; Inflammation; hemostasis; Norepinephrine; Platelets; Saliva; Lipocalin; Chagas' disease; Trypanosoma cruzi; Arthropoda; Ixodidae; Rhodnius prolixus
DO  - http://dx.doi.org/10.1107/S0907444912043326
ER  - 



TY  - JOUR
T1  - PubChem3D: conformer ensemble accuracy
AN  - 1285096564; 17593382
AB  - Background: PubChem is a free and publicly available resource containing substance descriptions and their associated biological activity information. PubChem3D is an extension to PubChem containing computationally-derived three-dimensional (3-D) structures of small molecules. All the tools and services that are a part of PubChem3D rely upon the quality of the 3-D conformer models. Construction of the conformer models currently available in PubChem3D involves a clustering stage to sample the conformational space spanned by the molecule. While this stage allows one to downsize the conformer models to more manageable size, it may result in a loss of the ability to reproduce experimentally determined "bioactive" conformations, for example, found for PDB ligands. This study examines the extent of this accuracy loss and considers its effect on the 3-D similarity analysis of molecules. Results: The conformer models consisting of up to 100,000 conformers per compound were generated for 47,123 small molecules whose structures were experimentally determined, and the conformers in each conformer model were clustered to reduce the size of the conformer model to a maximum of 500 conformers per molecule. The accuracy of the conformer models before and after clustering was evaluated using five different measures: root-mean-square distance (RMSD), shape-optimized shape-Tanimoto (ST super( ST-opt )) and combo-Tanimoto (ComboT super( ST-opt )), and color-optimized color-Tanimoto (CT super( CT-opt )) and combo-Tanimoto (ComboT super( CT-opt )). On average, the effect of clustering decreased the conformer model accuracy, increasing the conformer ensemble's RMSD to the bioactive conformer (by 0.18 plus or minus 0.12 Aa), and decreasing the ST super( ST-opt ), ComboT super( ST-opt ), CT super( CT-opt ), and ComboT super( CT-opt ) scores (by 0.04 plus or minus 0.03, 0.16 plus or minus 0.09, 0.09 plus or minus 0.05, and 0.15 plus or minus 0.09, respectively). Conclusion: This study shows the RMSD accuracy performance of the PubChem3D conformer models is operating as designed. In addition, the effect of PubChem3D sampling on 3-D similarity measures shows that there is a linear degradation of average accuracy with respect to molecular size and flexibility. Generally speaking, one can likely expect the worst-case minimum accuracy of 90% or more of the PubChem3D ensembles to be 0.75, 1.09, 0.43, and 1.13, in terms of ST super( ST-opt ), ComboT super( ST-opt ), CT super( CT-opt ), and ComboT super( CT-opt ), respectively. This expected accuracy improves linearly as the molecule becomes smaller or less flexible.
JF  - Journal of Cheminformatics
AU  - Kim, Sunghwan
AU  - Bolton, Evan E
AU  - Bryant, Stephen H
AD  - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Department of Health and Human Services, 8600 Rockville Pike, Bethesda, MD 20894, USA
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 1
PB  - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom
VL  - 5
IS  - 1
SN  - 1758-2946, 1758-2946
KW  - Biotechnology and Bioengineering Abstracts
KW  - Conformation
KW  - Informatics
KW  - Models
KW  - Molecular modelling
KW  - Sampling
KW  - W 30910:Imaging
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285096564?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cheminformatics&rft.atitle=PubChem3D%3A+conformer+ensemble+accuracy&rft.au=Kim%2C+Sunghwan%3BBolton%2C+Evan+E%3BBryant%2C+Stephen+H&rft.aulast=Kim&rft.aufirst=Sunghwan&rft.date=2013-01-01&rft.volume=5&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cheminformatics&rft.issn=17582946&rft_id=info:doi/10.1186%2F1758-2946-5-1
L2  - http://www.jcheminf.com/content/5/1/1
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Number of references - 53
N1  - Last updated - 2013-03-11
N1  - SubjectsTermNotLitGenreText - Molecular modelling; Informatics; Sampling; Conformation; Models
DO  - http://dx.doi.org/10.1186/1758-2946-5-1
ER  - 



TY  - JOUR
T1  - Correlated Biomarker Measurement Error: An Important Threat to Inference in Environmental Epidemiology
AN  - 1285091981; 17577552
AB  - Utilizing multiple biomarkers is increasingly common in epidemiology. However, the combined impact of correlated exposure measurement error, unmeasured confounding, interaction, and limits of detection (LODs) on inference for multiple biomarkers is unknown. We conducted data-driven simulations evaluating bias from correlated measurement error with varying reliability coefficients (R), odds ratios (ORs), levels of correlation between exposures and error, LODs, and interactions. Blood cadmium and lead levels in relation to anovulation served as the motivating example, based on findings from the BioCycle Study (2005-2007). For most scenarios, main-effect estimates for cadmium and lead with increasing levels of positively correlated measurement error created increasing downward or upward bias for OR > 1.00 and OR < 1.00, respectively, that was also a function of effect size. Some scenarios showed bias for cadmium away from the null. Results subject to LODs were similar. Bias for main and interaction effects ranged from -130% to 36% and from -144% to 84%, respectively. A closed-form continuous outcome case solution provides a useful tool for estimating the bias in logistic regression. Investigators should consider how measurement error and LODs may bias findings when examining biomarkers measured in the same medium, prepared with the same process, or analyzed using the same method.
JF  - American Journal of Epidemiology
AU  - Pollack, A Z
AU  - Perkins, N J
AU  - Mumford, S L
AU  - Ye, A
AU  - Schisterman, E F
Y1  - 2013/01/01/
PY  - 2013
DA  - 2013 Jan 01
SP  - 84
EP  - 92
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 1
SN  - 0002-9262, 0002-9262
KW  - Health & Safety Science Abstracts
KW  - Bioindicators
KW  - Epidemiology
KW  - Simulation
KW  - Cadmium
KW  - Lead
KW  - Blood levels
KW  - H 12000:Epidemiology and Public Health
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285091981?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Correlated+Biomarker+Measurement+Error%3A+An+Important+Threat+to+Inference+in+Environmental+Epidemiology&rft.au=Pollack%2C+A+Z%3BPerkins%2C+N+J%3BMumford%2C+S+L%3BYe%2C+A%3BSchisterman%2C+E+F&rft.aulast=Pollack&rft.aufirst=A&rft.date=2013-01-01&rft.volume=177&rft.issue=1&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws209
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2013-11-04
N1  - SubjectsTermNotLitGenreText - Bioindicators; Epidemiology; Simulation; Cadmium; Lead; Blood levels
DO  - http://dx.doi.org/10.1093/aje/kws209
ER  - 



TY  - JOUR
T1  - Risk of Total and Aggressive Prostate Cancer and Pesticide Use in the Agricultural Health Study
AN  - 1285090733; 17577555
AB  - Because pesticides may operate through different mechanisms, the authors studied the risk of prostate cancer associated with specific pesticides in the Agricultural Health Study (1993-2007). With 1,962 incident cases, including 919 aggressive prostate cancers among 54,412 applicators, this is the largest study to date. Rate ratios and 95% confidence intervals were calculated by using Poisson regression to evaluate lifetime use of 48 pesticides and prostate cancer incidence. Three organophosphate insecticides were significantly associated with aggressive prostate cancer: fonofos (rate ratio (RR) for the highest quartile of exposure (Q4) vs. nonexposed = 1.63, 95% confidence interval (CI): 1.22, 2.17; P sub(trend) < 0.001); malathion (RR for Q4 vs. nonexposed = 1.43, 95% CI: 1.08, 1.88; P sub(trend) = 0.04); and terbufos (RR for Q4 vs. nonexposed = 1.29, 95% CI: 1.02, 1.64; P sub(trend) = 0.03). The organochlorine insecticide aldrin was also associated with increased risk of aggressive prostate cancer (RR for Q4 vs. nonexposed = 1.49, 95% CI: 1.03, 2.18; P sub(trend) = 0.02). This analysis has overcome several limitations of previous studies with the inclusion of a large number of cases with relevant exposure and detailed information on use of specific pesticides at 2 points in time. Furthermore, this is the first time specific pesticides are implicated as risk factors for aggressive prostate cancer.
JF  - American Journal of Epidemiology
AU  - Koutros, Stella
AU  - Beane Freeman, Laura E
AU  - Lubin, Jay H
AU  - Heltshe, Sonya L
AU  - Andreotti, Gabriella
AU  - Barry, Kathryn Hughes
AU  - DellaValle, Curt T
AU  - Hoppin, Jane A
AU  - Sandler, Dale P
AU  - Lynch, Charles F
AU  - Blair, Aaron
AU  - Alavanja, Michael CR
Y1  - 2013/01/01/
PY  - 2013
DA  - 2013 Jan 01
SP  - 59
EP  - 74
PB  - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL  - 177
IS  - 1
SN  - 0002-9262, 0002-9262
KW  - Pollution Abstracts; Risk Abstracts; Health & Safety Science Abstracts
KW  - Prostate cancer
KW  - Insecticides
KW  - Organochlorine compounds
KW  - Organophosphates
KW  - Risk factors
KW  - Pesticides
KW  - Aldrin
KW  - Malathion
KW  - H 5000:Pesticides
KW  - P 6000:TOXICOLOGY AND HEALTH
KW  - R2 23110:Psychological aspects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285090733?accountid=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=Risk+of+Total+and+Aggressive+Prostate+Cancer+and+Pesticide+Use+in+the+Agricultural+Health+Study&rft.au=Koutros%2C+Stella%3BBeane+Freeman%2C+Laura+E%3BLubin%2C+Jay+H%3BHeltshe%2C+Sonya+L%3BAndreotti%2C+Gabriella%3BBarry%2C+Kathryn+Hughes%3BDellaValle%2C+Curt+T%3BHoppin%2C+Jane+A%3BSandler%2C+Dale+P%3BLynch%2C+Charles+F%3BBlair%2C+Aaron%3BAlavanja%2C+Michael+CR&rft.aulast=Koutros&rft.aufirst=Stella&rft.date=2013-01-01&rft.volume=177&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkws225
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-02-01
N1  - Last updated - 2014-05-15
N1  - SubjectsTermNotLitGenreText - Organochlorine compounds; Insecticides; Prostate cancer; Organophosphates; Risk factors; Aldrin; Pesticides; Malathion
DO  - http://dx.doi.org/10.1093/aje/kws225
ER  - 



TY  - JOUR
T1  - Bone mineral density and blood metals in premenopausal women
AN  - 1283722466; 17497686
AB  - Exposure to metals, specifically cadmium, lead, and mercury, is widespread and is associated with reduced bone mineral density (BMD) in older populations, but the associations among premenopausal women are unclear. Therefore, we evaluated the relationship between these metals in blood and BMD (whole body, total hip, lumbar spine, and non-dominant wrist) quantified by dual energy X-ray absorptiometry in 248 premenopausal women, aged 18-44. Participants were of normal body mass index (mean BMI 24.1), young (mean age 27.4), 60% were white, 20% non-Hispanic black, 15% Asian, and 6% other race group, and were from the Buffalo, New York region. The median (interquartile range) level of cadmium was 0.30 mu g/l (0.19-0.43), of lead was 0.86 mu g/dl (0.68-1.20), and of mercury was 1.10 mu g/l (0.58-2.00). BMD was treated both as a continuous variable in linear regression and dichotomized at the 10th percentile for logistic regression analyses. Mercury was associated with reduced odds of decreased lumbar spine BMD (0.66, 95% confidence interval: 0.44, 0.99), but overall, metals at environmentally relevant levels of exposure were not associated with reduced BMD in this population of healthy, reproductive-aged women. Further research is needed to determine if the blood levels of cadmium, lead, and mercury in this population are sufficiently low that there is no substantive impact on bone, or if effects on bone can be expected only at older ages.
JF  - Environmental Research
AU  - Pollack, A Z
AU  - Mumford, S L
AU  - Wactawski-Wende, J
AU  - Yeung, E
AU  - Mendola, P
AU  - Mattison
AU  - Schisterman, E F
AD  - Epidemiology Branch, Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, United States, pollacka@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 76
EP  - 81
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 120
SN  - 0013-9351, 0013-9351
KW  - Toxicology Abstracts; Calcium & Calcified Tissue Abstracts; Environment Abstracts
KW  - BMD
KW  - BMI
KW  - CI
KW  - Cd
KW  - CR
KW  - Hg
KW  - OR
KW  - Pb
KW  - Bone mineral density
KW  - Cadmium
KW  - Lead
KW  - Mercury
KW  - Women
KW  - Age
KW  - USA, New York, Buffalo
KW  - Heavy metals
KW  - Wrist
KW  - Dual energy X-ray absorptiometry
KW  - Regression analysis
KW  - Geriatrics
KW  - Races
KW  - Metals
KW  - USA, New York
KW  - Blood levels
KW  - Spine (lumbar)
KW  - Spine
KW  - Females
KW  - Body mass index
KW  - Minerals
KW  - Hip
KW  - ENA 03:Energy
KW  - X 24360:Metals
KW  - T 2025:Bone and Bone Diseases
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1283722466?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Bone+mineral+density+and+blood+metals+in+premenopausal+women&rft.au=Pollack%2C+A+Z%3BMumford%2C+S+L%3BWactawski-Wende%2C+J%3BYeung%2C+E%3BMendola%2C+P%3BMattison%3BSchisterman%2C+E+F&rft.aulast=Pollack&rft.aufirst=A&rft.date=2013-01-01&rft.volume=120&rft.issue=&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2012.06.001
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2014-02-01
N1  - Last updated - 2015-03-19
N1  - SubjectsTermNotLitGenreText - Age; Heavy metals; Wrist; Dual energy X-ray absorptiometry; Lead; Blood levels; Spine (lumbar); Bone mineral density; Geriatrics; Regression analysis; Mercury; Cadmium; Body mass index; Races; Hip; Metals; Spine; Females; Minerals; USA, New York, Buffalo; USA, New York
DO  - http://dx.doi.org/10.1016/j.envres.2012.06.001
ER  - 



TY  - JOUR
T1  - Effect of mother's dominance rank on offspring temperament in infant rhesus monkeys (Macaca mulatta)
AN  - 1282828469; 4393887
AB  - In humans, temperament plays an important role in socialization and personality. Some temperaments, such as behavioral inhibition are associated with an increased risk for psychopathology. Nonhuman primates can serve as a model for neurobiological and developmental contributions to emotional development and several recent studies have begun to investigate temperament in nonhuman primates. In rhesus monkeys, dominance rank is inherited from the mother and is associated with social and emotional tendencies that resemble differences in temperament. The current study assessed differences in temperament in infant rhesus monkeys as a function of maternal dominance rank. Temperament was assessed in 26 infants (13 males) from birth until 6 months of age with a battery that included Brazelton test, human intruder test, human intruder-startle, cortisol stress reactivity, and home cage observations of interactions with peers and the mother. Throughout testing, infants lived with their mothers and a small group of other monkeys in indoor/outdoor runs. Dominance rank of the mothers within each run was rated as either low/middle (N = 18, 9 male) or high/alpha (N = 8, 4 female). Infants of high-ranking mothers displayed more intruder-directed aggression and reduced startle potentiation in the human intruder tests. Dominant offspring also had reduced levels cortisol and startle across development and spent more time away from mothers in the interaction tests. These results suggest that dominance of the mother may be reflected in behavioral reactivity of infants early in life. These findings set up future studies, which may focus on contributing factors to both dominance and temperament such as genetics, rearing, and socialization. Such factors are likely to interact across development in meaningful ways. These results also suggest future human-based studies of a similar relationship may be warranted, although social dominance is clearly more complex in human than macaque societies. Am. J. Primatol. 75:65-73, 2013. Published 2012 by Wiley Periodicals, Inc.† Copyright John Wiley & Sons. Reproduced with permission. An electronic version of this article is available online at http://www.interscience.wiley.com
JF  - American journal of primatology
AU  - Suomi, Stephen J
AU  - Noble, Pamela L
AU  - Pine, Daniel S
AU  - Fox, Nathan A
AU  - Nelson, Eric E
AU  - Suarez-Jimenez, Benjamin
AU  - Hathaway, Amanda
AU  - Waters, Carlos
AU  - Vaughan, Kelli
AD  - National Institutes of Health ; National Institute of Child Health and Human Development ; University of Maryland
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 65
EP  - 73
VL  - 75
IS  - 1
SN  - 0275-2565, 0275-2565
KW  - Anthropology
KW  - Psychopathology
KW  - Aggression
KW  - Primates
KW  - Interactionism
KW  - Socialization
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282828469?accountid=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=American+journal+of+primatology&rft.atitle=Effect+of+mother%27s+dominance+rank+on+offspring+temperament+in+infant+rhesus+monkeys+%28Macaca+mulatta%29&rft.au=Suomi%2C+Stephen+J%3BNoble%2C+Pamela+L%3BPine%2C+Daniel+S%3BFox%2C+Nathan+A%3BNelson%2C+Eric+E%3BSuarez-Jimenez%2C+Benjamin%3BHathaway%2C+Amanda%3BWaters%2C+Carlos%3BVaughan%2C+Kelli&rft.aulast=Suomi&rft.aufirst=Stephen&rft.date=2013-01-01&rft.volume=75&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=American+journal+of+primatology&rft.issn=02752565&rft_id=info:doi/10.1002%2Fajp.22081
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 11977; 10409; 662; 6618 9161 9486; 10148
DO  - http://dx.doi.org/10.1002/ajp.22081
ER  - 



TY  - JOUR
T1  - Mann-Whitney test with adjustments to pretreatment variables for missing values and observational study
AN  - 1282039268; 4391522
AB  - Summary. The conventional Wilcoxon or Mann-Whitney test can be invalid for comparing treatment effects in the presence of missing values or in observational studies. This is because the missingness of the outcomes or the participation in the treatments may depend on certain pretreatment variables. We propose an approach to adjust the Mann-Whitney test by correcting the potential bias via consistently estimating the conditional distributions of the outcomes given the pretreatment variables. We also propose semiparametric extensions of the adjusted Mann-Whitney test which lead to dimension reduction for high dimensional covariates. A novel bootstrap procedure is devised to approximate the null distribution of the test statistics for practical implementations. Results from simulation studies and an economics observational study data analysis are presented to demonstrate the performance of the approach proposed. Reprinted by permission of Blackwell Publishers
JF  - Journal of the Royal Statistical Society
AU  - Chen, Song Xi
AU  - Qin, Jing
AU  - Tang, Cheng Yong
AD  - Peking University ; National Institute of Allergy and Infectious Diseases ; National University of Singapore
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 81
EP  - 102
VL  - 75
IS  - 1
SN  - 1369-7412, 1369-7412
KW  - Economics
KW  - Distribution
KW  - Economic performance
KW  - Simulation
KW  - Data analysis
KW  - Bias
KW  - Covariance
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1282039268?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=Mann-Whitney+test+with+adjustments+to+pretreatment+variables+for+missing+values+and+observational+study&rft.au=Chen%2C+Song+Xi%3BQin%2C+Jing%3BTang%2C+Cheng+Yong&rft.aulast=Chen&rft.aufirst=Song&rft.date=2013-01-01&rft.volume=75&rft.issue=1&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=13697412&rft_id=info:doi/10.1111%2Fj.1467-9868.2012.01036.x
LA  - English
DB  - International Bibliography of the Social Sciences (IBSS)
N1  - Date revised - 2013-06-12
N1  - Last updated - 2013-09-16
N1  - SubjectsTermNotLitGenreText - 2977 13249 10214 12224 971; 11670; 3279 971 3286; 3974 9390; 1565 1362 2688 2449 10404; 3641 12233
DO  - http://dx.doi.org/10.1111/j.1467-9868.2012.01036.x
ER  - 



TY  - JOUR
T1  - Pyocyanin-enhanced neutrophil extracellular trap formation requires the NADPH oxidase.
AN  - 1273805213; 23342104
AB  - Beyond intracellular killing, a novel neutrophil-based antimicrobial mechanism has been recently discovered: entrapment and killing by neutrophil extracellular traps (NETs). NETs consist of extruded nuclear DNA webs decorated with granule proteins. Although NET formation is an important innate immune mechanism, uncontrolled NET release damages host tissues and has been linked to several diseases including cystic fibrosis (CF). The major CF airway pathogen Pseudomonas aeruginosa establishes chronic infection. Pseudomonas imbedded within biofilms is protected against the immune system, but maintains chronic inflammation that worsens disease symptoms. Aberrant NET release from recruited neutrophils was found in CF, but the underlying mechanisms remain unclear. One of the most important Pseudomonas virulence factors is pyocyanin, a redox-active pigment that has been associated with diminished lung function in CF. Here we show that pyocyanin promotes NET formation in a time- and dose-dependent manner. Most CF Pseudomonas clinical isolates tested produce pyocyanin in vitro. Pyocyanin-derived reactive oxygen species are required for its NET release. Inhibitor experiments demonstrated involvement of Jun N-terminal Kinase (JNK) and phosphatidylinositol 3-Kinase (PI3K) in pyocyanin-induced NET formation. Pyocyanin-induced NETs also require the NADPH oxidase because NET release in chronic granulomatous disease neutrophils was greatly reduced. Comparison of neutrophils from gp91phox- and p47phox-deficient patients revealed that pyocyanin-triggered NET formation is proportional to their residual superoxide production. Our studies identify pyocyanin as the first secreted bacterial toxin that enhances NET formation. The involvement of NADPH oxidase in pyocyanin-induced NET formation represents a novel mechanism of pyocyanin toxicity.
JF  - PloS one
AU  - Rada, Balázs
AU  - Jendrysik, Meghan A
AU  - Pang, Lan
AU  - Hayes, Craig P
AU  - Yoo, Dae-Goon
AU  - Park, Jonathan J
AU  - Moskowitz, Samuel M
AU  - Malech, Harry L
AU  - Leto, Thomas L
AD  - Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America. radab@uga.edu
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 1
VL  - 8
IS  - 1
KW  - Reactive Oxygen Species
KW  - 0
KW  - Pyocyanine
KW  - 9OQM399341
KW  - NADPH Oxidase
KW  - EC 1.6.3.1
KW  - Index Medicus
KW  - Humans
KW  - Neutrophils -- metabolism
KW  - NADPH Oxidase -- metabolism
KW  - Reactive Oxygen Species -- metabolism
KW  - Pyocyanine -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273805213?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pyocyanin-enhanced+neutrophil+extracellular+trap+formation+requires+the+NADPH+oxidase.&rft.au=Rada%2C+Bal%C3%A1zs%3BJendrysik%2C+Meghan+A%3BPang%2C+Lan%3BHayes%2C+Craig+P%3BYoo%2C+Dae-Goon%3BPark%2C+Jonathan+J%3BMoskowitz%2C+Samuel+M%3BMalech%2C+Harry+L%3BLeto%2C+Thomas+L&rft.aulast=Rada&rft.aufirst=Bal%C3%A1zs&rft.date=2013-01-01&rft.volume=8&rft.issue=1&rft.spage=e54205&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0054205
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-08-02
N1  - Date created - 2013-01-23
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Med Microbiol Immunol. 2009 Nov;198(4):211-9 [19653000]
Trends Microbiol. 2009 Sep;17(9):406-13 [19726196]
Free Radic Biol Med. 2010 Mar 15;48(6):798-810 [20043988]
J Vis Exp. 2010;(36). pii: 1724. doi: 10.3791/1724 [20182410]
J Exp Med. 2010 Aug 30;207(9):1853-62 [20733033]
Nat Med. 2010 Sep;16(9):1018-23 [20818377]
Respirology. 2010 Oct;15(7):1037-56 [20723140]
Curr Top Microbiol Immunol. 2010;346:183-202 [20473789]
Future Microbiol. 2010 Nov;5(11):1663-74 [21133688]
N Engl J Med. 2010 Dec 30;363(27):2600-10 [21190454]
Nat Chem Biol. 2011 Feb;7(2):75-7 [21170021]
Cell Res. 2011 Feb;21(2):290-304 [21060338]
Mucosal Immunol. 2011 Mar;4(2):158-71 [20962773]
Sci Transl Med. 2011 Mar 9;3(73):73ra19 [21389263]
Sci Transl Med. 2011 Mar 9;3(73):73ra20 [21389264]
BMC Med. 2011;9:32 [21463524]
Leukemia. 2011 Jul;25(7):1064-79 [21436840]
PLoS One. 2011;6(9):e23637 [21909403]
J Biol Chem. 2011 Nov 25;286(47):40693-705 [21956105]
J Cyst Fibros. 2012 Mar;11(2):84-92 [21996135]
PLoS One. 2012;7(10):e46718 [23056420]
Nat Med. 2012 Sep;18(9):1386-93 [22922410]
Am J Respir Cell Mol Biol. 2012 Dec;47(6):738-45 [22865623]
J Immunol. 2002 Feb 15;168(4):1861-8 [11823520]
Clin Exp Rheumatol. 2003 Nov-Dec;21(6 Suppl 32):S95-100 [14740434]
Science. 2004 Mar 5;303(5663):1532-5 [15001782]
Infect Immun. 2004 Jul;72(7):4275-8 [15213173]
Blood. 2004 Nov 1;104(9):2947-53 [15251984]
Infect Immun. 1988 Sep;56(9):2515-7 [3137173]
Infect Immun. 1989 Sep;57(9):2591-6 [2547716]
Science. 1995 Aug 11;269(5225):847-50 [7543698]
Trends Mol Med. 2004 Dec;10(12):599-606 [15567330]
N Engl J Med. 2005 May 12;352(19):1992-2001 [15888700]
BioDrugs. 2005;19(3):135-44 [15984899]
Chest. 2006 May;129(5):1148-54 [16685004]
J Cell Biol. 2007 Jan 15;176(2):231-41 [17210947]
Curr Opin Microbiol. 2007 Feb;10(1):52-6 [17208512]
BMC Microbiol. 2007;7:45 [17521417]
Environ Sci Technol. 2008 Apr 1;42(7):2380-6 [18504969]
Contrib Microbiol. 2008;15:164-87 [18511861]
J Immunol. 2008 Oct 1;181(7):4883-93 [18802092]
J Cell Biol. 2009 Jan 26;184(2):205-13 [19153223]
Immunol Res. 2009;43(1-3):198-209 [18979077]
Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6226-31 [19339495]
Autophagy. 2009 Aug;5(6):887-9 [19550142]
Infect Immun. 2009 Dec;77(12):5300-10 [19805527]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1371/journal.pone.0054205
ER  - 



TY  - JOUR
T1  - Probing GPCR structure: adenosine and P2Y nucleotide receptors.
AN  - 1273775067; 23332701
AB  - The adenosine receptors (ARs) provide an example of how to accurately predict ligand recognition, even prior to the availability of a crystallographic structure. Homology modeling has been used to gain structural insight, in conjunction with site-directed mutagenesis, and structure-activity relationships of small molecular ligands. Recent X-ray structures greatly improved the accuracy of knowledge of AR ligand recognition and furthermore characterized conformational changes induced by receptor activation. Now, homology modeling extends these structural insights to related GPCRs and suggests new ligand structures. This strategy is also being applied to the eight subtypes of P2Y receptors for extracellular nucleotides, which lack X-ray structures and are best modeled by homology to the CXCR4 (peptide) receptor. Neoceptors, as studied for three of the four AR subtypes, create a molecular complementarity between a mutant receptor and a chemically tailored agonist ligand to selectively enhance affinity, implying direct physical contact and thus validating docking hypotheses. Copyright © 2013 Elsevier Inc. All rights reserved.
JF  - Methods in enzymology
AU  - Jacobson, Kenneth A
AU  - Costanzi, Stefano
AU  - Deflorian, Francesca
AD  - Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. kajacobs@helix.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 199
EP  - 217
VL  - 520
KW  - Purines
KW  - 0
KW  - Pyrimidines
KW  - Receptors, G-Protein-Coupled
KW  - Receptors, Purinergic P2Y
KW  - Adenosine
KW  - K72T3FS567
KW  - Index Medicus
KW  - Pyrimidines -- chemistry
KW  - Purines -- metabolism
KW  - Animals
KW  - Humans
KW  - Pyrimidines -- metabolism
KW  - Purines -- chemistry
KW  - Structure-Activity Relationship
KW  - Receptors, G-Protein-Coupled -- chemistry
KW  - Adenosine -- chemistry
KW  - Receptors, G-Protein-Coupled -- metabolism
KW  - Receptors, Purinergic P2Y -- metabolism
KW  - Receptors, Purinergic P2Y -- chemistry
KW  - Adenosine -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273775067?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+enzymology&rft.atitle=Probing+GPCR+structure%3A+adenosine+and+P2Y+nucleotide+receptors.&rft.au=Jacobson%2C+Kenneth+A%3BCostanzi%2C+Stefano%3BDeflorian%2C+Francesca&rft.aulast=Jacobson&rft.aufirst=Kenneth&rft.date=2013-01-01&rft.volume=520&rft.issue=&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Methods+in+enzymology&rft.issn=1557-7988&rft_id=info:doi/10.1016%2FB978-0-12-391861-1.00009-5
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-26
N1  - Date created - 2013-01-21
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Med Chem. 2005 Dec 29;48(26):8108-11 [16366591]
Med Res Rev. 2013 Mar;33(2):235-335 [22095687]
J Med Chem. 2006 Sep 7;49(18):5532-43 [16942026]
Pharmacol Rev. 2006 Sep;58(3):281-341 [16968944]
J Comput Aided Mol Des. 2006 Jul-Aug;20(7-8):417-26 [17016747]
Bioorg Med Chem Lett. 2007 Feb 1;17(3):761-6 [17088057]
J Mol Graph Model. 2007 Jan;25(5):740-54 [17095272]
Trends Pharmacol Sci. 2007 Mar;28(3):111-6 [17280720]
Biochemistry. 2007 Jun 26;46(25):7437-48 [17542617]
Biochem J. 2007 Jul 15;405(2):277-86 [17338680]
J Med Chem. 2008 Apr 10;51(7):2088-99 [18321038]
J Med Chem. 2008 May 22;51(10):2907-14 [18442228]
Nat Methods. 2008 Aug;5(8):673-8 [18668035]
Science. 2008 Nov 21;322(5905):1211-7 [18832607]
J Med Chem. 2009 May 14;52(9):2762-75 [19419204]
Biochem Pharmacol. 2009 Jul 1;78(1):11-20 [19447219]
Curr Opin Drug Discov Devel. 2010 May;13(3):317-25 [20443165]
J Med Chem. 2010 May 13;53(9):3748-55 [20405927]
Science. 2000 Aug 4;289(5480):739-45 [10926528]
J Med Chem. 2001 Nov 22;44(24):4125-36 [11708915]
J Med Chem. 2004 Oct 21;47(22):5393-404 [15481977]
Drug Des Discov. 1992;9(1):49-67 [1457698]
J Biol Chem. 1995 Mar 3;270(9):4185-8 [7876172]
J Biol Chem. 1995 Jun 9;270(23):13987-97 [7775460]
Drug Des Discov. 1995 Nov;13(2):133-54 [8872457]
J Med Chem. 1998 Apr 23;41(9):1456-66 [9554879]
Chem Biol. 2005 Feb;12(2):237-47 [15734651]
Bioorg Med Chem. 2010 Nov 15;18(22):7923-30 [20943397]
Science. 2010 Nov 19;330(6007):1066-71 [20929726]
Bioconjug Chem. 2009 Oct 21;20(10):1816-35 [19405524]
Science. 2011 Apr 15;332(6027):322-7 [21393508]
J Comput Aided Mol Des. 2011 Apr;25(4):329-38 [21461952]
J Med Chem. 2011 Jun 23;54(12):4018-33 [21528910]
Nature. 2011 Jun 23;474(7352):521-5 [21593763]
J Med Chem. 2011 Jul 14;54(13):4312-23 [21661720]
Structure. 2011 Sep 7;19(9):1283-93 [21885291]
Trends Pharmacol Sci. 2011 Nov;32(11):637-43 [21903279]
Expert Opin Investig Drugs. 2011 Dec;20(12):1591-609 [22017198]
ChemMedChem. 2011 Dec 9;6(12):2302-11 [22021213]
J Med Chem. 2012 Jan 12;55(1):538-52 [22104008]
J Med Chem. 2006 May 4;49(9):2689-702 [16640329]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/B978-0-12-391861-1.00009-5
ER  - 



TY  - JOUR
T1  - Charged-coupled device (CCD) detectors for Lab-on-a Chip (LOC) optical analysis.
AN  - 1273661022; 23329454
AB  - A critical element of any Lab-on-a-Chip (LOC) is a detector; among the many detection approaches, optical detection is very widely used for biodetection. One challenge for advancing the development of LOC for biodetection has been to enhance the portability and lower the cost for Point-of-Care diagnostics, which has the potential to enhance the quality of healthcare delivery for underserved populations and for global health. We describe a simple and relatively low cost charged-coupled device (CCD)-based detector that can be integrated with a conventional microtiter plate or a portable LOC assay for various optical detection modalities including fluorescence, chemiluminescence, densitometry, and colorimetric assays. In general, the portable battery-operated CCD-based detection system consists of four modules: (1) a cooled CCD digital camera to monitor light emission, (2) a LOC or microtiter plate to perform assays, (3) a light source to illuminate the assay (such as electroluminescence (EL) or light emitting diode (LED)), and (4) a portable computer to acquire and analyze images. The configuration of the fluorescence detector presented here was designed to measure fluorogenic excitation at 490 nm and to monitor emission at 523 nm used for FITC detection.The LOC used for this detection system was fabricated with laminated object manufacturing (LOM) technology, and was designed to detection activity of botulinum neurotoxin serotype A (BoNT-A) using a fluorogenic peptide substrate (SNAP-25) for botulinum neurotoxin serotype A (BoNT-A) labeled with FITC. The limit of detection (LOD) for the CCD detector is 0.5 nM (25 ng/ml). The portable system is small and is powered by a 12 V source. The modular detector was designed with easily interchangeable LEDs, ELs, filters, lenses, and LOC, and can be used and adapted for a wide variety of densitometry, florescence and colorimetric assays.
JF  - Methods in molecular biology (Clifton, N.J.)
AU  - Rasooly, Avraham
AU  - Kostov, Yordan
AU  - Bruck, Hugh A
AD  - Division of Biology, Office of Science and Engineering, FDA Center for Devices and Radiological Health (CDRH), Silver Spring, MD, USA. rasoolya@mail.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 365
EP  - 385
VL  - 949
KW  - Botulinum Toxins, Type A
KW  - EC 3.4.24.69
KW  - Index Medicus
KW  - Equipment Design
KW  - Spectrometry, Fluorescence
KW  - Botulinum Toxins, Type A -- analysis
KW  - Image Processing, Computer-Assisted
KW  - Botulinum Toxins, Type A -- chemistry
KW  - Electrical Equipment and Supplies
KW  - Optical Phenomena
KW  - Lab-On-A-Chip Devices
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273661022?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Charged-coupled+device+%28CCD%29+detectors+for+Lab-on-a+Chip+%28LOC%29+optical+analysis.&rft.au=Rasooly%2C+Avraham%3BKostov%2C+Yordan%3BBruck%2C+Hugh+A&rft.aulast=Rasooly&rft.aufirst=Avraham&rft.date=2013-01-01&rft.volume=949&rft.issue=&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-62703-134-9_23
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-26
N1  - Date created - 2013-01-18
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/978-1-62703-134-9_23
ER  - 



TY  - JOUR
T1  - Neem leaf glycoprotein is nontoxic to physiological functions of Swiss mice and Sprague Dawley rats: histological, biochemical and immunological perspectives.
AN  - 1273582794; 23178577
AB  - We have evaluated the toxicity profile of a unique immunomodulator, neem leaf glycoprotein (NLGP) on different physiological systems of Swiss mice and Sprague Dawley rats. NLGP injection, even in higher doses than effective concentration caused no behavioral changes in animals and no death. NLGP injection increased the body weights of mice slightly without any change in organ weights. NLGP showed no adverse effect on the hematological system. Moreover, little hematostimulation was noticed, as evidenced by increased hemoglobin content, leukocyte count and lymphocyte numbers. Histological assessment of different organs revealed no alterations in the organ microstructure of the NLGP treated mice and rats. Histological normalcy of liver and kidney was further confirmed by the assessment of liver enzymes like alkaline phosphatase, SGOT, SGPT and nephrological products like urea and creatinine. NLGP has no apoptotic effect on immune cells but induces proliferation of mononuclear cells collected from mice and rats. Number of CD4(+), CD8(+) T cells, DX5(+) NK cells, CD11b(+) macrophages and CD11c(+) dendritic cells is upregulated by NLGP without a significant change in CD4(+)CD25(+)Foxp3(+) regulatory T cells. Type 1 cytokines, like IFNγ also increased in serum with a decrease in type 2 cytokines. Total IgG content, especially IgG2a increased in NLGP treated mice. These type 1 directed changes help to create an anti-tumor immune environment that results in the restriction of carcinoma growth in mice. Accumulated evidence strongly suggests the non-toxic nature of NLGP. Thus, it can be recommended for human use in anti-cancer therapy.
          Copyright © 2012 Elsevier B.V. All rights reserved.
JF  - International immunopharmacology
AU  - Mallick, Atanu
AU  - Ghosh, Sarbari
AU  - Banerjee, Saptak
AU  - Majumder, Sayantani
AU  - Das, Arnab
AU  - Mondal, Bipasha
AU  - Barik, Subhasis
AU  - Goswami, Kuntal K
AU  - Pal, Smarajit
AU  - Laskar, Subrata
AU  - Sarkar, Koustav
AU  - Bose, Anamika
AU  - Baral, Rathindranath
AD  - Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute, 37 S. P. Mukherjee Road, Kolkata, India.
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 73
EP  - 83
VL  - 15
IS  - 1
KW  - Antineoplastic Agents
KW  - 0
KW  - Cytokines
KW  - Glycoproteins
KW  - Immunoglobulins
KW  - Immunologic Factors
KW  - Urea
KW  - 8W8T17847W
KW  - Creatinine
KW  - AYI8EX34EU
KW  - Aspartate Aminotransferases
KW  - EC 2.6.1.1
KW  - Alanine Transaminase
KW  - EC 2.6.1.2
KW  - Alkaline Phosphatase
KW  - EC 3.1.3.1
KW  - Index Medicus
KW  - Animals
KW  - Liver -- anatomy & histology
KW  - Phytotherapy
KW  - Cytokines -- immunology
KW  - Carcinoma, Ehrlich Tumor -- drug therapy
KW  - Creatinine -- blood
KW  - Rats
KW  - Tumor Burden -- drug effects
KW  - Liver -- drug effects
KW  - Apoptosis -- drug effects
KW  - Immunoglobulins -- immunology
KW  - Lymphocytes -- cytology
KW  - Lymphocytes -- drug effects
KW  - Urea -- blood
KW  - Cell Proliferation -- drug effects
KW  - Spleen -- cytology
KW  - Carcinoma, Ehrlich Tumor -- pathology
KW  - Kidney -- drug effects
KW  - Mice
KW  - Alkaline Phosphatase -- blood
KW  - Aspartate Aminotransferases -- blood
KW  - Alanine Transaminase -- blood
KW  - Rats, Sprague-Dawley
KW  - Plant Leaves
KW  - Female
KW  - Kidney -- anatomy & histology
KW  - Glycoproteins -- pharmacology
KW  - Azadirachta
KW  - Immunologic Factors -- therapeutic use
KW  - Immunologic Factors -- pharmacology
KW  - Antineoplastic Agents -- therapeutic use
KW  - Antineoplastic Agents -- pharmacology
KW  - Glycoproteins -- therapeutic use
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273582794?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neem+leaf+glycoprotein+is+nontoxic+to+physiological+functions+of+Swiss+mice+and+Sprague+Dawley+rats%3A+histological%2C+biochemical+and+immunological+perspectives.&rft.au=Mallick%2C+Atanu%3BGhosh%2C+Sarbari%3BBanerjee%2C+Saptak%3BMajumder%2C+Sayantani%3BDas%2C+Arnab%3BMondal%2C+Bipasha%3BBarik%2C+Subhasis%3BGoswami%2C+Kuntal+K%3BPal%2C+Smarajit%3BLaskar%2C+Subrata%3BSarkar%2C+Koustav%3BBose%2C+Anamika%3BBaral%2C+Rathindranath&rft.aulast=Mallick&rft.aufirst=Atanu&rft.date=2013-01-01&rft.volume=15&rft.issue=1&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=International+immunopharmacology&rft.issn=1878-1705&rft_id=info:doi/10.1016%2Fj.intimp.2012.11.006
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-24
N1  - Date created - 2013-01-16
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.intimp.2012.11.006
ER  - 



TY  - JOUR
T1  - A recombinant immunotoxin against the tumor-associated antigen mesothelin reengineered for high activity, low off-target toxicity, and reduced antigenicity.
AN  - 1273543933; 23136186
AB  - SS1P is a recombinant immunotoxin (RIT) engineered for the targeted elimination of malignant cells that express the tumor-associated antigen mesothelin. It is composed of an antimesothelin antibody variable fragment (Fv) linked to a cytotoxic fragment of Pseudomonas exotoxin A (PE) that includes domains II and III of native PE. The clinical use of SS1P is limited by its propensity to induce neutralizing antibodies and to cause a dose-limiting capillary leak syndrome (CLS) in patients. In this article, we describe a reengineered SS1P with improved properties that overcome these deficits. The redesign of SS1P consists of (i) removing the bulk of PE domain II (residues 251-273 and 284-394 of native PE), leaving only an 11-residue furin cleavage site, (ii) adding a Gly-Gly-Ser peptide linker after the furin cleavage site, and (iii) replacing eight highly solvent-exposed residues in the catalytic domain of PE. The new molecule, SS1-LR/GGS/8M, has cytotoxic activity comparable with SS1P on several mesothelin-expressing cell lines and remarkably improved activity on primary cells from patients with mesothelioma. In a mouse xenograft tumor model, high doses of SS1-LR/GGS/8M elicit antitumor activity superior to the activity of SS1P at its maximum-tolerated dose. In addition, SS1-LR/GGS/8M has greatly decreased ability to cause CLS in a rat model and reduced antigenicity or reactivity with antibodies to the sera of patients previously treated with SS1P.
JF  - Molecular cancer therapeutics
AU  - Weldon, John E
AU  - Xiang, Laiman
AU  - Zhang, Jingli
AU  - Beers, Richard
AU  - Walker, Dawn A
AU  - Onda, Masanori
AU  - Hassan, Raffit
AU  - Pastan, Ira
AD  - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 48
EP  - 57
VL  - 12
IS  - 1
KW  - Antigens, Neoplasm
KW  - 0
KW  - Antineoplastic Agents
KW  - GPI-Linked Proteins
KW  - Recombinant Fusion Proteins
KW  - SS1-LR-GGS-8M immunotoxin
KW  - mesothelin
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Capillary Leak Syndrome -- chemically induced
KW  - Cell Line, Tumor
KW  - Mice
KW  - Mice, Nude
KW  - Rats
KW  - Mutagenesis, Site-Directed
KW  - Half-Life
KW  - Tumor Burden -- drug effects
KW  - Rats, Wistar
KW  - Xenograft Model Antitumor Assays
KW  - Inhibitory Concentration 50
KW  - Maximum Tolerated Dose
KW  - Amino Acid Substitution
KW  - Female
KW  - Mesothelioma -- drug therapy
KW  - Antineoplastic Agents -- immunology
KW  - Recombinant Fusion Proteins -- adverse effects
KW  - GPI-Linked Proteins -- metabolism
KW  - Recombinant Fusion Proteins -- immunology
KW  - Recombinant Fusion Proteins -- genetics
KW  - Recombinant Fusion Proteins -- pharmacology
KW  - Mesothelioma -- pathology
KW  - Antineoplastic Agents -- pharmacology
KW  - GPI-Linked Proteins -- immunology
KW  - Antineoplastic Agents -- adverse effects
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273543933?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+recombinant+immunotoxin+against+the+tumor-associated+antigen+mesothelin+reengineered+for+high+activity%2C+low+off-target+toxicity%2C+and+reduced+antigenicity.&rft.au=Weldon%2C+John+E%3BXiang%2C+Laiman%3BZhang%2C+Jingli%3BBeers%2C+Richard%3BWalker%2C+Dawn+A%3BOnda%2C+Masanori%3BHassan%2C+Raffit%3BPastan%2C+Ira&rft.aulast=Weldon&rft.aufirst=John&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-12-0336
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-27
N1  - Date created - 2013-01-15
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
J Immunol. 2000 Dec 15;165(12):7150-6 [11120846]
Int J Cancer. 2001 Jun 15;92(6):861-70 [11351308]
J Mol Biol. 2001 Dec 7;314(4):823-37 [11734000]
Clin Cancer Res. 2002 Apr;8(4):995-1002 [11948105]
Nat Rev Mol Cell Biol. 2002 Oct;3(10):753-66 [12360192]
Hum Pathol. 2003 Jun;34(6):605-9 [12827615]
Nat Biotechnol. 1999 Jun;17(6):568-72 [10385321]
Clin Cancer Res. 2005 Feb 15;11(4):1545-50 [15746059]
Clin Cancer Res. 2005 May 15;11(10):3814-20 [15897581]
Gene Ther. 2005 Sep;12(18):1360-8 [15902276]
J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911]
J Immunol. 2006 Dec 15;177(12):8822-34 [17142785]
J Immunother. 2007 Sep;30(6):607-13 [17667524]
Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569]
J Clin Invest. 2007 Nov;117(11):3489-97 [17948127]
J Biol Chem. 1997 Dec 12;272(50):31707-11 [9395513]
Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):669-74 [9435250]
Cancer Res. 1998 Mar 1;58(5):968-75 [9500458]
Bioconjug Chem. 1998 Nov-Dec;9(6):736-43 [9815167]
Clin Cancer Res. 1996 Feb;2(2):245-52 [9816166]
Clin Cancer Res. 1997 Mar;3(3):339-45 [9815690]
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3957-62 [10097145]
Neuro Oncol. 2008 Jun;10(3):320-9 [18403491]
Blood. 2009 Apr 16;113(16):3792-800 [18988862]
Infect Immun. 2009 Jul;77(7):3090-9 [19380469]
J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673]
Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873]
Cancer Res. 2010 Feb 1;70(3):1082-9 [20103626]
Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554]
J Immunother. 2010 Apr;33(3):297-304 [20445350]
Ann Intern Med. 2010 Jul 20;153(2):90-8 [20643990]
J Immunol. 2011 Feb 1;186(3):1554-63 [21178016]
PLoS One. 2011;6(1):e14640 [21305058]
Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054]
Bioconjug Chem. 2011 Apr 20;22(4):736-40 [21410247]
FEBS J. 2011 Dec;278(23):4683-700 [21585657]
J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053]
Biochim Biophys Acta. 2012 Aug;1821(8):1050-8 [22265715]
Methods Mol Biol. 2004;248:503-18 [14970517]
Blood. 2004 Apr 1;103(7):2718-26 [14525789]
Am J Physiol. 1978 Jun;234(6):F455-60 [665772]
J Biol Chem. 1991 Sep 15;266(26):17376-81 [1910044]
J Biol Chem. 1993 Feb 5;268(4):2590-4 [8381410]
Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9514-8 [7937798]
Biochem J. 1995 Apr 1;307 ( Pt 1):29-37 [7717988]
Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):136-40 [8552591]
Nat Med. 1996 Mar;2(3):350-3 [8612238]
Semin Cancer Biol. 1996 Apr;7(2):87-95 [8740564]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1158/1535-7163.MCT-12-0336
ER  - 



TY  - JOUR
T1  - Both mucosal and cutaneous papillomaviruses are in the oral cavity but only alpha genus seems to be associated with cancer.
AN  - 1273449441; 23092620
AB  - Human papillomaviruses are associated with invasive cancers in the cervical, anogenital, and oropharyngeal areas. Persistent HPV infections, particularly with high-risk HPV such as HPV 16, are involved in the carcinogenesis of a subset of oropharyngeal cancers. The majority of published studies on HPV prevalence in these tumors concentrated on identifying high-risk mucosal types.
          To determine the HPV type specific prevalence in different samples collected from the oral cavity of three groups of patients: (A) healthy (n=25); (B) non-malignant lesions (n=47); and (C) cancers (n=78). To evaluate the prevalence of HPV genotypes in the oral cavity, samples were analyzed by PCR with: MY09/MY11 followed by GP5+/GP6+, CP65/CP70 followed by CP66/CP69, and FAP59/FAP64 primers. The presence of viral transcripts was ascertained by RT-PCR with specific primers for the E7 region.
          Mucosal HPV types were associated with the presence of cancers. This trend was statistically significant if the analysis was performed for HPV 16 (p=0.04), which is the most prevalent type detected in oropharyngeal cancers. Conversely, cutaneous HPVs were associated with non-malignant lesions (p=0.007). The multiple correspondence analysis confirmed these data. Viral transcripts of only mucosal HPVs were detected in non-malignant lesions and cancers. Different types of HPVs infect the oral epithelium, but only the mucosal types, particularly HPV 16, are clearly associated with tumors. The discovery that cutaneous HPVs are associated with potential malignant oral disorders brings other data to understand the significance of their presence in the oral cavity.
          Copyright © 2012 Elsevier B.V. All rights reserved.
JF  - Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
AU  - Paolini, Francesca
AU  - Rizzo, Consuelo
AU  - Sperduti, Isabella
AU  - Pichi, Barbara
AU  - Mafera, Barbara
AU  - Rahimi, Siavash S
AU  - Vigili, Maurizio G
AU  - Venuti, Aldo
AD  - Laboratory of Virology, Regina Elena National Cancer Institute, Rome, Italy.
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 72
EP  - 76
VL  - 56
IS  - 1
KW  - DNA Primers
KW  - 0
KW  - DNA, Viral
KW  - Index Medicus
KW  - Genotype
KW  - Young Adult
KW  - Polymerase Chain Reaction
KW  - DNA Primers -- genetics
KW  - Aged, 80 and over
KW  - Humans
KW  - Adult
KW  - Aged
KW  - Middle Aged
KW  - DNA, Viral -- genetics
KW  - Male
KW  - Female
KW  - Papillomaviridae -- pathogenicity
KW  - Oropharyngeal Neoplasms -- virology
KW  - Mouth -- virology
KW  - Papillomaviridae -- classification
KW  - Papillomaviridae -- isolation & purification
KW  - Papillomaviridae -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273449441?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+virology+%3A+the+official+publication+of+the+Pan+American+Society+for+Clinical+Virology&rft.atitle=Both+mucosal+and+cutaneous+papillomaviruses+are+in+the+oral+cavity+but+only+alpha+genus+seems+to+be+associated+with+cancer.&rft.au=Paolini%2C+Francesca%3BRizzo%2C+Consuelo%3BSperduti%2C+Isabella%3BPichi%2C+Barbara%3BMafera%2C+Barbara%3BRahimi%2C+Siavash+S%3BVigili%2C+Maurizio+G%3BVenuti%2C+Aldo&rft.aulast=Paolini&rft.aufirst=Francesca&rft.date=2013-01-01&rft.volume=56&rft.issue=1&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+virology+%3A+the+official+publication+of+the+Pan+American+Society+for+Clinical+Virology&rft.issn=1873-5967&rft_id=info:doi/10.1016%2Fj.jcv.2012.09.016
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-05-29
N1  - Date created - 2012-12-24
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.jcv.2012.09.016
ER  - 



TY  - JOUR
T1  - Reactivation of the silenced thyroid hormone receptor β gene expression delays thyroid tumor progression.
AN  - 1273431196; 23183175
AB  - That a knock-in mouse harboring a dominant-negative thyroid hormone receptor (TR)-β (Thrb) mutation develops metastatic thyroid cancer strongly suggests the involvement of TRβ in carcinogenesis. Epigenetic silencing of the THRB gene is common in human cancers. The aim of the present study was to determine how DNA methylation affected the expression of the THRB gene in differentiated thyroid cancer (DTC) and how reexpression of the THRB gene attenuated the cancer phenotypes. We used methylation-specific PCR to examine the expression and promoter methylation of the THRB gene in DTC tissues. Thyroid cancer cells with hypermethylated THRB were treated with the demethylating agents 5'-aza-2'-deoxycytidine (5'-aza-CdR) and zebularine to evaluate their impact on the cancer cell phenotypes. THRB mRNA expression in DTC was 90% lower than in normal controls, and this decrease was associated with a higher tumor/lymph node staging. The promoter methylation level of the THRB gene had a significant negative correlation with the expression level of the THRB gene. Treatment of FTC-236 cells with 5'-aza-CdR or zebularine induced reexpression of the THRB gene and inhibited cell proliferation and migration. FTC-236 cells stably expressing TRβ exhibited lower cell proliferation and migration through inhibition of β-catenin signaling pathways compared with FTC-236 without TRβ. 5'-Aza-CdR also led to suppression of tumor growth in an in vivo xenograft model using FTC-236 cells consistent with the cell-based studies. These finding indicate that TRβ is a tumor suppressor and could be tested as a potential therapeutic target.
JF  - Endocrinology
AU  - Kim, Won Gu
AU  - Zhu, Xuguang
AU  - Kim, Dong Wook
AU  - Zhang, Lisa
AU  - Kebebew, Electron
AU  - Cheng, Sheue-Yann
AD  - Laboratory of Molecular Biology, National Cancer Institute, 37 Convent Drive, Room 5128, Bethesda, MD 20892-4264, USA.
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 25
EP  - 35
VL  - 154
IS  - 1
KW  - Thyroid Hormone Receptors beta
KW  - 0
KW  - Cytidine
KW  - 5CSZ8459RP
KW  - pyrimidin-2-one beta-ribofuranoside
KW  - 7A9Y5SX0GY
KW  - Abridged Index Medicus
KW  - Index Medicus
KW  - Cell Proliferation -- drug effects
KW  - Animals
KW  - Humans
KW  - Mice, Nude
KW  - Mice
KW  - DNA Methylation -- genetics
KW  - Reverse Transcriptase Polymerase Chain Reaction
KW  - Cytidine -- analogs & derivatives
KW  - Blotting, Western
KW  - DNA Methylation -- drug effects
KW  - Cell Movement -- drug effects
KW  - Cytidine -- pharmacology
KW  - Xenograft Model Antitumor Assays
KW  - Immunohistochemistry
KW  - Cell Line
KW  - Male
KW  - Thyroid Hormone Receptors beta -- metabolism
KW  - Thyroid Neoplasms -- genetics
KW  - Thyroid Neoplasms -- metabolism
KW  - Thyroid Neoplasms -- pathology
KW  - Thyroid Hormone Receptors beta -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273431196?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reactivation+of+the+silenced+thyroid+hormone+receptor+%CE%B2+gene+expression+delays+thyroid+tumor+progression.&rft.au=Kim%2C+Won+Gu%3BZhu%2C+Xuguang%3BKim%2C+Dong+Wook%3BZhang%2C+Lisa%3BKebebew%2C+Electron%3BCheng%2C+Sheue-Yann&rft.aulast=Kim&rft.aufirst=Won&rft.date=2013-01-01&rft.volume=154&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/10.1210%2Fen.2012-1728
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-02-22
N1  - Date created - 2012-12-25
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Mol Cell Biol. 2001 Oct;21(20):6782-95 [11564863]
Physiol Rev. 2001 Jul;81(3):1097-142 [11427693]
Carcinogenesis. 2002 Jan;23(1):25-33 [11756220]
Cancer Res. 2002 Apr 1;62(7):1939-43 [11929806]
Oncogene. 2002 Jun 20;21(27):4307-16 [12082618]
J Mol Biol. 2002 Aug 23;321(4):591-9 [12206775]
Cancer Cell. 2004 Aug;6(2):151-8 [15324698]
Cancer Res. 1986 Sep;46(9):4831-6 [2425959]
Biochem Biophys Res Commun. 1995 May 16;210(2):464-71 [7538760]
Cancer Res. 1999 Apr 15;59(8):1811-5 [10213482]
Mol Carcinog. 1999 Sep;26(1):53-61 [10487522]
Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836]
Thyroid. 2005 Oct;15(10):1137-46 [16279847]
Int J Cancer. 2006 Apr 1;118(7):1653-9 [16231318]
Nat Rev Cancer. 2006 Apr;6(4):292-306 [16557281]
J Clin Invest. 2006 Nov;116(11):2972-84 [17039256]
Curr Opin Genet Dev. 2007 Feb;17(1):45-51 [17208432]
J Cell Physiol. 2007 Aug;212(2):330-44 [17458893]
J Clin Endocrinol Metab. 2007 Dec;92(12):4766-70 [17911173]
Mol Cell Biol. 2008 Jul;28(14):4598-608 [18474620]
J Endocrinol Invest. 2008 Aug;31(8):724-30 [18852534]
Epigenetics. 2009 Apr 1;4(3):185-93 [19430199]
Cancer Causes Control. 2009 Jul;20(5):525-31 [19016336]
Mol Cell Endocrinol. 2009 Aug 13;307(1-2):142-8 [19524134]
Lab Invest. 2009 Jul;89(7):791-9 [19506552]
Cancer Genet Cytogenet. 2010 Jan 15;196(2):140-5 [20082849]
Cancer Res. 2010 Feb 15;70(4):1389-97 [20124489]
Oncogene. 2010 Apr 1;29(13):1909-19 [20062085]
Endocr Rev. 2010 Apr;31(2):139-70 [20051527]
Ann Surg Oncol. 2010 Aug;17(8):2222-8 [20155399]
Trends Pharmacol Sci. 2010 Nov;31(11):536-46 [20846732]
J Clin Endocrinol Metab. 2011 Mar;96(3):E546-53 [21159845]
J Mol Endocrinol. 2011 Jun;46(3):R73-81 [21325372]
Clin Cancer Res. 2012 Mar 1;18(5):1281-90 [22271876]
Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13209-14 [11069286]
J Clin Endocrinol Metab. 2001 Nov;86(11):5572-6 [11701737]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1210/en.2012-1728
ER  - 



TY  - JOUR
T1  - Implications of global climate change for the assessment and management of human health risks of chemicals in the natural environment.
AN  - 1273256168; 23147420
AB  - Global climate change (GCC) is likely to alter the degree of human exposure to pollutants and the response of human populations to these exposures, meaning that risks of pollutants could change in the future. The present study, therefore, explores how GCC might affect the different steps in the pathway from a chemical source in the environment through to impacts on human health and evaluates the implications for existing risk-assessment and management practices. In certain parts of the world, GCC is predicted to increase the level of exposure of many environmental pollutants due to direct and indirect effects on the use patterns and transport and fate of chemicals. Changes in human behavior will also affect how humans come into contact with contaminated air, water, and food. Dietary changes, psychosocial stress, and coexposure to stressors such as high temperatures are likely to increase the vulnerability of humans to chemicals. These changes are likely to have significant implications for current practices for chemical assessment. Assumptions used in current exposure-assessment models may no longer apply, and existing monitoring methods may not be robust enough to detect adverse episodic changes in exposures. Organizations responsible for the assessment and management of health risks of chemicals therefore need to be more proactive and consider the implications of GCC for their procedures and processes.
          Copyright © 2012 SETAC.
JF  - Environmental toxicology and chemistry
AU  - Balbus, John M
AU  - Boxall, Alistair B A
AU  - Fenske, Richard A
AU  - McKone, Thomas E
AU  - Zeise, Lauren
AD  - National Institute of Environmental Health Sciences, Bethesda, MD, USA. john.balbus@nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 62
EP  - 78
VL  - 32
IS  - 1
KW  - Environmental Pollutants
KW  - 0
KW  - Index Medicus
KW  - Environment
KW  - Risk
KW  - Environmental Exposure -- statistics & numerical data
KW  - Humans
KW  - Climate
KW  - Models, Chemical
KW  - Risk Assessment
KW  - Environmental Pollutants -- toxicity
KW  - Climate Change
KW  - Environmental Pollutants -- analysis
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273256168?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology+and+chemistry&rft.atitle=Implications+of+global+climate+change+for+the+assessment+and+management+of+human+health+risks+of+chemicals+in+the+natural+environment.&rft.au=Balbus%2C+John+M%3BBoxall%2C+Alistair+B+A%3BFenske%2C+Richard+A%3BMcKone%2C+Thomas+E%3BZeise%2C+Lauren&rft.aulast=Balbus&rft.aufirst=John&rft.date=2013-01-01&rft.volume=32&rft.issue=1&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Environmental+toxicology+and+chemistry&rft.issn=1552-8618&rft_id=info:doi/10.1002%2Fetc.2046
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-23
N1  - Date created - 2012-12-20
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Exp Allergy. 2005 Sep;35(9):1113-24 [16164436]
Environ Sci Technol. 2005 Sep 1;39(17):6749-56 [16190235]
Environ Sci Technol. 2005 Dec 1;39(23):9033-8 [16382922]
Environ Health Perspect. 2006 Jan;114(1):A32-9 [16393645]
Toxicol Rev. 2005;24(4):271-8 [16499408]
Trends Microbiol. 2006 Apr;14(4):176-82 [16537105]
Sci Total Environ. 2006 Oct 1;369(1-3):163-77 [16914182]
Environ Health Perspect. 2006 Sep;114(9):1344-7 [16966086]
Int J Biometeorol. 2006 Nov;51(2):87-96 [16967305]
Bull World Health Organ. 2006 Dec;84(12):984-90 [17242835]
Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4248-51 [21368130]
Res Rep Health Eff Inst. 2010 Nov;(154):91-217 [21446212]
Am Psychol. 2011 May-Jun;66(4):265-76 [21553952]
J Environ Monit. 2011 Jun;13(6):1532-46 [21509380]
ISME J. 2011 Aug;5(8):1253-61 [21368907]
J Environ Monit. 2011 Oct;13(10):2728-34 [21869984]
Risk Anal. 2012 Jan;32(1):81-95 [21627672]
BMJ. 2000 Sep 16;321(7262):670-3 [10987770]
Am J Epidemiol. 2002 Jan 1;155(1):80-7 [11772788]
IARC Monogr Eval Carcinog Risks Hum. 2002;82:1-556 [12687954]
Chemosphere. 2007 Apr;67(7):1287-95 [17258268]
Arch Environ Occup Health. 2006 Jan-Feb;61(1):43-4; author reply 45-6 [17503620]
Environ Health Perspect. 2007 Aug;115(8):1140-6 [17687439]
Environ Res. 2007 Sep;105(1):87-100 [16930588]
Environ Res. 2007 Sep;105(1):67-86 [17451673]
Soc Sci Med. 2007 Oct;65(8):1792-806 [17658674]
Inhal Toxicol. 2007 Sep;19(12):1033-9 [17917919]
Environ Res. 2007 Nov;105(3):414-29 [17692309]
Environ Sci Technol. 2007 Sep 1;41(17):5967-72 [17937268]
Environ Sci Technol. 2007 Sep 1;41(17):5986-92 [17937271]
Int J Food Microbiol. 2007 Oct 20;119(1-2):109-15 [17881074]
Mar Pollut Bull. 2007 Dec;54(12):1845-56 [17963794]
Occup Environ Med. 2008 Apr;65(4):255-60 [17890300]
Environ Int. 2008 May;34(4):451-8 [17997483]
Am J Epidemiol. 2008 Jun 15;167(12):1476-85 [18408228]
Environ Health. 2008;7:41 [18671873]
Clin Exp Allergy. 2008 Aug;38(8):1264-74 [18537982]
Am J Ind Med. 2008 Dec;51(12):883-98 [18666136]
Environ Health Perspect. 2008 Nov;116(11):1449-55 [19057695]
Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):2077-82 [19188587]
Environ Int. 2009 Apr;35(3):647-54 [19110310]
Food Chem Toxicol. 2009 May;47(5):1009-21 [19353812]
Environ Health Perspect. 2009 Apr;117(4):508-14 [19440487]
Environ Int. 2009 Aug;35(6):971-86 [19375165]
Rev Environ Contam Toxicol. 2009;200:33-52 [19680610]
Environ Sci Technol. 2009 Aug 1;43(15):5818-24 [19731682]
Integr Environ Assess Manag. 2009 Oct;5(4):662-79 [19552503]
Lancet. 2009 Dec 5;374(9705):1917-29 [19942273]
Lancet. 2009 Dec 12;374(9706):2006-15 [19942282]
EXS. 2010;100:31-63 [20358681]
J Investig Allergol Clin Immunol. 2010;20(2):95-102; quiz following 102 [20461963]
Environ Health Perspect. 2010 Jun;118(6):847-55 [20519161]
Allergy. 2010 Sep;65(9):1073-81 [20560904]
Int J Environ Res Public Health. 2010 Aug;7(8):3006-21 [20948943]
J Occup Environ Med. 2010 Nov;52(11):1098-105 [21063187]
J Environ Monit. 2010 Dec;12(12):2252-8 [20941435]
Mt Sinai J Med. 2011 Jan-Feb;78(1):78-84 [21259264]
Photochem Photobiol Sci. 2011 Feb;10(2):280-91 [21253665]
Annu Rev Physiol. 2011;73:135-62 [21054169]
Environ Health Perspect. 2012 Jun;120(6):831-9 [22418651]
Environ Health Perspect. 2012 Nov;120(11):1520-6 [23124134]
Environ Toxicol Chem. 2013 Jan;32(1):93-101 [23097077]
Environ Toxicol Chem. 2013 Jan;32(1):13-9 [23097130]
Environ Toxicol Chem. 2013 Jan;32(1):32-48 [23136056]
Environ Toxicol Chem. 2013 Jan;32(1):20-31 [23136071]
Environ Toxicol Chem. 2013 Jan;32(1):49-61 [23147390]
Environ Toxicol Chem. 2013 Jan;32(1):79-92 [23161373]
Environ Res. 2003 May;92(1):1-7 [12706749]
Environ Res. 2003 May;92(1):48-53 [12706754]
Br Med Bull. 2003;68:199-208 [14757718]
Anal Bioanal Chem. 2004 Mar;378(5):1152-60 [14673562]
Toxicol Appl Pharmacol. 2005 Mar 15;203(3):273-89 [15737681]
Environ Health Perspect. 2005 May;113(5):521-6 [15866757]
Inhal Toxicol. 2005 Jun-Jul;17(7-8):343-53 [16020033]
Chem Res Toxicol. 2005 Aug;18(8):1253-61 [16097798]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/etc.2046
ER  - 



TY  - JOUR
T1  - Moderate alcohol consumption and breast cancer in women: from epidemiology to mechanisms and interventions.
AN  - 1273255602; 23072454
AB  - Epidemiologic studies indicate that moderate alcohol consumption increases breast cancer risk in women. Understanding the mechanistic basis of this relationship has important implications for women's health and breast cancer prevention. In this commentary, we focus on some recent epidemiologic studies linking moderate alcohol consumption to breast cancer risk and place the results of those studies within the framework of our current understanding of the temporal and mechanistic basis of human carcinogenesis. This analysis supports the hypothesis that alcohol acts as a weak cumulative breast carcinogen and may also be a tumor promoter. We discuss the implications of these mechanisms for the prevention and treatment of alcohol-related breast cancer and present some considerations for future studies. Moderate alcohol consumption has been shown to benefit cardiovascular health and recently been associated with healthy aging. Therefore, a better understanding of how moderate alcohol consumption impacts breast cancer risk will allow women to make better informed decisions about the risks and benefits of alcohol consumption in the context of their overall health and at different stages of their life. Such mechanistic information is also important for the development of rational clinical interventions to reduce ethanol-related breast cancer mortality.
          Copyright © 2012 by the Research Society on Alcoholism.
JF  - Alcoholism, clinical and experimental research
AU  - Brooks, Philip J
AU  - Zakhari, Samir
AD  - Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892-9304, USA. pjbrooks@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 23
EP  - 30
VL  - 37
IS  - 1
KW  - Carcinogens
KW  - 0
KW  - Central Nervous System Depressants
KW  - Ethanol
KW  - 3K9958V90M
KW  - Index Medicus
KW  - Central Nervous System Depressants -- adverse effects
KW  - Humans
KW  - Female
KW  - Ethanol -- adverse effects
KW  - Carcinogens -- pharmacology
KW  - Breast Neoplasms -- prevention & control
KW  - Breast Neoplasms -- etiology
KW  - Alcohol Drinking -- adverse effects
KW  - Breast Neoplasms -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273255602?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Moderate+alcohol+consumption+and+breast+cancer+in+women%3A+from+epidemiology+to+mechanisms+and+interventions.&rft.au=Brooks%2C+Philip+J%3BZakhari%2C+Samir&rft.aulast=Brooks&rft.aufirst=Philip&rft.date=2013-01-01&rft.volume=37&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=1530-0277&rft_id=info:doi/10.1111%2Fj.1530-0277.2012.01888.x
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-28
N1  - Date created - 2013-01-07
N1  - Date revised - 2017-01-14
N1  - SuppNotes - Cited By:
Ann Epidemiol. 2006 Mar;16(3):230-40 [16230024]
JAMA. 2001 Nov 7;286(17):2143-51 [11694156]
J Natl Cancer Inst. 2009 Mar 4;101(5):282-3 [19244170]
J Natl Cancer Inst. 2009 Mar 4;101(5):296-305 [19244173]
J Clin Invest. 2009 Jun;119(6):1420-8 [19487818]
J Epidemiol. 2009;19(5):244-50 [19667493]
Alcohol Clin Exp Res. 2010 Jan;34(1):19-31 [19860811]
Circulation. 2010 Apr 13;121(14):1589-97 [20351238]
J Mammary Gland Biol Neoplasia. 2010 Jun;15(2):253-60 [20354771]
J Stud Alcohol Drugs. 2010 Jul;71(4):515-25 [20553659]
PLoS Genet. 2010 Jul;6(7):e1001043 [20686660]
J Natl Cancer Inst. 2010 Sep 22;102(18):1422-31 [20733117]
Nature. 2010 Oct 28;467(7319):1114-7 [20981102]
Int J Cancer. 2011 Feb 1;128(3):533-40 [20715111]
Nat Rev Cancer. 2011 Jun;11(6):450-7 [21593786]
Br J Cancer. 2002 Nov 18;87(11):1234-45 [12439712]
Endocr Rev. 2003 Apr;24(2):152-82 [12700178]
Cancer Res. 2003 Jun 15;63(12):3092-100 [12810634]
Annu Rev Pharmacol Toxicol. 2004;44:27-42 [14744237]
Nat Med. 2004 Aug;10(8):789-99 [15286780]
Ann Clin Res. 1978 Oct;10(5):294-7 [104651]
Cancer. 1980 Apr 15;45(8):2198-2207 [7370960]
J Natl Cancer Inst Monogr. 1992;(12):45-9 [1616809]
Cancer. 1993 Jun 1;71(11):3547-51 [8490903]
Cancer Causes Control. 1993 Sep;4(5):441-8 [8218876]
Cancer Causes Control. 1994 Jan;5(1):53-60 [8123779]
N Engl J Med. 1995 May 11;332(19):1245-50 [7708067]
J Natl Cancer Inst. 1995 Jun 21;87(12):923-9 [7666482]
J Surg Oncol. 1995 Oct;60(2):137-46 [7564383]
Cancer Epidemiol Biomarkers Prev. 1995 Oct-Nov;4(7):721-5 [8672988]
J Surg Oncol. 1996 Jan;61(1):68-83 [8544465]
JAMA. 1996 Dec 4;276(21):1747-51 [8940324]
Alcohol Clin Exp Res. 1999 Jun;23(6):1108-10 [10397298]
Proc R Soc Med. 1965 May;58:295-300 [14283879]
Environ Mol Mutagen. 2005 Mar-Apr;45(2-3):206-13 [15672382]
J Steroid Biochem Mol Biol. 2011 May;125(1-2):39-45 [21356310]
N Engl J Med. 2011 Jun 23;364(25):2381-91 [21639806]
Nat Rev Cancer. 2011 Jul;11(7):523-32 [21677677]
IARC Monogr Eval Carcinog Risks Hum. 2010;96:3-1383 [21735939]
Br J Cancer. 2011 Aug 23;105(5):709-22 [21772329]
J Exp Clin Cancer Res. 2011;30:75 [21838876]
PLoS Med. 2011 Sep;8(9):e1001090 [21909248]
JAMA. 2011 Nov 2;306(17):1884-90 [22045766]
Alcohol Clin Exp Res. 2011 Dec;35(12):2101-12 [21919918]
Stroke. 2012 Apr;43(4):939-45 [22403048]
Alcohol Clin Exp Res. 2012 Apr;36(4):577-87 [21981381]
Toxicology. 2006 Feb 15;219(1-3):208-19 [16377051]
Cell. 2000 Jan 7;100(1):57-70 [10647931]
Alcohol Clin Exp Res. 2000 Apr;24(4 Suppl):117S-122S [10803793]
Nat Rev Cancer. 2007 Aug;7(8):599-612 [17646865]
N1  - Last updated - 2017-01-19
DO  - http://dx.doi.org/10.1111/j.1530-0277.2012.01888.x
ER  - 



TY  - JOUR
T1  - Interplay between apoptotic and autophagy pathways after exposure to cerium dioxide nanoparticles in human monocytes.
AN  - 1273250522; 23047327
AB  - Engineered nanomaterials, defined as having at least one dimension smaller than 100 nm, have revolutionized many technology sectors ranging from therapeutics and diagnostics to environmental monitoring and remediation. This has resulted in a rapid increase in their manufacture over the past few years, accompanied by an increased human exposure potential. However, understanding of the interactions of nanomaterials with biological systems is still rudimentary. We have described that an environmentally and medically relevant nano metal (cerium dioxide) can affect primary human monocyte viability and interact with programmed cell death pathways leading to apoptosis and autophagic cell death. Cerium dioxide nanoparticles (CeO 2 NPs)-induced autophagy acts as a prodeath mechanism and leads to increased cytotoxicity of human monocytes. A better understanding of the implication and biological significance of CeO 2 NPs-induced autophagy and apoptosis will help us understand the risks associated with its uses and develop safer nanomedicine.
JF  - Autophagy
AU  - Hussain, Salik
AU  - Garantziotis, Stavros
AD  - Clinical Research Program, National Institute of Environmental Health Sciences (NIEHS), National Institute of Health (NIH), Research Triangle Park, NC, USA. salik.hussain@nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 101
EP  - 103
VL  - 9
IS  - 1
KW  - Cerium
KW  - 30K4522N6T
KW  - ceric oxide
KW  - 619G5K328Y
KW  - Index Medicus
KW  - Phagosomes -- drug effects
KW  - Cells, Cultured
KW  - Humans
KW  - Mitochondria -- drug effects
KW  - Models, Biological
KW  - Autophagy -- drug effects
KW  - Metal Nanoparticles -- toxicity
KW  - Monocytes -- physiology
KW  - Apoptosis -- physiology
KW  - Apoptosis -- drug effects
KW  - Monocytes -- pathology
KW  - Monocytes -- drug effects
KW  - Cerium -- toxicity
KW  - Autophagy -- physiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273250522?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Autophagy&rft.atitle=Interplay+between+apoptotic+and+autophagy+pathways+after+exposure+to+cerium+dioxide+nanoparticles+in+human+monocytes.&rft.au=Hussain%2C+Salik%3BGarantziotis%2C+Stavros&rft.aulast=Hussain&rft.aufirst=Salik&rft.date=2013-01-01&rft.volume=9&rft.issue=1&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Autophagy&rft.issn=1554-8635&rft_id=info:doi/10.4161%2Fauto.22266
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-07-15
N1  - Date created - 2013-01-07
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.4161/auto.22266
ER  - 



TY  - JOUR
T1  - Polymorphisms in pattern-recognition genes in the innate immunity system and risk of non-Hodgkin lymphoma.
AN  - 1273170873; 23055202
AB  - The pattern-recognition pathway plays an important role in infection recognition and immune responses, and previous studies have suggested an association between genetic variation in innate immunity genes and non-Hodgkin lymphoma (NHL). We evaluated NHL risk associated with genetic variation in pattern-recognition genes using data from a case-control study of NHL conducted in Connecticut women. Single nucleotide polymorphisms (SNPs) in 27 pattern-recognition genes were genotyped in 432 Caucasian incident NHL cases and 494 frequency-matched controls. Unconditional logistic regression was used to compute odds ratios (ORs) for NHL and common NHL subtypes in relation to individual SNPs and haplotypes. A gene-based analysis that adjusted for the number of tagSNPs genotyped in each gene showed a significant association with overall NHL for the MBP gene (P = 0.028), with the diffuse large B-cell lymphoma (DLBCL) subtype for the MASP2 gene (P = 0.011), and with the follicular lymphoma (FL) subtype for DEFB126 (P = 0.041). A SNP-based analysis showed that MBP rs8094402 was associated with decreased risks of overall NHL (allele risk OR = 0.72, P-trend = 0.0018), DLBCL (allele risk OR = 0.72, P-trend = 0.036), and FL (allele risk OR = 0.67, P-trend = 0.021), while MASP2 rs12711521 was associated with a decreased risk of DLBCL (allele risk OR = 0.57, P-trend = 0.0042). We also observed an increased risk of FL for DEFB126 rs6054706 (allele risk OR = 1.39, P-trend = 0.033). Our results suggest that genetic variation in pattern-recognition genes is associated with the risk of NHL or specific NHL subtypes, but these preliminary findings require replication in larger studies. Copyright © 2012 Wiley Periodicals, Inc.
JF  - Environmental and molecular mutagenesis
AU  - Hu, Wei
AU  - Bassig, Bryan A
AU  - Xu, Jun
AU  - Zheng, Tongzhang
AU  - Zhang, Yawei
AU  - Berndt, Sonja I
AU  - Holford, Theodore R
AU  - Hosgood, H Dean
AU  - Leaderer, Brian
AU  - Yeager, Meredith
AU  - Menashe, Idan
AU  - Boyle, Peter
AU  - Zou, Kaiyong
AU  - Zhu, Yong
AU  - Chanock, Stephen
AU  - Lan, Qing
AU  - Rothman, Nathaniel
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892-7240, USA. wei.hu@nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 72
EP  - 77
VL  - 54
IS  - 1
KW  - DEFB126 protein, human
KW  - 0
KW  - MBP protein, human
KW  - Myelin Basic Protein
KW  - Receptors, Pattern Recognition
KW  - beta-Defensins
KW  - MASP2 protein, human
KW  - EC 3.4.21.-
KW  - Mannose-Binding Protein-Associated Serine Proteases
KW  - Index Medicus
KW  - Young Adult
KW  - Humans
KW  - Aged
KW  - Lymphoma, Large B-Cell, Diffuse -- immunology
KW  - Receptors, Pattern Recognition -- genetics
KW  - Lymphoma, Large B-Cell, Diffuse -- genetics
KW  - European Continental Ancestry Group -- genetics
KW  - Connecticut
KW  - Lymphoma, Follicular -- immunology
KW  - Lymphoma, Follicular -- genetics
KW  - Haplotypes
KW  - Aged, 80 and over
KW  - Logistic Models
KW  - Adult
KW  - Case-Control Studies
KW  - Middle Aged
KW  - Genetic Predisposition to Disease
KW  - Female
KW  - Lymphoma, Non-Hodgkin -- genetics
KW  - Polymorphism, Single Nucleotide
KW  - beta-Defensins -- genetics
KW  - Myelin Basic Protein -- genetics
KW  - Immunity, Innate -- genetics
KW  - Mannose-Binding Protein-Associated Serine Proteases -- genetics
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273170873?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Polymorphisms+in+pattern-recognition+genes+in+the+innate+immunity+system+and+risk+of+non-Hodgkin+lymphoma.&rft.au=Hu%2C+Wei%3BBassig%2C+Bryan+A%3BXu%2C+Jun%3BZheng%2C+Tongzhang%3BZhang%2C+Yawei%3BBerndt%2C+Sonja+I%3BHolford%2C+Theodore+R%3BHosgood%2C+H+Dean%3BLeaderer%2C+Brian%3BYeager%2C+Meredith%3BMenashe%2C+Idan%3BBoyle%2C+Peter%3BZou%2C+Kaiyong%3BZhu%2C+Yong%3BChanock%2C+Stephen%3BLan%2C+Qing%3BRothman%2C+Nathaniel&rft.aulast=Hu&rft.aufirst=Wei&rft.date=2013-01-01&rft.volume=54&rft.issue=1&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21739
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-04-19
N1  - Date created - 2013-01-03
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/em.21739
ER  - 



TY  - JOUR
T1  - A truncated peptide from p35, a Cdk5 activator, prevents Alzheimer's disease phenotypes in model mice.
AN  - 1273167202; 23038754
AB  - Alzheimer's disease (AD), one of the leading neurodegenerative disorders of older adults, which causes major socioeconomic burdens globally, lacks effective therapeutics without significant side effects. Besides the hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it has been reported that cyclin-dependent kinase 5 (Cdk5), a critical neuronal kinase, is hyperactivated in AD brains and is, in part, responsible for the above pathology. Here we show that a modified truncated 24-aa peptide (TFP5), derived from the Cdk5 activator p35, penetrates the blood-brain barrier after intraperitoneal injections, inhibits abnormal Cdk5 hyperactivity, and significantly rescues AD pathology (up to 70-80%) in 5XFAD AD model mice. The mutant mice, injected with TFP5 exhibit behavioral rescue, whereas no rescue was observed in mutant mice injected with either saline or scrambled peptide. However, TFP5 does not inhibit cell cycle Cdks or normal Cdk5/p35 activity, and thereby has no toxic side effects (even at 200 mg/kg), a common problem in most current therapeutics for AD. In addition, treated mice displayed decreased inflammation, amyloid plaques, NFTs, cell death, and an extended life by 2 mo. These results suggest TFP5 as a potential therapeutic, toxicity-free candidate for AD.
JF  - FASEB journal : official publication of the Federation of American Societies for Experimental Biology
AU  - Shukla, Varsha
AU  - Zheng, Ya-Li
AU  - Mishra, Santosh K
AU  - Amin, Niranjana D
AU  - Steiner, Joseph
AU  - Grant, Philip
AU  - Kesavapany, Sashi
AU  - Pant, Harish C
AD  - Laboratory of Neurochemistry, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 174
EP  - 186
VL  - 27
IS  - 1
KW  - Enzyme Activators
KW  - 0
KW  - Nerve Tissue Proteins
KW  - neuronal Cdk5 activator (p25-p35)
KW  - Index Medicus
KW  - Animals
KW  - Apoptosis
KW  - Phosphorylation
KW  - Molecular Sequence Data
KW  - Mice
KW  - Amino Acid Sequence
KW  - Mice, Transgenic
KW  - Nerve Tissue Proteins -- chemistry
KW  - Alzheimer Disease -- prevention & control
KW  - Enzyme Activators -- pharmacology
KW  - Nerve Tissue Proteins -- pharmacology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273167202?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=A+truncated+peptide+from+p35%2C+a+Cdk5+activator%2C+prevents+Alzheimer%27s+disease+phenotypes+in+model+mice.&rft.au=Shukla%2C+Varsha%3BZheng%2C+Ya-Li%3BMishra%2C+Santosh+K%3BAmin%2C+Niranjana+D%3BSteiner%2C+Joseph%3BGrant%2C+Philip%3BKesavapany%2C+Sashi%3BPant%2C+Harish+C&rft.aulast=Shukla&rft.aufirst=Varsha&rft.date=2013-01-01&rft.volume=27&rft.issue=1&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=1530-6860&rft_id=info:doi/10.1096%2Ffj.12-217497
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-07
N1  - Date created - 2013-01-03
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Neurosci. 2011 Nov 2;31(44):15751-6 [22049418]
Acta Neuropathol. 2012 Jan;123(1):133-51 [22083255]
J Biol Chem. 2012 Mar 2;287(10):7224-35 [22223639]
Bioorg Med Chem Lett. 2004 Nov 15;14(22):5521-5 [15482916]
Science. 1991 Feb 8;251(4994):675-8 [1899488]
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5384-8 [1376918]
Genes Dev. 1996 Apr 1;10(7):816-25 [8846918]
Science. 1996 Oct 4;274(5284):99-102 [8810256]
Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):11173-8 [8855328]
Nat Med. 1998 Jan;4(1):97-100 [9427614]
Science. 1999 Sep 3;285(5433):1569-72 [10477521]
Front Biosci. 2005 Jan 1;10:143-59 [15574357]
EMBO J. 2005 Jan 12;24(1):209-20 [15592431]
J Neurosci. 2005 Sep 28;25(39):8843-53 [16192374]
Neuron. 2005 Dec 8;48(5):825-38 [16337919]
J Neurosci Res. 2006 May 15;83(7):1252-61 [16511867]
J Neurosci. 2006 May 3;26(18):4717-28 [16672644]
CNS Neurol Disord Drug Targets. 2006 Jun;5(3):355-61 [16787235]
J Neurosci. 2006 Oct 4;26(40):10129-40 [17021169]
J Neurochem. 2006 Oct;99(2):353-70 [17029592]
J Neurosci. 2006 Oct 11;26(41):10536-41 [17035538]
Biotechnol J. 2007 Aug;2(8):941-8 [17597494]
Neuron. 2008 Mar 13;57(5):680-90 [18341989]
Acta Pharmacol Sin. 2009 Apr;30(4):379-87 [19343058]
Int Rev Neurobiol. 2009;84:151-65 [19501717]
Bioorg Med Chem Lett. 2009 Oct 1;19(19):5703-7 [19700321]
J Neurochem. 2009 Dec;111(6):1275-308 [20050287]
Am J Pathol. 2010 Jan;176(1):320-9 [19948833]
Expert Rev Neurother. 2010 Jul;10(7):1201-8 [20586698]
Neuropharmacology. 2010 Sep-Oct;59(4-5):290-4 [20394761]
Proc Natl Acad Sci U S A. 1985 Jun;82(12):4274-6 [3159022]
J Neuropathol Exp Neurol. 1986 Jan;45(1):56-64 [3510274]
Proc Natl Acad Sci U S A. 1986 Jun;83(11):4044-8 [2424016]
Proc Natl Acad Sci U S A. 1986 Jul;83(13):4913-7 [3088567]
Nature. 1999 Dec 9;402(6762):615-22 [10604467]
Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2910-5 [10706614]
J Cell Sci. 2000 Jun;113 ( Pt 11):1857-70 [10806097]
Nature. 2000 May 18;405(6784):360-4 [10830966]
Neurobiol Aging. 2000 May-Jun;21(3):383-421 [10858586]
Biochem Biophys Res Commun. 2000 Jul 21;274(1):16-21 [10903889]
Nat Med. 2000 Aug;6(8):916-9 [10932230]
Cancer Res. 2001 Jan 15;61(2):474-7 [11212234]
Eur J Biochem. 2001 Mar;268(6):1518-27 [11248668]
Trends Cell Biol. 2002 Jan;12(1):28-36 [11854007]
J Neurosci. 2002 May 1;22(9):3700-7 [11978846]
J Biol Chem. 2002 Jul 12;277(28):25493-501 [11964410]
FEBS Lett. 2002 Jul 17;523(1-3):58-62 [12123804]
Eur J Biochem. 2002 Sep;269(18):4427-34 [12230554]
J Mol Neurosci. 2002 Dec;19(3):267-73 [12540052]
Neuron. 2003 May 22;38(4):555-65 [12765608]
J Biol Chem. 2003 Jun 27;278(26):24026-32 [12695506]
Nat Cell Biol. 2003 Aug;5(8):701-10 [12855954]
Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):11035-40 [12958210]
Neurobiol Dis. 2003 Oct;14(1):89-97 [13678670]
J Cell Biol. 2003 Oct 13;163(1):83-95 [14557249]
Neuron. 2003 Oct 30;40(3):471-83 [14642273]
Neurosignals. 2003 Sep-Oct;12(4-5):209-14 [14673207]
Biochim Biophys Acta. 2004 Mar 11;1697(1-2):137-42 [15023356]
Am J Geriatr Psychiatry. 2004 Jul-Aug;12(4):358-69 [15249273]
Brain Res. 1988 Aug 2;457(1):12-20 [2458799]
J Neurosci. 1990 Oct;10(10):3295-304 [1698946]
Science. 1990 Oct 12;250(4978):279-82 [2218531]
J Biol Chem. 2010 Oct 29;285(44):34202-12 [20720012]
FASEB J. 2010 Nov;24(11):4396-407 [20624930]
Rev Neurosci. 2011;22(2):143-52 [21476938]
Prog Neurobiol. 2011 Jun;94(1):49-63 [21473899]
PLoS One. 2011;6(9):e25735 [21984943]
FASEB J. 2011 Nov;25(11):3896-905 [21828286]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1096/fj.12-217497
ER  - 



TY  - JOUR
T1  - Prediagnostic circulating adipokine concentrations and risk of renal cell carcinoma in male smokers.
AN  - 1273158694; 23042303
AB  - Despite a well-established link between obesity and renal cell carcinoma (RCC), the mechanism through which obesity acts to increase cancer risk is unclear. Adiponectin, leptin and resistin are adipocyte-secreted peptide hormones that may influence RCC development through their demonstrated effects on inflammation, insulin resistance and cell growth and proliferation. We conducted a nested case-control study to evaluate whether prediagnostic serum adiponectin, leptin and resistin levels are associated with RCC risk. This case-control study (273 cases and 273 controls) was nested within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of Finnish male smokers. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using conditional logistic regression models, with analyte levels modeled continuously and categorically (defined using quartiles among controls). High adiponectin levels were significantly associated with reduced RCC risk (Quartile 4 versus Quartile 1: OR = 0.52, 95% CI = 0.30-0.88; P trend = 0.01). This association remained upon additional adjustment for body mass index at blood collection and exclusion of cases diagnosed within the first 2 years of follow-up. In addition, model adjustment for adiponectin resulted in a substantial attenuation of the association between BMI and RCC (OR per 5 kg/m(2) changed from 1.19 to 1.05). No clear associations with RCC were observed for leptin or resistin. Our results suggest that elevated levels of circulating adiponectin are associated with decreased subsequent risk of RCC. These findings provide the strongest evidence to date, suggesting that the association between obesity and RCC is mediated at least in part through the effects of low adiponectin.
JF  - Carcinogenesis
AU  - Liao, Linda M
AU  - Weinstein, Stephanie J
AU  - Pollak, Michael
AU  - Li, Zhen
AU  - Virtamo, Jarmo
AU  - Albanes, Demetrius
AU  - Chow, Wong-Ho
AU  - Purdue, Mark P
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA. liaolm@mail.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 109
EP  - 112
VL  - 34
IS  - 1
KW  - Adipokines
KW  - 0
KW  - Index Medicus
KW  - Finland
KW  - Humans
KW  - Case-Control Studies
KW  - Middle Aged
KW  - Male
KW  - Kidney Neoplasms -- blood
KW  - Smoking -- blood
KW  - Adipokines -- blood
KW  - Kidney Neoplasms -- epidemiology
KW  - Carcinoma, Renal Cell -- blood
KW  - Carcinoma, Renal Cell -- epidemiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273158694?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prediagnostic+circulating+adipokine+concentrations+and+risk+of+renal+cell+carcinoma+in+male+smokers.&rft.au=Liao%2C+Linda+M%3BWeinstein%2C+Stephanie+J%3BPollak%2C+Michael%3BLi%2C+Zhen%3BVirtamo%2C+Jarmo%3BAlbanes%2C+Demetrius%3BChow%2C+Wong-Ho%3BPurdue%2C+Mark+P&rft.aulast=Liao&rft.aufirst=Linda&rft.date=2013-01-01&rft.volume=34&rft.issue=1&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs322
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-02-25
N1  - Date created - 2013-01-03
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
N Engl J Med. 2000 Nov 2;343(18):1305-11 [11058675]
Endocr Rev. 2005 May;26(3):439-51 [15897298]
J Natl Cancer Inst. 2005 Nov 16;97(22):1688-94 [16288122]
J Cell Physiol. 2006 Apr;207(1):12-22 [16110483]
Diabetologia. 2006 Apr;49(4):744-7 [16496121]
Br J Cancer. 2006 May 8;94(9):1221-5 [16570048]
Physiol Res. 2006;55(3):233-44 [16238454]
Nat Rev Immunol. 2006 Oct;6(10):772-83 [16998510]
J Clin Endocrinol Metab. 2007 Jan;92(1):255-63 [17062769]
Int J Cancer. 2007 Apr 1;120(7):1573-8 [17205522]
Horm Metab Res. 2007 May;39(5):314-21 [17533572]
Cytokine Growth Factor Rev. 2007 Jun-Aug;18(3-4):313-25 [17507280]
Am J Epidemiol. 2007 Oct 1;166(7):752-9 [17615089]
Am J Epidemiol. 2007 Oct 15;166(8):932-40 [17656615]
Chin Med J (Engl). 2007 Sep 20;120(18):1592-6 [17908478]
BMJ. 2007 Dec 1;335(7630):1134 [17986716]
Lancet. 2008 Feb 16;371(9612):569-78 [18280327]
Arch Physiol Biochem. 2008 Feb;114(1):71-83 [18465361]
Am J Epidemiol. 2008 Aug 1;168(3):268-77 [18544571]
J Clin Endocrinol Metab. 2008 Aug;93(8):3165-72 [18492747]
Int J Obes (Lond). 2008 Sep;32 Suppl 4:S7-12 [18719601]
Eur Urol. 2008 Oct;54(4):866-73 [18343565]
Am J Epidemiol. 2008 Nov 1;168(9):1047-55 [18801887]
Int J Obes (Lond). 2008 Dec;32 Suppl 7:S13-8 [19136982]
Cancer Prev Res (Phila). 2008 Oct;1(5):369-75 [19138981]
Hormones (Athens). 2009 Jan-Mar;8(1):39-46 [19278051]
Nat Rev Urol. 2010 May;7(5):245-57 [20448658]
Curr Opin Pharmacol. 2010 Dec;10(6):676-83 [20810317]
Handb Exp Pharmacol. 2011;(203):303-30 [21484577]
Cancer Causes Control. 2005 Nov;16(9):1099-106 [16184476]
Acta Oncol. 2002;41(4):381-8 [12234031]
J Clin Endocrinol Metab. 2003 Mar;88(3):993-7 [12629074]
Diabetologia. 2003 Apr;46(4):459-69 [12687327]
Oncol Rep. 2003 Nov-Dec;10(6):2015-21 [14534736]
Clin Cancer Res. 2003 Nov 15;9(15):5699-704 [14654554]
J Clin Endocrinol Metab. 2003 Dec;88(12):6098-106 [14671216]
J Clin Endocrinol Metab. 2004 Mar;89(3):1102-7 [15001594]
J Clin Endocrinol Metab. 2004 Mar;89(3):1160-3 [15001602]
Proc Natl Acad Sci U S A. 2004 Jul 13;101(28):10308-13 [15210937]
Nat Rev Cancer. 2004 Aug;4(8):579-91 [15286738]
Ann Epidemiol. 1994 Jan;4(1):1-10 [8205268]
Am J Clin Nutr. 2001 Sep;74(3):295-301 [11522551]
N Engl J Med. 1996 Feb 1;334(5):292-5 [8532024]
Biochem Biophys Res Commun. 1999 Apr 2;257(1):79-83 [10092513]
Cell Mol Life Sci. 2004 Oct;61(19-20):2485-96 [15526156]
Circulation. 2004 Nov 23;110(21):3335-40 [15545519]
Am J Epidemiol. 2004 Dec 15;160(12):1168-76 [15583369]
J Biol Chem. 2005 May 6;280(18):18341-7 [15734737]
Comment In:
J Urol. 2013 Sep;190(3):863 [23931186]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1093/carcin/bgs322
ER  - 



TY  - JOUR
T1  - Super-resolution characterization of TCR-dependent signaling clusters.
AN  - 1273120433; 23278738
AB  - Multi-molecular signaling complexes drive the earliest events of immune cell activation via immunoreceptors with unexplained specificity and speed. Fluorescence microscopy has shown that these complexes form microclusters at the plasma membrane of activated T cells upon engagement of their antigen receptors (TCRs). Although crucial for cell function, much remains to be learned about the molecular content, fine structure, formation mechanisms, and function of these microclusters. Recent advancements in super-resolution microscopy have enabled the study of signaling microclusters at the single molecule level with resolution down to approximately 20 nm. These techniques have now helped to characterize the size distributions of signaling clusters at the plasma membrane of intact cells and to shed light on the formation mechanisms that govern their assembly. Surprisingly, dynamic and functional nanostructures have been identified within the signaling clusters. We expect that these novel methodologies, combined with older techniques, will shed new light on the nature of signaling clusters and their critical role in T-cell activation.
          Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
JF  - Immunological reviews
AU  - Sherman, Eilon
AU  - Barr, Valarie
AU  - Samelson, Lawrence E
AD  - Laboratory of Cellular and Molecular Biology, CCR, NCI, NIH, Bethesda, MD 20892-4256, USA. samelsonl@helix.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 21
EP  - 35
VL  - 251
IS  - 1
KW  - Multiprotein Complexes
KW  - 0
KW  - Receptors, Antigen, T-Cell
KW  - Index Medicus
KW  - Microscopy -- trends
KW  - Lymphocyte Activation
KW  - Animals
KW  - Microscopy -- methods
KW  - Receptor Cross-Talk
KW  - Humans
KW  - Signal Transduction -- immunology
KW  - Receptor Aggregation
KW  - Receptors, Antigen, T-Cell -- metabolism
KW  - Receptors, Antigen, T-Cell -- immunology
KW  - T-Lymphocytes -- immunology
KW  - Nanostructures
KW  - Multiprotein Complexes -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273120433?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunological+reviews&rft.atitle=Super-resolution+characterization+of+TCR-dependent+signaling+clusters.&rft.au=Sherman%2C+Eilon%3BBarr%2C+Valarie%3BSamelson%2C+Lawrence+E&rft.aulast=Sherman&rft.aufirst=Eilon&rft.date=2013-01-01&rft.volume=251&rft.issue=1&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Immunological+reviews&rft.issn=1600-065X&rft_id=info:doi/10.1111%2Fimr.12010
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-06-28
N1  - Date created - 2013-01-02
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Annu Rev Biochem. 2009;78:993-1016 [19489737]
J Immunol. 2009 Dec 1;183(11):7352-61 [19917685]
Nat Immunol. 2010 Jan;11(1):90-6 [20010844]
Immunol Rev. 2010 Sep;237(1):191-204 [20727037]
Nature. 2010 Sep 23;467(7314):465-9 [20818374]
Nat Rev Immunol. 2011 Jan;11(1):47-55 [21127503]
Nat Rev Immunol. 2011 Jan;11(1):21-33 [21179118]
J Exp Med. 2011 May 9;208(5):1055-68 [21482698]
Nat Immunol. 2010 Jan;11(1):51-2 [20016513]
Immunity. 2010 Feb 26;32(2):187-99 [20171124]
Annu Rev Immunol. 2010;28:185-210 [20192804]
J Cell Biol. 2000 May 29;149(5):1131-42 [10831616]
J Biol Chem. 2000 Jul 28;275(30):23355-61 [10811803]
Science. 2000 Aug 25;289(5483):1349-52 [10958781]
Cold Spring Harb Perspect Biol. 2010 May;2(5):a002279 [20452964]
Sci Signal. 2010;3(121):ra36 [20460647]
J Biophotonics. 2010 Jul;3(7):446-54 [20148419]
EMBO J. 2010 Jul 21;29(14):2315-28 [20562827]
Cold Spring Harb Perspect Biol. 2010 Aug;2(8):a005512 [20610546]
Nat Immunol. 2011 Jul;12(7):655-62 [21642986]
Immunity. 2011 Jun 24;34(6):919-31 [21703543]
PLoS One. 2011;6(8):e23586 [21887278]
J Biol Chem. 2011 Sep 16;286(37):31993-2001 [21757710]
Immunity. 2011 Sep 23;35(3):375-87 [21903423]
Nat Methods. 2011 Nov;8(11):969-75 [21926998]
Immunity. 2011 Nov 23;35(5):705-20 [22055681]
Annu Rev Phys Chem. 2012;63:519-40 [22404589]
J Cell Biol. 2000 Oct 16;151(2):199-208 [11038169]
Cell. 2000 Oct 13;103(2):211-25 [11057895]
J Cell Biol. 2001 Aug 6;154(3):645-58 [11489921]
Science. 2002 Feb 22;295(5559):1539-42 [11859198]
Annu Rev Immunol. 2002;20:371-94 [11861607]
J Cell Biol. 2002 Sep 30;158(7):1263-75 [12356870]
J Cell Biol. 2003 Jan 20;160(2):165-70 [12527752]
Annu Rev Immunol. 2003;21:457-81 [12615889]
Nat Immunol. 2004 May;5(5):524-30 [15048111]
Mol Biol Cell. 2004 Jun;15(6):2580-92 [15034144]
Cell. 1998 Jan 9;92(1):83-92 [9489702]
Immunity. 1998 Aug;9(2):239-46 [9729044]
Science. 1999 Jul 9;285(5425):221-7 [10398592]
Semin Immunol. 2004 Dec;16(6):379-93 [15541653]
Nat Immunol. 2005 Jan;6(1):80-9 [15558067]
J Immunol. 2005 Feb 1;174(3):1385-92 [15661896]
Annu Rev Biophys Biomol Struct. 2005;34:351-78 [15869394]
Nature. 2005 Jun 2;435(7042):590-7 [15931211]
Cell. 2005 Jun 17;121(6):937-50 [15960980]
J Exp Med. 2005 Aug 15;202(4):493-503 [16087711]
J Exp Med. 2005 Oct 17;202(8):1031-6 [16216891]
Nat Immunol. 2005 Nov;6(11):1168-76 [16200067]
Micron. 2006;37(1):14-34 [16081296]
Expert Rev Mol Med. 2005 Dec 19;7(29):1-29 [16364187]
Nat Immunol. 2005 Dec;6(12):1253-62 [16273097]
EMBO J. 2006 Feb 22;25(4):774-84 [16467851]
Immunity. 2006 Jul;25(1):117-27 [16860761]
Traffic. 2006 Sep;7(9):1143-62 [16919152]
Nat Struct Mol Biol. 2006 Sep;13(9):798-805 [16906159]
Science. 2006 Sep 15;313(5793):1642-5 [16902090]
Mol Cell Biol. 2006 Oct;26(19):7155-66 [16980618]
Nat Methods. 2006 Oct;3(10):793-5 [16896339]
Proc Natl Acad Sci U S A. 2006 Dec 12;103(50):18992-7 [17146050]
Immunity. 2007 Jul;27(1):76-88 [17629516]
J Cell Sci. 2007 Aug 15;120(Pt 16):2763-73 [17652160]
Mol Cell Biol. 2007 Dec;27(24):8622-36 [17938199]
Nat Cell Biol. 2008 Aug;10(8):955-63 [18641640]
Immunity. 2009 Jan 16;30(1):44-55 [19135393]
Mol Membr Biol. 2009 Jan;26(1):80-92 [19115142]
Nature. 2009 Feb 26;457(7233):1159-62 [19098897]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1111/imr.12010
ER  - 



TY  - JOUR
T1  - Finite State Control of a Variable Impedance Hybrid Neuroprosthesis for Locomotion After Paralysis
AN  - 1272741077; 17574816
AB  - We have previously reported on a novel variable impedance knee mechanism (VIKM). The VIKM was designed as a component of a hybrid neuroprosthesis to regulate knee flexion. The hybrid neuroprosthesis is a device that uses a controllable brace to support the body against collapse while stimulation provides power for movement. The hybrid neuroprosthesis requires a control system to coordinate the actions of the VIKM with the stimulation system; the development and evaluation of such a controller is presented. Brace mounted sensors and a baseline open loop stimulation pattern are utilized as control signals to activate the VIKM during stance phase while simultaneously modulating muscle stimulation in an on-off fashion. The objective is twofold: reduce the amount of stimulation necessary for walking while simultaneously restoring more biologically correct knee motion during stance using the VIKM. Custom designed hardware and software components were developed for controller implementation. The VIKM hybrid neuroprosthesis (VIKM-HNP) was evaluated during walking in one participant with thoracic level spinal cord injury. In comparison to walking with functional neuromuscular stimulation alone, the VIKM-HNP restored near normal stance phase knee flexion during loading response and pre-swing phases while decreasing knee extensor stimulation by up to 40%.
JF  - IEEE Transactions on Neural Systems and Rehabilitation Engineering
AU  - Bulea, Thomas C
AU  - Kobetic, Rudi
AU  - Audu, Musa L
AU  - Schnellenberger, John R
AU  - Triolo, Ronald J
AD  - Functional and Applied Biomechanics Section, National Institutes of Health, Bethesda, MD, USA
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 141
EP  - 151
PB  - Institute of Electrical and Electronics Engineers, Inc., 3 Park Avenue, 17th Fl New York NY 10016-5997 United States
VL  - 21
IS  - 1
SN  - 1534-4320, 1534-4320
KW  - Biotechnology and Bioengineering Abstracts
KW  - Rehabilitation
KW  - Muscles
KW  - Walking
KW  - Spinal cord injury
KW  - Knee
KW  - Paralysis
KW  - Computer programs
KW  - software
KW  - Locomotion
KW  - Hybrids
KW  - Thorax
KW  - Prosthetics
KW  - W 30955:Biosensors
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272741077?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Neural+Systems+and+Rehabilitation+Engineering&rft.atitle=Finite+State+Control+of+a+Variable+Impedance+Hybrid+Neuroprosthesis+for+Locomotion+After+Paralysis&rft.au=Bulea%2C+Thomas+C%3BKobetic%2C+Rudi%3BAudu%2C+Musa+L%3BSchnellenberger%2C+John+R%3BTriolo%2C+Ronald+J&rft.aulast=Bulea&rft.aufirst=Thomas&rft.date=2013-01-01&rft.volume=21&rft.issue=1&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Neural+Systems+and+Rehabilitation+Engineering&rft.issn=15344320&rft_id=info:doi/10.1109%2FTNSRE.2012.2227124
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2015-03-19
N1  - SubjectsTermNotLitGenreText - Paralysis; Computer programs; software; Rehabilitation; Locomotion; Hybrids; Thorax; Muscles; Walking; Spinal cord injury; Knee; Prosthetics
DO  - http://dx.doi.org/10.1109/TNSRE.2012.2227124
ER  - 



TY  - JOUR
T1  - Designing endocrine disruption out of the next generation of chemicals
AN  - 1272716187; 17531893
AB  - A central goal of green chemistry is to avoid hazard in the design of new chemicals. This objective is best achieved when information about a chemical's potential hazardous effects is obtained as early in the design process as feasible. Endocrine disruption is a type of hazard that to date has been inadequately addressed by both industrial and regulatory science. To aid chemists in avoiding this hazard, we propose an endocrine disruption testing protocol for use by chemists in the design of new chemicals. The Tiered Protocol for Endocrine Disruption (TiPED) has been created under the oversight of a scientific advisory committee composed of leading representatives from both green chemistry and the environmental health sciences. TiPED is conceived as a tool for new chemical design, thus it starts with a chemist theoretically at "the drawing board." It consists of five testing tiers ranging from broad in silicoevaluation up through specific cell- and whole organism-based assays. To be effective at detecting endocrine disruption, a testing protocol must be able to measure potential hormone-like or hormone-inhibiting effects of chemicals, as well as the many possible interactions and signaling sequellae such chemicals may have with cell-based receptors. Accordingly, we have designed this protocol to broadly interrogate the endocrine system. The proposed protocol will not detect all possible mechanisms of endocrine disruption, because scientific understanding of these phenomena is advancing rapidly. To ensure that the protocol remains current, we have established a plan for incorporating new assays into the protocol as the science advances. In this paper we present the principles that should guide the science of testing new chemicals for endocrine disruption, as well as principles by which to evaluate individual assays for applicability, and laboratories for reliability. In a 'proof-of-principle' test, we ran 6 endocrine disrupting chemicals (EDCs) that act viadifferent endocrinological mechanisms through the protocol using published literature. Each was identified as endocrine active by one or more tiers. We believe that this voluntary testing protocol will be a dynamic tool to facilitate efficient and early identification of potentially problematic chemicals, while ultimately reducing the risks to public health.
JF  - Green Chemistry
AU  - Schug, T T
AU  - Abagyan, R
AU  - Blumberg, B
AU  - Collins, T J
AU  - Crews, D
AU  - DeFur, P L
AU  - Dickerson, S M
AU  - Edwards, T M
AU  - Gore, A C
AU  - Guillette, L J
AU  - Hayes, T
AU  - Heindel, J J
AU  - Moores, A
AU  - Patisaul, H B
AU  - Tal, T L
AU  - Thayer, KA
AU  - Vandenberg, L N
AU  - Warner, J C
AU  - Watson, C S
AU  - vom Saal, FS
AU  - Zoeller, R T
AU  - O'Brien, K P
AU  - Myers, J P
AD  - Division of Extramural Research and Training; Cellular, Organ and Systems Pathobiology Branch; National Institute of Environmental Health Sciences, Research Triangle Park; NC; USA; , schugt2@niehs.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 181
EP  - 198
PB  - Royal Society of Chemistry, c/o Springer-Verlag New York Inc. Secaucus New Jersey 07096 2485 United States
VL  - 15
IS  - 1
SN  - 1463-9262, 1463-9262
KW  - Health & Safety Science Abstracts; Risk Abstracts; Environment Abstracts; Sustainability Science Abstracts
KW  - Advisory committees
KW  - Chemicals
KW  - ENA 05:ENAironmental Design & Urban Ecology
KW  - H 12000:Epidemiology and Public Health
KW  - R2 23060:Medical and environmental health
KW  - M3:1010
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272716187?accountid=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=Green+Chemistry&rft.atitle=Designing+endocrine+disruption+out+of+the+next+generation+of+chemicals&rft.au=Schug%2C+T+T%3BAbagyan%2C+R%3BBlumberg%2C+B%3BCollins%2C+T+J%3BCrews%2C+D%3BDeFur%2C+P+L%3BDickerson%2C+S+M%3BEdwards%2C+T+M%3BGore%2C+A+C%3BGuillette%2C+L+J%3BHayes%2C+T%3BHeindel%2C+J+J%3BMoores%2C+A%3BPatisaul%2C+H+B%3BTal%2C+T+L%3BThayer%2C+KA%3BVandenberg%2C+L+N%3BWarner%2C+J+C%3BWatson%2C+C+S%3Bvom+Saal%2C+FS%3BZoeller%2C+R+T%3BO%27Brien%2C+K+P%3BMyers%2C+J+P&rft.aulast=Schug&rft.aufirst=T&rft.date=2013-01-01&rft.volume=15&rft.issue=1&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Green+Chemistry&rft.issn=14639262&rft_id=info:doi/10.1039%2Fc2gc35055f
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Number of references - 1
N1  - Last updated - 2014-02-21
N1  - SubjectsTermNotLitGenreText - Chemicals
DO  - http://dx.doi.org/10.1039/c2gc35055f
ER  - 



TY  - JOUR
T1  - A genetic polymorphism for translocator protein 18 kDa affects both in vitro and in vivo radioligand binding in human brain to this putative biomarker of neuroinflammation
AN  - 1272716106; 17515928
AB  - Second-generation radioligands for translocator protein (TSPO), an inflammation marker, are confounded by the codominant rs6971 polymorphism that affects binding affinity. The resulting three groups are homozygous for high-affinity state (HH), homozygous for low-affinity state (LL), or heterozygous (HL). We tested if in vitro binding to leukocytes distinguished TSPO genotypes and if genotype could affect clinical studies using the TSPO radioligand [ super(11)C]PBR28. In vitro binding to leukocytes and [ super(11)C]PBR28 brain imaging were performed in 27 human subjects with known TSPO genotype. Specific [ super(3)H]PBR28 binding was measured in prefrontal cortex of 45 schizophrenia patients and 47 controls. Leukocyte binding to PBR28 predicted genotype in all subjects. Brain uptake was similar to 40% higher in HH than HL subjects. Specific [ super(3)H]PBR28 binding in LL controls was negligible, while HH controls had similar to 80% higher binding than HL controls. After excluding LL subjects, specific binding was 16% greater in schizophrenia patients than controls. This difference was insignificant by itself (P=0.085), but was significant after correcting for TSPO genotype (P=0.011). Our results show that TSPO genotype influences PBR28 binding in vitro and in vivo. Correcting for this genotype increased statistical power in our postmortem study and is recommended for in vivo positron emission tomography studies.
JF  - Journal of Cerebral Blood Flow and Metabolism
AU  - Kreisl, William C
AU  - Jenko, Kimberly J
AU  - Hines, Christina S
AU  - Hyoung Lyoo, Chul
AU  - Corona, Winston
AU  - Morse, Cheryl L
AU  - Zoghbi, Sami S
AU  - Hyde, Thomas
AU  - Kleinman, Joel E
AU  - Pike, Victor W
AU  - McMahon, Francis J
AU  - Innis, Robert B
AD  - Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland, USA
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 53
EP  - 58
PB  - Nature Publishing Group
VL  - 33
IS  - 1
SN  - 0271-678X, 0271-678X
KW  - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts
KW  - Neuroimaging
KW  - Statistics
KW  - Gene polymorphism
KW  - Leukocytes
KW  - Brain
KW  - biomarkers
KW  - Inflammation
KW  - Schizophrenia
KW  - Mental disorders
KW  - Positron emission tomography
KW  - Radioisotopes
KW  - Cerebral blood flow
KW  - Cortex (prefrontal)
KW  - G 07880:Human Genetics
KW  - W 30910:Imaging
KW  - N3 11001:Behavioral and Cognitive Neuroscience
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272716106?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Cerebral+Blood+Flow+and+Metabolism&rft.atitle=A+genetic+polymorphism+for+translocator+protein+18+kDa+affects+both+in+vitro+and+in+vivo+radioligand+binding+in+human+brain+to+this+putative+biomarker+of+neuroinflammation&rft.au=Kreisl%2C+William+C%3BJenko%2C+Kimberly+J%3BHines%2C+Christina+S%3BHyoung+Lyoo%2C+Chul%3BCorona%2C+Winston%3BMorse%2C+Cheryl+L%3BZoghbi%2C+Sami+S%3BHyde%2C+Thomas%3BKleinman%2C+Joel+E%3BPike%2C+Victor+W%3BMcMahon%2C+Francis+J%3BInnis%2C+Robert+B&rft.aulast=Kreisl&rft.aufirst=William&rft.date=2013-01-01&rft.volume=33&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cerebral+Blood+Flow+and+Metabolism&rft.issn=0271678X&rft_id=info:doi/10.1038%2Fjcbfm.2012.131
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2013-10-21
N1  - SubjectsTermNotLitGenreText - Neuroimaging; Statistics; Gene polymorphism; Leukocytes; Brain; biomarkers; Inflammation; Schizophrenia; Mental disorders; Radioisotopes; Positron emission tomography; Cortex (prefrontal); Cerebral blood flow
DO  - http://dx.doi.org/10.1038/jcbfm.2012.131
ER  - 



TY  - JOUR
T1  - Regulatory Forum Opinion Piece*: Tox21 and Toxicologic Pathology
AN  - 1268655644; 17489871
AB  - Tox21 is a transformative effort on the part of several U.S. Federal agencies (the National Toxicology Program/National Institute of Environmental Health Sciences [NTP], the National Institutes of Health (NIH) Chemical Genomics Center/National Human Genome Research Institute [NCGC; now called the NIH Center for Translational Therapeutics, National Center for Advancing Translational Sciences] the Environmental Protection Agency's (EPA) National Center for Computational Toxicology, and recently the Food and Drug Administration) that are partnering to fundamentally change the science of safety toxicology. These agencies bring a comprehensive suite of capabilities and are working diligently together to develop, evaluate, and ultimately implement a new safety assessment paradigm. Toxicologic Pathology has an important ongoing role in establishing the validity of this transformation, and may ultimately benefit as a discipline through an enhanced understanding of chemically induced disease mechanisms.
JF  - Toxicologic Pathology
AU  - Bucher, John R
AD  - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA, bucher@niehs.nih.gov
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 125
EP  - 127
PB  - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL  - 41
IS  - 1
SN  - 0192-6233, 0192-6233
KW  - Toxicology Abstracts
KW  - Computer applications
KW  - Transformation
KW  - Translation
KW  - genomics
KW  - X 24310:Pharmaceuticals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1268655644?accountid=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+Tox21+and+Toxicologic+Pathology&rft.au=Bucher%2C+John+R&rft.aulast=Bucher&rft.aufirst=John&rft.date=2013-01-01&rft.volume=41&rft.issue=1&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623312450632
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Number of references - 5
N1  - Last updated - 2013-02-08
N1  - SubjectsTermNotLitGenreText - Transformation; Translation; genomics; Computer applications
DO  - http://dx.doi.org/10.1177/0192623312450632
ER  - 



TY  - JOUR
T1  - Mutational consequences of dNTP pool imbalances in E. coli
AN  - 1268651087; 17497324
AB  - The accuracy of DNA synthesis depends on the accuracy of the polymerase as well as the quality and concentration(s) of the available 5'-deoxynucleoside-triphosphate DNA precursors (dNTPs). The relationships between dNTPs and error rates have been studied in vitro, but only limited insights exist into these correlations during in vivo replication. We have investigated this issue in the bacterium Escherichia coli by analyzing the mutational properties of dcd and ndk strains. These strains, defective in dCTP deaminase and nucleoside diphosphate kinase, respectively, are characterized by both disturbances of dNTP pools and a mutator phenotype. ndk strains have been studied before, but were included in this study, as controversies exist regarding the source of its mutator phenotype. We show that dcd strains suffer from increased intracellular levels of dCTP (4-fold) and reduced levels of dGTP (2-fold), while displaying, as measured using a set of lacZ reversion markers in a mismatch-repair defective (mutL) background, a strong mutator effect for G.C arrow right T.A and A.T arrow right T.A transversions (27- and 42-fold enhancement, respectively). In contrast, ndk strains possess a lowered dATP level (4-fold) and modestly enhanced dCTP level (2-fold), while its mutator effect is specific for just the A.T arrow right T.A transversions. The two strains also display differential mutability for rifampicin-resistant mutants. Overall, our analysis reveals for both strains a satisfactory correlation between dNTP pool alterations and the replication error rates, and also suggests that a minimal explanation for the ndk mutator does not require assumptions beyond the predicted effect of the dNTP pools.
JF  - DNA Repair
AU  - Schaaper, Roel M
AU  - Mathews, Christopher K
AD  - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA, schaaper@niehs.nih.gov
Y1  - 2013/01/01/
PY  - 2013
DA  - 2013 Jan 01
SP  - 73
EP  - 79
PB  - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL  - 12
IS  - 1
SN  - 1568-7864, 1568-7864
KW  - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids
KW  - DNA replication fidelity
KW  - dNTP pools
KW  - DNA polymerase
KW  - dCTP deaminase
KW  - Nucleoside diphosphate kinase
KW  - DNA biosynthesis
KW  - Replication
KW  - Escherichia coli
KW  - Intracellular levels
KW  - Nucleoside-diphosphate kinase
KW  - Reversion
KW  - DNA repair
KW  - Transversion
KW  - J 02410:Animal Diseases
KW  - N 14820:DNA Metabolism & Structure
KW  - G 07770:Bacteria
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1268651087?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DNA+Repair&rft.atitle=Mutational+consequences+of+dNTP+pool+imbalances+in+E.+coli&rft.au=Schaaper%2C+Roel+M%3BMathews%2C+Christopher+K&rft.aulast=Schaaper&rft.aufirst=Roel&rft.date=2013-01-01&rft.volume=12&rft.issue=1&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=DNA+Repair&rft.issn=15687864&rft_id=info:doi/10.1016%2Fj.dnarep.2012.10.011
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2013-01-01
N1  - Last updated - 2016-04-13
N1  - SubjectsTermNotLitGenreText - DNA biosynthesis; Replication; Nucleoside-diphosphate kinase; Intracellular levels; Reversion; DNA repair; Transversion; dCTP deaminase; Escherichia coli
DO  - http://dx.doi.org/10.1016/j.dnarep.2012.10.011
ER  - 



TY  - JOUR
T1  - A multi-day environmental study of polycyclic aromatic hydrocarbon exposure in a high-risk region for esophageal cancer in China
AN  - 1257786507; 17482848
AB  - Linzhou, China has one of the highest rates of esophageal squamous cell carcinoma in the world. Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (BaP), may have a role in this increased risk. To better understand PAH sources, we measured PAHs in the air and food of 20 non-smokers over multiple days and compared the concentrations with a urinary PAH biomarker, 1-hydroxypyrene glucuronide (1-OHPG). Sampling occurred over 4 consecutive days. Kitchen air samples (days 2-3) and duplicate diet samples (days 1-4) were analyzed for 14 or more unique PAHs, including BaP. Daily urine samples (days 1-3) were analyzed for 1-OHPG. Mixed-effects models were used to evaluate the associations between air or food PAH concentrations and urine 1-OHPG concentrations. The median kitchen air BaP concentration was 10.2 ng/m super(3) (interquartile range (IQR): 5.1-20.2 ng/m super(3)). The median daily food BaP concentration and intake were 0.08 ng/g (IQR=0.04-0.16 ng/g) and 86 ng/day (IQR=41-142 ng/day), respectively. The median 1-OHPG concentration was 3.36 pmol/ml (IQR=2.09-6.98 pmol/ml). In mixed-effects models, 1-OHPG concentration increased with same-day concentration of food BaP (P=0.07). Although PAH concentrations in air were not associated with 1-OHPG concentrations, the high concentrations of PAHs in both air and food suggest that they are both important routes of exposure to PAHs in this population. Further evaluation of the role of PAH exposure from air and food in the elevated rates of esophageal cancer in this region is warranted.
JF  - Journal of Exposure Science and Environmental Epidemiology
AU  - Deziel, Nicole C
AU  - Wei, Wen-Qiang
AU  - Abnet, Christian C
AU  - Qiao, You-Lin
AU  - Sunderland, Deirdre
AU  - Ren, Jian-Song
AU  - Schantz, Michele M
AU  - Zhang, Yu
AU  - Strickland, Paul T
AU  - Abubaker, Salahaddin
AU  - Dawsey, Sanford M
AU  - Friesen, Melissa C
AU  - Roth, Mark J
AD  - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, Bethesda, Maryland, USA
Y1  - 2013/01//
PY  - 2013
DA  - Jan 2013
SP  - 52
EP  - 59
PB  - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL  - 23
IS  - 1
SN  - 1559-0631, 1559-0631
KW  - Risk Abstracts; Toxicology Abstracts; Pollution Abstracts; Health & Safety Science Abstracts
KW  - 1-Hydroxypyrene
KW  - Air sampling
KW  - Benzo(a)pyrene
KW  - Bioindicators
KW  - Cancer
KW  - Carcinogenicity
KW  - Diets
KW  - Environmental studies
KW  - Esophagus
KW  - Food
KW  - Kitchens
KW  - Polycyclic aromatic hydrocarbons
KW  - Risk factors
KW  - Risk groups
KW  - Sampling
KW  - Urine
KW  - biomarkers
KW  - squamous cell carcinoma
KW  - China, People's Rep.
KW  - H 11000:Diseases/Injuries/Trauma
KW  - P 0000:AIR POLLUTION
KW  - R2 23060:Medical and environmental health
KW  - X 24350:Industrial Chemicals
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257786507?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=A+multi-day+environmental+study+of+polycyclic+aromatic+hydrocarbon+exposure+in+a+high-risk+region+for+esophageal+cancer+in+China&rft.au=Deziel%2C+Nicole+C%3BWei%2C+Wen-Qiang%3BAbnet%2C+Christian+C%3BQiao%2C+You-Lin%3BSunderland%2C+Deirdre%3BRen%2C+Jian-Song%3BSchantz%2C+Michele+M%3BZhang%2C+Yu%3BStrickland%2C+Paul+T%3BAbubaker%2C+Salahaddin%3BDawsey%2C+Sanford+M%3BFriesen%2C+Melissa+C%3BRoth%2C+Mark+J&rft.aulast=Deziel&rft.aufirst=Nicole&rft.date=2013-01-01&rft.volume=23&rft.issue=1&rft.spage=52&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2012.73
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date revised - 2012-12-01
N1  - Last updated - 2013-02-08
N1  - SubjectsTermNotLitGenreText - Esophagus; Diets; Polycyclic aromatic hydrocarbons; Food; squamous cell carcinoma; biomarkers; Kitchens; Environmental studies; Urine; Risk factors; Risk groups; Benzo(a)pyrene; Sampling; 1-Hydroxypyrene; Bioindicators; Carcinogenicity; Air sampling; Cancer; China, People's Rep.
DO  - http://dx.doi.org/10.1038/jes.2012.73
ER  - 



TY  - JOUR
T1  - How to make a gonad: cellular mechanisms governing formation of the testes and ovaries.
AN  - 1239058997; 22614391
AB  - Sex determination of the gonad is an extraordinary process by which a single organ anlage is directed to form one of two different structures, a testis or an ovary. Morphogenesis of these two organs utilizes many common cellular events; differences in the timing and execution of these events must combine to generate sexually dimorphic structures. In this chapter, we review recent research on the cellular processes of gonad morphogenesis, focusing on data from mouse models. We highlight the shared cellular mechanisms in testis and ovary morphogenesis and examine the differences that enable formation of the two organs responsible for the perpetuation of all sexually reproducing species.
          Copyright © 2012 S. Karger AG, Basel.
JF  - Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation
AU  - Ungewitter, E K
AU  - Yao, H H-C
AD  - Reproductive Developmental Biology Group, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 7
EP  - 20
VL  - 7
IS  - 1-3
KW  - Index Medicus
KW  - Animals
KW  - Humans
KW  - Male
KW  - Female
KW  - Testis -- growth & development
KW  - Ovary -- growth & development
KW  - Ovary -- cytology
KW  - Cell Compartmentation
KW  - Morphogenesis
KW  - Testis -- cytology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1239058997?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Sexual+development+%3A+genetics%2C+molecular+biology%2C+evolution%2C+endocrinology%2C+embryology%2C+and+pathology+of+sex+determination+and+differentiation&rft.atitle=How+to+make+a+gonad%3A+cellular+mechanisms+governing+formation+of+the+testes+and+ovaries.&rft.au=Ungewitter%2C+E+K%3BYao%2C+H+H-C&rft.aulast=Ungewitter&rft.aufirst=E&rft.date=2013-01-01&rft.volume=7&rft.issue=1-3&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Sexual+development+%3A+genetics%2C+molecular+biology%2C+evolution%2C+endocrinology%2C+embryology%2C+and+pathology+of+sex+determination+and+differentiation&rft.issn=1661-5433&rft_id=info:doi/10.1159%2F000338612
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-09-16
N1  - Date created - 2012-12-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Biol Reprod. 2006 Nov;75(5):734-40 [16914692]
Nat Genet. 2006 Nov;38(11):1304-9 [17041600]
Sex Dev. 2008;2(3):128-33 [18769072]
Development. 2008 Nov;135(22):3731-43 [18927154]
Dev Biol. 2009 Feb 1;326(1):112-20 [19041858]
Dev Biol. 2009 May 1;329(1):96-103 [19268447]
Dev Dyn. 2009 May;238(5):1100-10 [19384968]
Development. 2009 Jun;136(11):1813-21 [19429785]
PLoS Biol. 2009 Sep;7(9):e1000196 [19753101]
Endocr Rev. 2009 Oct;30(6):624-712 [19776209]
Cell. 2009 Dec 11;139(6):1130-42 [20005806]
PLoS One. 2010;5(4):e10382 [20454446]
Proc Natl Acad Sci U S A. 2010 Jun 8;107(23):10526-31 [20498064]
Curr Top Dev Biol. 2010;90:231-62 [20691851]
Curr Top Dev Biol. 2010;90:263-90 [20691852]
Reproduction. 2010 Oct;140(4):489-504 [20628033]
Proc Natl Acad Sci U S A. 2011 Jan 4;108(1):167-72 [21173261]
Endocrinology. 2011 Apr;152(4):1199-208 [21248146]
Biol Reprod. 2012 Feb;86(2):37 [21976597]
Biol Reprod. 1993 Jul;49(1):13-23 [8353178]
J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):181-5 [11850223]
Endocrinology. 2002 Mar;143(3):1076-84 [11861535]
Development. 2002 Mar;129(5):1155-64 [11874911]
Biol Reprod. 2002 Apr;66(4):1134-50 [11906935]
Genes Dev. 2002 Jun 1;16(11):1433-40 [12050120]
Dev Biol. 2002 Jun 15;246(2):356-65 [12051821]
Hum Mol Genet. 2007 Dec 1;16(23):2795-804 [17728319]
Dev Biol. 2008 Feb 1;314(1):71-83 [18155190]
Hum Mol Genet. 2008 May 1;17(9):1278-91 [18250097]
Hum Mol Genet. 2008 May 1;17(9):1264-77 [18250098]
Proc Natl Acad Sci U S A. 2008 May 20;105(20):7212-7 [18480267]
Nature. 2008 Jun 12;453(7197):930-4 [18454134]
Science. 1999 Dec 17;286(5448):2328-31 [10600740]
Mol Reprod Dev. 2000 Jan;55(1):55-64 [10602274]
Development. 2000 Jan;127(1):65-73 [10654601]
Mol Reprod Dev. 2000 Aug;56(4):483-94 [10911398]
Mol Cell Endocrinol. 2000 May 25;163(1-2):3-9 [10963867]
Dev Biol. 2000 Sep 1;225(1):26-36 [10964462]
Biol Reprod. 2000 Dec;63(6):1617-28 [11090428]
Biol Reprod. 2000 Dec;63(6):1825-38 [11090455]
Cell. 2001 Mar 23;104(6):875-89 [11290325]
Dev Dyn. 2001 Jun;221(2):201-5 [11376487]
Mol Endocrinol. 2001 Jun;15(6):854-66 [11376106]
Biol Reprod. 2001 Nov;65(5):1392-402 [11673255]
Dev Biol. 2001 Dec 1;240(1):92-107 [11784049]
Genes Dev. 2003 Mar 15;17(6):800-10 [12651897]
Dev Biol. 2003 Jun 15;258(2):264-76 [12798287]
Dev Biol. 2003 Oct 15;262(2):303-12 [14550793]
Development. 2003 Dec;130(24):5895-902 [14561636]
Mol Cell Endocrinol. 2003 Dec 15;211(1-2):1-7 [14656469]
Development. 2004 Feb;131(4):933-42 [14736745]
Hum Mol Genet. 2004 Jun 1;13(11):1171-81 [15056605]
Dev Dyn. 2004 Jun;230(2):210-5 [15162500]
Nat Rev Genet. 2004 Jul;5(7):509-21 [15211353]
Mol Reprod Dev. 2004 Aug;68(4):422-8 [15236325]
Development. 2004 Aug;131(15):3627-36 [15229180]
J Anat. 1973 Nov;116(Pt 2):207-17 [4783416]
Dev Biol. 1975 May;44(1):1-21 [1132581]
J Reprod Fertil. 1975 Nov;45(2):201-9 [1239504]
Andrologia. 1978 Jan-Feb;10(1):1-21 [629409]
Biol Reprod. 1978 Nov;19(4):720-35 [743518]
Biol Reprod. 1979 May;20(4):773-8 [454765]
Prog Clin Biol Res. 1981;59B:383-92 [7279953]
J Embryol Exp Morphol. 1981 Jun;63:75-84 [7310296]
J Cell Biol. 1985 Jun;100(6):1941-7 [3889013]
Endocr Rev. 1985 Summer;6(3):371-99 [3896767]
J Cell Biol. 1985 Oct;101(4):1511-22 [4044644]
Dev Biol. 1986 Jan;113(1):119-34 [3943660]
Symp Soc Exp Biol. 1984;38:7-23 [6400220]
J Exp Zool. 1990 Jan;253(1):61-70 [2313242]
Nature. 1990 May 10;345(6271):167-70 [2336108]
Nature. 1990 Jul 19;346(6281):240-4 [1695712]
Nature. 1990 Jul 19;346(6281):245-50 [2374589]
Development. 1990 Jul;109(3):635-46 [2401216]
Nature. 1990 Nov 29;348(6300):450-2 [2247150]
Int Rev Cytol. 1991;124:43-101 [2001918]
Nature. 1991 May 9;351(6322):117-21 [2030730]
Bioessays. 1991 Apr;13(4):151-6 [1859392]
Development. 1990 Oct;110(2):521-8 [2133553]
Hum Genet. 1992 Feb;88(4):471-4 [1339396]
Dev Dyn. 1992 Jul;194(3):177-92 [1467554]
Development. 1993 Jan;117(1):273-81 [8223251]
Development. 1995 Jun;121(6):1603-14 [7600978]
Philos Trans R Soc Lond B Biol Sci. 1995 Nov 29;350(1333):263-8; discussion 268-9 [8570690]
Development. 1996 Sep;122(9):2813-22 [8787755]
Curr Biol. 1996 Mar 1;6(3):298-304 [8805249]
Nature. 1996 Oct 10;383(6600):531-5 [8849725]
Biol Reprod. 1997 Apr;56(4):938-45 [9096876]
Curr Biol. 1997 Dec 1;7(12):958-68 [9382843]
J Clin Endocrinol Metab. 1997 Dec;82(12):4243-51 [9398748]
Development. 1998 Sep;125(17):3323-8 [9693136]
Dev Biol. 1998 Nov 15;203(2):323-33 [9808783]
Nature. 1999 Feb 4;397(6718):405-9 [9989404]
Development. 1999 Jul;126(13):2883-90 [10357932]
Mol Endocrinol. 1999 Jun;13(6):1018-34 [10379899]
Exp Cell Res. 1961 Sep;24:495-507 [13871511]
Dev Biol. 2004 Dec 1;276(1):64-73 [15531364]
J Mol Endocrinol. 2004 Dec;33(3):705-15 [15591029]
Dev Biol. 2005 Nov 1;287(1):111-24 [16185683]
Biol Reprod. 2006 May;74(5):978-83 [16452457]
PLoS Biol. 2006 Jun;4(6):e187 [16700629]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1159/000338612
ER  - 



TY  - JOUR
T1  - Psychoactive 'bath salts': compounds, mechanisms, and toxicities.
AN  - 1151922083; 23147485
JF  - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
AU  - Lehner, Kurt R
AU  - Baumann, Michael H
AD  - Medicinal Chemistry Section, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA.
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 243
EP  - 244
VL  - 38
IS  - 1
KW  - Alkaloids
KW  - 0
KW  - Designer Drugs
KW  - Psychotropic Drugs
KW  - Street Drugs
KW  - cathinone
KW  - 540EI4406J
KW  - Index Medicus
KW  - Animals
KW  - Alkaloids -- chemistry
KW  - Humans
KW  - Alkaloids -- toxicity
KW  - Substance-Related Disorders -- metabolism
KW  - Substance-Related Disorders -- psychology
KW  - Psychotropic Drugs -- toxicity
KW  - Psychotropic Drugs -- chemistry
KW  - Street Drugs -- chemistry
KW  - Street Drugs -- toxicity
KW  - Designer Drugs -- toxicity
KW  - Designer Drugs -- chemistry
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1151922083?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Psychoactive+%27bath+salts%27%3A+compounds%2C+mechanisms%2C+and+toxicities.&rft.au=Lehner%2C+Kurt+R%3BBaumann%2C+Michael+H&rft.aulast=Lehner&rft.aufirst=Kurt&rft.date=2013-01-01&rft.volume=38&rft.issue=1&rft.spage=243&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.2012.162
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-05-02
N1  - Date created - 2012-11-13
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
Clin Toxicol (Phila). 2011 Jul;49(6):499-505 [21824061]
J Pharmacol Exp Ther. 2011 Nov;339(2):530-6 [21810934]
J Anal Toxicol. 2012 Jul;36(6):360-71 [22586208]
J Med Toxicol. 2012 Mar;8(1):33-42 [22108839]
Neuropsychopharmacology. 2012 Apr;37(5):1192-203 [22169943]
Fed Regist. 2011 Oct 21;76(204):65371-5 [22016903]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1038/npp.2012.162
ER  - 



TY  - JOUR
T1  - Heterogeneity of high-grade cervical intraepithelial neoplasia related to HPV16: implications for natural history and management.
AN  - 1124757807; 22488167
AB  - Factors associated with progression from cervical intraepithelial neoplasia (CIN) grades 2 and 3 to invasive cancer are not well understood; most CIN2 and CIN3 do not progress to cancer. Among carcinogenic human papillomavirus (HPV) types, infections with HPV16 have the highest risk of progressing to cancer. We evaluated the heterogeneity of risk factors, lesion size, colposcopic impression and colposcopic biopsy results in relation to HPV16 status among 627 women with CIN2 or CIN3 in women referred to colposcopy at the University of Oklahoma. Loop excision specimens were evaluated in 12 radial segments to estimate lesion size. The mean age at CIN3 was 27.7 years for HPV16-positive women (n = 225) and 33.6 years for HPV16-negative women (n = 104). The average lesion size did not differ by HPV16 status (p = 0.83). Among HPV16-positive women with CIN3, lesions were significantly larger in women 30 years and older (p = 0.03). Colposcopic impression was worse in women with HPV16 infections (p = 0.009), but the detection of CIN3 at the preceding biopsy was not improved in HPV16-positive women. CIN3 is detected at the same lesion size, but at much younger age in women with HPV16 infections, suggesting faster growth. CIN2 lesion size in women without HPV16 peaks below 30 years and then decreases, suggesting frequent regression, whereas HPV16-related CIN2 is more likely to persist. Lesion size seems to be an important determinant of colposcopy and biopsy performance. Genotyping for HPV16 in cervical cancer screening can improve risk stratification but may pose challenges to finding small lesions in colposcopy.
          Copyright © 2012 UICC.
JF  - International journal of cancer
AU  - Wentzensen, Nicolas
AU  - Walker, Joan
AU  - Schiffman, Mark
AU  - Yang, Hannah P
AU  - Zuna, Rosemary E
AU  - Dunn, S Terence
AU  - Allen, R Andy
AU  - Zhang, Roy
AU  - Sherman, Mark
AU  - Gold, Michael A
AU  - Wang, Sophia S
AD  - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20852-7234, USA. wentzenn@mail.nih.gov
Y1  - 2013/01/01/
PY  - 2013
DA  - 2013 Jan 01
SP  - 148
EP  - 154
VL  - 132
IS  - 1
KW  - Index Medicus
KW  - Genotype
KW  - Risk Factors
KW  - Humans
KW  - Electrosurgery -- methods
KW  - Adult
KW  - Disease Progression
KW  - Biopsy -- methods
KW  - Female
KW  - Colposcopy
KW  - Papillomavirus Infections -- pathology
KW  - Papillomavirus Infections -- diagnosis
KW  - Cervical Intraepithelial Neoplasia -- pathology
KW  - Human papillomavirus 16 -- isolation & purification
KW  - Cervical Intraepithelial Neoplasia -- surgery
KW  - Uterine Cervical Neoplasms -- diagnosis
KW  - Papillomavirus Infections -- virology
KW  - Cervical Intraepithelial Neoplasia -- virology
KW  - Uterine Cervical Neoplasms -- surgery
KW  - Uterine Cervical Neoplasms -- pathology
KW  - Uterine Cervical Neoplasms -- virology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1124757807?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Heterogeneity+of+high-grade+cervical+intraepithelial+neoplasia+related+to+HPV16%3A+implications+for+natural+history+and+management.&rft.au=Wentzensen%2C+Nicolas%3BWalker%2C+Joan%3BSchiffman%2C+Mark%3BYang%2C+Hannah+P%3BZuna%2C+Rosemary+E%3BDunn%2C+S+Terence%3BAllen%2C+R+Andy%3BZhang%2C+Roy%3BSherman%2C+Mark%3BGold%2C+Michael+A%3BWang%2C+Sophia+S&rft.aulast=Wentzensen&rft.aufirst=Nicolas&rft.date=2013-01-01&rft.volume=132&rft.issue=1&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27577
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-28
N1  - Date created - 2012-10-30
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Natl Cancer Inst. 2005 Jul 20;97(14):1072-9 [16030305]
Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):863-5 [19273486]
Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494]
Obstet Gynecol. 2010 Jul;116(1):177-85 [20567185]
J Natl Cancer Inst. 2010 Oct 6;102(19):1478-88 [20841605]
Int J Cancer. 2011 Feb 15;128(4):927-35 [20473886]
Int J Cancer. 2011 Mar 15;128(6):1354-62 [20506504]
Lancet Oncol. 2005 Apr;6(4):204 [15830458]
Am J Clin Pathol. 2011 Mar;135(3):468-75 [21350104]
Int J Cancer. 2007 Aug 1;121(3):621-32 [17405118]
Am J Obstet Gynecol. 2007 Jul;197(1):47.e1-8 [17618753]
J Low Genit Tract Dis. 2007 Oct;11(4):201-22 [17917566]
Lancet Oncol. 2008 May;9(5):425-34 [18407790]
Int J Cancer. 2009 Feb 15;124(4):964-9 [19030188]
Obstet Gynecol. 2009 Jan;113(1):18-25 [19104355]
Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):113-20 [19124488]
J Natl Cancer Inst. 2009 Apr 1;101(7):475-87 [19318628]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ijc.27577
ER  - 



TY  - JOUR
T1  - NOS2 enhances KRAS-induced lung carcinogenesis, inflammation and microRNA-21 expression.
AN  - 1124755639; 22618808
AB  - Mutant KRAS in lung cancers induces molecular pathways that regulate cellular proliferation, survival and inflammation, which enhance tumorigenesis. Inducible nitric oxide synthase (NOS2) upregulation and sustained nitric oxide generation are induced during the inflammatory response and correlate positively with lung tumorigenesis. To explore the mechanistic contribution of NOS2 to KRAS-induced lung tumorigenesis and inflammation, we used a genetic strategy of crossing NOS2 knockout (NOS2KO) C57BL6 inbred mice with a KRAS(G12D)-driven mouse lung cancer model. KRAS(G12D);NOS2KO mice exhibited delayed lung tumorigenesis and a longer overall survival time compared to that of KRAS(G12D);NOS2WT (wild-type) controls. Correspondingly, tumors in KRAS(G12D);NOS2KO mice had reduced tumor cell proliferation in adenomas and carcinomas. NOS2 deficiency also led to markedly suppressed inflammatory response by attenuation of macrophage recruitment into alveoli and within tumor foci. In contrast, FOXP3+ regulatory T cells were increased in tumors from KRAS(G12D) ;NOS2KO mice. We further analyzed the expression of microRNA-21 (miR-21), an oncogenic noncoding RNA involved in oncogenic Ras signaling, by quantitative reverse-transcription polymerase chain reaction and in situ hybridization. Lung carcinomas dissected from KRAS(G12D);NOS2KO mice showed a significantly reduced miR-21 expression along with decreased tumor cell proliferation, suggesting that NOS2 deficiency could attenuate RAS signaling pathways that transactivate miR-21 expression. Therefore, deletion of NOS2 decreases lung tumor growth as well as inflammatory responses initiated by oncogenic KRAS, suggesting that both KRAS and NOS2 cooperate in driving lung tumorigenesis and inflammation. Inhibition of NOS2 may have a therapeutic value in lung cancers with oncogenic KRAS mutations.
          Copyright © 2012 UICC.
JF  - International journal of cancer
AU  - Okayama, Hirokazu
AU  - Saito, Motonobu
AU  - Oue, Naohide
AU  - Weiss, Jonathan M
AU  - Stauffer, Jimmy
AU  - Takenoshita, Seiichi
AU  - Wiltrout, Robert H
AU  - Hussain, S Perwez
AU  - Harris, Curtis C
AD  - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Y1  - 2013/01/01/
PY  - 2013
DA  - 2013 Jan 01
SP  - 9
EP  - 18
VL  - 132
IS  - 1
KW  - Forkhead Transcription Factors
KW  - 0
KW  - Foxp3 protein, mouse
KW  - MIRN21 microRNA, mouse
KW  - MicroRNAs
KW  - Nitric Oxide Synthase Type II
KW  - EC 1.14.13.39
KW  - Nos2 protein, mouse
KW  - Kras2 protein, mouse
KW  - EC 3.6.5.2
KW  - Proto-Oncogene Proteins p21(ras)
KW  - Index Medicus
KW  - Pulmonary Alveoli -- pathology
KW  - Animals
KW  - Cell Growth Processes -- physiology
KW  - Inflammation -- genetics
KW  - Mice
KW  - T-Lymphocytes, Regulatory -- metabolism
KW  - Mice, Knockout
KW  - Forkhead Transcription Factors -- genetics
KW  - Pulmonary Alveoli -- metabolism
KW  - Mice, Inbred C57BL
KW  - Mutation -- genetics
KW  - Inflammation -- metabolism
KW  - Forkhead Transcription Factors -- metabolism
KW  - Inflammation -- pathology
KW  - Macrophages -- metabolism
KW  - Proto-Oncogene Proteins p21(ras) -- metabolism
KW  - Cell Transformation, Neoplastic -- pathology
KW  - Nitric Oxide Synthase Type II -- deficiency
KW  - MicroRNAs -- genetics
KW  - Cell Transformation, Neoplastic -- metabolism
KW  - MicroRNAs -- biosynthesis
KW  - Lung Neoplasms -- genetics
KW  - Nitric Oxide Synthase Type II -- metabolism
KW  - Nitric Oxide Synthase Type II -- genetics
KW  - Cell Transformation, Neoplastic -- genetics
KW  - Proto-Oncogene Proteins p21(ras) -- genetics
KW  - Lung Neoplasms -- pathology
KW  - Lung Neoplasms -- metabolism
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1124755639?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=NOS2+enhances+KRAS-induced+lung+carcinogenesis%2C+inflammation+and+microRNA-21+expression.&rft.au=Okayama%2C+Hirokazu%3BSaito%2C+Motonobu%3BOue%2C+Naohide%3BWeiss%2C+Jonathan+M%3BStauffer%2C+Jimmy%3BTakenoshita%2C+Seiichi%3BWiltrout%2C+Robert+H%3BHussain%2C+S+Perwez%3BHarris%2C+Curtis+C&rft.aulast=Okayama&rft.aufirst=Hirokazu&rft.date=2013-01-01&rft.volume=132&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27644
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-28
N1  - Date created - 2012-10-30
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
PLoS One. 2010;5(11):e15541 [21124965]
Oncogene. 2011 Jan 20;30(3):275-86 [20956945]
Nat Rev Genet. 2010 Sep;11(9):597-610 [20661255]
Cancer Cell. 2010 Sep 14;18(3):282-93 [20832755]
Cancer Res. 2010 Oct 15;70(20):8108-16 [20813833]
J Exp Med. 2010 Oct 25;207(11):2455-67 [20921282]
Cancer Res. 2010 Nov 1;70(21):8288-98 [20978195]
J Leukoc Biol. 2010 Dec;88(6):1157-62 [20807706]
Cell Cycle. 2011 Feb 15;10(4):619-24 [21293193]
CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855]
Clin Cancer Res. 2011 Apr 1;17(7):1875-82 [21350005]
J Natl Cancer Inst. 2011 Jul 20;103(14):1112-22 [21685357]
Int J Cancer. 2012 Apr 15;130(8):1733-44 [21544811]
Int J Cancer. 2012 Aug 1;131(3):760-5 [22042537]
Clin Cancer Res. 2000 Dec;6(12):4739-44 [11156228]
Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630]
Cancer Res. 2002 Dec 1;62(23):6850-6 [12460898]
Nat Rev Cancer. 2003 Jan;3(1):11-22 [12509763]
Int J Cancer. 2003 Aug 10;106(1):1-7 [12794750]
Cancer Res. 2004 Apr 1;64(7):2307-16 [15059877]
Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):8894-9 [15178764]
Gut. 2004 Sep;53(9):1250-5 [15306579]
Cancer Res. 2004 Oct 1;64(19):6849-53 [15466171]
Vet Pathol. 1990 Jul;27(4):274-81 [2169666]
Cancer Cell. 2004 Nov;6(5):447-58 [15542429]
Nat Med. 1998 Dec;4(12):1371-6 [9846573]
Br J Cancer. 1998 Aug;78(4):534-41 [9716040]
Cancer Res. 2005 Apr 15;65(8):3226-35 [15833854]
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460]
Cancer Cell. 2006 Mar;9(3):189-98 [16530703]
Oncogene. 2006 Mar 30;25(14):2105-12 [16288213]
Nat Rev Cancer. 2006 Jul;6(7):521-34 [16794635]
Vet Pathol. 2006 Sep;43(5):682-8 [16966445]
Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16472-7 [17060621]
Int J Cancer. 2007 Feb 15;120(4):796-805 [17096325]
Cancer Res. 2007 Jan 1;67(1):289-99 [17210710]
Genes Dev. 2007 Jul 15;21(14):1714-9 [17639077]
Nature. 2008 Jul 24;454(7203):436-44 [18650914]
Cancer Res. 2008 Sep 1;68(17):7130-6 [18757428]
N Engl J Med. 2008 Sep 25;359(13):1367-80 [18815398]
Oncogene. 2009 Jan 8;28(1):73-84 [18850008]
Am J Respir Cell Mol Biol. 2009 Apr;40(4):443-53 [18927348]
Curr Med Chem. 2009;16(19):2373-94 [19601787]
Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12085-90 [19597153]
Nat Cell Biol. 2009 Sep;11(9):1135-42 [19701195]
Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19455-60 [19892741]
Carcinogenesis. 2010 Jan;31(1):37-49 [19955394]
J Immunol. 2010 Feb 15;184(4):1799-809 [20083653]
Curr Pharm Des. 2010;16(4):411-20 [20236069]
Adv Cancer Res. 2010;107:57-117 [20399961]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1002/ijc.27644
ER  - 



TY  - JOUR
T1  - Oral and pharyngeal epithelial keratinocyte culture.
AN  - 1115527944; 23097101
AB  - Primary human oral epithelial cells are readily available and have been recently employed for tissue engineering. These cells are currently being widely utilized in multiple research efforts, ranging from the study of oral biology, mucosal immunity, and carcinogenesis to stem cell biology and tissue engineering. This chapter describes step-by-step protocols for the successful isolation and culture of human oral epithelial cells and fibroblasts, and techniques for their use in two-dimensional and three-dimensional culture systems. The described methods will enable to generate reconstituted tissues that resemble epithelial like structures in vitro, which can recapitulate some of the key features of the oral epithelium in vivo.
JF  - Methods in molecular biology (Clifton, N.J.)
AU  - Leelahavanichkul, Kantima
AU  - Gutkind, J Silvio
AD  - Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, Bethesda, MD, USA.
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 67
EP  - 79
VL  - 945
KW  - Collagen
KW  - 9007-34-5
KW  - Nitrogen
KW  - N762921K75
KW  - Index Medicus
KW  - Nitrogen -- chemistry
KW  - Animals
KW  - Humans
KW  - Fibroblasts -- cytology
KW  - Collagen -- chemistry
KW  - Cell Proliferation
KW  - Cryopreservation
KW  - Oropharynx -- cytology
KW  - Keratinocytes -- cytology
KW  - Cell Culture Techniques -- methods
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1115527944?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Oral+and+pharyngeal+epithelial+keratinocyte+culture.&rft.au=Leelahavanichkul%2C+Kantima%3BGutkind%2C+J+Silvio&rft.aulast=Leelahavanichkul&rft.aufirst=Kantima&rft.date=2013-01-01&rft.volume=945&rft.issue=&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-62703-125-7_5
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-03-28
N1  - Date created - 2012-10-25
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/978-1-62703-125-7_5
ER  - 



TY  - JOUR
T1  - AMPAKINE enhancement of social interaction in the BTBR mouse model of autism.
AN  - 1041140263; 22801296
AB  - Autism is a neurodevelopmental disorder in which the first diagnostic symptom is unusual reciprocal social interactions. Approximately half of the children diagnosed with an autism spectrum disorder also have intellectual impairments. General cognitive abilities may be fundamental to many aspects of social cognition. Cognitive enhancers could conceivably be of significant benefit to children and adults with autism. AMPAKINE compounds are a novel class of pharmacological agents that act as positive modulators of AMPA receptors to enhance excitatory glutamatergic neurotransmission. This class of compounds was reported to improve learning and memory in several rodent and non-human primate tasks, and to normalize respiratory abnormalities in a mouse model of Rett syndrome. Here we evaluate the actions of AMPA compounds in adult male and female BTBR mice, a well characterized mouse model of autism. Acute treatment with CX1837 and CX1739 reversed the deficit in sociability in BTBR mice on the most sensitive parameter, time spent sniffing a novel mouse as compared to time spent sniffing a novel object. The less sensitive parameter, time in the chamber containing the novel mouse versus time in the chamber containing the novel object, was not rescued by CX1837 or CX1739 treatment. Preliminary data with CX546, in which β-cyclodextrin was the vehicle, revealed behavioral effects of the acute intraperitoneal and oral administration of vehicle alone. To circumvent the artifacts introduced by the vehicle administration, we employed a novel treatment regimen using pellets of peanut butter for drug delivery. Absence of vehicle treatment effects when CX1837 and CX1739 were given in the peanut butter pellets, to multiple cohorts of BTBR and B6 control mice, confirmed that the pharmacologically-induced improvements in sociability in BTBR were not confounded by the administration procedures. The highest dose of CX1837 improved the cognitive deficit in novel object recognition in BTBR. No drug effects were detected on the high levels of repetitive self-grooming in BTBR. In open field tests, CX1837 and CX1739 did not induce hyperactivity or sedation in either strain. It is interesting to speculate that the ability of CX1837 and CX1739 to restore aspects of sociability in BTBR mice could utilize synaptic mechanisms regulating social cognition, suggesting a potential pharmacological target for interventions to treat symptoms of autism. This article is part of a Special Issue entitled 'Cognitive Enhancers'.
          Published by Elsevier Ltd.
JF  - Neuropharmacology
AU  - Silverman, J L
AU  - Oliver, C F
AU  - Karras, M N
AU  - Gastrell, P T
AU  - Crawley, J N
AD  - Laboratory of Behavioral Neuroscience, National Institute of Mental Health, Bethesda, MD 20892-3730, USA. jill.silverman@ucdmc.ucdavis.edu
Y1  - 2013/01//
PY  - 2013
DA  - January 2013
SP  - 268
EP  - 282
VL  - 64
KW  - 1-(1,4-benzodioxan-6-ylcarbonyl)piperidine
KW  - 0
KW  - Dioxoles
KW  - Drugs, Investigational
KW  - Excitatory Amino Acid Agonists
KW  - Nootropic Agents
KW  - Piperidines
KW  - Receptors, AMPA
KW  - Index Medicus
KW  - Social Behavior Disorders -- prevention & control
KW  - Animals
KW  - Cognition Disorders -- etiology
KW  - Random Allocation
KW  - Dose-Response Relationship, Drug
KW  - Drugs, Investigational -- adverse effects
KW  - Mice
KW  - Dioxoles -- administration & dosage
KW  - Piperidines -- adverse effects
KW  - Drugs, Investigational -- therapeutic use
KW  - Recognition (Psychology) -- drug effects
KW  - Mice, Inbred Strains
KW  - Behavior, Animal -- drug effects
KW  - Piperidines -- therapeutic use
KW  - Cognition Disorders -- prevention & control
KW  - Dioxoles -- adverse effects
KW  - Social Behavior Disorders -- etiology
KW  - Mice, Inbred C57BL
KW  - Piperidines -- administration & dosage
KW  - Drugs, Investigational -- administration & dosage
KW  - Dioxoles -- therapeutic use
KW  - Male
KW  - Female
KW  - Nootropic Agents -- administration & dosage
KW  - Excitatory Amino Acid Agonists -- therapeutic use
KW  - Social Behavior
KW  - Molecular Targeted Therapy
KW  - Autistic Disorder -- drug therapy
KW  - Excitatory Amino Acid Agonists -- administration & dosage
KW  - Disease Models, Animal
KW  - Nootropic Agents -- therapeutic use
KW  - Receptors, AMPA -- agonists
KW  - Excitatory Amino Acid Agonists -- adverse effects
KW  - Nootropic Agents -- adverse effects
KW  - Autistic Disorder -- physiopathology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1041140263?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=AMPAKINE+enhancement+of+social+interaction+in+the+BTBR+mouse+model+of+autism.&rft.au=Silverman%2C+J+L%3BOliver%2C+C+F%3BKarras%2C+M+N%3BGastrell%2C+P+T%3BCrawley%2C+J+N&rft.aulast=Silverman&rft.aufirst=J&rft.date=2013-01-01&rft.volume=64&rft.issue=&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=1873-7064&rft_id=info:doi/10.1016%2Fj.neuropharm.2012.07.013
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2013-02-11
N1  - Date created - 2012-09-18
N1  - Date revised - 2017-01-13
N1  - SuppNotes - Cited By:
J Autism Dev Disord. 2009 Nov;39(11):1613-9 [19572193]
J Psychiatry Neurosci. 2012 May;37(3):154-69 [22297065]
Sci Transl Med. 2012 Apr 25;4(131):131ra51 [22539775]
J Neurosci. 2012 May 9;32(19):6525-41 [22573675]
Neurobiol Dis. 2012 Aug;47(2):210-5 [22525571]
J Autism Dev Disord. 2012 Jul;42(7):1326-41 [21932156]
Prog Neuropsychopharmacol Biol Psychiatry. 2012 Aug 7;38(2):260-9 [22542870]
Behav Brain Res. 2012 Sep 1;234(1):33-7 [22677272]
Physiol Behav. 2012 Dec 5;107(5):649-62 [22245067]
Clin Pharmacol Ther. 2010 Feb;87(2):204-11 [19907420]
Neuropsychopharmacology. 2010 Mar;35(4):976-89 [20032969]
Neurosci Lett. 2010 Mar 3;471(2):63-5 [20036313]
Psychol Med. 2011 Mar;41(3):619-27 [21272389]
Autism Res. 2011 Feb;4(1):17-27 [20928844]
Genes Brain Behav. 2011 Mar;10(2):228-35 [21040460]
Brain Res. 2011 Mar 22;1380:34-41 [21078305]
Conscious Cogn. 2011 Mar;20(1):130-40 [20932779]
Pediatr Res. 2011 May;69(5 Pt 2):55R-62R [21289537]
Pharmacol Biochem Behav. 2011 Aug;99(2):116-29 [21215768]
Pharmacol Biochem Behav. 2011 Aug;99(2):146-54 [21334367]
Bioorg Med Chem Lett. 2011 Jul 1;21(13):3927-30 [21636273]
Bioorg Med Chem Lett. 2011 Jul 1;21(13):3923-6 [21636275]
Curr Protoc Neurosci. 2011 Jul;Chapter 8:Unit 8.26 [21732314]
Anat Rec (Hoboken). 2011 Oct;294(10):1713-25 [21905241]
J Neurosci. 2000 Mar 15;20(6):RC65 [10704519]
Neuron. 2000 Nov;28(2):355-63 [11144346]
J Cogn Neurosci. 2001 Feb 15;13(2):232-40 [11244548]
Synapse. 2001 May;40(2):154-8 [11252027]
Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11047-54 [11572967]
Brain. 2002 Apr;125(Pt 4):752-64 [11912109]
J Mol Neurosci. 2002 Feb-Apr;18(1-2):151-65 [11931346]
Arch Gen Psychiatry. 2002 Sep;59(9):809-16 [12215080]
Nat Neurosci. 2002 Nov;5 Suppl:1035-8 [12403980]
Psychopharmacology (Berl). 2003 Jan;165(3):260-9 [12417966]
J Autism Dev Disord. 2003 Aug;33(4):403-15 [12959419]
J Pharmacol Exp Ther. 2003 Oct;307(1):297-305 [12893840]
Neuroscience. 2003;121(2):509-21 [14522010]
Curr Opin Pharmacol. 2004 Feb;4(1):4-11 [15018832]
Pediatrics. 2004 May;113(5):e472-86 [15121991]
J Child Psychol Psychiatry. 2004 Sep;45(6):1115-22 [15257668]
Psychol Med. 2010 Apr;40(4):569-79 [19671209]
Behav Pharmacol. 2009 Oct;20(7):662-7 [19741506]
Nat Rev Neurosci. 2010 Jul;11(7):490-502 [20559336]
Behav Brain Res. 2010 Dec 25;214(2):443-9 [20600340]
Trends Cogn Sci. 2010 Oct;14(10):441-7 [20674467]
Behav Brain Res. 2011 Jan 1;216(1):446-51 [20816701]
Neuroscience. 2010 Dec 29;171(4):1197-208 [20888890]
J Neurochem. 2011 Jan;116(2):291-303 [21070242]
Behav Brain Res. 2011 Mar 1;217(2):302-8 [21055421]
J Autism Dev Disord. 2011 Feb;41(2):148-57 [20499148]
Genes Brain Behav. 2011 Feb;10(1):35-43 [20345893]
Genes Brain Behav. 2011 Feb;10(1):44-56 [20618443]
Genes Brain Behav. 2004 Oct;3(5):303-14 [15344923]
J Child Neurol. 1988;3 Suppl:S57-64 [3058787]
J Clin Exp Neuropsychol. 1993 Nov;15(6):933-46 [8120129]
J Child Psychol Psychiatry. 1995 Sep;36(6):1065-76 [7593399]
Psychol Bull. 1997 Jan;121(1):114-32 [9000894]
Behav Brain Res. 1997 Feb;83(1-2):15-23 [9062655]
J Neurosci. 1998 Apr 1;18(7):2740-7 [9502831]
J Neurosci. 1998 Apr 1;18(7):2748-63 [9502832]
J Med Chem. 2004 Nov 18;47(24):5829-32 [15537339]
Brain. 2005 May;128(Pt 5):1038-48 [15758039]
Int J Obes (Lond). 2005 Jun;29(6):607-14 [15795750]
PLoS Biol. 2005 Sep;3(9):e299 [16104830]
Bioorg Med Chem Lett. 2011 Oct 15;21(20):6170-5 [21889339]
PLoS One. 2011;6(10):e25322 [21998649]
Results Probl Cell Differ. 2012;54:297-335 [22009360]
Bioorg Med Chem Lett. 2011 Dec 15;21(24):7455-9 [22056742]
Neurosci Biobehav Rev. 2012 Jan;36(1):285-96 [21741402]
Annu Rev Psychol. 2012;63:287-313 [21838544]
Curr Alzheimer Res. 2011 Dec;8(8):876-82 [22171951]
Behav Brain Res. 2012 Feb 1;227(1):64-72 [22056750]
Neurosci Biobehav Rev. 2012 Feb;36(2):901-42 [22101112]
Arch Gen Psychiatry. 2012 Mar;69(3):306-13 [22065253]
Neurosci Biobehav Rev. 2012 Apr;36(4):1292-313 [22353426]
Trends Cogn Sci. 2012 Apr;16(4):231-9 [22425667]
J Clin Psychiatry. 2005;66 Suppl 10:3-8 [16401144]
Brain Res. 2006 Mar 24;1079(1):98-105 [16513097]
Trends Neurosci. 2006 Oct;29(10):554-62 [16890999]
Behav Brain Res. 2007 Jan 10;176(1):4-20 [16971002]
Behav Brain Res. 2007 Jan 10;176(1):21-6 [17097158]
Neuropsychopharmacology. 2007 Apr;32(4):745-56 [16936708]
Curr Drug Targets. 2007 May;8(5):583-602 [17504103]
Childs Nerv Syst. 2007 Jul;23(7):815-9 [17387490]
Learn Mem. 2007 Aug;14(8):533-8 [17686947]
J Neurosci. 2007 Oct 3;27(40):10912-7 [17913925]
Neuroimaging Clin N Am. 2007 Nov;17(4):495-509, ix [17983966]
Int J Dev Neurosci. 2007 Dec;25(8):515-21 [17980995]
Am J Psychiatry. 2008 Feb;165(2):203-13 [18172019]
Genes Brain Behav. 2008 Mar;7(2):152-63 [17559418]
Eur J Pharmacol. 2008 May 6;585(1):2-13 [18374328]
Brain Res. 2008 May 19;1210:179-88 [18417102]
Pharmacol Biochem Behav. 2008 Jul;90(1):58-64 [18455219]
PLoS One. 2008;3(8):e3067 [18728777]
Ann N Y Acad Sci. 2008 Dec;1145:283-99 [19076404]
J Child Psychol Psychiatry. 2009 Jan;50(1-2):108-15 [19220594]
Neuroscience. 2009 Mar 3;159(1):283-95 [19141314]
Proc Natl Acad Sci U S A. 2009 Mar 24;106(12):4906-11 [19264961]
Eur J Neurosci. 2009 Apr;29(8):1663-77 [19419429]
Philos Trans R Soc Lond B Biol Sci. 2009 May 27;364(1522):1377-83 [19528020]
Neuropsychologia. 2009 Oct;47(12):2515-26 [19410583]
Biochem Pharmacol. 2009 Oct 1;78(7):658-67 [19406107]
Respir Physiol Neurobiol. 2009 Aug 31;168(1-2):153-7 [19712906]
Psychopharmacology (Berl). 2009 Nov;206(4):631-40 [19390843]
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1016/j.neuropharm.2012.07.013
ER  - 



TY  - JOUR
T1  - Prolonged intravenous infusion of sodium nitrite delivers nitric oxide (NO) in humans.
AN  - 1033533994; 22890643
AB  - In preclinical studies, infusion of sodium nitrite delivers nitric oxide (NO) as treatment of vasospasm after subarachnoid hemorrhage. We evaluated safety and toxicity of intravenous nitrite administration in healthy volunteers infused with increasing doses of sodium nitrite for 48 h. Twelve volunteers (5 men, 7 women; mean age was 38.8 years, range 27-56 years) participated in the study. The starting sodium nitrite dose was 4.2 mg/kg/h, and it was doubled for each subsequent volunteer up to a maximal dose of 533.8 mg/kg/h at which a clinically silent dose-limiting toxicity (DLT) was observed. Toxicity included a transient decrease of mean arterial blood pressure or asymptomatic increase of methemoglobin level above 5%. The maximal tolerated dose (MTD) was 267 mg/kg/h. S-Nitrosothiols increased significantly in plasma, confirming in vivo sodium nitrite reduction to NO and encouraging its use against vasospasm and ischemia-reperfusion injury to the brain, kidneys, liver, and heart.
JF  - Acta neurochirurgica. Supplement
AU  - Pluta, Ryszard M
AD  - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. rysiek@ninds.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 49
EP  - 51
VL  - 115
SN  - 0065-1419, 0065-1419
KW  - Nitric Oxide
KW  - 31C4KY9ESH
KW  - Sodium Nitrite
KW  - M0KG633D4F
KW  - Index Medicus
KW  - Young Adult
KW  - Infusions, Intravenous
KW  - Humans
KW  - Adult
KW  - Middle Aged
KW  - Maximum Tolerated Dose
KW  - Time Factors
KW  - Male
KW  - Female
KW  - Sodium Nitrite -- administration & dosage
KW  - Arterial Pressure -- drug effects
KW  - Nitric Oxide -- blood
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033533994?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+neurochirurgica.+Supplement&rft.atitle=Prolonged+intravenous+infusion+of+sodium+nitrite+delivers+nitric+oxide+%28NO%29+in+humans.&rft.au=Pluta%2C+Ryszard+M&rft.aulast=Pluta&rft.aufirst=Ryszard&rft.date=2013-01-01&rft.volume=115&rft.issue=&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Acta+neurochirurgica.+Supplement&rft.issn=00651419&rft_id=info:doi/10.1007%2F978-3-7091-1192-5_11
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2012-12-18
N1  - Date created - 2012-08-14
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/978-3-7091-1192-5_11
ER  - 



TY  - JOUR
T1  - Non-human primate models of alcohol-related phenotypes: the influence of genetic and environmental factors.
AN  - 1030349927; 21706389
AB  - Because of their complex social structures, behaviors, and genetic similarities to humans, nonhuman primates are useful for studying how genetic factors influence alcohol consumption. The neurobiological systems that influence addiction vulnerability may do so by acting on alcohol response, reward pathways, behavioral dyscontrol, and vulnerability to stress and anxiety. Rhesus macaques show individual differences in alcohol response and temperament, and such differences are influenced by genetic variants that are similar functionally to those present in humans. Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (MAOA-LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (CRH-248C/T and -2232 C/G), Neuropeptide Y (NPY-1002 T/G), and the μ-opioid receptor (OPRM1 C77G). These provide opportunities for modeling how genetic and environmental factors (i.e., stress, individual's sex, or alcohol exposure) interact to influence alcohol consumption. Studies in primates may also reveal selective factors have driven maintenance or fixation of alleles that increase risk for alcohol use disorders in modern humans.
JF  - Current topics in behavioral neurosciences
AU  - Barr, Christina S
AD  - Section of Comparative Behavioral Genomics, NIH/NIAAA/LNG, Rockville, MD 20852, USA. cbarr@mail.nih.gov
Y1  - 2013
PY  - 2013
DA  - 2013
SP  - 223
EP  - 249
VL  - 13
SN  - 1866-3370, 1866-3370
KW  - Neuropeptide Y
KW  - 0
KW  - Receptors, Opioid, mu
KW  - Serotonin Plasma Membrane Transport Proteins
KW  - Monoamine Oxidase
KW  - EC 1.4.3.4
KW  - Index Medicus
KW  - Phenotype
KW  - Animals
KW  - Humans
KW  - Mutation -- genetics
KW  - Disease Models, Animal
KW  - Serotonin Plasma Membrane Transport Proteins -- genetics
KW  - Primates
KW  - Receptors, Opioid, mu -- genetics
KW  - Neuropeptide Y -- genetics
KW  - Monoamine Oxidase -- genetics
KW  - Alcohol-Related Disorders -- genetics
KW  - Gene-Environment Interaction
KW  - Alcohol-Related Disorders -- etiology
UR  - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1030349927?accountid=14244
L2  - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+behavioral+neurosciences&rft.atitle=Non-human+primate+models+of+alcohol-related+phenotypes%3A+the+influence+of+genetic+and+environmental+factors.&rft.au=Barr%2C+Christina+S&rft.aulast=Barr&rft.aufirst=Christina&rft.date=2013-01-01&rft.volume=13&rft.issue=&rft.spage=223&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+behavioral+neurosciences&rft.issn=18663370&rft_id=info:doi/10.1007%2F7854_2011_142
LA  - English
DB  - ProQuest Environmental Science Collection
N1  - Date completed - 2012-11-13
N1  - Date created - 2012-07-30
N1  - Date revised - 2017-01-13
N1  - Last updated - 2017-01-18
DO  - http://dx.doi.org/10.1007/7854_2011_142
ER  -