Institution
Virginia Commonwealth University
Education•Richmond, Virginia, United States•
About: Virginia Commonwealth University is a education organization based out in Richmond, Virginia, United States. It is known for research contribution in the topics: Population & Health care. The organization has 23822 authors who have published 49587 publications receiving 1787046 citations. The organization is also known as: VCU.
Topics: Population, Health care, Poison control, Medicine, Cancer
Papers published on a yearly basis
Papers
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Virginia Commonwealth University1, University of Rochester2, Duke University3, National Institutes of Health4, University of Southern California5, United States Environmental Protection Agency6, North Carolina State University7, Harvard University8, Old Dominion University9, University of Washington10, University of California, Irvine11, University of California, Los Angeles12, University of Maryland, Baltimore13, Icahn School of Medicine at Mount Sinai14
TL;DR: Recent findings that have established the effects of inhaled air pollutants in the brain, explore the potential mechanisms driving these phenomena, and discuss the recommended research priorities/approaches that were identified by the panel.
Abstract: Accumulating evidence suggests that outdoor air pollution may have a significant impact on central nervous system (CNS) health and disease. To address this issue, the National Institute of Environmental Health Sciences/National Institute of Health convened a panel of research scientists that was assigned the task of identifying research gaps and priority goals essential for advancing this growing field and addressing an emerging human health concern. Here, we review recent findings that have established the effects of inhaled air pollutants in the brain, explore the potential mechanisms driving these phenomena, and discuss the recommended research priorities/approaches that were identified by the panel.
434 citations
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TL;DR: The results with these Sphk1 null mice reveal that some key physiologic processes that require S1P receptor signaling, such as vascular development and proper lymphocyte distribution, can occur in the absence of SPHK1.
434 citations
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Raymond K. Walters1, Raymond K. Walters2, Renato Polimanti3, Emma C. Johnson4 +168 more•Institutions (48)
TL;DR: The largest genome-wide association study to date of DSM-IV-diagnosed AD found loci associated with AD and characterized the relationship between AD and other psychiatric and behavioral outcomes, underscoring the genetic distinction between pathological and nonpathological drinking behaviors.
Abstract: Liability to alcohol dependence (AD) is heritable, but little is known about its complex polygenic architecture or its genetic relationship with other disorders. To discover loci associated with AD and characterize the relationship between AD and other psychiatric and behavioral outcomes, we carried out the largest genome-wide association study to date of DSM-IV-diagnosed AD. Genome-wide data on 14,904 individuals with AD and 37,944 controls from 28 case-control and family-based studies were meta-analyzed, stratified by genetic ancestry (European, n = 46,568; African, n = 6,280). Independent, genome-wide significant effects of different ADH1B variants were identified in European (rs1229984; P = 9.8 × 10-13) and African ancestries (rs2066702; P = 2.2 × 10-9). Significant genetic correlations were observed with 17 phenotypes, including schizophrenia, attention deficit-hyperactivity disorder, depression, and use of cigarettes and cannabis. The genetic underpinnings of AD only partially overlap with those for alcohol consumption, underscoring the genetic distinction between pathological and nonpathological drinking behaviors.
434 citations
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University of Bonn1, Cardiff University2, Eli Lilly and Company3, Harvard University4, State University of New York Upstate Medical University5, NorthShore University HealthSystem6, University of California, San Diego7, National Institutes of Health8, Stanford University9, University of North Carolina at Chapel Hill10, Trinity College, Dublin11, Radboud University Nijmegen12, University of Pennsylvania13, University of St Andrews14, University of Western Australia15, University of California, Los Angeles16, Washington University in St. Louis17, University of Pittsburgh18, Johns Hopkins University19, Icahn School of Medicine at Mount Sinai20, University of Illinois at Urbana–Champaign21, University of Helsinki22, Université de Montréal23, University of Washington24, University of Toronto25, Vanderbilt University26, McMaster University27, University of Oslo28, University of Edinburgh29, University of Michigan30, University College London31, GlaxoSmithKline32, Indiana University33, Virginia Commonwealth University34, VU University Amsterdam35, University of Iowa36, University of California, San Francisco37, Howard University38, Institute of Physics39, QIMR Berghofer Medical Research Institute40, Columbia University41, Pfizer42, Rush University Medical Center43, Mayo Clinic44, Georgetown University45, Karolinska Institutet46, National Institute for Health and Welfare47, University of Queensland48, University of Aberdeen49, North Carolina State University50
TL;DR: GWAS methods have detected a remarkable number of robust genetic associations for dozens of common diseases and traits, leading to new pathophysiological hypotheses, although only small proportions of genetic variance have been explained thus far and therapeutic applications will require substantial further effort.
Abstract: Objective: The authors conducted a review of the history and empirical basis of genomewide association studies (GWAS), the rationale for GWAS of psychiatric disorders, results to date, limitations, and plans for GWAS meta-analyses. Method: A literature review was carried out, power and other issues discussed, and planned studies assessed. Results: Most of the genomic DNA sequence differences between any two people are common (frequency >5%) single nucleotide polymorphisms (SNPs). Because of localized patterns of correlation (linkage disequilibrium), 500,000 to 1,000,000 of these SNPs can test the hypothesis that one or more common variants explain part of the genetic risk for a disease. GWAS technologies can also detect some of the copy number variants (deletions and duplications) in the genome. Systematic study of rare variants will require large-scale resequencing analyses. GWAS methods have detected a remarkable number of robust genetic associations for dozens of common diseases and traits, leading to new pathophysiological hypotheses, although only small proportions of genetic variance have been explained thus far and therapeutic applications will require substantial further effort. Study design issues, power, and limitations are discussed. For psychiatric disorders, there are initial significant findings for common SNPs and for rare copy number variants, and many other studies are in progress. Conclusions: GWAS of large samples have detected associations of common SNPs and of rare copy number variants with psychiatric disorders. More findings are likely, since larger GWAS samples detect larger numbers of common susceptibility variants, with smaller effects. The Psychiatric GWAS Consortium is conducting GWAS meta-analyses for schizophrenia, bipolar disorder, major depressive disorder, autism, and attention deficit hyperactivity disorder. Based on results for other diseases, larger samples will be required. The contribution of GWAS will depend on the true genetic architecture of each disorder.
434 citations
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TL;DR: Intravenous ascorbic acid infusion was safe and well tolerated in this study and may positively impact the extent of multiple organ failure and biomarkers of inflammation and endothelial injury.
Abstract: Parenterally administered ascorbic acid modulates sepsis-induced inflammation and coagulation in experimental animal models. The objective of this randomized, double-blind, placebo-controlled, phase I trial was to determine the safety of intravenously infused ascorbic acid in patients with severe sepsis. Twenty-four patients with severe sepsis in the medical intensive care unit were randomized 1:1:1 to receive intravenous infusions every six hours for four days of ascorbic acid: Lo-AscA (50 mg/kg/24 h, n = 8), or Hi-AscA (200 mg/kg/24 h, n = 8), or Placebo (5% dextrose/water, n = 8). The primary end points were ascorbic acid safety and tolerability, assessed as treatment-related adverse-event frequency and severity. Patients were monitored for worsened arterial hypotension, tachycardia, hypernatremia, and nausea or vomiting. In addition Sequential Organ Failure Assessment (SOFA) scores and plasma levels of ascorbic acid, C-reactive protein, procalcitonin, and thrombomodulin were monitored. Mean plasma ascorbic acid levels at entry for the entire cohort were 17.9 ± 2.4 μM (normal range 50-70 μM). Ascorbic acid infusion rapidly and significantly increased plasma ascorbic acid levels. No adverse safety events were observed in ascorbic acid-infused patients. Patients receiving ascorbic acid exhibited prompt reductions in SOFA scores while placebo patients exhibited no such reduction. Ascorbic acid significantly reduced the proinflammatory biomarkers C-reactive protein and procalcitonin. Unlike placebo patients, thrombomodulin in ascorbic acid infused patients exhibited no significant rise, suggesting attenuation of vascular endothelial injury. Intravenous ascorbic acid infusion was safe and well tolerated in this study and may positively impact the extent of multiple organ failure and biomarkers of inflammation and endothelial injury. ClinicalTrials.gov identifier NCT01434121
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433 citations
Authors
Showing all 24085 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Kessler | 274 | 1332 | 328983 |
Carlo M. Croce | 198 | 1135 | 189007 |
Nicholas G. Martin | 192 | 1770 | 161952 |
Michael Rutter | 188 | 676 | 151592 |
Kenneth S. Kendler | 177 | 1327 | 142251 |
Bernhard O. Palsson | 147 | 831 | 85051 |
Thomas J. Smith | 140 | 1775 | 113919 |
Ming T. Tsuang | 140 | 885 | 73865 |
Patrick F. Sullivan | 133 | 594 | 92298 |
Martin B. Keller | 131 | 541 | 65069 |
Michael E. Thase | 131 | 923 | 75995 |
Benjamin F. Cravatt | 131 | 666 | 61932 |
Jian Zhou | 128 | 3007 | 91402 |
Rena R. Wing | 128 | 649 | 67360 |
Linda R. Watkins | 127 | 519 | 56454 |