Institution
Veterans Health Administration
Government•Washington D.C., District of Columbia, United States•
About: Veterans Health Administration is a government organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: Population & Veterans Affairs. The organization has 63820 authors who have published 98417 publications receiving 4835425 citations. The organization is also known as: VHA.
Papers published on a yearly basis
Papers
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TL;DR: In US hospitals between 2001 and 2008, a substantial decrease in CABG surgery utilization rates was observed, but PCI utilization rates remained unchanged.
Abstract: Coronary revascularization, comprising coronary artery bypass surgery (CABG) and percutaneous coronary intervention (PCI), is among the most common major medical procedures provided by the U.S. healthcare system, with over 1 million procedures performed annually.1 It is also among the most costly: Medicare inpatient payments to hospitals for coronary revascularizations exceeded $3.2 billion in fiscal year 2006,2 an amount larger than the reimbursement for any other medical or surgical procedure except for hip/knee replacement.
Several innovations in coronary revascularization, such as drug-eluting stents, minimally invasive CABG, and "off-pump" CABG, have been adopted widely in the past decade,3–5 with the promise of improved clinical outcomes compared to older revascularization technologies and techniques.5–7 In addition, publication of randomized controlled trial results from the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial (2007)8 and the Synergy between PCI with Taxus and Cardiac Surgery (SYNTAX) trial (2009)9 have provided important new information about both the potential clinical value of revascularization compared to pharmacotherapy, as well as the outcomes of CABG compared to PCI in the drug-eluting stent era. In addition, during the past decade updated appropriateness criteria for coronary revascularization have been issued and/or revised by the major cardiovascular societies.10–14
During this period of technological innovation, new published evidence, and updated guidelines, it is not well known whether or how the volume of coronary revascularization and its constituent types changed in the United States. Substantial changes in the overall volume of revascularizations and/or the relative use of CABG versus PCI would have important ramifications on clinical outcomes, healthcare costs, and the future organization and delivery of hospital-based cardiovascular care. Therefore, the goal of this study was to use a representative national sample of hospitalization claims to estimate temporal trends in the annual volume of coronary revascularization procedures during 2001–2008.
524 citations
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TL;DR: It is concluded that the LFP brain injury model is an appropriate tool to study the cellular and mechanistic aspects of human TBI that cannot be addressed in the clinical setting, as well as for the development and characterization of novel therapeutic interventions.
Abstract: This article comprehensively reviews the lateral fluid percussion (LFP) model of traumatic brain injury (TBI) in small animal species with particular emphasis on its validity, clinical relevance and reliability. The LFP model, initially described in 1989, has become the most extensively utilized animal model of TBI (to date, 232 PubMed citations), producing both focal and diffuse (mixed) brain injury. Despite subtle variations in injury parameters between laboratories, universal findings are evident across studies, including histological, physiological, metabolic, and behavioral changes that serve to increase the reliability of the model. Moreover, demonstrable histological damage and severity-dependent behavioral deficits, which partially recover over time, validate LFP as a clinically-relevant model of human TBI. The LFP model, also has been used extensively to evaluate potential therapeutic interventions, including resuscitation, pharmacologic therapies, transplantation, and other neuroprotective and neuroregenerative strategies. Although a number of positive studies have identified promising therapies for moderate TBI, the predictive validity of the model may be compromised when findings are translated to severely injured patients. Recently, the clinical relevance of LFP has been enhanced by combining the injury with secondary insults, as well as broadening studies to incorporate issues of gender and age to better approximate the range of human TBI within study design. We conclude that the LFP brain injury model is an appropriate tool to study the cellular and mechanistic aspects of human TBI that cannot be addressed in the clinical setting, as well as for the development and characterization of novel therapeutic interventions. Continued translation of pre-clinical findings to human TBI will enhance the predictive validity of the LFP model, and allow novel neuroprotective and neuroregenerative treatment strategies developed in the laboratory to reach the appropriate TBI patients.
524 citations
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Rosalind A. Eeles1, Ali Amin Al Olama2, Sara Benlloch2, Edward J. Saunders +153 more•Institutions (46)
TL;DR: In this paper, a custom Illumina array (iCOGS) was used to genotype 211,155 SNPs in blood DNA from 25,074 prostate cancer cases and 24,272 controls from the international PRACTICAL Consortium.
Abstract: Prostate cancer is the most frequently diagnosed cancer in males in developed countries. To identify common prostate cancer susceptibility alleles, we genotyped 211,155 SNPs on a custom Illumina array (iCOGS) in blood DNA from 25,074 prostate cancer cases and 24,272 controls from the international PRACTICAL Consortium. Twenty-three new prostate cancer susceptibility loci were identified at genome-wide significance (P < 5 × 10(-8)). More than 70 prostate cancer susceptibility loci, explaining ∼30% of the familial risk for this disease, have now been identified. On the basis of combined risks conferred by the new and previously known risk loci, the top 1% of the risk distribution has a 4.7-fold higher risk than the average of the population being profiled. These results will facilitate population risk stratification for clinical studies.
523 citations
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TL;DR: Advances in understanding the pathogenetic cascade of events that characterize AD provide a framework for early detection and therapeutic interventions, including transmitter replacement therapies, antioxidants, anti-inflammatory agents, estrogens, nerve growth factor, and drugs that prevent amyloid formation in the brain.
Abstract: Alzheimer's disease (AD) can be diagnosed with a considerable degree of accuracy. In some centers, clinical diagnosis predicts the autopsy diagnosis with 90% certainty in series reported from academic centers. The characteristic histopathologic changes at autopsy include neurofibrillary tangles, neuritic plaques, neuronal loss, and amyloid angiopathy. Mutations on chromosomes 21, 14, and 1 cause familial AD. Risk factors for AD include advanced age, lower intelligence, small head size, and history of head trauma; female gender may confer additional risks. Susceptibility genes do not cause the disease by themselves but, in combination with other genes or epigenetic factors, modulate the age of onset and increase the probability of developing AD. Among several putative susceptibility genes (on chromosomes 19, 12, and 6), the role of apolipoprotein E (ApoE) on chromosome 19 has been repeatedly confirmed. Protective factors include ApoE-2 genotype, history of estrogen replacement therapy in postmenopausal women, higher educational level, and history of use of nonsteroidal anti-inflammatory agents. The most proximal brain events associated with the clinical expression of dementia are progressive neuronal dysfunction and loss of neurons in specific regions of the brain. Although the cascade of antecedent events leading to the final common path of neurodegeneration must be determined in greater detail, the accumulation of stable amyloid is increasingly widely accepted as a central pathogenetic event. All mutations known to cause AD increase the production of beta-amyloid peptide. This protein is derived from amyloid precursor protein and, when aggregated in a beta-pleated sheet configuration, is neurotoxic and forms the core of neuritic plaques. Nerve cell loss in selected nuclei leads to neurochemical deficiencies, and the combination of neuronal loss and neurotransmitter deficits leads to the appearance of the dementia syndrome. The destructive aspects include neurochemical deficits that disrupt cell-to-cell communications, abnormal synthesis and accumulation of cytoskeletal proteins (e.g., tau), loss of synapses, pruning of dendrites, damage through oxidative metabolism, and cell death. The concepts of cognitive reserve and symptom thresholds may explain the effects of education, intelligence, and brain size on the occurrence and timing of AD symptoms. Advances in understanding the pathogenetic cascade of events that characterize AD provide a framework for early detection and therapeutic interventions, including transmitter replacement therapies, antioxidants, anti-inflammatory agents, estrogens, nerve growth factor, and drugs that prevent amyloid formation in the brain.
523 citations
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CEU San Pablo University1, National and Kapodistrian University of Athens2, University of Marburg3, Rush University Medical Center4, Toronto Western Hospital5, University of Toronto6, University of Pennsylvania7, Newcastle University8, University of Sydney9, University of New South Wales10, Centre national de la recherche scientifique11, Peking Union Medical College12, Columbia University13, University of Paris14, Aarhus University15, UCL Institute of Neurology16, National Institutes of Health17, Emory University18, San Francisco VA Medical Center19, University of California, San Francisco20, Veterans Health Administration21, Erasmus University Medical Center22, Baylor College of Medicine23, University of Kiel24, Hebrew University of Jerusalem25, University of Barcelona26, Columbia University Medical Center27, McGill University28, University of Alabama at Birmingham29, Northwestern University30, Icahn School of Medicine at Mount Sinai31, University of Perugia32, Vancouver Coastal Health33, University of British Columbia34
TL;DR: This multiple‐author article provides a historical state‐of‐the‐art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease.
Abstract: This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.
523 citations
Authors
Showing all 63886 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Karin | 236 | 704 | 226485 |
Paul M. Ridker | 233 | 1242 | 245097 |
Eugene Braunwald | 230 | 1711 | 264576 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
John Q. Trojanowski | 226 | 1467 | 213948 |
Fred H. Gage | 216 | 967 | 185732 |
Edward Giovannucci | 206 | 1671 | 179875 |
Rob Knight | 201 | 1061 | 253207 |
Frank E. Speizer | 193 | 636 | 135891 |
Stephen V. Faraone | 188 | 1427 | 140298 |
Scott M. Grundy | 187 | 841 | 231821 |
Paul G. Richardson | 183 | 1533 | 155912 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Dennis S. Charney | 179 | 802 | 122408 |
Kenneth C. Anderson | 178 | 1138 | 126072 |