scispace - formally typeset
Search or ask a question
Institution

Veterans Health Administration

GovernmentWashington 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
More filters
Journal ArticleDOI
TL;DR: Using a novel single-molecule PCR approach to quantify the total burden of mitochondrial DNA molecules with deletions, it is shown that a high proportion of individual pigmented neurons in the aged human substantia nigra contain very high levels of mtDNA deletions.
Abstract: Using a novel single-molecule PCR approach to quantify the total burden of mitochondrial DNA (mtDNA) molecules with deletions, we show that a high proportion of individual pigmented neurons in the aged human substantia nigra contain very high levels of mtDNA deletions. Molecules with deletions are largely clonal within each neuron; that is, they originate from a single deleted mtDNA molecule that has expanded clonally. The fraction of mtDNA deletions is significantly higher in cytochrome c oxidase (COX)-deficient neurons than in COX-positive neurons, suggesting that mtDNA deletions may be directly responsible for impaired cellular respiration.

832 citations

Journal ArticleDOI
TL;DR: The Aneurysm Detection and Management (ADAM) study is an ongoing randomized clinical trial comparing two strategies for the management of AAA in patients 50 to 79 years of age with asymptomatic AAAs.
Abstract: Background: Independent risk factors for abdominal aortic aneurysm (AAA) have not been clearly defined in multivariable analyses of large patient populations. Objective: To identify factors that ar...

830 citations

Journal ArticleDOI
22 Feb 2011-PLOS ONE
TL;DR: The data suggests the existence of a core pulmonary bacterial microbiome that includes Pseudomonas, Streptococcus, Prevotella, Fusobacterium, Haemophilus, Veillonella, and Porphyromonas within the same lung of subjects with advanced COPD.
Abstract: Although culture-independent techniques have shown that the lungs are not sterile, little is known about the lung microbiome in chronic obstructive pulmonary disease (COPD). We used pyrosequencing of 16S amplicons to analyze the lung microbiome in two ways: first, using bronchoalveolar lavage (BAL) to sample the distal bronchi and air-spaces; and second, by examining multiple discrete tissue sites in the lungs of six subjects removed at the time of transplantation. We performed BAL on three never-smokers (NS) with normal spirometry, seven smokers with normal spirometry (“heathy smokers”, HS), and four subjects with COPD (CS). Bacterial 16 s sequences were found in all subjects, without significant quantitative differences between groups. Both taxonomy-based and taxonomy-independent approaches disclosed heterogeneity in the bacterial communities between HS subjects that was similar to that seen in healthy NS and two mild COPD patients. The moderate and severe COPD patients had very limited community diversity, which was also noted in 28% of the healthy subjects. Both approaches revealed extensive membership overlap between the bacterial communities of the three study groups. No genera were common within a group but unique across groups. Our data suggests the existence of a core pulmonary bacterial microbiome that includes Pseudomonas, Streptococcus, Prevotella, Fusobacterium, Haemophilus, Veillonella, and Porphyromonas. Most strikingly, there were significant micro-anatomic differences in bacterial communities within the same lung of subjects with advanced COPD. These studies are further demonstration of the pulmonary microbiome and highlight global and micro-anatomic changes in these bacterial communities in severe COPD patients.

830 citations

Journal ArticleDOI
TL;DR: Long intergenic non-coding RNA genes have diverse features that distinguish them from mRNA-encoding genes and exercise functions such as remodelling chromatin and genome architecture, RNA stabilization and transcription regulation, including enhancer-associated activity.
Abstract: Long intergenic non-coding RNA (lincRNA) genes have diverse features that distinguish them from mRNA-encoding genes and exercise functions such as remodelling chromatin and genome architecture, RNA stabilization and transcription regulation, including enhancer-associated activity. Some genes currently annotated as encoding lincRNAs include small open reading frames (smORFs) and encode functional peptides and thus may be more properly classified as coding RNAs. lincRNAs may broadly serve to fine-tune the expression of neighbouring genes with remarkable tissue specificity through a diversity of mechanisms, highlighting our rapidly evolving understanding of the non-coding genome.

829 citations

Journal ArticleDOI
TL;DR: This study demonstrates that both selective and nonselective NSAIDs inhibit angiogenesis through direct effects on endothelial cells, and challenges the premise that selective COX-2 inhibitors will not affect the gastrointestinal tract and ulcer/wound healing.
Abstract: Angiogenesis, the formation of new capillary blood vessels, is essential not only for the growth and metastasis of solid tumors, but also for wound and ulcer healing, because without the restoration of blood flow, oxygen and nutrients cannot be delivered to the healing site. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, indomethacin and ibuprofen are the most widely used drugs for pain, arthritis, cardiovascular diseases and, more recently, the prevention of colon cancer and Alzheimer disease. However, NSAIDs produce gastroduodenal ulcers in about 25% of users (often with bleeding and/or perforations) and delay ulcer healing, presumably by blocking prostaglandin synthesis from cyclooxygenase (COX)-1 and COX-2 (ref. 10). The hypothesis that the gastrointestinal side effects of NSAIDs result from inhibition of COX-1, but not COX-2 (ref. 11), prompted the development of NSAIDs that selectively inhibit only COX-2 (such as celecoxib and rofecoxib). Our study demonstrates that both selective and nonselective NSAIDs inhibit angiogenesis through direct effects on endothelial cells. We also show that this action involves inhibition of mitogen-activated protein (MAP) kinase (ERK2) activity, interference with ERK nuclear translocation, is independent of protein kinase C and has prostaglandin-dependent and prostaglandin-independent components. Finally, we show that both COX-1 and COX-2 are important for the regulation of angiogenesis. These findings challenge the premise that selective COX-2 inhibitors will not affect the gastrointestinal tract and ulcer/wound healing.

829 citations


Authors

Showing all 63886 results

NameH-indexPapersCitations
Michael Karin236704226485
Paul M. Ridker2331242245097
Eugene Braunwald2301711264576
Ralph B. D'Agostino2261287229636
John Q. Trojanowski2261467213948
Fred H. Gage216967185732
Edward Giovannucci2061671179875
Rob Knight2011061253207
Frank E. Speizer193636135891
Stephen V. Faraone1881427140298
Scott M. Grundy187841231821
Paul G. Richardson1831533155912
Peter W.F. Wilson181680139852
Dennis S. Charney179802122408
Kenneth C. Anderson1781138126072
Network Information
Related Institutions (5)
Medical University of South Carolina
45.4K papers, 1.7M citations

85% related

University of Texas Health Science Center at Houston
42.5K papers, 2.1M citations

85% related

University of Maryland, Baltimore
64.7K papers, 2.9M citations

84% related

University of California, San Francisco
186.2K papers, 12M citations

84% related

Anschutz Medical Campus
28.1K papers, 1.4M citations

84% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202314
2022137
20216,161
20205,712
20195,171
20184,497