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: It is reported that mitochondria from mammalian cells contain intrinsic NAD-dependent deacetylase activity, which is inhibited by the NAD hydrolysis product nicotinamide, but not by trichostatin A, consistent with a class III de acetylase.
Abstract: The yeast silent information regulator (Sir)2 protein links cellular metabolism and transcriptional silencing through its nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase activity. We report that mitochondria from mammalian cells contain intrinsic NAD-dependent deacetylase activity. This activity is inhibited by the NAD hydrolysis product nicotinamide, but not by trichostatin A, consistent with a class III deacetylase. We identify this deacetylase as the nuclear-encoded human Sir2 homologue hSIRT3, and show that hSIRT3 is located within the mitochondrial matrix. Mitochondrial import of hSIRT3 is dependent on an NH2-terminal amphipathic α-helix rich in basic residues. hSIRT3 is proteolytically processed in the mitochondrial matrix to a 28-kD product. This processing can be reconstituted in vitro with recombinant mitochondrial matrix processing peptidase (MPP) and is inhibited by mutation of arginines 99 and 100. The unprocessed form of hSIRT3 is enzymatically inactive and becomes fully activated in vitro after cleavage by MPP. These observations demonstrate the existence of a latent class III deacetylase that becomes catalytically activated upon import into the human mitochondria.
541 citations
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TL;DR: The anatomy, physiology and biochemistry of opiomelanotropinergic neurons are reviewed and the implications of multi-neurotransmitter and multi-hormone neurons and cells are discussed.
540 citations
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TL;DR: The immunological events after trauma are described and important mediators and pathways of the inflammatory immune response are introduced to introduce important mediator and pathways in the initiation and persistence of the pro-inflammatory response after severe injury.
Abstract: Trauma is still one of the main reasons for death among the population worldwide. Mortality occurring early after injury is due to "first hits", including severe organ injury, hypoxia, hypovolaemia or head trauma. Massive injury leads to activation of the immune system and the early inflammatory immune response after trauma has been defined as systemic inflammatory response syndrome (SIRS). "Second hits" such as infections, ischaemia/reperfusion or operations can further augment the pro-inflammatory immune response and have been correlated with the high morbidity and mortality in the latter times after trauma. SIRS can lead to tissue destruction in organs not originally affected by the initial trauma with subsequent development of multi-organ dysfunction (MOD). The initial pro-inflammatory response is followed by an anti-inflammatory response and can result in immune suppression with high risk of infection and sepsis. Trauma causes activation of nearly all components of the immune system. It activates the neuroendocrine system and local tissue destruction and accumulation of toxic byproducts of metabolic respiration leads to release of mediators. Extensive tissue injury may result in spillover of these mediators into the peripheral bloodstream to further maintain and augment the pro-inflammatory response. Hormones like ACTH, corticosteroids and catecholamines as well as cytokines, chemokines and alarmins play important roles in the initiation and persistence of the pro-inflammatory response after severe injury. The purpose of this review is therefore to describe the immunological events after trauma and to introduce important mediators and pathways of the inflammatory immune response.
540 citations
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TL;DR: Alcohol use in chronic hepatitis C doubles the risk for HCC as compared with the risk in hepatitis C alone, and there may be synergism between alcohol and hepatitis C in the development of HCC, and in these patients HCC may occur at an earlier age and the H CC may be histologically more advanced.
540 citations
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TL;DR: Evidence supports efficacy of exposure therapy including the manualized version Prolonged Exposure (PE); cognitive therapy (CT), cognitive processing therapy (CPT), cognitive behavioral therapy (CBT)-mixed therapies ( moderate SOE); eye movement desensitization and reprocessing (EMDR) and narrative exposure therapy (low-moderate SOE).
540 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 |