E
Edwin A. Deitch
Researcher at Rutgers University
Publications - 112
Citations - 8823
Edwin A. Deitch is an academic researcher from Rutgers University. The author has contributed to research in topics: Lung injury & Lymph. The author has an hindex of 51, co-authored 112 publications receiving 8344 citations.
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MicroRNA-145, a novel smooth muscle cell phenotypic marker and modulator, controls vascular neointimal lesion formation.
Yunhui Cheng,Xiaojun Liu,Jian Yang,Ying Lin,Da Zhong Xu,Qi Lu,Edwin A. Deitch,Yuqing Huo,Ellise Delphin,Chunxiang Zhang +9 more
TL;DR: It is demonstrated that miR-145 is a novel VSMC phenotypic marker and modulator that is able of controlling vascular neointimal lesion formation and this finding may have extensive implications for the diagnosis and therapy of a variety of proliferative vascular diseases.
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Animal models of sepsis and shock : A review and lessons learned
TL;DR: The goal of this review article is to review the advantages and disadvantages of commonly used sepsis and shock models in light of lessons learned from these clinical trials.
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Role of the Gut in Multiple Organ Failure: Bacterial Translocation and Permeability Changes
Gregory M. Swank,Edwin A. Deitch +1 more
TL;DR: Even if the immune inflammatory system, rather than the gut, is the “motor of” MOF, the gut remains one of the major pistons that turns the motor.
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Adenosine inhibits IL-12 and TNF-[alpha] production via adenosine A2a receptor-dependent and independent mechanisms
György Haskó,David G. Kuhel,Jiang-Fan Chen,Michael A. Schwarzschild,Edwin A. Deitch,Jon G. Mabley,Anita Marton,Csaba Szabó +7 more
TL;DR: The notion that adenosinebased therapies might be useful in certain autoimmune and/or inflammatory diseases is supported, as the effect of the endogenous purine nucleosideadenosine on the production of IL‐12 was investigated.
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Gut-origin sepsis: evolution of a concept.
TL;DR: The goal of this review is to trace the evolution of gut-origin sepsis and gut-induced MODS and put these disorders and observations into clinical perspective and conclude that bacterial translocation occurs clinically and is responsible for increased infectious complications in patients undergoing major abdominal surgery.