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Michael S. Goligorsky

Researcher at New York Medical College

Publications -  178
Citations -  19116

Michael S. Goligorsky is an academic researcher from New York Medical College. The author has contributed to research in topics: Endothelial stem cell & Endothelium. The author has an hindex of 56, co-authored 174 publications receiving 17092 citations. Previous affiliations of Michael S. Goligorsky include Queens College & State University of New York System.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Endothelium-derived microparticles impair endothelial function in vitro

TL;DR: The data strongly suggest that circulating EMPs directly affect the endothelium and thus not only act as a marker for ECD but also aggravate preexisting ECD.
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Presence of the μ3 Opiate Receptor in Endothelial Cells COUPLING TO NITRIC OXIDE PRODUCTION AND VASODILATION

TL;DR: The data presented above reveal a novel site of morphine action, endothelial cells, where a mu3 receptor is coupled to nitric oxide release and vasodilation.
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Nitric oxide in acute renal failure: NOS versus NOS

TL;DR: The intricate relations between endothelial and epithelial cells are perturbed in renal ischemia primarily as a result of endothelial dysfunction precipitating epithelial injury.