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Kiichi Nakahira

Researcher at Cornell University

Publications -  80
Citations -  15607

Kiichi Nakahira is an academic researcher from Cornell University. The author has contributed to research in topics: Inflammasome & Autophagy. The author has an hindex of 43, co-authored 70 publications receiving 12640 citations. Previous affiliations of Kiichi Nakahira include Harvard University & Brigham and Women's Hospital.

Papers
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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.
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Mechanisms of cell death in oxidative stress.

TL;DR: Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke.
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The NASA Twins Study: A multidimensional analysis of a year-long human spaceflight.

Francine E. Garrett-Bakelman, +88 more
- 12 Apr 2019 - 
TL;DR: Given that the majority of the biological and human health variables remained stable, or returned to baseline, after a 340-day space mission, these data suggest that human health can be mostly sustained over this duration of spaceflight.
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Fatty Acids Modulate Toll-like Receptor 4 Activation through Regulation of Receptor Dimerization and Recruitment into Lipid Rafts in a Reactive Oxygen Species-dependent Manner

TL;DR: It is shown that TLR4 recruitment to lipid rafts and dimerization were coupled events mediated at least in part by NADPH oxidase-dependent reactive oxygen species generation, which provides a new insight in understanding the mechanism by which fatty acids differentially modulateTLR4-mediated signaling pathway and consequent inflammatory responses which are implicated in the development and progression of many chronic diseases.