scispace - formally typeset
C

Charles G. Cochrane

Researcher at Scripps Research Institute

Publications -  249
Citations -  22873

Charles G. Cochrane is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Receptor & Prekallikrein. The author has an hindex of 82, co-authored 249 publications receiving 22678 citations. Previous affiliations of Charles G. Cochrane include University of Pittsburgh & Brigham and Women's Hospital.

Papers
More filters
Journal ArticleDOI

Leukocyte-dependent histamine release from rabbit platelets the role of ige, basophils, and a platelet-activating factor

TL;DR: LDHR must be considered as an immediate hypersensitivity-type mechanism which may link allergic reactions with immunologic disease associated with severe structural injury.
Journal ArticleDOI

Mechanisms of oxidant-mediated cell injury. The glycolytic and mitochondrial pathways of ADP phosphorylation are major intracellular targets inactivated by hydrogen peroxide.

TL;DR: Both the estimated rates of ADP phosphorylation by glycolysis and mitochondria and the estimated rate of ATP hydrolysis by ongoing metabolism were utilized to model the approximate decline in intracellular ATP expected at 15-min exposure to various H2O2 concentrations.
Book ChapterDOI

Immune Complex Disease in Experimental Animals and Man

TL;DR: This chapter summarizes the data presented in two reviews of experimental acute and chronic immune complex disease produced by nonliving antigens and discusses in detail more recent studies.
Journal ArticleDOI

Oxidant injury of cells. DNA strand-breaks activate polyadenosine diphosphate-ribose polymerase and lead to depletion of nicotinamide adenine dinucleotide.

TL;DR: Results suggest that DNA damage induced within seconds after addition of oxidant may lead to stimulation of poly-ADP-ribose polymerase, and a consequent fall in NAD sufficient to interfere with ATP synthesis.
Journal ArticleDOI

Hydrogen peroxide-induced injury of cells and its prevention by inhibitors of poly(ADP-ribose) polymerase

TL;DR: In the current studies, inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide, nicotinamide, or theophylline in cells exposed to lethal concentrations of H2O2 prevented the sequence of events that eventually led to cell lysis--i.e., the decrease in NAD, followed by depletion of ATP, influx of extracellular Ca2+, actin polymerization and, finally, cell death.