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Matthew B. Grisham

Researcher at Texas Tech University Health Sciences Center

Publications -  351
Citations -  30238

Matthew B. Grisham is an academic researcher from Texas Tech University Health Sciences Center. The author has contributed to research in topics: Nitric oxide & Colitis. The author has an hindex of 92, co-authored 349 publications receiving 29002 citations. Previous affiliations of Matthew B. Grisham include University Medical Center New Orleans & LSU Health Sciences Center New Orleans.

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Journal ArticleDOI

Protective effects of O2 radical scavengers and adenosine in PMA-induced lung injury.

TL;DR: Vascular permeability and resistance are measured before and 1 h after PMA in five groups of blood-perfused dog lungs to find that, compared with PMA alone, catalase, deferoxamine, and adenosine provided significant protection, whereas the results with superoxide dismutase were variable.
Book ChapterDOI

Mechanisms of oxidant-mediated microvascular injury following reperfusion of the ischemic intestine.

TL;DR: Based on work from the laboratory and studies by others, the following hypothesis is proposed to explain the interaction among xanthine oxidase, PMNs, and tissue injury in the postischemic small intestine.
Journal ArticleDOI

Effects of reactive oxygen and nitrogen metabolites on MCP-1-induced monocyte chemotactic activity in vitro.

TL;DR: Peroxynitrite attenuated MCP-1-induced monocyte chemotactic activity (MCA) in a dose-dependent manner but did not attenuate leukotriene B4 or complement-activated serum MCA, which is consistent with nitration of tyrosine by peroxynite, with subsequent inhibition of M CP-1 binding to monocytes, and suggest that peroxysitrite may play a role in regulation of MCP
Journal ArticleDOI

Estrogen Receptor-α, Sexual Dimorphism and Reduced-Size Liver Ischemia and Reperfusion Injury in Mice

TL;DR: The data showed that untreated females or males treated with E2 survived RSL+I/R surgery indefinitely whereas all male mice given vehicle died within 3-5 days following surgery, and it was concluded that this protection may in part be due to the E2/ER-α-mediated activation of eNOS.