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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

Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease.

TL;DR: No one mouse model completely recapitulates the immunopathology of CD or UC, however each model possesses particular similarities to human IBD and offers advantageous for specific details of IBD pathogenesis.
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Role of Blood- and Tissue-Associated Inducible Nitric-Oxide Synthase in Colonic Inflammation

TL;DR: These findings implicate both blood cell- and tissue-derived iNOS in DSS-induced colonic inflammation, with tissue-associated iN OS making a larger contribution to the recruitment of inflammatory cells.
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Role of NADPH oxidase-derived superoxide in reduced size liver ischemia and reperfusion injury.

TL;DR: It is proposed that therapies directed toward scavenging of O(2)(-), inhibiting NADPH oxidase, and/or immuno-neutralizing TNF-alpha may prove useful in limiting the liver injury induced by surgical procedures that require resection and I/R such as split liver or living donor liver transplantation.
Journal Article

Monochloramine, a neutrophil-derived oxidant, stimulates rat colonic secretion.

TL;DR: At concentrations found in inflamed tissue, both NH2Cl and H2O2 increase Isc probably by stimulating release of arachidonate metabolites and neurotransmitter(s).NH2Cl also may act directly on the epithelial cell to stimulate Isc and evoke Cl- secretion.
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Role of neutrophils in acetic acid-induced colitis in rats.

TL;DR: The data demonstrate that infiltrating neutrophils do not mediate the mucosal injury and inflammation observed in acetic acid-induced colitis, and suggested that inflammatory neutrophil may mediate mucosal Injury and inflammation in this model of colitis.