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Hamish R. Michie

Researcher at Brigham and Women's Hospital

Publications -  12
Citations -  3117

Hamish R. Michie is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Cyclooxygenase pathway & Tumor necrosis factor alpha. The author has an hindex of 11, co-authored 12 publications receiving 3089 citations. Previous affiliations of Hamish R. Michie include Harvard University.

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Journal ArticleDOI

Detection of circulating tumor necrosis factor after endotoxin administration.

TL;DR: It is concluded that the response to endotoxin is associated with a brief pulse of circulating tumor necrosis factor and that the resultant responses are effected through the cyclooxygenase pathway.
Journal Article

Tumor necrosis factor and endotoxin induce similar metabolic responses in human beings.

TL;DR: TNF may represent the primary afferent signal that initiates many of the metabolic responses associated with sepsis and endotoxemia.
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Recombinant Human Tumor Necrosis Factor Administered as a 24-Hour Intravenous Infusion. A Phase I and Pharmacologic Study

TL;DR: The 24-hour infusions of rH-TNF were associated with significant decreases in serum cholesterol and high-density lipoprotein levels and Pharmacokinetic studies using an enzyme-linked immunosorbent assay demonstrated peak plasma rhTNF levels of 90-900 pg/mL, despite continuous infusion, no steady-state level was achieved.
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A Single Dose of Endotoxin Increases Intestinal Permeability in Healthy Humans

TL;DR: It is suggested that a brief exposure to circulating endotoxin increases the permeability of the normal gut, consistent with the hypothesis that during critical illness, prolonged or repeated exposure to systemic endotoxins or associated cytokines may significantly compromise the integrity of the gastrointestinal mucosal barrier.
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Inhibition of Cyclo-oxygenase Attenuates the Metabolic Response to Endotoxin in Humans

TL;DR: Data indicate that activation of the cyclooxygenase pathway is necessary to produce many of the metabolic changes observed during critical illness, including weight loss, hypermetabolism, and accelerated proteolysis.