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Charles A. Dinarello

Researcher at University of Colorado Denver

Publications -  1073
Citations -  152254

Charles A. Dinarello is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Interleukin & Cytokine. The author has an hindex of 190, co-authored 1058 publications receiving 139668 citations. Previous affiliations of Charles A. Dinarello include University of Guadalajara & Pennsylvania State University.

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Innate Cytokines Dictate the Fate of Acute Intestinal Inflammation

TL;DR: Findings clearly point to a pro-inflammatory role of IL-1α and a protective role ofIL-1β during acute inflammation/repair of the gut mucosa during acute colitis and restitution.
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Abstract 8603: Expression of Human Interleukine-37 Protects Mouse Heart Against Ischemic Injury Through Suppression of Monocyte Chemoattractant Protein-1-Mediated Mononuclear Cell Accumulation

TL;DR: In this paper, up-regulated chemokine expression and leukocyte accumulation contributes to the mechanism of myocardial injury and cardiac dysfunction, and IL-3 contributes to this mechanism.
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Soluble tumor necrosis factor receptors inhibit phorbol myristate acetate and cytokine-induced HIV-1 expression chronically infected U1 cells.

TL;DR: It is concluded that soluble TNF receptors can inhibit stimuli-induced HIV-1 expression and NK- kappa B DNA-binding activity in chronically infected U1 cells.
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P504Critical role IL-37 to ameliorate endotoxemic cardiac depression in aging mice: a critical role of suppression cardiodepressant cytokines

TL;DR: IL-37 has the therapeutic potential for cardiac protection in the elderly against functional injury associated with major surgeries through suppression of myocardial production of MCP-1 and cardiodepressant cytokines.
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Leukocyte endogenous mediator fails to alter protein dynamics in a model of liver dysfunction.

TL;DR: The findings confirm the catabolic effect of LEM in normal animals and identify the essential role of the liver in the acute phase response and suggest that indomethacin may modify the acutephase response by reducing plasma amino acid oxidation as well as enhancing the levels of some specific acute phase proteins.