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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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Expression of functional Toll-like receptors 2 and 4 in human aortic valve interstitial cells: potential roles in aortic valve inflammation and stenosis.

TL;DR: It is demonstrated for the first time that HAVICs express TLR2 and TLR4 and that stimulation of HAVics by PGN or LPS induces the expression of proinflammatory mediators and the upregulation of osteogenesis-associated factors.
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Interleukin-6 as an endogenous pyrogen: induction of prostaglandin E2 in brain but not in peripheral blood mononuclear cells.

TL;DR: Whether interleukin-6 (IL-6) stimulates PGE2 formation in a manner similar to IL-1 and TNF is examined and IL-6 was also pyrogenic in the cat by either the systemic or the intraventricular route.
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IL-32, a novel proinflammatory cytokine in chronic obstructive pulmonary disease.

TL;DR: This is the first study to demonstrate increased expression of IL-32 in lung tissue of patients with COPD, where it was colocalized with tumor necrosis factor-alpha and correlated with the degree of airflow obstruction.
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Identification of the most active interleukin‐32 isoform

TL;DR: A specific target will be provided to neutralize endogenous IL‐32, which may contribute to basic and clinical immunology and to produce recombinant protein with a high yield.
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Interleukin-1 homologues IL-1F7b and IL-18 contain functional mRNA instability elements within the coding region responsive to lipopolysaccharide

TL;DR: It is demonstrated that similar to IL-18, both mRNA and intracellular protein expression of IL-1F7b are up-regulated by LPS (lipopolysaccharide) in human monocytes and contains functional instability determinants within their coding region, which influence mRNA decay as a novel mechanism to regulate the expression ofIL-1 family members.