scispace - formally typeset
R

Richard Bucala

Researcher at Yale University

Publications -  622
Citations -  58697

Richard Bucala is an academic researcher from Yale University. The author has contributed to research in topics: Macrophage migration inhibitory factor & Cytokine. The author has an hindex of 119, co-authored 595 publications receiving 54607 citations. Previous affiliations of Richard Bucala include École Polytechnique Fédérale de Lausanne & Rockefeller University.

Papers
More filters
Journal ArticleDOI

Macrophage migration inhibitory factor is released from pituitary folliculo-stellate-like cells by endotoxin and dexamethasone and attenuates the steroid-induced inhibition of interleukin 6 release.

TL;DR: The results suggest that the FS cells are both a source of and a target for MIF and raise the possibility that MIF serves as a paracrine/autocrine factor in the pituitary gland that contributes to the protective neuroendocrine response to endotoxin.
Journal ArticleDOI

Null mutation in macrophage migration inhibitory factor prevents muscle cell loss and fibrosis in partial bladder outlet obstruction.

TL;DR: These studies implicate MIF in the sequence of events leading to detrusor muscle loss and fibrosis in obstruction and raise the possibility that strategies designed to antagonize MIF synthesis, release, or biological activity could prevent or delay DU and urinary retention.
Journal ArticleDOI

The non-mammalian MIF superfamily.

TL;DR: An overview of the non-mammalian MIF-like proteins that have been most well studied experimentally and how a combined targeting of both parasitic and host MIF could lead to more effective treatment strategies for parasitic diseases of socioeconomic importance.
Journal ArticleDOI

Efficient scavenging of fatty acid oxidation products by aminoguanidine.

TL;DR: AG was found to be an efficient scavenger of alpha,beta-unsaturated aldehydes when compared to nucleophilic amino acids, suggesting that one of its mechanisms of action in vivo is to protect tissue constituents from the damaging effects of oxidative stress.
Journal ArticleDOI

The role of advanced glycosylation end-products in the pathogenesis of atherosclerosis

TL;DR: It is proposed that these chemically reactive circulating AGE-peptides contribute to tissue injury by reattaching to susceptible target proteins both within and outside the vasculature, and that this process accelerates vascular pathology in diabetic patients.