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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.

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Macrophage migration inhibitory factor exhibits a pronounced circadian rhythm relevant to its role as a glucocorticoid counter-regulator

TL;DR: The beneficial role of macrophage migration inhibitory factor neutralization in models of inflammatory arthritis is explained, by antagonizing cortisol‐mediated pro‐inflammatory cytokine suppression may prolong the duration of early morning inflammation.
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Macrophage migration inhibitory factor.

TL;DR: Unique structural features of MIF, including an intrinsic catalytic activity, offer attractive opportunities for the discovery and design of therapeutic MIF inhibitors.
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The influence of macrophage migration inhibitory factor gene polymorphisms on outcome from community-acquired pneumonia

TL;DR: In this article, two distinct polymorphisms in the MIF promoter were analyzed: a G/C transition at -173 and a CATT repeat at -794; however, the 90-d mortality was lower for the high-expression C allele (P=0.003) and the hazard ratio was similar in different geographic sub-cohorts, and the association remained significant after adjusting for false discovery.
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Macrophage migration inhibitory factor (MIF) gene polymorphisms are associated with increased prostate cancer incidence.

TL;DR: Individuals with −173G/C, −173C/C and −794 7-CATT MIF genotypes have an increased incidence of CaP and these genotypes may serve as an independent marker for cancer recurrence.
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Macrophage migration inhibitory factor promotes cell death and aggravates neurologic deficits after experimental stroke.

TL;DR: It is concluded that MIF promotes neuronal death and aggravates neurologic deficits after experimental stroke, which implicates MIF in the pathogenesis of neuronal injury after stroke.