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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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MIF (Macrophage Migration Inhibitory Factor) Promoter Polymorphisms and Susceptibility to Severe Malarial Anemia

TL;DR: The findings demonstrate that variation in the MIF promoter influences susceptibility to SMA and peripheral MIF production, however, the Mif -173 and -794 polymorphisms appear to have both independent and interactive effects on different measures of disease severity, suggesting that MIF plays a complex role in malarial pathogenesis.
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Expression of Inducible 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase/PFKFB3 Isoforms in Adipocytes and Their Potential Role in Glycolytic Regulation

TL;DR: Anti-phospho-iPFK-2(Ser461) Western blotting revealed strong reactivity in insulin-treated 3T3-L1 adipocyte, suggesting that insulin induces the phosphorylation of PFKFB3 protein, expanding the role of these structurally unique iPFK- 2/PFKFB 3 isoforms in the metabolic regulation of adipocytes.
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A Plasmodium-encoded cytokine suppresses T-cell immunity during malaria

TL;DR: It is observed that the Plasmodium ortholog of macrophage migration inhibitory factor enhanced inflammatory cytokine production and also induced antigen-experienced CD4 T cells to develop into short-lived effector cells rather than memory precursor cells, indicating that PlasModia actively interfere with the development of immunological memory.
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MIF and D-DT are potential disease severity modifiers in male MS subjects

TL;DR: It is demonstrated that genetically controlled high MIF expression (and D-DT) promotes MS progression in males, suggesting that these two factors are sex-specific disease modifiers and raising the possibility that aggressive anti-MIF treatment of clinically isolated syndrome or RRMS males with a high-expresser genotype might slow or prevent the onset of progressive MS.