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.
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Circulating fibrocytes: collagen-secreting cells of the peripheral blood.
TL;DR: Fibrocytes are a rich source of inflammatory cytokines, growth factors, and chemokines that provide important intercellular signals within the context of the local tissue environment and may play an important etiopathogenic role in disease development.
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Immunochemical detection of advanced glycosylation end products in vivo.
TL;DR: It is suggested that tissue AGEs which form in vivo appear to contain a common immunological epitope which cross-reacts with A GEs prepared in vitro, supporting the concept that immunologically similar AGE structures form from the incubation of sugars with different proteins.
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Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency
Richard Bucala,Zenji Makita,Gloria Lena Vega,Scott M. Grundy,Theodor Koschinsky,Anthony Cerami,Helen Vlassara +6 more
TL;DR: Data indicate that AGE modification significantly impairs LDL-receptor-mediated clearance mechanisms and may contribute to elevated LDL levels in patients with diabetes or renal insufficiency.
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An agent cleaving glucose-derived protein crosslinks in vitro and in vivo
Vasan S,Xini Zhang,Aphrodite Kapurniotu,Jürgen Bernhagen,Saul Teichberg,John M. Basgen,Wagle D,Shih D,Terlecky I,Richard Bucala,A. Cerami,Egan J,P C Ulrich +12 more
TL;DR: A prototypic AGE crosslink 'breaker', N-phenacylthiazolium bromide (PTB), is described, which reacts with and cleaves covalent, AGE-derived protein crosslinks and offers a potential therapeutic approach for the removal of established AGECrosslinks.
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Sustained mitogen-activated protein kinase (MAPK) and cytoplasmic phospholipase A2 activation by macrophage migration inhibitory factor (MIF). Regulatory role in cell proliferation and glucocorticoid action.
TL;DR: It is indicated that the sustained activation of p44/p42 MAP kinase and subsequent arachidonate release by cytoplasmic phospholipase A2 are important features of the immunoregulatory and intracellular signaling events initiated by MIF and provide the first insight into the mechanisms that underlie the pro-proliferative and inflammatory properties of this mediator.