Richard S. Beard
Boise State University
28 Papers
72 Citations
Richard S. Beard is an academic researcher from Boise State University. The author has contributed to research in topics: Downregulation and upregulation & Inflammation. The author has an hindex of 15, co-authored 27 publications. Previous affiliations of Richard S. Beard include University of South Florida & Idaho State University.
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Papers
Hyperhomocysteinemia increases permeability of the blood-brain barrier by NMDA receptor-dependent regulation of adherens and tight junctions
TL;DR: Data provide the first evidence that the NMDAr is required for Hcy-mediated increases in blood-brain barrier permeability, and may present a novel therapeutic target in diseases associated with opening of the blood- brain barrier in HHcy.
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Vascular complications of cystathionine β-synthase deficiency: future directions for homocysteine-to-hydrogen sulfide research.
TL;DR: Findings from human and animal studies are included to identify important opportunities for future investigation that should be aimed at generating new basic and clinical understanding of the role of CBS and transsulfuration in cardiovascular and neurovascular disease.
116
Role of Neutrophil Extracellular Traps and Vesicles in Regulating Vascular Endothelial Permeability.
TL;DR: The current knowledge on neutrophil-induced changes in endothelial barrier structures is summarized, with a detailed presentation of recently characterized molecular pathways involved in the production and effects of neutrophils extracellular traps and extrace cellular vesicles.
Interleukin-1β-induced barrier dysfunction is signaled through PKC-θ in human brain microvascular endothelium
TL;DR: The interpretation is that inhibition of PKC-θ or inhibition of ZO-1 phosphorylation could be viable strategies for preventing blood-brain barrier dysfunction under a variety of neuroinflammatory conditions.
Palmitoyl acyltransferase DHHC21 mediates endothelial dysfunction in systemic inflammatory response syndrome
Richard S. Beard,Xiaoyuan Yang,Jamie E. Meegan,Jonathan W. Overstreet,Clement G.Y. Yang,John A. Elliott,Jason J. Reynolds,Byeong J. Cha,Christopher D. Pivetti,David A. Mitchell,Mack H. Wu,Robert J. Deschenes,Sarah Y. Yuan +12 more
TL;DR: Data suggest the involvement of DHHC21-mediated PLCβ1 palmitoylation in endothelial inflammation, as well as overexpression of wild-type, not mutant, PLC β1 augments barrier dysfunction.