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Stephen M. Taylor

Researcher at Government of Western Australia

Publications -  156
Citations -  8249

Stephen M. Taylor is an academic researcher from Government of Western Australia. The author has contributed to research in topics: C5a receptor & Receptor. The author has an hindex of 49, co-authored 155 publications receiving 7496 citations. Previous affiliations of Stephen M. Taylor include Heart of England NHS Foundation Trust & Department of Employment, Economic Development and Innovation.

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Pathophysiology, treatment, and animal and cellular models of human ischemic stroke

TL;DR: This review explores the etiology and pathogenesis of ischemic stroke, and provides a general model of such, and explores new and emerging approaches for the prevention and treatment of stroke.
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The role of the complement system in ischemia-reperfusion injury.

TL;DR: The use of specific inhibitors to block complement activation has been shown to prevent local tissue injury after I/R, and novel inhibitors of complement products may find wide clinical application because there are no effective drug therapies currently available to treat I-R injuries.
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Toll-like receptors in ischemia-reperfusion injury.

TL;DR: The contribution of TLR activation in hepatic, renal, cerebral, intestinal, and myocardial I/R injuries is discussed and the development of specific TLR-targeted therapeutics to treat these conditions is discussed.
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Low-Molecular-Weight Peptidic and Cyclic Antagonists of the Receptor for the Complement Factor C5a

TL;DR: A series of small molecules derived from the C-terminus of C5a are described, some of which are the most potent low-molecular-weight C 5a receptor antagonists reported to date for the human polymorphonuclear leukocyte (PMN) C5A receptor.
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Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease.

TL;DR: Oral delivery of a cyclic hexapeptide C5a receptor antagonist for 2–3 mo resulted in substantial reduction of pathological markers such as fibrillar amyloid deposits and activated glia in two mouse models of AD, suggesting a novel therapeutic target for reducing pathology and improving cognitive function in human AD patients.