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Steve Poole

Researcher at National Institute for Biological Standards and Control

Publications -  7
Citations -  1149

Steve Poole is an academic researcher from National Institute for Biological Standards and Control. The author has contributed to research in topics: Reperfusion injury & Vascular permeability. The author has an hindex of 7, co-authored 7 publications receiving 1087 citations.

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Involvement of resident macrophages and mast cells in the writhing nociceptive response induced by zymosan and acetic acid in mice

TL;DR: The results suggest that the nociceptive activity of zymosan and acetic acid in the writhing model is due to the release of TNF-alpha, interleukin 1beta and interleucin 8 by resident peritoneal macrophages and mast cells.
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The effect of photodynamic action on two virulence factors of gram-negative bacteria.

TL;DR: The ability of TBO-mediated PDA to reduce the activities of key virulence factors may be an additional benefit of using light-activated antimicrobial agents in the treatment of infectious diseases.
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Effects of inhibition of PDE4 and TNF-α on local and remote injuries following ischaemia and reperfusion injury

TL;DR: The capacity of PDE4 inhibitors to block the recruitment of neutrophils into tissues, the production of LTB4 and of the pro‐inflammatory cytokines TNF‐α, IL‐1ß and IL‐6 appear to underlie their anti‐inflammatory effects in the authors' model of I/R injury.
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Repertaxin, a novel inhibitor of rat CXCR2 function, inhibits inflammatory responses that follow intestinal ischaemia and reperfusion injury

TL;DR: CINC‐1 and possibly other CXC chemokines, acting on CXCR2, have an important role during I/R injury and drugs, such as Repertaxin, developed to block the function of the CX CR2 receptor may be effective at preventing reperfusion injury in relevant clinical situations.
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Leukemia Inhibitory Factor Is an Anti-Inflammatory and Analgesic Cytokine

TL;DR: The data show that upregulation of LIF during peripheral inflammation serves a key, early anti-inflammatory role and that exogenous LIF can reduce inflammatory hyperalgesia.