T
Thomas Bishop
Researcher at King's College London
Publications - 7
Citations - 646
Thomas Bishop is an academic researcher from King's College London. The author has contributed to research in topics: Schwann cell & Hyperalgesia. The author has an hindex of 5, co-authored 7 publications receiving 623 citations. Previous affiliations of Thomas Bishop include Wolfson Centre for Age-Related Diseases.
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Journal ArticleDOI
CCL2 is a key mediator of microglia activation in neuropathic pain states.
Michael Thacker,Michael Thacker,Anna K. Clark,Thomas Bishop,John Grist,Ping K. Yip,Lawrence D. F. Moon,Stephen W. N. Thompson,Fabien Marchand,Stephen B. McMahon +9 more
TL;DR: The chemokine CCL2, produced by both damaged and undamaged primary sensory neurons in neuropathic pain states in rats, is released in an activity dependent manner from the central terminals of these fibres and provides a mechanism for immune activation, which in turn regulates the sensitivity of pain signaling systems in neuropathy pain states.
Journal ArticleDOI
Neurotrophin-3-Mediated Regeneration and Recovery of Proprioception Following Dorsal Rhizotomy
Matt S. Ramer,Thomas Bishop,Peter Dockery,Makarim S. Mobarak,D O'Leary,John P. Fraher,John V. Priestley,Stephen B. McMahon +7 more
TL;DR: Investigation of the ability of intrathecal neurotrophin-3 (NT3) to promote axonal regeneration across the dorsal root entry zone (DREZ) and functional recovery in adult rats found it to allow sensory axons to overcome inhibition present at the DREZ and may serve to promote functional recovery following dorsal root avulsions in humans.
Journal ArticleDOI
Characterisation of ultraviolet-B-induced inflammation as a model of hyperalgesia in the rat.
Thomas Bishop,David W. Hewson,Ping K. Yip,M S Fahey,David Dawbarn,Antony R. Young,Stephen B. McMahon +6 more
TL;DR: It is concluded that UVB inflammation produces a dose‐dependent hyperalgesic state sensitive to established analgesics, which suggests thatUVB inflammation in the rat may represent a useful translational tool in the study of pain and the testing of analgesic agents.
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Ultraviolet‐B induced inflammation of human skin: Characterisation and comparison with traditional models of hyperlagesia
TL;DR: It is suggested that UVB inflammation, at least using moderate doses produces sensory changes primarily by sensitising peripheral pain processing in the relative absence of alterations in central pain processing.
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Ultraviolet-B-induced mechanical hyperalgesia: A role for peripheral sensitisation
TL;DR: It is concluded that UVB‐induced mechanical hyperalgesia may be explained by a net shift in peripheral nociceptor response properties and alteration in mechanical responses of A&dgr;‐ and heat‐insensitive C‐nocicePTors were particular to stronger stimuli.