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James J. Burston

Researcher at University of Nottingham

Publications -  49
Citations -  3788

James J. Burston is an academic researcher from University of Nottingham. The author has contributed to research in topics: Osteoarthritis & Cannabinoid receptor. The author has an hindex of 24, co-authored 47 publications receiving 3302 citations. Previous affiliations of James J. Burston include Virginia Commonwealth University & University of the West of England.

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Journal ArticleDOI

Evaluation of NHS carbamates as a potent and selective class of endocannabinoid hydrolase inhibitors.

TL;DR: It is demonstrated that NHS carbamate 1a (MJN110) alleviates mechanical allodynia in a rat model of diabetic neuropathy, marking NHS carbamates as a promising class of MAGL inhibitors.
Book ChapterDOI

The Role of the Endocannabinoid System in Pain

TL;DR: The general features of the EC system are described as related to pain and nociception and the wealth of preclinical and clinical data involving targeting theEC system is discussed, with focus on modulation of 2-AG signalling via specific enzyme inhibitors and the role of spinal CB2 in chronic pain states.
Journal ArticleDOI

The contribution of spinal glial cells to chronic pain behaviour in the monosodium iodoacetate model of osteoarthritic pain.

TL;DR: There is evidence for a contribution of spinal glial cells to pain behaviour, in particular distal allodynia, in this model of osteoarthritic pain, which may provide a novel analgesic target for the treatment of OA pain.
Journal ArticleDOI

Increased function of pronociceptive TRPV1 at the level of the joint in a rat model of osteoarthritis pain

TL;DR: Increased TRPV1 immunoreactivity in human OA synovium is demonstrated, confirming the diseased joint as a potential therapeutic target for TRPv1-mediated analgesia, and provides a clinical and mechanistic rationale for the future investigation of the therapeutic benefits of intra-articular administration of TRpV1 antagonists for the treatment of OA pain.
Journal ArticleDOI

Cannabinoid CB2 Receptors Regulate Central Sensitization and Pain Responses Associated with Osteoarthritis of the Knee Joint

TL;DR: New clinically relevant evidence that joint damage and spinal CB2 receptor expression are correlated combined with converging pre-clinical evidence that activation of CB2 receptors inhibits central sensitization and its contribution to the manifestation of chronic OA pain is provided.