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To compare pain intensity among individuals with idiopathic inflammatory myopathies (IIMs), other systemic autoimmune rheumatic diseases (AIRDs), and without rheumatic disease (wAIDs).
Learn More >Nerve injury significantly affects human motor and sensory function due to destruction of the integrity of nerve structure. In the wake of nerve injury, glial cells are activated, and synaptic […]
Learn More >The analgesic effects of delta-9-tetrahydrocannabinol (THC), the primary psychoactive compound in cannabis, have been widely promoted. Unfortunately, animal research is limited by the use of high doses and pain-evoked tests. […]
Learn More >Morphine diminishes pain, but its long-term use is compromised by tolerance and hyperalgesia. Studies implicate δ receptors, β-arrestin2 and Src kinase in tolerance. We examined whether these proteins are also […]
Learn More >P2X receptors are a family of ATP-gated cation channels comprising seven subtypes in mammals, which play key roles in nerve transmission, pain sensation and inflammation. The P2X4 receptor in particular […]
Learn More >Polymyalgia rheumatica (PMR) is an inflammatory joint disease in patients over 50 years of age with pain and prolonged morning stiffness in the shoulder and hip girdles and neck. The lack […]
Learn More >Despite the primary myelin-related pathophysiology, small fiber neuropathy (SFN) and axonal degeneration are also considered to be involved and associated with disabling symptoms and impaired quality of life in chronic […]
Learn More >μ-Conotoxin KIIIA, a selective blocker of sodium channels, has strong inhibitory activity against several Na isoforms, including Na1.7, and has potent analgesic effects, but it contains three pairs of disulfide […]
Learn More >NADPH oxidase isoform-2 (NOX2) has been implicated in the pathophysiology of neuropathic pain (NP), mostly through the modulation of neuroinflammation. Since it is also accepted that some neuroimmune mechanisms underlying […]
Learn More >Lipids, especially lysophosphatidylcholine LPC16:0, have been shown to be involved in chronic joint pain through the activation of acid-sensing ion channels (ASIC3). The aim of the present study was to […]
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