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Mashup Score: 17July 2025 - Volume 166 - Issue 7 : PAIN - 2 day(s) ago
PAIN publishes research on the nature, mechanisms and treatment of pain. The journal provides a forum for the dissemination of research in the basic and clinical sciences of multidisciplinary interest.
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Mashup Score: 0
ry, the expression and function of Kcnq4 channel in nociceptors remains unknown. Here we showed that Kcnq4 is substantially expressed by unmyelinated small-diameter DRG neurons in both human and mouse. In spite of a dispensable role in acute pain and chronic skin inflammation, Kcnq4 is specifically involved in the regulation of scratching behavior through controlling action potential firing properties, evidenced by the increased neuronal excitability in small-diameter DRG neurons isolated from Kcnq4 deficient mice. Moreover, genetic ablation of Kcnq4 in Trpv1-positive neurons exacerbates both acute and chronic itch behavior in mice. Taken together, our results uncover a functional role of Trpv1-lineage neuron-expressing Kcnq4 channel in the modulation of itch-specific neuronal excitation in the periphery….
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Mashup Score: 7
An abstract is unavailable.
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Mashup Score: 8Clinical proof-of-concept results with a novel TRPA1... : PAIN - 20 day(s) ago
ter Protocol was used to evaluate the safety and efficacy of LY3526318 in 3 randomized, placebo-controlled, proof-of-concept studies in knee osteoarthritis pain (OA), chronic low back pain (CLBP), and diabetic peripheral neuropathic pain (DPNP). Participants were randomized (1:2, placebo:LY3526318, 250 mg daily) into an 8-week double-blinded period. At 4 weeks, participants treated with LY3526318 transitioned to a placebo. The primary endpoint was the self-reported daily pain intensity measured using a Numerical Rating Scale (NRS) at 4 weeks. All endpoints were collected for up to 8 weeks. Change from baseline in average weekly NRS was analyzed using Bayesian mixed model repeated measures in the OA (N = 160), CLBP (N = 159), and DPNP (N = 154) studies. Baseline characteristics were balanced between treatment arms. Mean NRS change from baseline to week 4 did not differ significantly between placebo and LY3526318; however, a numerical improvement was observed in the CLBP, not in the OA o
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Mashup Score: 12
, these standard CPM within designs (baseline always preceding treatment) do not control for order effects, which might help to distinguish specific CPM inhibition from general habituation. To tackle this issue, we conducted 2 separate studies where we controlled for order effects to investigate whether CPM effects depend on the order of baseline and treatment. In both studies, a sample of 60 participants underwent 2 CPM test blocks: one standard order block (baseline before treatment) and one reversed order block (treatment before baseline), separated by a 20-minute break (randomized order across participants). Pain thresholds and pain ratings of phasic heat stimuli served as measures of TS. Cold water (study 1) and cuff pressure algometry (study 2) served as CS. We found significant CPM order effects in both studies and for both measures of TS (pain threshold and ratings). Only the standard CPM order (baseline before treatment) yielded robust pain inhibition effects, whereas the reve
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Mashup Score: 7N-methyl-D-aspartate receptor activation is downstream... : PAIN - 26 day(s) ago
nociceptive signals dependent on spinal NMDAR through several possible mechanisms. Through behavioral, pharmacological, and molecular approaches, our study in male rats has revealed several key findings: (1) neurons located in spinal cord laminae I and II express functional Panx1 channels in both neuropathic and sham rats. These channels can open (indicated by YOPRO-1 uptake) through the stimulation of NMDARs with intrathecal NMDA; (2) intrathecal NMDA leads to increased expression of pSrc and pPanx1 in dorsal horn neurons. This elevation exacerbates existing mechanical hyperalgesia in nerve-injured rats; (3) inhibition of Src with intrathecal PP2 or blockade of Panx1 with intrathecal 10Panx effectively mitigates NMDA-induced effects and reduces the spontaneous mechanical hyperalgesia of nerve-injured rats. Notably, while 10Panx successfully alleviates hyperalgesia, it does not alter pSrc expression; and (4) NMDA-stimulated YOPRO-1 uptake in neurons of laminae I-II of spinal cord slice
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In this week’s #PAIN Featured Image, Zepeda-Morales et al. depict Panx1 channel as a downstream effector of Src-mediated signaling after NMDAR activation (with NMDA or glutamate) in dorsal horn laminae I-II neurons during nerve-injured pain. Learn more at https://t.co/Z9XgUjqmqd https://t.co/BoKPTAIUCz
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Mashup Score: 7N-methyl-D-aspartate receptor activation is downstream... : PAIN - 26 day(s) ago
nociceptive signals dependent on spinal NMDAR through several possible mechanisms. Through behavioral, pharmacological, and molecular approaches, our study in male rats has revealed several key findings: (1) neurons located in spinal cord laminae I and II express functional Panx1 channels in both neuropathic and sham rats. These channels can open (indicated by YOPRO-1 uptake) through the stimulation of NMDARs with intrathecal NMDA; (2) intrathecal NMDA leads to increased expression of pSrc and pPanx1 in dorsal horn neurons. This elevation exacerbates existing mechanical hyperalgesia in nerve-injured rats; (3) inhibition of Src with intrathecal PP2 or blockade of Panx1 with intrathecal 10Panx effectively mitigates NMDA-induced effects and reduces the spontaneous mechanical hyperalgesia of nerve-injured rats. Notably, while 10Panx successfully alleviates hyperalgesia, it does not alter pSrc expression; and (4) NMDA-stimulated YOPRO-1 uptake in neurons of laminae I-II of spinal cord slice
Source: journals.lww.comCategories: General Medicine News, RheumatologyTweet-
In this week’s #PAIN Featured Image, Zepeda-Morales et al. depict Panx1 channel as a downstream effector of Src-mediated signaling after NMDAR activation (with NMDA or glutamate) in dorsal horn laminae I-II neurons during nerve-injured pain. Learn more at https://t.co/Z9XgUjqmqd https://t.co/BoKPTAIUCz
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Mashup Score: 5Performance of baseline quartile-stratified minimal... : PAIN - 28 day(s) ago
evaluate the performance of individual and baseline quartile-stratified MCIDs. The current study included data from 346 persons with baseline and 12-month postoperative outcome data from KASTPain, a no-effect randomized clinical trial conducted on persons with knee arthroplasty and pain catastrophizing. Subgroup trajectories from LCGC were used as a gold standard comparator. Minimal clinically important difference–specific trajectories of recovery were calculated for the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) Pain, Disability and EuroQol-5 Dimension Visual Analogue Scale of self-reported health. The latent Kappa (Kl) chance-corrected agreement between MCIDs and LCGCs were estimated to indicate which MCID method was best at detecting important change. For all 3 outcomes, the average latent class probabilities ranged from 0.90 to 0.99, justifying the use of LCGCs as a gold standard. The Kl for LCGC and individual MCIDs ranged from 0.21 (95% CI = 0.13, 0.28
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Mashup Score: 1A revisit of soreness and acidosis-related pain : PAIN - 29 day(s) ago
An abstract is unavailable.
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Mashup Score: 15
hared environmental or genetic factors might account for any observed association. Around 3000 participants from the TwinsUK with CWP information and measures of carotid–femoral pulse wave velocity (cfPWV), carotid intima–media thickness (cIMT), and plaque were considered. The relationship between CWP and cfPWV, cIMT, and plaque was determined. UK Biobank data were used to replicate the association. Cholesky decomposition and multivariate pathway twin models were examined. Using a 2-sample Mendelian randomisation approach, the causal association between CWP and coronary artery disease was assessed. TwinsUK participants demonstrated a significant association between CWP and increased cfPWV consistent with arterial stiffening (OR = 1.35, P-value = 0.012), as well as the presence of carotid plaque (OR = 1.45, P-value = 0.8e-5). The twin modelling showed a common latent component and pathway underlying CWP, cfPWV, and carotid plaque, with genetic factors accounting for 68% and 90% of the l
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Kazemi Naeini et al. find that a common latent factor mediates chronic widespread pain (CWP), arterial stiffness, and atheromatous plaque association, explaining 65% of CWP, 26% of carotid-femoral pulse wave velocity, 34% of plaque genetic variations #PAIN https://t.co/8q4wueo2am https://t.co/uBiVcnZuEx
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The July 2025 issue of #PAIN is now available! Catch up on the latest pain research at https://t.co/LmUhIkEEPE https://t.co/9sPnoBg9eB