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Mesenchymal stem cells (MSCs)-derived exosomes have shown promise as a cell-free therapeutic strategy for neuropathic pain. This study was conducted to explore the potential mechanisms underlying the analgesic effects of MSC-derived exosomes in treating neuropathic pain.

Both musculoskeletal pain and sleep disturbances are major health problems worldwide. Literature suggests that the two are reciprocally related and both may be associated with changes in C-reactive protein (CRP) levels. However, the relationships among musculoskeletal pain, sleep duration, and CRP remain unclear. In this cross-sectional study, we investigated the relationship between acute and chronic musculoskeletal pain, sleep, and inflammation using the data from the initial visit of the UK Biobank. 17,642 individuals with chronic musculoskeletal pain, 11,962 individuals with acute musculoskeletal pain, and 29,604 pain-free controls were included in the analysis. In addition, we validated the findings using data from the second visit assessment of the UK Biobank. We found that 1) chronic pain was associated with higher CRP levels compared to both acute pain and the pain-free controls; 2) chronic pain was associated with a lower sleep score (a measurement of sleep patterns), compared to acute pain and the pain-free controls; and acute pain was associated with lower sleep scores compared to the controls; 3) there was a significant negative association between the sleep score and CRP; 4) CRP may partially mediate the association between chronic pain and decreased sleep score. However, the effect size of the mediation was rather small, and the pathophysiological significance remains uncertain. Further validation is needed. These findings were partly replicated in the UK Biobank second visit assessment cohort with a smaller sample size. Our findings, which are based on the large UK Biobank dataset, support the interplay between musculoskeletal pain, sleep patterns, and the potential mediating role of CRP on this reciprocal relationship.

We aimed to describe the natural history leading to end-stage knee osteoarthritis (esKOA), focusing on knee symptoms, radiographic severity, and the presence of limited mobility or instability.

Studies of individuals with non-cancer-related chronic pain, find that higher levels of psychological flexibility (PF) are associated with less distress, better functioning, and a better response to treatment. People diagnosed with cancer are at significantly increased risk of developing chronic cancer-related pain, the presence of which is associated with poorer health outcomes. Little is known about whether PF is applicable to cancer pain. The current study investigates the relationship between chronic cancer-related pain, distress and functioning, and three theoretical processes proposed by the PF model: pain acceptance, present-moment focus, and committed action.

Dystrophic epidermolysis bullosa is a rare genetic blistering skin disease caused by mutations in , which encodes type VII collagen (C7). Beremagene geperpavec (B-VEC) is a topical investigational herpes simplex virus type 1 (HSV-1)-based gene therapy designed to restore C7 protein by delivering .

Chronic pain often leads to depression, increasing patient suffering and worsening prognosis. While hyperactivity of the anterior cingulate cortex (ACC) appears to be critically involved, the molecular mechanisms underlying comorbid depressive symptoms in chronic pain remain elusive. T cell lymphoma invasion and metastasis 1 (Tiam1) is a Rac1 guanine nucleotide exchange factor (GEF) that promotes dendrite, spine, and synapse development during brain development. Here, we show that Tiam1 orchestrates synaptic structural and functional plasticity in ACC neurons via actin cytoskeleton reorganization and synaptic N-methyl-d-aspartate receptor (NMDAR) stabilization. This Tiam1-coordinated synaptic plasticity underpins ACC hyperactivity and drives chronic pain-induced depressive-like behaviors. Notably, administration of low-dose ketamine, an NMDAR antagonist emerging as a promising treatment for chronic pain and depression, induces sustained antidepressant-like effects in mouse models of chronic pain by blocking Tiam1-mediated maladaptive synaptic plasticity in ACC neurons. Our results reveal Tiam1 as a critical factor in the pathophysiology of chronic pain-induced depressive-like behaviors and the sustained antidepressant-like effects of ketamine.

Pharmaceutical opioid consumption has been increasing worldwide, but disparities in access to these medications exist. Few countries of the WHO Eastern Mediterranean Region have well defined pain management policies.

In this study, two novel derivatives of naphthalene-2-sulfonic acid: 6-(((1S,5R)-3,5-dichloro-2,4,6-triazabicyclo [z3.1.0]hex-3-en-1-yl)amino)-5-((E)-phenyldiazenyl)naphthalene-2-sulfonic acid (DTPS1) and (E)-6-((4,6-dichloro-1,3,5-triazine2-yl)amino)-4-hydroxy-3-(phenyldiazenyl)naphthalene-2-sulfonic acid (DTPS2) have been synthesized and characterized using FT-IR, UV-vis, and NMR spectroscopic techniques. Applying density functional theory (DFT) at the B3LYP, APFD, PBEPBE, HCTH, TPSSTPSS, and ωB97XD/aug-cc-pVDZ level of theories for the electronic structural properties. In-vitro analysis, molecular docking, molecular dynamic (MD) simulation of the compounds was conducted to investigate the anti-inflammatory potential using COXs enzymes. Docking indicates binding affinity of -9.57, -9.60, -6.77 and -7.37 kcal/mol for DTPS1, DTPS2, Ibuprofen and Diclofenac which agrees with assay. Results of MD simulation, indicates sulphonic group in DTPS1 has > 30% interaction with the hydroxyl and oxygen atoms in amino acid residues, but > 35% interaction with the DTPS2. It can be said that the DTPS1 and DTPS2 can induce inhibitory effect on COXs to halt biosynthesis of prostaglandins (PGs), a chief mediator of inflammation and pain in mammals.Communicated by Ramaswamy H. Sarma.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic disease that lacks known pathogenesis, distinctive diagnostic criteria, and effective treatment options. Understanding the genetic (and other) risk factors associated with the disease would begin to help to alleviate some of these issues for patients.

Migraine involves central and peripheral nervous system mechanisms. Erenumab, an anti-calcitonin gene-related peptide (CGRP) receptor monoclonal antibody with little central nervous system penetrance, is effective for migraine prevention. The objective of this study was to determine if response to erenumab is associated with alterations in brain functional connectivity and pain-induced brain activations.