The journal of pain : official journal of the American Pain Society
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Hand-holding reduces experimentally induced acute pain and buffers against the development of mechanical secondary hypersensitivity, an indirect proxy of central sensitization. Here, we tested if verbal support from a stranger, a common occurrence in clinical contexts, exerts the same effects. In this preregistered study, 44 healthy female participants were assigned to an alone or support group whereby a supportive female stranger encouraged them through the painful procedure leading to secondary mechanical hypersensitivity. ⋯ PERSPECTIVE: Verbal support by a stranger during a painful procedure leading to secondary mechanical hypersensitivity attenuated the development of some measures of mechanical hypersensitivity and associated neural responses in healthy female participants. No evidence was found for the role of stress. DATA AVAILABILITY: The authors will make all data available upon request.
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Numerous genome-wide association studies have identified risk genes for chronic pain, yet the mechanisms by which genetic variants modify susceptibility have remained elusive. We sought to identify key genes modulating chronic pain risk by regulating brain protein expression. We integrated brain proteomic data with the largest genome-wide dataset for multisite chronic pain (N = 387,649) in a proteome-wide association study (PWAS) using discovery and confirmatory proteomic datasets (N = 376 and 152) from the dorsolateral prefrontal cortex. ⋯ This integrative proteogenomic approach identified 18 high-confidence causal genes for chronic pain, regulated by cis-effects on brain protein levels, suggesting promising avenues for treatment research and indicating a contributory role for the DRG. PERSPECTIVE: The current post genome-wide association study analyses identified 18 high-confidence causal genes regulating chronic pain risk via cis-modulation of brain protein abundance, suggesting promising avenues for future chronic pain therapies. Additionally, the significant expression of these genes in the DRG indicated a potential contributory role, warranting further investigation.
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Clinicians often ask people with chronic pain about their perceived benefit from interventions designed to improve their pain. The aim of this study is to identify factors that contribute to underestimating or overestimating perceived changes in daily pain intensity over a month of daily assessments. We examined data from individuals with chronic pain who provided at least 28 daily assessments using a pain app as secondary analyses. ⋯ This longitudinal study suggests that those who report greater levels of catastrophizing and anxiety and depression are more likely to underestimate any improvements in their pain over time but seem to engage more with a pain app. Future research will help in our understanding of what magnitude of perceived change in pain ratings is clinically meaningful. PERSPECTIVE: Those who report greater levels of pain, disability, anxiety, depression, and catastrophizing are most prone to underestimate improvements of their pain over time.
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Chronic pain often coincides with changes in gut microbiota composition. Yet, the role of gut microbiota in bone cancer pain (BCP) is still not fully understood. This study investigated the role of gut microbiota in BCP and the effect of oxymatrine (OMT) on gut microbiota in BCP. ⋯ Also, C butyricum or NaB improves BBB via PPARγ/COX-2. OMT, a BCP treatment, modifies microbiota by regulating PPARγ/COX-2, in turn improving pain and BBB integrity. These findings suggest a therapeutic approach, emphasizing clinical relevance in targeting gut microbiota and restoring butyric acid levels.
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The voltage-gated sodium channel β2 subunit protein (SCN2B) plays a crucial role in neuropathic pain. However, the role and mechanisms of SCN2B in orofacial neuropathic pain are still unclear. This study aimed to investigate the upstream regulatory mechanisms of SCN2B in the trigeminal ganglion (TG) underlying orofacial neuropathic pain. ⋯ PERSPECTIVE: This study points to the important role of SCN2B in orofacial neuropathic pain. Furthermore, miR-6954-3p is proven to regulate the expression of SCN2B by binding to the 3'-untranslated region of Scn2b mRNA. These findings indicate that SCN2B and miR-6954-3p are potential therapeutic targets for the treatment of orofacial neuropathic pain.