Scientific reports
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This study was conducted to explore underlying mechanism of microcirculation dysfunction and protectiverole of Xuebijing in heat stroke. Forty rats were divided into: control, vehicle + heat stress (HS), superoxide dismutase (SOD) + HS, and Xuebijing + HS groups. Rats in heat stress groups were subjected to continuous heat stress in infant incubator 1 h after tail vein injection of the tested compound and spinotrapezius preparation. ⋯ Xuebijing increased SOD activity, decreased ROS levels and exhibited a protective effect in terms of blood flow rate but was less protective than SOD. The survival time in Xuebijing + HS group was longer than that in vehicle group but shorter than that in SOD + HS group. The results suggested Xuebijing could decrease ROS levels and have protective effects in severe heat stroke.
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Randomized Controlled Trial Comparative Study
Exploring the effects of anodal and cathodal high definition transcranial direct current stimulation targeting the dorsal anterior cingulate cortex.
The dorsal anterior cingulate cortex (dACC) has been identified as a core region affected by many disorders, representing a promising target for neuromodulation. High Definition-transcranial Direct Current Stimulation (HD-tDCS) is a non-invasive neuromodulation technique that has already shown promising outcomes and has been tested to engage deeper structures. This study investigates whether it is possible to modulate dACC activity using anodal and cathodal HD-tDCS. ⋯ RsEEG showed changes: anodal HD-tDCS showed significant increase in beta frequency band activity in dACC, while cathodal HD-tDCS led to significant increase in activity at dorsal and rostral ACC in the theta frequency band. Behavioral changes were also found after anodal HD-tDCS in the cognitive Counting Stroop for incongruent trials and after cathodal HD-tDCS in the emotional Counting Stroop for emotional trials. This study demonstrated that HD-tDCS is able to modulate dACC activity, suggesting that it has the potential to be used as a treatment tool.
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Meta Analysis
Intra-articular dexmedetomidine in knee arthroscopy: A systematic review and meta-analysis.
The aim of this meta-analysis is to evaluate the analgesic effects of intra-articular dexmedetomidine (DEX) in arthroscopic knee surgery. A comprehensive literature search was conducted to identify randomized controlled trials (RCTs) comparing intra-articular DEX versus control for postoperative analgesia in knee arthroscopy. Trial sequential analysis (TSA) was applied to determine the reliability of the evidence. ⋯ Intra-articular DEX did not affect the incidence of postoperative nausea and vomiting, hypotension, bradycardia, or somnolence. This meta-analysis demonstrated that intra-articular administration of DEX improved pain outcomes in the early postoperative period after knee arthroscopy. Due to the limited number of trials and patients included in this meta-analysis, more evidence is required to confirm these findings.
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Voltage-gated sodium channels NaV1.7, NaV1.8 and NaV1.9 have been the focus for pain studies because their mutations are associated with human pain disorders, but the role of NaV1.6 in pain is less understood. In this study, we selectively knocked out NaV1.6 in dorsal root ganglion (DRG) neurons, using NaV1.8-Cre directed or adeno-associated virus (AAV)-Cre mediated approaches, and examined the specific contribution of NaV1.6 to the tetrodotoxin-sensitive (TTX-S) current in these neurons and its role in neuropathic pain. We report here that NaV1.6 contributes up to 60% of the TTX-S current in large, and 34% in small DRG neurons. ⋯ Although NaV1.8-Cre driven NaV1.6 knockout does not alter acute, inflammatory or neuropathic pain behaviors, AAV-Cre mediated NaV1.6 knockout in adult mice partially attenuates SNI-induced mechanical allodynia. Additionally, AAV-Cre mediated NaV1.6 knockout, mostly in large DRG neurons, significantly attenuates excitability of these neurons after SNI and reduces NaV1.6 accumulation at nodes of Ranvier at the neuroma. Together, NaV1.6 in NaV1.8-positive neurons does not influence pain thresholds under normal or pathological conditions, but NaV1.6 in large NaV1.8-negative DRG neurons plays an important role in neuropathic pain.
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Sigma-1 receptor (σ1R) knockout (KO) CD1 mice, generated by homologous recombination, and separate pharmacological studies in wild type (WT) mice were done to investigate the role of this receptor in the development of pain-related behaviours (thermal hyperalgesia and mechanical allodynia) in mice after spinal cord contusion injury (SCI) - a model of central neuropathic pain. The modulatory effect of σ1R KO on extracellular mediators and signalling pathways in the spinal cord was also investigated. In particular, changes in the expression of inflammatory cytokines (tumour necrosis factor TNF-α, interleukin IL-1β) and both the expression and activation (phosphorylation) of the N-methyl-D-aspartate receptor subunit 2B (NR2B-NMDA) and extracellular signal-regulated kinases (ERK1/2) were analysed. ⋯ Accordingly, treatment of WT mice with the σ1R antagonist MR309 (previously developed as E-52862; S1RA) after SCI exerted antinociceptive effects (i.e. reduced mechanical allodynia and thermal hyperalgesia). Attenuated nociceptive responses in σ1R KO were accompanied by reduced expression of TNF- α and IL-1β as well as decreased activation/phosphorylation of NR2B-NMDA receptors and ERK1/2. These findings suggest that σ1R may modulate central neuropathic pain and point to regulation of sensitization-related phenomena as a possible mechanism.