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Spinal cord injury (SCI) is a severe disease with motor and sensory function being destroyed, which leads to a poor prognosis and a serious financial burden. It is urgent to figure out the molecular and pathological mechanisms of SCI to develop feasible therapeutic strategies. This article aims to review documents focused on gene expression in SCI and summarize research hotspots and the development process in this field.

The aim: To investigate the clinical features of the chronic pancreatitis (CP) clinical course in patients with concomitant arterial hypertension.

Acid-sensing ion channels (ASICs) play a critical role in nociception in human sensory neurons. Four genes ( and ) encoding multiple subunits through alternative splicing have been identified in humans. Real time-PCR experiments showed strong expression of three subunits , , and in human dorsal root ganglia; however, their detailed expression pattern in different neuronal populations has not been investigated yet. In the current study, using an hybridization approach (RNAscope), we examined the presence of , , and mRNA in three subpopulations of human dorsal root ganglia neurons. Our results revealed that and were present in the vast majority of dorsal root ganglia neurons, while was only expressed in less than half of dorsal root ganglia neurons. The distribution pattern of the three subunits was the same across the three populations of dorsal root ganglia neurons examined, including neurons expressing the REarranged during Transfection (RET) receptor tyrosine kinase, calcitonin gene-related peptide, and a subpopulation of nociceptors expressing Transient Receptor Potential Cation Channel Subfamily V Member 1. These results strongly contrast the expression pattern of in mice since our previous study demonstrated differential distribution of among the various subpopulation of dorsal root ganglia neurons. Given the distinct acid-sensitivity and activity dynamics among different ASIC channels, the expression differences between human and rodents should be taken under consideration when evaluating the translational potential and efficiency of drugs targeting ASICs in rodent studies.

The skin is an important barrier that protects against invasion by foreign substances, including irritants and harmful microorganisms, and holds water in the body. Washing the skin with cleansers and shampoos containing anionic surfactants, for example sodium dodecyl sulfate (SDS), is important for maintaining skin homeostasis. However, surfactants can cause dermatitis, cutaneous hypersensitivity (e.g., alloknesis), and pruritus in humans. Our previous studies revealed an alloknesis response in the skin with SDS-induced dermatitis in C57BL/6 mice. In addition, we found that alloknesis responses and afterdischarge responses following stimulation with light touch are related because they are observed contemporaneously. In this study, we used Hos:HR-1 hairless mice to establish a mouse model to evaluate long-term drug application for alloknesis responses. Alloknesis was observed in HR-1 mice with SDS-induced dermatitis. The mean number of c-Fos (a marker of neural activity) immunopositive neurons was increased in the lamina 1-2 (L1-2) spinal dorsal horn, but not in L3-4, of SDS-treated HR-1 mice compared to vehicle-treated mice. We also discovered that afterdischarge responses were observed in neurons in L1-2. There was also a correlation between the intensity of the afterdischarge responses and depth of the recording site. Thus, the following were suggested: 1) neurons that mediate these afterdischarge responses are located on the superficial layer of the spinal cord; 2) afterdischarge responses can be an index of alloknesis responses, and 3) the mouse model of SDS-induced dermatitis is an appropriate alloknesis model.

Chronic subdural hematoma (CSH) in the posterior fossa is extremely rare and only a few cases have been reported in the literature. We report a case of CSH in the posterior fossa successfully treated with a single burr hole surgery.

Chronic neuropathic pain (NP) frequently occurs after spinal cord injury (SCI) but lacks effective therapeutic options in the clinic. Numerous evidence indicates the involvement of macrophages activation in the NP, and the modulation of macrophages is promising for NP treatment. In this study, we introduce Cerium oxide nanoparticles (CONPs) and aim to investigate whether it can relieve the NP by modulating macrophage polarization.

HIV-associated distal neuropathic pain (DNP) is one of the most prevalent, disabling, and treatment-resistant complications of HIV, but its biological underpinnings are incompletely understood. While data specific to mechanisms underlying HIV DNP are scarce, functional neuroimaging of chronic pain more broadly implicates the role of altered resting-state functional connectivity within and between salience network (SN) and default mode network (DMN) regions. However, it remains unclear the extent to which HIV DNP is associated with similar alterations in connectivity. The current study aimed to bridge this gap in the literature through examination of resting-state functional connectivity patterns within SN and DMN regions among people with HIV (PWH) with and without DNP. Resting state functional magnetic resonance imaging (rs-fMRI) scans were completed among 62 PWH with HIV-associated peripheral neuropathy, of whom 27 reported current DNP and 35 did not. Using subgrouping group iterative multiple estimation, we compared connectivity patterns in those with current DNP to those without. We observed weaker connectivity between the medial prefrontal cortex (MPFC) and posterior cingulate cortex (PCC) and stronger connectivity between the anterior cingulate cortex (ACC) and thalamus among those reporting DNP. Overall, these findings implicate altered within DMN (i.e., MPFC-PCC) and within SN (i.e., ACC-thalamus) connectivity as potential manifestations of adaptation to pain from neuropathy and/or mechanisms underlying the development/maintenance of DNP. Findings are discussed in the context of differential brain response to pain (i.e., mind wandering, pain aversion, pain facilitation/inhibition) and therapeutic implications.

Oxaliplatin (OXA) is a third-generation platinum compound with clinical activity in multiple solid tumors. Due to the repetition of chemotherapy cycle, OXA-induced chronic neuropathy presenting as paresthesia and pain. This study explored the neuropathy of chemotherapy pain and investigated the analgesic effect of 2-bromopalmitate (2-BP) on the pain behavior of OXA-induced rats. The chemotherapy pain rat model was established by the five consecutive administration of OXA (intraperitoneal, 4 mg/kg). After the establishment of OXA-induced rats, the pain behavior test, inflammatory signal analysis and mitochondrial function measurement were conducted. OXA-induced rats exhibited mechanical allodynia and spinal inflammatory infiltration. Our fluorescence and western blot analysis revealed spinal astrocytes were activated in OXA rats with up-regulation of astrocytic markers. In addition, NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome mediated inflammatory signal cascade was also activated. Inflammation was triggered by dysfunctional mitochondria which represented by increase in cyclooxygenase-2 (COX-2) level and manganese superoxide dismutase (Mn-SOD) activity. Intrathecally injection of 2-BP significantly attenuated dynamin-related protein 1 (Drp1) mediated mitochondrial fission, recovered mitochondrial function, suppressed NLRP3 inflammasome cascade, and consequently decreased mechanical pain sensitivity. For cell research, 2-BP treatment significantly reversed tumor necrosis factor-α (TNF-α) induced mitochondria membrane potential deficiency and high reactive oxygen species (ROS) level. These findings indicate 2-BP decreases spinal inflammation and relieves OXA-induced neuropathic pain via reducing Drp1-mediated mitochondrial dysfunction.

Endometriosis of the rectus abdominis muscle is an extremely rare form of extrapelvic localization of the disease. It is usually iatrogenic and develops after caesarean section or gynecological surgery. Preoperative diagnosis is very difficult and a challenge for gynecologists and surgeons; thus, the diagnosis is histological. The treatment of choice consists of wide local excision of the lesion on healthy margins. We cite a case of isolated endometriosis in the rectus abdominis muscles in a 46-year-old patient with a previous caesarean section, the diagnosis of which was made randomly when performing abdominal total hysterectomy for the treatment of chronic pelvic pain. Histological examination of the surgical specimen confirmed the diagnosis. Simultaneously, the surgical specimen of the uterus and ovaries was free of endometriosis. Postoperatively, the patient mentioned discharge of her symptoms. No further therapeutic intervention was deemed necessary, as it was considered that a complete resection of the endometrial tissue implantation from the muscles of abdominal wall was performed. The present case report lay emphasis on the significant difficulties involved in the preoperative diagnosis of endometriosis of the rectus abdominis muscle. Concurrently, it is pointed out that, despite its rarity, individual extrapelvic endometriosis located in the rectus abdominis muscle should be included among other pathological entities in the differential diagnosis of chronic pelvic pain in women of reproductive age, who gave birth by caesarean section or underwent gynecological surgery with abdominal or laparoscopic access.

To estimate the prevalence of chronic back pain (CBP) and its associated factors.