Rejected

Arsenic toxicity is a global health problem affecting millions of people. Contamination is caused by arsenic from natural geological sources leaching into aquifers, contaminating drinking water, and may also be caused by mining and other industrial processes. Acute arsenic poisoning is associated with nausea, vomiting, abdominal pain, and severe diarrhea. Chronic arsenic toxicity results in multisystemic diseases leading to central nervous system (CNS) impairments such as cognitive or intellectual deficits in children. Over the past ten years, arsenic contamination has been reported in northern Thailand. The Ministry of Public Health; Thailand, Forensic Science Institute Thammasat University, and the Research Center to Promote Safety and Prevent Injuries in Children at the Ramathibodi Hospital compiled a report on the health impact of the population within a 10 kilometer radius around a mine tailing in the Phichit, Phitsanulok, and Phetchabun Provinces of Thailand. It showed that more than 30 % of children (aged 8-13 years) had higher than normal arsenic contamination levels based on the Agency for Toxic Substances and Disease Registry (ATSDR). After the publication of that report, the mine was temporarily closed in 2016. Based on this data, this research aimed to follow arsenic contamination after the mining operation had stopped operation for three years. The study showed that 4.5 % of school aged children had levels of inorganic arsenic in their urine, higher than the normal range (ATSDR), showing clearly that inorganic arsenic contamination is still above the normal range in children living near an inactive mining site Therefore, monitoring heavy metal contamination in Thailand and the health effects on vulnerable children who live near mines during regular operation or after being temporarily suspended can prevent and mitigate possible health impacts.

Numerous studies have shown that mitochondrial dysfunction manifested by increased mitochondrial permeability transition pore (mPTP) opening and reactive oxygen species (ROS) level, and decreased mitochondrial membrane potential (MMP) plays an important role in the development of neuropathic pain. Sirtuin3 (SIRT3), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, has been shown to inhibit mitochondrial oxidative stress. However, the role of SIRT3 in neuropathic pain is unclear. In this study, we found that the protein and mRNA levels of SIRT3 were significantly downregulated in the spinal cords of spared nerve injury- (SNI-) induced neuropathic pain mice, while overexpression of spinal SIRT3 reversed SNI-induced pain hypersensitivity. Further study showed that SIRT3 overexpression reduced the acetylation level of lysine 166 (K166) on cyclophilin D (CypD), the regulatory component of the mPTP, inhibited the mPTP opening, decreased ROS and malondialdehyde (MDA) levels, and increased MMP and manganese superoxide dismutase (MnSOD) in SNI mice. Point mutation of K166 to arginine on CypD (CypD-K166R) abrogated SNI-induced mitochondrial dysfunction and neuropathic pain in mice. Moreover, inhibiting mPTP opening by cyclosporin A (CsA) improved mitochondrial function and neuropathic pain in SNI mice. Together, these data show that SIRT3 is necessary to prevent neuropathic pain by deacetylating CypD-K166 and further improving mitochondrial dysfunction. This study may shed light on a potential drug target for the treatment of neuropathic pain.

To investigate the analgesic mechanism of electroacupuncture (EA) in rats with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).

This study aimed to investigate the analgesic effect and mechanism of electroacupuncture (EA) in nicotine withdrawal-induced hyperalgesia rats.

We evaluated the long-term clinical status of pediatric patients after testing positive for COVID-19. We hypothesized that there are similar symptoms to those that have been described in adults and children and that pediatric patients with neurophysiologic symptoms still present 3-5 months after infection have psychological consequences that interfere with their adaptive functioning.

Increasing evidence has shown that noncoding RNAs perform a remarkable function in neuropathic pain (NP); nonetheless, the mechanisms underlying the modulation of competitive endogenous RNA in NP remain uncertain. The goal of this research was to investigate the molecular processes underlying NP.

A new thermostable Co(II)-based compound, namely [Co(L)(HTEA)] (, HL = isonicotinic acid, HTEA = triethanolamine), has been successfully synthesized by the isomicotinic acid ligand and HTEA anion. The photocatalytic property of was also investigated, indicating that it shows excellent photocatalytic activity for the degradation of Rhodamine B (MB) solution under the UV light irradiation. For the treatment of trigeminal neuralgia, the content of the inflammatory cytokines released into the trigeminal ganglion tissue fluid was measured with enzyme-linked immunosorbent assay (ELISA) assay. Then, the real-time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was conducted and the activation of the nuclear factor kappa-B (NF-κB) inflammatory signaling pathway was measured.

Neuropathic pain is a commonly seen symptom and one of the most intractable comorbidities following spinal cord injury (SCI). Acupuncture has been widely used for neuropathic pain after SCI in clinical settings. There is no systematic review or meta-analysis evaluating the efficacy of acupuncture in the treatment of SCI-induced neuropathic pain. Thus, this study aimed to conduct a systematic review and meta-analysis to assess the efficacy of acupuncture on SCI-induced neuropathic pain.

Type 2 diabetes (T2D) is the most common comorbidity of COVID-19, and both are related to the lack of circulating melatonin. In addition, chronic pain is a common sequela of both COVID-19 and T2D. Using a neuropathic pain model produced by sciatic nerve chronic constriction injury in Zucker diabetic fatty rats, a verified preclinical genetic T2D neuropathy animal model, this study aimed to show that transcutaneous auricular vagal nerve stimulation (taVNS) could elevate plasma melatonin concentration, upregulate the expression of melatonin receptors (MTRs) in the amygdala, and relieve peripheral neuropathic pain. Furthermore, taVNS would restore melatonin levels and relieve pain even in pinealectomized rats. On the contrary, intraperitoneally injected luzindole, a melatonin receptor antagonist, would attenuate the antinociceptive effects of taVNS. In conclusion, the mechanism of the therapeutic effect of taVNS on chronic pain involves the release of extrapineal melatonin and the positive regulation of the expression of central MTRs. This beneficial efficacy should be considered during COVID-19 rehabilitation in individuals with diabetes.

Dermatological reactions have been reported following Shingrix vaccine administration in previous published cases, but dermatomal rash after Shingrix vaccination has not been reported in the United States. This case describes a 73-year-old immunocompetent woman with a dermatomal rash after Shingrix recombinant vaccine administration. This case highlights the rare possibility of an acute reaction after Shingrix vaccine administration, which should be recognized. Nonetheless, the vaccine has been shown to be very effective at preventing varicella zoster virus reactivation and postherpetic neuralgia, so the benefit of receiving the vaccination significantly outweighs the risk.