Electromuscular Incapacitation Current Induced Neuromuscular Tissue Injury

Electrical stun devices (ESDs) serve a basic role in law enforcement and provide an alternative to lethal options for target control by causing electromuscular incapacitation (EMI). A fundamental concern is the adverse health consequences associated with their use. The capability of EMI electric field pulses to disrupt skeletal muscle cells (i.e. rhabdomyolysis) was investigated over the operational range commonly used in commercial EMI devices. Functional and structural alteration and recovery of muscle and nerve tissue were assessed. In an anesthetized swine model, the left thigh was exposed to 2 min of electrical pulses, using a commercially available ESD or a custom-made EMI signal power amplifier. Serum creatinine phosphokinase (CPK), troponin, aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels were monitored intermittently for 6 h post-EMI exposure. A standard external cardiac defibrillator served as a positive control. Muscle and nerve tissue histology adjacent to the EMI contacts were examined. Post-EMI shock skeletal muscle function was evaluated by analyzing the compound muscle action potentials (CMAPs) of the rectus femoris muscle. Maximal energy cardiac defibrillator pulses resulted in rhabdomyolysis and marked elevation of CPK, LDH, and AST 6 h post-shock. EMI field pulses resulted in the animals developing transient acidosis. CMAP amplitudes decreased approximately 50% after EMI and recovered to near-normal levels within 6 h. Within 6 h post-EMI exposure, blood CPK was mildly increased, LDH was normal, and no arrhythmia was observed. Minimal rhabdomyolysis was produced by the EMI pulses. These results suggest that EMI exposure is unlikely to cause extremity rhabdomyolysis in normal individuals. Bioelectromagnetics. © 2020 Bioelectromagnetics Society     

2000年以来有毒蘑菇研究新进展

误食毒蘑菇而中毒一直被认为是一个对人类健康造成威胁的全球性问题,也是我国食物中毒事件中导致死亡的最主要因素。对2000年以来在有毒蘑菇新种类、新毒素与新症状、有毒蘑菇鉴定及毒素检测新方法、有毒蘑菇中毒机理、毒素基因克隆、中毒治疗以及鹅膏肽类毒素治疗肿瘤等领域取得的新进展进行了综述,并对一些热点研究领域做了展望。     

MBD2 mediates renal cell apoptosis via activation of Tox4 during rhabdomyolysis-induced acute kidney injury

Our study investigated the role of Methyl-CpG–binding domain protein 2 (MBD2) in RM-induced acute kidney injury (AKI) both in vitro and in vivo. MBD2 was induced by myoglobin in BUMPT cells and by glycerol in mice. MBD2 inhibition via MBD2 small interfering RNA and MBD2-knockout (KO) attenuated RM-induced AKI and renal cell apoptosis. The expression of TOX high mobility group box family member 4 (Tox4) induced by myoglobin was markedly reduced in MBD2-KO mice. Chromatin immunoprecipitation analysis indicated that MBD2 directly bound to CpG islands in the Tox4 promoter region, thus preventing promoter methylation. Furthermore, siRNA inhibition of Tox4 attenuated myoglobin-induced apoptosis in BUMPT cells. Finally, MBD2-KO mice exhibited glycerol-induced renal cell apoptosis by inactivation of Tox4. Altogether, our results suggested that MBD2 plays a role in RM-induced AKI via the activation of Tox4 and represents a potential target for treatment of RM-associated AKI.