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Malignant hyperthermia (MH) is an autosomal dominant genetic condition of the skeletal muscle triggered by inhaled general anesthetic agents or succinylcholine and associated with a hypermetabolic state and skeletal muscle rigidity. Tachycardia, increased carbon dioxide production, hypercarbia, hyperthermia, acidosis, hyperkalemia, cardiac arrhythmias, muscle rigidity, and rhabdomyolysis are common symptoms of MH. As the progression of the syndrome could be rapid or less evident, even experienced physicians have difficulty in diagnosing MH, which can lead to delays in treatment and increased mortality. We report a rare case of a 36-year-old man, who underwent open reduction and internal fixation of the left clavicle after inhaled anesthetics. The patient developed dyspnea, hypotension, unremitting hyperthermia, tachycardia, and elevated serum myoglobin, and finally died of pyemia and disseminated intravascular coagulation. We reviewed the process of disease development, summarized the steps of diagnosis, and improved genetic testing. Exome sequencing revealed a new mutation c.8519G>A (p.arg2840 GLN) in the RYR1 gene that could be associated with MH. The gene mutation was also found in his daughter’s genetic test. This case emphasized the importance of the awareness of MH and its atypical clinical symptoms. The presence of dyspnea, hypotension, unremitting hyperthermia, tachycardia, and raised myoglobin in serum might further strengthen the clinical diagnosis of suspected MH.

Purpose: To investigate the neuroprotective effect of Shenxiong Drop Pill (SXDP) pretreatment on rats with middle cerebral artery occlusion (MCAO) in rats, and the mechanism involved.Methods: Ninety-nine SD rats were randomly assigned to 4 groups: control group, MCAO group, shamoperated group and SXDP group. The MCAO model was established via thread occlusion. Rats in the SXDP group was administered SXDP 7 days before induction of MCAO. Neurological deficit score (NDS) was determined using Bederson's neurological behavioral scoring method, while cerebral infarction volume was measured using TTC staining. Integrated optical density (IOD) of Nissl Body was evaluated via Nissl staining. Brain water content was measured using dry-wet method. The expression level of AQP4 in brain tissues was determined using immunocytochemistry.Results: The SXDP treatment resulted in significant reduction in NDS, marked improvement in IOD of Nissl Body, and significant reductions in cerebral infarction volume, brain water content, and expression level of AQP4, relative to control (p< 0.05).Conclusion: These results suggest that SXDP pretreatment exerts neuroprotective effect against cerebral ischemia in rats by decreasing in cerebral edema through a mechanism involving downregulation of the expression of AQP4. Keywords: Middle cerebral artery occlusion, Cerebral ischemia, Aquaporins-4, Cerebral edema, Neuroprotection

Purpose: To investigate the effect of Shenxiong Drop Pill (SXDP) on cerebral infarction (CI) in rats, and the involvement of anti-inflammatory response in the process.Methods: Rats were sacrificed at three different time points, viz, 24, 48 and 72 h after establishment of CI model. Neurological deficit score (NDS) was determined using Bederson’s neurological behavioral scoring method, whereas triphenyltetrazolium chloride (TTC) staining was used to show brain injury. The integrated optical density (IOD) of Nissl bodies and caspase-3-positive nerve cells were measured with Nissl staining and SP kit, respectively. The mRNA expression of intercellular adhesion molecule 1(ICAM-1) was determined using reverse transcription-polymerase chain reaction (RT-PCR).Results: SXDP produced neuroprotective effect at high, medium, and low doses. The infarct volumes in the high-, medium- and low-dose SXDP, and cyclophosphamide groups were significantly reduced at each time point. Different doses of SXDP significantly reduced the mRNA expression of ICAM-1 and the IOD of caspase-3.Conclusion: These results indicate that SXDP exerts neuroprotective effects against ischemic injury by negatively regulating ICAM-1/caspase-3 downstream of inflammatory and apoptosis pathways.

To observe the effective mechanism of electroacupuncture for chronic fatigue syndrome (CFS).The dynamic detection of chronobiology was used to test the event-related potentials in 20 healthy subjects and 20 CFS patients. P3a and P3b latencies at 4 equidistant time points (8:00, 14:00, 20:00, 2:00) within 24 hours were collected and analyzed.(1) Latency of P3a in CFS group was obviously prolonged at 14:00 compared to health group with statistical significance (P0.05), latency of P3b was decreased at 14:00 after electroacupuncture treatment with statistical significance compared to that of pre-treatment (P0.01). (2) There were obviously circadian rhythm in latency of P3a and P3b in health group (P0.05), which were not seen in CFS group (P0.05); the circadian rhythm latency of P3b restored after treatment (P0.05). (3) The latency acrophase of P3a and P3b pre-treatment obviously shifted backward compared to that of healthy subjects (P0.05), shifted forward after electroacupuncture treatment (P0.05).The event-related potential circadian rhythms are lost in CFS patients. Electroacupuncture at Shenshu (BL 23) and Zusanli (ST 36) can regulate the circadian rhythm of P3a and P3b latency and improve the cognition of the patients in daytime.