Objective To investigate the effects and mechanisms of median nerve electrical stimulation on synaptic plasticity in ischemic stroke rats.Methods 18 healthy male SD rats were randomly divided into Sham group(n = 6),ischemic stroke group(MCAO group,n = 6)and median nerve electrical stimulation group(MNES group,n = 6).The left middle cerebral artery occlusion model of rats was established by thread plug method.Thread plug was not inserted in sham group.The median nerve electrical stimulation group was given median nerve electrical stimulation intervention on the 3rd day after modeling,and intervention on the next day.After intervention for 7 times,behavioral detection,HE staining was used to detect median nerve injury.Nissl staining was used to detect cerebral infarction volume.Western blot was used for detection of the expression level of proteins related to synaptic plasticity,and electron microscopy was performed.Results HE staining showed that median nerve electrical stimulation did not cause damage to the median nerve in stroke rats,and the median nerve membrane was intact without obvious inflammatory cells.Compared with MCAO group,the neural function,motor function and coordination of the injured forelimb in MNES group were significantly improved(P<0.01).Compared with MCAO group,cerebral infarction volume in MNES group was significantly reduced(P<0.05),the pyknosis of Nissl bodies in ischemic penumbra decreased.Compared with MCAO group,the expression levels of synaptic plastication-related proteins PSD95 and synI in the cortex of MNES group were significantly up-regulated after median nerve electrical stimulation(P<0.05),the number of synapses in the ischemic cortex increased significantly(P<0.01).Conclusion Median nerve electrical stimulation is a safe and effective therapeutic measure to improve nerve function after stroke,and its mechanism is related to promoting synaptic plasticity.

After ischemic stroke, the key to reduce the mortality and disability rate is to restore the blood supply of brain tissue as soon as possible. However, the cerebral ischemia-reperfusion injury (CIRI) caused by blood flow restoration is also an important cause of brain tissue structural damage and dysfunction. Studies in recent years have shown that the activation of mitophagy at CIRI stage can reduce the volume of cerebral infarction and protect neurons from CIRI, while excessive or insufficient mitophagy can aggravate CIRI. This suggests that inducing moderate mitophagy may be a potential therapeutic target for neuroprotection after stroke. However, the neuroprotective mechanism of mitophagy has not yet been fully elucidated. This article reviews the neuroprotective mechanism and potential application of mitophagy in stroke, and discusses some problems of mitophagy as a therapeutic target for stroke.

Objective To analyze the process of intercomparison of national personal dose monitoring, evaluate the ability of personal dose monitoring, and ensure the accuracy and reliability of monitoring results in our laboratory. Methods In accordance with the intercomparison protocol for 2019—2021, an energy-discriminant thermoluminescence dosimeter was used for measurement at different doses. The uncertainty of measurement was evaluated and compared with the reference value. Results H_p(10) was measured for intercomparison in 2019—2021. In 2019, the single group performance difference was −0.02 to 0.02 and the comprehensive performance was 0.02. These values were 0.02-0.10 and 0.05 in 2020, and −0.02 to 0.02 and 0.01 in 2021. The intercomparison results were rated as excellent in the three consecutive years. Conclusion The personal dose monitoring system in our laboratory was in good condition, and the monitoring results were accurate and reliable. Improving the knowledge of personnel and cultivating a serious working attitude are important for intercomparison and personal dose monitoring.