Objective To examine the expression of inhibitory chondroitin sulfate proteoglycans (CSPGs) and in-vestigate their potential effects on neural plasticity in the peri-infarct cortex and ipsilateral thalamus after focal cerebral infarction in hypertensive rats. Methods Twenty-four adult renovascular hypertensive Sprague-Dawley rats per group were subjected to permanent right middle cerebral artery occlusion(MCAO) or sham operation. Twelve rats which were se-lected randomly from per group at each time point were decapitated and their brains were removed and cut into coronal sections at 7 and 14 days post MCAO. The expression of CSPGs, NG2 and Neurocan was examined using immunostaining and western blot. Results All rats displayed neurological deficits to varying degrees and the expression of CSPGs, NG2 and full length Neurocan was increased in the peri-infarct cortex and ipsilateral thalamus at 7 and 14 days (P<0.05). However, there were no significant difference in either expression of CSPGs, NG2 and full-length Neurocan between 7 and 14 days or the expression of C-terminal fragment Neurocan at 7 and 14 days (all P>0.05). Conclusions CSPGs may play a negative role in neural plasticity through induction of inhibitory environment in the peri-infarct cortex and ipsilat-eral thalamus following focal cerebral infarction in hypertensive rats.

Objective To investigate the dynamic levels of autophagy after intimal injury of carotid artery. Meth-ods In this study ,40 male SD rats were randomly assigned to operated(n=20)and control groups(n=20). Balloon inju-ry was induced in the left carotid artery in operated groups .Rats in control groups just received carotid artery exposure without injury. Western blot was used to detect the levels of Beclin-1, LC3 and p62 at the third and seventh days. Immu-nofluorescence was used to examine the expression of Beclin-1 and LC3 at the third and seventh days. Results The ex-pression levels of Beclin-1 and LC3 were increased while the levels of P62 were decreased at the third and seventh days after carotid balloon injury. Beclin-1 and LC3 were present in neointima and medintima. The numbers of both Beclin-1 positive cells and LC3 positive cells were increased at the third and seventh days after carotid injury. The numbers of Be-clin-1 positive cells were 18.60 ± 1.34 in neointima and 6.40 ± 0.55 in medintima at third day, (27.6 ± 2.19 in neointima and 6.40±0.55 in medinitima at the seventh day,(all P=0.000,n=5). The numbers of LC3 positive cells were 10.60±1.52 in neointima and 3.00 ± 0.71 in medintima at third day, (P=0.000,n=5;at the seventh day 21.20 ± 2.49;3.00 ± 0.71,P=0.000,n=5). Conclusions This study domenstrates that autophagy was activated after carotid injury and the chang is dy-namic, which may contribute to neointima formation.

Objective To investigate the clinical and electrophysiological features of patients with non-inflammatory myopathy with neurogenic lesions. Method The clinical and electromyography data was retrospectively collected from 110 patients who were diagnosed with myopathy and completed routine electromyography examination from 2015 to 2017. A retrospective analysis of clinical and electrophysiological features was conducted on 4 patients with non-inflammatory myopathy with neurogenic lesions. Result Of the 110 patients, 10 patients with neurogenic lesions and 4 of them were diagnosed to have non-inflammatory myopathy. These 4 patients had limb and trunk weakness with muscle atrophy and the electromyography showed neurogenic lesion with or without peripheral nerve lesion. Conclusion This study has revealed neurogenic lesions in a small number of non-inflammatory myopathy on the electromyography, suggesting that the electromyography alone may not be sufficient for diagnosis of myopathy.

Objective To investigate the loss of motor unit and it's influencing factors in the lower motor neurons after middle cerebral artery infarction. Method Forty patients with first onset and unilateral middle cerebral artery infarction were divided into cortical-basal ganglia(26)and basal ganglia(14)groups and 10 healthy controls were served as control group.All included patients were scored by National Institute of Health stroke scale(NIHSS),modified Rankin scale (mRS), Fugl-Meyer Assessment (FMA) at 48 hours of admission. Nerve conduction study on the limb and motor unit number estimation (MUNE) on abductor pollicis brevis were performed at 2-4 weeks after onset, and the data of single motor action potential (SMUAP) were collected. SPSS 20.0 software was used to statistical analysis. Result The MUNE on were significantly lower and the amplitude and area of SMUAP were significantly increased in ipsilateral than contralateral sides (cortical-basal ganglia group:95.85±26.82 vs. 143.65±38.86, P<0.001; basal ganglia group: 126.71± 44.13 vs. 157.36±56.72, P=0.001). The affected MUNE was significantly decreased in the cortex-basal ganglia than in basal ganglia groups (95.85±26.82 vs.161.40±48.90,P=0.027). The MUNE was negatively correlated with NIHSS score (r=-0.362,P=0.022)and mRS score(r=-0.339,P=0.032).NIHSS score(β=-1.603,P=0.032,95%CI:-3.064~-0.142)and mRS score(OR=2.885,P=0.025,95%CI:1.139~7.158)on admission could predict the loss of MUNE on the affected side. Conclusion This study reveals the loss of motor unit and the compensation of remained motor unit on the affected side after middle cerebral artery infarction,NIHSS score and mRS score on admission may predict the loss of MUNE after stroke.

Objective:To establish the reference values of stimulation single fiber electromyography (SFEMG) in orbicularis oculi, and to explore its sensitivity in repetitive nerve stimulation (RNS) negative ocular myasthenia gravis (OMG) patients, and the relationship between jitter and various clinical parameters.Methods:Thirty-two healthy volunteers were included to establish the reference value of normal controls from January 2019 to December 2019. From December 2019 to January 2023, 36 OMG patients with negative RNS were collected. Quantitative MG score (QMGS) was performed, neostigmine test and antibody titers as well as thymus CT results were recorded. One side of the orbicularis oculi muscle was tested with a disposable concentric needle electrode in stimulation SFEMG, and the mean consecutive difference (MCD) value was calculated, which was compared with the average MCD value and upper limit of individual values in normal controls to evaluate whether the jitter was abnormal. Spearman correlation analysis of abnormal mean MCD values with QMGS and antibody titer was conducted.Results:Among the 32 healthy volunteers, there were 13 males and 19 females, the age was (46.8 ±18.7) years, and the MCD was (19.0 ±4.4) μs. The upper limit of the reference value was 27.7 μs for average MCD, and 37.4 μs for 10% individual values. Among 36 OMG patients negative at RNS tests, 20 were male and 16 were female, with a age of (37.2 ±17.0) years. The MCD was (29.9 ±14.7) μs, and Jitter was abnormal in 29 patients (81%). Among them, 20 (20/25) patients were antibody positive, 6 (6/26) patients had thymic hyperplasia, and 7 (7/26) patients had thymoma. The QMGS was 3(2, 4). There were 7 patients (19%) with normal jitter, whose QMGS was 3(2, 4). Among the patients with normal Jitter, 5 (5/5) patients were antibody positive, 2 (2/6) patients had thymic hyperplasia. There was no statistically significant difference in clinical indicators between the two groups of patients with abnormal or normal jitter. There was no significant correlation in antibody titer or QMGS with abnormal mean MCD value. Conclusions:The upper limit of the mean MCD value in the normal controls is 27.7 μs. The upper limit of a single value is 37.4 μs. Its sensitivity for OMG patients with RNS negative is 81%, and the abnormal mean MCD value does not show a significant correlation with various clinical indicators. Abnormal jitter indicates dysfunction of neuromuscular junction transmission, which is an important neuroelectrophysiological indicator for MG patients and is suitable for RNS negative patients. Orbicularis oculi muscle stimulation SFEMG provides a reliable and sensitive electrophysiological means for functional evaluation of neuromuscular junction.