Objective To explore the influence of self-efficacy training on the memory and executive function of patients with ischemic stroke in the recovery stage.Methods A total of 80 cases were randomly divided into a self-efficacy training group and a control group,with 40 cases in each.The control group was given routine cognitive therapy,while the self-efficacy group was given cognitive interventions plus efficacy training.Before training and after training for 3 months,self-efficacy levels were examined using the general self-efficacy scale (GSES),memory and executive function were measured using the Behavioral Assessment of Dysexecutive Syndrome (BADS) and the Wechsler Memory Scale (WMS).Anxiety and depression were evaluated using the Self-rating Depression Scale (SDS) and Self-Rating Anxiety Scale (SAS).Results Inter-group comparison showed no significant differences in terms of GSES or BADS scores before treatment between the control and self-efficacy groups.After training,the total GSES and BADS scores in both groups were significantly higher than before.Both the average GSES and BADS scores in the self-efficacy group were significantly higher than in the control group.There were similarly no significant differences in WMS scores before treatment,but after training the WMS results were significantly better in the self-efficacy training group than in the control group.After training,the SDS and SAS scores had improved to a significantly greater extent in the self-efficacy group than in the control group.Conclusion Self-efficacy training can facilitate the recovery of memory and promote executive function in patients with ischemic stroke.

Objective To investigate the effects of grape seed proanthocyanidin(GSPE) on mitochondrial injury in hippocampus and learning-memory impairment after obstructive sleep apnea hypoxia in rats.Methods Male SD rats(n=80) were randomly divided into control group,model group,low dose of GSPE treatment group and high dose of GSPE treatment group.Rats in control group were exposed in air,the model group were suffered from intermittent hypoxia conditions (50 ml/L,8-hour-intermittent hypoxia everyday,and the duration of experiment 2 and 6 weeks,respectively).Mitochondrion pathology in hippocampal region was observed using electron microscope;malondialdehyde (MDA) contents and superoxide dismutase activity were detected by colorimetry and apoptotic cells was measured by TUNEL method.The cognitive function of rats in each group was assessed with the Morris water maze (MWM).Results After hypoxia,mitochondrion was significantly injured.The MDA contents were increased(79.86 ± 2.52,88.26 ± 2.86) and SOD level decreased (70.67 ± 6.70,64.26 ± 7.86).The number of neural apoptotic cells was significantly enhanced (9.68 ± 0.79,15.9 ± 2.92).MWM test showed that the escaping latency was prolonged and the frequency of crossing the platform was decreased (P ＜ 0.05).Compared with that in the model group,low dose of GSPE decreased MDA contents (76.38 ± 1.96,82.16 ±2.02),increased SOD level(76.20 ± 6.86,70.58 ± 6.86),and decreased apoptotic cells (6.60 ± 0.69,9.54 ±1.36).MWM test showed that the escaping latency was shortened and the frequency of crossing the platform was increased in GSPE treatment groups(P ＜ 0.05).Compared with low dose of GSPE,high dose of GSPE decreased MDA contents increased SOD level and decreased apoptotic cells.MWM test showed that the escaping latency was shortened and the frequency of crossing the platform was increased (P＜ 0.05).Conclusion GSPE can attenuate mitochondrial injury and improve learning-memory function after obstructive sleep apnea hypoxia.

Objective:To study the effect of endothelin receptor antagonist BQ-123 on the nerve function damage after subarachnoid hemorrhage (SAH)in the rats,and to explore the mechanisms.Methods:Total 120 male SD rats were divided into sham group,SAH group,low dose of BQ-123 group (50 μg· kg-1 )and high dose of BQ-123 group (75 μg·kg-1 ).The SAH rat models were established by injecting the autologous blood into cisterna magna twice.The morphological changes of hippocampus nerve cells of rat brain tissue were detected with HE staining, and the expressions of mTOR, Beclin-1 and LC3-Ⅱ in the hippocampus of rats were detected with immunohistochemistry and RT-PCR;the shuttle-box experiment was used to evaluate the abilities of learning and memory,and the holding power evaluation was used to evaluate the forelimb pulling force of the rats in various groups at each time point.Results:Compared with sham group,the morphological damages of neurons of the rats in SAH group were increased,the survival rate of neurons of the rats in SAH group was decreased (P <0.05),the expression levels of mTOR mRNA,Beclin-1 mRNA and LC3-Ⅱ mRNA in hippocampus tissue of the rats were increased (P < 0.05),and the abtilities of learning and memory and the values of holding power were decreased (P <0.05).Compared with SAH group,the morphological damages of neurons of the rats in BQ-123 groups were decreased,the survival rates of neurons of the rats in BQ-123 groups were increased (P < 0.05),the expression levels of mTOR mRNA of rats were decreased (P <0.05),the expression levels of Beclin-1 mRNA and LC3-ⅡmRNA in hippocampus tissue were increased (P <0.05),and the abilities of learning and memory and the values of holding power were increased (P < 0.05 ). The changes were more significant in high dose of BQ-123 group compared with low dose of BQ-123 group (P <0.05).Conclusion:BQ-123 can improve the nerve function damage after SAH in the rats,its mechanism may be related to regulating the mTOR/autophagy signaling pathway.

Objective To investigate the changes in the expression of phosphatidylinositol 3?kinase(PI3?K),mammalian target of rapamycin (mTOR)and Beclin?1 in the hippocampus of normal rats and intermittent hypoxia rats with cerebral ischemia/reperfusion ,so as to explore the role of PI3K/mTOR/autophagy pathway in global cerebral ischemia/reperfusion injury aggravated by intermittent hypoxia. Methods A total of 80 healthy male Wistar rats were randomly divided into sham operation group(SO group,n=20),merely ischemia/reperfusion group(I/R group,n=20),intermittent hypoxia for 7?day ischemia/reperfusion group(IH7+I/R group,n=20),and intermittent hypoxia for 21?day ischemia/reperfusion group(IH21+I/R group,n=20). IH7+I/R group and IH21+I/R group were respectively given intermittent hypoxia for 7 days and 21 days before ischemia/reperfusion. The cerebral ischemia/reperfusion model was established by modified Pulsinelli four?vessel occlusion method. The morpholog?ical changes of nerve cells in hippocampal CA1 region were observed by HE staining and electron microscope. The protein expressions of PI3?K, mTOR and Beclin?1 of nerve cells in hippocampal CA1 region were detected by immunohistochemical staining and RT?PCR. The learning memory capacity of rats were assessed by the Morris water maze test. Results Compared with SO group,I/R group increased the never cells morphology damages,reduced the number of survival neurons,and declined the ability of learning and memory(P<0.05). Immunohistochemistry showed that the number of PI3?K immunoreactive cell,mTOR immunoreactive cell and Beclin?1 immunoreactive cell increased in I/R group compared with S0 group(P<0.05). RT?PCR showed that the expressions of PI3?K,mTOR and Beclin?1 increased in I/R group compared with S0 group(P<0.05). Compared with I/R group,intermittent hypoxia groups increased the never cells morphology damages,decreased the number of survival neu?rons,and declined the ability of learning and memory(P<0.05). Immunohistochemistry showed that the number of PI3?K immunoreactive cell, mTOR immunoreactive cell and Beclin?1 immunoreactive cell increased in IH7+I/R and IH21+I/R groups compared with I/R group(P<0.05). RT?PCR showed that the expressions of PI3?K,mTOR and Beclin?1 increased in IH7+I/R and IH21+I/R groups compared with I/R group(P<0.05),and the changes were more significant in IH21+I/R group(P<0.05). Conclusion Intermittent hypoxia can aggravate neurological injury after ischemia,which is related to PI3K/mTOR/autophagy pathway activation.

Objective To investigate the influence of infarction location on the executive function and self-efficacy of patients with ischemic stroke. Methods 320 patients with cerebral infarction at basal ganglia, parietal-occipital lobe, frontal lobe and other areas (80 cases respectively)and 80 healthy people were assessed with Wisconsin Card Sorting Test (WCST), Clock Drawing Test (CDT), Self-rating Depression Scale (SDS), Self-Rating Anxiety Scale (SAS) and General Self-efficacy Scale (GSES). Results The scores of WCST, CDT and GSES were significantly worse in the patients than in the controls, especially in those with infarction at frontal lobe and basal ganglia. There was no significant difference in scores of SDS and SAS among all the subjects (P>0.05). Conclusion There are executive function and self-efficacy impairment in ischemic stroke patients, especially for those with the focus at frontal lobe and basal ganglia.

Objective To investigate the characteristics of Behavioral Assessment of Dysexecutive Syndrome (BADS) and Wisconsin Card Sorting Test (WCST) for executive function assessment in patients with cerebral infarction. Methods 706 patients with cerebral infarction were assessed with BADS, WCST and Mini-Mental State Examination (MMSE). Results There was significant difference in the scores of BADS and WCST among the patients with normal cognition, mild cognition impairment and severe cognition impairment (P<0.05). There was no significant difference in the scores of BADS among the patients with different focuses of infarction (P>0.05), but there was in the scores of WCST (P<0.05). Conclusion BADS and WCST can be used to assess the executive impairment in the patients with cerebral infarction, and the focuses may affect the outcome of WCST.

Objective To study the effects of integrative body-mind training with cognitive rehabilitation based on the sensory integration training theory on executive function and anxiety and depression mood in patients with traumatic brain injury.Methods 85 cases were randomly divided into the control group (42 cases) and the treatment group (43 cases).The control group took targeted cognitive rehabilitation with sensory integration training theory and the treatment group was given targeted integrative bodymind training based on this training.Before training and after 3 months,the cognitive function and executive function were detected by the Behavioral Assessment of Dysexecutive Syndrome (BADS); the cognitive dysfunction were evaluated by Loewenstein Occupation Therapy Cognitive Assessment (LOTCA); Anxiety and Depression were evaluated by Self-rating Depression Scale (SDS) and Self-Rating Anxiety Scale (SAS).Results There was no marked differences in BADS,LOTCA,SDS and SAS scores before treatment; Compared with the control group,they were much improved after training; Moreover,they were much more improved in the treatment group than those of the control group.Conclusions Integrative bodymind training with cognitive rehabilitation based on the sensory integration training theory can improve the executive function and regulate the mood on cognitive dysfunction in patients with traumatic brain injury.

Objective To investigate the expression of CD40 and intercellular adhesion molecule-1 (ICAM-1) treated with lipopolysaccharide (LPS) in rat peritoneal mesothelial cells(RPMC) and the role of NF-κB signal transduction pathway. Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were exposed respectively to different concentrations of LPS for 12 h or treated with LPS (5 μg/ml) for different time points. To observe the effect of LPS on the expression of CD40 and ICAM-1, the RPMCs were treated with LPS (5 μg/ml) for different time points. To observe the effect of LPS on the expression of NF-κB and p-NF-κB protein, the RPMCs were treated by LPS or pretreated with BAY11-7085 (5 μmol/L or 1 μmol/L ) for 3 h, then treated with LPS for another 3 h, respectively. Expression of CD40 and ICAM-1 mRNA was examined by RT-PCR. Expression of NF-κB and p-NF-κB protein was detected by Western blot. Results Compared with medium control group, stimulation of RPMCs with 1 μg/ml and 5 μg/ml of LPS resulted in a significant increase in the expression of CD40 and ICAM-1 mRNA(P<0.05). 10 μg/ml of LPS had strongest effect on CD40 and ICAM-1 expression compared with that of 1 μg/ml and 5 μg/ml of LPS. Treatment with 5 μg/ml of LPS resulted in time-dependent increase in the gene level of CD40 and ICAM-1, with the peak at 3 h. However, after that time point, the gene level of them was gradually attenuated. Following treatment with LPS (5 μg/ml), the level of p-NF-κB began to increase at 15 min, gradually reached the peak at 1 h, and then decreased. But the level of p-NF-κB at 2 h was still significantly higher than that of medium control. 5 μmol/L of BAY11-7085 decreased significantly the up-regulation of CD40 and ICAM-1 induced by LPS. Conclusion LPS enhanced the expression of CD40 and ICAM-1 on RPMCs in a concentration-dependent and a time-dependent manner. LPS induced expression of CD40 and ICAM-1 depend on the NF-κB signal transduction pathway.

Objective To investigate the effect of Lokomat Robotic Gait Training System on motor, gait and range of motion (ROM) for stroke patients with hemiplegia. Methods 80 stroke patients with hemiplegia were divided into treatment group (n=40) and control group (n=40). The control group accepted routine rehabilitation and the treatment group accepted robotic gain training. They were assessed with Fugl-Meyer Assessment, gait parameter and ROM of hip and knee before training and after 10 weeks of treatment. Results There was no significant difference on all the index before treatment (P>0.05), and improved more in the treatment group than in the control group after training (P<0.05). Conclusion Lokomat Robotic Gait Training System intervention can promote the recovery of walking in stroke patients with hemiplegia.

OBJECTIVE To observe the protection of vitamin C on the cardiac injury induced by 50 nm titanium dioxide inmice.METHODS Kunming mice were ad mistered by ig of vitamin C 100,200 and 400 mg·kg -1 for 2 d.And then the mice were ad mistered by ig of nano-TiO2 2 g·kg -1 and vitamin C (100.0,200.0 and 400.0 mg·kg -1 )for 3 d,the interval of treatment with nano-TiO2 and vitamin C was 4 h.The mice were scarified 24 h later after the last ad ministration.Electrocardiogra m (ECG)was determinated by physiological recorder.The myocardial enzy mes activities in serum and superoxide dismutase (SOD)and glutathione peroxidase(GSH-Px)activities in serum and myocardial tissue were determinated by bioche mical method.Cometassay was used to detect the DNA da mage of the heart. Heart tissue was used for histopathological exa mination by HE staining.RESULTS Co mpared with the control,ECG showed higher S-T and T-wave a mplitude of nano-TiO2 2 g·kg -1 (P<0.05).The myocar-dial enzy mes activities significantly increased and activities of SOD and GSH-Px significantly decreased in nano-TiO2 group,compared with the control group(P <0.05).Cometassay showed that olive tail mo ment (OTM)was significantly increased after nano-TiO2 2 g·kg -1 ,compared with the control group (P<0.05).The histopathology showed ede ma of myocardial cells,myofibril disorders and increasing infla mmatory cells.Vita min C 100,200 and 400 mg·kg -1 can decrease S-T in ECG,OTM,myocardial enzy mes activities,increase the SOD and GSH-Px activities in serum and myocardial tissue;reduce myocardial hypertrophy and infla mmatory cells.CONCLUSION nano-TiO2 can induce myocardial injury inmice and vitamin C can alleviate the da mage.The mechanism may be associated with the antioxidant ability of vitamin C inmyocardial tissue.