Objective To investigate the correhtion between cognitive impairment and cerebral atherosclerosis in patients with acute ischemic stroke.Methods Acute ischemic stroke patients without cognitive impairment were recruited before symptom onset.The Montreal cognitive assessment (MoCA) was used to evaluate the cognitive function.Magnetic resonance imaging (MRI) was used to identify the infarct locations and sides.Magnetic resonance angiography,CT angiography and digital subtraction angiography were used to identify atherosclerotic arteries.Resul~ A total of 101 patients with acute ischemic stroke were enrolled,including 75 (74.3％) with cognitive impairment.The proportions of age (54.54 ± 12.59 years vs.64.43 ± 10.37 years;t =-3.960,P ＜0.001),years of education ≤6 years (50.7％ vs.11.5％;x2 =12.257,P ＜ 0.001),and cerebral atherosclerosis (89.3％ vs.50.0％;x2 =18.137,P ＜0.001) of the cognitive impairment group were significantly higher than those of the normal cognitive function group.Multivariate logistic regression analysis showed that cerebral atherosclerosis was an independent risk factor for cognitive impairment in patients with acute ischemic stroke (odds ratio 1.720,95％ confidence interval 1.005-2.942;P=0.048).MoCA score was negatively correlated with the offending vessels (r=-0.365,P＜ 0.001) and the most severe vessels of atherosclerotic degree (r=-0.243,P =0.014).Conclusions Most patients with acute ischemic stroke had cognitive impairment in the early stage after onset,and the MoCA scores was negatively correlated with the degree of cerebral atherosclerosis.Cerebral atherosclerosis was an independent risk factor for cognitive impairment in patientswith acute ischemic stroke.

Objective To discuss the nursing intervention of Rey syndrome in children patients.so as to search effective nursing measures.Methods 12 children patients with Rey syndrome received comprehensive nursing treatment with reducing intracranial pressure and were under continuous close observation.Slightest changes were feeded back timely,then effective nursing measures were taken to stabilize their illness,patients also received dietary therapy,medication nursing and rehabilitation training,etc.Results All patients ameliorated after 3 to 7 days,and achieved clinical recovery after 20 to 30 days without sequelae.Conclusions Early diagnosis and correct effective nursing care can improve curative rate and avoid the occurrence of complications and sequelae.

Objective To investigate the characteristics and neural mechanisms of visual attention dysfunction in patients with hypertension using the event related potentials(ERPs).Methods Visual Oddball pattern was adopted to analyze P3a and P3b components of 15 essential hypertensives and 15 normotensives,and all the participants were submitted to cognitive assessment by Mini-Mental State Examination (MMSE).Results ①Novelty stimulus:the mean amplitude of N2 in hypertensive patients ((1.56± 1.15) μV) was decreased than normal controls ((-2.19±1.15) μV,P＜0.05),particularly at forehead-central sites (P＜0.05).In addition,the amplitude of P3a of hypertensive patients ((6.27± 1.01) μV) was different from normal controls ((7.09± 1.01) μV),but there was no statistical significance(P＞0.05).The latency of visual P3a was significantly longer in patients with hypertension group ((432.83 ± 8.22) ms) than that in control group ((403.10 ± 8.22) ms,P＞ 0.05).②Target stimulus:compared with control group ((6.75 ±0.90)μV),visual P3b amplitude in hypertension group ((4.08 ± 0.90) μV) was significantly declined (P＜ 0.05).Besides,the latency of visual P3b of hypertensive patients ((440.70 ± 6.42) ms) was different from normal controls ((436.91±6.42) ms),but there was no statistical significance(P＞0.05).③Compared with control group (27.31± 1.22),the M MSE score of patients with hypertension (24.55±2.42) was decreased (P＜0.05).The amplitude of visual P3b was positively correlated with MMSE scores in parietal region(r=0.51,P＜0.05).Conclusions The abilities of visual involuntary attention and voluntary attention are damaged in patients with hypertension,the impact degree of hypertension on two kinds of attention and the neural mechanisms are different.Moreover,there is a significant positive correlation between the amplitude of visual P3b and MMSE,which prompts that visual P3b for clinical early assessment of attention in patients with hypertension provides more objective neurophysiological basis.

Objective To investigate the effect of neurotrophin-3(NT-3)on the proliferation and apoptosis of bone marrow mesenchymal stem cells(BMSCs)in rats and possible mechanisms. Methods The NT-3 overexpression and lentiviral transfection of BMSCs were co-cultured with neuronal cells respectively and then they were divided into overexpression control group,NT-3 transfection group and shRNA-NT-3 transfection group(NT-3 silencing group).MTT assay was used to detect the cell culture for 24 h,48 h and 72 h. Cell cycle and apoptosis were detected by flow cytometry for 48 h. Real-time quantitative PCR was used to detect the expression of C/EBPβmRNA.The expression of C/EBPβprotein was detected by Western blot. Results MTT results showed that the proliferation ability of BMSCs in the NT-3 overexpres-sion group was significantly higher than that in the control group(0.650±0.042,0.826±0.074)at 48 h and 72 h(P<0.05).Compared with the control group(P<0.05),the cell cycle and apoptosis of BMSCs in NT-3 silencing group were significantly decreased at 48 h and 72 h(P<0.05). The results of 48 h cell cycle and apoptosis showed that the percentage of G1 phase in BMSCs was decreased,G2 and S were increased and the apoptosis was decreased. The percentage of G1 phase in G2-S phase and the increase of apoptosis were in-creased in NT-3 silencing group. The results of Western Blot showed that C/EBPβ mRNA and protein levels were significantly up-regulated in BMSCs of NT-3 overexpression group and significantly decreased in NT-3 silencing group(P<0.05).Conclusion NT-3 may promote the expression of C/EBP beta and affect the ex-pression of its downstream target genes,which can inhibit the apoptosis of BMSCs cells.