Objective To explore the teaching feasibility and practicability on team-based learning (TBL) and lecture-based learning (LBL) combined with PDCA circle teaching in clinical teaching of neurol-ogy, and evaluate its teaching effect. Method 100 cases clinical medical professional training students were chosen, divided into experiment group and control group, with 50 cases in each group. Control group used TBL and LBL teaching while experiment group used combined with PDCA circle teaching on the basis of control group. After the teaching, the teaching effects difference between two groups was evaluated and compared. Result The theoretical examination scores in experiment group (85.95 ±7.63) was higher than that in control group (77.31±5.38), and the difference was statistically significant (t=2.126, P=0.034). The practical operation scores in experiment group (82.37±5.15) was higher than that in control group (76.62± 4.35), and the difference was statistically significant (t=2.173, P=0.029). In anonymous satisfaction survey, the average coutent degree with teaching in experiment group is higher than control ( 92% vs . 82%) . Conclusion TBL and LBL combined with PDCA circle teaching improves the students' basic theory, prac-tical operation and doctor-patient communication ability, whose satisfaction has also significantly increased, which is worth popularizing in the clinical practice teaching of neurology.

Objective To evaluate the nutritional risk screening for younger patients with stroke and to explore risk factors of malnutrition. Methods Younger patients with stroke were enrolled in a prospective way. The patients were evaluated by nutritional risk screening 2002 (NRS 2002) at their admission for nutritional risk screening, and were divided into nutritional risk group and no nutritional risk group according to the evaluation results. Prealbumin less than 200 mg/L was defined as malnutrition. Demographic and baseline clinical characteristics of the patients were analyzed with multivariate logistic regression analysis to determine independent risk factors for malnutrition at the admission and the 14th day. Results (1) A total of 152 young stroke patients were enrolled, including 51 in nutritional risk group, 101 in no nutritional risk group, the rate of nutritional risk was 33.6%(51/152). (2) The rate of malnutrition at admission was 13.8%(21/152), the rate of malnutrition in nutritional risk group was 25.5%(13/51), and 7.9%(8/101)in no nutritional risk group on admission. While the rate of malnutrition was 32.2%(49/152), including the rate of malnutrition in nutritional risk group was 60.78%(31/51)and 17.8%(18/101)in no nutritional risk group was at the 14th day of admission. (3) Multivariate Logistic regression analysis showed that advanced age (from 36 to 45 years), sex, diabetes, hyperthyroidism were independent risk factors for malnutrition in younger patients with stroke. Recent history of surgery and smoking, stroke-associated pneumonia, post-stroke depression, swallowing disorder, sleep disorder, moderate and severe neurologic deficits were also risk factors for malnutrition. Conclusion The incidence of malnutrition in youngerpatients with stroke were higher, and earlier nutritional risk screening and nutritional support in these patients were urgent.

Objective To observe the efficacy and safety of rosuvastatin in the treatment of hyperlipidemia and carotid atherosclerotic plaque in young ischemic stroke patients.Methods In prospective study,264 young ischemic stroke patients with hyperlipidemia and carotid atherosclerotic plaque were randomly divided into low dose group,middle dose group,high dose group,88 cases in each group.All patients were given rosuvastatin immediately after dinner,in doses of 5mg,10mg,20mg,respectively,for eight months.Then,the changes of hyperlipidemia and carotid atherosclerotic plaque in the three groups were surveyed,and its safety by the observation of clinical symptoms and monitoring of adverse reactions after eight months were assessed.Results Before treatment,the blood fat and carotid atherosclerosis plaque index in the three groups had no statistically significant differences (all P >0.05). After treatment,the total cholesterol,triglycerides,low -density lipoprotein cholesterol of the high dose group were (1.67 ±0.68)mmol/L,(3.23 ±0.53)mmol/L,(1.83 ±0.62)mmol/L,which of the middle dose group were (1.93 ±0.74)mmol/L,(3.73 ±0.23)mmol/L,(2.24 ±0.73)mmol/L,which of the low dose group were (2.16 ± 0.77)mmol/L,(4.06 ±0.93)mmol/L,(2.93 ±0.35)mmol/L.These indicators were decreased than before treat-ment [(2.79 ±0.72)mmol/L,(5.40 ±0.67)mmol/L,(3.64 ±1.03)mmol/L,(2.75 ±0.81)mmol/L,(5.59 ± 0.95)mmol/L,(3.43 ±0.92)mmol/L and (2.83 ±0.53)mmol/L,(5.84 ±0.79)mmol/L,(3.83 ±0.88)mmol/L].The decrease of the high dose group was higher than the middle and low dose group,the difference was statistically significant(F =6.61,P <0.05).The effective rate of the high dose group was 85.23%.which of the middle dose group was 76.14%.The effective rate of the low dose group was 62.50%.The efficacy of the high dose group was better than the middle dose group and low dose group,the difference was statistically significant(χ2 =5.79,P <0.05).After treatment,the intima -media thickness,plaque area and Crouse score of the high dose group were (0.92 ±0.41)mm,(0.52 ±0.56 )mm,(3.07 ±0.58 )mm,which of the middle dose group were (1.11 ± 0.52)mm,(0.60 ±0.36)mm,(3.39 ±0.83)mm,which of the low dose group were (1.42 ±0.87)mm,(0.81 ± 0.91)mm,(4.09 ±0.77)mm,which were decreased than before treatment[(1.71 ±0.89)mm,(0.86 ±0.55)mm, (4.39 ±0.19)mm,(1.74 ±1.03)mm,(0.89 ±0.48)mm,(4.42 ±0.53)mm and (1.68 ±0.96)mm,(0.87 ± 0.61)mm,(4.38 ±0.22)mm].The decrease of the high dose group was higher than the middle and low dose group, the difference was statistically significant (F =5.83,P <0.05 ).The effective rate of the high dose group was 78.41%.The effective rate of the middle dose group was 52.27%.The effective rate of the low dose group was 30.68%.The efficacy of the high dose group was better than the middle dose group and low dose group,the difference was statistically significant(χ2 =5.37,P <0.05).There were 10 cases (11.36%)had adverse reaction in the low dose group,12 cases (13.64%)in the middle dose group,14 cases (15.91%)in the high dose group.There was no statistically significant difference in incidence of adverse reactions among the three groups (P >0.05),and no serious adverse reaction was found.Conclusion The high dose rosuvastatin treatment can reverse the nature of plaque, decrease the thickness of the plaques and lower blood lipid of young ischemic stroke with hyperlipidemia and carotid atherosclerotic plaque,which is better than middle and low dose,and has better security.There is no serious adverse reaction.It is worth for clinical promotion.

Objective To investigate effect of FK506 binding protein 51 (FKBP51) on the c-JunN-terminal kinase (JNK) pathway in cerebral ischemia-reperfusion injury.Methods Transient global cerebral ischemia rat models were made by four-vessel method.Healthy male SD (Sprague Dawley) rats were randomly divided into:sham group,ischemia/reperfusion group (I/R group),FKBP51 antisense oligonucleotide group (FKBP51 ASODN group),FKBP51 missense oligonucleotide group (FKBP51 MSODN group),and solvent control group (TE group).The effect of FKBP51 ASODN on expression of FKBP51 protein and JNK was detected,and c-Jun phosphorylation was detected by Western blot.Results (1) FKBP51 protein expression in the FKBP51 ASODN group was reduced.The change of FKBP51 protein expression between the FKBP51 ASODN and sham groups was statistically significant (P ＜ 0.05).(2) The expression differences of total JNK protein between all the groups were not statistically significant (P ＞ 0.05).The expression of p-JNK in sham group was significantly less than the other groups (P ＜ 0.05).The expressions of p-JNK in I/R 3d,TE,and FKBP51 MSODN groups were higher relative to Sham group; however,the differences among those three groups were not statistically significant (P ＞ 0.05).The expression of p-JNK in FKBP51 ASODN group was significantly less than FKBP51 MSODN group (P ＜ 0.05).(3) The expression differences of total c-Jun protein among all groups were not statistically significant (P ＞ 0.05).The expression of p-c-Jun in sham group was significantly less than the other groups (P ＜ O.05).The expressions of p-c-Jun in I/R 6 h,TE,and FKBP51 MSODN groups were higher relative to the sham group; however,the differences among those three groups were not statistically significant (P ＞ 0.05).The expressions of p-c-Jun in FKBP51 ASODN group was significantly less than FKBP51 MSODN group (P ＜ 0.05).Conclusions FKBP51 might activate JNK signaling pathway in cerebral ischemia-reperfusion injury.

Objective To investigate the neuralprotective effect of Rho kinase inhibitor fasudil hydrochloride in cerebral ischemia/reperfusion injury in rats.Methods The SD rats were randomly divided into four groups:the sham group,the ischemia/reperfusion group,the fasudil hydrochloride group and the physiological saline group.Fasudil hydrochloride were injected intraperitoneally 30 minutes before ischemia.And the physiological saline group were treated with the intraperitoneal injection of the same volume of saline.The phosphorylation and protein expression of GluR6 at 6 hours during reperfusion were detected using immunoprecipitation and immunoblotting analysis to examine the effect of Fasudil hydrochloride.Furthermore,TUNEL staining was used to examine the apoptosis of neurons in rat hippocampal CA1 regions after 3 days reperfusion.Results 1.Immunoprecipitation and immunoblotting analysis were used to analyze the phosphorylation of GluR6 in serine site.The results showed that the GluR6 serine phosphorylation level increased significantly at 6h of reperfusion compared with the sham group (P＜0.05).Fasudil hydrochloride group could inhibit the increased phosphorylation of GluR6 at 6h of reperfusion compared with the ischemia/reperfusion group and saline group,respectively (P ＜ 0.05).2.TUNEL staining was used to examine the apoptosis of neurons in 3 days after reperfusion in CA1 regions of hippocampus.The results indicated that significant numbers of TUNEL positive cells (40.20 ± 2.77) were observed 3 days after ischemia/reperfusion.The numbers of viable neurons per 1 mm length of CA1 pyramidal cells were quantitatively analyzed.Fasudil hydrochloride markedly decreased the neuronal loss compared with the ischemia/reperfusion group (19.80 ± 2.86) (P＜0.05).Conclusion Fasudil hydrochloride can inhibit induced phosphorylation of GluR6 by the ischemia/reperfusion.Fasudil hydrochloride can reduce the neurons apoptosis in hippocampal CA1 regions,and perform a neuralprotective effect on ischemia/reperfusion injury in rats.

ObjectiveTo investigate the effect of vitamin D supplementation on the outcome of acute ischemic stroke in young patients with vitamin D deficiency.MethodsThe prospective controlled study was used to select the consecutive young patients with acute ischemic stroke.Vitamin D deficiency was defined as 25-hydroxyvitamin D (25(OH)D) ≤50 nmol/L.The Patients with vitamin D deficiency were randomly divided into an intervention group and a routine treatment group according to the random number table method.Routine treatment group didn't receive the drug intervention for vitamin D deficiency, and the intervention group received daily oral alfacalcidol 0.5 μg.After 1 year of treatment, the 25(OH)D levels were examined again;the adverse reactions during the drug treatment were monitored;the modified Rankin Scale (mRS) was used to evaluate the functional outcome and 0-2 was defined as good outcome.ResultsThere are 94 patients (53.41%) with vitamin D deficiency among 176 young patients with acute ischemic stroke.They were randomly divided into either an intervention group or a routine treatment group (n=47 in each group).At the end of the follow-up, the good outcome rate (82.98% vs.63.83%;χ2=4.414, P=0.036) and serum 25(OH)D level (85.83±10.53 nmol/L vs.39.10±11.18 nmol/L;t=20.860, P<0.001) in the intervention group were significantly higher than those in the routine treatment group.During the follow-up period, there was no loss to follow-up or death events in both groups.Only 2 cases of nausea and 1 case of dizziness were observed, and the incidence of adverse reaction was 6.38% in the intervention group.ConclusionsVitamin D supplement can increase the vitamin D levels and improve functional outcome in young patients with acute ischemic stroke and vitamin D deficiency.

Objective To investigate the effect of Rho kinase inhibitor fasudil on taxed lineage kinase 3 (MLK3), c-Jun NH2-terminal kinase (JNK) phosphorylation, caspase-3expression, and neuronal injury in hippocampal CA1 region follwong cerebral ischemic rep erfusion in rats. Methods A total of 72 Sprague-Dawley rats were randomly divided into sham operation, ischemia-reperfusion, normal saline, and fasudil groups. A global cerebral ischemic model was prepared by four-vessel ligation. The levels of MLK3 and JNK phosphorylation, and caspase-3 expression were detected by Western blot analysis. Cresy1 violet staining was used to detect the numbers of survival neurons in hippocampal CA1 region. Results When 6 hours after ischemia-reperfusion, the level of MLK3 phosphorylation in the fasudil group (1.13 ± 0. 03)was significantly lower than that in the normal saline group (2. 08 ± 0. 01 ,P = 0. 000 3), while the levels of MLK3 was no significant difference. When 3 hours after ischemia-reperfusion, the level of JNK phosphorylation in the fasudil group (1.27 ±0. 02)was significantly lower than that in the normal saline group (2.09 ±0. 01, P=0. 000 2), while the levels of JNK was no significant difference. When 6 hours after ischemia-reperfusion, the expression level of caspase-3in the fasudil group (1.28 ± 0. 02) was significantly lower than that in the normal saline group (2. 10 ± 0. 01, P = 0. 000 6). When 5 days after ischemia-reperfusion, the pyramidal cells in hippocampal CA1 region almost completely disappeared in the ischemia-reperfusion group, and only a few cells left (9. 8 ±2. 1). The numbers of survival pyramidal cell (8. 28 ± 3.2) in hippocampal CA1 region in the fasudil group was significantly more than that in the normal saline group (11.8 ± 1.6, P ＜0. 05). Conclusions Fasudil may significantly inhibit the ischemia-reperfusion-induced phosphorylation of MLK3 and JNK, as well as the expression of caspase-3, and thus reduce neuronal injury in hippocampal CA1 region.

Objective To investigate the effects of the FKBP51 · PHLPP · AKT signal module on the phosphorylation of Akt and hippocampal neuronal injury after the cerebral ischemia / reperfusion induced neuronal death in rat hippocampus.Methods Transient(15 min)brain ischemia was induced by the four-vessel occlusion in Sprague-Dawley rats.6 rats were used in each group.The antisense oligodeoxynucletides(AS ODN)of PHLPP2 (PH domain and leucine rich repeat protein phosphatases) was used to suppress the assembly of FKBP51 · PHLPP · Akt signal module by intracerebroventricular infusion once per day for 3 days before ischemia.After 6 hours reperfusion,interactions of PHLPP2 and FKBP51 (FK506 binding protein 5) with Akt were detected by immunoprecipitation (IP) and the phosphorylation of Akt was detected by western blot (IB).After 5 days reperfusion,rats were perfusion-fixed with paraformaldehyde and Hematoxylin-Eosin staining was used to examine the survival number of CA1 pyramidal cells of hippocampus.Results Compared to PHLPP2 MS ODN group(1.24±0.24,1.68±0.11,0.58±0.01),PHLPP2 AS ODN suppressed the assembly of the FKBP51 · PHLPP · Akt signaling module(1.06±0.01,1.04±0.13),and increased the phosphorylation of Akt(0.76±0.02) (P＜0.05).Furthermore,compared to PHLPP2 MS ODN group (20.1±2.5),the number of surviving neurons significantly increased in PHLPP2 AS ODN group(88.3±2.7)(P＜0.05).Conclusion The increasing assembly of FKBP51 · PHLPP · Akt signal module can damage CA1 pyramidal cells of hippocampus by inhibiting the phosphorylation level of Akt.

Objective To explore the effect of FKBP51 acting on Caspase-3 and hippocampal CA1 area neu-ronal necrosis in cerebral ischemia reperfusion injury of rat.Methods SD rats were randomly divided into Sham group,ischemia reperfusion group ( I/R group ) , TE buffer group ( TE group ) , FKBP51 antisense oligonucleotide group (FKBP51 ASODN group) and FKBP51 missense oligonucleotide group (FKBP51 MSODN group).Transient global cerebral ischemia rats models were made by four-vessel method.We used Western blot to detect the expression of FKBP51,the effect of FKBP51 ASODN to FKBP51 expression and Caspase-3 activity;while we used HE staining technique to detect FKBP51 ASODN effect to rat hippocampal CA1 area neuronal necrosis.Results (1) In Sham group and I/R group (0min,15min,30min,1h,3h,6h,1d,3d),FKBP51 expressed,and the difference among the groups was no statistical significance (F=0.64,P>0.05).(2)The expression of FKBP51 in FKBP51 ASODN group was obviously reduced, and the difference was statistically significant compared with Sham group ( t =8.21, P <0.05).(3)The expression of Cleaved-Caspase-3 in Sham group obviously declined than the other groups,the differ-ence between them was statistically significant (F=12.31,P<0.05);The expression of FKBP51 in FKBP51 ASODN group was decreasing compared with FKBP51 MSODN group,and the difference was statistical significance(t=9.71, P<0.05).(4)HE staining showed:the number of Sham group (186.3 ±2.5) hippocampal CA1 pyramidal cells was most.The cells arranged densely,and nucleoli were large and round,the difference was statistically significant com-pared with the other groups (χ2 =81.91,P<0.05);The hippocampal CA1 pyramidal cells of I/R group (15.4 ± 2.6),TE group (18.5 ±2.2) and FKBP51 MSODN group (17.5 ±1.8) were almost completely disappeared,only left a few residual cells,a great quantity of denaturated cells which presented karyopykosis,tinctorialed endochylema, ruptured of membrane and released cell content;the hippocampal CA1 pyramidal cells FKBP51 ASODN group (92.8 ±2.6) survival increased significantly compared with other group,the difference was statistically significant (χ2 =52.36,P<0.05).Conclusion In cerebral ischemia reperfusion injury,FKBP51 can enhance the activation of Caspase-3 (Cleaved-Caspase-3) expression and inhibit the survival of the neurons.

Objective To analyze the efficacy of epley maneuver associated with vertigo calming for treating posterior semicircular canal benign paroxysmal positional vertigo (PC-BPPV) in young.Methods Two hundred and fifty-eight cases(age was 18-50 years old) with PC-BPPV were randomly divided into maneuver group(86 cases),betahistine group(86 cases) and vertigo calming group(86 cases).The maneuver group was treated by epley maneuver associated with placebo,2 pills per time,3 times daily for one month and follow up one month.The betahistine group and vertigo calming group were treated by epley maneuver with betahistine(12 mg/ time,Tid) or vertigo calming(2 piles/time,Tid),the same dose,period of treatment and follow-up as maneuver group.Results After one time treatment,199 cases were cured in 258 patients,including 68 cases in maneuver group,66 cases in betahistine group,65 cases in vertigo calming group,and the difference between groups was not statistically significant(x2 =0.308,P＞0.05).After treatments and followed up for one month,72 cases were cured,3 cases were effective,11 cases were invalid in maneuver group;74 cases were cured,3 cases were effective,9 cases were invalid in betahistine group;81 cases were cured,4 cases were effective,1 cases were invalid in vertigo calming group.Efficient of betahistine group,maneuver group and vertigo calming group were 89.5％,87.2％ and 98.8％,and the difference between maneuver group and betahistine group was not statistically significant(x2=58.65,P＞0.05),the difference of vertigo calming group between with other groups was statistically significant(P＜0.05).Conclusion The effects of vertigo calming in addition to Epley maneuver is significantly better than both Epley maneuver and Epley maneuver combined with betahistine in young PC-BPPV,while the effects of Epley maneuver combined with betahistine isn't better than Epley maneuver.