BACKGROUND:Exercises play an important role in the recovery of neurological function after stroke. Few studies concerned the amount of exercise in rats after stroke. Hippocampus is strongly associated with cognitive function, but no reports addressed the expression of repulsive guidance molecule A in the rat hippocampus after ischemia and reperfusion. OBJECTIVE:To explore the effects of exercise on repulsive guidance molecule A expression in the hippocampus on the ischemic side in rats after cerebral ischemia-reperfusion injury. METHODS:120 Sprague-Dawley rats were equal y and randomly divided into normal group, sham-operation group, and 7-, 14-, 28-day model groups. The model of right cerebral ischemia-reperfusion injury was induced by ligation with nylon monofilament in rats of 7-, 14-, 28-day model groups. Low exercise group received treadmil training of 5 m/min, 5 minutes;7 m/min, 5 minutes;9 m/min, 20 minutes. Moderate exercise group received treadmil training of 8 m/min, 5 minutes;10 m/min, 5 minutes;13 m/min, 20 minutes. High exercise group received treadmil training of 8 m/min, 5 minutes;11 m/min, 5 minutes;20 m/min, 20 minutes. RESULTS AND CONCLUSION:Repulsive guidance molecule A mRNA and protein expression was highest in the ischemic side of the hippocampus in the 7-day model group without excercise. Moreover, repulsive guidance molecule A relative expression gradual y reduced over time. Compared with non-exercise, repulsive guidance molecule A mRNA and protein expression significantly decreased in the 14-and 28-day model groups during moderate exercise (P<0.05), but repulsive guidance molecule A mRNA and protein expression increased during high exercise. Above data confirmed that moderate exercises could decrease repulsive guidance molecule A expression in the affected side of the hippocampus of rats with cerebral ischemia-reperfusion injury.

Aim To investigate the influence of the overexpression of CRMP2 on neural cell apoptosis after ischemia reperfusion injury in rats and its possible mechanism. Methods A total of 192 male adult SD rats were divided into four groups: sham group, cere-bral ischemia/reperfusion group( MCAO group) , cere-bral ischemia with blank plasmid control group( MCAO+GFP group ) , cerebral ischemia with CRMP2 eu-karyotic plasmid group ( MCAO + CRMP2/GFP group) . One day after injecting eukaryotic plasmid, the rats were operated for 120-min ischemia through MCA occlusion and reperfused. At 48 h and 1 wk, the expression of CRMP2 , p53 , Caspase-3 , Caspase-8 and BCL2 in brain tissue was tested by RT-PCR and West-ern blot. Apoptotic cells were observed by TUNEL test. TTC staining was use to detect cerebral infarction volume. The neural function of the rats were also eval-uated. Results Compared with the sham group, the expression levels of CRMP2 and BCL2 in MCAO group and MCAO +GFP group were significantly decreased ( P <0. 01 ) , while p53 , Caspase-3 , Caspase-8 and TUNEL positive cells were elevated(P<0. 01). Inter-vention of CRMP2 eukaryotic plasmid resulted in the increased expression of CRMP2 and BCL2 ( P<0. 01 ) and the decreased p53 , Caspase-3 and Caspase-8 ex-pression. In TUNEL test, overexpression of CRMP2 obviously decreased the number of TUNEL positive cells(P<0. 01). The expression of BDNF was upregu-lated after cerebral ischemic injury ( P<0. 01 ) , while overexpression of CRMP2 increased BDNF more signif-icantly ( P <0. 01 ) . TTC staining showed cerebral in-farction Volume of MCAO + CRMP2/GFP group was obviously decreased ( P <0. 01 ) , and neurologic defi-cits were significantly improved ( P <0. 01 ) . Conclu-sion The overexpression of CRMP2 reduces nerve cell apoptosis possibly by regulating the mitochondrial ap-optosis pathway after cerebral ischemia/reperfusion in-jury to protect nervous system.

Objective To establish an in vitro oxygen-glucose deprivation/reoxygenation axon injury model in rat hippocampal neurons in order to found a basis for research concerning the injury of oxygen glucose deprivation and axons regeneration. MethodsThe hippocampal neurons isolated from rats 24 h after born and cultured for 7 d were exposed to D-hanks solution with nitrogen gas instead of the original culture medium for 0.5, 1.0 and 1.5 h respectively, and then continue to be cultured in the original culture medium with oxygen. LDH content in the culture media was measured at 1, 5, 24, 48 and 72 h after reoxygenation. The morphological changes of neuron and axon were observed with inverted phase contrast microscopy. ResultsAfter oxygen-glucose deprivation/reoxygenation injury, hippocampal neurons became darker, swollen, and were with shorten axons. With the elapse of time, the LDH content was increased. The survival rate of hippocampal neurons was higher and the change of axon length was more obvious in the group of oxygen-glucose deprivation for 0.5 h than in the other groups. ConclusionAn in vitro oxygen-glucose deprivation/reoxygenation axon injury model in rat hippocampal neurons is successfully established.

Objective To explore the effects of low dose intravenous minocycline on neurological function and the expression of RGMa in rats after focal cerebral ischemia reperfusion. Methods Fifty-five adult male Sprague-Dawley rats were randomly divided into sham-operated group, cerebral ischemia/reperfusion (I/R) group and minocycline-treat?ed group. The cerebral ischemia/reperfusion model was established by 2 h of middle cerebral artery occlusion. At 2 weeks after ischemia reperfusion, the expression levels of RGMa and growth associated protein 43 (GAP-43) were ana?lyzed by using immunohistochemistry and Western blot, respectively. Neurological functional recovery was evaluated us?ing both the modified neurological severity score (mNSS) and staircase test at 2, 7,14 and 28 d after ischemia reperfusion. Results Minocycline at a dose of 3 mg/kg via the caudal vein significantly reduced the expression of RGMa protein (0.53± 0.08 vs. 1.17±0.15, P<0.05) and enhanced the expression of GAP-43 protein (0.94±0.10 vs. 0.57±0.09, P<0.05) in isch?emic cortex 2 weeks after ischemia reperfusion. Moreover, minocycline could reduce mNSS and improve forelimb motor function when compared to the I/R group (P<0.05). Conclusions Low dose intravenous minocycline (3 mg/kg) can im?prove neurological functional recovery in a rat model of focal cerebral ischemia reperfusion and the mechanism may be re? lated to the down-regulation of RGMa expression and up-regulation of GAP-43 expression.

The article introduced experience of class teaching of neurology from attending a lecture and preparing lessons,actively making use of multimedia teaching,applying combina-tionly many kinds of teaching methods and thoroughly stimulating learning interest.It is key point for improving teaching quality that the teacher strengthen their mixed ability.

Objective To investigate the effects of minocycline on cell viability and neurite outgrowth of pheochromocytoma cells (PC12) after oxygen‐glucose deprivation(OGD) injury .Methods PC12 cells were exposed to OGD insult for 2 ,4 ,6 ,8 h to estab‐lish a cerebral ischemia model in vitro .High‐differentiated PC12 cells were cultivated and randomly divided into three groups :con‐trol group ,OGD group and various doses of minocycline(0 .1 ,1 .0 ,10 .0 μM) treated group .24 h after OGD‐reperfusion ,PC12 cells viability was assessed by CCK‐8 assay ,the neurite was labeled with MAP‐2 by immunofluorescence and neurite length was meas‐ured by the Image‐Pro Plus 7 .0 software ,GAP‐43 protein expression was determined by Western blotting .Results Compared to the OGD groups ,minocycline induced a concentration‐dependent increase in cells viability [(46 .1 ± 2 .9)% vs .(77 .0 ± 2 .5)% ,P<0.01],improvedneuriteoutgrowthandincreasedtheexpressionofGAP‐43proteininPC12cellsafterOGDinjury([(0.34±0.04) vs .(2 .11 ± 0 .10) ,P<0 .01] .Conclusion Minocycline could protect against oxygen glucose deprivation injury and promote neurite outgrowth .This finding suggests minocycline may be a novel therapy for cerebral ischemia .

Objective To observe the effect of ischemic postconditioning on neuron structure plasticity and memory after global cerebral ischemia injury in rats and discuss the protection mechanism from aspect of Morphology. Methods A total of 36 SD male rats were randomly divided into sham operation group, global cerebral ischemia for 15 min group and global cerebral ischemia plus postconditioning group, 12 rats per group. The pullsinelli 4 vessel occlusion was applied to produce the models of global cerebral ischemia reperfusion injury, common carotid arteries (CCA) occlusion with 15 min and postconditioning with three cycles, of 15 sec release and 15 sec occlusion (15s/15s). Six rats from each group were evaluated by Morris Maze test for the ability of space learning and memory and the other six rats were evaluated by golgi stain for morphologic change of neuron. Results The ischemic postcondtioning group showed significant shorter mean escape latency compared with the sham operated group ( at day 3, P =0. 014; at day 4, P =0.040; at day 5, P =0.001 ). The density of dendritic spine in ischemic postcondtioning group was increased more significantly compared with ischemic group ( F = 562. 820,P ＜ 0. 01 ). Conclusion Ischemic postconditioning has obvious protective effect on cerebral ischemiainduced memory impairment, which may be related to alleviation of dendritic spine injury.

Objective To observe the survival of EAE rats after recombinant adenovirus NgR specific RNA interference(Ad-shRNA-NgR) transfected the brain tissue of the experimental autoimmune encephalomyelitis(EAE),and provide the basis for EAE intervention.Methods EAE rats were randomly divided into high,medium,low and control groups(20 rats in each group).The lateral ventricle of EAE rats were injected with a titer of 1×1011 pfu/mL,1×1010 pfu/mL and 1×109 pfu/mL Ad-shRNA-NgR.The survival of EAE rats at third and seventh days after injection was observed.Results The survival rate of EAE rats of the high titer group was significantly lower than those of the middle titer group and low titer group at third and seventh days after Ad-shRNA-NgR transfected into EAE brain tissue.There was no significant difference in survival rate in middle titer group,low titer group and control group.Conclusion The titer of Ad-shRNA-NgR is safe in the experiment of EAE rats from 1×1010 pfu/mL to the range of 1×109 pfu/mL.

Objective To analyze the magnetic resonance imaging(MRI)features of multiple sclerosis(MS)patients both in the brain and the spinal cord and to explore its relationship with factors such as quality of life,disability of MS patients and so on.Methods A total of 170 MS patients confirmed clinically underwent MRI examination and answered the questionnaires of Multiple Sclerosis Quality Of Life-54 instrument,Expanded Disability Status Scale,Hamilton Anxiety Scale and Hamilton Depression Scale.Results The lesions on brain MRI were usually seen in the white matter around the lateral ventricles,the centrum ovale majus and frontal lobe.The commonly seen length of the single lesions on the spinal cord was as long as that of 1-2 vertebral bodies,but that of the fused lesions was as long as that of 4-5 vertebral bodies.The distribution of the lesions was significantly correlated with the quality of life,the degrees of the disability,anxiety and depression.Conclusion MRI examination is useful for early and better diagnosis of MS and can provide guidance for treatment,and thus can improve the prognosis and the quality of life of patients.

Objective To detect the effect of olfactory bulb(OB)lesion on proliferation,migration and differentiation of the neural stem cells(NSCs)in the subventricular zone(SVZ).Methods Forty-two healthy female SD rats were enrolled and randomly divided into normal control group,isotonic saline group and OB lesion at day 3,at weeks 1,2,3 and 4 groups,six rats per group.OB lesion was induced by N-methyl-D-aspartic acid(NMDA)injection.Bromodeoxyuridine(BrdU)was injected intraperitoneally to label NSCs.Immunohistochemical staining was used to detect the proliferation of SVZ NSCs.In addition,another 18 rats were randomly divided into normal control group,isotonic saline group and lesion group,six rats per group.BrdU was injected intraperitoneally one week after OB lesion and then the animals were sacrificed four weeks after BrdU injection to detect the migration and differentiation of NSCs with immunohistochemistry and immunofluorescence.Results Three days after OB lesion,BrdU-positive cells in SVZ began to increase(26.33 ± 2.58,P ＜0.01),reached the maximum at week 1 (35.33 +3.01,P＜0.01)and still sustained a high level at week 4(19.50+ 2.26,P＞0.05).Five weeks after the OB lesion,the rostral migratory-stream(RMS)and the BrdU-positive cells in OB were significantly increased(86.50 + 5.09,P ＜ 0.01)and(52.83 + 3.87,P ＜ 0.01),respectively.By using fluorescence double staining,most of the BrdU-positive cells were co-localized with the neuronal nuclear antigen(Neun),with a portion of BrdU-positive cells expressing the glial fibrillary acidic protein (GFAP).Conclusions OB lesion can improve the proliferation of NSCs in SVZ and migration of NSCs to OB.The newborn cells can differentiate into not only neurons,but also gliocytes and may be involved in lesion repair.