Great Acupuncture is a special method to treat stroke patients on the relative health side, which reflects the whole view of the traditional Chinese medicine. With more and more clinical controlled trials reported recently, the origin, development and possible mechanisms of great acupuncture are worthy discussed for providing a neoteric method to treat cerebral apoplexy. The differences of great acupuncture and contralateral collateral needling were analyzed in this paper. Indications and attentions of great acupuncture were also summarized. Through comparing between the treatment of cerebral apoplexy by the great acupuncture and related techniques of the modern neurological rehabilitation, we found that the modern rehabilitation techniques focused on promoting the activities of the injured limbs, which might be much weaker in therapeutic intensity than great acupuncture. Therefore we believed that the concept of the great acupuncture of the traditional Chinese medicine is much advanced.

Objective To observe the clinical effect of treating atlanto-axial subluxation by manipulative reduction therapy. Methods 128 patients with atlanto-axial subluxation confirmed by cervical plain X ray were randomized into two groups: 64 in the treatment group treated by manipulative reduction therapy, and 64 in the control group treated by the routine cervical traction. The clinical effect was evaluated by both clinical and X-ray confirmation. Results The X-ray study showed that after treatment the reconstruction of excursion in odontoid process in the treatment group was better than that in the control group significantly (P<0.01). The improvement of vertebra basal artery blood flow in the treatment group was also better than that in the control group significantly (P<0.05). The total effective rate of the treatment group was 95.3%, while the control group was 78.1%. Conclusion The technique of manipulative reduction on atlanto-axial subluxation acts more directly on the cause of the disease than the routine traction, and exerts better results in restoring proper atlanto-axiai joint position and mechanics stability of cervical vertebra.. Thus it is the effective shortcut way with high safety and low cost.

Objective To investigate the effects of taurine on the expression of stem cell factor mRNA of the focal cerebral ischemia in rat.Methods 63 adult male rats were randomly divided into taurine-treated group (Taurine, 80 mg/kg, began at the day of MCAO and continuously intravenous injection for 10 min, daily for 7 days) and controlled group (0.9% normal saline, 1 ml, continuously intravenous injection for 10 min daily for 7 days). The rats received right middle cerebral artery occlusion at 2h and different hours of reperfusion. Expression of SCF was detected by in situ hybridization in the rats subjected to2h,24h,3d,7d, 14 d of reperfusion and sham-operated group (n=3). Results Low level SCF mRNA expressions were found in cortex, striatum and extraventricular zone in sham-operated group. The expression of SCF mRNA in ischemic hemisphere of controlled group increased markedly compared with sham-operated group (t=2.16~25.19, P＜ 0.05), besides that of 2 h in cortex, 2 h in striatum, 2h and 14d in extraventricular zone. SCF mRNA expression in the treatment group increased markedly in cortex,striatum and extraventricular zone at 3d and 7d(t=5.19~ 26.17,P＜0.05). Conclusion Taurine increased the SCF mRNA expression in MCAO rats, therefore it might promote the creation of neural stem cell.

AIM: To compare the clinical effect of Tianshu Capsule(Rhizoma Chuanxiong,Rhizoma Gastrodiae,efc) on migraine with Flunarizine. METHODS: 82 cases of patients with migraine were divided randomly into the treatment group(40 cases),which were treated with oral Tianshu Capsule,4 capsules(1.36 g),3 times daily after meals,and the control group(42 cases),which were treated with Flunarizine(Sibelium) 5 mg quaque nocte,for 2 months.One year follow-up was carried out.The frquency and duration of migraine were analyged before and after treatment,and duration of positive results after withdraw of drugs were also recorded.The body weight,blood and urine routine,liver and kidney function as well as electrocardiograph were compared before and after treatment. RESULTS: In the treatment group the frequency and duration of migraine decreased more than that of control group.The positive results remained longer in the Tianshu Capsule group(P

Oyecave:To observe the influence of nociceptin/orphanin FQ(N/OFO)on cerebral infarction volume and somatosellsOry evoked potential(SEP)in focal cerebral ischemia in rats.Methods:Forty one SD rats were randomly alloomed into middle artery occlusion(MCAO)sham-operation(n=5),isehemic(n=8),N/OFQ 10μg(n=7),N/OFQ 1 μg(n=7),N/OFQ0.1 μg(n=7),and artificiai cerebrospinal fluid(ACSF)(n=7)groups.A model of middle cerebral artery occlusion(MCAO)in rats was induced using intraluminal suture method.Reperfusion was performed 2 hours after MCAO.One hour after MCAO,N/OFQ 10 μg,N/OFQ 1 μg,N/OFQ O. 1 μg,and the same volume of ACSF were injected intraventricularly in the N/OFQ 10 μg,N/OFQ 1 μg,N/OFQ 0. 1 μg,and ACSF groups,respectively. The cerebral infarction volurne was detected 24 hours after reperfusion,and SEP was recorded. Results:1he amplitude of SEP P1 decreased in the sham-operation group. There was no significant change in P1 peak latencies.There were no significant differences hetween the N/OFQ 0. 1 μg group and the ACSF group in SEP amplitudes,P1 peak lantecies and cerebral infarction volume. As compared with the ACSF group,the SEP amplitudes were further decreased in the N/OFQ 1 μg and N/OFQ 10 μg groups,but there were no significant change in P1 peak lantecies. One hour after reperfusion,the SEP amplitude in the ACSF group almost returned to the level of preischemia,the recovery slowed down in the N/OFQ 1 μg group,and it still did not recovered 3 hours after reperfusion in the N/OFQ 10 μg group. The dose of N/OFQ and SEP response showed dose-effect relationship,The higher the dose,the deeper the SEP depression and the slower the recovery. At 24 hours after reperfusion,the cerebral infarction vlumes in the shamoperation,ACSF,N/OFQ 0. 1 μg,N/OFQ 1 μg,and N/OFQ 10 μg groups were 0 mm3,24.180 ±4.088 mm3,23.090±4.523 mm3,35.304 ± 6. 824 mm3,and 40. 806±6. 716 mm3,respectively. There was no significant difference between N/OFQ 0. 1 and ACSF groups. There were significant differences between N/OFQ 1 μg and 10 μg groups and ACSF group (all P ＜ 0.01 ). Conclusions:Intracerebroventricular injection of N/OFQ in the early stage of cerebral ischemia decreases the SEP amplitude,prolongs the time of recovery,and increases cerebral infarction volume,which shoves that it may aggravate cerebral ischemic injury.

Objective To explore the effect of picrodideⅡ on the expressions of Caspase-3 in brain tissue following cerebral ischemic reperfusion injury in rats. Methods The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in rats. Picrodide Ⅱ (10 mg/kg) was injected from tail vein for treatment. The neurological function was evaluated with Bederson's test. The brain structure was observed by hematoxylin-eosin (HE)stain and the apoptosis were counted by TUNEL immunofiuorescence assay. The expressions of Caspase-3 were detected with immunohistochemical and enzyme linked immunosorbent assay. Results After ischemia for 2 h and reperfusion for 22 h, the rats showed neurological function deficit. The expressions of Caspase-3 and the number of apoptotic cells in brain tissue increased significantly than those in the sham operative group (P＜ 0.01). In picroside, the Bederson's scores, the expressions of Caspase-3 and the number of apoptosis cells were significantly lower than those in the negative control group(P＜0.01).Conclusion Picroside Ⅱ might reduce the expressions of Caspase-3 to inhibit the neuronal apoptosis induced by cerebral ischemia reperfusion injury and improve the neurological function of rats.

AIM: This study was designed to investigate the inhibition of tanshinone ⅡA on C6 glioma cell line and its mechanism. METHODS: MTT was used to measure the levels of the proliferation of C6 cultured with tanshinone ⅡA at different concentrations. The effects of tanshinone ⅡA on cell cycle of C6 were observed by FCM. The change of DNA was observed by Sepharose electrophoresis. The expression of proto-oncogenes c-myc was measured by RT-PCR. RESULTS: The proliferation of C6 was obviously inhibited by tanshinone ⅡA in a dose-dependent manner. The outcome of FCM showed that the apoptotic cell rate was 7.7%, when cultured with tanshinone ⅡA at 1.0 mg/L for 3 days. The apoptotic cell rate was 21.6%, when cultured with tanshinone ⅡA at 2.0 mg/L in 3 days. CONCLUSION: Tanshinone ⅡA inhibits the proliferation of C6 cells, induces apoptosis and inhibits the expression of proto-oncogene c-myc.

Objective To investigate the anti-oxidant effect and the possible mechanisms ofpicrodide II in cerebral ischemia/reperfusion injuries in rats. Methods A total of 90 adult, healthy, mmale Wistar rats were used to established the middle cerebral artery occlusion reperfusion (MCAO/R) models by intraluminal monofilament suture on the left external-internal carotid artery. The treatment group and the positive control group were respectively injected with 1.0％ picroside II (10 mg/kg, 250 μl) and salvianic acid A sodium (10 mg/kg, 250 μl) via the tail vein, and the negative control group and sham-surgery group were injected with 0.1mol/L phosphate buffer saline (PBS) 250 μl. The neurological deficit scores were evaluated with Bederson's test. The cerebral infarction volume was observed with tetrazolium (TTC) staining. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase dUTP nick-end labeling and the expressions of inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) were detected with immunohistochemical assay.The concentration of iNOS and SOD proteins in brain tissue was detected by enzyme linked immunosorbent assay.Results Neurological behavioral malfunction appeared in all the rats with MCAO/R. The infarction focuses emerged in the ischemic hemisphere following the MCAO/R injuries. The number of apoptotic cells and the expression of iNOS increased while the SOD reduced after MCAO/R. After the treatment of picrodide Ⅱ, the nervous behavioral function (1.28±0.38)improved, the infarction volume(68.73±4.46)％ reduced, the number of apoptosis positive cells(6.10± 1.26), the expressions and the concentrations in brain tissue of iNOS(4.67+0.51)decressed while those of SOD (0.53 ±0.14) increased significantly compared with the negative control groups(t=3.16、 2.51、 4.15、3.12、 3.25, P＜0.05). Conclusion PicrodideⅡ might play a neuroprotective effect by inhibiting the neuronal apoptosis and the expressions of iNOS and SOD after cerebral ischemia/reperfusion injuries.

Objective To establish an ideal focal cerebral ischemia reperfusion model in monkeys.Methods Adult healthy rhesus monkeys(Macaca mulatta) 12 cases(male 6 and female 6),aged 4-7 years and weighted 4.8-7.5kg.were used in this study.The middle cerebral artery occlusion/reperfusion(MCAO/R) model was established by inserting a standard micro-balloon catheter intraluminally from the carotid common artery or femoral artery into the proximal segment of the middle cerebral artery(MCA).The regional cerebral blood flow of MCA was occluded by expanding the micro-balloon to cause ischemia,and withdrawing the micro-ballon catheter to reperfuse the MCA.The MCAO/R model was evaluated by angiography,magnetic resonance angiography(MRA),magnetic resonance imaging(MRI),tetrazolium chloride(TTC) staining and neurological behavoral function scores.Results By inserting a micro-balloon catheter intraluminally from the carotid common artery or femoral artery into the MCA,the micro-balloon catheter could be inserted into the MCA to occlude blood flow,and no image of MCA shown on TV screen.In MCA blood flow supplied area,magnetic resonance T1,T2 and DWI showed high signals,TTC staining showed cerebral ischemic infarction,and correspondly the monkeys showed neurological function disorders.This method used a simple operatire procedure had a high successful rate,and could be repeated.Conclusion We showed ideal method to establish the MCAO/R model in monkeys by inserting intraluminally a micro-balloon catheter into the MCA.

AIM: This study was designed to investigate the effect of ginsenoside Rg1 on the amyloid ?-protein precursor (APP) and neprilysin (NEP)expression induced by lipopolysaccharide (LPS) in C6 cell line in order to discover effectual Alzheimer's disease (AD)-treated drugs. METHODS: MTT colorimetric analysis was used to measure the survival rate of C6 cultured with ginsenoside Rg1 at different concentrations (2 5, 5, 10 and 20 ?mol?L -1) and LPS (100 mg?L -1). The expression of APP and NEP mRNA was measured by RT-PCR. RESULTS: LPS decreased the survival rate of C6, furthermore, the increase in APP expression and the decrease in NEP expression were observed. On the other hand, the above alteration induced by LPS was reversed by ginsenoside Rg1. CONCLUSION: This study demonstrates that LPS can cause cell damage, the increase in APP expression and the decrease in NEP expression. Ginsenoside Rg1 can exert a neuroprotective action, protect C6 cells against LPS-induced injury via inhibiting APP expression and increasing NEP expression.