Aim To investigate the effect taurine on ischemia-induced neuron apoptosis and its mechanisms. Methods Focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). After 6 h permanent MCAO, mRNA expressions of Caspase-3/8 of rat brain were detected with real-time quantitative reverse transcriptase-polymerase chain reaction (real-time QRT-PCR). Oxygen-glucose deprivation (OGD) was used to induce an in vitro ischemia model. Primarily cultured cortical neurons were exposed to 4 h OGD. Intracellular calcium concentrations([Ca~(2+)]_i) was measured with fluorescent Ca~(2+) sensitive probe fura 2 acetoxylmethyl ester (Fura 2/AM). Neuronal apoptosis was assayed with flow cytometry of FITC-annexinV/propidium iodide binding 24 h after OGD. Results mRNA expressions of Caspase-3/8 were upregulated in MCAO model. [Ca~(2+)]_i and neuronal apoptosis were markedly increased in OGD model. Taurine pretreatment reduced the upregulation of mRNA expression of Caspase-3/8 in vivo and ameliorated calcium overload and neuronal apoptosis in vitro. Conclusion Taurine has neuroprotective effect against ischema-induced neuronal apoptosis. This is partly due to its effects on Caspase-3/8 and [Ca~(2+)]_i

AIM To observe the protective effect of taurine on focal cerebral ischemia in rats. METHODS Male SD rats were divided at random into three groups, i.e. sham-operated, control and treatment group respectively. Before ischemia impairment, taurine(250 mg?kg -1?d -1)was administrated ip for one week in treatment group. A nylon suture was inserted into internal carotid artery to occlude the beginning of middle cerebral artery(MCAO). After 3 h permanent occlusion, neurology deficit score was evaluated. At 6 h, all animals were decapitated rapidly to get brain tissue. Brain infarct region was stained by 2,3,5-triphenyltetrazolium(TTC) and the size was measured by AUTOCAD. Contents of malondialdehyde(MDA) and nitric oxide synthase(NOS) and activity of superoxide dismetase(SOD) in brain tissue were detected by spectrophotometer. Expressions of iNOS and inter-cellular adhesion molecule-1 (ICAM-1) were observed through immunohistochemistry method. RESULTS Compared with the control group:Taurine can ameliorate neurological deficit score and decrease infarct volume induced by MCAO. Taurine improved the activity of SOD, but did not affect NOS activity in the infarct without affecting MDA content after 6 h MCAO. Taurine decreased the positive expression of ICAM-1 significantly in brain slice. CONCLUSION The results suggest that taurine may reduce expression of ICAM-1 and improve activity of SOD, and play an neuroprotective effect against middle cerebral artery occulusion.

It has been suggested that HCN1 is primarily expressed in hippocampus, however little is known about its effects on spatial learning and memory. In the present study, we investigated the effects of non-specific HCN1 blocker CsCl on spatial learning and memory by using Morris water maze and in situ hybridization in mice. The results showed CsCl 160 mg/kg ip for 4 days, and the mean escape latency was 34 s longer than that of normal control (P<0.01). In hippocampal tissues, staining for the HCN1 mRNA was stronger in the DG and CA1 region of the hippocampus (P <0.05, P<0.05, when CsCl-administration group was compared with normal group). Our results suggested that CsCl could significantly affect the spatial learning and memory in mice, and HCN channel is involved in the process of learning and memory.

Objective To investigate the effect of daurinoline on basilar artery vascular smooth muscle. Methods The tension of isolated basilar artery ring of rabbit was measured. The effects of daurinoline on the basilar artery contracted by methoxamine,5-hydroxytryptamine(5-HT),KCl and Histamine( His)were also examined. Dose-response curves of 5-HT and KCl were observed as well. Results Daurinoline exerted obvious relaxation effect on the basilar artery vascular ring contracted by methoxamine,5-HT,KCl and His in a concentration-dependent manner. IC50 of daurinoline in methoxamine,5-HT,KCl and His-treated rabbits was 8.67×10-5,1.78×10-6,6.79×10-7 and 4.98×10-4 mol·L-1,respectively. The change of concentration-response curves of methoxamine,5-HT,KCl and His showed that daurinoline was a non-competitive antagonist. Conclusion Daurinoline exerts marked relaxation effect on basilar artery of rabbits through non-competitive antagonism. The mechanism of relaxation action may be related to blockage of voltage-dependent or receptor-dependent calcium channels.

Objective To provide anatomical evidence for the repair of wounds of finger distal phalanx,espe-cially for the recovery of feeling. Methods 10 samples of fresh adult hand were dissected under microscope. The course,branches,distribution and external diameter of nerves and blood vessels in finger distal phalanx and morpho-logical relationship between nerves and vessels were measured. Results Proper palmar digital nerves mostly step over digital arteries at section starts of distal finger arterial arcades and go to finger pulps and latero-backs. Their thinks di-vide into 2 branches. Transverse diameters of interior and exterior branches are 0.8 ～ 1.2 mm and 0.9 ～ 1.4 mm re-spectively at liner semilunaris levels. Distributionsof left and right branches are reciprocal chiasmas. Conclusion Finger nerve mostly ramifies to finger pulp,finger tip and finger back at the level of phalangette bottom. Its branches are lower and thinner than concomitant arteries. The suitable anatomy region for anastomosis of nerves and blood ves-sels is the middle1/3 section from the distal interphalangeal joint to the nail during replanation of amputated finger pa-ratelum.

Objective To determine the neuroprotective effect of clonidine on primary cultured cortical neurons in rats exposed to oxygen-glucose deprivation ( OGD) injury. Methods Cortical neurons cultured for 8 days were randomly assigned to the three groups: normal control group, model control group, and clonidine pretreatment group. OGD injury model was established by chemical hypoxia and glucose deprivation in incubation liquid for 4 h. Clonidine (1. 0, 3. 0, 10 μmol·L-1 ) was added 24 h before OGD injury. Neuronal injury was evaluated by MTT staining and the release of lactate dehydrogenase ( LDH) . Results Under the microscope, primary cultured cortical neurons in normal control group presented great density, round size, smooth edge, and high diopter,The suvival rate of neurons and the percentage of LDH releasing were (100. 00±32. 12)% and (100. 00 ± 37. 51 )%, respectively. After exposure to OGD injury, cortical neurons showed karyopyknosis, incomplete cell membranes, low diopters and a significant reduction in optical density of MTT staining. In addition, the suvival rate of neurons and the percentage of LDH releasing were (53. 61±7. 62)% and (166. 07±9. 65)% separately compared with normal control group. In the group with pretreatment of different concentrations of clonidine (1. 0, 3. 0, 10μmol·L-1), morphological changes induced by OGD injury were significantly reversed and optical density of MTT staining was dose-dependently raised. The percentages of survival neurons much higher than that of model control group were [(67. 53±10. 54)%, (71. 50±9. 79)% and (87. 48±5. 29)%, separately] and the obvious reductions of LDH releasing were [(136. 45±25. 72)%, (130. 92±24. 94)%and (121. 63±32. 68)%, respectively]. Conclusion Clonidine can exert neuroprotection against OGD-induced injury in primary cultured cortical neurons in rats.

Objective: To study the relationships between the expressions of E-cadherin and ki-67 in the tissues of heatocellular carcinoma(HCC)and the prognosis of HCC patients after hepatectomy as well as their clinical pathology. Methods: We examine the expressions of E-cadherin and ki-67 in 255 HCC tissues by tissue microarray and PV-6000 two-step method of immunohistochemistry and analyze the correlations between their expressions and clinical pathological data, 1-year recurrent rate and overall survival time after hepatectomy. Results: The expression of E-cadherin correlated with the tumor size and the 1-year recurrent rate of positive group was higher than that of the negative group. The expression of ki-67 correlated with vascular invasion and differentiation of the tumor, the positive group showed a higher 1-year recurrent rate and a shorter overall survival time. Multivariate Cox regression analysis indicated that the expression of ki-67 was an independent risky factor. Conclusions: The negative expression of E-cadherin and the positive expression of ki-67 predict a higher recurrent rate of early stage. The expression of ki-67 is an independent risky factor which can be used to evaluate the prognosis of patients with HCC after hepatectomy.

Aim To study the effect of ZD7288 on synaptic transmission in the pathway from perforant pathway (PP) fibers to CA3 region in rat hippocampus. Methods The extracellular recording technique in vivo was used to record the CA3 region field potentials. High-performance liquid chromatography (HPLC) with fluorescence detection was applied to measure the content of amino acids in hippocampal tissues. The effect of ZD7288 and CsCl on the amplitudes of population spike (PS) in CA3 region evoked by stimulation (0.5 Hz) of the perforant pathway (PP) fibers, and the content of amino acids in hippocampal tissue were observed. Results Microinjection of ZD7288 (20, 100 and 200 nmol)and CsCl (1,5 and 10 μmol) into CA3 region decreased the population spike (PS) amplitudes in a dosedependent manner. The inhibitory effects appeared at 5 min after microinjection and lasted at least 90 min.In those rats treated with ZD7288 (100 nmol), the contents of glutamate, aspartate, glycine and GABA decreased significantly as compared to those of saline control ( all P＜0.01, except P＜0.05 for that of glycine). A similar decrease in the contents of amino acids was observed when the rats were microinjected with CsCl (5 μmol). Conclusion ZD7288 could obviously inhibit synaptic transmission in the pathway from PP fibers to CA3 region in rat hippocampus, and this action of ZD7288 may be associated with altered contents of amino acids.

AIM Taurine was reported neuroprotective under several ischemic models in vivo. In this study, the direct effect of taurine against oxygen-glucose deprivation (OGD) inducing acute neuronal injury and the underlying mechanisms in vitro were investigated. METHODSFour hours OGD was used to induce in vitro ischemic injury in rat cortical neurons. Taurine 5, 10 and 20 mmol·L-1 was added 20 h before and during 4 h OGD period respectively. Mortality rate of neuron was assayed by MTT and flow cytometry methods. Level of neuronal [Ca2+]i was detected by Fura 2/AM loading. Amino acid concentrations in culture media were measured by high performance liquid chromatography. RESULTS Under OGD conditions, neuronal death was markedly increased, and the levels of neuronal [Ca2+]i and extracellular glutamate level were enhanced obviously. Taurine pretreatment obviously decreased the percentage of neuronal death induced by OGD. In addition, abnormal elevation of neuronal [Ca2+]i and extracellular glutamate level induced by OGD both were markedly repressed by taurine. CONCLUSION Taurine can alleviate rat cortical neuron injury induced by OGD, the mechanisms were likely due to repressing calcium overload and inhibiting excessive release or leakage of glutamate under such conditions.

0.05). Conclusions HF could not only relax cerebral vessels, reduce the CVR and enhance the CBF, but also dilate the femoral vessels of CVS dogs. Nevertheless, the latter action was much weaker. Furthermore, there was no relationship between effects of HF on vascular relaxation and contraction activity and the blood vessel endothelium.