Objective To investigate the effects of tissue kallikrein on expressions of bradykinin, bradykinin Bl receptor (B1R) and bradykinin B2 receptor (B2R) in ischemic brain tissue following cerebral ischemia-reperfusion in rats. Methods Fifty-four SD rats were randomly divided into three groups: sham operation, normal saline (NS) (2 ml · kg-1 · d-1, for 3 days), and TK (IK 175 × 10-3 U· kg-1 · d-1,for3 days) groups (n = 18 in each group). After three days,the neurological deficit score and the measurement of cerebral infarct volume were performed,The concentration of bradykinin in the ischemic region was detected by the enzyme- linked imrnunosorbent assay (ELBA).reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to detect the mRNA and protein expressions of BlR, B2R in ischemic brain tissue, respectively. Results Compared with the NS group, the neurological deficit (6.17 ± 1. 17 vs. 8. 17 ± 1.33; t =2.000, P =0- 004) and the cerebral infarct volume (29. 67% ±3. 78% vs. 37. 50% ± 6. 72% ;t =0.078, P =0.005) in the TK group were reduced significantly; the concentration of bradykinin in ischemic brain tissue in the TK group was increased significantly (9.25 ± 1. 13 vs. 15.53 ± 1.68, t =6.283, P =0. 000); the expression of B2R mRNA was up regulated significantly (1. 21 ±0. 17 υs. 2.15 ±0.20; t =0.943,P =0- 000), but the up-regulation of the B2R mRNA expression was not obvious (0.51 ±0.05 υs. 0.57 ±0.06; t =0.058, P =0. 141); the expression of B2R protein in ischemic brain tissue was up-regulated significantly (1. 15 ±0. 16 vs. 1. 88 ± 0.21, t =0. 737, P =0. 000), but the up-regulation of BlR was not obvious (0. 50 ±0.04 vs. 0.53 ±0.05, t = 1.326, P =0. 214). Conclusions TK has protective effect on cerebral ischemia-reperfusion in rats. It may increase the bradykinin concentration in ischemic brain tissue, and up-regulate B2R expression, but it has little effect on Bl R expression.It is speculated that B2R may play a major role in TK protecting ischemic brain tissue.

Objective To study the risk factors of type 2 diabetes mellitus patients complicated with cerebral infarction.Methods 32 type 2 diabetes mellitus patients complicated with cerebral infarction(group A) and 30 type 2 diabetes mellitus patients (group B) were enrolled in the study. The living habit, history, blood lipids, blood glucose, body mass index and height were investigated, also common carotid artery intimal thickness (CCA-IMT) and plaque incidence rate were measured by two-dimensional color Doppler ultrasound, and the relationship between them was evaluated.Results There were significant differences between two groups in age, duration of smoking, course of diabetes, high density lipoprotein (HDL) and fasting blood glucose (FBG) (all P

The article describes the molecular structure and biological characteristics of thrombin and thrombin receptor.It manly discusses thrombin caused the mechanisms of cerebral edema formation after intracerebral hemorrhage by prormoting cell inflammtory reaction,neuron apoptosis and injurying blood-brain barrier.

AIM: To investigate the clinical effect and side-effects of paroxetine in the treatment of generalized anxiety (GA). 　METHODS: Ninety patients who met Chinese classification and diagnostic criteria of mental disorders, 2nd Rev Ed (CCMD-2-R) criteria for GA were randomly divided into paroxetine group of 30 patients (M 12, F 18; age 40 a±s 13 a) which was treated with paroxetine 20-40 mg, po, qd or bid, benzodiazepines group of 30 patients (M 13, F 17; age 37 a±13 a) among them, 16 patients were treated with alprazolam 0.4-0.8 mg, po, bid or tid, 14 patients were treated with clonazepam 1-2 mg, po, bid or tid and placebo group of 30 patients (M 11, F 19; age 37 a±13 a) which was treated with placebo 1 tablet, tid for 12 wk. Effects were evaluated with Hamailton anxiety scale (HAMA), self-rating anxiety scale (SAS), clinical global impression scales (CGI) and treatment emergent symptoms scale (TESS), before and after the wk 2,4,8,12 of treatment.　RESULTS: The excellent response rates of paroxetine group and benzodiazepines group were 90 % and 50 % (P<0.01). The side-effects of paroxetine group were dry mouth, constipation, nausea, but those were less than that of benzodiazepines group. 　CONCLUSION: The study suggests that paroxetine is an effective drug for the long treatment of GA and the side-effect is less.

Objective:To study the effect of Mg 2+ on glutamate and energy metabolites during focal cerebral ischemia and reperfusion in rats. Methods: Twelve male Wistar rats were divided into 2 groups(n=6):magnesium sulfate(100 mg/kg, i.p.) group and saline group.Cerebral ischemia was produced by occlusion of middle cerebral artery with a nylon thread for 60 min and followed by 60 min reperfusion.Microdialysis probes were stereotaxically implanted into the cortex; dialysates were collected every 15 min to determine the concentrations of glucose, lactic acid and glutamate. Results: There was a dynamic decrease of glucose and an increase of lactic acid and glutamate during ischemia and reperfusion in saline group.Glucose decreased slightly in magnesium sulfate group during ischemia and recovered to normal rapidly during reperfusion. The lactic acid levels in magnesium sulfate group were lower than that in saline group during early stage of ischemia(0-15 min) and reperfusion.There were significant attenuation in the elevation of glutamate during ischemia and reperfusion when magnesium sulfate was administered and recovered to normal after 30 min of reperfusion. Conclusion: The preservation of cellular energy metabolism,the decrease of lactacidosis and attenuation of glutamate level during ischemia and reperfusion may contribute to the neuroprotective effects of Mg 2+ .

Objective To study the effectiveness of Huperzine A,Nimodipine and the combinative utilization to age associated memory impairment(AAMI) and the influence of those to the plasma total antioxidant capacity(TAC) and calcium of platelet.Methods 140 patients with AAMI were randomly divided into 4 groups(35 cases in each group).Huperzine group administrated with Huperzine A 100 ?g thrice a day;Nimodipine group administrated with Nimodipine 30 mg thrice a day;combined group administrated with Huperzine A 100 ?g twice a day and Nimodipine 30 mg thrice a day;control group administrated with Vitamin B6 10 mg thrice a day.All the cases were treated for 6 weeks.Before and after treatment,the memory function were tested by WMS.The levels of plasma TAC and calcium of platelet were also measured at the same time.Results After treatment,the scores of WMS,the levels of plasma TAC and calcium of platelet in Huperzine A group,Nimodipine group and combined group were higher than before treatment and those in control group(all P

Objective To study the clinical features of hyperkalemic periodic paralysis (hyperKPP) and the relationship with SCN4A gene in a Chinese family Methods The clinical features of 7 patients in a Chinese family with hyperKPP were summarized All 24 exons of SCN4A gene were screened with denaturing high performance liquid chromatography (DHPLC) technology, and then sequence analysis was performed on those with abnormal elution peak Results This family showed typical clinical features of hyperKPP but without myotonia Three mutations were found in exon 13, 23 and 24 respectively Linkage analysis and direct sequencing showed the mutation in exon 24 was a synonymous mutation The mutation in exon 23 was a missense mutation, but proved to be a benign polimophism; the mutation in exon 13 was proved leading to the best known amino acid exchange Thr704Met Conclusion SCN4A gene should be related to hyperKPP, and Thr704Met be responsible for hyperKPP in this Chinese family

Objective To investigate the possible effects and underlying mechanisms of desferroxamine (DFO) preconditioning against hypoxia in neurons. Methods Cortical neurons were cultured in DFO under ischemia condition of oxygen-glucose deprivation (OGD). Cell viability was determined by cell counting kit-8 (CCK-8) method; apoptotic cell ratio was examined with Hoechst 33342 staining; the morphological change was observed. Middle cerebral artery was occluded with or without DFO administration to establish the cerebral ischemia rat model. Infarct sizes were examined by TIC staining, and the neurological severity score was evaluated. Meanwhile immunofluorescent staining was employed to detect the protein synthesis of hypoxia inducible factor-1 (HIF-1) and erythropoietin (EPO), RT-PCR was performed to detect the mRNA expression of HIF-1 and EPO as well Results Neuronal viability kept in 49% (OGD group was 25%, t =8. 544, P<0. 05), the rate of apoptosis was 38% (OGD group was 30%, t = 4. 409, P <0.05 ) after administration of DFO (post-DFO) , the morphology of neurons improved. In the model of focal cerebral ischenfia of 30 mg/kg group, neurological severity score was reduced, the percentage of brain infarct decreased 8.5% (t=4.649, P<0.05) 3 days post-DFO(vs control). In the 100 mg/kg group, neurological severity score was 7.44 ±0.39 (t=2.903, P<0.05 ) ,5.60±0.47 (t=10.143, P < 0.01 ) ,6.97 ±0.73 (t=3.142, P<0.05 ), the percentage of brain infarct decreased 12. 0% (t=5.056, P<0.05), 32.3% (t =10.993, P<0.01), 10.6% (t =4.385, P<0.05)2,3 and7 days post-DFO(vs control), respectively. Immunofluorescent staining found synthesis of HIF-1α and EPO in cultured cortex neurons after DFO pretreated; HIF-1α and EPO were upregulated in the neurons of rat brain after DFO pretreated. The mRNA of HIF-1α and EPO upregulated in vivo and in vitro. Conclusion DFO preconditioning can protect the brain against ischemic damage, which is related to the protective effect on neurons. The mechanism of DFO preconditioning may be involved in the expression of HIF-1α and EPO in vivo and in vitro.

0.05). Conclusion In our samples, this two polymorphisms in A2M might play similar roles in the susceptibilities to PD and AD.

AIM: To study the difference in glucose and lactate levels between brain extracellular fluid (ECF) and plasma in rabbits in the different blood glucose levels. METHODS: Using intracerebral microdialysis technology, brain ECF levels of glucose and lactate were measured in every 10 min under basal conditions and during a hyperglycemia-hypoglycemia clamp study. RESULTS: Under basal condition, brain ECF glucose levels were markedly lower than ambient plasma levels (30% of plasma), whereas ECF lactate levels were substantially higher (165% of plasma). During the hyperglycemia-hypoglycemia clamps, the relationship between plasma and ECF levels of glucose remained similar, but changes in ECF glucose lagged about 30 min. There were no substantially changes in ECF levels of lactate during dynamical study. CONCLUSION: There are striking differences in glucose and lactate levels between brain ECF and plasma. Lactate may involve in the metabolic process of central nervous system.