Objective To explore the effect on the differentiatiation of bone marrow mesenchymal stem cells(BMSCs) induced by Ganglioside(GM1) into neural cells.Methods Rat BMSCs were isolated on the basis of its ability to adhere to the culture plate,passaged three times,and finally added GM1 to induce its differentiation.The morphologic changes of BMSCs were observed under phase-contrast microscopy,then neuron specific enolase(NSE) and glial fibrillary acidic protein(GFAP) expression were determined by immunocytochemistry way.Never growth factor(NGF) mRNA and brain-derived neurotrophic factor(BDNF) mRNA expression were detected with RT-PCR and then compared with those of FBS control group and blank control group.Results In GM1 induction group,BMSCs appeared round-shaped,with some dendrite and axon interlaced.(29.47%?3.26)% BMSCs showed positive staining to NSE,while(2.32?0.18)% were positive to GFAP.(6.97?0.56)% and(10.6?0.75)% BMSCs were positive to NSE in FBS control group and blank control group respectively,while(1.41?0.35)% and(1.21?0.35)% BMSCs were positive to GFAP in FBS group and blank control group respectively.NGF mRNA and BDNF mRNA levels in GM1 induction group were significant higher than those in the FBS group(all P

Objective To investigate the change and its clinical significance of plasma insulin and leptin level in the patients with cerebral infarction.Methods The plasma leptin, insulin, glucose levels and insulin sensitivity index(ISI) of 31 patients with atherothrombotic cerebral infarction (ACI), 30 patients with lacunar infarction (LI) and 21 cases of healthy controls were determined. Results Compared with those in the controls, there were elevation of plasma insulin level (6.17 ? 4.33 ?IU/ml, P

Objective To investigate the relationship between plasma resistin level and insulin resistance in the patients with cerebrovascular disease.Methods Fasting plasma resistin and insulin (INS) protein levels were determined by ELISA method in 50 patients with atherothrombotic cerebral infarction (ACI), 36 patients with lacunar infarction (LI), 36 patients with intracerebral hemorrhage (ICH) and 46 healthy control subjects. Blood glucose, blood lipid, blood pressure, height and weight were measured. Body mass index (BMI) and quantitative insulin sensitivity check index (QUICKI) were caculated as well.Results Compared with the control subjects, there were significantly higher fasting plasma insulin protein level and lower QUICKI in the ACI and ICH patients ( P

Objective To establish a rapid determination of sodium valprate in plasma by capillary zone electrophoresis.Method Plasma was acidized by 1 mol/L HCl, VPA was extracted into organic phase (n-Hexane), then re-extracted into aqueous phase (0.05 mmol/L NaOH solution including 15% Ethanol). Capillary clone was 75 ?m(id)?37 cm. Electrolyte consisted of 15 mmol/L sodium salicylate, 0.5 mmol/L CTAB and 15% Ethanol (pH 5.7).Separating voltage was 20 kV, detection wave was 214 nm, temperature was 20℃,injection time was 5 s by press in negative.Result The linear ranger of concentration for standard drug was between 25~200 ?g/ml (r=0.999),the limit of detection was 0.35 ?g/ml, the average recovery of VPA was 87.4%,the average inter-day and intar-day CV were less than 4% and 6%. Conclusion This method is simple, rapid, reliable and correct, for determination of VPA in plasma.

0.05).Conclusion The gene polymorphism of MMP-9/C1562T may be unrelated with IS.

AIM To explore the antioxidation of metabotropic glutamate receptors (mGluRs)ligand on rat models of Parkinson disease. METHODS The rat models of Parkinson disease were established by employing 6 hydroxydopamine to lesion unilateral substantia nigral. The serum total antioxidative capability (T AOC), reactive oxygen species (ROS) inhibition competence and content of glotathione (GSH) were measured with chemical colorimetry. RESULTS Compared with control group, serum T AOC and GSH and ROS inhibition competence increased in all treatment groups, mGluRs antagonist (SIB 1893) group, mGluRs agonists (APDC ) group, mGluRs agonists ( L SOP) group and L DOPA group. The effect of APDC was most prominent. CONCLUSION mGluRs antagonist and mGluRs agonists may exert a partial antioxidation effect on unilateral substantia nigral 6 hydroxydopamine lesioned rat and may be beneficial to the body for alleviating the oxdative stress.

To analyze maternal and neonatal complications among late preterm birth cases and to investigate risk factors of late preterm birth. Methods This was a retrospective analysis of 258 late preterm cases (late preterm group) born in Peking University First Hospital from January 1, 2009 to December 31, 2010. Maternal comorbidity and complications, delivery modes, and neonatal complications of these 258 late preterm infants were compared with 308 term cases (term group) during the same period. Statistical analysis was performed usingχ2 test, Fisher's exact probability test, t test and logistic regression. Results In Peking University First Hospital, late preterm births accounted for 3.9%(258/6 695) of live births and 60.1%(258/429) of preterm births. The incidence of the following maternal complications among the late preterm group was higher than that among term group(all P<0.05): severe pre-eclampsia [7.4%(19/258) vs 1.0%(3/308), χ2=15.35]; preterm rupture of membrane [42.6%(110/258) vs 15.3%(47/308), χ2=52.49];cervical insufficiency [1.9%(5/258) vs 0.0%(0/308), Fisher's exact test];placenta previa[3.5%(9/258) vs 0.6%(2/308), Fisher's exact test] and placental abruption [2.7%(7/258) vs 0.3%(1/308), Fisher's exact test]. Severe pre-eclampsia was the major risk factor leading to late preterm birth. The incidence of the following neonatal complications among the late preterm group was higher than that among term group (all P<0.05):respiratory distress syndrome (NRDS) [11.6%(30/258) vs 1.6%(5/308), χ2=24.22]; hyperbilirubinemia [64.3%(166/258) vs 39.6%(122/308),χ2=34.36];electrolyte disturbance [12.8%(33/258) vs 1.6(95/308),χ2=27.96];hypothermia [7.0%(18/258) vs 2.9%(9/308),χ2=5.08];infectious pneumonia[13.6%(35/258) vs 3.2%(10/308), χ2=20.43]; leukoencephalopathy [3.1%(8/258) vs 0.3%(1/308), χ2=5.25]; low body temperature [18.6%(48/258) vs 3.6%(11/308),χ2=33.98] and neonatal asphyxia [6.2%(16/258) vs 1.0%(3/308),χ2=11.86]. The incidence of the following neonatal complications among late preterm infants born at<35 weeks gestation was higher than that among late preterm infants born at≥35 weeks gestation (all P<0.05):NRDS [30.4%(14/46) vs 7.5%(16/212) ,χ2=19.26];hyperbilirubinemia [91.3%(42/46) vs 58.5%(124/212), χ2=17.74]; electrolyte disturbance [21.7%(10/46) vs 10.8%(23/212), χ2=4.02]; intracranial hemorrhage [8.7%(4/46) vs 1.9%(4/212),χ2=3.88];leukoencephalopathy [10.9%(5/46) vs 1.4%(3/212),χ2=8.32] and neonatal asphyxia [15.2%(7/46) vs 4.2%(9/212), χ2=6.05]. Conclusions Severe pre-eclampsia is the major risk factor leading to late preterm birth. The incidence of complications among late preterm infants is higher than that among term infants. If a pregnancy has to be terminated because of maternal disorders, the pregnancy period should be extended to 35 weeks if it permits.

Objective To investigate influence of Ang-(1-7) on the inducible nitric oxide synthase (iNOS) activity and gene expression following focal cerebral ischemia/reperfusion in rats. Methods Cerebral ischemia/reperfusion injury was induced by intraluminal thread occlusion of middle cerebral artery in the adult male Sprague-Dawley (SD) rats. Ang-(1-7) or artificial cerebrospinal fluid (aCSF) was continuous administrated by implanted Alzet osmotic minipumps into lateral cerebral ventricle after reperfusion. Experimental animals were divided into sham-operated group ( sham operation + aCSF), aCSF treatment group(MCAO+aCSF)and ang-(1-7)treatment groups(MCAO+Ang-(1-7))at low(1 pmol·0.5 μl-1·h-1),medium (100 pmol·0.5 μl-1·h-1)or hith(10 nmol·0.5 μl-1·h-1)dose levels.The activity of iNOS in ischemic tissues were measured by iNOS detection kits. Reverse transcription( RT)-PCR was used to determine messenger RNA (mRNA) of the iNOS in ischemic tissues. Results The cerebral ischemic lesion resulted in a significant increase of iNOS expression compared with sham operation group. The high-dose Ang-(1-7) markedly enhanced (iNOS) activity ( 160. 83 vs 116. 75 U/mg, F = 19. 22,P＜0.01; 151.87 vs 113.07 U/mg, F=63.52,P＜0. 01) and gene expression(0.43 vs 0.38, F=21.83,P ＜ 0. 01; 0. 40 vs 0. 35, F = 19.49, P ＜ 0. 01 ) compared with aCSF treatment group at 24 hours and 48hours after reperfusion, whereas medium and low-dose Ang-( 1-7 ) didn't stimulate iNOS activation.Conclusions The obtained results suggest that high-dose Ang-(1-7) upregulate iNOS expression following ischemic stroke.Moreover,overdose Ang-(1-7)(10 nmol·0.5 μl-1·h-1)may have Ang Ⅱ-like effects in iNOS expression increase.

Objective To investigate the expression of endothelin converting enzyme (ECE) mRNA in patients with acute cerebral infarction (ACI) and its clinical significance.Methods Blood samples from 40 patients with ACI (patient group) within 72 hours after the onset of ACI and 28 gender and age-matched healthy subjects (control group) were collected on admission. Plasma concentrations of endothelin-1 (ET-1) as well as the serum levels of cholesterol, triglyceride, low density lipoprotein,high density lipoprotein, apoA1, apoB, lipoprotein a and fasting plasma glucose in each sample were measured and analyzed. Additionally, semi-quantitative RT-PCR was performed to check the ECE mRNA level in the blood cells. European stroke scale (ESS) was used to evaluate ACI patients' neurological deficit on admission.Results (1) ECE mRNA could be detected in every blood sample from either patient group or control group. However, the ECE mRNA level increased significantly in the patient group compared with that in the control group (0.31?0.092 versus 0.25?0.10, t=2.46, P=0.016). (2) The plasma ET-1 concentration in patient group was also significantly higher than that of control subjects (183.27?56.63pg/ml versus 156.47?34.24 pg/ml, t=2.23, P=0.029). (3) Plasma ET-1 concentration was negatively correlated with ECE mRNA level in the control group (r=-0.452, P=0.021). However, the result in the patient group was not the same as the control group. (4) The ET-1 concentration and ECE mRNA level in the patients had histories of hypertension, diabetes mellitus and stroke were not significantly different from those in the patients without these histories. (5) No significant correlation existed between plasma ET-1 concentration and ECE mRNA level and age of the patient, ESS score, fasting plasma glucose and serum lipid. Conclusions ECE mRNA level is significantly increased in the early stage of ACI, which may be associated with the acute-phase reaction of cerebral infarction and may have deleterious effects on the development of neuronal injury. Our results suggest the protective reflection in the endothelin system of normal human body may be disturbed by the onset of ACI. The relationship between ECE mRNA level and neurological deficit degree, stroke risk factors is worthy for further study.

Objective To study the effects of hyperglycemia plasma glucose and insulin intervention on the cerebral injury after ischemia-reperfusion in rats.Methods 160 male SD rats were randomly divided into four groups:sham operation group,normal plasma glucose group,hyperglycemia group and insulin intervention group(40 rats in each group).The rats of hyperglycemia and insulin intervention groups were given STZ to induce hyperglycemia model.All the rats except for those in the sham operation group were subjected to right middle cerebral artery occlusion and then reperfusion.The reperfusion was started at 1 h,6 h,12 h and 24 h after 2 h ischemia.The neurologic functional scores,infarct volume and numbers of neuron apoptosis of the rats were analyzed with the neurological severity score(NSS),TTC staining assay and TUNEL method,respectively after the 2ats wake up.Results Compared with normal plasma glucose group,worse neurological function score,larger infarct size and more number of apoptotic neurons were found in hyperglycemia group at the same reperfusion time(all P