Objective To explore the expression and significance of adhesion molecules ?2 integrin CD11c, CD18 in the polymorphonuclear neutrophils (PMN) and mononuclear leukocytes (MNL) of peripheral blood in patients with acute ischemic stroke (AIS).Methods Using indirect immunofluorescence and adopting a flow cytometry, the expressions of CD11c, CD18 in PMN and MNL in peripheral blood were measured within 72 h and 7 d after onset in 28 patients and 28 healthy controls.Results In AIS group, the expressions of CD11c, CD18 in PMN and MNL within 72 h ( 20.82?5.88, 218.25?89.00, 34.78?14.56 and 286.75?95.50, respectively) and at 7 d ( 18.60?5.52, 185.52?68.44, 31.97?14.47and 247.00?88.06, respectively) were significantly higher than those of normal control group ( 15.63?3.01, 150.76?41.20, 20.20?8.50 and 186.38?52.97, respectively)(all P

Vascular dementia is the primary cause of senile dementia in our country,which is the only preventable type of dementia now.qqais article reviews the advances in research on pathophysiology and imaging of vascular dementia.

Objective To study the protective effects of total glycosides of Pacony(TGP) on acute myocardial infarction in dogs.Methods Thirty domestic dogs were randomly divided into 5 groups(6 in each group): model control group,positive control group(ISM),and TGP groups with doses of 2.0,4.0,and 8.0 mg?kg~(-1),respectively.The descending branch of left coronary artery was ligated to construct the model of myocardial infarction in the anesthetic thoraco-opened dogs.The effect of TGP on epicardium electrocardiogram(EECG),myocardial infarction size(MIS) and serum myocardial enzymes were observed.Results Compared with controls,the ischemia degree(∑-ST,P

Aim An HPLC method was established for the study on pharmacokinetics and bioequivalence of oxaprozin enteric tablet in healthy volunteers.Methods The oxaprozin in plasma was determined using HPLC method following a single oral dose of 400 mg of oxaprozin given respectively to 18 healthy male volunteers in an open randomized crossover design.The pharmacokinetic parameters and relative bioavailability were calculated to evaluate the bioequivalence of 2 preparations.Results AUC_(0-240 h) of oxaprozin tested tablet and reference tablet were(2852.86?871.00)and (2992.84?854.02)?g?L~(-1)?h,C_(max) were(33.48?11.36)and (32.70?7.30)?g?L~(-1),T_(max) were(12.1?5.7)and(13.8?5.8)h,T_(1[]2ke) were(57.11?8.51)and(60.98?7.97)h,respectively.These main pharmacokinetic parameters obtained showed no statistically significant difference between the 2 products.Conclusion The method is simple and sensitive.Both preparations are bioequivalent.

Objective To investigate the mechanism of myocardial ischemia and reperfusion-induced acute lung injury (ALl) and protective effect of ischemic postconditioning.Methods Forty SD rats were allocated to sham group,myocardial ischemia/reperfusion group (reperfusion group),ischemic postconditioning group (postconditioning group),and ischemic postconditioning + phosphatase and tensin homolog deleted on chromosome ten (PTEN) inhibiting group (inhibitor group) according to the random number table,with 10 rats per group.Myocardial ischemia/reperfusion was induced by left anterior descending coronary artery occlusion.Postconditioning was performed within 1 minute before reperfusion consisting of 3 10 s cycles of reperfusion followed by 10 s occlusion.Lung was immediately removed 120 minutes after reperfusion for HE stain,immunohistochemical detection of inflammatory factors and apoptosis factors,TUNEL assay of cell apoptosis,and Western blot of protein kinase B (Akt),phospho-Akt (p-Akt),glycogen synthase kinase-3β (GSK-3β),and phospho-GSK-3β (p-GSK-3β).Results Down-regulated B-cell lymphoma-2 (Bcl-2) and IL-10 and up-regulated Bcl-2 associated X protein (Bax),cysteinyl aspartate specific proteinase-3 (Caspase-3),IL-6 as well as IL-8 were observed in other 3 groups compared with sham group (P ＜0.01).Moreover,down-regulated Bax,Caspase-3,IL-6,IL-8 as well as TUNEL and up-regulated Bcl-2 as well as IL-10 were observed in reperfusion group compared to postconditioning group and tensor group (P ＜ 0.01).No statistical differences were found among the four groups in levels of Akt,p-Akt,and GSK-3β,but level of p-GSK-3β was significantly down-regulated in reperfusion group compared to other 3 groups(P ＜ 0.01).Conclusion Development of ALI may relate to down-regulation of p-GSK-3β evoked directly by the release of inflammation factors in early period of myocardial ischemia/reperfusion and ischemic postconditioning may attenuate the condition.

Objective To evaluate the effects of ischemic postconditioning on brain injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Diabetes mellitus was induced by intraperitoneal streptozotocin 60 mg/kg and confirmed by blood glucose level ＞ 16.7 mmol/L.Thirty male Sprague-Dawley rats,weighing 220-280 g,in which diabetes mellitus was successfully induced,were randomly allocated into 3 groups (n =10 each) using a random number table:group sham operation (group S),group I/R and group ischemic postconditioning (group P).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery in I/R and P groups.Group P received 3 cycles of 10 s reperfusion followed by 10 s ischemia at the end of myocardial ischemia.The rats were sacrificed at 120 min of reperfusion and the brains were removed for microscopic examination and for determination of cell apoptosis (by TUNEL) and expression of interleukin-6 (IL-6),IL-8,IL-10,glycogen synthase kinase-3 beta (GSK-3β) and phosphorylated GSK-3β (pGSK-3β) (by immuno-histochemistry).Apoptotic index was calculated.Results Compared with group S,apoptotic index was significantly increased,IL-6 and IL-8 expression was up-regulated,and IL-10 and pGSK-3β expression was downregulated in I/R and P groups (P ＜ 0.01).Compared with group I/R,apoptotic index was significantly decreased,IL-6 and IL-8 expression was down-regulated,and IL-10 and pGSK-3β expression was up-regulated in group P (P＜0.01).There was no significant difference in GSK-3β expression among the 3 groups (P ＞ 0.05).The pathologic changes were significantly attenuated in group P as compared with group I/R.Conclusion Ischemic postconditioning can attenuate brain injury induced by myocardial I/R in diabetic rats,and inhition of activity of GSK-3β may be involved in the mechanism.

Objective To study the effects of ShaJi on the indexes of oxygen metabolism such as coronary blood flow in myocardium of anesthetized thoraco-opened dogs. Methods Dogs were randomly divided into control group,4 and 16 mg?kg-1 ShaJi groups,and positive control group(n=6).The anesthetized thoraco-opened dog models were set up.The administration of intravenous injection was used by femoral vein.The blood pressure,heart rate and coronary blood flow(CBF) were measured.Coronary resistance,myocardial oxygen uptake rate,myocardial oxygen consumption index and myocardial oxygen consumption were calculated.Results Compared with control group,the CBF was increased (P0.05).Conclusion ShaJi can significantly ameliorate oxygen metabolism in myocardium of anesthetized thoraco-opened dogs.

Objective To investigate the prevalence of Alzheimer's disease (AD) in first-degree relatives of patients with affective disorders,and to evaluate the risk of AD in first-degree relatives of the patients with affective disorders.Methods Patients with affective disorders meeting DSM-Ⅳ-TR criteria (affective disorders group) and their healthy spouses (conrol group) were recruited in this study (n=109 each).The first-degree relatives inclusion criteria were biological relatives of both probands aged over 55 years.Subjects were investigated by neuropsychological assessment,imaging and clinical examinations,and were diagnosed as AD according to the criteria of the United States of America neuropathy language disorders and stroke research institute and Alzheimer's disease and Related Disorders Association (NINCDS-ADRDA).Results 284 first-degree biological relatives of affective disorders patients and 274 first-degree relatives of control group were selected.There were no statistically significant differences in demographic characteristics of the first-degree relatives between the two groups.The prevalence of Alzheimer's disease in the first-degree relatives had a significant difference between affective disorders group and control group [10.6％ (30/284) vs.4.4％ (12/ 274),x2=7.47,P=0.006].The prevalence of AD in the first-degree relatives was higher in bipolar disorder and depressive disorder patients than in control group [11.2％ (14/125) vs.4.4％(12/274),20.0％ (15/75) vs.4.4％(12/274),x2=6.80,20.56,OR=2.60,4.63,both P＜0.05],while there was no significant difference in the prevalence of AD in the first-degree relatives between mania patients and control group [1.1％ (1/87) vs.4.4％ (12/274),x2 =1.99,P＞0.05].Conclusions There is a high risk for Alzheimer' s disease in first-degree relatives of patients with affective disorders,particularly in first-degree relatives of patients with depression and bipolar disorders.

Objective To investigate the effects of ischemic pre- and postconditioning on cerebral glycogen synthase kinase-3 beta (GSK-3β) activity in a rat model of global cerebral ischemia-reperfusion (I/R).Methods Forty male Wistar rats weighing 200-230 g were randomly allocated into 4 groups (n =10 each) : Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPR) and Ⅳ group ischemic postconditioning (group IPO). The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g. Global cerebral ischemia was induced by four-vessel-occlusion in group Ⅱ , Ⅲ and Ⅳ. Bilateral vertebral arteries were cauterized and bilateral carotid arteries were occluded for 10 min. In group IPR cerebral ischemia was preceded by 3 cycles of 10 s ischemia followed by 30 s reperfusion. The group IPO received 3 cycles of 30 s reperfusion followed by 10 s ischemia at the end of 10 min cerebral ischemia. The animals were killed 2 days later. The brains were immediately removed for determination of neuronal apoptosis in the cortex (by TUNEL), the infarct size (by TTC), p-GSK-3β activity (by spectrum assay) and the expression of Bcl-2, Bax and Caspase-3 (by SP). Linear correlation of p-GSK-3β activity with the number of apoptotic neurons in the cortex and cerebral infarct size was analyzed. Results Cerebral I/R significantly increased the number of apoptotic neurons in the cortex and infarct size, decreased p-GSK-3β activity, down-regulated Bcl-2 expression and up-regulated Bax and Caspase-3 expression in group I/R as compared with group S. Ischemic pre- and postconditioning significantly attenuated these cerebral I/R-induced changes. The p-GSK-3β activity was negatively correlated with the number of apoptotic neurons in the cortex and cerebral infarct size. Conclusion Ischemic pre- and postconditioning reduces cerebral I/R injury through inhibiting the activity of GSK-3β.