Objective: To elucidate the effect of cervical multi-infarction on memory function. Method: Homogenous microthrombi were injected into internal carotid artery(ICA) through external carotid artery of Sprangue-Dawlay rat to get unilateral,bilateral or recurrent embolic cerebral multi-infarcction model. Water maze and passive-avoidance tests were used to assess the memorial function. Brain histopathological changes were also conducted. Result: Memorial function was severely injured,on the contrast to the pseudo-operational rats. Among the three models, unilateral,bilateral and recurrent ones, recurrent multi-infarction model is the worst on the memorial function, while the bilateral group is worse. Conclusion: Cerebral multi-infarction can cause memorial dysfunction. The degree of memorial function is closely related to the degree of ischemic severity.

Objective To investigate the effects of peroxisome proliferator-activated receptor-? (PPAR?) agonist Pioglitazone on treating the vascular dementia (VD) model.Methods SD rats were randomly divided into the sham-operated group,VD group,Pioglitazone high-dose group [20 mg/(kg?d)] and low-dose group [5 mg/(kg?d)].The VD models were made by modified Pulsinelli four-vessel occlusion method,and each group received corresponding treatment for 7 d.Then,Morris water maze test was applied to examine the place navigation escape latency.The number of PPAR? positive neurons and expression of PPAR? in the cerebral tissue were detected by immunohistochemistry.Results Compared to the VD group,the place navigation escape latencies in the two Pioglitazone treated groups were significantly shorter(all P

Purpose To analyze the perfusion differences of different pancreatic diseases using the low-dose whole organ dynamic volume CT perfusion imaging, and to provide the evidence for the clinical application. Materials and Methods Twenty-eight patients suspected as pancreatic disease were applied by 640 layer volume CT perfusion imaging for the pancreas. Data were collected at the same time of bolus injection of contrast agent, then were analyzed by spatial alignment and perfusion calculation using the perfusion software. The time-density curve, blood perfusion flow diagram and tissue artery blood flow were obtained using the maximum slope method. Results Normal pancreatic tissue (n=9) blood flow was (117.04±12.05) ml/(min?100 ml), pancreatitis organizations (6 cases with acute pancreatitis and 3 cases with chronic pancreatitis) (118.67±37.18) ml/(min?100 ml), pancreatic carcinoma tissue (n=10) was (67.16±18.94) ml/(min?100 ml). There was significant difference among three groups (F=8.59, P<0.001);the difference was demonstrated in pancreatic cancer vs. normal pancreas and pancreatic cancer vs. pancreatitis group (q=3.70, P<0.05), which could be clearly demonstrated by blood perfusion flow diagram. The difference was not statistically revealed pancreatitis and normal pancreas group (q=2.91, P>0.05). The total dose of X-rays in the whole scanning process was 21.5-23.9 mSv. Conclusion Low-dose whole pancreas organ CT perfusion scan can quantitatively analyze the hemodynamic changes in pancreatic disease, which be of great value for evaluating changes in microcirculation during the treatment of pancreatic cancer.

Objective To study the correlation between intermedin 1-53 (IMD 1-53) with hypertension and formation of carotid atheromatous plaques.Methods One hundred and thirty-eight patients with 1-2 degree hypertension admitted to our hospital for carotid ultrasonography were divided into atheromatous plaques group (n =98) and atheromatous plaques-free group (n=40) with 30 subjects undergoing physical examination served as a control group in this study.Their serum IMD 1-53 level,blood pressure,and carotid IMT were measured and compared.Results The SBP [(158.57±13.55)mm Hg and (145.16±14.54)mm Hg vs (125.24±10.64)mm Hg,1 mm Hg=0.133 kPa],DBP[(95.23±5.62)mm Hg and (87.15±4.72)mm Hg vs (80.31±4.62)mm Hg] and carotid IMT[(1.26±0.38)mm and (1.05±0.28)mm vs (0.87±0.38)mm] and serum IMD 1-53 level (7.20±1.62 ng/L vs 5.05±1.85 ng/L,P＜0.01) were significantly higher in atheromatous plaques group and atheromatous plaques-free group than in control group and in atheromatous plaques group than in atheromatous plaques-free group.Conclusion IMD 1-53 is involved in the formation of carotid atheromatous plaques and can resist or delay the formation of carotid atheromatous plaques.

Objective To explore the effect ofhypoxia on CXCR4 expression in N9 microglia cells and the role of CXCR4 in hypoxia-induced N9 cell migration.Methods N9 microglia cells were cultured in normoxia and hypoxia conditions; total cell RNA and protein were prepared,real-time PCR was used to detect the CXCR4 mRNA expression,and Western blotting was employed to detect the protein expressions ofhypoxia-inducible factor-1α (HIF-1α) and CXCR4.After cells were transfected with siRNA targeting HIF-1α or CXCR4,the CXCR4 expression was detected again.The migration ability of N9 cells in normoxia and hypoxia conditions were detected by Transwell assay.After cells were treated with CXCR4 siRNA,the migration ability of N9 cell in hypoxia was measured again.Results As compared with cell cultured in normoxia condition,the CXCR4 expression was significantly increased as compared with cells cultured in hypoxia condition (P＜0.05); however,the hypoxia-induced CXCR4 up-regulation was prevented by HIF-1α silencing.The migration ability of N9 cells in hypoxia condition was significantly higher than that of cells cultured in normoxia condition (number of transmembrane cells:(63.00±5.57) and (20.33±2.08),respectively,P＜0.05); however,the N9 cell migration ability promoted by hypoxia was obviously inhibited by CXCR4 silencing (number of transmembrane cells:63.00±4.00 in si-Control cells and 19.33±3.21 in CXCR4 siRNA cells,P＜0.05).Conclusion Hypoxia can promote the migration ability of N9 cells through inducing CXCR4 expression.

Objective To investigate the role of Notch signaling in hypoxia-induced pro-inflammatory cytokine secretion in N9 microglia by inhibiting Notch signaling with a γ-secretase inhibitor,DAPT.Methods N9 cells cultured in vitro were divided into normoxia group,normoxia+10 μmol/L DAPT treatment group,hypoxia group and hypoxia+10 μmol/L DAPT treatment group;10 μmol/L DAPT was added to the media of treatment groups;normoxia group and hypoxia group were added the same amount of solvent.Then,cells in the hypoxia group and hypoxia+10 μmol/L DAPT treatment group were changed into hypoxia conditions (3％ O2) for 12 h.The mRNA and protein were extracted among the four groups;real-time PCR was used to observe the mRNA expression levels of interleukin (IL)-6,IL-1 β and tumor necrosis factor (TNF)-α,Western blotting was applied to detect the protein levels of N1ICD,Hes1 and Hey1,and ELISA was used to determine the secretion levels of IL-6,IL-1 β and TNF-α among four groups.Results DAPT had an inhibitory effecton mRNA expression and protein secretion of the inflammatory cytokines IL-6,IL-1β and TNF-α,and the inhibition effect gradually increased with the increase of DAPT doses.As compared with those in the normoxia group,the mRNA and protein secretion levels of IL-6,IL-1 β and TNF-α and Notch signaling molecules N1ICD,Hes1,Hey1 protein levels were significantly increased in the hypoxia group (P＜0.05).As compared with those in the hypoxia group,the mRNA and secretion levels of IL-6,IL-1β and TNF-α and Notch signaling molecules N1ICD,Hes1,Hey1 protein levels were significantly decreased in hypoxia+DAPT group (P＜0.05).There were no significant differences in the mRNA and protein secretion levels of IL-6,IL-1β and TNF-α and Notch signaling molecules N1ICD,Hes1,Hey1 protein levels between normoxia group and nomoxia+DAPT group (P＞0.05).Conclusion Notch signaling mediates hypoxia induced pro-inflammatory cytokine secretion in microglia.

Objective To explore the role ofperoxisome proliferator-activated receptor (PPAR)-γ in hypoxia-induced secretion of inflammatory cytokine and migration of N9 microglia cells by activating PPAR-γsignaling with pioglitazone and its mechanism.Methods N9 microglia cells cultured in vitro were divided into normoxia group,hypoxia group,pioglitazone+hypoxia group and T0070907 (PPAR-γ pathway inhibitor)+pioglitazone+hypoxia group.Total cell RNA and protein were prepared,Western blotting was employed to detect the protein expressions of hypoxia-inducible factor-1 (HIF-1α).Real-time PCR was used to detect the interleukin (IL)-1 β,IL-6 and TNF-α mRNA expressions.The migration ability of N9 cells was detected by Transwell assay.The HIF-1α protein expression in N9 cells was detected by immunofluorescence.Results As compared with cells from normoxia group,cells from the hypoxia group had significantly increased HIF-1α protein expression,markedly enhanced migration ability and significantly increased mRNA levels of IL-1β,IL-6 and TNF-α (P＜0.05).As compared with those in the cells from the hypoxia group,the HIF-1α protein expression,migration ability and IL-1β,IL-6 and TNF-α mRNA levels were significantly decreased in the cells from pioglitazone+hypoxia group (P＜ 0.05).T0070907+pioglitazone+hypoxia group had significantly increased HIF-1α protein expression,migration ability and IL-1β,IL-6 and TNF-o mRNA levels as compared with pioglitazone+hypoxia group (P＜0.05).Conclusion Activation of PPAR-γ pathway could inhibit the hypoxia-induced secretion of inflammatory cytokine and migration ability of N9 microglia cells via down-regulation of HIF-1α protein and IL-1β,IL-6 and TNF-α mRNA expressions.