Objective To observe the expression of uPA, tPA and PAI-1 in whole blood of rat membranous ne-phropathy ( MN) models induced by cationic bovine serum albumin ( C-BSA) , and to explore the effect of fibrinolytic sys-tem on podocyte apoptosis and pathological changes. To explore the possible preventive and therapeutic effects and the pos-sible mechanisms of early prevention of fibrinolysis. Methods We developed a MN model with the modified Border meth-od. At the end of the 1st, 2nd, 3th, and 4th week of immunization, respectively, the levels of whole blood uPA, tPA and PAI-1 were determined by ELISA. The rat kidney tissues were examined by light microscopy and electron microscopy to i-dentify the pathological changes. The expression levels of nephrin and WTl were detected with immumofluorescence staining and their correlation was analyzed. Results Compared the treatment group with control group, the levels of whole blood uPA, tPA and PAI-1 of the model group were decreased, while PAI-1 was elevated, showing a significant difference ( P<0. 05). The degree of renal interstitial fibrosis was more serious. Correlation analysis showed that the whole blood tPA and uPA levels were positively correlated with the changes of nephrin protein expression in the kidney tissue, while the whole blood PAI-1 level was negatively correlated with the nephrin protein expression in the kidney tissue. Conclusions In the process of MN development, the fibrinolytic system may have important significance for podocyte apoptosis. Determination of early phase of MN podocyte injury may be another therapy target for prevention of the disease development, and then pro-vide new ideas for clinical research and drug development for MN.

Objective To investigate the CT perfusion imaging and the pathological features on the disturbance of regional cerebral microcirculation in a pre-infarction period, and to evaluate the relationship between the astrocytes and regional cerebral microcirculation. Methods Dynamic CT perfusion imaging of the models with regional cerebral hypoperfusion and astrocytic swelling in rats was performed to assess the presence or absence of the disturbance of regional cerebral microcirculation. Then, the histopathologic examination was made for both models, respectively. The ratios of side-to-side were measured at hypoperfusion areas in the models of regional cerebral ischemia. Results Regional hypoperfusion was revealed by regional cerebral blood flow (rCBF) and mean transit time (MTT) maps in the group of hypoperfusion for 6 hours. Regional cerebral blood volume (rCBV) and time-to-peak (TTP) maps were normal in that group. The ratios of rCBF, rCBV, MTT and TTP were 0 39-0 55, 0 92-1 00, 1 20-1 50 and 1 00-1 00 respectively. Astrocytic swelling pressing the capillary wall was obvious and subtle neuronal reversible degeneration was occasionally found. TTC stain was normal. In the tACPD group of astrocytic swelling, the abnormal hemodynamic regions on rCBF and MTT maps were found. The rCBV maps of 3 rats in the tACPD group showed the area of reduced rCBV. In 2 rats of tACPD group, the areas of delayed TTP were also found. The ratios of rCBF, rCBV, MTT and TTP were 0 25-0 44, 0 70-1 01, 1 20-2 00 and 1 02-1 45 respectively. TTC stain was negative. Electron microscope study revealed remarkable swelling of astrocytes, especially endfoot processes of astrocytes around capillaries. The abnormal hemodynamic region on rCBF and MTT maps matched with abnormal extent on histopathologic examination. The rCBV and TTP maps appeared normal. Conclusion The astrocytes can react in a way faster than the neurons in the pre-infarction period, viz. astrocytic swelling. The swelling of astrocytic foot, which pressed capillary vessel, induced the disturbance of regional cerebral microcirculation, and then aggravated hypoxic ischemic state in regional brain parenchyma. Perfusion CT and its parameters' analysis may play an increasing role to delineate the reversible hypoperfusion areas in pre-infarction period. Analyzing the relationship of rCBF and rCBV is very helpful to know the status of the capillary vessels in regional cerebral hypoperfusion area.

Objective To study cost-effectiveness of primary cerebral infarction patients. Methods The neural function of primary cerebral infarction patients was studied by the National Institutes of Health Stroke Scale (NIHSS) with rank test and multiple regression analysis. Results After treatment in hospitals of different grades, no obvious difference was detected in the NIHSS score, but difference was found in therapy cost and therapy time; the NIHSS score and therapy time of primary cerebral infarction patients in different attack positions were obviously different, but therapy cost had no significant statistical difference. The NIHSS score of primary cerebral infarction patients with different treatments was obviously different, but therapy cost and therapy time was not. Conclusions Patients are advised to choose grade hospitals in nearby cities for treatment. Clinician are expected to choose low-cost treatment plan to relieve patients' economic burden.

Mitochondrial dysfunction has been implicated in the aetiology of sporadic Parkinson's disease but its role in the disease mechanism remains unclear.To investigate the effect of synuclein on mitochondrial dysfunction induced by rotenone.The human dopaminergic SH-SY5Y cells were used as a cell model.The cells over-expressed the wild-type ?-synuclein were treated with complex I inhibitor rotenone.The cell viability,complex I activity,Mitochondrial swelling and O2-content were tested at different time point-1w,2w,4w after rotenone treated.CCK-8 test results showed that the cell viability of overexpressed ?-synuclein(SH-SY5Y-Syn)was much lower than the control group(SH-SY5Y-Ctr).After administrating with rotenone about 1w or 2w the cell viability of SH-SY5Y-Syn became higher than that of SH-SY5Y-Ctr.On the 4th week the results were contrary to the first 2 weeks.Similar results were got when test the mitochondrial function.In the first 2 weeks after roteoone administrating,the mitochondrial function of SH-SY5Y-Syn was better than that of SH-SY5Y-Ctr.This suggest that the ?-synuclein could protect the mitochondrial against the injury induced by rotenone in the early stage-1w,2w,while this effect disappeared in the final stage-4w.

Child, Preschool ; Coronary Aneurysm ; etiology ; pathology ; Coronary Vessels ; pathology ; Female ; Humans ; Infant ; Male ; Mucocutaneous Lymph Node Syndrome ; complications ; pathology

Animals ; Brain Injuries ; drug therapy ; metabolism ; Cerebral Cortex ; metabolism ; Male ; Malondialdehyde ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Taurine ; pharmacology ; therapeutic use

Objective To observe the effects of recruitment maneuver (RM) and tidal volume with different amount of gas after RM ventilation on lung diastole function in rats with acute lung injury (ALI). Method ALI rat models were induced by intravenous infusion of lipopolysaccharide (LPS) in dose of 6 mg/kg. Twenty-five rats were randomly(random number) divided into control group ( n = 5), ALI group ( n = 5), low tidal volume group (LV group,VT= 6 mL/kg, n = 5), sustained inflation (SI) with low tidal volume (SI+ LV group, VT=6 mL/kg, n = 5), and SI with moderate tidal volume group (SI+ MV group, VT= 12 mL/kg, n = 5). The RM carried out by using SI with airway pressure 30 cmH-2O for 30 seconds, and the positive end-expiratory pressure (PEEP)was set at 5 cmH2O. Lung tissue was taken after mechanical ventilation for 5 hours. The mean arterial pressure (MAP) was monitored throughout the entire course of experiment. Endothelin-1 ( ET-1 ), endothelial nitricoxide synthase (eNOS), and acetylcholine-(Ach-) induced endothelium-dependent relaxation response of isolated pulmonary artery rings were investigated after mechanical ventilation for 5 hours. Results The LPS increased the ET-1 level in lung tissue, decreased the level of eNOS in lung tissue, and impaired the Ach-induced endothelium-dependent relaxation response in pulmonary vassals, without obvious influence on systemic hemodynamics. SI + LV significantly reduced LPS-induced elevation of ET-1 level, and increased the level of eNOS, and significantly lessened endothelial dysfunction and ameliorated dysfunction od endothelium-dependent relaxation in pulmonary vas sals. Conclusions RM with high tidal volume or lowtidal volume ventilation could improve the lung vascular endothelial function of rats with acute lung injury, and RM with low tidal volume ventilation could lessen more the injury of lung vascular endothelial diastole function in rats with acute lung injury.

Adolescent ; Adult ; Benzene ; poisoning ; Female ; Humans ; Male ; Occupational Exposure ; Thrombocytopenia ; chemically induced ; immunology

Objective To explore the changes of Sema3A and it′s receptor Npl in temporal lobe epilepsy(TLE)rat brain and the roles in epileptogenesis mechanism.Methods TLE model was established with male healthy SD rats,in which mossy fiber sprouting(MFS)was verified using Neo-Timm staining method.Sema3A mRNA,Npl mRNA and protein was respectively analyzed by immunohistochemistry and in situ hybridization in the entorhinal cortex(EC)or dentate gyrus(DG)at different time after LiCL-PILO induced TLE.Results There were Mossy fiber sprouting(7d:0.70?0.42,15d:1.50?0.52,30 d:2.20 ?0.41,60 d:2.50?0.51)in DG inner molecular layer(IML)of TLE rat compared with those of controls (P

Objective To analyse the causes of perinatal death and explore the preventive measures to reduce the perinatal mortality.Methods The cases with perinatal death in this hospital from January 2005 to December 2006 were reviewed to analyse the causes of death by categorization and sum-up.Results There were 166 cases with perinatal death and the mortality rate was 27.08‰,including 126 cases with fatal death,which accounted for 75.90%.In the analysis of dead causes,the first one was birth defects,which suffered 69 cases,41.57% of all,and mostly were with fetus edema syndrome.The cord factors had been elevated to the second cause,which suffered 51 cases,30.72% of all.Conclusion Improving the consciousness of gestational monitoring and self-care,strengthening the prenatal diagnosis and genetic counseling,controlling the perinatal birth defects,monitoring mother and fetus by poly-parameter and stopping the pregnancy in time can reduce perinatal death effectively.