Objective:To investigate the anti-gout capsule ( AGC) effect on acute gouty arthritis ( AGA) rat tumor necrosis factor-α(TNF-α)level.Methods: Selected 60 SD rats,were randomly divided into normal group,model group,colchicine group(0.8 mg/kg),AGC low dose group (0.3 g/kg) and AGC high dose group (1.2 g/kg),12 rats in each group,detected each group articular cartilage,serum and synovial fluid TNF-αcontent,observed rats ankle swelling.Results: The model group 24 h,48 h gait behavior scores were(2.57±0.43)point and(2.11±0.50)point,significantly higher than other groups (P<0.05);colchicine group,AGC low dose group and AGC high dose group 24 h,48 h gait behavior score were significantly lower than that of model group (P<0.05).The model group began to swell after modeling 2 h,reached the peak at 12-24 h.The rats in the modeling 72 h each period ,the model group ankle swelling rate were significantly higher than the normal group , the difference was statistically significant ( P<0.05 ) .Colchicine group 12 h,24 h and 48 h ankle swelling rate was significantly lower than that of model group ( P<0.05 ) ,AGC high dose group 12 h,24 h,48 h and 72 h ankle swelling rate was significantly lower than that of model group ( P<0.05 ) ,AGC low dose group ankle swelling rate was lower than that of the model group only in 24 h ( P<0.05 ) .The model group articular cartilage TNF-αexpression significantly increased compared with normal group ( P<0.05 ) ,but model group and colchicine group difference were no statistically significant ( P>0.05 );AGC high dose group and low dose group articular cartilage TNF-αexpression significantly decreased than model group ( P<0.05).The model group serum and synovial fluid TNF-αcontent were significantly higher than the normal group (P<0.05);colchicine group,AGC low dose group and AGC high dose group serum and synovial fluid TNF-αcontent reduced compared with the model group (P<0.05);AGC low dose group and AGC high dose group serum TNF-αwere(0.81±0.27)ng/ml and(0.79±0.31)ng/ml,lower than the colchicines group ( P<0.05 ).Conclusion:AGC can significantly improve the joint symptoms of AGA rats ,decrease AGA rats articular cartilage tissue ,serum and synovial fluid TNF-αlevel.

Objective Recent.studies have found a strong association of insulin resistance, which might occur during ischemia reperfusion in vitro in the experimental dogs, with disturbed function of cardiomyocytes. Obvious acute insulin resistance, along with glucose dysmetabolism in the reperfused cardiomyocytes, was furher observed in the study performed with ischemia-reperfused ventric- ular myocytes of rats. We tried to investigate preliminarily the molecular mechanisms of insulin resistance in the cardiomyocytes after ischemia reperfusion. Methods An experimental model of insulin-stimulated ischemia reperfusion (SI/R) was created by isolating cardiomyocytes from adult rats. Glucose uptake of the cardiomyoctyes was evaluated with isotope-labeling technique. Glucose trans- porter 4 (GLUT4) translocation induced by insulin was investigated with Western blot analysis, and the intracellular level of free Ca2+ ([Ca2+]I) was measured quantitatively with Ca2+ indicator Fura-2. Results Insulin can stimulated glucose uptake by cardiomyo- cytes, indicating that these cells were insulin-sensitive. Cardiomyocytes were demonstrated notable acute insulin resistmce during reperfusion. Insulin-stimulated GLUT4 translocation in the cardiomyocytes 15 minutes after reperfusion was 72.2% of that in the con- trol group(P<0.05), in which the GLUT4 content in plasma membrane remained unchanged. The finding suggested that a disturbed GLUT4 translocation might happen in the cardiomyocytes during insulin-stimulated ischemia-reperfusion. Calcium overload was identi- fied in the cardiomyocytes with ischemia reperfusion. At 15 minutes of reperfusion, [Ca2+]I was significantly higher in the reperfused cardiomyocytes than that in the control cardiomyocytes[(318.66±23.06)vs(130.70±0.82) nmol/L, P<0.05], and kept at a higher level [(177.79±17.46) nmol/L] at 60 minutes of reperfusion (P<0.05, vs control). Partial correlation analysis revealed a negative correlation of[Ca2+]I with insulin-induced ghcose uptake in the cardiomyoctyes (r = -0.557,P=0.006). Conclusion Disturbed GLUT4 translocation and decreased intrinsic activity may be important molecular mechanisms for the development of insulin resistance in the cardiomyocytes of rat during insulin-simulated ischemia reperfusion,. [Ca2+]I overload may account for the de- creased intrinsic activity d GLUT4.

Objective To discuss pathogens findings in children with severe pneumonia.Methods Bacteria was detected by using sputum culture and blood culture in sterile culture media.Viruses and atypical pathogenic antibodies were detected by using indirect immunofluorescence.Influenza A (H1N1) virus RNA were tested using RT-PCR.According to the results of bacterial culture and drug sensitive test,we can guide the use of antibiotics,and individualize treatment was carried out,including anti-inflammatory,organ function support.Results Bacteria was found in 69 children by using sputum culture.Gram negative bacteria accounted for 57.47％.Gram positive bacteria accounted for 42.53％.Escherichia coli(14.94％),Haemophilus influenzae (20.96％) and klebsiella pneumoniae(13.79％) were the main strains of Gram negative bacteria,Staphylococcus aureus (21.84％)and Streptococcus pneumonia(16.1％)were the main strains of Gram positive bacteria.Bacteria was found in 7 (8.00％) children by using blood culture.Virus were identified in 11 out of 123 patients,including 2 cases of respiratory syncytial virus antibody positive,2 cases of adenovirus antibodies positive,4 cases of influenza B virus antibody positive,2 cases of parainfluenza virus antibody positive and influenza A(H1N1) virus from only one case,Mycoplasma pneumonia agents were identified in 8 patients.Eighty-nine children (72.36％) complicated with sepsis,85 children (69.11％) with respiratory failure,48 children (39.02％) with gastrointestinal dysfunction,32 children (26.02％) with heart failure,18 children(14.63％) with septic shock,13 cases (10.57％) with toxic encephalopathy,5 children (4.07％) with disseminated intravascular coagulation.Among them,17 children (13.82％) complicated with multiple organ dysfunction syndrome.In the 123 children with severe pneumonia,46 cases (37.4％) were cured,73 cases (59.35％) improved,and 4 cases died (3.25％) with critical multiple organ dysfunction syndrome.Conclusion The detection rate of pathogen is high in this study.We should pay more attention to individualize therapy for complication,so that the cure rate could be increased.

Objective:To investigate the efficacy of Silybinin meglumine on hepatic fibrosis rats and possible mecha -nisms.Methods:The liver fibrosis rats were randomly divided into 4 groups,the model group,Silybinin meglumine 120 mg/kg group, Silybinin meglumine dose group 60 mg/kg and Silybinin meglumine low dose group 30 mg/kg,and the control group.All groups had been treated for 4 groups.Results:No deaths rat.Compared with the control group ,the reduced body weight ,less dynamic,dark hair, decreased liver and spleen indexes ,increased ALT,AST,TBIL,TG,TC and LDLC,and the decreased ALB, and the increased LXRαand SREBP1c had been observed in the model group (P<0.05).Compared with the model group ,better activity and body weight ,the in-creased liver and spleen indexs decreased ALT ,AST,TBIL,TG,TC and LDLC,and the increased ALB , and the decreased LXRαand SREBP1c had been observed in the Silybinin meglumine groups (P<0.05),in a way of dose-depended.Conclusion: The Silibinin meglumine can treat liver fibrosis ,by improving liver function,lowing lipid and decreaseing LXRαand SREBP1c expression in liver tis-sue.But the mechanism of two proteins reduced remains for further investigation .

0.05,vs control).Insulin stimulated glucose transport into cardiomyocytes in a dose-dependent fashion.Glucose uptake stimulated by insulin into cardiomyocytes was both decreased significantly in 15 mins reperfusian group and in 60 mins reperfusion group (P

Mechanical environment seems to be one of the most important surviving environment for vessel conduit and vascular endothelial cells(ECs), while adhesion is one of the most important physical characteristics of ECs. In this study, Flow chambers of steady laminar and turbulent flow are made and improved. Different flow-derived VCAM-1, ICAM-1 expressions are detected by laser confocal microscope. Spacial and temporal curves of the adhesion molecules are protracted. In laminar flow, expression of VCAM-1 is dramatically elevated, whereas the expression of ICAM-1 is transiently elevated and it immediately falls back to the baseline. In turbulent flow, expression of VCAM-1 declines, while expression of ICAM-1 slowly rises to a peak. These results indicate that such pathological flow field as turbulence exerts different influence on the adhesion of vascular ECs from laminar flow, and turbulence could be one of the most important reasons of the ECs structural and functional lesion.
Cell Adhesion ; Cells, Cultured ; Endothelium, Vascular ; cytology ; metabolism ; Epithelial Cells ; cytology ; metabolism ; Humans ; Intercellular Adhesion Molecule-1 ; biosynthesis ; Microscopy, Confocal ; Stress, Mechanical ; Umbilical Veins ; cytology ; Vascular Cell Adhesion Molecule-1 ; biosynthesis

In mankind, the circulation system is a closed pressure-loaded system; the pressure in circulation flow field would change with the variation of natural or pathological geometry of the local bloodvessel, and the pressure shift induced by the variation of vascular geometry would lead to a series of physiological and pathological changes in the endothelial cells (ECs). This experiment is designed to elucidate the effects of different pressure shift on F-actin alignment and expression in cultured endothelial cells in vitro, and to investigate the relationship between the altered pressure shift and the expression intensity of Vascular adhesion molecule (VCAM) and Integrin alphaVbeta3. Non-activated cultured ECs and single shear stress loaded ECs as control group were set, the double-immuno-fluoro-cytochemistry, laser confocal scanning microscopy and image analysis system were used to observe the expression of VCAM, Integrin alphaVbeta3 and F-actin in endothelial cells which were exposed to levels of pressure shift in an improved parallel plate flow chamber. When exposed to different decreased pressure shift, the expression intensity of VCAM, Integrin alphaVbeta3 and F-actin showed regular changes. The decreased pressure shift resulted in changes in cell alignment and cytoskeleton F-actin, and also affected ECs adhesion function and transmembrane mechanotransduction function which were represented by VCAM and Integrin alphaVbeta3 respectively.
Actins ; genetics ; metabolism ; Cell Adhesion ; Cells, Cultured ; Endothelial Cells ; cytology ; metabolism ; Hemodynamics ; Humans ; Integrin alphaVbeta3 ; genetics ; metabolism ; Pressure ; Umbilical Veins ; cytology ; Vascular Cell Adhesion Molecule-1 ; genetics ; metabolism

To understand the local hemodynamics of modified TF-AHCB carotid bifurcation model, using particle image velocimetry technique to measure the instantaneous velocity distribution of the model attatched to a circuit. The velocity was controlled by regulating the height of the reservoir. The working fluid consists of glycerine and water mixture with viscosity of 3.75 mPa.s similar to human blood. Instantaneous velocity fields were obtained by PIV and the shear stresses were calculated according to the velocity. The results showed that inside the model, there were a large flow separation and an anticlockwise rotating vortex on the lateral wall of ICA, The location and distance of the vortex changed with the flow velocity. The higher the flow velocity, the smaller the vortex distance, and the farther the location. The shear stresses on the lateral wall were significantly lower in all work condition. And there a low shear stress kernel when the velocity was lower than 0.839 m/s. The location of the low shear stress was just the position of atherosclerosis. The flow pattern inside the model consists of large flow separation and vortex zones. And there are low shear stress zones at the lateral wall of ICA, Where are thought to be associated with the genesis of atherosclerosis.
Blood Flow Velocity ; Carotid Arteries ; physiology ; Models, Cardiovascular ; Pulsatile Flow ; Regional Blood Flow ; physiology ; Rheology ; methods ; Stress, Mechanical

OBJECTIVE: To investigate a revision of the Trauma and Injury Severity Score (TRISS) weight coefficients in order to overcome the inference from foreign coefficients on Chinese trauma scoring. METHODS: The data of 1 297 Chinese trauma patients were studied for trauma scoring with the Revised Trauma Score-Injury Severity Score-TRISS (RTS-ISS-TRISS) system to get a serial of new weight coefficients through analyzing a multivariation logical regression between the outcome and the injury severity. RESULTS: ISS was higher but the Age Score and probability of survival (Ps) of the death group were lower than those of the survival group. New values of RTS-ISS-Age coefficients differed from the Major Trauma Outcome Study (MTOS) ones, through which the constant b(0) decreased its negative value, and ISS weight b(2) increased its negative value, but RTS weight b(1) and age weight b(3) changed with the trauma types. MTOS's values and new values of weight coefficients were used on 1297 patients for prognosis by calculating Ps. The accuracy of new values (90.13%) was a little higher than that of MTOS's (89.5%), with a promotion in specialization but a loss in sensitivity. CONCLUSIONS: A revision of TRISS's weight coefficients is either necessary or feasible. To achieve this purpose, a Chinese trauma database with large capacity is recommended.

Objective: To establish an animal model of hypoxia-induced bronchopulmonary dysplasia asso-ciated with pulmonary hypertension (BPD-PH). Methods: C57BL/6 male and female specific pathogen free mice mated and female mice with their offspring mice were randomly divided into normoxic group and hypoxia group by way of numerical method.Normoxic group was placed in the indoor environment directly.Hypoxia group was placed in 120 mL/L oxygen concentration environment within 12 hours after birth.Body weight gain and mortality of the neonatal mice were recorded.The mice lungs and hearts were harvested on day 14 for immunofluorescence staining and HE staining, and Western blot was used to observe the morphological changes and vascular endothelial growth factor (VEGF) protein level. Results: The mortality rates of normoxic group and hypoxic group were 11.8% and 47.3%, respectively.Compared with the normoxic group, body weight of hypoxia group increased slowly, as the final body weight of 2 groups were (12.40±2.33) g and (5.50±0.32) g, respectively, and the difference was significant (χ²=13.38, t=20.50, all P<0.01). Hypoxia group showed higher right ventricular hypertrophy index [(96.00±0.15)% vs.(40.40±4.00)%, t=41.67, P<0.01], fusion of alveolar, diminished microvasculature, thickening alveolar septal, decreased alveolar radiation coefficient (RAC)(19.73±2.33 vs.10.90±1.85) and increased mean linear intercept(MLI) (33.2±4.33 vs.58.70±7.27) with statistical significance, respectively (t=16.27, 9.53, all P<0.01). In the lung HE staining, pulmonary arterial thickening, pulmonary smooth muscle cell proliferation and intimal roughness in immunofluorescence, significantly decreased expression of VEGF protein level by Western blot were observed in hypoxic group (0.41±0.04 vs.1.19±0.08, t=15.10, P<0.01). Conclusions Hypoxia-induced mouse BPD-PH model was consistent with the pathophysiological process of pulmonary vascular remodeling of pulmonary hypertension, which increase pulmonary vascular resistance eventually leading to right ventricular hypertrophy.