Objective:To analyze the effect of global budget of New Rural Cooperative Medical System (NCMS) on the per-visit inpatient compensations,inpatient compensation ratios,per-visit inpatient out-of-pocket expenses and inpatient out-of-pocket rates.Methods:The difference in difference method was used to control the non-intervention factors and estimate the net impact of global budget.Results:Global budget of NCMS decreased the per-visit inpatient compensations by 14.37 yuan,but it had no statistical significance.The compensation ratio of hospitalization increased by 5.23％,the average hospitalization self-payment decrease by 141.51 yuan,the self-payment decreased by 5.23％,which all had statistical significance while there were differences on the effects for specific diseases.Conclusion:Global budget of NCMS increased the inpatient benefit,but the effect was varies by conditions.In addition,measurement of global budget's standard still needed to be scientific and reasonable.

Objective To determine the role of activated status of peroxisome proliferator-activated receptorγ/nuclear factor-κB ( PPAR-γ/NF-κB ) in coagulation disorders induced by sepsis. Methods Forty male Sprague-Dawley ( SD ) rats were randomly divided into four groups, n = 10 in each group: control group, lipopolysaccharide ( LPS ) challenged group, rosiglitazone ( ROSI, selective agonist of PPAR-γ) pretreatment group, and GW9662 ( PPAR-γ antagonist ) pretreatment group. The sepsis model was reproduced by injection of 6 mg/kg LPS via sublingual vein, and the rats in control group were injected with 2 mL/kg normal saline. The rats in ROSI pretreatment group were given 0.3 mg/kg ROSI by sublingual venous injection followed by injection of LPS 30 minutes later;and in GW9662 pretreatment group rats were given 0.3 mg/kg GW9662 by sublingual venous injection followed by 0.3 mg/kg ROSI 15 minutes later, followed by injection of LPS 30 minutes later. Blood was collected at 4 hours after LPS administration, and the expressions of PPAR-γ and NF-κBp65 in peripheral blood mononuclear cell ( PBMC ) were determined with immunocytocheminal technique and graph analysis. Plasma prothrombin time ( PT ), activated partial thromboplastin time ( APTT ), fibrinogen ( FIB ), and D-dimer were determined simultaneously. Results① PPAR-γ/NF-κB pathway: the expressions of PPAR-γ and NF-κBp65 were lowered in control group, and they were expressed in cytoplasm. In LPS challenged group the expression of PPAR-γ ( gray value ) was slightly increased but with no significant difference as compared with control group ( 111.01±4.06 vs. 98.46±5.99, P >0.05 ). In ROSI pretreatment group the expression of PPAR-γ( gray value ) was significantly higher than that in LPS challenged group ( 214.38±5.79 vs. 111.01±4.06, P<0.01 ), with dislocation into nuclei. In GW9662 pretreatment group the expression of PPAR-γ ( gray value ) was lowered but without significant difference compared with that of control group ( 44.21±2.64 vs. 98.46±5.99, P>0.05 ). In LPS challenged group the expression of NF-κBp65 ( gray value ) was significantly higher than that in control group ( 249.48±6.86 vs. 105.81±10.19, P < 0.01 ), and it was translocated into the nuclei. In ROSI pretreatment group the expression of NF-κBp65 ( gray value ) was significantly lower than that in LPS challenged group ( 102.47±8.05 vs. 249.48±6.86, P < 0.01 ), and it lied in cytoplasm. In GW9662 pretreatment group the expression of NF-κBp65 ( gray value ) showed no significant difference as compared with that of LPS challenged group ( 214.84±7.91 vs. 249.48±6.86, P>0.05 ).②Coagulation:compared with control group, PT and APTT were significantly prolonged, FIB was significantly decreased, and D-dimer was significantly increased in LPS challenged group [ PT ( s ):18.32±2.03 vs. 12.22±1.38, APTT ( s ):40.05±2.72 vs. 26.64±2.73, FIB ( g/L ): 1.65±0.51 vs. 3.60±0.37, D-dimer ( mg/L ): 2.58±0.73 vs. 0.37±0.06, all P < 0.01 ]. Compared with LPS challenged group, APTT and PT were significantly shortened, FIB was significantly increased, and D-dimer was significantly lowered in ROSI pretreatment group [ PT ( s ):13.93±1.67 vs. 18.32±2.03, APTT ( s ):30.29±0.86 vs. 40.05±2.72, FIB ( g/L ):3.18±0.69 vs 1.65±0.51, D-dimer ( mg/L ):0.40±0.12 vs. 2.58±0.73, all P<0.01 ]. All parameters in GW9662 pretreatment group showed no significant difference as compared with those of LPS challenged group. Conclusions PPAR-γagonist ROSI may ameliorate coagulation disorders in septic rats. PPAR-γ/NF-κB transduction pathway plays an important role in septic coagulopathy.

Objective To investigate the central neurotoxicity induced by nucleoside analog reverse transcriptase inhibitors (NRTIs)-stavudine (D4T).Methods Mouse primary cortical neurons were cultured and treated with different concentrations of stavudine.Neuron apoptosis was analyzed by calcein/acetomethoxy/propidium iodide (AM/PI) staining. Morphological change of neuron was confirmed by immunofluorescence.Mitochondrial DNA copies which were usually evaluated through Cycloxygenase 2 (COX-2) and thymidine kinase2 (TK2) mRNA were determined by real-time quantitative polymerase chain reaction.Chi-square test,student t test and Wilcoxon nonparameter test were used to analyze the data.Results Neuronal apoptosis observed in 50 μmol/L D4T treatment group was more significant than that in 0μmol/L D4T treatment group and 25 μmol/L D4T treatment group (51.3％±12.4％ vs 24.9％±8.2％ and 26.5％±10.6％,respectively; x2 =7.25 and 6.93,respectively; both P＜0.01).The average neurite numbers of each neuron were 11.2±3.6 in 0μmol/L D4T treatment group,8.6±2.8 in 25 μmol/L D4T treatment group and 4.3±2.4 in 50 μmol/L D4T treatment group.The difference was statistically significant between 25 μmol/L D4T treatment group and 0 μmol/L D4T treatment group (t=4.06,P＜0.01) and between 50 μmol/L D4T treatment group and 25 μmol/L D4T treatment group (t =4.35,P＜ 0.01). Furthermore,the average lengths of neuritis were (319.9±100.2) μm in 0 μmol/L D4T treatment group,(298.3±83.9) μm in 25 μmol/L D4T treatment group and (258.4±82.2) μm in 50 μmol/L D4T treatment group.The difference was statistically significant between 25 μmol/L D4T treatment group and 0 μmol/L D4T treatment group (t=4.58,P＜0.01) and between 50 μmol/L D4T treatment group and 25 μmol/L D4T treatment group (t=4.65,P＜0.01).TK2 mRNA expression dramatically decreased along with the increasing D4T concentration.The fold changes were 0.34 in 25 μmol/L D4T treatment group and 0.08 in 50 μmol/L D4T treatment group. The difference was statistically significant between 25 μmol/L D4T treatment group and 0μmol/L D4T treatment group (Z=- 3.28,P＜0.01) and between 50 μmol/L D4T treatment group and 25 μmol/L D4T treatment group (Z=-4.25,P＜0.01).Compared with 0μmol/L D4T treatment group,the relative fold changes of COX-2 copies were 1.01 in 25 μmol/L D4T treatment group and 1.12 in 50 μmol/L D4T treatment group.The differences were not significant among the three groups (Z=0.98 and 1.24,respectively; both P＞0.05).Conclsion It suggests that short-term exposure to D4T may result in neuron apoptosis,neurite shrink and down-regulated expression of TK2,but the level of mitochondrial DNA copies keeps stable.

AIM: To investigate the effect of dapagliflozin on myocardial injury in type 1 diabetes mice and its mechanism. METHODS: Normal C57BL / 6J male mice were randomly divided into normal control group (Control), diabetes cardiomyopathy group (DCM) and dapagliflozin group (DAPA). The model of diabetes was induced by streptozotocin (STZ) and given maintenance feed. DAPA group was given 10 mg · kg