Literature review to build optional indexes pool,Delphi method to screen indexes,fuzzy model used to calculate the weight,for building such a system.An index system centering on public wellbeing is thus constructed,comprising three level 1 indicators,six level 2 indicators,40 level-3 indicators.The system can satisfactorily reflect the vision of county-level public hospitals reform,and showcase outcomes of such a reform.

Objective To explore the clinical application of pereutaneous transluminal angioplasty(PTA) and endovascular bracket to treat lower extremity arteriosclorotic occlusion.Methods The clinical data of 36 patients(41 affected limbs)with lower extremity atherosclerotic occlusion who were treated with PTA and bracket implantation from Jan 2008 to Dee 2008 were summarized.Results The initial successful rate of PTA wag 95.1% (39/41).The clinical symptoms were considerably improved in 37 affected limbs,representing of pain disappearing,skin temperature increasing and the healing of refractory ulcer.The index of ankle to brachial significantly increased from 0.54±0.11 to 0.79±0.15(before v.s.after therapy).However,no improvement was observed in 3 affected limbs,and one affected limb Wag re-operated by the amputation.In the following 3 to 15 months.three superficial femorsI arteries were re-obstructed at the 5th,6th,12th month,respectively.One arteria tibialis pesterior was re-obstructed at the 8th month.The cumulative cure rate was 89.7%(35/39).Conclusions PTA is effective in treating atherosclerotic occlusive diseases.The endovascular bracket can increase the cumulative cure rate.PTA and endovascular bracket are safe and effective in treating lower extremity arteriosclerotie occlusion.

OBJECTIVE: To observe the effects of Qingdan Capsule (QDC) and Yanggan Lidan Granule (YGLDG), two kinds of compound traditional Chinese herbal medicines, on biochemical parameters in guinea-pigs with pigment gallstones. METHODS: An animal model of pigment gallstones was established in male guinea-pigs by hypodermic injection of lincomycin. The guinea-pigs were randomly divided into blank control group, untreated group, QDC group and YGLDG group. There were 8 guinea-pigs in each group. After ten-day treatment, animals were sacrificed and sampled to calculate the rate of stone formation, total bilirubin (TB), unconjugated bilirubin (UCB) and Ca2+ density in bile of the four groups. RESULTS: In comparison with the untreated group, the rates of stone formation in the QDC and YGLDG groups were significantly decreased (P<0.01). TBIL, UCB and Ca2+ content of bile in both QDC and YGLD groups was also significantly decreased (P<0.05, P<0.01). CONCLUSION: QDC and YGLD have good effects on biochemical changes of animal model of pigment gallstone in reversing the lithogenesity of bile by reducing the content of TB, UCB and Ca2+, hence resulting in clinical treatment and prevention of pigment gallstone disease.

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BACKGROUND:Previous studies have reported that rapamycin can affect the proliferation, migration and adhesion abilities of endothelial progenitor cels, but there is no report on the effect of autophagy, as wel as the interaction between autophagy and apoptosis. OBJECTIVE: To observe the effect of rapamycin activated autophagy activation on the proliferation, apoptosis, and cycle of endothelial progenitor cels. METHODS:Density gradient centrifugation was used to obtain mononuclear cels from bone marrow, and the mononuclear cels were inoculated on human fibronectin-coated culture plate.Then after cultured for 7 days the adherent cels colected were the endothelial progenitor cels. Different concentrations of rapamycin (0.01, 0.1, 1 and 10 μg/L) were added and cultured for 24 hours. Western blot was used to detect the LC3-II protein expression and monitor the induction of autophagy, flow cytometry was used to observe the cel cycle progression and apoptosis changes, and methylthiazolyldiphenyl-tetrazolium bromide colorimetric assay was used to observe the proliferation ability. Meanwhile, the ultrastructural changes were observed under transmission electron microscope. RESULTS AND CONCLUSION:Compared with the control group, there was no significant increasing of LC3-II protein expression of endothelial progenitor cels in 0.01 μg/L rapamycin group, and the LC3-II protein expression was in the high level. The LC3-IIprotein expression in the 1 μg/L and 10 μg/L rapamycin groups was higher than that in the control group, but lower than that in the 0.01 μg/L rapamycin group, which indicated that autophagywas particularly active when the concentration of rapamycin was 0.01 μg/L. The apoptosis of endothelial progenitor cels was increased with the increasing of concentration of rapamycin, and the proliferation rate was decreased with the increasing of concentration of rapamycin. The results indicate that activation of autophagy by bapamycin can promote the cel apoptosis, change the cel cycle significantly, and can inhibit the proliferation of endothelial progenitor cels.

Background and purpose:The prognosis in patients with early breast cancer(EBC) was poorly defined by clinical and histopathological features.There were more than 200 genes that might be correlated with development,progression,recurrence and prognosis of breast cancer in the published literature.This study evaluated the prognosis of patients with EBC at molecule level according to the protein expressions of 16 selecting genes(HER2,ER,PR,BCL2,Ki-67,BMYB,Cyclin B1,STK15,MMP11,BAG1,NM23,PTEN,P53,P27,VEGF,PCN A).Methods:The immunohistochemical method was used to detect the protein expressions of these genes in 76 patients with EBC and the statistical analysis was performed by COX proportional hazards model.Results:COX proportional hazard model revealed that BCL2,VEGF and STK15 were independent prognostic factors for patients with EBC.A formula of PI was set up according the three genes.The predictive outcomes with PI were compared with the actual follow-up outcomes in 48 patients with EBC.As a result,the predictive accuracy of good and bad prognosis was 86.67% and 91.67%,respectively.Conclusion:A formula of PI derived from protein expressions of the 16 genes correlated with breast cancer was ultimately set up and might be used to predict the outcomes of the patients with EBC.

Objective To observe the effect of apigenin on acute lung injury (ALI) induced by lipopolysaccharide(LPS)in mice,and to discuss its possible mechanism. Methods Forty healthy male Kunming mice were randomly divided using random number table into control group,model group and low,medium,high dose groups of apigenin intervention,and each group consisted of 8 mice. The model of ALI was reproduced by intraperitoneal injection of 5 mg/kg LPS. Mice of the low,medium and high-dose intervention groups were given intraperitoneal injection of apigenin 10,25,50 mg/kg,respectively,1 hour before LPS modeling. Pathological changes in right upper lobe of lung tissue were examined after hematoxylin and eosin(HE)staining and pathology score was observed at 6 hours after modeling. Right inferior lung was weighed to measured wet/dry ratio(W/D). Intercellular adhesion molecule-1(ICAM-1)and tumor necrosis factor-α(TNF-α)in serum and bronchoalveolar lavage fluid (BALF)were determined by enzyme linked immunosorbent assay(ELISA). The mRNA expressions of p38 mitogen-activated protein kinase(p38MAPK),ICAM-1,and TNF-α were determined by reverse transcription-polymerase chain reaction(RT-PCR). Results Compared with control group,lung W/D ratio in model group was significantly increased(17.79±2.89 vs. 5.56±0.37,P<0.05),and the pathology score was significantly elevated(10.32±0.23 vs. 1.87±0.54,P<0.05),ICAM-1 and TNF-α contents,in serum and BALF were increased〔ICAM-1(ng/L) in serum:21.4±2.7 vs. 14.3±3.5,TNF-α(ng/L)in serum:254.8±10.6 vs. 142.3±13.7;ICAM-1(ng/L)in BALF:20.3±2.4 vs. 11.5±3.2,TNF-α(ng/L)in BALF:230.3±5.8 vs. 110.5±11.2,all P<0.05〕,and the mRNA expressions of p38MAPK,ICAM-1 and TNF-α were also increased significantly(the mRNA expression of p38MAPK,ICAM-1 and TNF-αwere 4.42±0.37,4.89±0.27,3.28±0.13,respectively,all P<0.05). Different doses of apigenin could obviously alleviate the damaging effect to the lung,and the most obvious effect was seen in the medium dose group,in which lung W/D ratio was 13.28±1.21,ICAM-1 in serum was(18.5±4.3)ng/L,TNF-αin serum was(169.4±20.8)ng/L,ICAM-1 in BALF was(17.8±3.5)ng/L,TNF-αin BALF was(150.4±7.1)ng/L, the mRNA expression of p38MAPK,ICAM-1 and TNF-αin lung tissue was 2.99±0.28,3.97±0.17,2.87±0.27, respectively. Statistically significant difference was found when they were compared with that of model group(P<0.05 or P<0.01). Conclusion Different doses of apigenin have some antagonistic effect against LPS in producing ALI in mice,the best improvement effect was seen in the medium dose group,and the protective effect may be related to inhibition of p38MAPK signaling pathway activity and reduction of pro-inflammatory factors such as TNF-αand ICAM-1 expression.

Objective To explore the effects of Dimethyloxalyl Glycine(DMOG)on isehemic acute renal failure(iARF)in mice and its relationship with activation of hypoxia inducible factor 1α(HIF-1α).Method Twenty five C57/BL male mice were divided into 5 groups randomly:control group,DMOG group,sham operation group,ischemia/reperfusion(I/R)group and DMOG pretreated group(DMOG+I/R).Ischemia/reperfusion injury was induced in mice by clamping both renal pedicles for 30 minutes.The expression of HIF-1α was determined by Western blot.Renal function was reflected by blood urea nitrogen(BUN)and serum creatinine(Scr).Morphologic changes were evaluated under light microscopy.Apoptosis in the kidney was detected by TUNEL staining.Expression of Vimentin,a marker of tubulointerstitial damage was detected by immunohistochemistry.Results The elvated levels of of BUN((65.8±2.6) vs (13.6±0.7),P＜0.01],and Scr[(229.5±11.2) vs (6.5±0.8),P＜0.01]andwere found morphological injury were induced by the ischemic insult in I/R group.Administration of DMOG dramatically improved renal function[BUN,(26.3±6.5)vs(65.8±2.6);Scr,(27.0±14.1)vs(229.5±11.2),P＜0.01]associated with amelioration of tubulointerstital damage.In the DMOG treated group,the protein level of HIF-1α in the kidney of mile was also up-regulated significantly.Conclusions The protection against iARF in mice by DMOG administration is mediated by activation of HIF-1α.

Objective To examine the association between residual renal function at initiation of dialysis and prognosis in maintenance dialysis patients.Methods Incident patients with end-stage renal diseases initiating dialysis between 1 January 2005 and 30 September 2009,followed up to 31 March 2010 were enrolled in this study.Residual renal function was evaluated using eGFR estimated by the abbreviated MDRD equation.Patients were classified into four groups according to eGFR of ≥10.5,8 to ＜10.5,6 to ＜8,＜6 ml·min-1·(1.73 m2)-1.The outcome was all-cause and cardiocerebral vascular mortality.Results (1) A total of 562 patients were included.The median eGFR at initiation of dialysis was 5.60 (2.26-12.62) ml·min-1·(1.73 m2)-1.The median follow-up time was 17 (0-58) months from initiation of dialysis and 141 patients died within this period.The median survival time was 45.48 (43.05-47.90) months.With eGFR declined,Scr,BUN,serum uric acid,serum prealbumin,phosphorus,calcium and phosphate product,iPTH,mean arterial pressure (MAP) at initiation of dialysis increased (P＜0.05),and hemoglobin,proportion of male,proportion of diabetes comorbidity,proportion of the Charlson comorbidity index ≥5 decreased (P＜0.05).Though there was no significant difference among the four groups,the proportion of left ventricular hypertrophy comorbidity increased when eGFR declined.(2) There was no significant difference of all-cause mortality among four groups using Kaplan-Meire survival curve.Cox regression model indicated no significant difference of all-cause mortality in levels of eGFR (HR=1.012,95％CI 0.961-1.065,P=0.654).Without patients died in the first 3 months,the multivariate Cox regression model indicated eGFR at initiation of dialysis was the protective factor to 1 year survival (HR=0.791,95％CI 0.669-0.935,P＜0.01).(3) The multivariate Cox regression model indicated the risk of overall and 1 year cardiocerebral vascular death decreased with eGFR at initiation of dialysis increased (HR=0.868,95％CI 0.777-0.971,P＜0.05; HR=0.937,95％CI 0.851-0.992,P＜0.05,respectively).(4) The multivariate Cox regression model indicated eGFR at initiation of dialysis was benefit to survival of patients treated by peritoneal dialysis,with all-cause death risk decreased by 10％ when eGFR increased by 1 ml·min-1·(1.73 m2)-1 (HR=0.90,95％CI 0.81-0.99,P＜0.05).In hemodialysis patients,Kaplan-Meire survival curve was significantly different among the four groups (Log-rank test,P=0.047); the survival of the group of 8 to ＜10.5 ml·min-1·(1.73 m2)-1 was lower as compared to the groups of 6 to ＜8 (Log-rank test,P=0.033) and ＜6 ml·min-1(1.73 m2)-1 (Log-rank test,P=0.005); but the multivariate Cox regression model indicated no relationship between survival and eGFR.In the subgroup of chronic glomerulonephritis as primary renal disease,the eGFR at initiation of dialysis was the benefit factor,with all-cause death risk decreased by 16.6％ (HR=0.834,95％CI 0.736-0.946,P＜0.01) and cardiocerebral vascular death risk decreased by 18.2％ (HR=0.818,95％CI 0.669-0.999,P＜0.05) when eGFR increased by 1 ml ·min-1 ·(1.73 m2)-1.In the subgroup of chronic glomerulonephritis treated by peritoneal dialysis,the all-cause death risk decreased by 32.1％ with eGFR increased by 1 ml·min 1·(1.73 m2)-1 (HR=0.679,95％CI 0.535-0.862,P＜0.01).Conclusions Early initiation of dialysis may not be associated with improved overall survival,but may reduce cardiocerebral vascular and 1 year all-cause mortality,improve the survival of chronic glomerulonephritis patients and peritoneal dialysis patients.

Objective To investigate the effect of proliferation,apoptosis and cell cycle of 3-MA on rat endothelial progenitor cells. Methods Bone marrow-derived mononuclear cells were isolated from rat bone marrow by ficoll. There were five groups. The control group and four 3-MA concentration groups: 1. 25 mmol/L,2. 5 mmol/L,5 mmol/L, 10 mmol/L. MTT was used to measure the proliferation of endothelial progenitor cells. Flow cytometry ( FCM) was used to detect cell apoptosis and cell cycle. Results (1)5 mmol/L 3-MA promotes proliferation of endothelial progenitor cells, while 10 mmol/L 3-MA inhibits the proliferation of endothelial progenitor cells (P ＜ 0. 05). (2) 10 mmol/L 3-MA promotes apoptosis of endothelial progenitor cells, compared with the control, the difference was significant ( P ＜ 0. 05 ). (3) 3-MA at the concentration of 5 mmol/L reduces cells at G0/G1 phase and increases S and G2/M phase cells; 10 mmol/L 3-MA induces endothelial progenitor cells blockade at S phase, G2/M phase cells decreased, compared with the control, the difference was significant (P ＜ 0. 05). Conclusions 5 mmol/L 3-MA promotes the proliferation of endothelial progenitor cells. 10 mmol/L 3-MA inhibits the proliferation and promotes apoptosis of endothelial progenitor cells.