Objective: To study the urban and rural difference impacts of aging on health care expenditure. Methods: Using 2002-2011 panel data of 31 provinces throughout the country to build fixed effect models for the urban and rural areas and make comparative analysis. Results: For urban and rural areas, there are significant differences in the impact of aging on health care expenditure, the estimated coefficients are 0.13 and 0.48 respectively. Conclusion:Under the background of the aging process, it needs to strengthen the construction of rural medical insurance system in China, increase financial support and rural health resource allocation.

Objective:To investigate the effects and mechanisms of interleukin-22(IL-22) on inhibiting liver fibrosis induced by HSC,and explore the role of Wnt/β-catenin pathway in the activation of hepatic stellate cells(HSC).Methods:Rat HSC was activated by TGF-β1,and the mRNA and protein levels of β-catenin and α-SMA were detected by q-PCR and Western blot,respectively.HSC was treated with different hours and concentration of recombinant rat protein IL-22.The cell proliferation rates were detected by CCK8,cell apoptosis rates were tested by flow cytometry.HSC were treated with optimal concentration of IL-22 after activated by TGF-β1,the cell proliferation rates,mRNA and protein levels of β-catenin and α-SMA were compared of before and after intervention.Results:The mRNA and the protein levels of β-catenin and α-SMA were significantly increased after activated by TGF-β1(P<0.05).IL-22 inhibiting the proliferation of HSC in a dose-and time-dependent manner (P<0.05) and decreased the mRNA and the protein expression level of β-catenin and α-SMA(P<0.05),but had no significant effect on apoptosis rates(P>0.05).IL-22 significantly inhibited the activation of HSC induced by TGF-β1 and remarkably decreased the mRNA and the protein expression level of β-catenin and α-SMA(P<0.05).Conclusion:The Wnt/β-catenin pathway may participates in the process of HSC activation and α-SMA secretion,and IL-22 inhibits biological function of HSC in a dose-and time-dependent manner.This effect probably via inhibited the Wnt/β-catenin signal pathway.

Objective:To explore the effects and mechanism of anti IL-9 antibody on malignant ascites ( MA) of hepatic carci-noma in mice.Methods:A mouse model of MA was established by mouse H 22 cell line.45 mice were divided randomly into experi-mental group,negative control group and blank control group at 24 hours after modeling,with 15 mice in each group.The experimental group was injected intraperitoneally with anti IL-9 antibody;the negative control group was injected with isotype IgG antibody;the blank control group was injected with normal saline .The weight and behavior of the mice were measured before each injection .Five mice of each group was sacrificed at 24 hours after the last injection to measure the volume of MA .The level of VEGF,MMP-2,IL-9 and IFN-γin MA were determined with ELISA assay;the survival time of rest mice were recorded and compared .Results:The mean volume of MA of experimental group,negative control group and blank control group were (6.70±1.52)ml,(10.28±1.75)ml,(10.36±2.30) ml,respectively,the MA volume of experimental group were lower as compared to negative control group and blank control group ( P<0.05).The mean survival time of experimental group was (17.2±2.1)d,which was significantly prolonged compared with the negative control group (14.5±1.2)d and the blank control group (14.8±1.4)d (P<0.05).The levels of VEGF of MA in experimental group was significantly lower compared to the negative control group and blank control group (P<0.05).The levels of IL-9 of MA in experi-mental group was significantly lower compared to the negative control group (P<0.05).The levels of MMP-2 and IFN-γin experimental group had no significant difference compared with the negative control group and blank control group ( P>0.05 ) .Conclusion:Intraper-itoneal injection anti IL-9 antibody on H22 ascites-bearing mice can effectively inhibit the generation of the MA .The mechanism may be related to the inhibition of the expression of the VEGF and IL-9.

Objective To analyze risk factors of acute respiratory failure(ARF)in patients with hypertriglyceridemia acute pancreatitis(HTG-AP)and construct a risk prediction model.Methods A total of 222 HTG-AP patients were included in this study and divided into the non-ARF group(176 cases)and the ARF group(46 cases)according to diagnostic guidelines for ARF.Clinical data of the two groups were compared and the predictive factors were screened.These selected factors were then utilized in a multivariate Logistic regression analysis to construct a Logistic regression model.Subsequent evaluation of the model′s predictive ability,accuracy and clinical utility was conducted through ROC,curve analysis,calibration plot examination and decision curve analysis(DCA),respectively.Results Compared with the non-ARF group,the levels of high density lipoprotein cholesterol(HDL-C),low density lipoprotein cholesterol(LDL)-C and albumin(ALB)were decreased in the ARF group(P＜0.05),while the levels of creatinine(Cr),urea nitrogen(BUN),aspartate aminotransferase(AST)and C-reactive protein(CRP)were increased,and the incidence of pleural fluid and ascites was also increased(P＜0.05).Multivariate Logistic regression analysis showed that higher levels of Cr and AST,lower levels of ALB,HDL-C and ascites were independent risk factors for HTG-AP complicated ARF(P＜0.05).Based on these results,a column-line prediction model for HTG-AP complicated ARF was established.After internal verification,the area under curve(AUC)of receiver operating characteristic(ROC)curve of the nomogram model was 0.952(95%CI:0.923-0.981),the Youden index was 0.808 and the sensitivity and specificity were 93.33%and 87.43%,respectively.The calibration curve showed that the probability of HTG-AP concurrent ARF predicted by the model was in good agreement with the actual probability.The DCA curve showed that the model had certain clinical value.Conclusion The nomogram prediction model combined could provide a scheme for the clinical prevention of HTG-AP complicated with ARF.