OBJECTIVE:To compare the clinical efficacy and safety of rivaroxaban and low molecular weight heparin calcium (LMWHA)in the prevention of deep venous thrombosis(DVT)after total hip arthroplasty(THA). METHODS:A total of 100 THA patients selected from orthopedics department of our hospital as research objects were divided into control group and observa-tion group according to random number table,with 50 cases in each group. Control group was treated with LMWHA injection 0.4 mL subcutaneously,qd;observation group was given Rivaroxaban tablet 10 mg orally,qd. Both groups received treatment on the first day after surgery,for consecutive 14 d. Coagulation indexes(PT,APTT,Fib,TT,D-D),VAS score,the incidence of DVT and PE were observed in 2 groups. The postoperative bleeding volume and ADR as hematoma and gastrointestinal bleeding were compared between 2 groups. RESULTS:Before treatment,there was no statistical significance in coagulation indexes or VAS scores between 2 groups(P>0.05). After treatment,PT,APTT,TT and D-D levels,VAS scores of 2 groups were decreased sig-nificantly,while Fib levels were increased significantly;VAS score of observation group was significantly lower than that of con-trol group,with statistical significance(P<0.05). There was no statistical significance in coagulation indexes between 2 groups (P>0.05). The incidence of DVT and PE in observation group were 8.00% and 7.50% ,which were significantly lower than 12.00% and 4.00% of control group,with no statistical significance(P>0.05). The postoperative bleeding volume of observation group was(298.31±52.18)mL,which was significantly lower than(327.40±54.20)mL of control group,with statistical signifi-cance(P<0.05). There was no statistical significance in the incidence of hematoma or gastrointestinal bleeding between 2 groups (P>0.05). CONCLUSIONS:Rivaroxaban and LMWHA can significantly improve coagulation state,prevent the generation of DVT after THA. While rivaroxaban is better in shortening pain time without increasing the risk of ADR.

Objective To explore the action mechanism of tauroursodeoxycholic acid(TUDCA)promoting intracellular clearance of Burkholderia pseudomallei(B.pseudomallei)in RAW264.7 macrophages.Methods After TUDCA of different concentrations were used to treat RAW264.7 cells pre-infected with B.pseudomallei for 8 h or not,flow cytometry was applied to detect the apoptosis of the infected and control cells.In addition,another endoplasmic reticulum stress(ERS)inhibitor 4-PBA was used to detect the apoptosis and proliferation of host cells after B.pseudomallei infection with Annexin-V/PI double staining and MTT cell proliferation assay.Furthermore,after transfected with CHOP siRNA,Western blotting and flow cytometry were employed to detect the effect of TUDCA on the expression levels of Caspase-3 and Caspase-12 and the changes in apoptotic rate after B.pseudomallei infection,respectively.Finally,the effect of TUDCA on intracellular multiplication of infected RAW264.7 cells were observed to estimate the CFU value in the presence and absence of CHOP siRNA.Results Under different concentrations of TUDCA,100 or 200 μmol/L TUDCA significantly reduced B.pseudomallei-induced apoptosis in RAW264.7 cells(P＜0.05).Meanwhile,both TUDCA and 4-PBA treatment could decrease the apoptosis induced by B.pseudomallei infection by ERS(P＜0.05).Further,the expression levels of Caspase-3 and Caspase-12 were obviously increased after B.pseudomallei infection compared with uninfected groups,but their expression levels in the siCHOP group was significantly lower than that in the siC group.Besides,flow cytometry also showed that TUDCA could reduce apoptosis induced by B.pseudomallei infection(P＜0.05),but no significant effect of TUDCA on apoptosis was observed under CHOP knockdown.Finally,intracellular CFU assay indicated that TUDCA treatment promoted the host cell clearance of B.pseudomallei(P＜0.05),but no such effect was observed in siCHOP group.Conclusion In B.pseudomallei infected RAW264.7 cells,TUDCA promotes the intracellular clearance of the bacteria by inhibiting ERS-induced apoptosis.