AIM: To study the effects of oxidative modification lipoproteins on blood coagulation and fibrino (lysis) in vitro. METHODS: Normal human plasma VLDL, LDL and HDL, which were isolated by density gradient ultracentrifugation method, were oxidatively modified by Cu~(2+) and HOCl method. N-VLDL, Ox-VLDL, N-LDL, Ox-LDL, N-HDL, Ox-HDL were added to the reaction system which consisted of mixed fresh normal plasma respectively, prothrombin time (PT), activated partial thrombplastin time (APTT), plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (t-PA) and platelet aggregation were measured according to the direction of the kits. RESULTS: The relative electrophoretic mobility (REM), absorbance at 234nm and TBARS of oxidized VLDL, LDL and HDL mediated by HOCl or Cu~(2+) were significantly higher than that of the control group (P

Objective To explore the efficacy and adverse reactions of diminishing scheme of cefaclor sustained re-lease tablets in the treatment of recurrent urinary tract infection(RUTI).Methods 60 RUTI patients in a hospital were divided into treatment group(n=30)and control group (n=30),patients in treatment group were treated with diminishing scheme of cefaclor sustained release tablets,patients in control group were treated with diminishing scheme of levofloxacin tablets,clinical therapeutic efficacy and adverse reactions of two groups were observed. Results The curative rate in treatment group was higher than control group ([80.00%,n =24]vs [53.33%,n =16])(χ2 =4.80,P =0.028).The incidence of RUTI in treatment group was lower than control group ([6.67%,n=2]vs [26.67%,n=8])(χ2 =4.32,P =0.038).Incidence of adverse reactions in treatment group was lower than control group (16.67% vs 50.00%)(χ2 =7.50,P =0.006).Conclusion The diminishing scheme of cefaclor sus-tained release tablets in the treatment of RUTI has good curative efficacy,low recurrence rate,fewer adverse reac-tions,and can be used for the treatment of recurrence of RUTI.

Objective To observe the interfering effect of different doses of penehyclidine hydrochloride (PHC) on the mRNA expressions of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the lung tissue of rats with traumatic shock so as to investigate the protective role of PHC in secondary long injury following traumatic shock and the underlying mechanism.Methods The traumatic shock model was established.A total of 104 Wistar rats were randomly divided into four groups:control group,shock group,low dose PHC group ( P1 group) and high dose PHC group ( P2 group).At the beginning of resuscitation,the rats in P1 and P2 groups were given transjugular intravenous injection of 2 ml/kg isotonic saline containing 0.15 mg/kg and 0- 45 mg/kg PHC respectively,while the rats in shock and control groups were injected only isometric isotonic saline.The rats in the four groups were killed at 2 h,6 h,12 h and 24 h after resuscitation respectively to detect the mRNA expressions of NF-κB and iNOS by using RT-PCR and determine the lung wet/dry weight (W/D) ratio,lung permeability index (LPI) and lung injury score (LIS).Results The mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS at all the time intervals in the shock,P1 and P2 groups were all significantly increased as compared with those in the control group (P＜0.05).Howerver,the P2 group showed significant reduction in aspects of the mRNA expressions of NF- κB and iNOS,lung W/D ratio,LPI and LIS at all time points and P1 group also had significant decrease regarding the mRNA expressions of NF-κB and iNOS,lung W/D ratio at2 h,6 h,and LPI and LIS at 2 h,6 h,12 h,as compared with the shock group.Meanwhile,P2 group showed evident decrease at 6 h concerning the mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS as compared with P1 group (P ＜ 0.05 ).Conclusions PHC,especially at a large dosage,can significantly mitigate the long injury secondary to traumatic shock,and the mechanism may be associated with the inhibition of mRNA expressions of NF-κB and iNOS.

Objective To investigate the effects of exosomes derived from human dental pulp mes-enchymal stem cells ( hDPSC-exosomes) on the maturation and function of dendritic cells ( DC) stimulated by lipopolysaccharide ( LPS ) , and to evaluate their regulatory effects on the immune system. Methods Adult permanent teeth-derived dental pulp mesenchymal stem cells were cultured in vitro to extract exosomes in the cell culture medium. The morphology and sizes of the exosomes were observed under transmission electron microscopy. Expression of CD9 and CD63 on the surface of the exosomes was detected by Western blot. PBS, LPS and LPS+hDPSC-exosomes were respectively used to stimulate mouse bone marrow-derived dendritic cells (DC2. 4) for 24 h. A blank control group was set up accordingly. Expression of co-stimulato-ry molecules and cytokine secretion were detected by flow cytometry and ELISA, respectively. Expression of TLR2, TLR4 and NF-κB at mRNA level was detected by RT-PCR. Changes in the functions of DC were evaluated by mixed lymphocyte reaction ( MLR) . Results Adult permanent teeth-derived dental pulp mes-enchymal stem cells were successfully isolated. Up-regulated CD73 and CD90, and down-regulated CD45 were detected on the surface of the cells. Under electron microscopy ( SEM ) , hDPSC-exosomes showed round or oval microcapsule bodies about 50-80 nm in diameter with positive surface markers of CD9 and CD63. hDPSCs-exosomes could significantly reduce the LPS-induced expression of co-stimulatory molecules CD11c and CD86 on DC surface. Moreover, hDPSCs-exosomes increased TGF-β expression and decreased IL-4. They could also significantly inhibit the proliferation of splenic lymphocytes that was induced by DC af-ter LPS stimulation. Compared with the blank control group, hDPSC-exosomes could promote the expression of TLR2 and TLR4 on DC surface and up-regulate the expression of NF-κB. Conclusions This study showed that hDPSC-exosomes could inhibit the activation and functional maturation of DC, promote the de-velopment towards tolerant DC through TLR-NF-κB signaling pathway, and induce immune tolerance to regu-late immune balance.