OBJECTIVE:To observe therapeutic efficacy and safety of Danshen chuanxiongqin injection combined with flunari-zine hydrochloride in the benign prevention and treatment of paroxysmal positional vertigo (BPPV) and lower extremity deep ve-nous thrombosis (DVT) in post-operative long-term bedridden patients with lower limb fractures. METHODS:300 post-operative long-term bedridden patients with lower limb fractures were selected and randomly divided into observation group and control group,with 150 cases in each group. Control group was given Flunarizine hydrochloride capsules orally 10 mg,qd;observation group was additionally given Danshen chuanxiongqin injection 10 ml+5% Glucose injection 250 ml,ivgtt,qd. The incidence of BPPV and DVT were observed in 2 groups after intervention,and the circumference of lower limb,blood coagulation indexes, blood rheology indexes and inflammatory factor were observed before and after intervention,and the incidence of ADR was com-pared. RESULTS:The incidence of BPPV and DVT in observation group were 18.0% and 16.7%,which were significantly lower than in control group(48.7% and 52.7%),with statistical significance(P<0.05);after intervention,the circumference of lower limb,blood rheology indexes and the levels of inflammatory factors in 2 groups were decreased significantly, while the coagula-tion indicators were significantly improved;the observation group was better than the control group,with statistical significance (P<0.05). There was no statistical significance in the incidence of ADR between 2 groups(P>0.05). CONCLUSIONS:Danshen chuanxiongqin injection combined with flunarizine hydrochloride is effective in the prevention of BPPV and DVT in long-term bed-ridden patients with lower limb fractures,with low incidence of ADR.

Objective To investigate the incidence of non-infectious diseases at different stages of a prolonged escort missiononboard the frigate.Methods The constituent ratio of non-infectious diseases occurred at different stages of a prolonged escort missionby a certain frigate was calculated,and the incidence of various non-infectious diseases at different stages was compared accordingly.Results For non-infectious diseases occurred during the whole course of the mission,the top 3 non-infectious diseases were lumbarmuscle strain,insomnia and motion sickness.Then came dermatitis,dental ulcer,xerophthalmia,trauma and cardiovascular diseases.The onset stages (early,middle and late stages)of various non-infectious diseases were different from one another.The incidence oflumbar muscle strain,insomnia,dermatitis,dental ulcer and xerophthalmia at late stage of the mission was significantly higher than thatat the early stage(P <0.01),and the incidence of motion sickness at the early stage was significantly higher than that at late stage(P <0.01).Conclusion With the extension of the escort mission,the incidence of lumbar muscle strain,insomnia,dermatitis,dentalulcer and xerophthalmia increased,while the incidence of motion sickness decreased.

Objective To investigate the effects of macrophage inflammatory protein-1α (MIP-1α) combined with molecule 4-1BB L on the tumorigenicity of hepatocellular carcinoma cells in vivo. Methods Mouse MIP-1α (mMIP-1α) expressed Hepa 1-6 cells were transfected with m4-1BBL recombinant retrovirus, the anti-histidinol cells clones were selected and amplified. The expression of m4-1BB L was confirmed by flow cytometry. The growth curve of Hepa 1-6 cells transfected with mMIP-1α and m4-1BBL alone or together was drawn and compared. C57B/L Mice were randomly divided into 7 groups, 9 mice in each group, injected with mMIP-1α+m4-1BB L Hepa 1-6 cells, m4-1BB L Hepa 1-6 cells, mMIP-1α Hepa 1-6 cells, Hepa 1-6 cells, pLXSHD Hepa 1-6 cells or PBS respectively. The tumorigenicity of hepatocellular carcinoma cells and the mice survival rate were compared between each groups. Results Hepa 1-6 mMIP-1α+m4-1BB L cells which expressed both mMIP-1α and m4-1BB L were successfully established. The expression of mMIP-1α and m4-1BB L alone or together did not affect the growth curve of Hepa 1-6 cells. Observed for 5 weeks, no tumor developed in Hepa 1-6 mMIP-1α+m4-1BB L injected mice. The tumorigenicity of Hepa 1-6 mMIP-1α+m4-1BB L was lower than that of Hepa 1-6 mMIP-1α or Hepa 1-6 m4-1BB L in vivo. The survival rate of Hepa 1-6 mMIP-1α+m4-1BBL injected mice(9/9) was higher than that of Hepa 1-6 m4-1BB L injected mice (6/9)or Hepa 1-6 mMIP-1α injected mice (1/9). Conclusion Chemokine MIP-1α combined with costimulatory 4-1BB L lowered the tumorigenicity of hepatocellular carcinoma cells in vivo, and prolonged the mice survival period.

Objective: To investigate the effects of andrographolide on extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and tumor necrosis factor-α (TNF-α) expression in lipopolysaccharide (LPS)-activated macrophages. Methods: LPS-activated mouse peritoneal macrophages were cultured in media with different concentrations of andrographolide. Cytotoxicity of andrographolide was detected by cell counting kit-8. The macrophages were lysed, and then expressions of phosphorylated ERK1/2, JNK and p38 and nuclear factor-κB inhibitor (IκBα) protein were detected by Western blotting and TNF-α mRNA expression was detected by reverse transcription-polymerase chain reaction. Supernatants of the macrophages were used to detect content of TNF-α protein by enzyme-linked immunosorbent assay. Results: Andrographolide at 1-100 μg/mL showed no cytotoxicity on LPS-activated mouse peritoneal macrophages. Andrographolide inhibited ERK1/2 phosphorylation in LPS-activated murine peritoneal macrophages, which was concentration-dependent (P<0.01). Andrographolide at 1-25 μg/mL had no effects on phosphorylation levels of JNK and p38 and IκBα degradation in LPS-stimulated mouse peritoneal macrophages. In activated macrophages, TNF-α expression was inhibited by 12 μg/mL andrographolide and 20 μmol/L PD98059 (inhibitor of ERK1/2 signaling pathway) at both mRNA expression and protein secretion levels. Conclusion: In LPS-activated macrophages, andrographolide may inhibit the expression of TNF-α by inhibiting ERK1/2 signaling pathway.