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Background: Preventing suicide is a global imperative. Although the effects of social and individual risk factors of suicide have been widely investigated, evidence of environmental effects of exposure to air pollution is scarce. We investigated the effects of ambient air pollution on suicide mortality in Guangzhou, China during 2003-2012.Methods: A conditional logistic regression analysis with a time-stratified case-crossover design was performed to assess the effects of daily exposure to three standard air pollutants, including particulate matter less than 10 μm in aerodynamic diameter (PM10), sulphur dioxide (SO2) and nitrogen dioxide (NO2), on suicide mortality, after adjusting for the confounding effects of daily mean temperature, relative humidity, atmospheric pressure and sunshine duration. Further analyses were stratified by season, gender, age group, educational attainment and suicide type.Results: Between 2003 and 2012, there were a total of 1 550 registered suicide deaths in Guangzhou. A significant increase in suicide risk were associated with interquartile-range increases in the concentration of air pollutant, with an odds ratio of 1.13 (95 % confidence interval (CI): 1.01, 1.27) and 1.15 (95 % CI: 1.03, 1.28) for PM10 and NO2 at lag 02, and 1.12 (95 % CI: 1.02, 1.23) for SO2 at lag 01, respectively. The suicide risks related to air pollution for males and people with high education level were higher than for females and those with low education level, respectively. Significant air pollution effects were found on violent suicide mortality and in cool season but not on non-violent suicide mortality or in warm season.Conclusions: Suicide risk was positively associated with ambient air pollution levels. This finding would provide important information for the health impact assessment of air pollution and for the development of effective strategies and interventions for the prevention of suicide. [ABSTRACT FROM AUTHOR]

PrME and NS1 gene were the two main immuneprotect proteins of Japanese encephalitis virus (JEV), and they were also N-linked glycosylation proteins. To clear the effect of N-glycosylation on JEV immunity, the N-glycosylation site of prME and NS1 gene were eliminated by site-directed mutant PCR, subtituting the N to Q. And the the mutant genes were subcloned into eukaryotic expression plasmid. Four-weeks female mice were immuned with the wildtype and mutant gene by twice. The antibodies against prME were detected by ELISA and the neutralization antibodies were tested by viral neutralizing assay. The immunoprotection were determined by attack with JEV virulent strain. Compare with the wild-type gene immuned-groups, one N-glycan eliminated prME gene could induce a little higher ELISA antibody, neutralization antibody and immunoprotection, but the immunity of gene with both N-glycan absence was decreased. The similar status were observed in the wildtype and mutant NS1 groups. Thus these results show that the N-linked glycosylation in the prME and NS1 gene were correlated with the immunity, one glycan absent would enhance the immunity but both two loss would impair it.

Objective: To construct eukaryotic expression vectors of two mutants of hypoxia-inducible factor-1 (HIF-1alpha) and study their expressions in human microvascular endothelial cells (HMVECs)., Methods: Site-directed mutagenesis was performed to induce the mutation of the codons for the residue Pro564 (ccc) in HIF-1alpha into gcc (Ala) in pcDNA3.1(+)-HIF-1alphato obtain single-site-mutated vector pcDNA3.1(+)-HIF-1alpha-564Ala, which was then subjected to a second site-directed mutagenesis to convert the codons for Asn803 into that of Ala (gct) to acquire double-site-mutated pcDNA3.1(+)-HIF-1alpha-564Ala-803Ala. After lipofectin-mediated transient transformation of HMVECs with the 3 recombinant plasmids including the two plasmids containing the mutations and the one without mutation, respectively, the expression levels of HIF-1alpha mRNA and protein were determined using RT-PCR, immunofluorescent staining and Western blotting., Results: DNA sequence analysis demonstrated success of the two-step mutagenesis and the two plasmids of pcDNA3.1+-HIF-1alpha-564Ala and pcDNA3.1(+)-HIF-1alpha-564Ala- 803Ala were obtained, both of which could produce HIF-1alpha protein resistant to oxidation degradation in HMVECs as compared with the non-mutated one., Conclusion: The recombinant plasmids pcDNA3.1(+)-HIF-1alpha-564Ala and pcDNA3.1(+)-HIF-1alpha- 564Ala-803Ala have been successfully constructed with efficient expressions in HMVECs.

To enhance the immuogenicity of DNA vaccines expressing the GP5 protein of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), the tegument protein VP22 (encoded by VP22 gene) of Bovine Herpesvirus 1 (BHV-1), which has been demonstrated to exhibit the unusual protein transduction property, was fused to N-terminus of GP5 of DNA vaccine construct pCI-ORF5M, resulting in pCI-VP22-ORF5M expressing VP22-GP5 fusion protein. The expression of VP22-GP5 fusion protein was confirmed by both indirect immunofluorescence assay (IFA) and Western blot. To investigate its immunogenicity, BALB/c mice were immunized with the fusion expression plasmid pCI-VP22-ORF5M and non-fusion expression plasmid pCI-ORF5M, respectively. The GP5-specific ELISA antibodies, neutralizing antibodies and lymphocyte proliferative responses were evaluated at various time points after primary immunization. The results showed that GP5-specific ELISA antibodies, neutralizing antibodies, and lymphocyte proliferative responses induced by DNA vaccine pCI-VP22-ORF5M were higher significantly than those of DNA vaccine pCI-ORF5M, indicating that fusion expression with BHV-1 VP22 significantly enhances the immuogenicity of DNA vaccine expressing the PRRSV GP5 protein, and that this strategy may also be useful to develop more efficient DNA vaccines against other pathogens.

Objective: To investigate the effect of C-reactive protein (CRP) on expression of hypoxia-inducible factor-1alpha (HIF-1alpha)., Methods: Using CoCl(2) (100 micromol/L) to simulate hypoxic condition for culturing human umbilical vein endothelial cells (HUVECs), we examined the effects of CRP on expression of HIF-1alpha. The proteins were extracted from the cells after a 24-hour exposure of the cells to CRP of varied concentrations in the presence of CoCl(2), and Western blotting was performed for quantification of HIF-1alpha expression, the results were analyzed statistically with SPSS software., Results: CRP at the concentration of 5 microg/ml decreased the expression of HIF-1alpha (P<0.001), producing the maximum inhibitory effect at the concentration of 100 microg/ml, an effect exhibiting dose-dependence., Conclusion: CRP inhibits the expression of HIF-1alpha in HUVECs subjected to hypoxic condition, which serves as an important evidence for the inhibitory effect of CRP on angiogenesis in hypoxic condition.