[The effects of adenovirus 5 latent infection on pulmonary inflammation caused by biomass fumes in guinea pigs].

OBJECTIVE: To explore the effects of adenovirus 5 (Ad5) latent infection on oxidized injury and inflammation of the lungs caused by exposure to biomass fumes in guinea pigs. METHODS: Forty-six albino guinea pigs were randomly divided into 2 groups. One group (n = 26) was infected intranasally with Ad5, and the other group (n = 20) was sham-infected with sterile PBS as control. After 22 days, the living animals (n = 20 each) were randomly divided into 2 subgroups. One subgroup was exposed to biomass fumes for 3 weeks, and the other subgroup was exposed to room air. At the end of the experiment, all animals were sacrificed and their lung tissues were examined histopathologically. The levels of interleukin (IL)-8, IL-6, and cell adhesion molecule-1 (CAM-1) in bronchoalveolar lavage fluid (BALF) were measured. The results were analyzed using a two-way analysis of variance (ANOVA) with two crossed factors. The level of significance was P < 0.05. RESULTS: The exposure to biomass fumes and the latent infection of Ad5 were associated with a significant increase in the total number of airway inflammatory cells in the BALF [(37.1 +/- 5.5) x 10(6)/L and (16.8 +/- 2.3) x 10(6)/L], F = 208.947, 22.687, all P < 0.01). The exposure to biomass fumes was associated with a significant increase in the concentration of IL-8, IL-6, and CAM-1 in the BALF [(0.38 +/- 0.06), (0.188 +/- 0.021) and (6.5 +/- 1.6) mg/kg], F = 13.525 - 69.021, all P < 0.01). The latent infection of Ad5 was associated with a significant increase in the concentration of IL-8, and CAM-1 in the BALF [(0.37 +/- 0.05) and (8.2 +/- 2.1) mg/kg] (F = 11.964, 57.162, all P < 0.01). Ad5 infection had a synergistic effect on the IL-8 and CAM-1 production caused by biomass fume exposure. CONCLUSIONS: Biomass fumes caused severe histopathological changes and inflammation in lungs of guinea pigs, and Ad5 latent infection aggravated these changes. Increased production of inflammatory cytokines may play an important role in this process.

Characterization of complete chloroplast genome and phylogenetic analysis of sweet cherry Cerasus avium (L.) Moench (Prunoideae, Rosaceae).

Sweet cherry (Cerasus avium (L.) Moench) belonging to family Rosaceae, is an important economical fruit crop worldwide. In this study, the complete chloroplast (cp) genome of sweet cherry was generated by De novo assembly with low coverage whole-genome sequencing data. The genome size was 157,987 bp in length consisting of a typical quadripartite structure; a large single-copy region (LSC, 85,975 bp), a small single-copy region (SSC, 19,121 bp) and a pair of inverted repeat regions (IRs, 26,445 bp each). A total of 115 genes were predicted including 82 protein-coding genes, 29 tRNA genes and four rRNA genes. Phylogenetic analysis based on 12 reported complete chloroplast genome indicated the monophyly of the genus Creasus including newly sequenced C. avium, which is conform to the traditional classification.

[Association of tumor necrosis factor alpha 308 G/A gene promoter polymorphism with the presence of chronic obstructive pulmonary disease: a meta-analysis].

OBJECTIVE: To investigate the association between the polymorphism of tumor necrosis factor alpha 308 gene (TNF-alpha-308) promoter and the risk of chronic obstructive pulmonary disease (COPD) using the method of meta-analysis. METHOD: The database of Medline and the Chinese biomedicine disc (CBM) were searched for published case-control studies of the association between the polymorphism of TNF-alpha-308 gene promoter and COPD. Data were extracted using a standardized form and the meta-analysis was performed. RESULTS: Eighteen case-control studies, comprising 1606 patients with COPD and 2551 controls (the oriental population: 666 patients with COPD and 898 controls; the Caucasian: 940 patients with COPD and 1653 controls) were included in the meta-analysis. Using a fixed effect model, the pooled result in the oriental population showed that the TNF2 allele was associated with the susceptibility to COPD [odds ratio (OR) = 2.62, 95% confidence interval (95% CI) 2.00 to 3.43]. The OR for COPD susceptibility in TNF1/2 population was significantly increased at 2.44 (95% CI 1.79 to 3.33) compared to the TNF1/1 population. The OR for COPD susceptibility in the TNF1/2 plus TNF2/2 population was significantly increased at 2.78 (95% CI 2.06 to 3.75) compared to the TNF1/1 population. When adjusted for smoking, the result was similar. However, in the Caucasian population, the TNF2 allele was not associated with the susceptibility to COPD (OR = 0.97, 95% CI 0.84 to 1.14). There was no association between the genotype of TNF-alpha-308 and COPD (OR = 0.96, 95% CI 0.79 to 1.16, and OR = 1.03, 95% CI 0.86 to 1.25), compared between the TNF1/2 population, the TNF1/2 plus the TNF2/2 population and the TNF1/1 population respectively. When adjusted for smoking, the result was similar. CONCLUSION: In the oriental population, the TNF2 allele confers a significant risk for developing COPD. There is no association between the polymorphism of TNF-alpha-308 gene promoter and COPD in the Caucasian population.