Objective: To evaluate the curative effects of zinc medicine in the treatment of recurrent aphthous ulcers(RAU). Methods: The randomized controlled trials (RCTs) about the zinc medicine in the treatment of RAU were retrieved from PubMed, CENTRAL, EMbase, CNKI and WANFANG from January 1, 1980 to June 1, 2016, the references included in the study were manually selected. After quality evaluation and material extraction by the reviewer, Meta analysis was done according to the documents and materials by software Stata. Results: 4 RCTs involving 156 patients were included in the study, with 74 cases in the zinc medicine treatment group and 82 cases in the placebo control group. Meta analysis showed that zinc medicine was effective in the treatment of RAU(P＜ 0. 05). Conclusion: Zinc medicine is safe and effective in the treatment of RAU. Zinc deficiency is a risk factor of RAU.

Objective To study the genotoxicity of triptolide ,an important active component of Tripterygium wilfordii Hook f .Methods Ames test ,in vitro chromosomal aberration test of CHO cell and in vivo micronucleus assay were per-formed to investigate the genotoxicity of triptolide .Results The Ames test showed that triptolide did not increase mutagenicity for TA97 ,TA98 ,TA100 ,TA102 and TA1535 strains at the dosage of 1 .6~1000 μg per plate with and without metabolic ac-tivation system S9 .Results of in vitro CHO cell chromosomal aberration test indicated that there was no statistical difference between the triptolide groups (doses of 0 .01 ,0 .02 and 0 .04 μg/ml) and the solvent control group with and without metabolic activation system S9 .However ,triptolide significantly increased polychromatophilic erythrocyte micronucleus formation at the dosage of 720 μg/kg in ICR mice .Conclusion Triptolide did not induce genetic toxicity based on the Ames test and chromo-somal aberration test ,but could increase micronucleus formation at the dosage of 720 μg/kg .These results indicated that trip-tolide may have potential genotoxicity on human health .

Uncovering the risk factors of pulmonary hypertension and its mechanisms is crucial for the prevention and treatment of the disease.In the current study,we showed that experimental periodontitis,which was established by ligation of molars followed by orally smearing subgingival plaques from patients with periodontitis,exacerbated hypoxia-induced pulmonary hypertension in mice.Mechanistically,periodontitis dysregulated the pulmonary microbiota by promoting ectopic colonization and enrichment of oral bacteria in the lungs,contributing to pulmonary infiltration of interferon gamma positive(IFNγ+)T cells and aggravating the progression of pulmonary hypertension.In addition,we identified Prevotella zoogleoformans as the critical periodontitis-associated bacterium driving the exacerbation of pulmonary hypertension by periodontitis,and the exacerbation was potently ameliorated by both cervical lymph node excision and IFNγ neutralizing antibodies.Our study suggests a proof of concept that the combined prevention and treatment of periodontitis and pulmonary hypertension are necessary.