BACKGROUND:In oral warm and moisture circumstance, al oy which contains Be is easily to be eroded to release Be2+. But there is stil no research focusing on beryl ium influence on genotype of Porphyromonas gingivalis fimbriae gene cluster. OBJECTIVE:To investigate Be 2+effect on genotype of Porphyromonas gingivalis fimbriae gene cluster. METHODS:The revived Porphyromonas gingivalis was resuscitated for 48 hours in the anaerobic culture medium with different concentration of Be 2+(10×10-6, 5×10-6, 1.25×10-6). Through PCR amplification and sequencing, we investigated the effects of Be2+RESULTS AND CONCLUSION:(1) When Be on genotypes of Porphyromonas gingivalis fimbriae gene cluster. 2+concentration was 5×10-6, we found the peak of 217 and 257 sites on DNA sequence expressing G/A overlap peak, different from G single peak of the other groups, suggesting the suspicious bases changes, part of the single base G mutated into A. (2) On al concentrations, we found a base group composed of seven A bases was inserted into the 101 site of DNA sequence. Up to now, there is no direct contacts of the mutations occurring to Be2+concentration. Changes of gene may lead to the shifting of the reading frame, the abnormal synthesis of proteins, the change of Porphyromonas gingivalis fimA gene toxicity, and lastly the unbalance of the micro-ecological environment.

Objective To investigate the predictive value of plasma cystatin C (CysC) in patients with acute coronary syndrome (ACS) after pereutaneous coronary intervention (PCI).Methods A total of 660 patients with ACS admitted to cardiovascular department were enrolled in this study from January 2009 to June 2010.The enrollment criteria were:(1) the stenosis degree was above 75％ in at least one coronary artery checked by coronary angiography and successful PCI; (2) normal renal function or mild dysfunction with glomerular filtration rate (GFR) ＞ 60 ml/ ( min · 1.73 m2 ).Exclusion criteria were severe liver and renal insufficiency,malignancies and valvular heart diseases.The plasma CysC levels were examined by the latex enhanced immune turbidity method within 24 hours after admission.The relevant clinical data were recorded.The patients were followed up by out-patient interview or telephone from March to June 2011 and adverse cardiovascular events were recorded.The patients were divided into four groups according to CysC level:Q1 (CysC＜1.02 mg/L),Q2 (1.02 mg/L≤＜CysC ＜1.17 mg/ L),Q3 (1.17 mg/L ≤ CysC ＜1.35 mg/L) and Q4 (CysC ≥ 1.35 mg/L).Univariate and multivariate Cox hazards regressions were established to analyze the factors related to prognosis.The proportion differences between four groups were tested by x2.The survival ratio was estimated using the Kaplan-Meier method.Statistical significance was established at a P value of less than 0.05.Results ① A total of 606 ( 91.7％ ) patients successfully accepted follow-up.Mean follow-up time was ( 14.3 + 1.7 ) months.Of them,95 patients were subjected to adverse cardiovascular events ( 15.7％ ).②The incidences of adverse cardiovascular events in Q2,Q3,Q4 were significantly higher than those in Q1 ( P ＜ 0.001 ).The rates of mortality,nonfatal myocardial infarction and target lesion revascularization in Q4 were higher than those in Q1 ( P ＜ 0.05 ).The incidences of heart failure in Q3 and Q4 were higher than that in Q1 ( P ＜ 0.05 ).③Univariate analysis demonstrated that CysC,creatinine,LVEF,age,history of PCI and NYHA grade ≥3 were the risk factors of poor prognosis (P ＜ 0.05 ).④ Multivarite cox hazards regression revealed that the elevation of CysC level remained an independent predictor of adverse cardiovascular events.The relative risk of Q3 and Q4 were 3.930 (95％ CI 1.306-11.829,P =0.015 ) and 6.380 (95％ CI 2.171-18.751,P =0.001 ) compared with Q1.⑤　The cumulative rates of survival without adverse cardiovascular events in Q2,Q3 and Q4 decreased compared with Q1 (P ＜ 0.001 ).Conclusions High plasma CysC concentration is an independent predictor of adverse cardiovascular events in patients with ACS after PCI.

Environmental chemical pollutants are increasing, which brings various harms to human health. Epigenetics may be an important medium between exposure to environmental chemical contaminants and adverse health effects. Many environmental chemical pollutant exposures can regulate gene expression and promote disease occurrence and development through epigenetic mechanisms. This review outlines the mechanisms of epigenetics and the latest research advances in exposure and epigenetics of several environmental chemical substances (heavy metal arsenic, bisphenol A, dioctyl phthalate and benzene). To further understand and study the relationship between environmental chemical pollutant exposures and epigenetics in order to elucidate the mechanisms of disease occurrence and development.

Environmental chemical pollutants are increasing, which brings various harms to human health. Epigenetics may be an important medium between exposure to environmental chemical contaminants and adverse health effects. Many environmental chemical pollutant exposures can regulate gene expression and promote disease occurrence and development through epigenetic mechanisms. This review outlines the mechanisms of epigenetics and the latest research advances in exposure and epigenetics of several environmental chemical substances (heavy metal arsenic, bisphenol A, dioctyl phthalate and benzene). To further understand and study the relationship between environmental chemical pollutant exposures and epigenetics in order to elucidate the mechanisms of disease occurrence and development.