Objective To study the genotoxicity of bromate,a chief by-product of ozonated drinking water.Methods Genotoxicity at gene,DNA and chromosome levels induced by bromate DBP was determined using Ames test,unscheduled DNA synthesis(UDS)assay and micronucleus test(MNT)of mice bone marrow polychromatic erythrocytes respectively.Results In Ames test,bromate showed no mutagenic effect on salmonella typhimurium TA98and TA100strains with or without S9(rat liv-er metabolic activation system)compared with the negative control group,but the results of UDS assay showed that bromate could induce unscheduled DNA synthesis in rat primary hepatocytes and the results of MNT indicated that bromate increased the micronucleus rate of bone marrow polychromatic erythrocytes of mice.Conclusion It was suggested that bromate DBP might have genotoxicity at DNA and chromosome levels.

Objective To explore the role of IEGs in the central neurotoxicity of mice induced by anatoxin-a ANTX-A. Methods 80 Kunming mice were divided into groups and treated with ANTX-A at 200, 50 and 12.5 ?g/kg respectively i.p. for one month, 0.9% sodium chloride solution was used as the control. The expression of c-fos and NGFI-A genes and CREB protein in mouse brain were determined by using RT-PCR and immunocytochemical methods. Results The expression of c-fos gene significantly increased in the females of 50, 200 ?g/kg groups and in the males of 200 ?g/kg group compared with the control group. The expression of C-FOS and CREB-1 protein was significantly higher in 200 ?g/kg group than that in the control group. In all ANTX-A treated groups, the expression of NGFI-A gene did not show a significant difference compared with the control. Conclusion c-fos and CREB-1 genes may play a role in the central neurotoxicity induced by anatoxin-a.

OBJECTIVETo find a potential link among ABO blood group, lipid profiles and coronary artery disease (CAD) and to estimate the effect size of connection using mediation analysis model.

METHODSA total of 898 consecutive patients undergoing coronary angiography were enrolled, and divided into CAD group and non-CAD group according to angiographic findings. According to ABO blood group, patients were divided into O blood group and non-O blood group, as well as A blood group and non-A blood group. Baseline characteristics among various groups were compared and the association of ABO blood group, CAD and lipid profile was explored.

RESULTSSubjects of blood type A had higher concentration of total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) compared with that of non-A type (TC: (4.43 ± 1.12) mmol/L vs. (4.18 ± 1.09) mmol/L, LDL-C: (2.79 ± 0.99) mmo/L vs. (2.59 ± 1.01) mmol/L, all P < 0.01). TC and LDL-C were significantly higher while high density lipoprotein cholesterol (HDL-C) and ApoA I levels were significantly lower in CAD group than in non-CAD group (TC: (4.36 ± 1.05) mmol/L vs. (4.13 ± 1.16) mmol/L, LDL-C: (2.61 ± 0.87) mmol/L vs. (2.47 ± 0.94) mmol/L; ApoA I: (1.38 ± 0.29) mmol/L vs. (1.45 ± 0.33) mmol/L; all P < 0.01). After adjustment for traditional cardiovascular risk factors, blood group A and TC remained significantly associated with the risk of CAD (OR = 1.88, 95% CI 1.280-2.774, P < 0.01; OR = 1.03, 95% CI 1.018-1.033, P < 0.01, respectively). Specially, mediation analysis indicated that 10.5% of the effect of A blood group on CAD was mediated by TC levels (P < 0.01).

CONCLUSIONOur data indicate that there is an association between ABO blood group, TC levels and risk of CAD. Around 10.5% of the effect of A blood group on CAD is mediated by TC levels.

Apolipoprotein A-I ; blood ; Blood Group Antigens ; blood ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Coronary Angiography ; Coronary Artery Disease ; blood ; Humans ; Risk Factors ; Triglycerides ; blood