[25] that determines:

(1) relative excess risk due to interaction (RERI); (2) attributable proportion due to interaction Inhibitor Library cost (AP) and (3) synergy index (S). RERI is the excess risk due to an interaction relative to the risk without exposure. AP refers to the attributable proportion of disease among individuals exposed to both factors that is due to the factors’ interaction. S is the excess risk from both exposures when there is an additive interaction, relative to the risk from both exposures without an interaction. RERI = 0, AP = 0 or S = 1 means no interaction or strict additivity; RERI > 0, AP > 0 or S > 1 means positive interaction or more than additivity; and RERI < 0,

AP < 0 or S < 1 means negative interaction or less www.selleckchem.com/products/BIBW2992.html than additivity [26]. If any of the null values (0 in RERI and AP or 1 in S) falls outside the 95% CI of its respective measurement, then, the additive interaction is considered statistically significant. Excluding the calculation of linkage disequilibrium and statistical power, all statistical analyses were performed using STATA/SE software version 12.0 (StataCorp, College Station, TX, USA). The characteristics of cases and controls are shown in Table 1. Compared with control subjects, cases were more likely to live in a prefecture other than Fukuoka in Kyushu. There were no differences between cases and control subjects with regard to age at oral examination, education, smoking, toothbrushing frequency or use of an interdental brush. Among our control subjects, the genetic distributions of VDR SNPs rs731236, rs7975232, rs1544410 and rs2228570 did not deviate from the Hardy–Weinberg equilibrium (P = 0.76, 0.11, 0.54 and 0.42, respectively). Of the six SNP pairs, three pairs were in strong linkage disequilibrium: D’ between rs731236 and rs7975232, D’ between rs731236 and rs1544410 and D’ between rs7975232 and

rs1544410 Mirabegron were 0.99, 0.98 and 0.97, respectively (Table 2). In the multivariate model, compared with a reference group of women with the AA genotype of SNP rs731236, those with the GG genotype had a significantly increased risk of periodontal disease, while the AG genotype was not significantly associated with the risk of periodontal disease: the adjusted OR for the GG genotype was 3.68 (95% CI: 1.06–12.78) (Table 3). No evident relationships were observed between SNP rs7975232, rs1544410 or rs2228570 and periodontal disease. With respect to SNP rs1544410, the statistical power calculation revealed that using our sample size, we could detect the gene–disease association for an OR of 1.697 with an accuracy of more than 80% at a significance level of 0.05 with a two-side alternative hypothesis under the log-additive model.