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Natural log transformation was applied to 25(OH)D and total IgE to calculate geometric means and to improve the approximation of normal distribution. All models were adjusted for sex, month of measurement, and region (Scotland or South, Middle or North of England). For analyses including SNPs, a further adjustment was made for the genotyping platform. All carriers of minor alleles were grouped together to improve the stability of the estimates. A cut-off value of 50?nmol/L was used to define VDD [22], and individuals with 25(OH)D?>?135?nmol/L (n?=?33) were excluded to reflect the nonlinear relationship between 25(OH)D and total IgE [4]. Interactions between each SNP and VDD were assessed using the likelihood ratio test. A stratified analysis was performed when significant interactions were detected. A genetic risk score was constructed by combining the risk genotypes of SNPs that were found to interact DAPT secretase datasheet with VDD (rs2443250 and rs512555), Proteasome inhibitor with risk genotypes defined as the groups in which VDD was associated with increasing total IgE levels. A chi-square goodness of fit test was used to assess deviation from Hardy�CWeinberg equilibrium (P?>?0.01 for all SNPs). All P-values were derived from two-sided tests. Multiple testing was corrected for all single SNP and exploratory interaction analyses using the false discovery rate method [(��0.05?��?27?SNPs)/rank]. All analyses were carried out using STATA, version 12 [23]. The characteristics of the study participants are presented in the Table?1. Total IgE concentrations appeared higher in participants with VDD (Tolmetin sample. We investigated the association of the 27 SNPs with total IgE and specific IgE and found that only four SNPs [rs2427837 (FCER1A), P?