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1 of the original SNP. When no SNPs met these criteria, then the SNP with the highest r2 was chosen from all SNPs within 20?kb. The complete list of SNPs tested is provided in Supplemental Table 1. Genotyping was performed using the iPLEX genotyping assays on the MassARRAY platform, which is based on allele-specific http://www.selleckchem.com/products/azd9291.html primer extension with mass-modified terminators (Sequenom, Inc., San Diego, CA, USA). The average missing rate for the genotyping assays was 2.1%, with a range from 0.6% to 8.2% (Supplemental Table 1). Using one randomly selected individual in each family, each SNP was tested for significant (p? http://www.selleckchem.com/products/ch5424802.html for those regions where the previous associations were replicated, the data were augmented with those generated by the genome-wide association study. Genotyping was performed on the Human610Quadv1_B (Illumina, San Diego, CA, USA) by the Center for Inherited Disease Research (CIDR) using the Illumina Infinium II assay protocol. Genotype calls were made when a genotype yielded a quality metric (Gencall score) of 0.15 or higher. Blind duplicate reproducibility was 99.99% based on 36 paired samples. Samples having genotypes for at least 98% of the SNPs were included in the analyses. Our final analytic sample included 1524 women from 762 different families. This data set demonstrated minimal evidence of stratification, as indicated by a lack of inflation in genome-wide association study p values (��?=?1.003) for both the spine and neck BMD phenotypes. SNPs with a call rate of 98% or greater (n?=?581,255) were included and subjected to further quality-control analyses. From these, SNPs were removed if either the minor allele frequency was less than 0.01 in this data set (n?=?32,948) http://www.selleck.cn/products/Everolimus(RAD001).html or there was significant deviation (p?