Tintle NL; Ahn K; Mendell NR; Gordon D; Finch SJ, Characteristics of replicated single-nucleotide polymorphism genotypes from COGA: Affymetrix and Center for Inherited Disease Research, BMC Genetics [BMC Genet] 2005; Vol. 6 Suppl 1, pp. S154. Date of Electronic Publication: 2005 Dec 30.
Genetic investigation Workshop 14 supplied re-genotyped single-nucleotide polymorphism (SNP) data. Specifically, both Center for Inherited infection Research (CIDR) and Affymetrix genotyped the identical 11,560 SNPs from the Affymetrix GeneChip Mapping 10K Array marker set on the same 184 individuals from the Collaborative Study on the Genetics of Alcoholism database. While the inconsistency rate between CIDR and Affymetrix (two different genotypes for the identical subject) was low (0.2%), the non-replication rate (two distinct genotypes for the identical subject or one identified genotype and one missing genotype) was considerable (9.5%). The missing facts and figures could be from no-call districts, which is inconsistent with latest recommendations about the use of no-call regions in association tests. In supplement, no-call districts would propose that the actual inconsistency rate is higher than reported. A high inconsistency rate has important influence on power in related hypothesis tests. In supplement, the facts and figures are reliable with assumptions made in a lately suggested likelihood ratio test of association for re-genotyped facts and figures.
Thapar A; Harold G; Rice F; Ge X; Boivin J; Hay D; van den Bree M; Lewis A, Do intrauterine or genetic leverages interpret the foetal origins of chronic disease? A novel experimental method for disentangling effects, BMC Medical Research Methodology [BMC Med Res Methodol] 2007; Vol. 7, pp. 25. Date of Electronic Publication: 2007 Jun 22.
There are many clues to propose that risk for common clinical disorders begins in foetal life. Exposure to environmental risk factors although is often not random. Many routinely utilized indicators of prenatal adversity (e.g. maternal gestational tension, gestational diabetes, fuming in pregnancy) are influenced by maternal genes and genetically leveraged maternal behavior. As mother supplies the baby with both genes and prenatal natural environment, associations between prenatal risk components and offspring infection maybe attributable to factual prenatal risk consequences or to the "confounding" consequences of genetic liability that are distributed by mother and offspring. Cross-fostering concepts, including those that engage embryo move have proved helpful in animal studies. However disentangling these consequences in humans poses important problems for customary genetic epidemiological study designs. METHODS: We present an innovative study scheme aimed at disentangling maternally supplied pre-natal ecological and inherited genetic effects. Families of children elderly 5 to 9 years born by aided reproductive technologies, expressly homologous IVF, sperm donation, egg donation, embryo donation and gestational surrogacy were contacted through fertility clinics and mailed a package of questionnaires on wellbeing and mental health associated risk components and outcomes. Further data were got from antenatal records. RESULTS: To designated day 741 families from 18 fertility clinics have take part. The degree of association between maternally supplied prenatal risk factor and progeny outcome in the group of families where the woman undergoing pregnancy and offspring are genetically associated (homologous IVF, sperm ...