tailieunhanh - Báo cáo y học: " A model of gene-gene and gene-environment interactions and its implications for targeting environmental "

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: " A model of gene-gene and gene-environment interactions and its implications for targeting environmental | BioMed Central Theoretical Biology and Medical Modelling Research Open Access A model of gene-gene and gene-environment interactions and its implications for targeting environmental interventions by genotype Helen M Wallace Address GeneWatch UK The Mill House Tideswell Buxton Derbyshire SK17 8LN UK Email Helen M Wallace Corresponding author Published 09 October 2006 Received 13 April 2006 Theoretical Biology and Medical Modelling 2006 3 35 doi 1742-4682-3-35 Accepted 09 October 2006 This article is available from http content 3 1 35 2006 Wallace licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The potential public health benefits of targeting environmental interventions by genotype depend on the environmental and genetic contributions to the variance of common diseases and the magnitude of any gene-environment interaction. In the absence of prior knowledge of all risk factors twin family and environmental data may help to define the potential limits of these benefits in a given population. However a general methodology to analyze twin data is required because of the potential importance of gene-gene interactions epistasis geneenvironment interactions and conditions that break the equal environments assumption for monozygotic and dizygotic twins. Method A new model for gene-gene and gene-environment interactions is developed that abandons the assumptions of the classical twin study including Fisher s 1918 assumption that genes act as risk factors for common traits in a manner necessarily dominated by an additive polygenic term. Provided there are no confounders the model can be used to implement a topdown approach to quantifying the potential utility of

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