Faculty Opinions recommendation of Different data from different labs: lessons from studies of gene-environment interaction.

Author(s):  
Laurence H. Tecott
1997 ◽  
Vol 78 (01) ◽  
pp. 457-461 ◽  
Author(s):  
S E Humphries ◽  
A Panahloo ◽  
H E Montgomery ◽  
F Green ◽  
J Yudkin

2020 ◽  
Vol 16 (5) ◽  
pp. 457-470 ◽  
Author(s):  
Mohammad H. Zafarmand ◽  
Parvin Tajik ◽  
René Spijker ◽  
Charles Agyemang

Background: The body of evidence on gene-environment interaction (GEI) related to type 2 diabetes (T2D) has grown in the recent years. However, most studies on GEI have sought to explain variation within individuals of European ancestry and results among ethnic minority groups are inconclusive. Objective: To investigate any interaction between a gene and an environmental factor in relation to T2D among ethnic minority groups living in Europe and North America. Methods: We systematically searched Medline and EMBASE databases for the published literature in English up to 25th March 2019. The screening, data extraction and quality assessment were performed by reviewers independently. Results: 1068 studies identified through our search, of which nine cohorts of six studies evaluating several different GEIs were included. The mean follow-up time in the included studies ranged from 5 to 25.7 years. Most studies were relatively small scale and few provided replication data. All studies included in the review included ethnic minorities from North America (Native-Americans, African- Americans, and Aboriginal Canadian), none of the studies in Europe assessed GEI in relation to T2D incident in ethnic minorities. The only significant GEI among ethnic minorities was HNF1A rs137853240 and smoking on T2D incident among Native-Canadians (Pinteraction = 0.006). Conclusion: There is a need for more studies on GEI among ethnicities, broadening the spectrum of ethnic minority groups being investigated, performing more discovery using genome-wide approaches, larger sample sizes for these studies by collaborating efforts such as the InterConnect approach, and developing a more standardized method of reporting GEI studies are discussed.


Author(s):  
Andrey Ziyatdinov ◽  
Jihye Kim ◽  
Dmitry Prokopenko ◽  
Florian Privé ◽  
Fabien Laporte ◽  
...  

Abstract The effective sample size (ESS) is a metric used to summarize in a single term the amount of correlation in a sample. It is of particular interest when predicting the statistical power of genome-wide association studies (GWAS) based on linear mixed models. Here, we introduce an analytical form of the ESS for mixed-model GWAS of quantitative traits and relate it to empirical estimators recently proposed. Using our framework, we derived approximations of the ESS for analyses of related and unrelated samples and for both marginal genetic and gene-environment interaction tests. We conducted simulations to validate our approximations and to provide a quantitative perspective on the statistical power of various scenarios, including power loss due to family relatedness and power gains due to conditioning on the polygenic signal. Our analyses also demonstrate that the power of gene-environment interaction GWAS in related individuals strongly depends on the family structure and exposure distribution. Finally, we performed a series of mixed-model GWAS on data from the UK Biobank and confirmed the simulation results. We notably found that the expected power drop due to family relatedness in the UK Biobank is negligible.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jacinta I. Kalisch-Smith ◽  
Nikita Ved ◽  
Dorota Szumska ◽  
Jacob Munro ◽  
Michael Troup ◽  
...  

AbstractCongenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene–environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women.


Author(s):  
David M. Wineroither ◽  
Rudolf Metz

AbstractThis report surveys four approaches that are pivotal to the study of preference formation: (a) the range, validity, and theoretical foundations of explanations of political preferences at the individual and mass levels, (b) the exploration of key objects of preference formation attached to the democratic political process (i.e., voting in competitive elections), (c) the top-down vs. bottom-up character of preference formation as addressed in leader–follower studies, and (d) gene–environment interaction and the explanatory weight of genetic predisposition against the cumulative weight of social experiences.In recent years, our understanding of sites and processes of (individual) political-preference formation has substantially improved. First, this applies to a greater variety of objects that provide fresh insight into the functioning and stability of contemporary democracy. Second, we observe the reaffirmation of pivotal theories and key concepts in adapted form against widespread challenge. This applies to the role played by social stratification, group awareness, and individual-level economic considerations. Most of these findings converge in recognising economics-based explanations. Third, research into gene–environment interplay rapidly increases the number of testable hypotheses and promises to benefit a wide range of approaches already taken and advanced in the study of political-preference formation.


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