scholarly journals A study of gene-environment interaction on the gene for angiotensin converting enzyme: a combined functional and population based approach

2004 ◽  
Vol 41 (2) ◽  
pp. 99-103 ◽  
Author(s):  
F A Sayed-Tabatabaei
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Population Based ◽  
Environment Interaction ◽  
Converting Enzyme ◽  
Gene Environment Interaction ◽  
Gene Environment

Gene-environment interaction in atopic diseases: a population-based twin study of early-life exposures

2014 ◽  
Vol 9 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Niklas Kahr ◽  
Vibeke Naeser ◽  
Lone Graff Stensballe ◽  
Kirsten Ohm Kyvik ◽  
Axel Skytthe ◽  
...  
Keyword(s):  
Twin Study ◽  
Early Life ◽  
Population Based ◽  
Environment Interaction ◽  
Atopic Diseases ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Early Life Exposures

scholarly journals A Gene–Environment Interaction Between Smoking and Gene polymorphisms Provides a High Risk of Two Subgroups of Sarcoidosis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Natalia V. Rivera ◽  
Karina Patasova ◽  
Susanna Kullberg ◽  
Lina Marcela Diaz-Gallo ◽  
Tomoko Iseda ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Smoking Status ◽  
Interaction Model ◽  
Population Based ◽  
Environment Interaction ◽  
Additive Interaction ◽  
Swedish Population ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Löfgren’S Syndrome

AbstractThe influence and effect of cigarette smoking in sarcoidosis is unclear. Here, we evaluated gene-environment interaction between multiple genetic variants including HLA genes and smoking in sarcoidosis defined by two clinical phenotypes, Löfgren’s syndrome (LS) and patients without Löfgren’s syndrome (non-LS). To quantify smoking effects in sarcoidosis, we performed a gene-environment interaction study in a Swedish population-based case-control study consisting of 3,713 individuals. Cases and controls were classified according to their cigarette smoking status and genotypes by Immunochip platform. Gene-smoking interactions were quantified by an additive interaction model using a logistic regression adjusted by sex, age and first two principal components. The estimated attributable proportion (AP) was used to quantify the interaction effect. Assessment of smoking effects with inclusion of genetic information revealed 53 (in LS) and 34 (in non-LS) SNP-smoking additive interactions at false discovery rate (FDR) below 5%. The lead signals interacting with smoking were rs12132140 (AP = 0.56, 95% CI = 0.22–0.90), p = 1.28e-03) in FCRL1 for LS and rs61780312 (AP = 0.62, 95% CI = 0.28–0.90), p = 3e-04) in IL23R for non-LS. We further identified 16 genomic loci (in LS) and 13 (in non-LS) that interact with cigarette smoking. These findings suggest that sarcoidosis risk is modulated by smoking due to genetic susceptibility. Therefore, patients having certain gene variants, are at a higher risk for the disease. Consideration of individual’s genetic predisposition is crucial to quantify effects of smoking in sarcoidosis.

Gene-Environment Interaction in the Determination of Levels of Haemostatic Variables Involved in Thrombosis and Fibrinolysis

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