References
- Cheng S, Pallaud C, Grow M A, Scharf S J, Erlich H A, Klitz W, Pullinger C R, Malloy M J, Kane J P, Siest G, Visvikis S. A multilocus genotyping assay for cardiovascular disease. Clin. Chem. Lab Med. 1998; 36(8)561–566
- Siest G, Visvikis S, Herbeth B, Gueguen R, Vincent-Viry M, Sass C, Beaud B, Lecomte E, Steinmetz J, Locuty J, Chevrier P. Objectives, design and recruitement of a familial and longitudinal cohort for studying gene-environment interactions in the field of cardiovascular risk: The Stanislas Cohort. Clin. Chem. Lab Med. 1998; 36(1)35–42
- Miller S A, Dykes D D, Polesky H F. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res. 1988; 16: 1215
- Bohnet K, Régis-Bailly A, Vincent-Viry M, Schlenck A, Gueguen R, Siest G, Visvikis S. Apolipoprotein E genotype ϵ4/ϵ2 in the STANISLAS Cohort Study-Dominance of the ϵ2 allele ?. Ann. Hum. Genet. 1996; 60: 509–16
- Hallman D M, Visvikis S, Steinmetz J, Boerwinckle E. The effect of variation in the apoli-porpotein B gene on plasma lipid and apolipoprotein B levels. Ann. Hum. Genet. 1994; 58: 35–64
- Zaiou M, Visvikis S, Gueguen R, Parra H J, Fruchart J C, Siest G. DNA polymorphisms of human apolipoprotein A-IV gene: frequency and effects on lipid, lipoprotein and apolipoprotein levels in a french population. Clin. Genet. 1994; 46: 248–254
- Salah D, Bohnet K, Gueguen R, Siest G, Visvikis S. Combined effects of lipoprotein lipase and apolipoprotein E polymorphisms on lipid and lipoprotein levels in the Stanislas Cohort. J. Lipid Res. 1997; 38: 904–912
- Georges J L, Régis-Bailly A, Salah D, Rakotovao R, Siest G, Visvikis S, Tiret L. Family study of lipoprotein lipase gene polymorphisms and plasma triglyceride levels. Genetic Epidemiol. 1996; 13: 179–192
- Lange K, Weeks D, Boehnke M. Programs for pedigree analysis: Mendel, fisher, and d gene. Genetic Epidemiol 1988; 5: 471–472
- Lange K, Westlake J, Spence M A. Extensions to pedigree analysis. III. Variance components by the scoring method. Ann. Hum. Genet. 1976; 39: 485–491
- Tenkanen H, Lukka M, Jauhiainen M, Mesto J, Baumann M, Pelton L, Ehnholm C. The mutation causing the common apolipoprotein A-IV polymorphism is a glutamine to histidine substitution of amino acid 360. Arterioscler. Thromb. 1991; 11: 851–856
- Tenkanen H, Ehnholm C. Molecular basis for apo A-IV polymorphisms. Ann. Med. 1992; 24: 369–374
- Von Eckardstein A, Funke H, Schulte M, Erren M, Shulte H, Assmann G. Nonsynonymous polymorphic sites in the apolipoprotein (apo) A-IV gene are associated with changes in the concentration of apo B and apo A-I containing lipoproteins in a normal population. Am. J. Hum. Genet. 1992; 50: 1115–1128
- Zaiou M, Visvikis S, Gueguen R, Steinmetz J, Parra H J, Fruchart J C, Siest G. Sources of variability of human plasma apolipoprotein A-IV levels and relationships with lipid metabolism. Genetic Epidemiol 1994; 11: 101–114
- Boerwinkle E, Visvikis S, Welsh D, Steinmetz J, Hanash S, Sing C F. The use of measured genotype information in the analysis of quantitative phenotypes in man. II. The role of the apolipoprotein E polymorphism in determining levels, variability and covariability of cholesterol, beta-lipoprotein and triglycerides in a sample of unrelated individuals. Ann of Hum Genet 1987; 27: 567–82