References: 

1) Andrew et al., Nonrandom association between Huntington disease and two loci separated by about Mb on chromosome 4p16.3. Genomics 12, 301-308 (1992).
2) Weber JL & May PE. Abundant class of human DNA polymorphisms which can be typed using the polymerase chain reaction. Am J Hum Genet 44, 388-396 (1989).
3) Fries JF. Aging, natural death and the compression of morbidity. N Engl J Med 303, 130-135 (1980).
4) Ordovas JM et al., Apolipoprotein E isoform phenotyping methodology and population frequency with identification of ap and ap isoforms. J lipid Res 31, 1203-1216 (1990).
5) Utermann G et al., Genetic control of human apolipoprotein E polymorphism: comparison one- and two-dimensional techniques of isoprotein analysis. Hum Genet 60, 244-249 (1982).
6) Boemi M et al., Gender differences in a type (non-insulin-dependent) diabetic population with respect to apolipoprotein E phenotype frequencies. Diabetologia 34, 845-849 (1991).
7) Jeunemaitre X et al., Absence of linkage between the angiotensin converting enzyme locus and human essential hypertension. Nature Genet 1, 72-75 (1992).
8) Ehlers MRW & Riordan JF. Angiotensin-converting enzyme: new concepts concerning its biological role. Biochemistry 28, 5311-5318 (1989).
9) Costerousse O et al., The angiotensin-converting enzyme (kininase II): molecular organization and regulation of its expression in humans. J Cardiovasc Pharmacol 20 Suppl 9, S34-S39 (1992).
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