Abstract The cardiovascular diseases exert widely differing contributions to the total burden of mortality and morbidity in extant human populations. To a large extent these differences are a reflection of the variable distribution of specific antecedent risk factors. For one such risk factor, blood pressure, there is considerable variability in its distribution between different ethnic groups, especially between traditional and nontraditional societies. Intensive epidemiological studies in Western societies, together with a number of cross‐cultural comparisons, suggest that the major determinants of high blood pressure are likely to be a constellation of sociocultural factors, with genetic determination being limited to the interaction between genotype and environment. Studies of populations in sociocultural transition offer an unique opportunity to identify the relative influence of specific sociocultural factors on the rate of change of blood pressure. In addition, when the study of such populations is placed in a quasi‐experimental context, genetic‐environmental interactions may also be detected. This strategy is illustrated by a study of the changing blood pressure distribution in Tokelauan migrants. Such an approach requires the initial definition of a response variable which measures change in blood pressure as a consequence of migration. The response variable, which identifies the relative influence of concomitants such as weight, age, and obesity, can then be subjected to genetic analysis. In the Tokelau case, blood pressure response tends to be positive in migrants but negative in non‐migrants. Further statistical analysis indicates that there is a small proportion of high responders in both populations and that these cluster in families in the migrant population. However, estimates of the transmission parameter suggest that sociocultural transmission, rather than Mendelian segregation, is responsible. To date there is little evidence that genetic‐environmental interactions have had any impact on the development of hypertension in this migrant population.
Twenty‐four alleles have been defined for HLA‐DPB based on their second exon sequences. This paper describes a novel method, co‐digested amplified fragment length polymorphisms (CAFLP), for assigning these alleles to heterozygous patients, as well as to homozygous cell lines. The method depends on co‐digestion of amplified DNA by restriction endonucleases and separation of the resultant fragments with polyacrylamide gel electrophoresis. Co‐digestion by selected restriction enzymes produces a set of readily discernible fragments that are unique for a given haplotype because the selected restriction sites occur in cis. Consequently, this method provides haplotype information not available from independent digests and allows all known heterozygous genotypes to be identified. Analysis of 103 trios of mother, father, and child, plus 120 normal caucasians, demonstrates the reliability and simplicity of this procedure. This simple typing method results in unambiguous assignment of all current HLA‐DPB genotypes in random samples with a high proportion of heterozygous individuals.
Real time compression of skinfolds was measured at three sites (triceps, abdominal medial calf), using a Slim Guide skinfold caliper adapted by the addition of a potentiometer, on eight males and eight females (age range 18-40 years). An average of eight trials for each subject at each site was used in modeling the compression curves. A mechanical model was developed, comprised of two parallel spring and viscous components in series with each other. $ Tt = Tinitial + F \left( { 1 \over k_1 } - \left\lceil { e { -k_1 t \over b_1 } \over k_1 } \right\rceil \right) + F \left( { 1 \over k_2 } - \left\lceil { e { -k_2 t \over b_2 } \over k_2 } \right\rceil \right) $ where: Tt = thickness at time t; Tinitial = intial skinfold thickness; F = force exerted by caliper; k(1) and k(2) = coefficients of elasticity; b(1) and b(2) = coefficients of viscosity. This two-component model was the best fitting model in comparison to one or three component alternatives. The coefficients of the model were different by sex and skinfold site. Coefficients for females showed greater elasticity and less viscosity compared to those for males. Further, there appeared to be a systematic site difference with the triceps having less elasticity and viscosity in both sexes. Am. J. Hum. Biol. 11:531-537, 1999. Copyright 1999 Wiley-Liss, Inc.
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