Abstract The magnitude and rates of growth have been compared among two cross‐sectional samples of Tokelau children on the basis of 26 anthropometric dimensions. One of the samples consisted of children living on the Tokelau Islands. The migrant sample consisted of children of Tokelau descent who were living in New Zealand. The comparison between samples suggest significant differences in the rate of linear growth at the younger ages. However, most differences were not significant among 17 year olds. The results support the hypothesis that even when the original environment is favorable, qualitative changes in the environment may affect the general pattern of growth. The effects of an accelerated growth pattern cannot be determined at this time.
Data from various laboratories have indicated associations of various alleles determined by RFLPs within or adjacent to several apolipoprotein genes with abnormalities in plasma lipids and/or premature coronary artery disease (CAD). In order to assess such relationships we have examined allele frequencies of 8 different RFLPs within or adjacent to the apo A-I, C-III and A-IV gene complex on the long arm of chromosome 11 (MspI, 5′ to the apo A-I gene; MspI, within the apo A-1 gene; PstI, 3′ to the apo A-I gene; SstI, 3′ to the apo C-III gene; PvuII, within the apo C-III gene; PvuII, 5′ to the apo C-III gene; XbaI, within the apo A-IV gene; and XbaI, 3′ to the apo A-IV gene) in 202 patients with CAD (50% narrowing of one or more coronary arteries) prior to age 60 and 145 normal controls. None of the allele frequencies of these RFLPs were significantly different in cases as compared to controls. With regard to associations with plasma lipids and apolipoprotein levels, the rare allele determined by the absence of the PstI site was associated with elevated triglyceride levels (P < 0.05) in cases, but not in controls. In contrast, the rare MspI allele 5′ to the apo A-I gene was associated with elevated triglyceride levels (P < 0.05) in controls but not in cases. In both cases and controls, subjects with the uncommon SstI allele had triglyceride levels that were 9 and 38% higher than in those without this allele. These differences were significant (P < 0.05) only in controls. Our data indicate that the rare allele determined by the SstI site within this gene complex deserves further study in order to understand its association with elevated triglycerides in Caucasian populations. However, at the present time all these DNA markers lack sufficient specificity to be clinically useful for CAD risk assessment.
Background Although both genetic and nongenetic factors contribute to the pathogenesis of coronary artery disease, the identification of specific genetic lesions has lagged behind the identification of critical environmental risk factors. A reported association between myocardial infarction (MI) and the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene in European men suggests a critical role for this genomic region. However, the generality of this association remains to be determined. It also is not clear at what stage in disease progression the association with the ACE I/D polymorphism becomes important. Methods and Results We evaluated the ACE I/D polymorphism in patients who had undergone coronary angiography (402 men and 295 women) and in 203 representative control subjects. After polymerase chain reaction amplification, genotypes were determined by agarose gel sizing and by hybridization with allele-specific oligonucleotides. After patients were categorized by the degree of coronary artery stenosis and the occurrence of an MI, the distribution of ACE I/D genotypes was evaluated by log linear analysis. Patients were genetically representative of the regional population, and patients with >60% stenosis of their coronary arteries had the same distribution of ACE I/D genotypes as did patients with <10% stenosis. However, among patients with stenosis, the occurrence of an MI was significantly associated with the D allele in all patients (odds ratio [OR], 1.59; P =.002) and in men alone (OR, 1.63; P =.006). The lack of significance in women (OR, 1.40; P =.263) is probably due to the fact that only 36 women in the present study had experienced an MI. Furthermore, the association between MI and the ACE I/D polymorphism was independent of blood pressure, smoking habits, and body mass index. Conclusions Segregation of the ACE I/D polymorphism is a pervasive genetic risk factor for MI in whites but has no evident effect on the events leading to stenosis of the coronary arteries. This suggests that risk of MI is influenced by two independent processes—atherogenesis that leads to coronary stenosis followed by conversion to MI. The renin-angiotensin system appears to confer significant risk of infarction by influencing the conversion to MI but has no apparent effect on the development of atherostenosis.
The aim of this study was to examine strategies for selecting a criterion value during anthropometric data assembly and their resilience to imposed error. Sixty-seven women aged 16–60 years were subjected to three separate series of measurements, which included six skinfolds and three girths. A random error term was added to the first of the three series of measurements to produce a pseudo-series containing error, termed the ‘erroneous replicated series’. Five strategies were then used to determine the criterion value of each of the replication series: the first measurement, the mean of the first two measurements, the mean of all three measurements, the mean of the closest two measurements and the median of the three measurements. The technical error between the criterion values of the true and the flawed replication series for each of the selection strategies was calculated. We found that, for five of the skinfolds and all of the girths, the median value provided the smallest technical error of measurement between the criterion values for the true and erroneous replication series. We conclude that the strategy of selecting the median of three measurements is the most resilient to imposed error.
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