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J A Morrison

Publications and source records attributed to J A Morrison.

At least 91 records · Page 5Linked to original sources
PubMed1982

The Clinical Lipid Research Clinic Family Study: familial determinants of plasma uric acid.

Commingling analysis of plasma uric acid levels in a random sample of 160 nuclear families supports the hypothesis that there is a mixture of three distributions. Assuming one, two, and three components in the underlying distribution, we obtained the corresponding p-values (for power transformation) as 0.059, 1.040, and 1.643, respectively. Path analysis with p = 0.059, 1.040, and 1.643 respectively. Path analysis with p = 0.059 gives genetic (h2) and cultural (c2) heritabilities as 0.256 and 0.199, without much support for intergenerational differences, assortative mating, or maternal effects. Complex segregation analysis with p = 0.059 supports multifactorial inheritance, consistent with the findings of Gulbrandsen et al. (1979) and Morton (1979) in other populations. This study also fails to support a major locus hypothesis, contrary to earlier reports.

Adolescent↗
PubMed1982

The Cincinnati Lipid Research Clinic family study: cultural and biological determinants of lipids and lipoprotein concentrations.

A general linear model is described here for cultural and biological inheritance of lipids and lipoproteins. This model involves 10 parameters to be estimated from a total of 17 correlations, leaving ample degrees of freedom to test the goodness of fit. The model fits very well to each of the five lipid and lipoprotein variables analyzed here from a Lipid Research Clinic family data set. Both genetic and cultural inheritance are significant for each trait with the single exception that triglyceride levels fail to support genetic inheritance. Under the most parsimonious hypothesis, the genetic heritability (h2) ranges from .194 +/- .092 for triglyceride to .624 +/- .093 for low-density lipoprotein-cholesterol. Cultural heritability ranges from .070 +/- .030 for total cholesterol to .149 +/- .034 for triglyceride.

Adult↗
PubMed1981

Lipid and lipoprotein distributions in black adults. The Cincinnati Lipid Research Clinic's Princeton School Study.

To provide population data on levels of plasma cholesterol, triglyceride, and high- and low-density lipoprotein-cholesterol (HDL-C and LDL-C) in black adults, 627 black adults, aged 20 to 59 years, 206 men and 421 women, were studied in the Cincinnati Lipid Research Clinic's Princeton School Study. Comparisons were made with 2,493 white adults, aged 20 to 59 years, 1,111 men and 1,382 women, from the Princeton School Study. Black men had total plasma cholesterol levels that were comparable with those in whites; plasma cholesterol levels were higher in black than white women. Black men had lower levels of plasma triglycerides, higher HDL-C levels, and lower LDL-C levels than white men. Black women not taking exogenous sex steroid hormones had higher total cholesterol and HDL-C levels, and lower triglyceride and LDL-C levels than white women not taking exogenous sex steroid hormones. Black women taking exogenous sex steroid hormones had lower plasma cholesterol and triglyceride levels and slightly higher HDL-C and lower LDL-C levels than white women taking exogenous sex steroid hormones. These differences not only require the use of race-specific lipoprotein distribution tables for characterization of individual subjects, but are consistent with putatively reduced risk for coronary heart disease in blacks when compared with whites.

Adult↗
PubMed1981

Spontaneous imitations of Down's syndrome children: a lexical analysis.

This study describes the spontaneous imitations produced by four Stage 1 Down's syndrome children. The imitative speech of the children was compared to their spontaneous productions to determine whether words imitated are different from those produced spontaneously. The findings suggest that Down's children are similar to normal-language learners in that they selectively imitate model utterances during this linguistic stage.

Child↗
PubMed1981

Parent-child coronary heart disease risk factor associations.

The aim of this study was to assess parent-child interactions of coronary heart disease risk factors (total cholesterol, high and low density lipoprotein cholesterols, systolic and diastolic blood pressures, and relative ponderosity) in parents and their pediatric-aged children in the Princeton School study. The study population included 430 parent-child pairs from 301 families. Forty-seven of these 301 families were "nuclear" (both parents and at least one child) and included 118 parent-child pairs. Univariate analyses of covariance were used to assess parent-child risk factor interactions and interrelationships. Interdependent coronary heart disease risk factor relationships were extensively shared by parents with their children. Knowledge of parental risk factor levels and their relationships and interactions with children's risk factor levels should be useful in identifying children at presumptively increased long-term risk as adults, and should illuminate metabolic relationships between parents and children for coronary heart disease risk factors.

Adolescent↗
PubMed1981

Coronary risk factors in the young.

The exceptional growth in risk factor assessment and the efficacy of primary prevention in childhood of atherosclerotic and hypertensive diseases is the subject of entire books that have recently collated the results of multiple investigators (58, 59). It is a topic well beyond the constraints of this review. It appears that the major "adult" CHD risk factors, including elevated total plasma and low-density lipoprotein cholesterol, elevated triglyceride, reduced high-density lipoprotein cholesterol, high blood pressure, obesity, and initiation of cigarette smoking can usually be recognized in children. There are, as yet, no longitudinal studies that control for one or more of these CHD risk factor variables to determine whether future development of CHD could be prevented or ameliorated. In the absence of unequivocal longitudinal studies of efficacy of intervention, prudent, safe, and well-supervised interventions should be carried out only after exhaustive proof of diagnosis (58). The recently summarized data suggest that they hyperlipoproteinemias, high blood pressure, obesity, and initiation of cigarette smoking can (with varying degrees of success) be dealt with during childhood and adolescence.

Adolescent↗
PubMed1981

Alcohol intake, cigarette smoking and plasma lipids and lipoproteins in 12--19-year-old children. The Collaborative Lipid Research Clinics Prevalence Study.

The relationship of alcohol intake to plasma lipids and lipoproteins was assessed in 1603 white children, ages 12-19 years, from six Lipid Research Clinics as part of the Lipid Research Clinics Collaborative Population Studies. Of the 1603 children, 933 came from a randomly recalled group and 660 from a group recalled because of elevated cholesterol or triglyceride or both (the hyperlipidemic recall group). Using multiple regression analysis, the relationships of lipoproteins (as dependent variables) to alcohol, smoking, age and body mass (as explanatory variables) are assessed in both recall groups. In the random recall group, high-density lipoprotein (HDL) cholesterol was positively related to alcohol intake, independent of the other variables considered; for every ounce of alcohol intake, HDL cholesterol was 0.55 mg/dl higher in males and 1.04 mg/dl higher in females. HDL cholesterol was strongly and inversely related to smoking and body mass in both males and females and was inversely related to age in males. In females, plasma low-density lipoprotein (LDL) cholesterol, triglycerides and very low density lipoprotein (VLDL) cholesterol were all positively related to alcohol intake. In the hyperlipidemic recall group of children, alcohol intake had a weak positive relationship with HDL cholesterol in males; in the females, for every ounce of alcohol intake, HDL cholesterol was higher by 1.5 mg/dl. Alcohol intake was positively related to triglyceride levels in hypertriglyceridemic male children. In each recall group, alcohol intake had a small, significant, positive association with HDL cholesterol levels in 12--19-year-old children, and a less consistent positive association with triglyceride and VLDL cholesterol. If low HDL cholesterol concentrations in children are undesirable, attention should first be focused reduction of smoking (inversely associated with HDL cholesterol) and weight (inversely associated with HDL cholesterol, positively associated with LDL cholesterol, triglyceride and VLDL cholesterol), as measures that may modify HDL cholesterol levels.

Adolescent↗