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Multiple strategies are available to affect children's cardiovascular health. From clinic-based high-risk counseling to broad-based school or community programs, intervention strategies are being developed and tested to find the most effective means of changing the risk factors of youth to assure a healthier future for our children. Since adoption of new behaviors is improved by consistent messages from multiple sources, a concerted effort is needed. The involvement of health professionals, educators, community organizations, industry, and government together will be important to support the adoption of healthy lifestyles for succeeding generations. Intervention through cardiovascular health promotion for school children may well be the future direction for preventive cardiology.

The distributions of serum creatinine levels and their relationship with selected anthropometric and cardiovascular risk variables have been described in 3983 children and young adults, aged 5 to 26 years, obtained from a biracial population, Bogalusa, Louisiana. For both blacks and whites serum creatinine levels increased slowly with age, until 11 years of age when a steeper increase occurred to around 19 years of age. Before this age there was a significant age by sex interaction (p less than 0.0001) in the distributions of serum creatinine. After the age of 19 years mean serum creatinine levels were significantly higher in black men than in white men (1.16 mg/dl vs 1.09 mg/dl, p less than 0.0005) and in black women than in white women (0.87 mg/dl vs 0.84 mg/dl, p less than 0.08). Creatinine levels were also significantly higher in men than in women (1.11 mg/dl vs 0.85 mg/dl, p less than 0.0001). Creatinine clearance, estimated from an equation using serum creatine, age, and weight, showed a steady increase until 13 years of age when a maximum range of 120 to 140 ml/min was reached. By the age of 19 years the clearance had declined to a relatively constant range of 100 to 120 ml/min. Black men had the highest correlation of serum creatinine concentration with height, weight, and lean body mass after adjusting for age. White men had the highest correlation of serum creatinine concentration with uric acid. Diastolic blood pressure becomes an important determinant of creatinine levels by the age of 11 years. The race-sex differences in serum creatinine levels in children and young adults are likely related to body mass.

The robust or model-free method for detecting linkage developed by Haseman and Elston for data from sib pairs is extended to incorporate observations of multiple traits on each individual. A method is proposed that estimates the linear function that results in the strongest correlation between the squared pair differences in the trait measurements and identity by descent at a marker locus. The method is illustrated by the study of apolipoprotein and cholesterol levels in individuals from a large family that had many members diagnosed with coronary heart disease.

At the initial meeting on “Evolution of the Atherosclerotic Plaque” in 1963, the importance of specific glycosaminoglycans (GAG) (acid mucopolysaccharides) in atherosclerosis was shown (1). These complex sugars were noted to be an integral part of the arterial wall connective tissue matrix that changes with the type of atherosclerotic lesion. Although complex sugars were isolated from aorta about a century ago, it was not until the decade 1950–1960 (2) that characterization of the GAG fractions provided the opportunity to explore a pathobiologic role of these substances. Histochemical studies stimulated interest in complex sugars in atherosclerosis but did not allow their characterization. The considerable information that is now available from a variety of studies indicates that early in the formation of atherosclerotic lesions changes of GAG is part of the vascular connective tissue, followed by extensive lipid deposition and progression of lesions.

Many advances have now been made in understanding the early natural history of coronary artery disease and essential hypertension, an understanding that these diseases begin in childhood and that CVD relates to clinical cardiovascular risk factors. Methods have now been established to determine risk factors in the pediatric age and, with a family history, to begin to identify children at potential risk for premature heart disease. Advances have also been made in developing models for intervention and beginning prevention through both high-risk and population strategies directed at schoolchildren. Obviously, both approaches are needed and complement each other. An impressive future is ahead for effective preventive cardiology beginning with children by incorporation of cardiovascular health education and health promotion in elementary schools. Applying behavioral concepts to intervention programs can strengthen their chances of success. The overall good of having children adopt healthy life-styles with an understanding of their necessity is now attainable. It will be the responsibility of physicians to guide the direction of programs being promoted for children.

Arterial wall structure and function, an important determinant of cardiovascular (CV) disease, are influenced by CV risk factors, especially high levels of blood pressure and low-density lipoprotein cholesterol (LDLC). However, the differential impact of these two risk factors on arterial structure and function in healthy, asymptomatic younger adults is not clear. This aspect was examined in 1003 black and white adults aged 23-43 years enrolled in the Bogalusa Heart Study. Carotid artery intima-media thickness (IMT) (an average of common, bulb and internal carotid on both sides) and aorta-femoral pulse wave velocity (PWV) measured by B-mode ultrasound were used as indicators of artery structure and function. Values of IMT (0.83 mm) and PWV (5.4 m/sec) in blacks were significantly higher than IMT (0.80 mm) and PWV (5.2 m/sec) in whites, respectively (p

That cardiovascular (CV) risk variable levels tend to track in the same ranking over time is well recognized. However, information on tracking of CV risk variables over a long period of time from childhood to adulthood and the changes in tracking with increasing intervals is limited. This aspect was examined in a biracial (black-white) cohort of 7770 individuals (63% white, 46% male) who were examined repeatedly 2-12 times with 31500 observations over an average follow-up period of 12 years (range: 1-28 years). Pearson correlations of pairs of two consecutive values measured 1 to 28 years apart decreased progressively regardless of risk variables as the intervals between the two observations increased. Intraclass correlation, an overall measure of tracking, was estimated using 4 serial measurements over 20-25 years, 2 in childhood (4-17 years), and 2 in adulthood (18-43 years). Body mass index showed the greatest intraclass correlation (0.74 for whites; 0.73 for blacks), followed, in order, by low-density lipoprotein cholesterol (0.56; 0.58), systolic blood pressure (0.43; 0.38), high-density lipoprotein cholesterol (0.35; 0.36), diastolic blood pressure (0.30; 0.34), and triglycerides (0.36; 0.28). Both the Pearson and intraclass correlations of all risk variables did not differ by race and sex groups and remained essentially the same when adjusted for body mass index. Thus, CV risk variables measured in childhood are predictive of adulthood levels over a period of 2-3 decades. These results underscore the value of measuring childhood CV risk variables in identification of high-risk individuals, which is important for early prevention and intervention.

Cigarette smoking, an established cardiovascular (CV) disease risk factor, is known to adversely influence atherosclerosis and its relationship to other risk factors in middle-aged and older adults. However, information is limited in this regard in younger adults. This aspect was examined in a sample of 697 cigarette smokers and 311 nonsmokers, aged 25-44 years, from a biracial (black-white) community. Carotid intima-media thickness (IMT), a surrogate measure of coronary atherosclerosis, was measured by B-mode ultrasonography to obtain the mean value of far wall readings of carotid artery segments (common, bulb, internal) on both sides. Smokers vs nonsmokers showed lower levels of body mass index (27.1 vs 29.5 kg/m2, p

It is necessary to examine lipid abnormalities at a macromolecular level, with emphasis on the transport lipoproteins rather than on cholesterol and triglyceride values alone. Methods for determining serum lipoproteins, which can be adapted for a small laboratory, are now available and are recommended for general clinical use. It is becoming increasingly apparent that the process of atherosclerosis has a long natural history that begins in childhood, and that it is now possible to study children for potential risk.

Parent-child associations of height, weight, subscapular skinfold thickness, blood pressure, and serum lipids and lipoproteins were observed in a cohort of 440 infants and their parents in Bogalusa, LA. The infants were examined according to a standardized protocol six times from birth to 7 years of age, and the parents were examined when the child was 2 years old. Regression analyses were performed with the value of the cardiovascular risk factor variable for the child as the dependent variable and race, sex of child, and either mother's value, father's value, or both mother's and father's values as the independent variables. The most significant relationship between parents and their children was for height (P < .005 at all ages of the child) and weight (P < .05 from age 1 year for father's regression coefficient and at all ages for mother's regression coefficient). Regression coefficients for parental serum lipids and lipoproteins tended to increase with the child's age. Child-father regression coefficients and child-mother regression coefficients were generally significant (P < .05) after age 2 years for total cholesterol. Less association was noted for triglycerides and lipoproteins. Parental diastolic BP was a poor predictor of children's values; the regression coefficients for systolic BP were higher and more significant. The longitudinal nature of this cohort study allows for examination of the changing patterns of familial association with aging and may provide insight as to the best age for examining children for cardiovascular risk factors to determine their relative risk for heart disease.

We separately evaluated split specimens of serum for lipoprotein cholesterol in 38 five- to 14-year-old children, by the heparin/Ca2+ precipitation method and the ultracentrifugation/dextran sulfate precipitation method. Statistical analysis of the results indicated an excellent agreement (especially in beta- and alpha-lipoprotein cholesterol values) between results by the two methods. The percentage of alpha-lipoprotein cholesterol (mean +/- SD: 38.6 +/- 5.0) in children further confirmed the earlier observations that cholesterol derived from alpha-lipoprotein in children constitutes a relatively greater part of the serum total cholesterol than is true of adults.

The genetic determination of high-density-lipoprotein cholesterol (HDL-C) levels was evaluated using segregation analysis techniques in a large multigenerational kindred with a high prevalence of coronary heart disease and myocardial infarction. Univariate segregation analysis of HDL-C levels with the effects of age and sex removed by regression provided evidence of a Mendelian mode of inheritance for a portion of the variability in HDL-C levels. Subsequent analyses included low-density-lipoprotein cholesterol (LDL-C) levels and several behavioral and anthropometric variables that affect HDL-C levels. Pedigree discriminant analysis was used to find the linear functions of the variables that maximized the likelihood given the pedigree structure and assuming monogenic segregation. The best linear function was found to be approximately equivalent to the log of the HDL-C to LDL-C ratio, with concomitant and environmental effects removed by regression. Genetic hypotheses were tested by cross-validation; linear functions derived from data on each side of the kindred were used to test hypotheses on the other side of the kindred. On one side of the kindred, all hypotheses were accepted. On the other side of the kindred, only Mendelian inheritance of the linear function was indicated. Segregation of the age- and sex-adjusted HDL-C values, and of the linear function, was evaluated using a regressive model that allows for intrafamilial correlations in addition to a monogenic effect. All analyses provide evidence for levels of HDL-C being controlled by a major locus with neither dominant nor recessive expression.

The "Report of the National Heart, Lung, and Blood Institute's Task Force on Blood Pressure Control in Children" (Pediatrics suppl, May 1977) is a serious and long-needed attempt at establishing guidelines for practitioners in monitoring blood pressure levels in children and diagnosing early primary hypertension. Further, and importantly, it includes a consideration of prevention of future hypertensive disease, encouraging greater research and clinical interest in blood pressure in the pediatric age group. Specifically it encourages the physician examining children to include observations of blood pressure as a routine part of a physical examination.

We evaluated glycosylation of hemoglobin (HbA + HbA1) in 25 control subjects and in 133 diabetic patients who were in various stages of blood glucose control, by measuring ketoamine-linked hexoses in hemoglobin. These hexoses were converted by digestion with 10 mol/L acetic acid for 16 h at 100 +/- 5 degrees C to 5-hydroxymethylfurfuraldehyde, which was quantitated by reaction with 2-thiobarbituric acid. Glycosylation of hemoglobin was expressed as micromoles of hydroxymethylfurfuraldehyde per gram of globin protein (the "HMF index"). A mean HMF index of 1.67 (SD = 0.23) was obtained for controls; that for diabetic patients was 2.93 (SD 0.95). The index correlated well (r = 0.83, p < 0.001) with average blood glucose concentration as measured during the preceding 16 weeks, over a wide range of glucose values (1 to 6 g/L). It correlated even better (r = 0.92, p < 0.001) when corrected for variations in hemoglobin concentration. Thus measurement of ketoamine-linked hexoses of hemoglobin or HMF index provides an independent and useful alternative to the currently used methods that measure only HbA1 or HbA1c.

Summary Specimens of dead skin from various sites of the body were studied to determine the rate of passive diffusion of water under certain environmental atmospheric states. Effects of dry heat, relative humidity, radiant heat, ultraviolet irradiation, air currents and protection of skin by lipid coverings were observed. These factors influence the rate of water loss by diffusion through the skin in a predictable manner. The importance of these observations in relation to acclimatization to a tropical and subtropical environment was discussed. Since the inhibition of the transfer of water through human skin resides in the epidermis, the effects of chemical alteration of constituents of epidermis were also observed. The superficial layer of cells of the epidermis apparently inhibits water diffusion through skin by virtue of diffuse lipid or fat phase supported in a keratin-rich framework. This inhibiting material was not identified or studied in detail.

SummaryStudies on the liver involved with increasing amounts of amyloidosis and control tissues indicate that there is a marked increase in MPS content with severe amyloid infiltration. The increase of MPS was accounted for by increases in heparitin sulfate, chondroitin sulfate B, and somewhat less of chondroitin sulfates A and C. The consistent increase of heparitin sulfate in the liver of the ducks was similar to that observed in amyloidosis in humans and in experimentally induced disease. This remarkable increase of chondroitin sulfate B suggests a link to other vascular diseases and genetic connective tissue defects. The Pekin duck serves as an interesting model to study spontaneously occurring amyloidosis.

Diets of four groups of 10-year-old children (no. = 871) from a biracial community were examined to document eating patterns and to note temporal trends in energy, protein, fat, and carbohydrate intakes. A 24-hour dietary recall method, incorporating numerous quality controls, was adapted for interviewing children. Protein provided 13%, fat 38%, and carbohydrate 49% of calories. Few racial differences in eating patterns were detected. Boys had higher energy intakes than girls, but after diets were adjusted per 1,000 kcal, no other sex differences in intake were found. Snacks yielded roughly one-third of daily energy intake, one-fifth of the day's protein, one-third of the fat, and two-fifths of the total carbohydrate intake. Density of macronutrients within the children's diets was consistent over time. Diets of children in the Bogalusa study typify the American eating pattern and are comparable with those found in major national surveys.

We studied the effect of low-density lipoproteins (LDL) on the synthesis and secretion of proteoglycans by cultured human umbilical-vein endothelial cells. Confluent cultures were incubated with [35S]sulphate or [3H]glucosamine in lipoprotein-deficient serum in the presence and in the absence (control) of LDL (100-400 micrograms/ml), and metabolically labelled proteoglycans in culture medium and cell layer were analysed. LDL increased accumulation of labelled proteoglycans in medium and cell fractions up to a concentration of 200 micrograms/ml. At this concentration of LDL the accumulations of proteoglycans in medium and cell layer were 65% and 32% respectively above control for 35S-labelled proteoglycans, and 55% and 28% respectively above control for 3H-labelled proteoglycans. At concentrations above this LDL was found to depress the accumulation of proteoglycans in medium and cell layer. Gel filtration on Sepharose CL-4B showed that in both control and LDL-treated cultures the cell layer contained a large (Kav. = 0) and a small (Kav. = 0.35) heparan sulphate proteoglycan, whereas the culture medium contained a large heparan sulphate proteoglycan (Kav. = 0) and a smaller isomeric chondroitin sulphate proteoglycan (control, Kav. = 0.35; LDL-treated, Kav. = 0.17). The relative increase in hydrodynamic size of the isomeric chondroitin sulphate proteoglycan (Mr 150,000 compared with 90,000) in the medium of cultures exposed to LDL was partly attributable to the larger size of the glycosaminoglycan side chains (Mr 39,000 compared with 21,000). The isomeric chondroitin sulphate proteoglycan in LDL-treated culture was relatively enriched in chondroitin 6-sulphate compared with that in control cultures (39% compared with 29%). Pulse-chase studies showed that LDL treatment did not alter the turnover rate of proteoglycans as compared with controls, implying that the elevation in proteoglycan accumulation in LDL-treated cultures was due to enhanced synthesis. These results demonstrate that LDL can modulate proteoglycan synthesis by cultured vascular endothelial cells, resulting in the secretion of a larger isomeric chondroitin sulphate proteoglycan enriched in chondroitin 6-sulphate.

Social and behavioral learning methods, combined with nutrition counseling and innovative education modules, provide a well-rounded approach to eating behavior intervention. Dietitians can apply this multifaceted approach in various settings to maximize eating behavior change.

Height, weight, and skinfold measurements were obtained on a cohort of 447 children from birth (weight) or 6 months of age (height and skinfold) and monitored yearly thereafter until 7 years of age. At age 7 years, 250 remained for follow-up screening. A significant degree of tracking was found for all variables from age 1 to age 7 years. Height and weight tracked most strongly (age 1- to 7-year correlations = .42 and .44, respectively), whereas skinfold tracked somewhat lower (.28). Earlier levels of each anthropometric variable were the best predictor of later levels of that parameter. Implications for early detection and treatment of growth abnormalities are discussed.

A large pedigree (N = 356) with a high prevalence of heart disease and associated adverse lipoprotein phenotype was studied. The adverse lipoprotein phenotype is characterized by both low levels of high-density-lipoprotein cholesterol (HDL-C) alone (16.3%) and in combination with other adverse lipoprotein levels (12.8%). In all, 44.2% of all pedigree members had at least one adverse lipoprotein level. Analysis of mating types showed that all lipids and lipoproteins possess familial clustering with 25-36% of offspring above median levels when both parents had levels below the median, while 67-83% had levels above the median when both parents had levels above the median. Using adjusted lipid and lipoprotein levels, a statistically significant linear trend was found between the degree of relationship to pedigree members with heart disease, and both the low-density-lipoprotein cholesterol/high-density-lipoprotein cholesterol (LDL-C/HDL-C) ratio (P less than .05), and the very-low-density-lipoprotein cholesterol (VLDL-C; P less than .01) level. A similar analysis using the prevalence of adverse lipoprotein levels as the dependent variable and degree of relationship to heart diseased pedigree numbers as the independent variable showed significant (P less than .05) relationships with VLDL-C and the LDL-C/HDL-C ratio. Further genetic analyses of this pedigree may reveal genetic mechanisms responsible for the familiality of lipoprotein levels in this pedigree.

The concept of injury as a mechanism leading to atherosclerosis has been fostered by numerous studies of initiating factors and by observation of the response of cardiovascular connective tissue, ie, cellular and extracellular matrix components. Carbohydrate-protein macromolecules of the extracellular matrix are a complex group of biologically important substances that play a crucial role in mesenchymal tissue repair following injury, a process needed to maintain arterial wall integrity. Of particular interest are the proteoglycans that enter into a variety of roles, from that of inhibiting atherosclerosis and helping to maintain fibrillar structures to that of taking part in lipid deposition in the development of atherosclerosis.

Glycoproteins were extracted from human atherosclerotic lesions by a phosphate buffered heparin solution and by 0.15 M NaCl, followed by sequential digestion of the tissue by collagenase and elastase. Proteins obtained from the extracts by fractional precipitation by (NH4)2SO4 at 40%, 60% and 100% saturation of the salt at pH 4.0 were analyzed for total protein and for fibronectin and laminin by immunodiffusion. Greater amounts of proteins were extracted from atherosclerotic lesions than from uninvolved tissue. The buffered heparin solution extracted several-fold more protein than 0.15 M NaCl. Fibronectin was found in most protein fractions from every extract, but the presence of laminin was noted only in the protein fractions precipitated at 40% saturation of (NH4)2SO4 in the extracts of the tissue by heparin.

Cardiovascular risk factor variables were examined in a cohort of 440 infants from birth through 7 years of age. Anthropometric measures, BP, serum lipid and lipoprotein values, and dietary intake data were obtained according to detailed protocols. Various quality controls to ensure the collection of valid and reliable data were instituted. Participation remained high throughout the study with 80% of the children examined at 6 months and 60% at 7 years of age. Rates were slightly higher for black than for white children. Children born in the private hospital were more likely to continue in the study than children born in the charity hospital. Children of parents examined when the child was 2 years of age were more likely to be examined during the preschool phases, but parental examination was not related to child examination when the child was 7 years of age. As in studies of school-aged children, measurement errors were lowest for height, weight, and serum total cholesterol. Measurement errors for BP were highest at the younger ages, particularly for diastolic BP. Examination of a newborn cohort throughout time affords the opportunity to study early development of relationships and tracking of cardiovascular risk factors.

To assess relationships between increases in triceps skin-fold thickness (TRSF) and changes in levels of serum lipids and lipoproteins in early life, a biracial sample of 1,598 five to 12 year olds were reexamined five years after an initial examination. Significant positive correlations, controlled for age, were observed between changes in TRSF and changes in levels of serum total cholesterol, serum triglycerides, and low- and very low-density lipoprotein cholesterol. Inverse associations between changes in TRSF and high-density lipoprotein cholesterol were weaker, but also statistically significant. Although females showed the largest increases in TRSF, most associations were stronger in males. Increases in estimated percentage body fat and ponderal index (kilograms per cubic meter) were highly associated with changes in TRSF, but showed slightly different associations with the serum lipids and lipoproteins. Results show that increases in obesity in youth are accompanied by an increasingly atherogenic lipoprotein profile.

Eighty per cent of all identified children 2 1/2-5 1/2 years old in a total geographic community in Bogalusa, Louisiana, were examined for cardiovascular disease risk factor variables, including blood pressure (BP), anthropometric measurements, and blood lipids. Blood pressure was measured by three instrument types, each with three readings, according to a rigid, randomized design. Results from the three instruments were compared, and potential biases for each instrument are listed. All observations on the children were analyzed by multiple regression with BP as the dependent variable. After controlling for the mood of the child, the authors found that some index of body size was positively related to BP, whereas age, race, and serum lipids were not consistently related. The regressions of blood pressure on height as well as on log weight fit straight lines. These results conform with the findings for the 5- to 14-year-olds in this community. The basal or fundamental reference blood pressure is likely to rise gradually from birth to the age of incipient adult stature, and to be linearly related to height and to log weight. Changes observed over time are needed to relate BP levels in childhood to the early natural history of essential hypertension.

We used a combination of heparin micro-affinity column chromatography and heparin-Mn2+/dextran sulfate (DS) precipitation procedures to measure directly the total high-density lipoprotein (HDL)-cholesterol and HDL3-cholesterol in serum. The value for HDL2-cholesterol was obtained by subtracting the value for HDL3-cholesterol from that for total HDL-cholesterol. Results of this methodology and of the original heparin-Mn2+/DS double-precipitation method were compared with those of preparative ultracentrifugation. Concentrations of HDL- and HDL2-cholesterol by the original double-precipitation method were respectively 26 and 33 mg/L lower than by the ultracentrifugation method (p less than 0.001). Corresponding values by the micro-affinity/precipitation method were 36 and 29 mg/L higher than by the ultracentrifugation method (p less than 0.001). The values for HDL3-cholesterol by ultracentrifugation and by precipitation differed only by 7 mg/L (p greater than 0.05). Micro-affinity/precipitation and double-precipitation results both correlated well with those by ultracentrifugation (r = 0.84 to 0.94); the y-intercept of the comparison with the micro-affinity/precipitation method was close to zero. Use of the micro-affinity/precipitation method with samples from black or white adolescents showed that the blacks had higher concentrations of HDL2-(p less than 0.01) and HDL3-cholesterol (p less than 0.02) than did the whites.

Changes of arterial wall lipid and connective tissue components were studied under various regression regimes on experimental high fat-cholesterol diet induced atherosclerosis in non-human primates. Levels of plasma lipids and aorta tissue lipids were closely related, while an inverse relationship between plasma cholesterol levels was noted with the ratio of aorta tissue free/ester cholesterol. Although the total content of glycosaminoglycan increased slightly with increasing disease, changes of individual glycosaminoglycans were most closely related to the severity of aorta atherosclerosis associated with both induction and regression of disease. With increasing atherosclerosis hyaluronic acid tended to decrease, while chondroitin sulfates decreased. Heparan sulfate decreased considerably with increasing severity of atherosclerosis. Consequently, regression regimens reducing the severity reversed the glycosominoglycan changes. Withdrawal of the dietary stimulus and cholestryamine produced the greatest reversal of atherosclerosis. In contrast, D-thyroxine treatment resulted in severe aorta atherosclerosis comparable to controls receiving no treatment. The effectiveness of regression depends on favorably altering plasma lipids but without adversely affecting the arterial wall structural elements.

Although differences in hemoglobin levels between blacks and whites may be due in part to genetic influences, low hemoglobin levels in black girls of childbearing age may nevertheless constitute a health hazard. To study this problem, hemoglobin levels were examined in children of a biracial community not only before but also during and after puberty and menarche. At the same time, 24-hour dietary recalls of a representative group of 13-year-olds in the same population were examined with respect to the intake of iron and nutrients influencing iron absorption. In black girls, hemoglobin levels dropped after menarche, accompanied by a diet marginal in iron and in iron-absorption-promoting nutrients. Questions as to hemoglobin levels compatible with optimum health remain, and racial differences and genetic influences on levels should not be an excuse for failure to address this problem. More investigational studies are also needed to observe responses to an optimum dietary iron intake.

The incorporation of 35S into proteoglycans (PG) of bovine aorta segments maintained in short term culture was investigated. The labeled PG were isolated by 4.0 M guanidinium chloride extraction and collagenase and elastase digestion and specific activities determined. The culture medium contained about 10% of the total uronate. In the sequential extraction of tissue PG, elastase treatment released the most uronate material. Guanidinium chloride extracted PG showed the highest degree of sulfation while the elastase solubilized PG had the lowest sulfate content. In the culture medium the highest specific activity was noted in heparan sulfate PG, followed by the chondroitin sulfates PG and then dermatan sulfate PG. Among the PG from tissue extracts, dermatan sulfate chains from guanidinium chloride extracted and collagenase solubilized PG showed similar specific activity. The highest specific activity of haparan sulfate was observed in the elastase solubilized PG. The specific activity of chondroitin sulfate chains was the lowest in all tissue PG preparations. These studies provide further evidence of the metabolic heterogeneity of aorta PG.

The gene frequencies of a polymorphism in the 5'-flanking region of the insulin gene and its relationship to cardiovascular disease risk were studied in a well defined population of children (mean age 5.5 years) from a biracial community. The BglII endonuclease was used for digestion of the DNA around this polymorphic region. The risk factors studied included parental and grandparental self-reported histories of myocardial infarction and diabetes mellitus, fasting glucose and insulin levels, lipoprotein, cholesterol, and triglyceride levels, and skinfold thicknesses and weight. Four alleles were observed at this locus, with the class 2 allele being significantly more common among blacks than whites. Among white children, the class 3 allele was associated with increased risk for grandparental diabetes mellitus. White children with 2 copies of the class 3 allele had significantly higher levels of glucose. Black children with a copy of the class 3 allele had significantly higher levels of insulin. This study indicates that the class 3 allele is potentially associated with risk for diabetes mellitus and coronary heart disease that can be observed in childhood.

Although the significance of Yudkin’s (1972) observation relating morbidity from coronary heart disease (CHD) to excessive intake of dietary sucrose remains controversial, the metabolic effects of sucrose on CHD risk factor variables such as serum lipids, glucose and insulin are well recognized. We observed that the average intake of sucrose in Bogalusa children constituted 50% of the total carbohydrate (Frank et al. 1978). It is also generally accepted that excessive salt intake is an etiologic factor in the development of hypertension, another major CHD risk factor. In rats dietary sucrose has been shown to potentiate salt induced hypertension (Hall and Hall 1966). While manipulation of dietary fat and cholesterol continues to be extensively applied in experimental atherosclerosis, only a few studies have been concerned with the effect of dietary sucrose on the accepted CHD risk factors, viz., hyperlipidemia and hypertension, under experimental conditions, especially in nonhuman primates. In these studies we investigated the response of different nonhuman primates to the potentiating effects of sucrose on hyperlipoproteinemia and salt induced hypertension (Srinivasan et al. 1978, 1979a, 1979b).

Glycoproteins from bovine aorta intima were isolated by a sequential digestion of the tissue with collagenase and elastase after extration of the tissue with saline. The proteins in the extracts were precipitated by (NH4)2SO4 and fractionated by Con-A sepharose affinity chromatography. The fractions were analyzed for their carbohydrate composition and by polyacrylamide disc gel electrophoresis. These studies show that considerable heterogeneity of aorta glycoproteins exists. Some of the glycoprotein materials are likely intimately associated with fibrous structures, collagen and elastin, of the aorta intima.

During the past 10 years, much clinical information has been obtained on cardiovascular (C-V) risk factors in pediatric populations. Impetus to study C-V risk in children for adult heart diseases evolved naturally from adult population studies, i.e., Framingham, Tecumseh, Evans County and others. The major medical advance was made in documenting clinical parameters that predict morbid C-V events. It became apparent that similar clinical parameters could be observed in children. Equally important to the clinical observations has been recognition that atherosclerotic lesions are already present in early life. ZEEK (1), HOLMAN et al. (2) noted atherosclerotic lesions developed early, even in infancy. Findings of coronary artery lesions in soldiers necropsied in the Korean War (3), and later in Vietnam (4), were impressive. The nature of coronary artery lesions, occurring early and gradually increasing during a subclinical phase, is now well recognized. As an outgrowth to this history, it became important as part of an epidemiology program, to study the early natural history of coronary artery disease in children (5) and to correlate anatomic changes along with clinical C-V risk factors.