Early feeding patterns and atherosclerosis.
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Biomedical subjects
Publications and source records attributed to K Burton.
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Relationships between nutrient intakes and plasma lipids and lipoproteins were studied in 949 randomly selected children, ages 6--19, in the biracial, suburban, Princeton School District. While nutrient intake increased with age in males, such age-associated increases in nutrient ingestion were much less consistent or were not significant for females. Primarily in the 6--9 and 10--12 yr age groups, white children ingested more total calories, more saturated fat, and a lower ratio of polyunsaturated to saturated (P/S) fat, more total carbohydrates, sucrose, starch, and other carbohydrates, and more protein than black children. After adjusting for age, race, sex, weight, and height, several nutrient-lipid and lipoprotein partial correlation coefficients were significant, but of relatively low magnitude. There were weak but significant inverse correlations between dietary P/S ratios and dietary carbohydrates with both total (r = -.07, -0.7) and low-density lipoprotein cholesterol (C-LDL), (r = -.07, -.08). Plasma high-density lipoprotein cholesterol (C-HDL) was inversely and significantly correlated with dietary sucrose (r = -.07); plasma triglyceride correlated positively with dietary sucrose (r = .08). Potential relationships between nutrients and lipids-lipoproteins were also examined in children at the extremes of, and in the middle of, lipid-lipoprotein distributions. After covariance adjustment for age, sex, race, and Quetelet index, children having the highest levels of C-HDL had the lowest intake of dietary carbohydrate and total calories. After further covariance adjustment for total calories, children at the highest end of the plasma cholesterol distribution had a greater intake of cholesterol and total protein than did children in the lowest end of the distribution. Nutrient intake may play a small but significant role relative to lipids and lipoproteins in children, and as such, may have importance relative to pediatric precursors of atherosclerosis.
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Relationships between nutrient intakes and plasma lipids and lipoproteins were studied in 1,669 schoolchildren, aged 6 to 19 years; 948 were selected by random recall and 721 because of elevated plasma cholesterol or triglyceride (hyperlipidemic recall). Nutrient intake data was collected by using a 24-hour dietary recall. Median dietary cholesterol intakes for 6 to 9-year-old boys and girls in the random recall group were 222 and 230 mg/day, with polyunsaturated/saturated fat ratios of 0.34 and 0.33. For boys and girls, aged 10 to 12 years, median dietary cholesterol intakes were 296 and 235 mg/day, for 13 to 15 year olds, 343 and 237, and for 16 to 19 year olds, 418 and 221 mg/day. The dietary polyunsaturated/saturated fat ratios did not change appreciably with age. Partial correlation coefficients describing relationships between lipids, lipoproteins, and nutrients after adjustment for age, sex, race, and Quetelet index (W/H2) were calculated for all children (random and hyperlipidemic recall) after excluding children having plasma cholesterol, triglycerides, and calories less than or equal to the first or greater than or equal to the 99th percentiles for the random recall children. Plasma cholesterol was inversely and triglyceride positively correlated with dietary sucrose. Plasma low density lipoprotein cholesterol was inversely and triglyceride positively correlated with the dietary polyunsaturated/saturated fat ratio, total carbohydrate, and sugar. Potential relationships between nutrients and lipids-lipoproteins were also examined in children having low (first to tenth percentile), intermediate (45th to 55th percentile), and high (90th to 99th percentile) nutrient intake, after covariance adjustment for age, race, sex, and Quetelet index. Total plasma cholesterol fell as sucrose intake increased. Triglyceride rose along with caloric intake, total carbohydrate intake, and sucrose intake, while high density lipoprotein cholesterol levels fell with increasing caloric and sucrose intake. As dietary polyunsaturate ingestion rose from low to intermediate to high, plasma low density lipoprotein cholesterol increased. Nutrient intake may play a small but significant role relative to lipids and lipoproteins in children and, as such, may have importance relative to pediatric precursors of atherosclerosis.
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During the preparation of spheroplasts, adenine phosphoribosyltransferase (EC 2.4.2.7) and hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) were released in parallel with cytidine deaminase (EC 3.5.4.5) and uridine phosphorylase (EC 2.4.2.3), which, on other evidence, are considered to be located intracellularly. The two phosphoribosyltransferases and uridine phosphorylase were not significantly associated with purified membrane fractions as was purine nucleoside phosphorylase (EC 2.4.2.1). The effects of the poorly permeable enzyme-inactivating reagents, 4-diazoniumbenzenesulphonate, 7-diazonium-1,3-naphthalene-disulphonate and 2,4,6-trinitrobenzenesulphonate, on Escherichia coli indicate that all the above-mentioned enzymes and also the xanthine-guanine phosphoribosyltransferase [Miller, Ramsey, Krenitsky & Elion (1972) Biochemistry 11, 4723--4731] are located intracellularly.
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In 1972, the University of Minnesota, the Minnesota Dental Association, and the State Board of Dentistry implemented a program known as the Dental Information Service Center. An important component of this effort was a set of computerized programs aimed at facilitating placement of recent graduates of the University's dental school. Although use of the computerized program has grown substantially during the four-year study period, personal contacts remain the source of information most frequently responsible for initial placements; they accounted for 60% of such placements. The computerized referral program accounted for 27% of first placements for the class of 1976. The program has been influential in increasing student awareness of underserved areas. Overall career satisfaction was high among recent graduates, and their subjective evaluation of the program was generally positive.
Uptake of adenine, hypoxanthine and uracil by an uncA strain of Escherichia coli is inhibited by uncouplers or when phosphate in the medium is replaced by less than 1 mM-arsenate, indicating a need for both a protonmotive force and phosphorylated metabolites. The rate of uptake of adenine or hypoxanthine was not markedly affected by a genetic deficiency of purine nucleoside phosphorylase. In two mutants with undetected adenine phosphoribosyltransferase, the rate of adenine uptake was about 30% of that in their parent strain, and evidence was obtained to confirm that adenine had then been utilized via purine nucleoside phosphorylase. In a strain deficient in both enzymes adenine uptake was about 1% of that shown by wild-type strains. Uptake of hypoxanthine was similarly limited in a strain lacking purine nucleoside phosphorylase, hypoxanthine phosphoribosyltransferase and guanine phosphoribosyltransferase. Deficiency of uracil phosphoribosyltransferase severely limits uracil uptake, but the defect can be circumvented by addition of inosine, which presumably provides ribose 1-phosphate for reversal of uridine phosphorylase. The results indicate that there are porter systems for adenine, hypoxanthine and uracil dependent on a protonmotive force and facilitated by intracellular metabolism of the free bases.
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The heat of the reaction NAD(+)+propan-2-ol=NADH+acetone+H(+) was determined to be 42.5+/-0.6kJ/mol (10.17+/-0.15kcal/mol) from equilibrium measurements at 9-42 degrees C catalysed by yeast alcohol dehydrogenase. With the aid of thermochemical data for acetone and propan-2-ol the values of DeltaH=-29.2kJ/mol (-6.99kcal/mol) and DeltaG(0)=22.1kJ/mol (5.28kcal/mol) are derived for the reduction of NAD (NAD(+)+H(2)=NADH+H(+)). These values are consistent with analogous but less accurate data for the ethanol-acetaldehyde reaction. Thermodynamic data for the reduction of NAD and NADP are summarized.
1. In many instances, there was no change in the rate of oxygen consumption per cell when adenine was withdrawn from purine auxotrophs of Escherichia coli and Salmonella typhimurium. 2. However, adenine deficiency inhibited the metabolism of glucose, mannitol or glycerol in a purA(-) strain, in purB(-) or purH(-) strains in the absence of histidine and in purB(-) mutants supplied with hypoxanthine. These are all instances where reactions occur to consume adenine nucleotides. 3. The inhibition of glucose oxidation is accompanied by the accumulation of fructose 1,6-diphosphate and dihydroxyacetone phosphate. 4. Insufficiency of ADP for phosphoglycerate kinase is the most probable cause of the inhibition.
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1. The synthesis of nucleic acids and the content of purine nucleotides have been studied in selected purine-requiring strains of Escherichia coli including a purB(-) strain and a purB(-)guaA(-) strain. 2. When the exogenous purines can be converted into GTP but not into ATP, RNA is synthesized at the expense of intracellular ATP, ADP and AMP. 3. Net synthesis of RNA as measured by the incorporation of uracil can be correlated with the availability of GTP except when ATP falls to a very low concentration. 4. Nicotinamide nucleotides are not an important reservoir of adenine nucleotides for RNA synthesis.
1. Experiments with rifampicin and stringent strains of Escherichia coli (pro(-)purB(-)rel(+)) indicate that purine deficiency does not decrease and may considerably increase the potential for RNA synthesis by RNA polymerase molecules that are bound to DNA and have already commenced transcription. 2. DNA-RNA hybridization experiments indicate that purine starvation increases the distribution of bound RNA polymerase molecules between the cistrons for mRNA and those for stable RNA. 3. Synthesis of beta-galactosidase mRNA is more dependent on the ability to synthesize guanine nucleotides than on the ability to synthesize adenine nucleotides. 4. Amino acid starvation tends to decrease the potential for RNA synthesis by RNA polymerase molecules bound to DNA. 5. Since this effect differs from that due to purine starvation, amino acid control of RNA synthesis does not appear to operate solely by causing a deficiency of purine nucleotides. 6. The results are discussed in terms of the ability to initiate RNA chains and to extend them under different circumstances.
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