Calculator assisted monitoring of nutrition, fluids, and electrolytes.
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Biomedical subjects
Publications and source records attributed to K Kelly.
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Treatment of rabbits with sterile solutions of bovine Cu-Zn superoxide dismutase according to schedules recommended for radiation cystitis and radiation side effects has elicited the production of antibodies to the enzyme, detected in rabbit sera by a sensitive and specific radioimmunoassay. No antibodies were detected after a single treatment. However, on repeated administration of the enzyme all animals, including those that received 4 Gy whole body radiation prior to treatment, produced detectable antibody. Titers of antibody in sera rose progressively with repeated injections of the enzyme. Irradiation served merely to delay the onset of the immune response. In addition, human and bovine Cu-Zn superoxide dismutase have been found to be antigenically distinct when examined by competitive inhibition radioimmunoassay. These antigenic differences and the immunogenicity of the bovine enzyme in rabbits raise reasonable doubt as to the safety of administration of bovine superoxide dismutase to human patients. It is recommended that such patients be monitored for antibody production, preferably by radioimmunoassay.
Localization of thyroid-mediated decrease of lactase activity along the villus-crypt unit in adult rat jejunum was studied 24 and 48 h after first injection of L-thyroxine (200 micrograms/100 g body wt) every 24 h. [3H]thymidine was also given at time of first thyroxine injection. Serum thyroid-stimulating hormone, food intake, and body weight were significantly decreased within 24 h. Total jejunal protein and villus-crypt height were unchanged during the time period studied. Lactase activity (expressed both as per tissue protein and per intestinal segment) was significantly decreased in jejunum and midjejunum within 24 h. Serial sectioning of the jejunal villus-crypt unit in a cryostat showed that the site of decrease in lactase activity at 24 h was in the apical villus and by 48 h extended along the entire height of the villus. Epithelial cell migration measured both by histoautoradiography and scintillation counting of [3H]thymidine in cryostat sections revealed no difference between control and thyroid-treated animals at both 24 and 48 h. The decrease in lactase activity at 24 h was in advance of the leading edge of radioactivity, indicating that the thyroid-evoked response occurred in mature enterocytes already on the villus.
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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.
The effect of superoxide dismutases from five species upon phospholipid bilayers has been investigated. The uptake by egg phosphatidylcholine bilayers of the holo and apo forms of bovine superoxide dismutase increases with enzyme concentration and only a fraction of each is removed by treatment with trypsin. These uptake data indicate that both forms of the enzyme associate with and are embedded within lipid bilayers. From the spectrum of the spin label 2-(3-carboxypropyl)-4,4-dimethyl-2-tridecyl-3-oxazolidinyloxyl, the binding of superoxide dismutase to egg phosphatidylcholine bilayers can be shown to disorder the lipid packing. The disordering by the bovine holoenzyme is small but increases with increasing enzyme concentration and period of incubation. The disordering effects of the apoenzyme are much larger and are reversible by Cu2+, Zn2+ reconstitution of the apoenzyme. The disordering effect of the apoenzyme is further confirmed by differential scanning calorimetry. The gel to liquid crystalline phase transition of egg phosphatidylcholine is lowered 7 degrees C by 25% by weight apo-superoxide dismutase to lipid. Human, dog, swordfish and yeast superoxide dismutases also disorder, and to a greater extent than the bovine enzyme. The greatest perturbation is produced by yeast superoxide dismutase; a 20% decrease in the order parameter by 50% by weight enzyme to lipid.
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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.
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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.
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Age reliably predicted performance of 120 volunteers, 20 to 84 yr. old, on the Memory-for-Designs test. Scoring employed both the Graham-Kendall and a modified scoring technique in which each of 15 designs was rated within six error categories (reversal, distortion, omission, rotation, embellishment, perseveration). Inter-rater reliability of four raters indicated a marked scoring consistency and the error category scoring interacted with age, i.e., older persons (greater than 60 yr.) made more omission and distortion errors than younger persons (less than 40 yr.) who committed proportionally more reversal errors. Concomitant performance on the WAIS Block Design accounted for only part of the age differences in errors. The error category scoring was more sensitive to age differences in visual memory than the usual Graham-Kendall scoring method. In addition, it provided much needed age norms.
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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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Interrelationships between nutrient intakes (dietary cholesterol, total carbohydrate, saturated and polyunsaturated fat, and total calories) of parents and children were examined in 294 families (60 black, 234 white) which included at least one parent and one child in the Princeton School survey of parents and their children, ages 6 to 19. The nutrient data were collected by means of the standardized Lipid Research Clinics' collaborative 24-hr dietary recall; simple correlations and analysis of covariance were used to assess parent-child nutrient intake (per kg body weight) relationships. There were significant positive simple correlations between nutrient intake of parents and children for total carbohydrate (r = 0.28, P < 0.0001), saturated fat (r = 0.15, P < 0.01), polyunsaturated fat (r = 0.19, P < 0.001), and calories (r = 0.24, P < 0.0001); parents' intake of cholesterol did not correlate with that of their children (r = 0.004, P > 0.1). By analysis of covariance with adjustment for sex, race, age, and recall group, the parent-child association of cholesterol intake was significant (P = 0.001), and the remaining parent-child nutrient intake relationships were congruent with those observed by simple correlations. The proportion of variation of the children's nutrient intake accounted for by parental nutrient intake varied from a low of 23% for parent-child cholesterol intakes (all parents-all children) to a high of 97% for carbohydrate intake in black fathers over age 40 and their children. The multiple Rs2 for black parents-black children for nutrient intakes were higher than those for white parents-white children for carbohydrate, saturated fat, and calories. Close parent child nutrient interrelationships not only suggest that a considerable portion of lipid-lipoprotein variability may be nutritionally-environmentally determined, but may contribute to clustering of coronary heart disease risk factors in families.