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Biomedical subjects

D W Edington

Publications and source records attributed to D W Edington.

At least 19 recordsLinked to original sources
PubMed1992

Prediction of prospective medical claims and absenteeism costs for 1284 hourly workers from a manufacturing company.

Multivariate regression models were developed to predict the employer's economic costs (medical claims payments and loss from employees' absenteeism) from selected health-related measures among 1284 hourly employees. Twelve health-related measures, mainly from a Health Risk Appraisal (HRA) completed in 1985, were selected as predictors. Regression models were developed according to the economic measures for the three subgroups (men under 35, men 35 or older, and women). All the regression models significantly predicted economic costs from selected health-related measures with a multiple R2 range of .23 to .13 (P less than .001).

Absenteeism↗
PubMed1991

Comparing the predictive accuracy of health risk appraisal: the Centers for Disease Control versus Carter Center program.

BACKGROUND: From 1986 to 1987 the Carter Center of Emory University joined with the Centers for Disease Control (CDC) to develop a new, probability-based, adult health risk appraisal (HRA) instrument for the public domain. This new instrument is compared with the CDC HRA version to determine which is a more accurate predictor of mortality. METHODS: We compared predicted mortality risks from the CDC HRA and the Carter Center HRA with the observed mortality among 3135 smokers and never-smoking persons, aged 25 to 60, followed from 1959 to 1979 as part of the Tecumseh Community Health Study. RESULTS: When individuals were classified according to the difference between their actual age and risk age, for the CDC HRA, there was a progressively increasing risk of 10-year mortality as the difference increased. The Carter Center HRA did not show this trend. An analysis using relative operating characteristic curves showed that the mortality risk predictions for both programs were very similar for men and women. However, differences between actual age and risk age for the two programs were not similar for men or women, particularly older men. Therefore, actual age minus risk age for the CDC program was a more accurate predictor of 10-year mortality than was this difference for the Carter Center program. CONCLUSIONS: The results from both types of analyses suggest that the validity of risk ages obtained from the Carter Center version may not be sufficient to justify updating programs for those currently using the CDC instrument.

Adult↗
PubMed1987

The accuracy of health risk appraisal in predicting mortality.

In order to determine the accuracy of the Centers for Disease Control/Health Risk Appraisal (CDC/HRA) program, the authors compared observed to predicted mortality for the 3,135 persons followed from 1959-79 as part of the Tecumseh Community Health Study. The analysis was limited to smokers and never-smokers aged 25-60 whose 1959 questionnaires included at least the minimal variables for prediction using the CDC/HRA (age, sex, race, height, weight, and smoking habits). For men and women overall and in each age group, the observed proportion dying over 20 years of follow-up increased as the difference between 1959 age and risk age increased. CDC/HRA predicted 10-year risks of mortality appeared to improve upon age-sex-race predicted risks of mortality when compared to the observed proportion dying over 10 years and when predictors were used in a logistic regression model with vital status after 10 years as the dependent variable. Thus, CDC/HRA may be an appropriate method for identifying high-risk populations for health interventions.

Adult↗
PubMed1987

Protein synthesis in skeletal muscle from normal and diabetic rats following increased contractile activity in situ.

Protein synthesis was measured in rat skeletal muscle after one hour of heavy work. Direct, supramaximal electrical stimulation in situ under anesthesia resulted in an increase in the in vitro rate of protein synthesis in the soleus and gastrocnemius muscles during the next two hours. Most of the increase was located in the nuclear-connective tissue fraction. No increase was observed in the actomyosin, microsomal or soluble fractions. The same pattern was also observed in the flacid contralateral soleus. Passive stretch of the same muscle group did not result in such changes in protein synthesis. The response was obliterated by rendering the rat diabetic. The observed increase in protein synthesis may represent the initial stages of the adaptive response to increases in muscular activity.

Animals↗
PubMed1985

Tissue coenzyme Q (ubiquinone) and protein concentrations over the life span of the laboratory rat.

The coenzyme Q (ubiquinone) concentrations of a number of tissues have been determined over the life span of the male laboratory rat. Coenzyme Q increased between 2 and 18 months and decreased significantly at 25 months in the heart and kidney, and the gastrocnemius, oblique and deep aspect (red) vastus lateralis muscles. The coenzyme Q concentration of liver increased over the life span, while it remained relatively constant in brain, lung, and the superficial aspect (white) of the vastus lateralis muscle. Data are also included for organ weights and protein contents of tissues over the life span. The various roles of coenzyme Q in cellular electron transfer and its regulation, energy conservation in oxidative phosphorylation, and its clinical efficacy in diseases of energy metabolism are discussed. It is hypothesized that coenzyme Q serves as a free radical quencher in the mitochondrion, a major site of free radical formation, in addition to its other roles in cellular energy metabolism, and that its cellular diminution may contribute to the loss of cellular function accompanying ageing.

Aging↗
PubMed1984

Exercise-induced reversal of age-related declines of oxidative reactions, mitochondrial yield, and flavins in skeletal muscle of the rat.

The ability of gastrocnemius muscle homogenates to catalyze the oxidation of succinate, glutamate + malate, pyruvate + malate, palmitoyl-coenzyme A, decanoylcarnitine and palmitoylcarnitine in the presence of ADP decreased by approximately 32% in sedentary male Sprague-Dawley rats between the ages of 9 and 25 months. Following 21 weeks of treadmill training (running), such homogenates from 25-month-old animals catalyzed oxidations 55% more rapidly than those from 25-month-old sedentary rats, and 17% faster than those from 9-month-old sedentary rats. Total and peptide-bound flavin of gastrocnemius muscles also declined between 9 and 25 months of age and were elevated in the 25-month-old endurance trained rats to levels greater than both 9- and 25-month-old sedentary animals. The yield of protein in the mitochondrial fraction from the quadriceps femoris muscle decreased between 9 and 25 months and was restored to the 9-month level by endurance training. The kinetic characteristics of the isolated mitochondria were not influenced by age or exercise. These data indicate that 2-year-old rats retain the capacity to increase skeletal muscle oxidative capacity and mitochondrial population density in response to endurance training.

Aging↗
PubMed1983

Effects of dietary carnitine on myocardial palmitate oxidation in the aging rat.

Aging is associated with decreases in myocardial fatty acid oxidation and carnitine concentration. The purpose of this study was to investigate the effects of dietary carnitine manipulation on myocardial palmitate oxidation and carnitine content in young adult and middle-aged rats. Rats were fed either a carnitine-free or a carnitine-supplemented diet for nine weeks and killed at ages 6.5 and 18 months. Myocardial carnitine content was unaffected by age or diet. However, in 18 months rats fed a carnitine-free diet, myocardial palmitate oxidation was 77% higher, carnitine palmitoyltransferase activity 39% higher, and lipid droplet volume density 55% higher compared to 18 month rats fed a carnitine-supplemented diet. In 6.5 month rats, dietary carnitine had no effect on these variables. These results indicate that dietary carnitine restriction increases myocardial fatty acid metabolism in middle-aged but not in young adult rats.

Aging↗
PubMed1983

Myocardial protein synthesis during aging and endurance exercise in rats.

Rates of protein synthesis, and RNA and cytochrome c concentrations, were assayed in hearts of 9- and 25-month-old sedentary rats and 25-month-old rats trained to run 5 days/week for 21 weeks. Isolated working hearts were perfused with modified Krebs-Henseleit bicarbonate buffer labelled with [14C]phenylalanine. Protein synthesis rate decreased with age, as did RNA content and efficiency of protein synthesis, an indication of the activity per ribosome. None of these three parameters were altered by endurance training. Cytochrome c concentration, which also decreased significantly between 9 and 25 months, was increased in the 25-month-old endurance trained heart to the level of the 9-month-old sedentary heart. We conclude that the depressed protein synthetic system of aged animals is less of a liability in the endurance trained than in the sedentary animal as a consequence of the associated improvement in functional capacity that serves to minimize homeostatic disequilibrium in response to environmental challenges.

Aging↗
PubMed1983

Myocardial adaptations to endurance exercise in aged rats.

Isolated perfused working hearts of 25-mo-old male Sprague-Dawley rats trained to run for 16 wk were compared with hearts from 9- and 25-mo-old sedentary animals. Under low work load conditions, systolic and diastolic aortic pressures, aortic flow, and oxygen consumption of the three groups were similar. Under high work load, systolic pressure of trained old and 9-mo groups were higher than the 25-mo sedentary values, but diastolic pressures were similar. At a systolic pressure of 150 mmHg, coronary flow of the old trained heart was higher than that of the age-matched controls, although not equal to the 9-mo sedentary group. The oxygen consumption of the intact hearts under the latter conditions follows the same quantitative trend. Left ventricular cytochrome c concentrations and rates of oxidation of glutamate-malate, palmitoylcarnitine, and succinate were increased in the older rats by training but not to the level of the 9-mo old. These data indicate that appropriate exercise in aged animals improves myocardial function and aerobic energy metabolism.

Aging↗
PubMed1981

Selected biochemical parameters of two sizes of rat skeletal and heart muscle mitochondria at selected intervals of a 16-week endurance training program.

Increases in oxidative capacity of skeletal muscle which has undergone training is well documented. The concomitant shifts in mitochondrial size and cytochrome content have varied with different investigations. In this study the shifts in oxidative capacity, SDH activity, thiolase activity, was measured in two sizes of heart and skeletal muscle mitochondria of rats undergoing 4, 8, and 16 weeks of training. In addition cytochrome content was measured in both sizes of mitochondria of the skeletal muscle. The small mitochondria of skeletal muscle showed the significant gains in number during the first 8 weeks of training while the large mitochondria increased in number during the last 8 weeks of training. The oxygen consumption, SDH activity, thiolase activity and cytochrome content all showed varying peaks in activity and content in the different sizes of mitochondria over the 16 weeks of training. In evaluating training regimes' effects on skeletal muscle it appears important to take into consideration the shifts in size of mitochondria as well as oxidative capacity and enzymatic activity alterations. There were no alterations observed in mitochondrial size in cardiac tissue.

Acetyl-CoA C-Acyltransferase↗
PubMed1981

Effects of age and cardiac work in vitro on mitochondrial oxidative phosphorylation and (3H)-leucine incorporation.

Mitochondria isolated from in vitro perfused rat heart preparations were used to study the combined effects of age and physical stress. Age-related declines in oxidative phosphorylation catalyzed by mitochondria from nonperfused hearts were not observed. Low work load perfusion resulted in decreased respiration by mitochondria from 24-month-old hearts (p less than .01) but not 10-month old hearts, while high work load perfusion resulted in decreased respiration in both ages. However, the decrease by the 24-month-old hearts was significantly greater than those in the younger hearts (p less than .01). Compared to age-matched low work load hearts, 5- and 10-month-old high work load hearts increased mitochondrial protein synthesis by 86% and 93%, respectively, 15-month-old hearts increased by 60%, and 24-month-old hearts by 13%. The results of this study provide evidence that the ability of the heart to respond appropriately so as to adapt to stress decreases with age, becoming apparent in the laboratory rat between 10 and 15 months of age.

Aging↗