Publications by authors named "HA Eder"

The Bronx Aging Study is a 10-year prospective investigation of very elderly volunteers (mean age at study entry, 79 years; range, 75-85 years) designed to assess risk factors for dementia and coronary and cerebrovascular (stroke) diseases. Entry criteria included the absence of terminal illness and dementia. All subjects (n = 350) included in this report had at least two lipid and lipoprotein determinations.

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The Bronx Aging Study is a longitudinal investigation of nondemented, nonterminally ill, community-residing, old old volunteer subjects, designed to assess risk factors for the development of dementia and coronary and cerebrovascular diseases. During the first five annual evaluations, total cholesterol, high-density (HDL) and low-density lipoprotein (LDL), and triglyceride levels were measured. Mean cholesterol values (+/- standard error of the mean) for subjects at baseline were significantly higher for women than for men.

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A colony of Hartley guinea pigs that exhibit hyperglycemia, glucosuria, and hypertriglyceridemia characteristic of human diabetes mellitus was developed. Initially, a group of guinea pigs that had normal serum glucose concentrations (less than or equal to 200 mg/dL of serum) at 3 to 4 weeks of age was obtained; however, in some of the animals progressively severe hyperglycemia (300 to 500 mg/dL of serum) and glucosuria (greater than 2 g of glucose/24 h) occurred as the animals matured. In addition, the animals exhibiting hyperglycemia and glucosuria had plasma insulin concentrations that were similar to those animals that were not hyperglycemic.

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To better characterize the severity and course of hyperlipidemia in diabetic ketosis and ketoacidosis, we measured plasma triglyceride and cholesterol concentrations in 50 episodes in 46 adults hospitalized on a municipal hospital medical service. Moderate hypertriglyceridemia was common: 32 patients (64%) had triglyceride levels above the 95th percentile (adjusted for age and sex), and 18 patients (36%) had cholesterol levels above the 95th percentile. Severe hypertriglyceridemia (levels above 5.

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The receptor-mediated uptake of very low density lipoprotein (VLDL) remnants by the rat liver was studied. Livers were perfused with native 125I-VLDL remnants, radiolabeled apo E-deficient remnants, and radiolabeled remnants that contained reductively methylated apo B and unmodified apo E. The specific uptake of the apo E-deficient remnants was 20% of that for the native remnants, whereas the specific uptake of the remnants containing unreactive apo B was 78% of the control value.

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We have used a preparation of rat liver plasma membranes to study the binding of rat apolipoprotein E-deficient HDL to rat liver. The membranes were found to bind HDL by a saturable process that was competed for by excess unlabeled HDL. The binding was temperature-dependent and was 85% receptor-mediated when incubated at 4, 22 and 37 degrees C.

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The uptake of the 125I-labeled apolipoprotein and 3H-labeled cholesteryl ester components of rat apolipoprotein E-deficient HDL by the perfused liver was studied. The uptake of the cholesteryl ester moiety was 4-fold higher than that of apolipoprotein. The concentration-dependent uptake of labeled protein was saturable and competed for by an excess of unlabeled HDL.

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This cross-sectional study evaluated high-density lipoprotein subclasses measured by a precipitation technique before and after treatment in men and women with types I and II diabetes. Total high-density lipoprotein cholesterol was lower in subjects of both sexes with untreated type I and type II diabetes, the change occurring primarily in subclass 2. Insulin therapy raised total and subclass 2 high-density lipoprotein levels in men and women with type I and type II diabetes, the predominant rise occurring in subclass 2.

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The effects of glipizide on HDL subclass levels were prospectively evaluated in 7 women and 2 men with non-insulin dependent (Type 2) diabetes. Total HDL, HDL2 and HDL3 levels were unchanged during the treatment period. Baseline HDL levels were lower when compared to a control population which may have been due to the elevated body weight present in most subjects.

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Apolipoprotein A-IV was isolated from the d less than 1.21 g/ml fraction of rat serum by gel filtration followed by heparin-Sepharose affinity chromatography; this method also facilitated the preparation of apolipoprotein A-I and apolipoprotein E. The apolipoprotein A-IV preparation was characterized by SDS-gel electrophoresis, isoelectric focusing, amino acid analysis and immunodiffusion.

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Apolipoprotein (apo) E-deficient rat high-density lipoproteins (HDL) bind to isolated rat hepatocytes at 4 degrees C by a process shown to be saturable and competed for by an excess of unlabeled HDL. Uptake (binding and internalization) at 37 degrees C was also saturable and competed for by an excess of unlabeled HDL. At 37 degrees C the HDL apoprotein was degraded as evidenced by the appearance of trichloroacetic acid-soluble radioactivity in the incubation media.

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Studies were performed to determine the mechanism of hepatic removal of a cholesterol-rich beta-migrating lipoprotein. This fraction, designated IDLc, was isolated from the serum of cholesterol-fed diabetic rats by ultracentrifugation at d 1.006-1.

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Although a great deal has been learned about HDL as a protective factor, our understanding of the role of HDL is far less comprehensive than that of LDL. Until such knowledge is available, efforts directed at altering HDL levels must be tentative and subject to revision, as indicated by experience. There is no evidence to warrant the use of drugs whose primary effect is to raise HDL.

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Studies in recent years have suggested that measurement of high density lipoprotein (HDL) subclasses may provide significant information beyond that provided by measurement of total HDL. However, conventional methodology for separation of HDL subclasses involves various types of ultracentrifugation that are time-consuming, costly, and not suitable for many clinical or epidemiological studies. We have developed a simple precipitation method for the separation of HDL subclasses in human plasma.

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The consistent body of evidence supporting a relationship between high density lipoproteins and coronary heart disease is examined. However, an actual causal relationship has yet to be demonstrated. Methods of measuring HDL are presented and the difficulties with clinical measurement and evaluation are explored.

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This report summarizes the current state of knowledge concerning the cardiovascular system in various animal models of diabetes and presents their major strengths and weaknesses for studying the important research questions in the field. Nonhuman primates have many desirable features for studies on the macrovascular and cardiac complications of the disease as well as risk factor alterations, but their availability, cost, and maintenance present practical disadvantages. The spontaneous rodent models of diabetes currently are not considered very useful for cardiovascular research, but they have not been well characterized with respect to most aspects of their cardiovascular system.

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Receptor-mediated hepatic uptake of low density lipoproteins (LDL) conjugated to colloidal gold was studied by perfusion of livers from rats treated for 5 d with 17 alpha-ethinylestradiol. Estrogen treatment resulted in a marked decrease in serum lipid and lipoprotein concentrations. After 15 min of perfusion the conjugate was bound to the hepatic microvilli of both control and estrogen-treated rats; the estrogen-treated rats showed an 8- to 11-fold greater number of membrane-bound conjugates.

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