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Biomedical subjects

D Seidel

Publications and source records attributed to D Seidel.

At least 181 records · Page 10Linked to original sources
PubMed1988

Incidence rates of fatal and nonfatal myocardial infarction in relation to the lipoprotein profile: first prospective results from the Göttingen Risk, Incidence, and Prevalence Study (GRIPS).

In a screening investigation in 1982, which included medical history, clinical examination, general laboratory investigation, and quantification of lipids, lipoproteins, and apoproteins A1 and B, 5020 male subjects aged 40 to 59 years took part. All subjects were free of any heart or vascular disease at the basic examination. Of them 40 suffered fatal or nonfatal myocardial infarction (MI) during the first 3-year observation period between January 1982 and December 1984 (incidence cases), the others remained free of heart or vascular diseases (reference group). Comparison with the reference group revealed a strong relationship between MI-incidence rate and LDL cholesterol (correlation coefficient according to univariate regression analysis r = +0.248; P value according to Chi-square test P less than 0.001). The relationship was less strong but significant for age (r = +0.189; P less than 0.001), total serum cholesterol (r = +0.197; P less than 0.001), and apoprotein B (r = +0.195; P less than 0.001). Although statistically significant, the relationships to the MI-incidence rate were comparatively weak for HDL cholesterol (r = -0.09; P less than 0.01), apo-A1 (r = -0.09; P less than 0.01), systolic blood pressure (r = +0.067; P less than 0.05), and blood glucose level (r = +0.066; P less than 0.05). Body mass index, diastolic blood pressure, and plasma levels of uric acid, triglycerides, and VLDL did not exert relevant influences on the MI-incidence rate in our study population.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Isolation of apolipoprotein-B-48 from chylomicrons by high-performance liquid chromatography.

Apolipoprotein-B-48 (B-48) is a component of chylomicrons and chylomicron remnants and originates in the human gut wall. Its molecular weight represents 48% of the hepatic apolipoprotein-B-100 (B-100). So far, immunochemical assays are only available for B-100 and do not permit the specific determination of B-48. As a convenient immunochemical method is necessary for clinical and biochemical investigations of chylomicron remnants, we isolated B-48 in amounts sufficient to permit the production of monoclonal antibodies. After delipidation of the chylomicron fraction from 3 1 of human chylous ascites, size-exclusion chromatography was performed by using two serially connected TSK columns. B-48 was eluted as a second peak at about 35% of the total volume, well separated from B-100 (eluted as a first peak). After detection by UV absorption at 280 nm, the fractions collected from 25 automated runs were combined, ultrafiltered and examined for their protein composition by sodium dodecyl sulphate polyacrylamide gel electrophoresis. This indicated that we were able to isolate rapidly 3.4 mg of B-48 in a purity sufficient to perform immunization.

Apolipoprotein B-48↗
PubMed1987

Selective removal of low density lipoproteins (LDL) by precipitation at low pH: first clinical application of the HELP system.

The first clinical application of a new extracorporeal procedure (HELP) for the selective elimination of low-density lipoproteins by heparin precipitation at acid pH is described. Plasma, obtained by filtration of whole blood through a 0.2 mu filter, is continuously mixed with an equal volume of an acetate buffer (pH 4.85) containing heparin. After removal of the precipitated heparin complex by filtration, excess heparin is adsorbed to a specially developed filter and the clear plasma filtrate is subject to bicarbonate dialysis/ultrafiltration to restore physiologic pH and remove excess fluid. The calculated efficiency for the elimination of low-density lipoproteins from plasma by HELP is 100% and is therefore comparable to conventional plasmapheresis. The HELP system shows a high degree of specificity with over 80% of total protein being returned to the patient. Over 130 treatment procedures have now been performed. Patient compliance and acceptance have been excellent and no major complications have been observed.

Adult↗
PubMed1987

Automated measurements of cerebral atrophy in multiple sclerosis.

An automated method of measuring cerebral atrophy is introduced. Using this method we studied patients with multiple sclerosis and a control group showing premature cerebral atrophy in multiple sclerosis (P = 1,32 x 10(-8) for male and P = 3,6 x 10(-14) for female). There was only a weak correlation between cerebral atrophy and psychological deficits. Multivariate analysis did not show any significant correlation between cerebral atrophy, duration of disease, clinical manifestations and progression of disease. We conclude that our method to measure cerebral atrophy is more accurate and less time-consuming than the use of linear indices. It might be appropriate for further investigations in evaluating atrophic processes in cerebro-vascular, degenerative and exogen-toxic disease of brain.

Adult↗
PubMed1987

The beneficial influence of nifedipine on the regression of the cholesterol-induced atherosclerosis in rabbits.

Nifedipine has been implicated as an inhibitor of dietary induced atherosclerosis in rabbits. This study was designed to examine the effect of nifedipine on the regression of atherosclerotic lesions in this animal model. NZ-rabbits were fed a cholesterol-enriched diet (1.5%) for 4.8 months. A control group A was killed and the aorta removed for planimetry of the vessel wall lesions. The remaining animals were divided into two groups, group P receiving a placebo solution and group N a nifedipine solution (2 X 20 mg/day). They were maintained on a standard chow for a further 4.5 months. In the nifedipine-treated group N, sudanophilia of the aorta was reduced by more than 20% as compared to the cholesterol-fed control group A and was 50% lower than in the placebo-treated group. Total cholesterol of the aortic tissue was lowest in group N. No significant differences in plasma cholesterol, triglycerides or the platelet half-life time were observed between the placebo- and the nifedipine-treated group. These data indicate that nifedipine can stimulate regression of pre-existing atherosclerotic lesions in rabbits.

Animals↗
PubMed1987

Fish oil feeding results in an enhancement of cholesterol-induced atherosclerosis in rabbits.

We investigated the influence of fish oil on cholesterol induced atherosclerosis in rabbits. Group I, a control group was fed a cholesterol-free diet, group II was fed a diet supplemented with 1.5% cholesterol, group III received in addition to cholesterol supplementation a purified fish oil concentrate (Maxepa, 2 ml/d). The animals received these diets for 5 months (100 g/d). Aortic atherosclerosis as measured by planimetry of sudanophilic lesions was significantly higher (+59%) in group III as compared with group II, even though serum cholesterol levels were comparable. No differences were found in platelet half-life times between groups II and III, but these values were significantly lower than the half-life of platelets in the control group I. Total serum peroxide levels, expressed as malondialdehyde equivalents were significantly elevated in the fish oil-treated group. This may be due to malondialdehyde modification of the lipoproteins and may be responsible for the enhanced development of atherosclerosis in these animals.

Animals↗
PubMed1987

Structural relationship of an apolipoprotein (a) phenotype (570 kDa) to plasminogen: homologous kringle domains are linked by carbohydrate-rich regions.

At least six allelic forms of apolipoprotein(a), differing in molecular mass, could be detected by immunoblot analysis. One of these phenotypes with a molecular mass of 570 kDa has been investigated. After reduction and carboxymethylation it was digested with trypsin and the resulting peptides were separated by gel filtration and reverse phase HPLC. The tryptic fragments sequenced comprised a total of 356 amino acids. The N-terminus of apo(a) was highly homologous to the start of the kringle 4 domain from human plasminogen and the majority of the tryptic peptides isolated was also homologous to sequences from this kringle. At least five homologous "kringle 4" domains are present in apolipoprotein(a) whereby one domain occurs more frequently than the others. A carbohydrate-rich peptide was also obtained in high yield. This glycopeptide connects two "kringle 4" domains and contains one N-glycoside within the kringle and six potential O-glycosides in the linking region. From the recovery it can be estimated that this peptide occurs several times within the whole apolipoprotein (a) sequence. The high carbohydrate content is in sharp contrast to that of human plasminogen. Other peptides sequenced indicate that apo (a) also contains domains homologous to the kringle 5 and protease regions of plasminogen. No unique peptides were found. These studies suggest that apolipoprotein (a) could have arisen through duplication of specific regions from the human plasminogen gene. The size heterogeneity of apo (a) might then be explained by differences in the numbers of gene duplications.

Amino Acid Sequence↗
PubMed1987

Lipoproteins in liver disease.

Liver disease is associated with profound and characteristic changes in lipoprotein composition and metabolism. The most pronounced alterations are the formation of lipoprotein-X in intra- and extrahepatic cholestasis, the decrease of apolipoproteins A-I and A-II and the increase of apolipoprotein E. These alterations impair the activities of both lipoprotein lipase and lecithin: cholesterol acyltransferase. They are also responsible for an abnormal receptor mediated uptake of the lipoproteins from plasma. The abnormal lipid and apolipoprotein composition of the lipoproteins in liver disease appears to affect various important functions of cell membranes. The understanding of how these changes occur and their significance in the pathogenesis of other metabolic disturbances secondary to the abnormal lipid metabolism are important challenges for future research.

Lipoproteins↗
PubMed1987

Medroxyprogesterone acetate and lipid metabolic changes.

Lipid metabolic changes under oral treatment with medroxyprogesterone acetate (MPA) were investigated in four groups of patients: group I; 10 patients aged 25-45 (mean 38) years received 50 mg MPA daily for pelvic endometriosis. Group II; 21 patients aged 55-77 (mean 62) years received 200 mg MPA daily for surgically treated endometrial carcinoma stage I. Group III; 14 praemenopausal patients aged 37-52 (mean 47) years received 1000 mg MPA daily for metastasized breast cancer. Group IV; 27 post-menopausal patients aged 53-78 (mean 68) years were treated with 1000 mg MPA daily for metastatic breast cancer as well. A fifth group of initially 86 patients aged 40-86 (mean 63) years after surgery for endometrial carcinoma stage I served as untreated control for groups II and IV. Cholesterol and triglyceride concentrations were measured enzymatically lipoproteins were determined by quantitative electrophoresis and precipitation and apolipoproteins A1 and B were quantified by kinetic rate nephelometry. Whereas in patients of group I no changes of lipid and lipoprotein parameters were observed, daily oral doses of 200 mg MPA and more led to a marked fall in alpha-lipoprotein-, HDL-cholesterol and apolipoprotein A1 levels. beta-Lipoprotein-, LDL-cholesterol and apolipoprotein B concentrations rose significantly in Groups III and IV. The relevance of these findings in terms of athero-genicity is discussed.

Adult↗
PubMed1986

[Serum magnesium concentration in myocardial infarct].

Serum magnesium concentrations were followed during the course of coronary infarction and were correlated to the event on the basis of the creatinine kinase activity E.C. no. 2.7.3.2. Those patients admitted to the hospital at a very early stage of the infarction showed initial high serum magnesium concentrations which fell during the event to subnormal values and then normalized later. In the case of severe coronary infarction (maximum CK activity greater than 700 U/1) the subsequent decrease in serum magnesium concentration was more pronounced than in subjects with lower CK activity. Patients suffering from angina pectoris had normal serum magnesium values which did not show any concentration change during a clinical follow-up. The previously postulated correlation between low serum magnesium and high risk for myocardial infarction may be questioned in the light of our observations.

Aged↗
PubMed1986

The association between serum Lp(a) concentrations and angiographically assessed coronary atherosclerosis. Dependence on serum LDL levels.

Lipoprotein(a) concentrations were measured by radial immunodiffusion in a cohort of 40-60 year males who had been classified by coronary angiography as CAD+ with 50% stenosis of one or more of the major coronary arteries or CAD- with no signs of coronary lesions. Sample odds ratios were calculated as a measure of association between serum Lp(a) values and the presence of coronary artery disease. An odds ratio of 2.706 (P less than 0.001) was derived for elevated (greater than or equal to 30 mg/dl) Lp(a) levels vs low (less than 5 mg/dl) Lp(a) levels indicating a strong association between the presence of coronary artery disease and elevated Lp(a) concentrations. This association was independent of the known risk factors smoking, hypertension and diabetes as well as the serum concentrations of total triglycerides, HDL-cholesterol, alpha-Lp-cholesterol and pre-beta-Lp-cholesterol. In contrast to these variables the association between Lp(a) and coronary artery disease was dependent upon the serum concentrations of LDL-cholesterol, beta-Lp-cholesterol and total cholesterol. At concentrations below the respective median for each variable, odds ratios of between 1.42 and 1.67 were calculated whereas at concentrations above the respective medians the odds ratios ranged from 4.50 to 6.33 (P less than 0.001). Our data, therefore, suggest that increasing LDL concentrations markedly increase the risk of coronary artery disease due to elevated Lp(a) levels.

Adult↗