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D Seidel

Publications and source records attributed to D Seidel.

At least 199 records · Page 11Linked to original sources
PubMed1986

Analytical performance of the random access analyser Hitachi 737. A multicentre evaluation.

The selective multitest analyser Hitachi 737 was examined according to the ECCLS guidelines in a multicentre evaluation involving 4 laboratories. Twenty routine parameters, including the electrolytes, sodium, potassium and chloride, were measured at 37 degrees C. All of the measured values were included for evaluation without correcting for outliers. The trial, which lasted 4 months and involved over 70 000 analyses, basically yielded the following results: The precision can be termed very good. For the majority of the methods, the day-to-day coefficients of variation were below 2%. The highest coefficient of variation was 6.3% (for creatine kinase) and the lowest below 0.1% (for gamma-glutamyltransferase). The recovery of the assigned values of control sera was very good for most of the parameters (between 95% and 105%). Only with bilirubin, phosphate and chloride did greater deviations occur in a few control sera. Excellent agreement was found between the results obtained from the instruments used in the comparison: the Hitachi 705, a flame photometer and a chloride meter. No drift effects were observed. The same applied to carryover effects, provided that Boehringer Mannheim's recommendations concerning method combinations are observed. Because of the large measuring range, it is necessary to repeat analyses only in exceptional cases. During the entire period of the trial there were no stoppages due to the instrument malfunction. As a result of its reliability, the Hitachi 737 is well suited for routine operation and emergency analysis in medium to large-sized laboratories.

Autoanalysis↗
PubMed1985

Effects of medrogestone and conjugated oestrogens on serum lipid and lipoprotein concentrations.

Twenty patients, aged 30-60 yr, who had undergone bilateral ovariectomy, were treated orally with 5 mg medrogestone (6,17-dimethylpregna-4,6-diene-3,20-dione) and 1.25 mg conjugated oestrogens per day, according to a constant dosage pattern during the cycle (22 + 6 days). The lipids and lipoproteins were determined twice before the start of therapy and 3, 6 and 12 mth thereafter. The lipids were quantified enzymatically and the lipoproteins by quantitative lipoprotein electrophoresis. Whilst cholesterol and triglyceride concentrations showed no detectable change, a slight but significant increase was seen in the high-density alphalipoprotein (HDL) cholesterol concentrations. The low-density beta-lipoprotein (LDL) cholesterol level showed a moderate fall. There was a resultant reduction in the beta/alpha-lipoprotein ratio. Accordingly, the apoprotein A1 concentrations were found to be elevated, while apoprotein B tended to fall to lower levels during therapy. When these changes are measured by the lipid metabolism risk criterion for the occurrence of coronary heart disease applicable to post-menopausal patients, the effects of the above-mentioned combination may be regarded as entirely favourable.

Adult↗
PubMed1985

[Changes in serum lipoproteins under hormonal therapy of breast carcinoma and other endocrine-dependent tumors].

The higher the low-density-lipoprotein cholesterol (beta lipoprotein) level, the greater the risk that coronary heart disease will develop, alpha-lipoprotein fractions (high-density-lipoproteins) are considered to be protective factors. Medroxyprogesterone acetate is responsible for characteristic changes of the lipoprotein patterns indicating enhanced coronary risks. Medroxyprogesterone acetate is applied in the therapy of breast, uterus and ovarian cancer. A statistically significant decrease was observed in alpha-lipoproteins whereas beta-lipoproteins increased without statistical significance. A similar reaction can be observed under the combination therapy of aminoglutethimide and medroxyprogesterone acetate, whereas the combination of cortisone and aminoglutethimide has a distinct influence on beta-lipoproteins but the alpha-lipoprotein level remains uninfluenced. According to these data the effect of an adjuvant application of these drugs must be carefully evaluated due to an increase of coronary risks.

Aminoglutethimide↗
PubMed1985

Isolation, characterization, and uptake in human fibroblasts of an apo(a)-free lipoprotein obtained on reduction of lipoprotein(a).

Treatment of native human Lp(a) under nondenaturing conditions with dithiothreitol yielded both a lipoprotein particle and a lipid-free protein component that could be separated by either ultracentrifugation at d 1.063 g/ml or heparin-Sepharose chromatography. The protein component only showed antigenicity against anti-Lp(a) but not against anti-B. It was heterogeneous according to SDS polyacrylamide gel electrophoresis (PAGE) consisting of two bands, a major band with molecular weight similar to apoB and a minor band with slightly lower molecular weight. The lipoprotein particle was similar to LDL with regard to its electrophoretic mobility, lipid-protein composition, its apparent molecular weight according to gel-exclusion chromatography, and its apoprotein content; only apoB was found to be present by SDS-PAGE and immunochemical analysis. This lipoprotein also proved to be identical to LDL in its uptake by the receptor-mediated LDL-pathway in cultured human fibroblasts as shown by the similarity of the concentration-dependent binding, internalization, and degradation curves at 37 degrees C of the 125I-labeled lipoproteins. Normal Lp(a) was not taken up as readily as either its reduced lipoprotein component or LDL in the various steps of the receptor-mediated pathway. The maximal capacity for Lp(a) in the degradation assay was only 25% of that of LDL and it had a fourfold higher Km. It is therefore probable that the LDL-receptor-mediated pathway is not a major route for the clearance of Lp(a) in vivo. These studies suggest that Lp(a) is, in essence, an LDL-particle to which the protein (a) is attached through disulfide bonds to apoB.

Chromatography, Affinity↗
PubMed1985

[Automated platelet count in thrombocytopenic patients--a comparison of methods].

157 EDTA blood samples from thrombocytopenic patients (platelets less than 100 X 10(9)/1) were measured and the platelet counts compared using the various blood cell counters of the central laboratory, University Clinic, Göttingen. Using the H 6000, Hemalog 8 (both Technicon) and ELT-8 (Ortho Instruments), product-moment correlation coefficients (r) ranging from 0.88 to 0.92 were obtained between the different counters. The correlation coefficients of the thrombocounter (Coulter) to the other instruments were only 0.84 and 0.85. Discrepant platelet counts (difference greater than 40 X 10(9)/1) were reinvestigated using the Neubauer chamber. From a total of 354 platelet measurements, falsely high concentrations were observed only in three cases and falsely low concentrations in seven cases.

Edetic Acid↗
PubMed1985

[Comparative hemolysis studies of various dialysis technics].

In simultaneous experiments the haemolysis in the double-needle dialysis was investigated in comparison to the single-needle technique. As SN-technique the 2-clamp technique with permanently going and start-stop function of the blood pump, respectively, was used. Another technique without arterial and with retarded venous clamp was tested. Furthermore, the pressure limits in the SND were varied. A slight increase of the haemolysis in the SND in comparison to the DND was stated. In the different SN-techniques no essential differences in the haemolysis could be proved, whereas an increase of the pressure limits led to a clear increase of the haemolysis.

Hemolysis↗
PubMed1984

Computed tomography in late-onset metachromatic leucodystrophy.

In late-onset metachromatic leucodystrophy (MLD), early clinical diagnosis is difficult since initial symptoms frequently consist of misleading nonspecific psychopathological alterations. On cranial computed tomography (CT), however, symmetrical attenuation decrease of the white matter and mild cerebral atrophy can already be found in an early stage of the disease, and may even precede clinical symptoms. On the basis of observations in four patients with late-onset MLD who were followed between 1 and 5 years, characteristic CT appearances in different stages of the disease are outlined and compared with the literature.

Adolescent↗
PubMed1984

[Lipoprotein changes during hormonal treatment of endometriosis with lynestrenol and danazol].

The Lipoprotein profile of 24 patients with endometriosis was determined before, during and after the treatment with the two steroid hormones Lynestrenol (10 mg/day) and Danazol (600-800 mg/day). The total cholesterol triglycerides, beta-, prebeta-, and Alphalipo -protein bound to cholesterol were determined. Both hormones cause a marked lowering of the Alpha-Lp-cholesterin. In addition, the beta-LP-cholesterin was elevated and the beta-alpha-LP-ratio was elevated. In the dosage used by us, Lynestrenol showed less effect on the Lipoprotein profile. Danazol caused changed in the beta- and alpha-lipoprotein pattern of highly pathological atherogenic types. The total cholesterol was not influenced. Since women in the fertile age group will suffer a higher risk of arteriosclerosis from an elevation of the beta-LP-cholesterin, the treatment with Danazol calls for a sophisticated monitoring of the lipid metabolism and care in the indication for long term treatment with Danazol or with Lynestrenol.

Adult↗
PubMed1984

Role of lipoprotein-X in the pathogenesis of cholestatic hypercholesterolemia. Uptake of lipoprotein-X and its effect on 3-hydroxy-3-methylglutaryl coenzyme A reductase and chylomicron remnant removal in human fibroblasts, lymphocytes, and in the rat.

Cholestasis is accompanied by the appearance of lipoprotein-X (LP-X) in plasma. This lipoprotein has a high content of unesterified cholesterol and phospholipids and appears to be ineffective in suppressing the enhanced hepatic cholesterogenesis of cholestasis. Its role as a possible causative factor for cholestatic hypercholesterolemia was investigated. When 125I-LP-X was injected into rats, it disappeared rapidly from the circulation. Calculated on the basis of gram wet weight, spleen took up more LP-X than liver. Prior ligation of the bile duct reduced the uptake in spleen. Experiments with isolated perfused rat liver showed that nonparenchymal cells (NPC) took up over eightfold more 125I-LP-X than hepatic parenchymal cells (PC). Incubation of PC, NPC, human lymphocyte suspensions, or fibroblast cultures with LP-X showed that NPC bound more LP-X than PC or fibroblasts. Lymphocytes took up 20-fold more LP-X than PC and the activity of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase was depressed by LP-X. Lymphocytes isolated from cholestatic patients showed low activity of this enzyme. The activity was increased by LP-X in isolated perfused livers, but suppressed in isolated microsomes. LP-X competitively inhibited the uptake of chylomicron remnants in isolated perfused livers and hepatocytes. In contrast, degradation of LDL by perfused livers, which were isolated from ethinyl estradiol-treated rats or human fibroblast cultures, remained unchanged in the presence of LP-X. The results indicate that cholesterol transported by LP-X is mainly taken up by the cells of the reticuloendothelial system. It increases the activity of hepatic HMG-CoA reductase and suppresses remnant uptake, thus emphasizing a major role of LP-X in cholestatic hypercholesterolemia.

Animals↗
PubMed1984

Influence of smoking on the plasma lipoprotein profile.

Smoking and hypercholesterolemia, or more specifically hyper-beta-lipoproteinemia, are well established risk factors for the early development of atherosclerotic disease. The presence of both factors augments the potential risk. The question arises, therefore, as to whether cigarette smoking has a direct effect on the plasma lipoproteins and, in particular, on the atherogenetic low density lipoproteins. In this study, the influence of cigarette smoking on the lipoprotein profile was investigated in a defined cohort of 6,543 male industrial workers aged 40-59 years, consisting of 2,434 smokers and 3,975 non-smokers. The effect of smoking on the lipoprotein profile showed no significant changes in LDL and only slight changes in the other lipoprotein fractions. Other factors, such as alcohol intake, body weight, and general life style seem to have a greater influence on HDL-cholesterol than smoking. It is concluded that smoking does not significantly alter lipid metabolism and that minor differences observed between smokers and non-smokers are due to a variety of factors, rather than a reflection of a direct metabolic relationship.

Adult↗
PubMed1984

Influence of smoking on cellular lipid metabolism.

Smoking and hyper-beta-lipoproteinemia, are well-established risk factors for the early development of atherosclerotic disease. The presence of both factors augments the potential risk. Since the influence of smoking on the plasma lipoprotein profile in humans seems to be either absent or minor, we were interested in whether cigarette smoking develops a direct influence on lipid metabolism at the cellular level. Our findings showed that smoking has no effect on either the high affinity LDL receptor activity or on the activity of HMG-CoA reductase, acid lipase, or cholesterol ester hydrolase.

Adult↗
PubMed1984

[Plasma lipoproteins in humans: metabolism and relation to atherosclerosis].

For a better understanding of atherogenesis it is important to consider the results from basic research in pathophysiology, pathobiochemistry and clinical research with special focus on the endothelium, the smooth muscle cells, macrophages, platelets and the plasma lipoproteins. The penetration of low-density lipoproteins through the endothelium, the contact of these particles with the potential foam cells, the effect of various cellular migratory and growth factors, the prostaglandin system and the hormonal status are important factors in the mechanisms leading to the formation of the atherosclerostic plaque. Disturbances in lipid metabolism are rarely recognized by signs such as formation of xanthomata. Even the measurement of plasma lipids does not always allow conclusions to be drawn with regard to the complicated relationship between lipoprotein concentrations and their potential risk. To estimate this risk biochemical and clinical interpretation must be performed individually and under consideration of various factors. This also holds true for the choice of therapeutical management. The therapy of lipid metabolism has to be an approach to the therapy of atherosclerosis with reduction of elevated low-density lipoprotein concentrations as the most important goal. Therapeutic management should be individually assessed, taking all known risk factors into account.

Arteriosclerosis↗
PubMed1983

Chromatofocusing of human high density lipoproteins and isolation of lipoproteins A and A-I.

Using chromatofocusing, a column chromatography method with an internally generated pH gradient and focusing effects, human plasma high density lipoproteins (HDL) were fractionated into six subclasses within an interval of less than 1 pH unit (pH 5.1-4.2). All fractions floated in the ultracentrifuge at density = 1.21 g X ml-1, retained a typical HDL electron micrographic morphology and as a single band, alpha-migration on agarose electrophoresis. Compositional analysis of the subclasses revealed an inverse relationship between cholesterol ester and cholesterol on a molar basis. Distinct differences in the distribution of the apolipoproteins between the fractions were found. Two of the subclasses contained only apolipoprotein A-I and were therefore considered to be two forms of the lipid-combined form of apolipoprotein A-I, i.e., lipoprotein A-I. One subclass contained only apolipoproteins A-I + A-II and was, therefore, lipoprotein A. One subclass contained apolipoproteins A-I + A-II + D, and the two remaining contained additionally apolipoproteins C and E. Lipoprotein A-I was also demonstrated after immunoabsorption of apolipoprotein A-II-containing lipoproteins from whole serum. It is suggested that this method, which allows the fractionation of HDL into subclasses with distinct differences in apolipoprotein composition, offers new avenues for the study of the structural and metabolic heterogeneity of HDL.

Apolipoprotein A-I↗