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Biomedical subjects

G Assmann

Publications and source records attributed to G Assmann.

At least 325 records · Page 18Linked to original sources
PubMed1987

The Prospective Cardiovascular Münster Study: prevalence and prognostic significance of hyperlipidemia in men with systemic hypertension.

The ongoing Prospective Cardiovascular Münster (PROCAM) trial was initiated to identify risk factors for coronary artery disease (CAD). By comparing patients' long-term cardiac status (clinical signs of atherosclerosis, myocardial infarction, stroke or death due to atherosclerotic disease) with results from entrance questionnaires, physical examinations, blood pressure measurements, electrocardiograms at rest and blood analyses, the characteristics and strategies for identifying people in the general population who are at risk for developing CAD were to be determined. From PROCAM trial data, 3 predictive criteria for identifying such people have been determined: They are a total cholesterol/high density lipoprotein (HDL) cholesterol ratio of 6.5 was determined to be the threshold for CAD risk. Combined analysis of lipid parameters identified high-risk patients as those with cholesterol values of greater than or equal to 300 mg/dl, and low-risk patients as those with cholesterol and triglyceride values less than 200 mg/dl. The remaining subjects are classified according to their HDL cholesterol values. If the HDL cholesterol value is less than 35 mg/dl, the subject is considered to be at high risk, if HDL cholesterol is greater than or equal to 35 mg/dl the patient is considered to be at average risk. The upper 20% of risk was computed by means of a multiple logistic function based on statistics for age, total cholesterol and HDL cholesterol levels, systolic blood pressure, angina pectoris, diabetes mellitus, cigarette smoking and family history of myocardial infarction. A further analysis was the risk incurred by hypertension. Hypertension was observed in 16.5% of men and 13.9% of women.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Characterization of an apolipoprotein C-III mutant by high-performance liquid chromatography and time-of-flight secondary ion mass spectrometry.

Apolipoprotein (apo) C-III isoforms from a patient with a mutant apo C-III and from controls were isolated to homogeneity by isoelectric focusing and subjected to proteolytic digestion. The peptides obtained were separated by reversed-phase high-performance liquid chromatography, and their molecular masses were determined by time-of-flight secondary ion mass spectrometry. Molecular masses of peptides derived from apo C-III0, C-III1 and C-III2 were indistinguishable from control preparations, whereas the mutant apo C-III contained a COOH-terminal, carbohydrate-containing peptide with an abnormal retention time in high-performance liquid chromatography and a molecular mass higher by 291 daltons owing to oversialation at position 74 of the amino acid sequence (apo C-III3).

Amino Acid Sequence↗
PubMed1987

Dimorphic markers for the human apolipoprotein CII gene locus.

Two restriction-site polymorphisms (RSP) have been detected when using a human apolipoprotein CII (apoCII) cDNA clone as a hybridization probe. These include a BanI and a TaqI RSP. Frequencies of the more common allele have been determined in a German population of 100 individuals and are 0.66 (BanI RSP) and 0.56 (TaqI RSP). Corresponding polymorphic information content (PIC) values are 0.36 and 0.37 for individual sites, and 0.58 for the BanI-TaqI pair of sites, making this locus a very informative (PIC-rich) marker for this region of chromosome 19. Haplotype studies also indicate the presence of allelic association (linkage disequilibrium) at the human apoCII gene locus.

Alleles↗
PubMed1987

Different substrate specificities of plasma lecithin: cholesterol acyl transferase in fish eye disease and Tangier disease.

Esterification of plasma free cholesterol is mediated by lecithin:cholesterol acyl transferase (LCAT). The free cholesterol of plasma high density lipoproteins (HDL) is considered to be the preferred substrate for LCAT. It therefore appeared as a paradox that plasma cholesterol esterification, both in vivo and in vitro, is normal in fish eye disease and Tangier disease, two familial conditions with extremely low plasma HDL levels. Fish eye disease plasma, however, was shown to have LCAT activity primarily acting on combined very low (VLDL) and low (LDL) density lipoproteins, denominated beta-LCAT, while it lacked LCAT activity esterifying HDL cholesterol (alpha-LCAT). Here we show that Tangier plasma, in contrast, has both alpha- and beta-LCAT. Thus, in both fish eye and Tangier diseases it is beta-LCAT that explains the apparent normal plasma cholesterol esterification. We also show that Tangier plasma, having alpha-LCAT activity, normalizes the low cholesteryl ester content as well as the abnormally small size of fish eye disease HDL particles during incubation.

Cholesterol↗
PubMed1987

Detection of a new Msp I restriction fragment length polymorphism in the apolipoprotein A-I gene.

We report the existence of a Msp I restriction fragment length polymorphism in the first intron of the apolipoprotein A-I gene that is different from the one described by Seilhamer et al. (DNA 3, 309 (1984)). Size comparison of the newly discovered Msp I fragment with a restriction map of the apolipoprotein A-I gene revealed that most likely the cutting site at the 5'-end of the normally seen 673 bp fragment is lost giving rise to the observed 719 bp Msp I fragment. Based on analyses of 136 DNAs of healthy and non-related caucasians the allelic frequency was determined to be 0.06. The observed Msp I genotype frequencies are in Hardy-Weinberg equilibrium.

Apolipoprotein A-I↗
PubMed1987

VLDL cholesterol and VLDL apolipoprotein B. Preliminary cross-sectional data of the prospective epidemiological study of company employees in Westphalia.

VLDL cholesterol concentrations were determined in 1641 male and 608 female and VLDL apolipoprotein B concentrations in 505 male and 211 female company employees in Westphalia aged 17-70 years. VLDL cholesterol and VLDL apolipoprotein B values were found to be distributed with positive skew in both sexes but were higher in men than in women (median in men: VLDL cholesterol 0.30 mmol/l, VLDL apolipoprotein B 0.066 g/l, median in women: VLDL cholesterol 0.18 mmol/l, VLDL apolipoprotein B 0.047 g/l). In males VLDL cholesterol and VLDL apolipoprotein B were closely correlated to each other (r = 0.757) as well as to triacylglycerols (VLDL cholesterol: r = 0.673, VLDL apolipoprotein B: r = -0.419). In females these observed correlations were weaker. The VLDL cholesterol/VLDL apolipoprotein B ratio was also higher in men (median 4.28 mmol/g) than in women (median 3.15 mmol/g). The ratio correlated to triacylglycerols (men: r = 0.591, women: r = 0.321). The results suggest that the composition of VLDL may be related to triacylglycerols in serum.

Adolescent↗
PubMed1987

Flow-cytometric determination of high-density-lipoprotein binding sites on human leukocytes.

In this method, leukocytes were isolated from 6 mL of EDTA-blood by density-gradient centrifugation and subsequently incubated with rhodamine isothiocyanate (RITC)-conjugated high-density lipoproteins (HDL). The receptor-bound conjugate particles were determined by fluorescent flow cytometry and compared with 125I-labeled HDL binding data for the same cells. Human granulocytes express the highest number of HDL binding sites (9.4 X 10(4)/cell), followed by monocytes (7.3 X 10(4)/cell) and lymphocytes (4.0 X 10(4)/cell). Compared with conventional analysis of binding of 125I-labeled HDL in tissue-culture dishes, the present determination revealed significantly lower values for nonspecific binding. In competition studies, the conjugate competes for the same binding sites as 125I-labeled HDL. With the use of tetranitromethane-treated HDL3, which fails to compete for the HDL receptor sites while nonspecific binding is not affected, we could clearly distinguish between 37 degrees C surface binding and specific 37 degrees C uptake of RITC-HDL3, confirming that the HDL receptor leads bound HDL particles into an intracellular pathway rather than acting as a "docking" type of receptor. Patients with familial dysbetalipoproteinemia showed a significantly higher number of HDL binding sites in the granulocyte population but normal in lymphocytes and monocytes, indicating increased uptake of cholesterol-containing lipoproteins. In patients with familial hypercholesterolemia, HDL binding was increased in all three cell types, indicating increased cholesterol uptake and increased cholesterol synthesis. The present method allows rapid determination of HDL binding sites in leukocytes from patients with various forms of hyper- and dyslipoproteinemias.

Binding, Competitive↗
PubMed1987

Interaction of Tangier lipoproteins with cholesteryl ester-laden mouse peritoneal macrophages.

Cholesterol efflux was studied from cholesteryl esterladen mouse peritoneal macrophages in the presence of Tangier lipoproteins derived from fasting and postprandial sera of three patients homozygous for Tangier disease (analphalipoproteinemia). The d greater than 1.063 g/ml fractions isolated from fasting patients and 3 hr and 18 hr after an oral fat load were all effective in cellular cholesterol removal. By contrast, the d greater than 1.063 g/ml fractions isolated 6 hr and 12 hr after fat ingestion did not affect net removal of cellular cholesterol. The d greater than 1.21 g/ml protein fractions derived from fasting as well as postprandial sera were all effective in removing cholesterol. D 1.063-1.21 g/ml fractions from fasting Tangier patients contained HDLT. In the corresponding postprandial fractions, in addition to HDLT, apoB-100- and apoB-48-containing lipoproteins were present. Furthermore, the 6 hr and 12 hr postprandial Tangier HDL fractions contained apoB-immunoreactive proteins of lower molecular weight. The abnormal activity of the elastase/alpha 1-antitrypsin proteolytic system and the abnormal fibronectin concentration we found in Tangier plasma suggests a possible relationship to the in vivo degradation of apoB. The peculiar type of membrane-bound lipid droplets in Tangier splenic macrophages points to a lipoprotein source of lipid accumulation which possibly originates from the uptake of chylomicrons or chylomicron-derived particles. It is concluded that cholesteryl ester storage in Tangier macrophages results from an imbalance of cholesterol influx and efflux. In the absence of HDL, the net increase of cholesterol caused by abnormal lipoproteins in certain postprandial states cannot be fully compensated by effective efflux and ultimately leads to macrophage cholesteryl ester accumulation.

Adult↗