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Biomedical subjects

G Assmann

Publications and source records attributed to G Assmann.

At least 379 records · Page 21Linked to original sources
PubMed1984

The effects of cigarette smoking on serum levels of HDL cholesterol and HDL apolipoprotein A-I. Findings of a prospective epidemiological study on employees of several companies in Westphalia, West Germany.

In preventive studies of company employees in Westphalia, HDL cholesterol was measured in the sera of 4933 men and 2365 women, as well as HDL apolipoprotein A-I in the sera of 3509 men and 1648 women. Three subgroups were compared: non-smokers = persons who have never smoked; ex-smokers = persons who do not smoke at present but did in the past; smokers = persons who smoke cigarettes at present. Mean values for HDL cholesterol and for HDL apolipoprotein A-I were significantly lower in smokers than in non-smokers or in ex-smokers, while there were no differences between the last two groups. These differences appeared in both sexes but were more pronounced in women than in men. To answer the question whether the observed differences are caused by the consumption of cigarettes by itself or whether they are caused by the presence of other risk factors, further subgroups were compared to assess the influence of the risk factors obesity, hypertension, hypercholesterolaemia, hyperglycaemia and hyperuricaemia. It was found that - regardless of the presence of no, one, two or more risk factors - the frequency of probands with low HDL cholesterol values (less than 0.907 mmol/l (men); less than 1.166 mmol/l (women] was about 10% higher in smokers than in non-smokers or ex-smokers. Subgroups based on the number of risk factors did not exhibit the same clear distribution for apolipoprotein A-I values as were seen for HDL cholesterol. The results are interpreted in the light of the existing literature.

Apolipoprotein A-I↗
PubMed1984

HDL phosphatidyl choline and risk-factors of coronary heart disease.

As part of our epidemiological study of employees in Westphalia, the concentration of HDL phosphatidyl choline was measured in 1546 men and 778 women. The results were analysed in relation to the corresponding HDL cholesterol values, as well as the various risk factors for coronary heart disease. HDL phosphatidyl choline values were found to be age independent, higher in women than in men (p les than 0.001), and lognormally distributed in both sexes (men: mean 1.162 mmol/l, median 1.13 mmol/l, minimum 0.60 mmol/l, maximum 2.46 mmol/l; women: mean 1.370 mmol/l, median 1.34 mmol/l, minimum 0.55 mmol/l, maximum 2.46 mmol/l). A positive correlation (p less than 0.001) was found in both sexes between HDL phosphatidyl choline and HDL cholesterol (men: r = 0.588; women r = 0.605). A negative correlation was found in both sexes between HDL phosphatidyl choline values and body weight (men: r = -0.102 (p less than 0.001) women: r = -0.129 (p less than 0.001); and in men, but not in women, there was a negative correlation between HDL phosphatidyl choline values and triglycerides (men: r = -0.190 (p less than 0.001) women: r = -0.042). A negative correlation between HDL phosphatidyl choline and cigarette smoking was found only in female smokers (r = -0.121 (p less than 0.05). The correlation coefficients between HDL cholesterol and triglycerides as well as HDL cholesterol and relative body weight in both sexes were clearly higher than the corresponding correlation coefficient of HDL phosphatidyl choline. In men as well as in women the HDL phosphatidyl choline/HDL cholesterol ratio decreased with increasing HDL cholesterol values or decreasing triglyceride values in blood serum.

Adolescent↗
PubMed1984

Frequency of apolipoprotein A-I mutants in the German population.

A randomly chosen population in the area of Westphalia (West Germany) was screened for apolipoprotein A-I mutants. About 5000 individuals were investigated and compared with a group of 1300 patients who had undergone coronary angiography. Four electrophoretically different apolipoprotein A-I-mutants (named Münster-1 to 4) were discovered. Five non-related probands were observed in the group of the unselected patients and three non-related probands in the group of coronary angiography patients. In most cases the familial nature of the abnormality was confirmed by pedigree analysis.

Adult↗
PubMed1984

The relationship of lipoprotein (a) (Lp(a)) to risk factors of coronary heart disease: initial results of the prospective epidemiological study on company employees in Westfalia.

Lp(a) concentrations were determined in 987 male and 477 female company employees in Westfalia, in the age range 17-70 years. These values were then related to age and to the following risk factors: obesity, smoking, hypertension, hypertriglyceridaemia, hypercholesterolaemia, hyperbetalipoproteinaemia, hypoalphalipoproteinaemia, hyperglycaemia and hyperuricaemia. The Lp(a) values showed a similar markedly skewed distribution for both men and women. The median for men was 0.039 g/l, for women 0.050 g/l. In both sexes only about 25% of all Lp(a) values were above 0.10 g/l. Raised Lp(a) values (greater than 0.30 g/l) were found in 6.5% of males and in 6.1% of females. A significantly higher frequency of raised Lp(a) values (greater than 0.30 g/l) was found in: post-menopausal women (11.3% as against 4.1%, p less than 0.01); females with hypercholesterolaemia (19.0% when cholesterol values were greater than or equal to 6.73 mmol/l, 10.8% when cholesterol values were between 5.70-6.72 mmol/l, 3.0% when cholesterol values were less than 5.70 mmol/l, p less than 0.001); and females with hyperbetalipoproteinaemia (22.6% when LDL cholesterol values were greater than or equal to 4.92 mmol/l, 5.0% when LDL cholesterol values were less than 4.92 mmol/l, p less than 0.001). 12.0% of men with hypoalphalipoproteinaemia (HDL cholesterol values less than 0.907 mmol/l) had Lp(a) values greater than 0.30 g/l, as against 5.5% of men with HDL cholesterol values greater than or equal to 0.907 mmol/l (p less than 0.01). This percentage rate increased to 16.9% when hypertriglyceridaemia (greater than or equal to 2.28 mmol/l triglycerides) was also present. All other risk factors which were examined and their combinations had no significant influence on the prevalence of raised Lp(a) concentrations.

Adult↗
PubMed1984

Lipid binding properties of the Tangier apolipoprotein A-I and its isoproteins.

The apolipoprotein A-I was isolated from the plasma of normal individuals and of three homozygous patients with Tangier disease by immunoprecipitation. The apoA-I isoforms were further fractionated by isofocusing on polyacrylamide gels. The physicochemical behavior of normal and Tangier apoA-I and of the isoproteins-2 and -4 was studied by monitoring the tryptophanyl fluorescence emission as a function of temperature, pH, and under exposure to guanidinium (guanidine) hydrochloride (GdmCl). Lipid-apoprotein complexes were generated by incubation with dimyristoylphosphatidylcholine and isolated by density gradient ultracentrifugation. Our results show that normal apoA-I and its isoprotein-4 associate with lipids to yield a complex containing 150-200 mol lecithin/mol apoA-I. The isoprotein-2 of normal apoA-I and the isoprotein-4 of Tangier apoA-I generate lipid-rich complexes with lecithin, while the isoprotein-2 of Tangier apoA-I shows only a limited association with lipids. ApoA-I normal and Tangier and their isoproteins-4 undergo a structural transition around 45 degrees C, which is not observed in the lecithin-apoA-I complexes. This transition is accompanied by an increased exposure of the tryptophanyl residues to the solvent. This transition was observed for the isoprotein-2 of apoA-I Tangier both in its lipid-free form and in the presence of lecithin. The pH denaturation of apoA-I and of the isoprotein-4 between pH 9 and 13 and between pH 7 and 2 is accompanied by a similar conformational transition. The transition occurs around pH 10.8 for the native apoproteins and is shifted towards respectively higher and lower pH's as result of the protective action of lipid binding on the protein conformation. Such an effect was not observed with the isoprotein-2 of apoA-I Tangier which is denatured at lower pH's both in its native form and in a lipid-protein mixture. Finally the denaturation of apoA-I by GdmCl indicates that apoA-I normal and Tangier undergo structural changes around 1 M GdmCl, whereas the apoA-I-Tangier-lecithin complex is more susceptible to denaturation than the complex with apoA-I normal. These data suggest that the apoA-I normal and Tangier and their isoproteins-4 are able to associate with lipids although the association between apoA-I Tangier with lecithin is weaker than that of apoA-I normal. The isoprotein-2 of normal apoA-I associates to a greater extent with lipids than the isoprotein-2 of Tangier apoA-I, whose structure differs from that of the isoprotein-4.(ABSTRACT TRUNCATED AT 400 WORDS)

Apolipoprotein A-I↗
PubMed1984

HDL phosphatidyl choline and cigarette smoking.

The influence of cigarette smoking on the concentration of HDL phosphatidyl choline was tested in 1,546 male and 778 female employees in Westfalia, and the results were compared with the influence of cigarette smoking on the concentration of HDL cholesterol. Three subgroups were established for comparison: non-smokers = persons who had never smoked; ex-smokers = persons who had in the past been smokers but were now non-smokers; and smokers = persons who at present smoked cigarettes. Neither male nor female smokers proved to have different HDL phosphatidyl choline values when compared to non-smokers or ex-smokers, whereas male and female smokers were found to have decreased HDL cholesterol values when compared to non-smokers (p less than 0.01) or ex-smokers (p less than 0.05). In female smokers a correlation was found between HDL phosphatidyl choline values and the number of cigarettes smoked every day (r = -0.12, p less than 0.05).

Adolescent↗
PubMed1984

Apolipoprotein E polymorphism and hyperlipidemia.

We tested apolipoprotein E phenotypes in 1557 normolipidemic factory workers and 822 hyperlipidemic hospital patients. We distinguished six different apolipoprotein E phenotypes and determined their frequencies in normolipidemia (factory workers), hypertriglyceridemia, hypercholesterolemia, and mixed hyperlipidemia. For the three homozygous phenotypes E3/3, E4/4, and E2/2, the percentage distribution in the normolipidemic group was 62.2%, 2.2%, and 0.9%, respectively; for the three heterozygous phenotypes E4/3, E3/2, and E4/2, we determined frequencies of 19.9%, 11.7%, and 2.9%, respectively. A higher prevalence of E2/2 homozygosity was observed in hypertriglyceridemic persons (2.5%) and persons affected by mixed hyperlipidemia (5.0%). E4/4 homozygosity occurred more often among hypercholesterolemic patients (5.0%) than normolipidemic persons (2.2%). These data suggest that E2/2 homozygosity and E4/4 homozygosity both predispose to hyperlipidemia. Patients affected by mixed hyperlipidemia should be investigated for their apolipoprotein E polymorphism because of the possible linkage of apolipoprotein E2/2 homozygosity, hyperlipidemia, and atherosclerosis.

Adult↗
PubMed1983

Turbidimetric kinetic method for serum low density lipoprotein quantitation.

A turbidimetric kinetic fixed-time method for the rapid determination of serum low density lipoprotein (LDL) has been developed. It is based on specifically precipitating this lipoprotein with the use of a combination of heparin, Ca2+, EDTA and lipase. The method has been adapted to the Eppendorf spectrum line photometer and to the ENI Gemsaec centrifugal analyzer. It yielded satisfactory results with regard to linearity and precision. The values agreed closely to those obtained by conventional procedures for LDL-cholesterol and LDL-apolipoprotein B. The predictive value of this new method for the assessment of the individual risk of vascular disease remains to be proven by clinical and epidemiological studies.

Calcium↗
PubMed1983

Effect of 10 weeks endurance training on the concentration of lipids and lipoproteins as well as on the composition of high-density lipoproteins in blood serum.

The effect of 10 weeks endurance training on the concentration of serum lipids and lipoproteins, particularly on the composition of high-density lipoproteins, was measured in nine 22--28-year-old male volunteers at weekly intervals during training as well as 5 and 10 weeks following the exercise program. A control group consisted of six male subjects between the ages of 22 and 37 years. The endurance program consisted of running for approximately 30 min three times a week covering about 5--7 km per session. Two participants discontinued the program after 6 weeks while the remaining seven completed the training in the course of 10 weeks. After the end of the exercise program, all subjects showed a 20%--25% decrease in free cholesterol as well as a 40% decrease in triglycerides while esterified cholesterol remained unchanged. Only in subjects with HDL cholesterol/total cholesterol ratios of less than 0.3 at the start of the exercise program was a statistically significant increase in HDL cholesterol values (P less than 0.05) following training observed. In all subjects HDL phosphatidyl choline values were elevated by a mean of 20% at the end. With the exception of two participants, the HDL triglyceride concentration was diminished after the exercise program. The concentrations of HDL apolipoprotein A-I and A-II were unaffected by exercise. In the control group, no statistically significant changes of the measured parameters could be observed. Our results suggest that short-term physical training produces changes in cholesterol ersterification and/or cholesterol-ester transport as well as in HDL composition.

Adult↗
PubMed1983

Tangier disease: defective recombination of a specific Tangier apolipoprotein A-I isoform (pro-apo A-i) with high density lipoproteins.

Isoforms of apolipoprotein A-I (apo A-I) from subjects with Tangier disease were characterized, and their ability to recombine with normal high density lipoproteins (HDL) was studied. In contrast to normal serum, in which isoprotein 4 is the dominant species [79 +/- 1.8% (mean +/- SD)], the Tangier serum contained much less total apo A-I (approximately equal to 1% of that in normal serum), and isoproteins 2 and 4 were present in roughly equivalent amounts (35.3 +/- 2.5% and 42.7 +/- 3.6%, respectively). The Tangier isoprotein 2 was shown to correspond to pro-apo A-I, having a six-amino acid amino-terminal extension with the sequence: Arg-His-Phe-Trp-Gln-Gln-. The Tangier isoprotein 4 had the same amino-terminal sequence as normal circulating plasma apo A-I. Its association with normal HDL (70%) was similar to the association of normal apo A-I with HDL (80-90%) in recombination experiments. In marked contrast to this behavior, very little (less than 10%) of Tangier isoprotein 2 (pro-apo A-I) associated with HDL in recombination experiments. These results suggest that the underlying defect in Tangier disease may be a faulty conversion of pro-apo A-I to mature apo A-I, either due to a defect in the converting enzyme activity or to a further specific structural defect in Tangier apo A-I. The failure of Tangier pro-apo A-I to associate with HDL may be at least partially responsible for the HDL deficiency in Tangier subjects.

Amino Acid Sequence↗
PubMed1983

Competitive enzyme immunoassay for apolipoprotein A-II.

A competitive enzyme immunoassay for apolipoprotein A-II was developed. Microtitre plates were used as a solid phase and coated with anti-apolipoprotein A-II antibodies. Purified apolipoprotein A-II, labelled with horseradish peroxidase was used as competing ligand. The assay was examined with respect to the optimal amounts of specific anti-apolipoprotein A-II antibodies and apolipoprotein A-II-enzyme conjugate. The displacement curves showed a good parallelism between serum and purified apolipoprotein A-II. Delipidation of serum did not affect the content of apolipoprotein A-II. Cross-reactivity with apolipoprotein A-I was minimal. The intra- and inter-assay coefficients of variation in the medium range were 9.0 and 11.8% respectively. The assay might be well-suited for clinical routine.

Antibodies↗
PubMed1983

An economical assay for HDL phosphatidyl choline.

An economical enzymatic assay for HDL phosphatidyl choline is described, as adapted for the Cobas-Bio analyser (Hoffmann LaRoche). This method entails the enzymatic cleavage of phosphatidyl choline by phospholipase C from B. cereus, hydrolysis of phosphoryl choline and enzymatic determination of choline with choline oxidase by an enzymatic colour test. This method provides consistent values and is, by comparison to the enzymatic UV method (assaying choline with choline kinase in an optical test procedure), simpler to perform, more precise, and less expensive.

Alcohol Oxidoreductases↗
PubMed1983

HDL sphingomyelin determinations in normal individuals and patients with type IV-hyperlipoproteinaemia.

In 138 men and 79 women sphingomyelin values in the supernatant of sera obtained by precipitation of apolipoprotein B-containing lipoproteins ( = high density lipoprotein-sphingomyelin, HDL sphingomyelin) were determined using an enzymatic method. In men, lower HDL sphingomyelin values were obtained (0.22 +/- 0.06 mmol/l) than for women (0.24 +/- 0.05 mmol/l) (p less than 0.05). In both sexes HDL sphingomyelin values were independent of age, with the exception that in men greater than or equal to 55 years, HDL sphingomyelin concentrations were lower. The correlation coefficients calculated for HDL sphingomyelin and hypertriglyceridaemia and relative body weight were lower than the correlation coefficients calculated for the corresponding HDL cholesterol values and both risk factors. In women with hypertriglyceridaemia (greater than or equal to 2.28 mmol/l) HDL sphingomyelin values were lower than those for normotriglyceridaemic women within the same age group, while in male hypertriglyceridaemic patients within the same age group there were no differences in HDL sphingomyelin values in comparison to normotriglyceridaemic male subjects. In both sexes the differences measured between hypertriglyceridaemic and normotriglyceridaemic subjects for HDL sphingomyelin were lower than for the corresponding HDL cholesterol values. The results obtained show that HDL sphingomyelin values are not simply a reflection of HDL cholesterol values.

Adolescent↗
PubMed1983

Determination of HDL phosphatidyl choline by an enzymatic method.

A routine method is described for the enzymatic determination of phosphatidyl choline in the apolipoprotein B-free supernatant after precipitation of blood sera with phosphotungstic acid/MgCl2. The principle of this method is based on the specific cleavage of phosphatidyl choline by purified phospholipase C from B. cereus, and the enzymatic determination of choline by choline kinase after hydrolysis of phosphoryl-choline. The enzymatic method provides HDL phosphatidyl choline values which coincide with those of the conventional chemical method. Furthermore, the values obtained with the enzymatic method for the HDL fraction isolated by ultracentrifugation (1.063--1.21 kg/l) also closely coincide with those of the apolipoprotein B-free supernatant fraction. The precision, linearity and sample stability were also checked. The findings obtained show that the enzymatic assay introduced here is suitable for the routine determination of phosphatidyl choline in the apolipoprotein B-free supernatant.

Aging↗
PubMed1983

[The physiology of lipoprotein metabolism].

The physiology of lipoprotein metabolism is discussed. Emphasis is given to the presentation of the structure and the metabolism of apolipoproteins (A-E) and their relevance to the metabolism of lipoproteins (chylomicrons, very low density lipoproteins, low density lipoproteins, high density lipoproteins). With the consistent transformation our our concept of lipid emulsion with this new physiological and pathophysiological knowledge, improvements in artificial nutrition can be expected.

Apolipoproteins↗
PubMed1983

Isoproteins of human apolipoprotein A-II: isolation and characterization.

In human serum, polymorphism of apoA-II predominantly in HDL3 could be demonstrated. HDL3-apoA-II was composed of four isoproteins, each with a molecular weight of 8600 (reduced form) and identical immunological properties. The isoproteins are designated apoA-II-1 (pI 5.16), apoA-II-2 (pI 4.89) corresponding to the already known apoA-II monomer band, apoA-II-3 (pI 4.58), and apoA-II-4 (pI 4.31). The amino acid compositions of the A-II isoproteins were virtually identical with the published data for apoA-II. Treatment with acid phosphatase, alkaline phosphatase, or neuraminidase before electrophoresis did not alter the apoA-II pattern. The apoA-II isoprotein pattern was studied in ten male and ten female normolipidemic volunteers, in two patients with Tangier disease, and in three patients with abetalipoproteinemia. The isoelectric focusing patterns of apoA-II appeared virtually identical in all subjects. However, in Tangier disease, due to the low apo-A-II concentration, only apoA-II-1 and apoA-II-2 were detectable, and in abetalipoproteinemia a different relative distribution pattern of the individual isoforms was found as compared to normal HDL3. Our studies indicate that apoA-II, similar to apoA-I, exists in several isoforms. The relationship of these isoforms to each other is at present unclear. They may originate from relatively basic isoproteins that are modified in charge by post-translational processes such as proteolytic cleavage, sequential deamidation, or other mechanisms.

Abetalipoproteinemia↗