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Biomedical subjects

D Seidel

Publications and source records attributed to D Seidel.

At least 235 records · Page 13Linked to original sources

[Oestrogen as a risk factor for the vascular system (author's transl)].

Plasma oestradiol and testosterone concentrations were measured in 44 men with angiographically proven coronary heart disease, 66 men without evidence of coronary heart disease serving as control. Another group consisted of 28 men with renal failure. Those with coronary heart disease had a significantly higher oestradiol concentration than the control group. This increased value also was present in patients with renal failure. There was a relationship between the level of oestradiol on one hand and glucose tolerance, ratio of beta to alpha-lipoproteins and blood pressure, on the other, in both the patients with coronary heart disease and the healthy controls. These results indicate the oestradiol may in males be an indicator of a risk constellation of vascular damage. Perhaps, it may be the cause of an abnormal carbohydrate and fat metabolism, which then leads to hypertension and degenerative vascular lesions.

Adult↗

Cerebrospinal fluid lipids in demyelinating disease. I. Sphingolipids.

The lipid composition of CSF, serum and lymphocytes from patients without demyelinating disease (controls) as well as from patients with acute and chronic MS is analyzed. Individual lipid fractions are isolated by TLC and their fatty acid composition determined. Lipid and fatty acid composition of normal CSF resembles the results found in lymphocytes and it is deduced that CSF lipids are derived mainly from lymphocytes rather than white matter (myelin) or serum. There is an increase of CSF sphingomyelin in patients with acute MS (showing pleocytosis) which is apparently derived from disintegrated lymphocytes; there is also an increase of linoleic acid concentration which could come from serum because of dysfunction of the blood-brain barrier. The role of the CNS in contributing to CSF lipids is considered negligible both in controls and in patients with demyelination.

Demyelinating Diseases↗

Cerebrospinal fluid lipids in demyelinating disease. II. Linoleic acid as an index of impaired blood-CSF barrier.

The absolute linoleic acid concentration in CSF was determined and the findings of MS patients (n = 10) and controls (n = 12) were compared. The linoleic acid content of control CSF (1.6 +/- 0.8 nMol/ml) is considerably lower than the corresponding serum value (2.5--4.1 muMol/ml). Although CSF from MS patients contains a significantly higher linoleic acid concentration than controls the close correlation between CSF linoleic acid and CSF albumin is maintained. The high CSF concentration of cholesterol esters rich in linoleic acid, which are abundant in serum but represent only traces in CNS lipids, points towards an impaired BBB function as the cause of CSF linoleic increase. We are able to show that both albumin and linoleic acid are suitable as "serum markers" and also as reference parameters for the overproportional IgG concentration in the CSF of MS patients. On the basis of these results it can be assumed that changes in CSF linoleic acid content are an expression of dysfunction of the blood-CSF barrier in MS and not, as had previously been postulated, the result of altered myelin metabolism.

Adult↗

Adult metachromatic leukodystrophy. III. Clinical course, final stages and first biochemical results.

Continuing the previously published clinical development of a case of adult metachromatic leukodystrophy (MLD), we now describe the terminal phase and death (at 46 years of age) of our patient. The final phase was characterized clinically by progression of generalized peripheral neuropathy, advanced extrapyramidal and pyramidal tract symptomatology, dementia and brainstem dysfunction. First biochemical results show a moderate relative increase (3- to 5-fold) of sulfatides in the frontal lobe white matter but not in the cortex. The analysis of fatty acids in total lipid extract shows a decrease of long-chained fatty acids in favor of short-chained fatty acids, this change is more pronounced in white matter in the cortex. The clinical course and biochemical results are discussed in relation to previous cases analyzed by us. Epidemiological aspects especially emphasize routine serach for MLD amongst patients with neuropsychiatric symptomatology showing unusual psychoses, presenile dementias or unspecific disturbance of motor coordination possibly with electroneurographic evidence of peripheral neuropathy.

Age Factors↗

Adult metachromatic leukodystrophy. IV. Ultrastructural studies on the central and peripheral nervous system.

Ultrastructural studies on the central and peripheral nervous system of 2 patients with adult onset metachromatic leukodystrophy (MLD), dead at the ages of 46 and 51 years, showed MLD-specific inclusions, tufaceous and prismatic structures, a wide spectrum of membranous arrangements within lysosomal residual bodies, and the intimate admixture of sulfatides and other membranous material with lipopigments. Oligodendrocytes and Schwann cells were foremost affected but membranous inclusions could also be verified in neuronal perikarya and astrocytes. The varying ultrastructural spectrum of lysosomal residual bodies in adult onset MLD and the association with lipopigments, chiefly in nerve cells, exceed the fine structural observations on late infantile and juvenile MLD and may reflect morphological differences between these subtypes of MLD that are also known from clinical and biochemical observations.

Adipose Tissue↗

[The problems of lipid metabolism. Demands for diagnostically improved insight into the function of lipoproteins (author's transl)].

In the course of a follow-up of 87 subjects with known hyperlipoproteinemia a new, simplified method was tested for quantification of the individual lipoprotein fractions capable of being performed by every larger laboratory, in contrast to the expensive ultracentrifugation. The LDL/HDL ratio proved to be the conclusive parameter for daily diagnosis in hospital and general practise. This enabled the most important aspects of the lipid metabolic situation of a patient to be recognized immediately.

Arteriosclerosis↗

Basic findings and current developments in sphingolipidoses.

Sphingolipidoses are caused by recessively inherited deficiencies of lysosomal hydrolases. The clinical backgrounds of and current biochemical and genetic approaches to the different forms and variants of gangliosidoses, trihexosylceramidosis (Fabry's disease), galactosylceramidosis (Krabbe's disease), sulfatidoses (metachromatic leukodystrophies), glucosylceramidosis (Gaucher's disease), sphingomyelinoses (Niemann-Pick disease) and ceramidosis (Farber's disease) are presented.

Fabry Disease↗

[Survival of Cochliobolus miyabeanus in the soil (author's transl)].

Survival of C. miyabeanus in irrigated soils of rice fields was higher in infected rice straw (70 days) than in infected rice leaves (40 days). The fungus survived longer in soil depth of 30 cm as in a depth of 15 cm. Between the survival of the fungus and the destruction of infected plant material exist a correlation. In infected rice seeds survived the fungus longer by 5--8 degrees C than by 26--33 degrees C.

Ascomycota↗

Influence of bile acids and free fatty acids on physicochemical properties of LP-X.

In this study it is demonstrated, that incubation of both, bile acids and free fatty acids with LP-X, the abnormal plasmalipoprotein found in patients suffering from cholestasis or LCAT-deficiency, results in striking alterations of the physico-chemical and immunological properties of LP-X: 1. The cathodic mobility in agar is changed into an anodic mairation of the material. 2. The unique appearance of LP-X on electronmicrographs is altered by the incubation revealing fingerprint like structures. 3. The albumin portion of LP-X becomes immunologically detectable. 4. Bile salts cause marked changes in the hydrated density of the material as determined by zonal ultracentrifugation. 5. In vitro incubation of LP-X with postheparin plasma causes a complete disappearance of LP-X as judged by its typical migration on agar electrophoresis. All these alterations can be prevented or reversed by the addition of albumin in appropriate concentrations. These findinga are important in the light of studies designed to investigate the catabolic action of plasma lipolytic enzymes on LP-X, as well as for follow up studies of LP-X concentrations during the course of disease.

Bile Acids and Salts↗