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Biomedical subjects

G Hoffmann

Publications and source records attributed to G Hoffmann.

At least 163 records · Page 9Linked to original sources
PubMed1989

Quantitative analysis for organic acids in biological samples: batch isolation followed by gas chromatographic-mass spectrometric analysis.

This new method for qualitative and quantitative determination of organic acids, aldehydes, and ketones in biological samples is effective for use with urine, plasma, and amniotic fluid, and it requires no deproteinization. Isolation by batch-wise liquid partition chromatography on silicic acid follows formation of the O-(2,3,4,5,6-pentafluorobenzyl)oximes of oxoacids, aldehydes, and ketones. The total organic acid content of the sample provides a rapid screening test for metabolic abnormality. A wide-bore, bonded-phase capillary column was used for quantitative gas chromatographic-mass spectrometric analysis, followed by automated identification and quantification. Analytical recoveries were quantitative for a wide variety of metabolites. Gas-chromatographic retention indices, discriminating ions, and control ranges in amniotic fluid, plasma, and urine of adult subjects were determined for 61 biologically important compounds.

Adult↗
PubMed1989

[Size differences in Demodex bovis (Acari)].

Demodex bovis females were isolated from the skin surface of an experimentally infected calf. The were designated "Size Variation 'Short"' (GVK). With a length of 132...149 microns they were significantly smaller than D. bovis females isolated from skin nodules of the same calf. These mites were 154...168 microns long and named "Size Variation 'Normal"' (GVN). All measurings were carried out in living mites.

Animals↗
PubMed1988

[Pedicled fibroma of the extrahepatic bile ducts].

It is reported on the very rare occurrence of a benign tumor in common hepatic bile duct of a 33-year-old woman, associated with obstructive jaundice. Clinical diagnosis and treatment are described, histological typing like fibroblastic tumor with neurogenic parts are discussed and a short review of the literature is given.

Adult↗
PubMed1988

Lack of insulinotropic effect of endogenous and exogenous cholecystokinin in man.

Intraduodenal phenylalanine administration (333 mg/min over 60 min) released endogenous cholecystokinin in healthy young subjects as demonstrated radioimmunologically and by intraduodenal bilirubin and pancreatic enzyme output. Concomitantly, there was only a small increase over basal in circulating immunoreactive-insulin and immunoreactive-C-peptide concentrations. In healthy volunteers intraduodenal infusions of saline (10 ml/min), glucose (333 mg/min) or phenylalanine (333 mg/min) were performed for 60 min when plasma glucose was clamped at approximately 8 mmol/l. Phenylalanine enhanced immunoreactive-insulin and immunoreactive-C-peptide responses three-fold more than did the same amount of glucose. Immuno-reactive gastric inhibitory polypeptide responses were small and not different after glucose and phenylalanine administration. Immunoreactive cholecystokinin was significantly stimulated to 9.4 +/- 1.4 pmol/l only by intraduodenal phenylalanine. Plasma phenylalanine concentrations increased into the supraphysiological range (approximately 1.5 mmol/l). Intravenous infusions of phenylalanine achieving plasma concentrations of 1.2 mmol/l stimulated insulin secretion at elevated plasma glucose concentrations (approximately 8 mmol/l clamp experiments), but had no effect at basal plasma glucose concentrations. A small increase in cholecystokinin also was observed. Intravenous infusions of synthetic sulphated cholecystokinin-8 leading to plasma concentrations in the upper postprandial range (8-12 pmol/l) did not augment the immunoreactive-insulin or immunoreactive-C-peptide levels during hyperglycaemic clamp experiments, in the absence or presence of elevated plasma phenylalanine concentrations. It is concluded that the augmentation of the glucose-induced insulin release by intraduodenal administration of phenylalanine cannot be related to cholecystokinin release, but rather is explained by the combined effects of elevated glucose and phenylalanine concentrations. In man, cholecystokinin does not augment insulin secretion caused by moderate hyperglycaemia, elevations of phenylalanine concentrations, or combinations thereof.

Adult↗
PubMed1988

Mevalonate kinase deficiency in a child with cerebellar ataxia, hypotonia and mevalonic aciduria.

Mevalonate kinase deficiency has been documented in an 8-year-old child who presented with cerebellar ataxia, hypotonia and mevalonic aciduria. The activity of mevalonate kinase in extracts of cultured skin fibroblasts derived from the patient was approximately 2% of the mean value for controls. Family studies were carried out on the mother, the father and a sister, all of whom were clinically well. Mevalonate kinase activity in extracts of cultured skin fibroblasts and transformed lymphoblasts derived from the parents of the patient were 43%-52% of the mean control values. These data are consistent with an autosomal recessive mode of inheritance for mevalonate kinase deficiency.

Carboxy-Lyases↗
PubMed1988

4-Hydroxybutyric aciduria in a patient without ataxia or convulsions.

A child presenting with mild psychomotor retardation, hypotonia, microcephaly and hyperkinesis is described. Urinary organic acid analysis by combined gas chromatography-mass spectrometry revealed 4-hydroxybutyric aciduria. Succinic semialdehyde dehydrogenase activity in extracts of white cells derived from the patient was less than 10% of control values.

Ataxia↗
PubMed1988

[Biotransformation of meclozine in the human body].

After oral administration of 1-[(4-chlorophenyl)-phenylmethyl]-4-[3-methylphenyl)-methyl]-piperazine (1, Meclozine) eleven compounds were isolated from human urine and faeces. The structural elucidation of the metabolites was accomplished by comparison of their spectral data with those of the synthetic reference compounds. The metabolites were identified as: Meclozine (1), N-[(4-chlorophenyl)-phenylmethyl]-piperazine (2), 3-(4-[(4-chlorophenyl)-phenylmethyl]-piperazino)-methyl-benzoic acid (3), 3-(4-[(4-chlorophenyl)-phenylmethyl]-piperazino)-methyl-benzamide] (4), 2-[3-(4-[(4-chlorophenyl)-phenylmethyl]-piperazino)-methyl-benzoyl ]-amino- ethanesulphonic acid (5), 3-(4-[(4-chlorophenyl)-3'-hydroxy-4'-methoxyphenylmethyl]-piper azino)- methyl-benzoic acid (6), 1-[(4-chlorophenyl)-phenylmethyl]-4-[(3-methylphenyl)-methyl]- piperazine-N4-oxide (7), 1-[(4-chlorophenyl)-phenylmethyl]-4-[(3-methylphenyl)-methyl]- piperazine-N,N'-dioxide (8), 3-methyl-benzoic acid (9), 3-methyl-hippuric acid (10) and 3-methyl-benzoic acid-glucuronide (11). The structure of compound 11 was confirmed after enzymatic cleavage and identification of the aglycon. A further metabolite was detected, but not identified.

Biotransformation↗
PubMed1987

Biological efficacy of partial hepatectomy and hepatopoietin in long-term selenium-deficient mice.

After partial hepatectomy the normal low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormone, the so-called hepatopoietin. This glycoprotein is organ-specific but not species-specific, i.e. an extract from rats is also active in mice. In order to examine the influence of selenium on liver cell proliferation, male albino NMRI mice were fed a selenium-deficient diet containing less than 10 ppb Se for at least 2 months (Se-). In the plasma protein profile and in the basic DNA synthesis rate of Se(-)-animals, no significant changes were observed compared to controls. However, liver cell proliferation induced by hepatopoietin or by partial hepatectomy was increased about 3-fold in Se-deficient mice. We assume a compensated metabolic Se-deficiency state in mice under these nutritional conditions, which leads to expression of enhanced metabolic capacity when induced by stress.

Animals↗