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Biomedical subjects

B Schmid

Publications and source records attributed to B Schmid.

At least 73 records · Page 4Linked to original sources
PubMed1992

The complete sequences of trout (Salmo gairdneri) thymosin beta 11 and its homologue thymosin beta 12.

Two forms of beta-thymosins, designated thymosin beta 11 and thymosin beta 12, were isolated from trout (Salmo gairdneri) spleen. This suggests that the presence of two beta-thymosins, previously thought to be a property of mammalian tissues only, is a more general phenomenon in vertebrate species. Both trout beta-thymosins were found to be N-terminally blocked by a group identified as acetyl by m.s. Automated protein sequencing of tryptic, thermolytic and Staphylococcus aureus in 41-residue V8 proteinase fragments revealed that one of the two beta-thymosins corresponds to the previously reported 41-residue-long sequence of thymosin beta 11 with two substitutions at positions 5 and 7, i.e. Asn instead of Asp, and Glu instead of Gln, whereas the other beta-thymosin, designated thymosin beta 12, was found to be a 42-residue polypeptide closely similar in sequence to thymosin beta 11, with five substitutions (i.e. at positions 5, 7, 10, 11 and 41, with Asp, Ala, Ser, Asn and Thr instead of Asn, Glu, Ala, Ser and Ser respectively) and one addition at position 42 (Ala). Comparison of the known six sequences of beta-thymosins together with the sequences reported here showed that the sequence similarity of the two beta-thymosins in trout (86%) is greater than that of the two beta-thymosins in mammalian species (74%) and that residues at 28 positions are identical in all beta-thymosins, the longer conserved segments located at positions 16-26 and 31-38.

Amino Acid Sequence↗
PubMed1992

Metabolism of GM1 ganglioside in cultured skin fibroblasts: anomalies in gangliosidoses, sialidoses, and sphingolipid activator protein (SAP, saposin) 1 and prosaposin deficient disorders.

Cultured skin fibroblasts from controls and patients with lysosomal storage diseases were loaded with GM1 ganglioside that had been labelled with tritium in its ceramide moiety. After a 65-h or 240-h incubation, a large percentage of this ganglioside remained undegraded in GM1 gangliosidoses, whereas in the other storage diseases studied, one of its metabolites accumulated by 2-4 fold relative to controls. Labelled GM2 ganglioside accumulated in 4 variants of GM2 gangliosidosis, whereas labelled GM3 ganglioside accumulated in sialidosis, galactosialidoses and sphingolipid activator protein 1 (SAP-1, saposin B) and prosaposin (saposin A, B, C and D) deficient lipidoses. The reduced degradation of GM3 ganglioside in the SAP-1 and prosaposin deficiencies was attributed to the deficient function of SAP-1. The prosaposin deficient cells also showed a reduced re-utilization of radioactive metabolites from GM1 ganglioside (i.e. sphingosine and fatty acid) for phospholipid biosynthesis compared with fibroblasts from the SAP-1 deficient patient or normal controls. This anomaly was ascribed to the previously shown defect in ceramide degradation in prosaposin deficiency.

Child, Preschool↗
PubMed1992

Plasminogen activator in human gingival tissue adjacent to dental implants.

The installment of endosseous dental implants has become an accepted treatment procedure, and the long-term clinical results appear excellent. The composition of the soft tissue environment, however, is different from that around natural teeth. One characteristic of original junctional epithelium is its association with plasminogen activator (PA) activity. In 11 patients with a total of 30 ITI hollow-screw titanium dental implants, 16 biopsies were taken. Histologic cryostat sections were assayed for the presence of PA in the junctional epithelium. The results demonstrated that junctional epithelium around titanium implants yields PA activity in a manner very similar to that of natural teeth. The ability to produce this enzyme activity is not related to the developmental origin of the junctional cells, but to their position and function at the base of the gingival sulcus.

Biopsy↗
PubMed1991

Sphingolipid activator protein 1 deficiency in metachromatic leucodystrophy with normal arylsulphatase A activity. A clinical, morphological, biochemical, and immunological study.

A 7-year-old boy had clinical features of metachromatic leucodystrophy (MLD), however, an increased urinary sulphatide excretion was found in the presence of normal arylsulphatase A (and alpha-galactosidase A) activity. A rectal biopsy showed metachromatically staining storage macrophages as well as nonmetachromatic, but PAS-positive, submucosal neurons filled with membranous cytoplasmic bodies. These two types of storage material led to testing for a sphingolipid activator protein (SAP) deficiency. Loading tests with sulphatide and globotriaosylceramide showed deficient turnover of both sphingolipids in cultured fibroblasts. Using the Ouchterlony method, there was no reactivity between a described anti-SAP 1 antiserum and the patient's fibroblast extracts. This new case of SAP-1 deficient MLD was compared with the four cases of this variant known from the literature. Our results indicate that rectal biopsy morphology and lipid loading biochemistry should prove useful for the screening of SAP defects.

Biopsy↗
PubMed1991

Synthesis and proaggregatory activity of 1-O-(2-methyloctadecyl)-2-O-acetyl-rac-glycero-3-phosphocholine.

Racemic 1-O-(2-methyloctadecyl)-2-O-acetyl-glycero-3-phosphocholine, a branched chain PAF species, was prepared by chemical synthesis and investigated for biological activity on human blood platelets in vitro. The synthesis started from 2-O-benzylglycerol and 2-methyloctadecyl-1-methyl sulfonate and was accomplished in five reaction steps. A comparison with 'octadecyl-rich' PAF showed that the PAF species described here exerts a 22-fold weaker proaggregatory activity. Based on [3H]PAF-binding studies, an obstruction of PAF-binding or the signal transduction by the branched alkyl chain in C-1 position of the glycerol backbone is suggested.

Humans↗
PubMed1991

Inter-laboratory ring trial of in vitro DNA repair tests using rat hepatocytes: further testing and conclusive remarks.

The results of the extension of a collaborative study for the detection of chemical-induced DNA damage in rat hepatocytes in vitro are presented in this report. Three coded compounds, i.e. 1,4-butanediol dimethanesulphonate, hydrazine sulphate and sodium dichromate, were tested for DNA repair synthesis by seven different laboratories, either using autoradiographic procedures or the liquid scintillation counting technique. Inter-laboratory standardization was intentionally not requested in order to investigate the validity of each study design under routine conditions. 1,4-Butanediol dimethanesulphonate was clearly positive in most laboratories; sodium dichromate was generally positive, while the results on hydrazine sulphate were contradictory.

Animals↗
PubMed1986

Indication against genetic localisation of the human transcobalamin II gene (TC2) on chromosome 16.

The genetic locus of human transcobalamin II (TC2) is not yet known. The mouse transcobalamin II gene has been assigned to mouse chromosome 11, linked to hemoglobin A. This fact suggested a similar linkage of transcobalamin II in man, assigning it thus to human chromosome 16. Our linkage investigation in a family material of more than 600 individuals demonstrated absence of linkage between transcobalamin II and phosphoglycolate phosphatase, which is very closely linked to hemoglobin A on chromosome 16. Additionally we confirmed absence of linkage with the chromosome 16 gene marker system haptoglobin. These two gene marker systems are located far from each other, and the total length of chromosome 16 is estimated only about 100 cM. Together with recent results of investigations in somatic mouse-man cell hybrids, we conclude that TC2 is not located on chromosome 16. Additionally we found absence of linkage between transcobalamin II and 6-phosphogluconate dehydrogenase, rhesus blood group (both on chromosome 1), GC (chromosome 4), Esterase D (chromosome 13) and AG; absence of close linkage with "debrisoquin polymorphism".

Animals↗
PubMed1986

Pharmacogenetics of dextromethorphan O-demethylation in man.

The metabolism of dextromethorphan has been investigated from the aspect of genetically determined intersubject differences of oxidative drug metabolism in man. For this purpose, the urinary elimination of dextromethorphan and dextrorphan, which is the major O-demethylated metabolite in urine, has been studied in selected drug hydroxylation phenotypes. Dextromethorphan O-demethylation co-segregates with polymorphic debrisoquine hydroxylation, whereas no such co-segregation exists with the independently controlled mephenytoin polymorphism in man. The urinary dextromethorphan over dextrorphan metabolic ratio was validated for linearity of O-demethylation vs dose administered, and for varying urine collection intervals at different urinary pH values. A 94% repeatability of the dextromethorphan metabolic ratio could be established in extensive and poor metabolizer phenotypes. In a preliminary study, different rates of N-, O- and N,O- demethylation of dextromethorphan to yield D-methoxymorphinane, dextrorphan and D-hydroxymorphinane, respectively, were found in extensive- (Sprague-Dawley) and poor-metabolizer (female dark Agouti) rat strains. The observed interphenotype differences in man and the interstrain variations in an experimental animal model indicate that dextromethorphan O-demethylation is catalysed by the debrisoquine-type cytochrome P-450 isozyme. Therefore, the common genetic control of debrisoquine and dextromethorphan metabolism indicates that dextromethorphan might be used as a safe and innocuous substitute for debrisoquine in future routine phenotyping in the field of human pharmacogenetics of oxidative drug metabolism.

Adult↗
PubMed1986

In vitro teratogenicity of acetylsalicylic acid on rat embryos: studies with various culture conditions.

Rat embryos taken at day 9.5 of gestation were exposed in vitro to acetylsalicylic acid (aspirin) using various culture conditions. It was observed that embryos were sensitive to aspirin emulsified in olive oil at concentrations greater than or equal to 150 micrograms/ml. Between 43% and 66% of the embryos exhibited multiple malformations depending on the culture medium, 100% homologous rat serum or Waymouth medium supplemented with 50% rat serum, respectively. At concentrations greater than or equal to 400 micrograms/ml aspirin induced further toxic effects on embryo growth and differentiation. When gelatin was used as the drug-delivery system, aspirin at concentrations of greater than or equal to 150 micrograms/ml induced some malformations (mainly irregular somite shapes) in 57% of the embryos cultured in Waymouth medium, but in only 13% of the embryos grown in 100% serum. At concentrations which were greater than or equal to 400 micrograms/ml aspirin induced dysmorphogenic effects in all embryos, without any concomittant toxicity.

Animals↗
PubMed1985

Pharmacokinetics of amiodarone, desethylamiodarone and other iodine-containing amiodarone metabolites.

In 23 patients treated with the iodine-containing antiarrhythmic drug amiodarone, the plasma concentrations of amiodarone, desethylamiodarone and iodine have been studied. Besides amiodarone and desethylamiodarone, a pool of iodine-containing substances, NANDAI (non-amiodarone-, non-desethylamiodarone-iodine), was present. At steady state the iodine content of NANDAI amounted to 64% and the iodine content of amiodarone plus desethylamiodarone to 36% of total serum iodine. At steady state 26% of the NANDAI fraction was made up of inorganic iodide, the average plasma concentration of which was at least 40 times above the upper limit of the normal range. The serum elimination half-life of NANDAI of 57-160 days exceeded that of amiodarone (35-68 days) and of desethylamiodarone (31-110 days). At steady state the serum concentration of desethylamiodarone appears to be related to the concentration of amiodarone by a Michaelis-Menten type function, yielding a Km of amiodarone of 2.45 mumol/l and a maximal desethylamiodarone concentration of 3.61 mumol/l.

Adolescent↗
PubMed1985

Limitations of 24-hour intraesophageal pH monitoring in the hospital setting.

Prolonged intraesophageal pH monitoring is considered by some to be the most sensitive and specific test of gastroesophageal reflux. We prospectively examined the ability of the test to discriminate 64 hospitalized patients with typical reflux symptoms from 20 age-matched hospitalized control subjects. Patients were subdivided based on endoscopic findings into two groups: group 1, normal endoscopy (n = 30); group 2, erosive esophagitis (n = 34). Six different individual reflux variables and a scoring system were evaluated. Total esophageal acid exposure time and the number of reflux episodes requiring longer than 5 min to clear were each found to have greater discriminatory power than other variables and the scoring system. Although the 64 patients had significantly more acid reflux than controls, only 48% had abnormal results (defined as 2 SD from the control mean). Group 1 patients had significantly more reflux than controls, though only 21% had abnormal results. Group 2 patients were significantly different than both controls and group 1, but 29% had normal studies. Ninety-three percent of the group 1 patients with normal studies responded to antireflux therapy, and only 1 patient had another explanation for the symptoms. The finding that 24-h pH monitoring was normal in half of the individuals presenting with reflux symptoms and in 29% of the patients with erosive esophagitis indicates that negative test results must be interpreted with caution. The insensitivity of the test may relate to the manner in which the study has traditionally been performed in the hospital, and outpatient ambulatory monitoring may improve its reliability.

Aged↗
PubMed1985

Polymorphic dextromethorphan metabolism: co-segregation of oxidative O-demethylation with debrisoquin hydroxylation.

Dextromethorphan hydrobromide, 25 mg po, was given to 268 unrelated Swiss subjects to study urinary drug and metabolite profiles. Rates of O-demethylation yielding the main metabolite dextrorphan were expressed by the urinary dextromethorphan/dextrorphan metabolic ratio. We found a bimodal distribution of this parameter in our population study, which indicates that there are two phenotypes for dextromethorphan O-demethylation. The antimode at a metabolic ratio of 0.3 separated the poor metabolizer (PM; n = 23; prevalence of 9%) from extensive metabolizer (EM) phenotypes. Urinary output of dextrorphan was less than 6% of the dose in all PMs and was 50% in the 245 EMs. Pedigree analysis of 14 family studies revealed an autosomal-recessive transmission of deficient dextromethorphan O-demethylation. In these families, 37 heterozygous genotypes could be identified; however, through use of the urinary drug and metabolite analysis it was not possible to identify the heterozygous genotypes within the EM phenotype group. Co-segregation of dextromethorphan O-demethylation with debrisoquin 4-hydroxylation was also studied. Complete concordance of the two phenotypic assignments was obtained, with a Spearman rank correlation coefficient of rs = 0.78 (n = 62; P less than 0.0001) for dextromethorphan and debrisoquin metabolic ratios. Presumably the two drug oxidation polymorphisms are under the same genetic control. Thus the innocuousness and ubiquitous availability of dextromethorphan render it attractive for worldwide pharmacogenetic investigations in man.

Administration, Oral↗
PubMed1983

[Does HDL-cholesterol determination facilitate the assessment of risk in coronary patients?].

Serum lipids (cholesterol, triglycerides, HDL-cholesterol) were analyzed in 153 patients with proven coronary heart disease (CHD) with the target to characterize the risk potential of HDL-cholesterol. It turns out, that the specificity of HDL-C is low (too many unexpected high values in CHD). Consequently this parameter is of little use in evaluating the individual risk for CHD.

Aged↗