Search PubMed⌕ Search

Biomedical subjects

G Kaufmann

Publications and source records attributed to G Kaufmann.

At least 91 records · Page 5Linked to original sources
PubMed1979

RNA ligase reaction products in plasmolyzed Escherichia coli cells infected by T4 bacteriophage.

Searching for a physiological role of T4 RNA ligase [polyribonucleotide synthetase (ATP); poly(ribonucleotide):poly(ribonucleotide) ligase (AMP-forming), EC 6.5.1.3] activity, we developed an acellular system of plasmolyzed Escherichia coli cells infected by T4 bacteriophage. Upon incubation of this system with [gamma-32P]ATP, 32P was transferred into a large number of polyribonucleotides, mostly up to 300-400 residues long. The bulk of 32P in the product polyribonucleotides was found in 5'-terminal phosphate groups, suggesting that they originated by a phosphorylation reaction catalyzed by the endogenous polynucleotide kinase (EC 2.7.1.78). Indeed, these products were not seen in an acellular system from uninfected cells, and their amount and complexity increased with the progress of infection. Analysis of the 32P-labeled polyribonucleotide products by gel electrophoresis, either before or after digestion with alkaline phosphatase (EC 3.1.3.1), revealed that a small fraction of the 32P resided in phosphodiester bonds of several tRNA-sized chains. This specific 32P transfer from [gamma-32P]ATP into phosphodiester bonds was apparently catalyzed by successive polynucleotide kinase and RNA ligase reactions. The possible relationship of the 32P transfer to RNA ligase was investigated next by using a system from cells infected with T4 am M69 (an amber mutant deficient in RNA ligase). Transfer of 32P from [gamma-32P]ATP into phosphodiester bonds was not detected in the am M69 system. However, addition of purified RNA ligase to the am M69 system restored the specific 32P transfer. A system from cells infected with T4 psu-b delta 33 (a deletion mutant lacking the entire tRNA region) sustained the specific 32P transfer into tRNA-sized products, indicating that they were not derived from transcripts of T4 tRNA genes. These data may reflect a role of RNA ligase in posttranscriptional conversion of presumably host polyribonucleotides into novel tRNA species during T4 infection.

Adenosine Triphosphate↗
PubMed1979

Inhibition of the 3 beta-hydroxysteroid oxidoreductase of Pseudomonas testosteroni by steroids.

55 Steroids of the estratriene and androstane type with substituents in pos. 16 alpha, 17 alpha or 17 beta were tested for inhibition of the 3beta-hydroxysteroid oxidoreductase of Pseudomonas testosteroni. Estratrien-3-ols were strong and competitive inhibitors (Ki less than 1 micron). Substituents in pos. 16 alpha of estradiol influenced the inhibitory activity distinctly. Substituents in 17 alpha- or 17 beta-position were of slight influence. 3-Methoxy estratrienes gave no inhibition of the enzymic 3 beta-OH-dehydrogenation. The 4-unsaturated 3-oxo-steroids tested were moderate inhibitors (Ki 2.4-70 micron). The activity was slightly influenced by 17 alpha-substituents. It was increased by 10 beta-substituents in the order H less than CH3 less than N3. The inhibition test can be used to select and eliminate very strong synthetic inhibitors, which are known to disturb the metabolism of steroid hormones.

3-Hydroxysteroid Dehydrogenases↗
PubMed1978

Okazaki pieces grow opposite to the replication fork direction during simian virus 40 DNA replication.

Simian virus 40 replicating DNA was pulse labeled with alpha-32P-dATP using an acellular DNA replication system. Nascent DNA chains of less than 200 nucleotides (Okazaki pieces) were then isolated from the denatured replicating DNA by electrosieving through a polyacrylamide gel column. The purified Okazaki pieces were hybridized to separated strands of Bg1(1)+Hpa1 simian virus 40 DNA restriction fragments immobilized on nitrocellulose filters. Only strands with polarity of the DNA replication fork direction hybridized with Okazaki pieces. Hence, Okazaki pieces in simian virus 40 are synthesized against the DNA replication fork direction.

DNA Replication↗
PubMed1977

[Serum digoxin concentration: dependence on body weight and age].

In patients of a cardiological practice, 121 digoxin serum concentrations were determined by radioimmunoassay (RIA). Some drugs were suspected of interfering with the RIA or with the pharmacokinetics of digoxin. Patients having such additional drugs or patients with elevated serum creatinine were not included. The daily maintenance dose of digoxin was roughly adjusted to body weight. Patients with 0.5 mg digoxin daily showed unexpectedly low serum digoxin levels not fully explained by the relatively high body weight. This dose group was not included in the following correlations. At a maintenance dose of 0.25 and 0.375 mg digoxin and in the age groups 40-69 years (n = 66) there was an approximately inverse proportionality between serum digoxin concentration (per 0.25 mg digoxin daily) and body weight. When all age classes from 20 to 89 years were included (n = 96), a week positive correlation between serum digoxin concentration (per 0.25 mg digoxin daily and per 69.28 kg body weight) and age was found. A similar positive correlation resulted between serum digoxin concentration (per 0.25 mg digoxin daily) and the reciprocal of the nomographically determined creatinine clearance, always within the normal serum creatinine range. Based on these correlations, two simplified formulas are presented to predict the serum concentration and therapeutic maintenance dose of digoxin. The formulas are valid for the normal serum creatinine range and for digoxin tablets of optimal bioavailability.

Adult↗
PubMed1976

[Drug therapy of tachycardial arrhythmias].

In recent years the antiarrhythmic armamentarium has been widened by several new drugs. The effects and side effects of amiodarone, verapamil, prenylamine and prajmalium bitartrate are described. With the introduction of the newer drugs, new recommendations have to some extent emerged with regard to treatment of tachyarrhythmias. For a national understanding of antiarrhythmic agents, regard must be had to their effects on both normal and damaged cells.

Amiodarone↗
PubMed1975

[Microbial 3-O-demethylation and 3-O-methylation of estratrienes].

Estradiol-3-methylether, estrone-3-methylether, 17alpha-ethinyl-estradiol-3-methylether and other 17alpha-substituted estratrienes were 3-O-demethylated to free 3-hydroxy compounds by fermentation with Corynebacterium sp. A hydroxy groupp in position 6alpha or 6beta prevented the reaction. The opposite reaction, methylation of the 3-hydroxy group of estratrienes, was performed using Mycobacterium smegmatis. The substrate specifity of this methylation was low. Analogies of these microbial reactions to steroid metabolism in mammalian organism are discussed.

Chemical Phenomena↗
PubMed1975

[Microbial hydroxylation of estratrienes].

Incubation of the synthetic estrogen 17alpha-ethinyl-estradiol-3-methylether (mestranol) with cultures of Penicillium chrysogenum gave 6alpha-hydroxy-17alpha-ethinylestradiol-3-methylether and 6beta-hydroxy-17alpha-ethinylestradiol-3-methylether. The corresponding 3-demethylated compound, 17alpha-ethinylestradiol, gave the 6alpha- and 6beta-hydroxy derivatives in lower yields. If the 6-hydroxy compounds were incubated, they were partially isomerized to a mixture of the 6alpha- and 6beta-hydroxy compounds. Estradiol, estrone and the corresponding methylethers were not hydroxylated. By incubation with cultures of Streptomyces olivaceus, estradiol, estrone and the corresponding methylethers were hydroxylated to 16alpha-hydroxy derivatives. 17alpha-Ethinyl compounds were not hydroxylated. 17alpha-Azidomethyl estradiol gave 17alpha-hydroxymethyl estradiol. Structures were established by chromatographical comparison and by IR and NMR spectra. Relations between metabolism of estratrienes by the mentioned microorganisms and the mammalian metabolism are discussed

Chemical Phenomena↗