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Biomedical subjects

W Kersten

Publications and source records attributed to W Kersten.

At least 55 records · Page 3Linked to original sources

[Therapy in bronchial asthma].

A division into two main groups is made: causal and symptomatic treatment. The first group includes elimination and avoidance of allergens and the specific hyposensitization according to own experiences. The second group is divided into medicamentous treatment (bronchodilatators, DNCG, corticosteroids, secretolytics, antibiotics, tranquilizers) and into a nonmedicamentous treatment like physiotherapy, climate therapy and psychotherapy.

Adrenal Cortex Hormones↗

[Diagnostic measures in bronchial asthma].

The diagnostic steps for in five groups divided forms of bronchial asthma are listed and are discussed. The diagnosis includes: 1. the anamnesis. 2. the clinical examination including X-ray, lung function tests, bronchologic inspection a.s.o., 3. special examinations for allergy including skin tests, provocation tests and pharmacodynamic tests, 4. serological-immunological methods of examination including determination of total IgE, specific IgE and several serum proteins.

Asthma↗

[Classification of bronchial asthma].

The bronchial asthma disease is divided into 5 groups: 1. bronchial asthma caused by allergy, 2. bronchial asthma caused by infection, 3. bronchial asthma caused by physicochemical irritants, 4. bronchial asthma caused by exercise, 5. combination between the groups 1--4. Etiological factors, immunologic phenomena so far as known and pathogenic mechanisms are listed for each group and discussed.

Aspirin↗

Metabolism of protein and RNA in liver of rats deprived of tryptophan.

Rat lost body weight after the second day of feeding a tryptophan free diet. After 15 days of tryptophan deprivation, they had lost 17% of body weight, whereas pair-fed controls had gained weight. Liver weights of deprived rats were significantly lower than those of controls. Water, protein, RNA, and DNA in the livers were not significantly changed after 15 days of tryptophan deprivation. Amounts of free typtophan and alanine in livers of derpived rats decreased to 40% of the controls after 15 days, whereas amounts of most other amino acids were nearly constant. Protein synthesis in livers of deprived rats for 15 days was impaired to about 55% of controls. Incorporation of orotic acid into different types of cytoplasmatic and nuclear RNA remained unaffected up to the tenth day. After 15 days of deprivation, more orotic acid had been incorporated into RNA fractions that correspond to the precursor ribosomal fractions.

Amino Acids↗

7-Methylguanine specific tRNA-methyltransferase from Escherichia coli.

A 7-methylguanine (m7G) specific tRNA methyltransferase from E. coli MRE 600 was purified about 1000 fold by affinity chromatography on Sepharose bound with normal E. coli tRNA. The purified enzyme catalyzes exclusively the formation of m7G in submethylated bulk tRNA of E. coli K12 met- rel-. The purified enzyme transfers the methyl group from S-adenosyl-methionine to initiator tRNA of B. subtilis and 0.8 moles m7G residues are formed per mole tRNA. It is suggested that the enzyme specifically recognizes the extra arm unpaired guanylate residue.

Electrophoresis, Disc↗

Inhibition of leucyl-tRNA synthetase in Escherichia coli by the cytostatic 5,8-dioxo-6-amino-7-chloroquinoline.

At concentrations of 1-1.6 mug/ml, 5,8-dioxo-6-amino-7-chloroquinoline causes auxotrophy for leucine in Escherichia coli MRE 600. With increasing concentrations of this quinone additional amino acids are required for growth. The amount of leucine in the pool of free amino acids is not decreased after treatment of E. coli with the quinone. Transfer RNALeu, however, is charged with leucine less than 10% in quinone-treated cells of E. coli, whereas in control cells the degree of aminoacylation is about 85%. From these data we conclude that the quinone causes auxotrophy for leucine by interacting with the charging process of tRNALeu. Quinone was found to inhibit leucyl-tRNA synthetase activity in purified extracts of E. coli with E. coli tRNA as substrate.

Amino Acids↗

Quinone induced stringent control. Accumulation of ppGpp and inhibition of RNA synthesis in stringent Escherichia coli by 5,8-dioxo-6-amino-7-chloroquinoline.

The mode of action of a synthetic cytostatic quinone was studied in Escherichia coli. 1. At concentrations of 1.5-6 mug/ml, 5,8-dioxo-6-amino-7-chloroquinoline rapidly inhibits growth and protein synthesis in E. coli. The synthesis of RNA is immediately affected in E. coli rel+ whereas in E. coli rel- the accumulation of RNA can proceed on addition of the quinone. This indicates that the inhibition of RNA synthesis in the stringent strain is a consequence of the regulatory phenomenon governed by the rel gene. 2. Chloramphenicol, known to abolish the stringent control mechanism, added simultaneously with the quinone allows the accumulation of RNA to proceed in the stringent strain. 3. Guanosine tetraphosphate accumulates in quinone-treated E. coli rel+ but not in the relaxed mutant strain. 4. Addition of amino acids reverses all inhibitory effects observed in quinone treated stringent and relaxed cells. 5. It is concluded that the bacteriostatic effect of 5,8-dioxo-6-amino-7-chloroquinoline on E. coli is caused by an apparent intracellular amino acid starvation.

Alanine↗

Inhibition of leucyl-transfer ribonucleic acid synthetasymol.

The bacteriostatic effect of low concentrations of the antibiotic granaticin on Bacillus subtilis is relieved by the addition leucine to the growth medium. In cells treated with granaticin, aminoacylation of leucine tRNA is specifically decreased, but the content of free leucine is not. It is concluded that granaticin interferes with the charging process of leucine tRNA in B. subtilis leading to leucine auxotrophy.

Amino Acids↗

Stringent control of ribonucleic acid synthesis in Bacillus subtilis treated with granaticin.

The antibiotic granaticin interferes in Bacillus subtilis with the charging process of tRNALeu causing both the arrest of protein synthesis and bacteriostasis [A. Ogilvie, K. Wiebauer & W. Kersten (1975) Biochem. J. 152, 511-515]. A concomitant inhibition of RNA synthesis is observed. This inhibition was studied with mutant strains of B. subtilis. 2. Granaticin inhibits protein and RNA synthesis in stringently controlled B. subtilis (rel+) to about the same extent. In a relaxed mutant strain (rel-) of B. subtilis, protein synthesis is also inhibited, but the accumulation of RNA continues after the addition of the drug. 3. Chloramphenicol, which is known to abolish the stringent control mechanism, added simultaneously with granaticin, allows the synthesis of RNA to proceed in the stringent strain. 4. Guanosine tetraphosphate (ppGpp) and guanosine pentaphosphate (pppGpp) accumulate in granaticin-treated stringently controlled B. subtilis but not in the rel- mutant. 5. It is concluded that the inhibition of RNA synthesis granaticin can adequately be explained as a stringent response caused by the interference by the drug with leucyl-tRNA synthetase.

Anti-Bacterial Agents↗