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K Hosono

Publications and source records attributed to K Hosono.

At least 73 records · Page 4Linked to original sources
PubMed1983

Acylpeptides, the inhibitors of cyclic adenosine 3',5'-monophosphate phosphodiesterase. I. Purification, physicochemical properties and structures of fatty acid residues.

An inhibitor of cyclic adenosine 3',5'-monophosphate (cAMP) phosphodiesterase was isolated from the culture filtrate of Bacillus subtilis C-756 isolated from soil. It was purified and finally separated into three fractions by reverse-phase HPLC. The respective fractions were designated as APD-I, -II and -III in the order eluted and the relative quantities of APD-I, -II and -III were approximately 10%, 40% and 50%, respectively. They were acylpeptides composed of beta-hydroxy fatty acid residues and heptapeptide. Though the amino acid compositions of the peptides were the same, the fatty acid residues were all different. APD-I contained a mixture of 3-hydroxy-11-methyldodecanoic acid (i-C13h3) and 3-hydroxy-10-methyldodecanoic acid (a-C13h3). APD-II contained 3-hydroxytetradecanoic acid (n-C14h3). APD-III contained a mixture of 3-hydroxy-13-methyltetradecanoic acid (i-C15h3) and 3-hydroxy-12-methyltetradecanoic acid (a-C15h3).

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

Acylpeptides, the inhibitors of cyclic adenosine 3',5'-monophosphate phosphodiesterase. II. Amino acid sequence and location of lactone linkage.

Bacillus subtilis C-756 produced three kinds of inhibitors of cyclic adenosine 3',5'-monophosphate (cAMP) phosphodiesterase. Each was an acylpeptide consisting of a beta-hydroxy fatty acid residue and heptapeptide. By the application of mass spectrometry, the amino acid sequence of peptide was determined to be beta-hydroxy fatty acid-Glu-Leu-Leu-Val-Asp-Leu-Leu in all three cases. Each had a lactone linkage between the carboxyl group of C-terminal leucine and the beta-hydroxyl group of the fatty acid moiety. The total structures of these inhibitors were thus established.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

Acylpeptides, the inhibitors of cyclic adenosine 3',5'-monophosphate phosphodiesterase. III. Inhibition of cyclic AMP phosphodiesterase.

Acylpeptides, APD-I, -II and -III, were inhibitors of cyclic adenosine 3',5'-monophosphate (cAMP) phosphodiesterase, and their inhibition types were non-competitive. The inhibitory activity of APD-II was the most potent among them. Opening of the lactone linkage reduced the inhibitory activity to about half. The activity almost disappeared when an inhibitor or a derivative with opened lactone linkage was methylated with diazomethane. The activity was, however, restored by the addition of metal ions such as Ca2+, Mn2+, Fe2+, and Co2+. This suggests that the inhibition may be caused by a chelating action of the free carboxyl groups of glutamic acid and aspartic acid in the peptide.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

[Antibacterial potency of cefotiam based on the clinical effect, MIC and decrement of organisms in the sputum].

To evaluate the antibacterial potency of cefotiam (CTM) clinical and laboratory studies were carried out and the results were as follows. Clinical evaluation and adverse reaction CTM was given to total of 23 patients, 10 with bronchopneumonia, 10 with bronchitis and one each with cystitis, enteritis and suspected sepsis. Overall efficacy rate was 78.3% (18/23) (excellent 9, good 9, fair 3, poor 2). Only 1 case showed a side effect of slightly elevated GOT and GPT. Antibacterial activities MIC of CTM against isolates from sputum was investigated on those patients mentioned above and was compared with MIC of CEZ and CMZ. CTM showed superior antibacterial activity against almost all strains. Especially on Haemophilus and Klebsiella antibacterial activity of CTM was impressive. Organisms in sputum Four out of 8 causative bacteria disappeared and 1 out of 8 decreased after administration of CTM. Thus CTM is considered to be the useful drug for the treatment of respiratory infection.

Adult↗
PubMed1982

Effects of new calcium channel blocker of niludipine on the coronary hemodynamics, diastolic properties, and metabolic responses to tachycardia stress in patients with coronary disease.

A new calcium channel blocker, niludipine, was administered intravenously to nine patients with coronary artery disease in order to investigate its effects on left ventricular systolic and diastolic function, coronary sinus blood flow, and myocardial lactate metabolism. Coronary sinus pacing was performed in all patients and produced angina in six patients. Niludipine increased the resting heart rate from 75+/-3 beats/min (mean+/-SEM) to 82+/-3 (NS) and decreased the left ventricular systolic pressure from 155+/-4.7 mm Hg to 134+/-2.8 (p less than 0.05). Coronary sinus blood flow increased by 9%(NS). During pacing after niludipine, clinical improvement occurred in the six patients who had initially experienced angina. The extent of ischemic ST segment depression was decreased (-1.56+/-0.27 mm to -0.78+/-0.38, p less than 0.02) and myocardial lactate metabolism was improved. When pacing was terminated, niludipine suppressed the elevation of left ventricular end-diastolic pressure compared to pretreatment values (16.2+/-2.5 mm Hg vs 8.5+/-0.9, p less than 0.05) and decreased the left ventricular time constant T(26.4+/-3.6 msec to 20.2+/-2.4 p less than 0.05). The results suggest that niludipine appears to be beneficial in reducing systolic and diastolic work of the left ventricle during pacing induced angina without a significant change in total coronary sinus blood flow. Niludipine appears to have less of a hypotensive and reflex tachycardic effect than nifedipine.

Adult↗