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Biomedical subjects

S Matsui

Publications and source records attributed to S Matsui.

At least 361 records · Page 20Linked to original sources
PubMed1984

[A case of giant prostatic hypertrophy].

This report deals with a case of an 82-year-old male with a giant prostate that weighted 270 grams. Retropubic prostatectomy was performed successfully. The removed prostate adenoma consisted of adenomatous hyperplasia on pathology. Though the nomenclature of "giant prostatic hypertrophy" is not clear, we reviewed cases of over 200 grams of hypertrophy so far reported in Japan were as giant prostatic hypertrophy. Twenty two cases of giant prostatic hypertrophy have been reported in the Japanese literature to date and our case was the sixth heaviest ever reported in Japan.

Aged↗
PubMed1984

Nifedipine in hypertension and heart failure.

The use of nifedipine in patients with hypertension, heart failure, and acute myocardial infarction is discussed. Data from over a ten-year period are presented. Results indicate that nifedipine, although frequently prescribed as an antianginal agent, is also useful as an antihypertensive agent, especially when used concomitantly with other drugs. Its ability to cause fluctuations in blood pressure remains a shortcoming, however.

Adult↗
PubMed1984

[Parathyroid carcinoma--a case report and a review of the Japanese literature].

The patient, a 42-year-old female, presented with bone pain and a cervical tumor. The tumor was operated at another hospital under a diagnosis of thyroid adenoma and the bone pain subsequently disappeared. Three years later, a cervical tumor was palpated just under the operative scar; the patient experienced nausea, vomiting. The tumor and the left thyroid lobe were removed and modified radical neck dissection was performed. The histological diagnosis of the resected specimen was parathyroid carcinoma.

Adult↗
PubMed1983

Hemodynamic effects of dibutyryl cyclic AMP in congestive heart failure.

To evaluate the hemodynamic effects of dibutyryl cyclic AMP (DBcAMP) in congestive heart failure (CHF), right-sided cardiac catheterization was performed in 11 patients with CHF, and hemodynamic variables were investigated before and after infusion of various doses of DBcAMP at a rate of 0.025 to 0.2 mg/kg/min (mean 0.14 +/- 0.077 [standard deviation]). DBcAMP reduced total systemic vascular resistance index from 3,171 +/- 1,158 to 1,880 +/- 554 dynes s cm-5 X m2 (mean +/- standard deviation) and pulmonary arterial end-diastolic pressure from 23 +/- 13 to 20 +/- 11 mm Hg, and increased cardiac index from 2.24 +/- 0.60 to 3.41 +/- 1.02 liters/min/m2. Mean arterial blood pressure decreased from 91 +/- 14 to 84 +/- 13 mm Hg, and heart rate increased from 91 +/- 16 to 99 +/- 13 beats/min. The increase in cardiac index was accompanied by a proportional decrease in total systemic vascular resistance index in all patients except 1. In 8 patients the decrease in pulmonary arterial end-diastolic pressure was accompanied by an increase or no change in the left ventricular stroke work index. In 6 patients, DBcAMP was given in incremental doses of 0.05, 0.1, and 0.2 mg/kg/min every 20 minutes, and 5 of 6 patients tolerated the full dose and showed dose-related hemodynamic changes for the incremental doses of DBcAMP. These data suggest that DBcAMP has powerful vasodilating effects on resistance vessels in patients with CHF; hence, it can be a useful vasodilating agent for treatment of CHF.

Aged↗
PubMed1983

Congenital coronary arterial aneurysm without arteriovenous fistula resulting in myocardial infarction--case report and review of the literature.

A 38-year-old woman with coronary arterial aneurysm, which resulted in myocardial infarction, was reported. By coronary arteriography, an aneurysm of the left anterior descending branch was found, but no arteriovenous shunt could be revealed. The patient has neither clinical history of severe febrile inflammatory disease nor any coronary risk factors. The etiology of her coronary arterial aneurysm was considered to be congenital. The patient underwent aorto-coronary saphenous vein bypass graft surgery successfully. We believe that this is the first case report in Japan on congenital aneurysm of the coronary artery without arteriovenous fistula, which was diagnosed during life by coronary arteriography.

Adult↗
PubMed1983

Studies on concurrent alpha- and beta-adrenoceptor blocking action of S-596 (arotinolol).

The effects of a therapeutic dose of oral S-596 upon the cardiovascular response to intravenous isoproterenol and noradrenaline were studied in 2 hypertensive and 4 normotensive subjects in order to evaluate the drug's mode of action. After oral administration of S-596, mean blood pressure rose slightly and the heart rate decreased. In addition, cardiac output decreased considerably and total peripheral resistance increased. However pulmonary arterial end-diastolic pressure and right atrial pressure were not affected by S-596 administration. Before S-596, intravenous isoproterenol increased both heart rate and pulse pressure in a dose-dependent manner. Similarly, intravenous noradrenaline increased both systolic and diastolic pressures. Following 15 mg of S-596, the effects of isoproterenol were antagonized such that the cumulative log-dose-response curves of the mean isoproterenol-induced increases in heart rate and reductions in diastolic pressure were shifted in parallel to the right. At the same time, the mean noradrenaline-induced increases in blood pressure were also antagonized in a competitive manner. The mean ratio of alpha- and beta-components was calculated as: (formula: see text) From this result it can be suggested that the alpha-adrenoceptor blockade potency of this drug is approximately one-eight of its beta-adrenoceptor blockade potency.

Adrenergic alpha-Antagonists↗
PubMed1983

Clonal chromosome changes in stimulated lymphocytes of untreated human B-cell leukemias.

The chromosome constitution of peripheral blood lymphocytes from nine cases of B-cell chronic lymphocytic leukemia and one case of B-cell prolymphocytic leukemia were studied at diagnosis following stimulation by B- and T-cell activators. Chromosome analysis with banding techniques revealed an extra chromosome 12 (trisomy 12) in 4 B-cell chronic lymphocytic leukemia cases and complicated abnormalities, i.e., trisomy 12, 6q-, 14q+, and a translocation between chromosomes 6 and 12, [t(6; 12)] in the prolymphocytic leukemia case. These findings suggest that trisomy 12 is a prototypic change in B-cell leukemia, particularly in B-cell chronic lymphocytic leukemia. Based on sister chromatid exchange studies of unstimulated lymphocytes, it appears that some leukemia cells with a normal karyotype not only divide but also proliferate in vitro.

Aged↗
PubMed1982

Isopeptidase: a novel eukaryotic enzyme that cleaves isopeptide bonds.

In an attempt to clarify the regulatory mechanism that accounts for the shift of protein A24 in the mitotic cycle, we demonstrated the existence of an enzyme, provisionally termed isopeptidase, that cleaves A24 stoichiometrically into histone H2A and ubiquitin. Properties of this enzyme are (i) most eukaryotes, including mammals, amphibia, chicken, and yeast, contain isopeptidase in the cytoplasm; (ii) a significant increase in enzyme binding to chromatin occurs when cells enter mitosis; (iii) Escherichia coli does not contain isopeptidase; (iv) isopeptidase has a molecular weight of 38,000; (v) at an ionic strength that induces globular conformation of H2A, isopeptidase activity is repressed; (vi) a SH group is an essential cofactor; and (vii) most divalent cations (except Mg2+ and Ca2+) are inhibitory. In view of the stoichiometric conversion of A24 into H2A and ubiquitin by isopeptidase in vitro, A24 probably contains a Gly-Gly dipeptide in isopeptide linkage but no other intervening polypeptides. Since ubiquitin in various eukaryotes binds to protein other than H2A, and is proteolytically released, isopeptidase probably acts on isopeptide bonds in general and not uniquely on those of A24. Inasmuch as isopeptidase is present throughout the cell cycle, the level of A24 in chromatin appears to be controlled by a balance between isopeptidase and an as yet unestablished H2A-ubiquitin ligase.

Animals↗