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Biomedical subjects

T Matsubara

Publications and source records attributed to T Matsubara.

At least 541 records · Page 30Linked to original sources
PubMed1977

A case of (13q;18q) translocation with proximal 13q monosomy.

A case of partial monosomy of the 13p terminal to 13q12, associated with a de novo 13/18 translocation, is reported. The symptoms appeared to be derived from both 18q- and partial monosomy 13, the latter giving rise to: high arched palate, epicanthus, antimongolian slant, small eye fissure, flat nasal bridge, hypoplastic helix, and large clitoris. Serum Ig-A and Ig-M levels were normal in our case.

Abnormalities, Multiple↗
PubMed1977

Colloid degeneration of the skin--a case report.

A patient with multiple nodules on the chin and scalp is presented. Histologically, the nodules were composed of amorphous materials which also completely filled up the whole dermis. Histochemical observation indicated that the amorphous material in the nodule was a kind of glycoprotein. Electron microscopic examination revealed that the material consists of short wavy fibrils, 60 to 100 A in diameter, and of a low electron-dense amorphous substance. Biochemical examination supported the view that the amorphous material is so-called sialomucoid. The nodules were finally diagnosed as colloid degeneration of the skin (nodular type).

Aged↗
PubMed1977

Hepatic aminopyrine N-demethylase system: further studies of assay procedure.

Rat hepatic aminopyrine N-demethylase activity was measured by detecting the amount of formaldehyde produced from aminopyrine. Some optimal conditions for the N-demethylation were determined using both isolated microsomes and whole homogenates, and the standard assay method is described. Formaldehyde production from the substrate by microsomal enzyme system was linear to the amount of microsomes added during 3 min reaction time, whereas long-time incubation caused a decrease in the apparent activity of aminopyrine N-demethylation. The N-demethylase activity observed in normal rat liver homogenate was quite similar to that in microsomes when the activity was expressed on the basis of cytochrome P-450 as molecular activity. Pretreatment of animals with typical inducers, phenobarbital and 3-methylcholanthrene, resulted in alteration of the aminopyrine N-demethylase system, which was detectable in both microsomes and whole homogenates.

Aminopyrine↗
PubMed1977

Analysis of hypotensive mechanisms of pindolol, a beta-adrenoceptor blocking drugs in rats.

The hypotensive mechanisms of pindolol in anesthetized and conscious rats were investigated. Pindolol caused a fall in blood pressure in anesthetized, conscious and spinal rats, though in conscious rats a higher dose of the drug was required to produce such a response. This hypotension with pindolol in anesthetized and conscious rats was markedly inhibited by pretreatment with the drug itself or other beta-adrenoceptor blocking drugs. A similar phenomenon also occurred when isoproterenol was injected intravenously in anesthetized and conscious rats. The relationship between the hypotensive actions of four beta-adrenoceptor blocking drugs in anesthetized rats and their intrinsic beta-sympathomimetic actions in isolated catecholamine-depleted tracheal preparations was determined. Order of hypotensive potencies was the same as that of their intrinsic beta-sympathomimetic action, namely, pindolol greater than carteolol greater than bufetolol in equilibrium propranolol (p less than 0.05). These results suggest that the hypotension with pindolol is mediated through a decrease in the peripheral vascular resistance due to an intrinsic beta-sympathomimetic action of the drug.

Adrenergic beta-Antagonists↗
PubMed1977

Hepatic aminopyrine N-demethylase system: effect of cyanide on microsomal N-demethylase activity.

Cyanide, an inhibitor of many hemoproteins, was shown to affect a number of microsomal drug-metabolizing activities catalyzed by cytochrome P-450. The N-demethylation reaction of aminopyrine was inhibited noncompetitively by this inhibitor in microsomal preparations from rats. The binding reaction of aminopyrine with microsomal cytochrome P-450 was also modified by cyanide, and an abnormal aminopyrine-induced difference spectrum of microsomes by cyanide, and an abnormal aminopyrine-induced difference spectrum of microsomes appeared when cyanide was added to the reaction mixture. Partial dissociation of cytochrome P-450. Cyanide complex by aminopyrine was observed by spectrophotometrical and epr spectroscopic methods. These results suggest that aminopyrine and cyanide reciprocally affect binding with cytochrome P-450 and modification by cyanide of aminopyrine binding reaction with the hemoprotein produces an inhibition of N-demethylase activity.

Aminopyrine↗
PubMed1977

Electrocardiographic studies in acute pericarditis with specific reference to ventricular involvement of non-specific pericarditis.

The authors investigated electrocardiographic changes minutely in five cases of acute pericarditis, and especially in two cases of non-specific pericarditis. The results indicated that the amplitudes of the R and S waves increased progressively immediately after the disease reached a peak, which was reached after abnormal heart shadow in the chest x-ray returned to normal. This increased curve of amplitude varied in association with changes in the ST segment and T wave, suggesting an inflammatory dilatation of the myocardium. On the other hand, however, the curve was indistinct and took a long time to reach a maximum in case of systemic lupus erythematosus pericarditis, and was found to decrease and remain stationary in cases of pericarditis secondary to lung cancer and/or tuberculosis. These facts should become a useful guideline for diagnosis of acute non-specific pericarditis (due to virus origin). Ischemic changes of the ST segment and T wave were manifested by an exercise test during recovery from acute pericarditis when ST segment and T wave abnormalities had already improved and high voltage was the only abnormal finding on the ECG. In the healing stage, regarding the finding of high voltage, it should be pointed out that the myocardium remains as yet with residual damage revealed by loading with exercise, and treatment may be necessary until the abnormal finding has improved.

Acute Disease↗
PubMed1976

Temperature dependence of cytochrome P-450 reduction. A model for NADPH-cytochrome P-450 reductase:cytochrome P-450 interaction.

The NADPH-dependent reduction of rat hepatic microsomal cytochrome P-450 has been studied as a function of temperature. In the temperature range 4-37 degrees the reduction reaction was found to be biphasic and composed of two concurrent first order processes. This phenomenon was observed with microsomes from untreated and phenobarbital-induced animals in the presence or absence of exogenous Type I substrates. The amount of cytochrome P-450 reduced in the fast phase comprised approximately 70% of the total cytochrome P-450 at temperatures above 20 degrees. The temperature dependence of the fast phase was unusual for a membrane-bound enzyme system in that it lacked a discontinuity in the Arrhenius plot at a presumed phase transition temperature for the microsomal membrane. The slow phase of reduction behaved in a normal fashion for a membrane-bound enzyme system with a break in the Arrhenius plot at about 20 degrees. The data presented here combined with previous observations which include (a) the ratio of cytochrome P-450 to NADPH cytochrome P-450 reductase (NADPH:ferricytochrome oxidoreductase, EC 1.6.2.4) is 20:1, (b) the catalytic portion of the reductase molecule probably protrudes above the surface of the membrane, and (c) the cytochrome P-450 molecules are presumably embedded in the membrane support the hypothesis that the hepatic microsomal drug-metabolizing system exists as clusters with most of the cytochrome P-450 molecules arranged about a central reductase molecule. This central flavoprotein reductase is able to randomly reduce those cytochrome P-450 molecules within the cluster without translational motion through the microsomal membrane. The slow phase of reduction represents the reduction of those molecules not directly associated with the clusters.

Animals↗
PubMed1976

alpha-L-Fucopyranosylceramide, a novel glycolipid accumulated in some of the human colon tumors.

A fucosylceramide was isolated from a ceramide monohexoside fraction of human colon carcinomas by acetylation followed by preparative thin layer chromatography on Silica Gel G developed with butylacetate. It contained only fucose as the carbohydrate component and the ceramide moiety was characterized as N-palmitoyloctadecasphingenine as a predominant component. The structure of the compound was determined as alpha-L-fucopyranosylceramide by methylation analysis, mass spectrometry of permethylated and reduced glycolipid, and by enzymatic hydrolysis with alpha-L-fucosidase. The chemical concentration of this compound in colon tumor tissue depends on degree of malignancy: highly malignant metastatic deposits from colon cancers were 3 to 70 ng/mg of residue protein, whereas that of localized colon tumor was 0 to 2 ng/mg of protein residue. The present observation offers additional support for the occurrence of metabolic abnormality of fucolipids as membrane phenotype of malignancy as was suggested in previous studies (Yang, H-J., and Hakomori, S. (1971) J. Biol. Chem. 246, 1192-1200; Steiner, S., Brennan, P.J., Melnick, J. L. (1973) Nature New Biol. 245, 19-21).

Cerebrosides↗