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Biomedical subjects

Y Omori

Publications and source records attributed to Y Omori.

At least 199 records · Page 11Linked to original sources

[Tl-201 single-photon emission computed tomography for clinical assessment of dilated cardiomyopathy].

In some cases of dilated cardiomyopathy (DCM) perfusion defects are demonstrable by Tl-201 imaging at rest. This study clarified the mechanism by which the Tl scan can show myocardial perfusion defects in patients with DCM by means of Tl-201 single-photon emission computed tomography (ECT) utilizing a rotating gamma camera to assess three-dimensional T1 distribution in the myocardium. Thirteen patients with DCM were studied by conventional planar and ECT imaging, and the degree of defects was determined visually. Perfusion defects were observed in 11 of 13 cases (85%) by planar imaging and in all 13 (100%) by ECT imaging. The mean defect score was higher in ECT than in planar imaging (4.15 +/- 1.46 vs 2.23 +/- 1.46, p less than 0.025). A comparative study of defect scores and left ventricular ejection fractions (EF) using gated cardiac blood pool scans established a negative correlation on ECT imaging (r= -0.64), and no correlation on planar imaging (r= -0.38). There was no statistically significant correlation between perfusion defects on planar imaging and regional wall motion abnormalities as observed by two-dimensional echocardiography (2-DE). In contrast, most of the segments with severe defects (defect score greater than or equal to 2) on ECT images showed high grade wall motion abnormalities on 2-DE. Both perfusion defects and wall motion abnormalities in DCM may be closely related to the fibrosis or scar formation in the myocardium. These results indicated that T1-201 myocardial scintigraphy, especially ECT imaging, is of great value in the clinical assessment of patients with DCM.

Adult↗

[Clinical usefulness of exercise-nitroglycerin myocardial imaging using dual administration of thallium-201].

In order to differentiate transient myocardial ischemia from infarction, the delayed thallium-201 myocardial imaging (redistribution image) is widely utilized, however, the precise mechanism of redistribution remains unsolved. In the present study, we proposed a new method to elucidate myocardial ischemia on images. In normal subjects, patients with old myocardial infarction (OMI) without angina pectoris (AP) and patients with AP, 1.4 mCi of thallium-201 (Tl-201) was intravenously injected at the peak exercise, and immediately myocardial images were obtained in the three projections. Then, 0.3 mg of nitroglycerin (NTG) was sublingually given, and 0.6 mCi of Tl-201 was readministered. NTG myocardial images were analyzed in the left anterior oblique projection and evaluated visually and quantitatively. There was no significant difference in the relative activity on exercise to NTG images in normal subjects and patients with OMI, while patients with AP showed increased activity on exercise to NTG images. Furthermore, the increase in relative activity done by the exercise-nitroglycerin study was greater than that by the conventional exercise-redistribution study in patients with AP. It was concluded that a new method in the present study is able to image myocardial ischemia distinctly and could be useful in clinical studies.

Adult↗

The heterogeneity of arylhydrocarbon hydroxylase in fetal liver microsomes of rats.

The characteristic of arylhydrocarbon hydroxylase system in fetal liver microsomes of rat was investigated. NADH-synergistic effect on NADPH-dependent arylhydrocarbon hydroxylase was observed in fetal liver microsomes of rat but not in maternal liver microsomes. NADH-synergistic effect decreased in parallel with the decrease of the ratio of cytochrome b5/cytochrome P-450 in liver microsomes. The cytochrome P-450 in arylhydrocarbon hydroxylase system in fetal liver microsomes of rat seemed to be different from that in offspring liver microsomes in respect of its dependency on cytochrome b5 system for its maximum activity.

4-Chloromercuribenzenesulfonate↗

Simultaneous determination of aminopyrine hydroxylation and aminopyrine N-demethylation in liver microsomes by high-performance liquid chromatography.

Aminopyrine and its metabolites, including 3-hydroxymethyl-2-methyl-4-dimethylamino-1-phenyl-3-pyrazoline-5-one which is a hydroxylated metabolite of aminopyrine, were separated on a reversed-phase (C8) Radial-Pak column using a mobile phase of methanol-triethylamine-water (30:1:69) adjusted to pH 5.40 with acetic acid. Detection of the peak was performed by an ultraviolet detector at 254 nm. By the rapid and simple method, aminopyrine hydroxylation as well as aminopyrine N-demethylation in liver microsomes can be examined simultaneously.

Aminopyrine↗

Cytotoxic effects of methylnitrosourea on developing brain.

The effect of methylnitrosourea (MNU) on cerebellar and cerebral DNA, RNA, protein, lysosomal enzymes (acid DNase, RNase, phosphatase, and beta-glucuronidase), and 2',3'-cyclic nucleotide 3'-phosphohydrolase (2',3'-CNPase) activities was studied in rats from birth through 12 days of age. Subcutaneous injection of MNU in a dose of 0.625 mmol/kg caused a suppression of increase in weights and content of DNA, RNA, and protein of cerebellum, but no changes in those of the cerebrum or in body weight. Ratios of protein and RNA to DNA were substantially elevated by MNU in the cerebellum but not in the cerebrum. Acid DNase and acid RNase activities of MNU-treated rats were significantly elevated beyond the increase of these activities in controls in the cerebellum, but no change in these activities by MNU was observed in the cerebrum. A slight elevation in acid phosphatase activity was observed in the cerebellum but not in the cerebrum after MNU pretreatment. Beta-glucuronidase and 2',3'-CNPase activities were not changed in the cerebellum or in the cerebrum. These results suggest that in the developing brain, especially in the cerebellum at the mitotic stage, MNU caused cell damage and inhibited cell mitosis.

Acid Phosphatase↗

New method for quantitative measurement of N-nitrosodimethylamine formation in the whole mouse.

A simple method for the quantitative estimation of the formation of N-nitrosodimethylamine (NDMA) in mice has been developed. Mice were frozen in liquid nitrogen and homogenized. NDMA was then extracted and analyzed by a gas chromatograph equipped with a thermal energy analyzer. In normal mice NDMA (100 nmole) administered orally was rapidly metabolized and recovery of NDMA was about 10% after 60 min. However, when pyrazole (300 mg/kg) was injected i.p. to mice 60 min before the administration of NDMA, more than 80% of the administered NDMA could be recovered within 60 min. This result suggested that in pyrazole pretreated mice the accurate amount of NDMA formed could be estimated. Therefore the NDMA formation was measured in the pyrazole pretreated mice. When 0.25 mumole of aminopyrine and from 0.25 to 2.0 mumole of sodium nitrite were simultaneously administered orally, the amount of the NDMA formation in 20 min was found to be from 8.2 to 60.3 nmole. These values are equal to about from 30 to 200 micrograms/kg of body weight which are nearly daily doses expected to cause the carcinogenic effect on mice or rats. This method of measuring NDMA in pyrazole pretreated mice appears to be useful for investigating the in vivo formation of NDMA quantitatively.

Aminopyrine↗

Effect of phenobarbital and 3-methylcholanthrene on the hepatic microsomal metabolism of N-nitrosodimethylamine, N-nitrosomethylbutylamine and N-nitrosomethylbenzylamine.

The effect of phenobarbital (PB) and 3-methylcholanthrene (MC) pretreatment on dealkylations of N-nitrosodimethylamine (NDMA), N-nitrosomethylbutylamine (NMBuA) and N-nitrosomethylbenzylamine (NMBeA) was investigated in rat hepatic microsomes. PB increased the demethylation and the debutylation of NMBuA and the debenzylation of NMBeA. MC increased the debutylation of NMBuA and the debenzylation of NMBeA. However, MC decreased the demethylation of NMBeA. The demethylation of NDMA was not changed by the pretreatment of the inducers. These results suggest that the dealkylations of these nitrosamines are catalyzed by several enzymes, which probably depend on different cytochrome P-450 species.

Animals↗

A new device for the determination of microsomal cytochrome P-450 in renal tissue preparations from various species contaminated with mitochondria and hemoglobin.

Using a spectrophotometer connected to a microcomputer, the carbon monoxide difference spectrum of renal microsomal dithionite-reduced cytochrome P-450 was measured avoiding the effects of the contaminating mitochondrial cytochromes and hemoglobin by subtracting the CO difference spectrum of a succinate-treated microsomal suspension from that of a dithionite-treated one. By this method, we quantitatively determined the microsomal cytochrome P-450 in kidneys from various species. The absorption peak of the renal microsomal cytochrome P-450 was about 452 nm in rats and about 450 nm in mice, hamsters, rabbits, guinea pigs, dogs, and pigs. Compared with the renal cytochrome P-450 contents in rats, the contents on a g tissue basis were greater in pigs, dogs, and mice and were about the same in hamsters and rabbits. The renal cytochrome P-450 contents in guinea pigs were less than those in rats.

Animals↗

Insulin-receptor autoantibody detected by the human placental membrane method: six patients with insulin-receptor autoantibody in japan.

Insulin-receptor antibodies were detected in six patients out of 61 diabetics from all over Japan during 1975 to 1979 using the human placental membrane method. These 61 patients were divided into three categories: (1) Those whose diabetes control needed more than 80 units of insulin a day; (2) those whose fasting IRI was higher than 50 microU/ml even with glucose intolerance; and (3) those who had hypoglycemia of unknown origin. Controls consisted of 11 serum samples from 11 healthy women and six diabetics treated with insulin and thus having insulin antibodies in their sera. The sera from healthy subjects did not suppress 125I-insulin binding with human placental membrane in either the direct or the preincubation method. 125I-insulin binding in the direct method was markedly suppressed, however, by the sera of insulin-treated diabetics, although no such suppression was observed with the preincubation method. In six of the 61 subjects (two males and four females), inhibition of binding was proved by both direct and preincubation methods for the protein fraction of the sera, particularly for the IgG fraction in five cases. Three of the six had Sjögren syndrome; one of these also had acanthosis nigricans. Four of the six showed insulin resistance, and two did not. A follow-up showed that antibodies decreased relatively quickly in three of the six cases, with the degree of inhibition paralleling patients' clinical courses.

Adult↗

Studies on nitrosamine formation by the interaction between drugs and nitrite. I. Measurement of the amount of nitrosamine formed in rat and guinea pig stomachs.

The amounts of nitrosamine formed by the interaction of several drugs and nitrite in rat and guinea pig stomachs were estimated. The nitrosamine formation from aminopyrine and nitrite was much more in guinea pig stomachs than in rat stomachs. It seemed that this result was due to the difference in gastric contents of these animals. As the nitrosamine formation was also indicated in the interaction of a clinically prescribed dose of aminopyrine and very low doses of nitrite in rat and guinea pig stomachs, there is a possibility that the nitrosation of aminopyrine takes place in human stomachs, too. Minocycline also interacted with nitrite and formed N-nitrosodimethylamine. However, the amount of nitrosamine formed was less in minocycline than in aminopyrine. Oxytetracycline was not found to form nitrosamine in the stomachs of these animals. The effects of several compounds on the nitrosamine formation by the interaction of aminopyrine and nitrite were also investigated. Ascorbic acid, sodium erythorbate, propyl gallate and butylated hydroxyanisole reduced the nitrosamine formation but the effect of alpha tocopherol, sorbic acid and butylated hydroxytoluene was not observed in the stomach.

Aminopyrine↗