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Biomedical subjects

T Hishinuma

Publications and source records attributed to T Hishinuma.

At least 73 records · Page 4Linked to original sources
PubMed1990

Severe atrophy of amygdala and hippocampus in both Alzheimer's disease and multi-infarct dementia.

Alzheimer's disease and multi-infarct dementia are the two main diseases entirely different from each other producing almost the same abnormalities as dementia syndrome. With magnetic resonance imaging, severe atrophy of amygdala and hippocampus in both Alzheimer's disease and multi-infarct dementia was observed. There was no essential difference on the atrophic findings between Alzheimer's disease and multi-infarct dementia. This result therefore suggest that the quantitative measurement of amygdaloid and hippocampal atrophy predicts dementia.

Aged↗
PubMed1989

Synthesis of C-labeled imipramine and its biodistribution in mice: a potential tracer for positron emission tomography.

A tricyclic antidepressant, C-labeled imipramine was synthesized by N-methylation of desipramine with 11CH3I to assist in the imaging of the human imipramine receptor by positron emission tomography. The radiochemical yield after purification of 11C-imipramine by high performance liquid chromatography was 28-63% at a specific activity of 26-53 Ci/mmol. The time required for synthesis, including purification was 30 min from the end of 11CH3I trapping. The organ distribution of 11C-imipramine was investigated in mice at various times after i.v. injection. The main accumulation of radioactivity was in the kidney, followed by the lung and the heart. In the brain, the radioactivity levels in the hypothalamus and striatum were the highest and remained constant, differentiating them from other portions of the brain. Furthermore, the result of a binding assay with 3H-labeled imipramine suggested that the regional distribution of 11C-imipramine in the same mouse brain correlated to that of the high affinity imipramine binding site.

Animals↗
PubMed1989

Expression forms and characteristics of Carr-Purcell-Meiboom-Gill sequence magnetic resonance images.

We propose two expression forms of Carr-Purcell-Meiboom-Gill (CPMG) sequence magnetic resonance images using the imaging parameters of recovery time (Tr), echo interval (Te), echo number (n) from 1 to N (number of echoes). An echo image can be expressed as a form of CPMG (Tr, Texn) and the other image synthesized by summing consecutive echo images numbered from n1 to n2 (l less than or equal to n1 less than n2 less than or equal to N) as a form of CPMG (Tr, Te x n1-n2). The CPMG (Tr, Te x n) images are weighted by T1, T2 or proton density and show the better morphological representation and contrast resolution of brain tumor lesion. The difference of signal intensities among the tissues is enhanced on the synthesized CPMG (Tr, Te x n1-n2) images with the increased signal-to-noise ratio. The calculated T2 images are also observed. These forms expound the scanning conditions and image characteristics and make easy to be compared with the spin echo images.

Brain Neoplasms↗
PubMed1989

A modified signal intensity equation of Carr-Purcell-Meiboom-Gill pulse sequence for MR imaging.

The signal intensity equation of Carr-Purcell-Meiboom-Gill (CPMG) pulse sequences for magnetic resonance imaging was modified to: S(n) = k.M0.exp (-n.Te/T2) [1-exp (-Tr/T1)] where S(n) is a signal intensity of "n-th" echo; k, constant; M0, initial longitudinal magnetization; n, echo number; Te, echo interval; and Tr, recovery time [Tr = TR-(N-1/2).Te; TR, repetition time; N, number of echoes]. To evaluate the accuracies of T1 and T2 values calculated from this modified equation, a phantom experiment using five tubes filled with 0.5 to 8 mM copper sulfate solutions was performed using a 0.14-T resistive whole-body MR scanner and a spectrometer system. The differences between the image values by this equation and the bulk values by the spectrometer were less than 6.2% (mean +/- S.D., 3.3 +/- 2.1%) in T2 and 15.6% (10.4 +/- 4.9%) in T1 (except 8 mM). By this modification, not only the image T2 value with a high accuracy but the image T1 value can be obtained simultaneously.

Magnetic Resonance Imaging↗
PubMed1989

[A case of huge duodenal leiomyosarcoma].

A case of duodenal leiomyosarcoma with large central necrosis was reported. Tumor was 15 X 10 X 10 cm in size. Ultrasonography showed a cystic tumor with thick wall in the right upper abdomen. CT scan revealed a gas formation in the central cystic cavity of the tumor. The gas formation was probably caused by bacterial infection. The diagnosis was confirmed histologically.

Aged↗
PubMed1987

Induction of cytochrome P-448 isozyme(s) in primary cultured rat hepatocytes by drugs which induce different isozymes in vivo.

Effect of 2-methoxy-4-aminoazobenzene (2-MeO-AAB) and 3-methylcholanthrene (MC) on the induction of microsomal cytochrome P-448 isozymes in primary cultured rat hepatocytes was examined by means of immunochemical methods such as protein A-enzyme-linked immonosorbent assay and immuno-blots using anti-rat cytochrome P-448 monoclonal antibodies and by means of bacterial mutation tests. Although 2-MeO-AAB selectively induced cytochrome P-448H and MC induced both cytochrome P-448H and a low spin form of cytochrome P-448 (P-448L) in the liver of rats, addition of these chemicals to primary cultured rat hepatocytes resulted in selective induction of cytochrome P-448L, as determined by the immunological methods. This was substantiated by the bacterial mutation test using Salmonella typhimurium TA 98 bacteria and two aromatic amine substrates with different specificities to the cytochrome P-448 isozymes. These results suggest that the responses of rat hepatocytes to cytochrome P-450 inducers are different in in vivo and in vitro.

Animals↗
PubMed1987

Species, sex and organ differences in induction of a cytochrome P-450 isozyme responsible for carcinogen activation: effects of dietary hepatocarcinogenic tryptophan pyrolysate components in mice and rats.

Both sexes of BALB/c X DBA/2 F1 mice and F344 rats were treated for 1 week with a diet containing 0.02% of hepatocarcinogenic tryptophan pyrolysate component (Trp P-1 or Trp P-2), and changes in the carcinogen activation enzyme activity in various organs were examined comparatively using a mutation test with Salmonella typhimurium TA98 as a tester bacterium. Hepatic enzymes from untreated mice and rats showed a definite catalytic activity for mutagenic activations of Trp P-1 and Trp P-2, whereas the activities of other organs--such as lung, kidney, small intestine and colon--were undetectable or very low. In both mice and rats either the Trp P-1 or Trp P-2 feeding resulted in induction of cytochrome P-450 isozyme(s), which could mediate in the liver but not in other organs the mutagenic activation of the carcinogen itself. As to the sex difference, the induction of the activation enzyme(s) was greater in the female animals than in the males. Species difference in the activity of hepatic enzymes catalyzing the Trp P-1 and Trp P-2 mutageneses was also observed in animals treated with the basal diet; the activity was higher in mice than in the sex-matched rats (Trp P-1, approximately 1.5-fold; Trp P-2, approximately 7-fold). When diet containing Trp P-1 or Trp P-2 was fed for 1 week, the activity of the rat liver for Trp P-1 mutagenesis was of a level similar to that of the sex-matched mice, but for Trp P-2 mutagenesis it was less than half that in the mice. The induced hepatic enzymes in mice and rats were suggested to be 3-methylcholanthrene-inducible cytochrome P-448 isozymes as determined by mutation tests with Trp P-1, Trp P-2 and two other substrates and by immunochemical analyses of rat hepatic cytochrome P-450 using monoclonal antibodies against rat cytochrome P-448 isozymes. These results indicate that a form of cytochrome P-450 responsible for activation of Trp P-1 and Trp P-2 is inducible by dietary treatment of mice or rats with these carcinogens and that the amount of the cytochrome P-450, including resident and induced forms, is related to the species, sex and organ differences in their carcinogenic susceptibility to these chemicals.

Animals↗
PubMed1987

Organ selective induction of cytochrome P-448 isozymes in the rat by 2-methoxy-4-aminoazobenzene and 3-methylcholanthrene.

Male Sprague Dawley rats were injected intraperitoneally with 2-methoxy-4-amino-azobenzene (2-MeO-AAB) or 3-methylcholanthrene (MC), and then the expression of microsomal cytochrome P-450 isozymes in liver and extrahepatic tissues was investigated by means of immunological methods and a bacterial mutation test. The results of protein A-enzyme-linked immunosorbent assaying and immunoblotting using anti-rat cytochrome P-448 monoclonal antibodies showed that MC induced at least two microsomal cytochrome P-448 isozymes, a high spin form (cytochrome P-448H) and a low spin form (cytochrome P-448L), in liver, but that it induced only cytochrome P-448L in extrahepatic tissues such as lung, kidney, small intestine, and colon. The results also indicated that, in contrast to MC, 2-MeO-AAB selectively induced microsomal cytochrome P-448H in liver but did not induce any cytochrome P-448 isozymes in extrahepatic tissues. The activities of 9,000 X g supernatants from the individual organs, as to the mutagenic conversion of 3 aromatic amines (3-amino-1-methyl-5H-pyrido(4,3-b)indole, 2-amino-6-methyldipyrido(1,2-a: 3',2'-d)-imidazole and 3-methoxy-4-aminoazobenzene), toward Salmonella typhimurium TA 98 bacteria were dependent upon the quantity and/or quality of the microsomal cytochrome P-448 isozymes in the organs.

Amines↗
PubMed1987

Immunochemically detected nuclear envelope-associated cytochrome P-450 component(s) in rat hepatocyte culture lines.

The presence and location of cytochrome P-450 in Donryu rat hepatocyte culture lines, Ac2F cells and 3 other cell lines were assessed by indirect immunofluorescence examination using anti-cytochrome P-450 monoclonal antibodies. Ac2F cells and other hepatocyte cell lines were selectively stained at their nuclear envelope, but not the cytoplasm, with a monoclonal antibody selective to a high-spin form of cytochrome P-448 (P-448H), although this monoclonal antibody stained primary cultured normal rat hepatocytes at both cellular components and did not stain hepatoma cells of 2 transplantation lines. The results of unscheduled DNA synthesis assay with Ac2F cells using several carcinogenic aromatic amines (4-aminoazobenzene derivatives and amino acid pyrolysis products) suggested that this nuclear envelope-associated cytochrome P-450 activates a restricted portion of these aromatic amines, i.e., a tryptophan pyrolysis component and a glutamic acid pyrolysis component. These results indicate that rat hepatocyte culture lines lack (or contain a reduced amount of) the cytoplasmic cytochrome P-450 but maintain a characteristic type of cytochrome P-450, probably a kind of cytochrome P-448H in their nuclear envelope, and this may be involved in oxidative metabolism of a restricted portion of aromatic amines.

Animals↗
PubMed1986

Malignant transformation of rat liver cells by N-benzoyloxy-3'-methyl-4-methylaminoazobenzene and its related compound.

N-Benzoyloxy-3'-methyl-4-methylaminoazobenzene-(N-benzoyloxy-3'-Me-MAB) was highly toxic to rat liver epithelial cells (Ac2F) and induced many more chromosome aberrations and unscheduled DNA synthesis than did 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB). N-Benzoyloxy-3'-Me-MAB and its related compound, N-acetoxy-4-methylaminoazobenzene, efficiently induced malignant transformation of the cells, but 3'-Me-DAB was not so effective. The cells transformed by N-acyloxy-4-methylaminoazobenzene (N-acyloxy-MAB) derivatives showed significant increases in plating efficiency in liquid medium and in the size of aggregates in rotation culture. Such increases were not seen in the 3'-Me-DAB-transformed cells. The results indicate that the N-acyloxy form of the 4-dimethylaminobenzene derivatives seems very likely to be the ultimate metabolite.

Animals↗
PubMed1985

3-Methoxy-4-aminoazobenzene, a selective inducer for a high spin form of cytochrome P-448 in rat liver microsomes.

Treatment of Sprague Dawley rats with 3-methoxy-4-aminoazobenzene (3-MeO-AAB) resulted in striking increase of the activity of hepatic microsomal cytochrome P-450s which could efficiently catalyze the mutagenic activation of hepatocarcinogenic aromatic amines such as a tryptophan-pyrolysate component, Trp P-2, and a glutamic acid-pyrolysate component, Glu P-1. The 3-MeO-AAB-induced cytochrome P-450 (3-MeO-AAB-P-450) was examined for the molecular character by immuno-Western blotting using monoclonal antibody to 3-methylcholanthrene-induced cytochrome P-448 (P-448H; m.w. 54,000).

Animals↗