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Biomedical subjects

M Tada

Publications and source records attributed to M Tada.

At least 325 records · Page 18Linked to original sources
PubMed1993

Sequential observation of rat prostate lesion development induced by 3,2'-dimethyl-4-aminobiphenyl and testosterone.

3,2'-Dimethyl-4-aminobiphenyl (DMAB), when combined with high doses of testosterone propionate (TP) induces invasive adenocarcinomas with metastatic potential in the rat prostate. The processes underlying this tumor development, including the involvement of atypical hyperplasias, were sequentially investigated in F344 rats. DMAB was given subcutaneously at a dose of 50 mg/kg body weight 10 times at 2-week intervals. TP was administered chronically (in Silastic tubes) from the beginning of the experiment or after the DMAB administration until termination (week 60). Invasive adenocarcinomas were induced in the lateral and anterior prostate as well as the seminal vesicles. Atypical hyperplasias appeared from an early stage, with the later appearance of cancers being closely associated with such foci of morphological alteration. The findings confirm that combined administration of DMAB and pharmacological doses of TP yields invasive adenocarcinomas in the rat prostate and provide further support for the conclusion that atypical hyperplasias are premalignant lesions.

Aminobiphenyl Compounds↗
PubMed1993

Sublethal ischemia alters myocardial antioxidant activity in canine heart.

We examined antioxidant activity in the pre-conditioned canine myocardium with four 5-min episodes of regional ischemia and reperfusion. Immediately after repetitive brief ischemia, mitochondrial Mn-superoxide dismutase (SOD) activity in the ischemic myocardium significantly increased compared with that in the nonischemic myocardium (18.7 +/- 2.1 vs. 14.9 +/- 1.0 U/mg protein, P < 0.05). Although no difference was seen in the activity between these regions after 3 h of the sublethal ischemia, a significant increase in the activity of the ischemic myocardium reappeared after 24 h compared with that of the nonischemic myocardium (26.7 +/- 0.9 vs. 20.8 +/- 0.9 U/mg protein, P < 0.05). Mn-SOD content increased gradually in the ischemic myocardium after sublethal ischemia, with a peak after 24 h (2.8 +/- 0.1 vs. 2.1 +/- 0.1 microgram/mg protein, P < 0.05). There were no differences in the activity and content of Cu, Zn-SOD between these regions after sublethal ischemia. Activities of glutathione peroxidase and reductase were significantly higher and lower, respectively, in the ischemic myocardium than those of the nonischemic myocardium immediately after repetitive brief ischemia, but no differences between these regions were seen in activities after 3 or 24 h. These results indicate that a brief ischemic insult alters myocardial antioxidant activity not only immediately after but also 24 h after sublethal ischemia.

Animals↗
PubMed1993

Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia.

The infarct-limiting effect of ischemic preconditioning is believed to be a transient phenomenon. We examined the delayed effects of repetitive brief ischemia on limiting infarct size in an open-chest dog model by an occlusion (90 minutes) of the left anterior descending coronary artery (LAD) followed by reperfusion (5 hours). The dogs were preconditioned with four brief repeated ischemic episodes induced by 5-minute LAD occlusions with subsequent reperfusion. The size of infarcts initiated by a sustained occlusion immediately or 24 hours after preconditioning was significantly smaller when compared with infarcts in sham-operated dogs (for the immediate occlusion, 14.4 +/- 2.0% versus 39.0 +/- 3.7%, respectively [p < 0.01]; and for the delayed occlusion, 18.8 +/- 3.4% versus 35.1 +/- 4.6%, respectively [p < 0.05]); however, when the infarction was induced 3 hours (31.2 +/- 3.7% versus 37.5 +/- 4.2%, respectively) or 12 hours (25.4 +/- 4.8% versus 35.0 +/- 5.3%, respectively) after repetitive ischemia, the infarct size did not differ. No differences were seen in regional myocardial blood flow or rate-pressure products between the two groups. These results indicate that an infarct-limiting effect of brief repeated ischemia can be observed 24 hours after sublethal preconditioning.

Animals↗
PubMed1993

Intramedullary disseminated capillary hemangioma with localized spinal cord swelling: case report.

A case of intramedullary disseminated capillary hemangioma in the cervical spinal cord is presented. The patient showed progressive neurological deficits. Magnetic resonance imaging showed localized swelling of the spinal cord. This case was initially misdiagnosed at another institution as syringomyelia. Decompression of the posterior fossa and a syringo-subarachnoid shunt operation were performed. However, the operative findings in the authors' institution showed edematous tissue with no apparent neoplastic characteristics. Pathological findings revealed angiomatous nests consisting of small capillary-like vessels, telangiectatic vessels, and aggregated venules scattered in the edematous and partially necrotic spinal cord tissue. The edema and necrosis of the cervical cord were considered to have been caused by circulatory disturbances in the spinal cord parenchyma resulting from these vascular lesions.

Diagnostic Errors↗
PubMed1993

X chromosome retains the memory of its parental origin in murine embryonic stem cells.

A cytogenetic and biochemical study of balloon-like cystic embryoid bodies, formed by newly established embryonic stem (ES) cell lines having a cytogenetically or genetically marked X chromosome, revealed that the paternally derived X chromosome was inactivated in the majority of cells in the yolk sac-like mural region consisting of the visceral endoderm and mesoderm. The nonrandomness was less evident in the more solid polar region containing the ectodermal vesicle, mesoderm and visceral endoderm. Since the same was true in embryoid bodies derived from ES cells at the 30th subculture generation, it was concluded that the imprinting responsible for the preferential inactivation of the paternal X chromosome that was limited to non-epiblast cells of the female mouse embryos, was stably maintained in undifferentiated ES cells. Differentiating epiblast cells should be able to erase or avoid responding to the imprint.

Animals↗
PubMed1993

Dystrophic axonal formation (spheroid body) in central neurocytoma--case report.

A 30-year-old female presented with a central neurocytoma manifesting as positional headache. Magnetic resonance imaging showed a large calcified mass in the right lateral ventricle. The tumor was completely removed surgically. Light microscopy showed a linear arrangement of well-defined cells (beaded-string pattern) containing small round nuclei with abundant perikarya. A perinuclear halo reminiscent of oligodendroglioma was prominent in some cell groups. The tumor was entirely amitotic and free of atypia. Large, plump spheroid bodies lacking nuclei but containing coarse brown pigments were present among the tumor cells. The tumor cells were immunoreactive to neuron-specific enolase and synaptophysin but not glial fibrillary acidic protein or neurofilament. The ultrastructure of the tumor cells included abundant spheroid bodies containing secretory granules around neurons, indicating a dystrophic or aborted process of neuronal differentiation rather than a completely-differentiated central neurocytoma.

Adult↗
PubMed1993

Human glioblastoma cells produce granulocyte-macrophage colony-stimulating factor in vitro, but not in vivo, without expressing its receptor.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) production and receptor expression by human glioblastomas was studied. Enzyme-linked immunosorbent assay showed four of 10 glioblastoma cell lines spontaneously released GM-CSF (2.9-9.2 pg GM-CSF protein/ml culture medium), which was enhanced by stimulation with tumor necrosis factor-alpha (TNF) (10 U/ml) up to 410 pg/ml. TNF also induced secretion of GM-CSF by another cell line. Northern blot analysis identified increasing GM-CSF gene expression by cells following TNF stimulation. However, no GM-CSF protein was detectable in the cerebrospinal fluid of three malignant glioma patients. Intratumoral administration of TNF in the patients also failed to stimulate GM-CSF levels in the cerebrospinal fluid. A binding assay using flow cytometry with biotinylated GM-CSF and Scatchard analysis using 125I-labeled GM-CSF failed to demonstrate GM-CSF receptor expression on the 13 cell lines. Exogenous GM-CSF stimulation had no effect on production of prostaglandin E2, interleukin-6, or interleukin-8 by glioma cells. Human glioblastoma cells secrete GM-CSF without expressing the receptor in vitro, but there was no evidence of GM-CSF production in vivo.

Glioblastoma↗
PubMed1993

TV game play and obesity in Japanese school children.

A survey conducted in 9 cities in Japan indicated for 1517 boys and 1546 girls there was more use of TV games for longer periods when children were classified as obese than when classified as moderate or lean. More boys than girls played although most children had experience and many owned TV game machines.

Body Mass Index↗
PubMed1993

Identification of N4-(guanosin-7-yl)-4-aminoquinoline 1-oxide and its possible role in guanine C8 adduction.

A novel base adduct of the carcinogen, 4-nitroquinoline 1-oxide, N4-(guanin-7-yl)-4-amino-quinoline 1-oxide was identified from RNA, which was bioactivated 4-hydroxyaminoquinoline 1-oxide. In addition of base adducts, we uncovered the formation of 8-hydroxyguanine residue (8-OH-G) in DNA and RNA after treatment of 4NQO, in vivo and in vitro. A conceivable mechanism of formation of 8-OH-G and guanine C8-substituted quinoline adducts is proposed.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1993

4-Hydroxyaminoquinoline 1-oxide can convert the Z-form of poly(dG-m5dC).poly(dG-m5dC) back to B-form-DNA.

Reactions between the chemical carcinogen 4-hydroxyaminoquinoline 1-oxide (4HAQO) and poly(dG-dC).poly(dG-dC), poly(dG-m5dC).poly(dG-m5dC) and poly(dG-br5dC).poly(dG-br5dC) were studied under B-form and Z-form conformation conditions. 4HAQO bound covalently to both B-form and Z-form-DNA. The extent of the B-form to Z-form-DNA transition was diminished by 4HAQO, as inferred by spectroscopic methods. Moreover, conversion of the Z-form-DNA back to a right handed DNA close to the B-form was observed with this carcinogen.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1993

[Calcium release channel of cardiac muscle sarcoplasmic reticulum].

Cardiac muscle contractility is controlled by myoplasmic calcium (Ca) concentration. Sarcoplasmic reticulum plays an essential role in the regulation of [Ca]. Depolarization of the sarcolemma induces Ca release from the sarcoplasmic reticulum, leading to the muscle contraction. On the other hand, Ca uptake by the sarcoplasmic reticulum into the lumen results in the muscle relaxation. The Ca release from the sarcoplasmic reticulum is mediated by Ca release channel. Using ryanodine as a molecular probe, the calcium release channel has been isolated, purified and characterized. Morphological studies have confirmed its identity with the feet structure which spans between the transverse tubule and the junctional face of the sarcoplasmic reticulum. The cardiac Ca release channel cDNA encodes 4969 amino acids with a molecular weight of 564,711. The analysis of the sequence indicates that 10 potential transmembrane sequences in the COOH-terminal fifth of the molecule and two additional nearer to the center of the molecule could contribute to the formation of the Ca conducting pore. The remainder of the molecule is hydrophilic and constitutes the cytoplasmic domain which corresponds to the feet structure. Northern blot analysis has shown that the cardiac Ca release channel is expressed in heart and brain. The channel is modulated by Ca, ATP, calmodulin, and phosphorylation. A potential modulator binding domain has been identified in the molecule by searching consensus sequences and investigation of a causal mutation for malignant hyperthermia, the primary defect of which exists in the skeletal Ca release channel.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Reoperation in patients with thymoma].

For past seven years, reoperations were carried out for six patients with thymoma and myasthenia gravis (MG). Of six patients, five patients were suspected recurrent thymoma and remaining one patient was diagnosed as the residual thymus after thymothymectomy or thymomectomy. Myasthenia gravis has been progressing in five patients after initial operation except for one patient. Two cases of pleural dissemination tumors, one case of local recurrent thymoma and one case of the residual thymus were confirmed by surgery, remaining two patients had no recurrent tumor. As surgical procedure, median sternotomy using for reoperation has a great surgical risk, because left brachiocephalic vein closely adhered to the sternum is apt to be injured. Clinical symptoms of MG were improved in all the patients after reoperation regardless of recurrent tumor.

Adult↗
PubMed1993

High accumulation of 2-deoxy-2-fluorine-18-fluoro-D-galactose by well-differentiated hepatomas of mice and rats.

The potential application of 2-deoxy-2-[18F]fluoro-D-galactose for the detection and evaluation of hepatomas with PET was examined in mouse and rat liver tumor models. Biodistribution studies showed that uptake of this marker was high in well-differentiated, spontaneous hepatoma of C3H mice at almost 92% of the normal liver level. The uptake by well-differentiated Morris rat hepatoma (5123D) was relatively high and second to that of the C3H hepatoma. On the other hand, uptake values for poorly differentiated mouse hepatoma (MH129P), rat hepatomas (AH109A, AH272), mouse melanoma (B-16) and mammary carcinoma (FM3A) were very low and only 14%-18% of that in the normal liver. The results suggest that while well-differentiated hepatomas maintain a high galactose metabolic activity, poorly differentiated hepatomas or other tumors lose this to a large extent. Consequently, this radiopharmaceutical can be used with PET for biochemical characterization of hepatomas and the differential diagnosis between hepatomas and other cancers.

Animals↗