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Biomedical subjects

M Tada

Publications and source records attributed to M Tada.

At least 523 records · Page 29Linked to original sources
PubMed1985

Altered metabolism of thromboxane A2 and prostacyclin in the pathogenesis of coronary vasospasm and thrombosis.

This chapter documents the significance of TXA2 and PGI2 in the pathologic events associated with active coronary artery disease. We suggest that altered metabolism of these prostanoids may result in disintegration of platelet and vascular wall reactivities accompanying coronary spasm or intravascular thrombosis associated with myocardial cell necrosis. Further studies should be carried out to determine if coronary circulatory disorders and subsequent myocardial cell injury can be affected by disintegration of the lipoxygenase system that plays a pivotal role in maintaining homeostasis in vascular endothelium and blood components.

Coronary Vasospasm↗
PubMed1985

Intraoperative sonography for brain tumor surgery.

Intraoperative ultrasonography was performed during craniotomies for nine cases of primary brain tumor. B-mode real-time linear scanner with a small probe head has proven to be extremely useful for detecting and localizing subcortical or deep seated brain tumors. The sonography clearly showed the tumors as hyperechogenic mass except in one case, calcifications as more echogenic particles, cyst as hypoechogenic area. Physical principles of echogenicity are discussed, and major advantages and disadvantages of intraoperative ultrasonography in neurosurgery are mentioned.

Adult↗
PubMed1985

Sphenoethmoidal encephalomeningocele and midline anomalies of face and brain.

An autopsy case of sphenoethmoidal encephalomeningocele associated with anophthalmia, agenesis of the corpus callosum, cleft palate and nasal septum defect is presented. A small colloid cyst and a cyst of unknown nature were found in the third ventricle. Based on a review of the literature, a peculiar association of sphenoethmoidal encephalomeningocele with callosal defect and midline facial anomalies seems not to be fortuitous and we proposed to call it "Sakoda complex" as a distinctive disease entity. Pathogenetic mechanism and significance of separation of this syndrome are discussed from a embryological standpoint. Anophthalmia and the cyst of unknown nature are interpreted as midline anomalies that may be attributed to the same pathogenetic cause.

Abnormalities, Multiple↗
PubMed1985

Reaction of nucleic acids bases and their derivatives with peroxodisulfate ion.

Reaction with peroxodisulfate ion was investigated, that is, reaction of 1,3-dimethyluracil, 1,3-dimethylthymine, and caffeine with carbon radicals formed from decarboxylation of carboxylic acids, oxidation of the methyl group at 5-position of thymines, and halogenation of nucleic acids bases and their derivatives with alkali halides.

Caffeine↗
PubMed1984

Growth rates of colorectal carcinoma and adenoma by roentgenologic follow-up observations.

During the last 15 years, seventeen patients with polypoid lesions or carcinoma in the colon or rectum were repeatedly examined with barium enemas. The doubling time of these colorectal tumors was calculated according to Spratt's theory of the growth rate of neoplasms. The doubling times of 6 carcinomas varied from 92.4 to 1032.2 days with those of early carcinomas being much shorter than those of advanced lesions. Advanced lesions of the proximal colon had a shorter doubling time than those of the distal colon. The doubling times of 6 adenomatous polyps ranged from 146.5 to 398.5 days, thus coinciding with the time interval of the carcinomas. However, 5 other adenomatous polyps did not grow during the follow-up period which ranged from 420 to 816 days. There was no definite correlation between the doubling time and the histology of the tumors. The difference in the doubling time of carcinomas correlated more with location than the histological grade of malignancy.

Adenocarcinoma↗
PubMed1984

Antagonizing effect of 3-aminoharman on induction of sister-chromatid exchanges by mutagens.

3-Aminoharman (3AH, 3-amino-1-methyl-9H-pyrido[3,4-b]indole), which has been reported as a novel substance with an antagonistic effect on induction of sister-chromatid exchange (SCE) by polycyclic mutagens in the presence of the metabolic activation system, was examined with a cultured human lymphoblastoid cell line, NL3, for its effect on SCE induction by direct-acting mutagens such as mitomycin C (MMC), nitrogen mustard N-oxide (NMO), methyl methanesulfonate (MMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitroquinoline 1-oxide (4NQO) and 3-hydroxyamino-1-methyl-5H-pyrido[4,3-b]indole (OH-Trp-P-2), and also by ultraviolet light (UV) irradiation. The results obtained on simultaneous treatment with 3AH and mutagens were as follows: (1) 3AH suppressed more than 50% of SCEs induced by MMC, NMO and OH-Trp-P-2; (2) 4NQO- and MNNG-induced SCEs were also suppressed by 3AH but to a lesser degree; (3) MMS-induced SCEs were not, however, altered by 3AH; and (4) the suppression of SCE by 3AH was dose-dependent. Treatment of cells with 3AH for 2 h immediately before MMC exposure suppressed SCE induction to a significant degree similar to the simultaneous treatment, but post-treatment with 3AH was much less effective. 3AH inhibited SCE induction by NMO when 3AH treatment was carried out either before or after NMO treatment, to an extent similar to the simultaneous treatment. Treatments with 3AH either before or after UV exposure did not change the UV-induced SCEs. Results with these direct-acting mutagens ruled out the relevance of metabolic activation as a necessary step for the antagonizing effect of 3AH.

Biotransformation↗
PubMed1984

Reduction of prostacyclin synthesis as a possible cause of transient flow reduction in a partially constricted canine coronary artery.

Coronary blood flow decreases cyclically in a partially occluded coronary artery of anesthetized dogs. Spontaneous aggregation and deaggregation of platelet plugs in the constricted artery have been indicated to be responsible for this phenomenon. A current hypothesis is that platelet aggregation may be determined by a balance between proaggregatory platelet product, thromboxane A2 (TXA2), and antiaggregatory substance, prostacyclin (PGI2). To elucidate the relationship between the cyclical reduction of coronary flow (CRCF) and metabolic alterations of TXA2 and PGI2, we attempted to determine the plasma levels of their stable catabolites, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), in the coronary circulation of 69 dogs. Of 40 cases, 20 cases exhibited CRCF accompanying a significant increase in TXB2 in the coronary sinus (CS) (P less than 0.05) and constant levels of 6-keto-PGF1 alpha in the CS and aorta (Ao). Another 20 cases did not exhibit CRCF that accompanied a marked increase in 6-keto-PGF1 alpha (P less than 0.05) with virtually no change in TXB2 in the CS and Ao. A higher dose of indomethacin (10 mg/kg, i.v.) was capable of evoking CRCF in cases not exhibiting CRCF spontaneously. Under these conditions, a significant decrease in 6-keto-PGF1 alpha was seen both in the CS and Ao compared with lower doses of indomethacin (1 to 3 mg/kg, P less than 0.01), that produced less pronounced reduction of 6-keto-PGF1 alpha without CRCF. Intravenous infusion of PGI2 (0.1 microgram/kg/min.) completely abolished spontaneously and indomethacin-induced CRCF with a marked elevation of 6-keto-PGF1 alpha in the CS and Ao. Although OKY-1580, a TXA2 synthetase inhibitor, relieved spontaneously-evoked CRCF with a marked increase in 6-keto-PGF1 alpha and a slight reduction of TXB2, indomethacin-induced CRCF was not abolished by this agent. These results are consistent with the hypothesis that the reduction of endogenous PGI2 synthesis in the vascular wall is related to the occurrence of CRCF after partial constriction of coronary artery and indomethacin.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Biomimetic preparation and structure determination of QGI, one of the quinoline-DNA base adducts formed in cells treated with 4-nitroquinoline 1-oxide.

One of the quinoline-DNA base adducts, QGI, formed in cells treated with 4-nitroquinoline 1-oxide, was readily prepared in vitro from GMP or dGMP and 4-hydroxy-aminoquinoline 1-oxide in the presence of ATP, L-serine, and seryl tRNA synthetase. Synthetic seryl-AMP could be substituted for the enzymatic activation system for QGI formation. Chemical and spectral analyses of the adduct thus prepared revealed that QGI can be formulated as N4-(guan-8-yl)-4-aminoquinoline 1-oxide, the structure of which is identical with the modified base structure involved in the deoxyguanosine-quinoline adduct, dGIII (nomenclature of Loucheux-Lefebvre et al.) obtained by the chemical modification of deoxyguanosine with monoacetyl and diacetyl derivatives of 4HAQO.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1984

Arrest of DNA elongation by DNA polymerases at guanine adducts on 4-hydroxyaminoquinoline 1-oxide-modified DNA template.

In vitro modification of M13 phage single-stranded DNA with 4-hydroxyaminoquinoline 1-oxide (4HAQO) resulted in four kinds of adducts: three guanine adducts, QGI, QGII, and QGIII; and one adenine adduct, QA, at ratios of 16.4 47.3, 13.7, and 22.6, respectively. The carcinogen-modified DNA, initiated with a sequence-defined oligodeoxynucleotide primer, was replicated in vitro with Escherichia coli DNA polymerase I (Klenow fragment) and calf thymus DNA polymerases alpha and beta. The reaction products were analyzed on a DNA-sequencing gel. DNA elongation by DNA polymerase I was arrested at putative guanine adducts on the template in three ways: at one base prior to guanine; at positions opposite to guanine; and at one base beyond guanine. Similar patterns of elongation arrest were also obtained with the mammalian DNA polymerases alpha and beta. In contrast to guanine adducts, the adenine adduct, QA, might lack the capacity to arrest DNA chain elongation by DNA polymerases.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1984

[Autofluorescence of gastric cancer--study by flow cytometry].

Autofluorescence from cancer cells and non-cancerous cells of the stomach was measured by flow cytometry. The number of cells with fluorescence and its intensity was higher in cancer than in the surrounding mucosa. Preliminary results suggest that, if fluorescence emission from non-cellular substances is eliminated, measurement of fluorescence excited by laser illumination would permit earlier detection of gastric cancer.

Aged↗