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Biomedical subjects

T Takano

Publications and source records attributed to T Takano.

At least 685 records · Page 38Linked to original sources
PubMed1980

The effects of various chemicals on the development of hyperplastic liver nodules in hepatectomized rats treated with N-nitrosodiethylamine or N-2-fluorenylacetamide.

The effects of various hepatocarcinogenic, non-hepatocarcinogenic and non-carcinogenic chemicals on the induction of hyperplastic liver nodules by N-nitrosodiethylamine (DEN) or N-2-fluorenylacetamide (2-FAA) as an initiator were studied in male Fischer 344 rats. Rats were injected intraperitoneally with 200 mg of DEN/kg body weight or were fed on basal diet containing 200 ppm of 2-FAA for 2 weeks, and then given various test chemicals starting from week 3. They were also partially hepatectomized in week 3. All animals were killed at the end of week 8 and examined histologically. For quantitative analysis, hyperplastic nodules in the liver were measured with a color video image processor, VIP-21C. The effect of various chemicals in rats treated with DEN or with 2-FAA were compared. The production of hyperplastic liver nodules was greatest in rats treated with strong hepatocarcinogens, and less in rats treated with weak hepatocarcinogens. Very few hyperplastic nodules were produced after treatment with non-hepatocarcinogens or noncarcinogens. Hyperplastic nodules were formed in rats treated with phenobarbital, which is a hepatopromoter. Saccharin, which is a urinary bladder promoter, did not enhance the production of hyperplastic nodules in the liver. These results indicate that many hepatocarcinogens enhance liver carcinogenesis. The classification of chemicals as liver carcinogens is discussed on the basis of the results.

2-Acetylaminofluorene↗
PubMed1980

Effect of hyperbaric oxygen on cyanide intoxication: in situ changes in intracellular oxidation reduction.

To evaluate the efficacy of hyperbaric oxygen on cyanide intoxication, changes in the intracellular oxidation-reduction state of the renal cortex were observed in situ in 16 New Zealand white rabbits by detecting the reduced pyridine nucleotide fluorescence that represents the degree of cyanide blockade of the respiratory chain. The data indicated that 100% oxygen at 2 ATA exerted both prophylactic and therapeutic antagonistic effects on the cyanide poisoning. Administration of hyperbaric oxygen could constitute a significant treatment if proper chemical treatment is carried out concomitantly.

Animals↗
PubMed1979

Mutagenic activity of selenium compounds.

The mutagenicities of selenate (SeO2/4-) and selenite (SeO2/3-) were determined by two bacterial assay systems: Kada's rec-assay and Ames's Salmonella test. In both assays, these compounds were found to be weak mutagens. In the Salmonella test, selenate (0.05 revertants/nmole) and selenite (0.2 revertants/nmole) gave rise to base-pair substitution.

Bacillus subtilis↗
PubMed1979

Evidence for bactericidal activity of polymorphonuclear leukocytes without phagocytosis.

The relationship between phagocytosis and bactericidal action of polymorphonuclear leukocytes was examined by comparing the functions of cytochalasin D-treated leukocytes with those of the control. Measurement of phagocytotic and bacterial DNA-degrading activities using Escherichia coli prelabeled with [3H]thymidine revealed that phagocytosis and bacterial DNA degradation were inhibited by treatment with cytochalasin D to about 50 and 10% of the control, respectively. Nevertheless, the bactericidal activity of the cytochalasin D-treated leukocytes was almost the same as that of the control leukocytes; almost all the bacteria were phagocytized by the latter leukocytes. Under the same experimental conditions, the production and release of superoxide anions and hydrogen peroxide, which are both known to be involved in the bactericidal action of the leukocytes, were markedly increased by cytochalasin D. Release of several lysosomal hydrolases was also increased markedly by cytochalasin D treatment, except for myeloperoxidase. However, lactate dehydrogenase, a typical cytosolic marker, was not released by the same treatment. Thus, it is unlikely that the increase in the release of the above-mentioned bactericidal factors was due to decomposition of the leukocytes. These results indicate that the site of bactericidal action of cytochalasin D-treated leukocytes is not necessarily intracellular but may be around the external surface of the cells.

Animals↗
PubMed1979

Fatty acid composition of cholesteryl esters in cholesterol-fed rabbits treated with lipid-lowering agent (ethyl 2-(p-chlorophenoxy) isobutyrate).

Regression mechanism of Ethyl 2-(p-chlorophenoxy) isobutyrate (CPIB) in the arterial wall was studied for elucidation in terms of fatty acid-compositional change in cholesterol-fed rabbits. The following evidence was obtained: (1) The amount of cholesterol and cholesteryl ester in the atheromatous aorta were reduced after CPIB treatment. (2) CPIB resulted in a significant increase in the ratio of linoleate to oleate in both the arterial wall and serum after withdrawal of the cholesterol diet. It is suggested that there is a preferential hydrolysis of linoleate-rich cholesteryl ester in both the arterial wall and the serum.

Animals↗
PubMed1979

Changes in blood level of kininogen, prostaglandin E and hemodynamics during experimental acute myocardial ischemia with and without FOY-007.

Changes in kininogen, prostaglandin E and hemodynamics were studied during 2 hours after left anterior descending artery ligation in 19 anesthetized dogs with and without FOY-007, an inhibitor of kinin forming enzyme. Significant decrease in kininogen in aorta and great cardiac vein (aorta greater than great cardiac vein) and increase in prostaglandin E in great cardiac vein were observed after ligation, indicating release of kinin and prostaglandin E from ischemic area. Both kininogen and prostaglandin E changes were inhibited by FOY-007 but further decrease in cardiac output and increase in systemic vascular resistance were observed. In summary, myocardial release of both kinin and prostaglandin E was inhibited by FOY-007, with increase of afterload of the heart.

Animals↗
PubMed1978

Cardiac arrhythmias associated with treadmill claudication testing.

Eighty-one consecutive patients of an average age of 58 years with suspected lower limb arterial disease underwent standard 5-minute treadmill claudication testing. Prior to, during, and after testing the patients were monitored electrocardiographically. The number of electrocardiographic abnormalities seen in 81 patients undergoing study increased from 33 (40.6%) at rest to 49 (60.5%) with exercise. The commonest abnormalities encountered with exercise were the development and increased incidence of paroxysmal beats and ST-T wave changes which, in some instances, became life-threatening, aborting the test. Since the principal hazard for patients with claudication appears to derive from an increase propensity to cardiac mortality and morbidity, rather than from the consequences of impaired circulation to the limb, electrocardiographic monitoring during treadmill claudication testing, though little practiced, is strongly advised.

Adolescent↗
PubMed1977

Mechanism of defective lysogenization by phage P1 in a lon-mutant of Escherichia coli K-12.

Phage P1 cannot lysogenize a lon- mutant of Escherichia coli K-12, which is defective in the regulation of cellular division cycle to result in snake formation (14). P1 mutants, called P1pla, can lysogenize the lon- host. These mutations have been classified into two complementation groups: one is cis-dominant; the other is trans-dominant. A temperature-sensitive lon- mutant was isolated, which exhibited the lon- phenotype at 42 C but not at 33 C. A temperature-shift experiment of the P1-lysogenic derivative of the lon- ts mutant showed lysis of the culture and induction of the phage production. It is proposed that P1 plasmid may be under a certain regulatory circuit of the division cycle of the host bacterium by indirectly regulating the production of P1 immune repressor, or alternatively by directly derepressing the functions of P1 prophage.

Cell Division↗