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Biomedical subjects

N Yoshimi

Publications and source records attributed to N Yoshimi.

At least 145 records · Page 8Linked to original sources
PubMed1988

Minute esophageal granular cell tumor: a case report with immunohistochemical and ultrastructural examination.

A small granular cell tumor (GCT) of the esophagus, which developed in a 44-year-old Japanese man and was removed by endoscopic polypectomy, is presented. Histopathologically, the tumor, located in the submucosa, was composed of uniform neoplastic cells with nuclei and abundant round or oval cytoplasm containing eosinophilic granules. An immunohistochemical examination showed positive reactions with S-100 protein, especially the beta subunit, and neuron specific enolase in the neoplastic cells. Electron microscopic observation revealed abundant electron-dense or light granules and myelin-like structures in the cytoplasm. These findings support the concept that esophageal GCT is derived from Schwann cells.

Adult↗
PubMed1988

[A study on the DNA histogram pattern of hepatocellular carcinoma--application of a high resolution analytical system using a charge couple device (CCD)].

In 25 cases of primary hepatocellular carcinomas, the relationships between clinical, pathological features and DNA histogram patterns were investigated. Nuclear DNA histogram that represents cell cycle and indicates biological malignancy of carcinoma was analyzed by rapid image sensor analytical system scanning enable to measure the density, area and perimeter of nuclei even on thin tissue sections. Histograms of over 65 years old patients showed low ploidy pattern rather than that of less than 65 patients whose AFP values are over 1000 ng/ml showed statistically higher ploidy pattern compared to those of under 10 ng/ml. No significant relations were verified between pathological findings and DNA histogram patterns. But patients who died within 18 months after hepatectomy showed broad and high ploidy histogram patterns compared to patients who lived over 18 months. These results suggested that DNA histogram analysis is useful for evaluate the biological malignancy of primary hepatocellular carcinoma.

Adult↗
PubMed1988

A case of double cancer (pancreatic and ovarian adenocarcinomas) diagnosed by exfoliative and fine needle aspiration cytology.

A case of double cancer (pancreatic and ovarian adenocarcinomas) in a woman suggested by exfoliative and fine needle aspiration (FNA) cytology is reported. Exfoliative cytology, including immunohistochemical findings of the biliary juice and those of clinical image examinations indicated tubular adenocarcinoma of the pancreatic body. FNA cytologic findings with immunohistochemical observation and those of ultrasound examination showed mucinous adenocarcinoma of the right ovary. As a rare event, pancreatic cancer metastasized to ovarian carcinoma.

Adenocarcinoma↗
PubMed1987

Genotoxicity of a variety of nitroarenes and other nitro compounds in DNA-repair tests with rat and mouse hepatocytes.

Genotoxicity of a variety of nitroarenes and other compounds was examined in DNA-repair tests with rat or mouse hepatocytes. Out of 15 nitroarenes tested, 9 compounds, i.e., 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene, 1-nitro-3-acetoxypyrene, 3-nitrofluoranthene, 2-nitrofluorene, 2,7-di-nitrofluorene and 5-nitroacenaphthene elicited positive response of DNA repair in the tests with rat and mouse hepatocytes. Among the positive chemicals, the DNA-repair level of the 3 dinitropyrene isomers was much higher than other nitroarenes. The results indicate that a number of nitroarenes are metabolically activated in the primary culture of rodent hepatocytes, and suggest potential carcinogenicity of 1-nitropyrene and 1-nitro-3-acetoxypyrene the carcinogenicity of which is either not clear or unknown. Of the other nitro compounds, 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide as well as 4-nitroquinoline 1-oxide were clearly genotoxic in the assays with hepatocytes of both species. However, 5-nitro-2-furaldehyde semicarbazone was negative in both assays with hepatocytes of 2 species.

Animals↗
PubMed1987

Genotoxicity of a variety of nitroarenes in DNA repair tests with human hepatocytes.

The genotoxicities of 8 nitroarenes, i.e., 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene, 2,7-dinitrofluorene, 3-nitrofluoranthene, 1-nitro-3-hydroxypyrene and 1-nitro-3-acetoxypyrene, were examined in DNA repair tests using human isolated hepatocytes. Out of the tested nitroarenes, 5 compounds, i.e., 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene and 1-nitro-3-acetoxypyrene, clearly elicited positive responses of DNA repair. Among the chemicals which elicited positive responses, the levels of unscheduled DNA synthesis induced by the three dinitropyrene isomers were much higher than those of the other nitroarenes. Three chemicals, i.e., 2,7-dinitrofluorene, 3-nitrofluoranthene and 1-nitro-3-hydroxypyrene, elicited negative responses. The negative responses of 2,7-dinitrofluorene and 3-nitrofluoranthene, which had been positive in DNA repair tests with rodent hepatocytes, suggest some species differences between humans and rats in the metabolic activity of hepatocytes toward these agents.

Carcinogens↗
PubMed1986

Genotoxicity in the hepatocyte/DNA repair test and toxicity to liver mitochondria of 1-hydroxyanthraquinone and several dihydroxyanthraquinones.

1-Hydroxyanthraquinone and dihydroxyanthraquinones (alizarin, quinizarin, anthrarufin and chrysazin) were examined for genotoxicity in the hepatocyte/DNA repair test and for effects on oxidative phosphorylation in isolated rat liver mitochondria. Of the anthraquinone compounds tested, 1-hydroxyanthraquinone and 1,8-dihydroxyanthraquinone (chrysazin) induced DNA repair synthesis in rat hepatocytes, indicating their genotoxic activity. Only 1,2-dihydroxyanthraquinone (alizarin) exerted an uncoupling and inhibitory effect on mitochondrial respiration. The possible relationships of the genotoxic potencies and the uncoupling activities of these anthraquinones to their chemical structures are discussed.

Animals↗
PubMed1986

Genotoxic effects of a variety of sterigmatocystin-related compounds in the hepatocyte/DNA-repair test and the Salmonella microsome assay.

The genotoxicity and mutagenicity of 11 fungal metabolites structurally related to sterigmatocystin were examined in the hepatocyte primary culture/DNA-repair test and the Salmonella microsome assay. 10 out of the mycotoxins, i.e. dihydrosterigmatocystin, 5-methoxysterigmatocystin, 5-methoxydihydrosterigmatocystin, 5,6-dimethoxysterigmatocystin, 5,6-dimethoxydihydrosterigmatocystin, sterigmatin, O-methylsterigmatocystin and O-acetylsterigmatocystin showed a positive response for DNA repair, suggesting their carcinogenic potency. 5-Methoxysterigmatocystin, 5,6-dimethoxysterigmatocystin demethylsterigmatocystin and O-acetylsterigmatocystin were mutagenic in TA100 of the bacterial mutagenicity assay with liver S9.

Acetylation↗
PubMed1986

Genotoxicity of a variety of azobenzene and aminoazobenzene compounds in the hepatocyte/DNA repair test and the Salmonella/mutagenicity test.

Genotoxicity of 39 azo dye compounds of azobenzenes, aminoazobenzenes, and diaminoazobenzenes was examined in the hepatocyte primary culture/DNA repair test. Azobenzene (AzB) and 3,3'- or 4,4'-substituted azobenzenes such as (CH3)2AzB, (CH2OH)2AzB, (CH2OCOCH3)2AzB, and (CH2Cl)2AzB did not generate DNA repair, indicating lack of genotoxicity of these compounds. In contrast, all of 24 aminoazobenzenes, including those of unknown carcinogenicity, i.e., 3'-methyl-4-aminoazobenzene, 3'-CH2OH-aminoazobenzene, 3'-hydroxymethyl-N-methyl-4-aminoazobenzene, 3'-COOH-methylaminoazobenzene, 4'-formyl-N,N-dimethyl-4-aminoazobenzene, 3'-CH2Cl-dimethylaminoazobenzene, 4'-CH2Cl-dimethylaminoazobenzene, and 2'-, 3'-, or 4'-CH2OCOCH3-dimethylaminoazobenzene, elicited DNA repair synthesis. A positive DNA repair response was obtained for the 3 of 6 tested diaminoazobenzenes, i.e., N'-acetyl-N'-methyl-4-amino-dimethylaminoazobenzene, N'-acetyl-N'-methyl-4-amino-methylaminoazobenzene, and N'-acetyl-N'-methyl-4-amino-N-acetyl-methylaminoazobenzene, which are known to be carcinogenic. These results indicate that the amino group is functional for the expression of genotoxicity of azobenzene compounds. Twenty-one azobenzenes of these 3 classes were also examined for their mutagenicity in the Salmonella/mutagenicity assay. These results were almost identical with those of the DNA repair test except for several azo dyes such as AzB and 4,4'-(CH2Oacetyl)2AzB of the azobenzenes and N'-acetyl-4-amino-dimethylaminoazobenzene and N'-acetyl-N-methyl-4-amino-N-acetyl methylaminoazobenzene of the diaminoazobenzenes.

Animals↗
PubMed1986

Carcinogenicity of chrysazin in large intestine and liver of mice.

The carcinogenicity of chrysazin (1,8-dihydroxy-9,10-anthracenedione) was examined by dietary administration to C3H/HeN mice. All of the effective mice (17) which were given 0.2% chrysazin diet and which survived more than 500 days developed adenomatous hyperplasia with cystic glands of the cecum. Similar lesions were also seen in the colon of mice in this group. These intestinal lesions were not obtained in any effective mouse (19) of the control group. The incidence of hepatocellular carcinoma of mice given chrysazin (4/17) was significantly higher than that of the controls (0/19). These results indicate that chrysazin is carcinogenic in mice as well as in rats. Some mechanistic aspects of the causation of these intestinal lesions and liver neoplasms are also discussed.

Animals↗
PubMed1985

Genotoxicity of carcinogenic N-nitrosopropylamine derivatives in the hepatocyte primary culture/DNA-repair test.

The genotoxicity of N-nitrosodipropylamine, 8 of its oxidized derivatives and N-nitroso-2,6-dimethylmorpholine was examined in the hepatocyte primary culture (HPC)/DNA repair test. Nine N-nitrosamines which are known to be carcinogenic and mutagenic were clearly positive in the HPC/DNA-repair test. N-Nitroso(2,3-dihydroxypropyl) (2-hydroxypropyl)amine did not elicit DNA repair, but showed a borderline mutagenic response in the Salmonella/microsome test. Thus, the HPC/DNA-repair test displays a comparable capacity to the bacterial mutagenesis test for detecting the genotoxic effects of this class of carcinogens.

Animals↗
PubMed1985

Reduced DNA repair response of cells from carcinogen-induced rat liver altered foci exposed to chemical carcinogens in culture.

Cells were cultured from rat livers containing enzyme-altered foci induced by N-2-fluorenylacetamide and the level of DNA repair synthesis in response to several carcinogens was compared in gamma-glutamyl transpeptidase-positive foci cells and in enzyme-negative hepatocytes from the same livers. The level of unscheduled DNA synthesis elicited in foci cells by either the activation-dependent carcinogens N-2-fluorenylacetamide and diethylnitrosamine or the activation-independent carcinogens N-methyl-N'-nitro-N-nitrosoguanidine and 1-methyl-1-nitrosourea was significantly lower than that in hepatocytes. The results suggest that the repair of DNA damage by these altered cells is abnormal.

2-Acetylaminofluorene↗
PubMed1985

Genotoxicity of a variety of pyrrolizidine alkaloids in the hepatocyte primary culture-DNA repair test using rat, mouse, and hamster hepatocytes.

Seventeen pyrrolizidine alkaloids were studied with the hepatocyte primary culture-DNA repair test using rat hepatocytes. DNA repair synthesis was elicited by 15 alkaloids, including 11 of unknown carcinogenicity, i.e., senecionine, seneciphylline, jacobine, epoxyseneciphylline, senecicannabine, acetylfukinotoxin, syneilesine, dihydroclivorine, ligularidine, neoligularidine, and ligularizine. The positive results with these alkaloids of unknown carcinogenicity suggest that they are possibly genotoxic carcinogens. The two pyrrolizidine alkaloids that did not elicit DNA repair were retronecine which lacks a necic acid component and ligularinine which lacks the unsaturated double bond at the 1,2-position of the pyrrolizidine ring. Five pyrrolizidine alkaloids, retronecine, monocrotaline, seneciphylline, senkirkine, and clivorine, were also tested in the DNA repair test with hamster or mouse hepatocytes. These alkaloids, except retronecine, showed a positive response in the test with hamster hepatocytes, but in the test with mouse hepatocytes clivorine in addition to retronecine was also negative. The results indicate a species difference in liver bioactivation of pyrrolizidine alkaloids, implying that there could be species differences in their carcinogenic activities.

Animals↗
PubMed1984

A cytochemical study of lactic dehydrogenase (LDH) isoenzymes in human lung cancer.

The cytochemical and electrophoretic LDH isoenzyme patterns in cells from lung cancer tissues were examined with 2.6 M urea treatment and the correlation between the LDH isoenzyme pattern and histopathological entities of lung cancer was also studied. The zymograms of the nonlesional lung tissues indicated the main peak at LDH3, with the M/H ratio 0.74. In tumor tissues, epidermoid carcinoma, adenocarcinoma, and large cell carcinoma showed almost similar patterns of isoenzymes with LDH4 peak. Though small cell carcinomas had a peak at LDH3, they indicated lower activity of %LDH1 and %LDH2 than those in nonlesional lung tissues. Most of the tumor tissues showed a high M/H ratio, more than 1.0. In cytochemical stain for LDH, no inhibitory effect of urea treatment was seen in the nonlesional lung tissues. On the other hand, in the cells obtained from three types of lung cancer, except for small cell carcinoma, urea inhibition was noticed. Cytochemical stainability for LDH-M subunits corresponded well to the results of LDH zymogram. These results suggest that the LDH stain with urea treatment is a useful method for detecting malignancy in cytological specimens.

Adenocarcinoma↗
PubMedDate not supplied

Oxidized phosphatidylcholine in alveolar macrophages in idiopathic interstitial pneumonias.

It has been suggested that oxidative stress plays a pathogenic role in idiopathic interstitial pneumonias. Macrophage- or neutrophil-derived oxidants seem to be important sources of oxidative stress in this group of inflammatory disorders. Recent experimental studies have revealed that oxidative injury during inflammation or apoptosis can change phosphatidylcholine of cell membrane into its oxidized form, which serves as a ligand for macrophage scavenger receptor CD36. Recently, we developed a monoclonal antibody against oxidized phosphatidylcholine. Using this novel antibody, we performed an immunohistochemical investigation to clarify the localization of oxidized phosphatidylcholine in lung tissues of idiopathic interstitial pneumonias and a relationship between oxidized phosphatidylcholine localization and CD36 expression. Lung specimens obtained from patients with desquamative (n = 8) or usual interstitial pneumonia (n = 15) were studied. Thirteen normal lung tissues were also examined as controls. Antibodies against oxidized phosphatidylcholine, CD36, epithelial cells, macrophages, and neutrophils were used as primary antibodies. The positive cell number was counted by computer-aided morphometry. While there were no oxidized phosphatidylcholine-positive cells in normal lungs, lungs of desquamative or usual interstitial pneumonia contained large numbers of oxidized phosphatidylcholine-positive cells in the alveolar spaces. Double-staining analysis revealed that most oxidized phosphatidylcholine-positive cells were macrophages. The oxidized phosphatidylcholine-positive cells were increased in association with the increase in the densities of macrophages (Rs = 0.87, p < 0.0001) and neutrophils (Rs = 0.89, p < 0.0001). Accumulated macrophages also showed distinct CD36 expression. These findings suggest that oxidative stress and the related product, oxidized phosphatidylcholine, play an important role in the pathophysiology of idiopathic interstitial pneumonias.

Aged↗
PubMedDate not supplied

Application of telomerase activity for screening of primary lung cancer in broncho-alveolar lavage fluid.

Telomerase is a ribonucleoprotein that synthesizes telomeric DNA onto chromosomal ends using an RNA component as a template. Extension of telomeric repeats by telomerase prevents telomere shortening with cell divisions and contributes to chromosomal stability, possibly leading to immortalization of the cells. In the present study, we used a telomerase assay to detect primary lung cancer in broncho-alveolar lavage fluid (BALF). A total of 58 BALF samples were examined by telometric repeat amplication protocol assay. Thirty-five (29 cancers, 2 salcoidoses, 2 pulmonary tuberculoses and 2 normal samples) of 58 (60.3%) cases were found to be positive for telomerase activity. The sensitivity of telomerase activity was 78.4%, compared with 64.7% of BALF cytology. Among 37 primary lung cancer patients diagnosed histopathologically, 24 had positive cytology and 29 had positive telomerase activity. The number increased to 32 patients when cytodiagnosis and telomerase activity were considered. Of patients in whom the presence of primary lung cancer was strongly suspected clinically, although there was no histopathological evidence, two were telomerase-positive, initially diagnosed as normal by cytological examination and histological examination but finally diagnosed as primary lung cancer (adenocarcinoma) in subsequent histological examination using operation specimens. These findings suggest that telomerase assay using BALF samples might be a useful screening method for primary lung cancer especially when combined with BALF cytology.

Aged↗