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Biomedical subjects

S Sugihara

Publications and source records attributed to S Sugihara.

At least 181 records · Page 10Linked to original sources
PubMed1983

Concurrent malignant lymphoma of the jejunum and multiple synchronous colon cancers.

This paper describes a unique case of combined malignant lymphoma of the jejunum and multiple synchronous carcinomas of colon and rectum. The jejunal tumor developed obstructive growth without regional lymph node involvement. Histologically, it was a malignant lymphoma corresponding to medium-sized cell type of follicular lymphoma, suggesting B cell origin in the bowel wall. In the colon and rectum, except for the transverse segment, there were three encircling, annular infiltrative tumors, and six polyps with malignant change. They developed independently, separated by an intact mucosa suggesting multiple synchronous cancers. Histologically they showed adenocarcinoma with or without mucus production, adenosquamous cell carcinoma, and villotubular adenocarcinoma. A case report is presented with a brief review of the incidence and pathogenesis of both jejunal and colonic tumors.

Adenocarcinoma↗
PubMed1976

Electron microscopic observations on the morphogenesis of renal cell carcinoma induced in rat kidney by dimethylnitrosamine and N-(3,5-dichlorophenyl)succinimide.

Renal cell carcinoma was induced in rats by p.o. administration of dimethylnitrosamine, 500 ppm daily, followed by N-(3,5-dichlorophenyl) succinimide (NDPS), 5000 ppm daily. Fine structural changes of the proximal convoluted tubule cells were observed by sequential examinations of the kidney cortices at 3, 5, 12, and 24 weeks after drug administration. Early prominent structural changes of the cells induced by dimethylnitrosamine alone were the appearance of microspherules in nucleoli and of numerous lamellar bodies on the membrane structure of the cells. With the addition of NDPS, the cells exhibited edematous cytoplasm that, in contrast to the relatively intact nuclear structure, contained numerous bodies small vesicles and dark mitochondria, with markedly disarranged microvilli. After prolonged treatment with these drugs, some of the cells showed regenerating features, while others became necrotic. In the former case, large clear nuclei appeared with enlarged nucleoli containing a large amount of granular components. Ribosomes in the cytoplasm also increased in number in accordance with nucleolar changes, and edema in cytoplasm and microvilli markedly decreased. However, a considerable number of vesicles still remained in some cells. Mitochondria decreased in number and showed pleomorphism and relatively high electron density. At 24 weeks, when clear cell carcinoma was induced, the cells in the cancer tissue exhibited a variety of features in their nuclei and cytoplasm. Some cells showed intact nuclear structure and dark cytoplasm containing a large number of vesicles; others had large round clear nuclei with enlarged nucleoli and clear cytoplasm containing no vesicles. Among these cells were mixed populations of large clear cells, showing a structure similar to the cells at 12 weeks, 2.e., to nodular hyperplastic cells. The starting point of malignant transformation seemed to be 1 week after treatment with NDPS (i.e., cells at 5 weeks) and, or the precancerous stage, at 12 weeks. These results suggest that the proximal convoluted tubule cells previously damaged by dimethylnitrosamine treatment were marked for mutation and were transformed to cancer cells by additional treatment with NDPS in such a way as to disturb the permeability of the membrane system of the cell and to condense chromatin fibers.

Adenocarcinoma↗
PubMed1976

Reversibility and irreversibility of liver tumors in mice induced by the alpha isomer of 1,2,3,4,5,6-hexachlorocyclohexane.

The characteristics of liver tumors in mice induced by the alpha isomer of 1,2,3,4,5,6-hexachlorocyclohexane (alpha-BHC), were studied with emphasis on their reversibility of irreversibility. Male 8-week-old DDY mice were fed basal diet supplemented with 500 ppm of alpha-BHC for 16, 20, 24, and 36 weeks and then were fed basal diet without alpha-BHC for 4, 8, 12, 16, 24, or 36 weeks. At various intervals, 13 to 20 mice were killed for light and electron microscopic observations. The incidences of liver tumors in mice induced by alpha-BHC increased progressively on continuous administration of alpha-BHC, but when its administration was discontinued some tumors disappeared. Histologically, after alpha-BHC administration for 24 weeks, most tumors were nodular hyperplasias, and there were only a few well-differentiated hepatocellular carcinomas. However, 60 or 72 weeks after the beginning of the experiment, most of the liver tumors were hepatocellular carcinomas and there were only a few nodular hyperplasias. At a later stage, 60 or 72 weeks, the liver parenchymal tissue in nontumorous areas was essentially normal, but small foci were occasionally seen in nontumorous areas that were composed of remaining hyperplastic nodular cells, phagocytic cells, Kupffer cells, and leukocytes. These findings suggest that the reversible tumors were usually nodular hyperplasias whereas the irreversible tumors were hepatocellular carcinomas. After alpha-BHC administration was stopped, many mesenchymal cells infiltrated the nodular hyperplastic lesions, and degenerated liver cells were found. These observations indicate that mesenchymal cell elements may be important in reversing the growth of liver tumors induced by alpha-BHC.

Animals↗
PubMed1976

Combination effect of citrinin and other chemicals on rat kidney tumorigenesis.

Histological studies were made on the nephrotoxic effect of citrinin on the kidneys of rats, with or without previous treatment with the nephrotoxic chemicals, N-(3,5-dichlorophenyl)succinimide (NDPS) and N-nitrosodimethylamine (DMN). Oral administration of 0.02% or 0.05% citrinin alone caused signs of kidney injury but did not induce kidney tumors. On treatment with DMN alone, 8 of 14 rats (57.1%) developed kidney tumors; two (14.3%) were renal cell tumors, eight (57.1%) embryonal cell tumors, and one (7.1%) hemangioendothelioma. On the other hand, kidney tumors developed in 18 of 19 rats (94.7%) and 13 of 15 rats (86.7%) by the administration of 0.02% and 0.05% citrinin, respectively, after DMN. The tumors in these two groups were diagnosed histologically as renal cell tumors in 18 (94.7%) in group IV and 13 (86.7%) in group III, and as embryonal cell tumors in 14 (73.7%) in group IV and 9 (60.0%) in group III. Thus, in groups treated with citrinin after DMN the incidence of renal cell tumors was much greater and the incidence of embryonal cell tumors slightly greater than in the group treated with DMN alone. Kidney tumors developed in 4 of 18 rats (22.2%) treated with 0.02% citrinin after NDPS, but treatment with NDPS alone did not induce kidney tumors. Thus, treatment with citrinin changes the histological type and incidence of kidney tumors in rats induced by DMN. Moreover, this study confirms that citrinin in combination with NDPS can induce kidney tumor in rats, which was renal cell tumor (adenoma) histologically.

Animals↗
PubMed1975

Pathologic analysis of chemical nephritis in rats induced by N-(3,5-dichlorophenyl)succinimide.

The effects of N-(3,5-dichlorophenyl)succinimide (NDPS) administration to rats were studied by blood chemical, histopathologic, histochemical, and ultrastructural examinations. Administration of 5000 p.p.m. of NDPS induced severe damage of the kidneys, but did not affect other organs. Administration of 2500 p.p.m. of NDPS had little effect, even on the kidneys. Chemical analysis of the blood showed that the urea nitrogen level increased with the increase in the period of NDPS administration. Histopathologic examination showed intensive cell infiltration, mainly of lymphocytes, into the renal interstitium after NDPS administration for only 4 weeks. After NDPS administration for 12 weeks or more, typical interstitial nephritis was observed. Histochemical analysis showed that after only 1 week various enzymatic activities in the proximal convoluted tubules were markedly decreased whereas their activities in the distal convoluted tubules were relatively well preserved for at least 4 weeks. These results indicate that NDPS predominantly attacked the proximal convoluted tubules. After 4 weeks, the most prominent ultrastructural changes were seen in the proximal convoluted tubules where the epithelial cells lost their polarity and had a very abnormal arrangement. These cells showed well developed, edematous microvilli, poorly developed basal infoldings, swollen mitochondria of various sizes, aggregated beta-type glycogen granules, and debris of erythrocytes. Development of the endoplasmic reticulum, Golgi complex, ribosomes, and lysosomes was poor in the cytoplasm. These investigations indicate that NDPS affects the function of the proximal convoluted tubules. NDPS is a selective nephrotoxic substance. That is, it initially damages the proximal convoluted tubules, and subsequently causes interstitial nephritis. It is suggested that nephritis induced by NDPS is useful as a model of interstitial nephritis in man.

Animals↗
PubMed1975

Development of hepatocellular carcinomas in rats treated with benzene hexachloride.

The effects of prolonged oral administration of the alpha-, beta-, and gamma-isomers of benzene hexachloride (BHC) on rat liver were examined histologically. Well-differentiated hepatocellular carcinomas were observed in the liver of rats fed a basal diet containing 1,500 or 1,000 parts per million (ppm) of alpha-BHC for 72 weeks. Many typical nodular hyperplasias developed in all groups given 1,500 or 1,000 ppm alpha-BHC. In non-neoplastic areas, slight oval cell infiltration and bile duct proliferation were seen. No neoplastic changes or other abnormal findings, such as oval cell infiltration, fatty changes, fibrosis, or bile duct proliferation of the liver, were observed in groups receiving 500 ppm alpha-, beta-, gamma-, or gamma-BHC.

Administration, Oral↗