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Biomedical subjects

H Endo

Publications and source records attributed to H Endo.

At least 523 records · Page 29Linked to original sources
PubMed1980

Selective activation of diaphyseal chondrocytes by parathyroid hormone, calcitonin and N6,O2-dibutyryl adenosine 3',5'-cyclic monophosphoric acid in proteoglycan synthesis of chick embryonic femur cultivated in vitro.

We have found that the developmental stage of chondrocytes in the chick embryo femur is sensitive to the action of PTH, CT and dibutyryl cyclic AMP in stimulating proteoglycan synthesis as estimated by the incorporation of radioactive inorganic sulfate. PTH treatment of the cartilage resulted in dramatic stimulation of the proteoglycan synthesis in the diaphysis, which is composed of rather old non-dividing hypertrophied chondrocytes with much lower proteoglycan-synthesizing activity than younger dividing cells in the epiphysis and metaphysis. No or slight stimulation was observed the epiphysis and metaphysis. Dibutyryl cyclic AMP produced much the same effect. CT also stimulated the proteoglycan synthesis only in the diaphysis but the stimulation was less potent (133% of control) than PTH (650% of control) or dibutyryl cyclic AMP (625% of control). The hormones and dibutyryl cyclic AMP, therefore, seem to activate the proteoglycan synthesis specifically in rather old chondrocytes of the diaphysis. A synergistic effect of PTH and CT suggesting a different stimulating mechanism was observed in the diaphysis.

Animals↗
PubMed1980

Formation of a transplacental mutagen, 1,3-Di(4-sulfamoylphenyl)triazene, from sodium nitrite and sulfanilamide in human gastric juice and in the stomachs of hamsters.

1,3-Di(4-sulfamoylphenyl)triazene was abundantly produced by incubation of sulfanilamide (SA) and NaNO2 in human gastric juice. This reaction also occurred in acetate buffer (pH approximately 4) at 37 degrees C as well as in hydrochloric acid (pH < 1) under ice cooling, with the product forming in almost the same amount. This phenomenon indicated the broad range of conditions under which the reaction occurs. The intragastric formation of this triazene was also demonstrated in Syrian golden hamsters by the concurrent administration of SA and NaNO2. Mutants resistant to 8-azaguanine were induced in a dose-dependent manner in the culture of embryo cells that were derived from pregnant hamsters 24 hours after ip injection of this triazene.

Animals↗
PubMed1979

Fulminant hepatic failure during remission from leukemia: three cases associated with massive liver cell necrosis and hepatitis B virus.

Three patients at various stages of remission from leukemia died following the development of massive liver necrosis within only 4-6 days. All had either hepatitis B surface antigen or antibody in their sera, and two of them experienced severe epigastric pain before the onset of liver injury. Hepatitis B surface antigen appeared in two of these patients after remission from leukemia. Serum gamma-globulin levels increased with decreasing doses of prednisolone and other antileukemic drugs, and hepatic cell necrosis occurred extensively. Localization of hepatitis B surface antigen in their livers revealed a strong positive reaction in the phagocytic cells. These observations strongly suggest that hepatitis B virus may be causally related to the fulminant hepatic failure at least in two of the reported leukemic patients.

Adolescent↗
PubMed1979

Biochemical and morphological study on hepatotoxicity of azathioprine in rat.

Sprague-Dawley rats given azathioprine in the diet for 3 to 4 weeks developed severe liver damage. Elevations of serum alkaline phosphatase and gamma-glutamyl transpeptidase activities were associated with increased hepatic glucose 6-phosphate dehydrogenase levels and decreased liver glucose 6-phosphatase activities, i.e., conditions which were commonly observed in various hepatotoxin-induced liver injuries. Light and electron microscopic observations revealed centrolobular necrosis with large scars and the proliferation of the mitochondria and rough endoplasmic reticulum. This model could be used to study the mechanisms of azathioprine-induced liver damage and its prevention.

Animals↗
PubMed1979

Formation of methylnitrosocyanamide from methylguanidine and sodium nitrite in simulated gastric juice and in stomachs of rats: quantitative estimation by a mutagenicity assay.

The formation of methylnitrosocyanamide (MNC), a carcionogenic N-nitroso compound, from methylguanidine (MG) and NaNO2 in simulated gastric juice (SGJ) and in the stomachs of rats was quantitatively investigated. With a reverse mutation assay in which a tester strain of Salmonella typhimurium was used, MNC formation was shown to increase linearly for about 40--60 minutes after the incubation of MG with NaNO2 in SGJ. However, it decreased rapidly thereafter. The initial rate of MNC formation was directly proportional to the initial molar ratio of MG to NaNO2, but the yields of MNC depended only on the amount of MG added and were fairly constant (0.3--0.5% of the initial MG). MNC did not form at a pH above 2.5 or in the presence of 2% casein in SGJ at pH 1.2. It decomposed rapidly in SGJ at pH 1.2 with a half-life of approximately 2 minutes, whereas it was stable in phosphate buffer at pH 7.0. Following concurrent administration of MG and NaNO2 via stomach tube, MNC formation was detected in the pylorus-ligated stomachs of rats preconditioned with a casein-free dextrin diet but not in those of rats preconditioned with a casein-containing or synthetic diet. The yields of MNC observed 40--60 minutes after administration of reactants ranged from 0.02 to 0.05% of the initial MG. The possible environment significance of MNC formation in vivo was considered.

Animals↗
PubMed1978

The synthesis and degradation of presumptive messenger RNA in cultured mouse leukemia cells during the inhibition of protein synthesis.

RNA synthesis in mouse leukemia L5178Y cells was inhibited depending upon the time of treatment by blasticidin S or by ricin, which inhibits specifically protein synthesis. When blasticidin S or ricin blocked protein synthesis by more than 90% of the control, marked accumulation of monosome was accompanied by the decrease of pulse-labeled RNA (20% of that in the control) in the polysomes and monosome fraction. The size distribution of pulse-labeled RNA among polysomal fractions including monosome obtained from the cells treated with either blasticidin S, ricin of L-asparaginase showed that the size of presumptive mRNA was shifted from 18 S to 9--10 S. TReatment of a blasticidin S-resistant (Bla-R) subline derived from L5178Y cells (Kuwano, M., Matsui, K., Takenaka, K., Akiyama, S. and Endo, H. (1977) Int. J. Cancer 20, 296--302) with L-asparaginase or ricin induced smaller size (9--10 S) RNA, but treatment of Bla-R cells with blasticidin S did not. Such shorter RNA fragments could not be observed even when cellular protein synthesis was inhibited by treatment for short time with blasticidin S (40--80% of the control activity). Smaller RNA fragments accumulated after drastic inhibition of protein synthesis were composed of 74% of polyadenylate sequence lacking poly(A)(-)RNA with peak of approx. 10 S and 26% of polyadenylate sequence containing poly(A)(+)RNA with a peak of 18 S, whereas cytoplasmic polysomal RNA of the control contained 46% poly(A)(+) with a peak of 18 S and 54% poly(A)(-)RNA with a 10--18 S peak. Cytoplasmic poly(A)(+)RNA degraded biphasically with half-lives of approx. 2 h and 8--10 h in exponentially growing mouse cells. However, in degradation of poly(A)(+)RNA molecules being formed in the cells pretreated with blasticidin S for 3 h, the rapid phase of decay with a half-life of approx. 2 h was interrupted by successively appearing poly(A)(+)RNA with a longer half-life of 8--10 h in cytoplasm. However, when the cells were pretreated with blasticidin S for 6 h, there appeared no poly(A)(+)RNA population with the rapid-decay in cytoplasm.

Animals↗
PubMed1978

An ultrastructural study of localized lymphangioma circumscriptum.

An electron microscopic study was performed on the lymphatic vessel (lv) of localized lymphangioma circumscriptum (Lc), which was found clinically typical but histologically not associated with hemangioma and inflammation. The lv of Lc was morphologically divided into two types. The first type was situated at the upper dermis of the lesion and the other, at the deep dermis. The former had certain similarities to lv of experimentally induced lymph-stasis, whereas the latter was morphologically similar to lv of the normal skin. From the findings of the present study and those reported in literature, Lc could not be considered as a mere benign overgrowth of lv, but as one of pathological results induced by a long-standing lymph-stasis.

Adult↗
PubMed1978

Mode of mutagenic action of 4-benzoylamido- and 4-acetamido-4-carboxamido-n(N-nitroso)-butylcyanamide.

The mode of mutagenic action of 4-benzoylamido- and 4-acetamido- 4-carboxamido-n(N-nitroso)-butylcyanamide (BCNBC, ACNBC) was studied using Escherichia coli K12 strains. The strains carrying defects in DNA-repair mechanism, AB2463 (recA) and P3478 (polA) were more sensitive than their parent strains to both compounds, while AB1886 (uvrA) showed the same sensitivity as the parental strain. About 90% of tryptophan revertants from BE1043 (trpambphoamb) by both compounds were due to mutation in suppressor genes. Suppressor analysis by using BE1047 (trpambphooch) revealed that the most frequently occurring reversion was due to a mutation in suppressor gene, supE. This implies that these two alkylnitrosocyanamides predominantly induce GC leads to AT transition.

DNA Repair↗
PubMed1978

Isolation and characterization of amphotericin B-resistant cell lines in Chinese hamster cells.

Amphotericin B is a polyene macrolide antibiotic which interacts specifically with sterols in mammalian cell membranes. Amphotericin B-resistant (AMBr) lines of stable phenotype have been isolated from cultured Chinese hamster (V79) cells. Three AMBr clones (AMBr-1, -2 and -3) isolated independently after treatment with nitrosoguanidine were resistant to greater than or equal to microgram/ml of the antibiotic, while DNA synthesis as well as the colony-forming ability of the parental V79 cells was blocked by greater than 80% of control in the presence of 20--50 microgram/ml amphotericin B. The AMBr cell line also exhibited increased resistance to other polyene macrolide antibiotics such as nystatin and pentamycin. Other agents, however, such as cytosine arabinoside or ricin, blocked DNA synthesis in AMBr cells to the same extent as in V79 cells. The amphotericin B resistance phenotype was stably retained even after AMBr cells were cultured in the absence of the drug for over 200 generations. The control of free cholesterol or its esters was significantly decreased in all three resistant clones. Furthermore, cholesterol synthesis from acetate as well as mevalonate was partly defective in AMBr cells, compared with that in V79 cells.

Amphotericin B↗