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Biomedical subjects

M Enomoto

Publications and source records attributed to M Enomoto.

At least 127 records · Page 7Linked to original sources
PubMed1988

Intracellular transport of cholesteryl esters from lysosomes to cytoplasm in macrophages.

The mechanism through which nonmembranous lipid inclusion bodies consisting of cholesteryl esters accumulate in the cytoplasm was studied. Most lipid inclusion bodies in macrophages after 24 h incubation with anisotropic cholesteryl oleate liquid crystals were surrounded by a limiting membrane. The limiting membrane, however, could not be observed after further incubation for 48 h in the presence of esterastin, which is known to be an inhibitor of lipase and esterase. Under these conditions, the levels of hydrolysis and re-esterification of cholesteryl esters were less than 15% and 5% of the control ones, respectively. These results suggest that the inclusion bodies were transferred from lysosomes to the cytoplasm, with partial hydrolysis of cholesteryl esters, in addition to through the pathway via microsomes.

Animals↗
PubMed1988

An autopsy case of histiocytic medullary reticulosis presenting with marked hepatosplenomegaly for 13 years before the onset.

A 32-year-old male was hospitalized with high fever, pancytopenia and hepatosplenomegaly. No atypical cells were found in the peripheral blood. Bone marrow aspiration resulted in dry taps. Superficial lymph node swelling was not observed. He had been treated twice for high fever, hepatosplenomegaly and leukopenia that were very similar to the present illness, 13 and 3 years before the onset and hepatosplenomegaly had been noted by the patient for 13 years. The patient died after a rapid course of 20 days. Histiocytic medullary reticulosis (HMR) was diagnosed at the autopsy, which revealed atypical histiocytic infiltration showing erythrophagocytosis in the liver, spleen, left adrenal, and mesenterial and pulmonary hilar lymph nodes. This patient had shown the same clinical signs and hepatosplenomegaly 13 years before the onset of HMR, which suggest a possible latent stage and acute exacerbation of HMR.

Adult↗
PubMed1987

Transformation of macrophages into foam cells in vitro induced by cholesteryl oleate liquid crystals.

Transformation of macrophages into foam cells after the uptake of cholesteryl oleate anisotropic liquid crystals was studied. A new technique to enhance the uptake of the liquid crystals by macrophages using an inverted petri dish was developed. Uptake of lipid droplets was found to increase in parallel with the amount of liquid crystals in the medium. A lysosomal enzyme was shown (by using lysosomotropic chloroquine) to be involved in the hydrolysis of the liquid crystals. About 47 and 72% of the [3H]cholesterol in liquid crystal-laden cells had disappeared after chase for 24 and 48 h, respectively. Thus the 50% clearance time of the liquid crystals by the macrophages was about 24 h, which was longer than that of denatured lipoprotein. A possible model of transformation of macrophages to foam cells is discussed.

Animals↗
PubMed1987

Gross and microscopic characteristics of liver lesions induced by direct injection of pentobarbital sodium into rats.

The hepatotoxic effects of anesthetics brought about by their faulty intraperitoneal application was investigated. Using a syringe with a 26G needle, we injected 0.05 ml/rat of a 50 mg/ml solution of pentobarbital sodium directly into the livers of Sprague-Dawley rats. The animals were killed at 15, 30, or 45 minutes after injection. Massive hemorrhagic necrosis of the liver was seen in all animals injected, while focal necrosis accompanied by inflammatory cell infiltration was observed in the rats killed at 30 and 45 minutes after injection. The histological characteristics of these liver lesions were composed of three types, namely, massive hemorrhagic necrosis, focal cell infiltration separate from the necrosis, and focal necrosis with inflammatory cell infiltration. The infiltrates were composed of both neutrophils and lymphocytes. The characteristic liver lesions closely resembled the hepatic lesions produced by captopril (Helliwel et al., 1985), cyclopiazonic acid (Morrissey et al., 1985), as well as spontaneous liver lesions. The study of serum transaminase levels showed that the elevation of both SGPT and SGOT activities was correlated with the time after injection. Also, a significant increase in the total bilirubin level was noted in all animals treated.

Alanine Transaminase↗
PubMed1987

A factor in conditioned medium of rabbit costal chondrocytes inhibits the proliferation of cultured endothelial cells and angiogenesis induced by B16 melanoma: its relation with cartilage-derived anti-tumor factor (CATF).

Serum-free medium conditioned by exposure to rabbit costal chondrocytes in culture inhibited the proliferation and DNA synthesis of bovine pulmonary endothelial cells in culture. The factor in conditioned medium did not inhibit DNA synthesis in B16 melanoma cells, L1210 cells or 3T3 fibroblasts in culture, but it inhibited angiogenesis in the chorioallantoic membrane of chick embryos induced by B16 melanoma and growth of the tumor transplanted onto the membrane. These findings strongly suggest that rabbit costal chondrocytes produce an anti-angiogenesis factor that is similar to cartilage-derived anti-tumor factor (CATF).

Angiogenesis Inhibitors↗
PubMed1986

A naturally occurring large chromosomal inversion in Escherichia coli K12.

Strain 1485IN and its derivatives were found to have a large inversion extending to about 35% of the chromosome. Because of this, the question arose as to whether 1485IN had arisen from an Escherichia coli strain other than K12. However, 1485IN had a flagellar antigen and a restriction-modification system indistinguishable from those of W3110, a major line of K12, and had retained an amber suppressor and lambda sensitivity that are characteristics of W1485 from which this strain seems to have arisen. Strain 1485IN had acquired proline auxotrophy, but showed the same growth rate as W1485 in nutrient broth at 37 degrees C. Interrupted matings with Hfr strains of 1485IN revealed a gene arrangement of nalA-gal-trp-his-lac-proA-thrleu-ilv, in which gal, trp, and his were on the inverted segment. The termini of the inversion were inferred to be situated between tsx (9.5 min) and purE (12 min) and between his (44 min) and cdd (46.5 min).

Chromosome Inversion↗
PubMed1986

Magnesium-dependent plaque formation by bacteriophage P1cinC(-) on Escherichia coli C and Shigella sonnei.

Phage P1C(-), in a state of the phage not infective to Escherichia coli K12, was able to form plaques on a wild-type strain of E. coli C and on Shigella sonnei in the presence of Mg2+. Citrobacter freundii, Enterobacter aerogenes, and a Salmonella typhimurium galE mutant were not lysed by, but were lysogenized with P1cinC(-), whereas Klebsiella pneumoniae, Proteus rettgeri, and S. typhimurium LT2 were not susceptible to either P1cinC(-) or P1cinC(+). The lipopolysaccharide structure of E. coli C and Sh. sonnei is discussed with reference to receptors for P1cinC(-) and P1cinC(+).

Bacteriophages↗
PubMed1986

Comparison of inhibition by a tumor promoter (12-O-tetradecanoylphorbol-13-acetate) of expression of the differentiated phenotype of chondrocytes in rabbit costal chondrocytes in culture with inhibition by retinoic acid.

Both retinoids and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibit expression of the differentiated phenotype by rabbit costal chondrocytes in culture, as judged by morphological changes and decreased sulfation of glycosaminoglycans (GAG). However, the inhibition of the differentiated phenotype of chondrocytes in TPA-treated cells is restored by parathyroid hormone (PTH), while the inhibition by retinoids is not [Takigawa et al. (1982) Mol. Cell. Biochem. 42, 145-153; Takigawa et al. (1983) Cell Differ. 13, 283-291]. In the present study, we examined the difference between TPA-treated chondrocytes and retinoic acid-treated chondrocytes to determine the mechanism of the restoration of the differentiated phenotype in de-differentiated cells treated with TPA. PTH increased the activity of ornithine decarboxylase [ODC; EC 4.1.1.17], a rate limiting enzyme of polyamine biosynthesis, and proteoglycan synthesis in chondrocytes pretreated with TPA as well as in normal chondrocytes. The maximal stimulations of ODC activity and GAG synthesis were observed 4 h and 24-36 h, respectively, after addition of PTH. The dose-response curve for ODC induction by PTH was parallel to that of PTH-stimulated proteoglycan synthesis both in TPA-treated chondrocytes and in normal chondrocytes. PTH also increased the intracellular cyclic AMP level after 2 min in TPA-treated cells as in normal cells. Addition of dibutyryl cyclic AMP (DBcAMP) induced ODC and restored proteoglycan synthesis in TPA-treated cells. The dose-response curve for induction of ODC by DBcAMP was parallel to that of DBcAMP-stimulated proteoglycan synthesis in both TPA-treated chondrocytes and normal chondrocytes. On the other hand, the increases by PTH in the intracellular cyclic AMP level, ODC activity, and proteoglycan synthesis were inhibited in chondrocytes pretreated with a combination of TPA and retinoic acid as well as in those pretreated with retinoic acid alone. TPA stimulated the syntheses of DNA and RNA in chondrocytes but did not increase the cyclic AMP level or ODC activity. PTH and DBcAMP inhibited the syntheses of DNA and RNA both in TPA-treated cells and in normal cells. These results suggest that ODC induction mediated by elevation of cyclic AMP plays an important role in re-differentiation of de-differentiated cells pretreated with these agents.

Animals↗
PubMed1986

[Pathological study on nephrocalcinosis in Fischer 344/Du Crj rats].

Histopathological examinations on nephlocalcinosis of the Fischer 344 (F344) rats were carried out. As the results of comparison on its appearance among F344, Wistar and SD strains of rats, F344 female rats showed the most severe nephrocalcinosis. Nephrocalcinosis developed between 4 weeks and 8 weeks and was likely to keep its appearance through 108 weeks of the survival period of the rats. Histologically, mineral deposit was always observed at cortico-medullary junction. It seemed to locate at the outer portion of the basement membrane of the tubular epithelium, adjacent to the capillary wall in the connective tissue. Four weeks after ovariectomy at 4 weeks of age, the rats showed a decrease in degree of nephrocalcinosis. In contrary, the rats treated with estorone following ovariectomy revealed an increase in degree of nephrocalcinosis. It was suggested that the oestrogen-type sex hormone appeared to give a role in nephlocalcinosis.

Animals↗
PubMed1986

The effect of ubenimex on N-methyl-N'-nitro-N-nitrosoguanidine-induced stomach tumor in rats.

The effect of ubenimex on the progression of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced stomach tumor in rats was studied. Tumor induction was performed by giving MNNG via drinking water for 34 weeks. Ubenimex was ip administered twice a week at 0.5 mg/kg for 84 weeks in one group and 49 weeks in another starting from the first and 36th weeks after initiation of MNNG administration, respectively. The stomachs were endoscopically examined 2 times. At the 64th week after initiation of MNNG administration tumorous lesions were observed with about 70% of the rats in both ubenimex administration groups. In the ubenimex non-administration group nearly 90% of the rats had the lesions. After completion of ubenimex administration almost all the rats had the lesions in the three groups but the sizes were much smaller with the two ubenimex administration groups. Almost all of these lesions were histopathologically identified as tumorous. The tumor volume per rat in the two ubenimex administration groups from the 1 and 36th weeks was 21.0 and 19.2% of the volume in the control group, respectively. Tumor number per rat was similar among the three groups. The natural killer activity of rats was also examined after completion of the above experiment. The activity markedly increased when ubenimex was administered from the 36th week after initiation of MNNG administration. When ubenimex was administered from the first week, the activity did not increase demonstratively. From all the results described above we conclude that ubenimex exerts an inhibitory action against the progression of MNNG-induced stomach tumor in rats. Contribution of the increase of natural killer activity to ubenimex antitumor action may be dependent on schedule of ubenimex administration.

Animals↗
PubMed1985

Expression of an Escherichia coli flagellin gene, hag48, in the presence of a Salmonella H1-repressor.

An Escherichia coli K12 flagellin gene, hag48, was found to be expressed in the presence of the Salmonella rh1 gene product. The strains which had hag48 on a chromosome or on an F' factor were constructed from strains H2-e,n,xon-off rh1+ and fixed H2-e,n,xon rh1+ in which rh1+ is cotranscribed with H2 in its "on" state. Motility of these strains in semisolid medium was inhibited by anti-H48 serum and motile clones (swarms) that escaped from it were hag mutants in case of the hag48 e,n,xon-off strain tested. H48 flagellin was detected by electrophoresis, though its amount was less than e,n,x flagellin, from all the strains that were nonmotile in the presence of anti-H48 serum.

Bacterial Proteins↗