[The contents of chronic subdural hematoma and its CT density, with special reference to differentiation from subdural hygroma].
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Biomedical subjects
Publications and source records attributed to J Sato.
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Primary mass cultures of isolated liver cells, which prepared from normal adult rat by a collagenase-liver-perfusion technique, were treated with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) to study the production of transformed liver cells. Enzymatically isolated liver cells had high sensitivity to 3'-Me-DAB in primary culture. By 2- or 6-day treatment, mature hepatocytes remarkably decreased in their numbers due to cytotoxic effect of 3-Me-DAB, but thereafter active proliferation of epithelial-like clear cells was observed. Six-day treatment induced epithelial-like clear cells with gross chromosomal abnormalities, although 2-day treatment failed to induce transformed cells. However, the transformed epithelial-like clear cells with chromosomal abnormalities were negative for gamma-glutamyl-transpeptidase (GGT).
Isolated liver cells, which were prepared from adult rats by a trypsin-liver-perfusion technique, were treated with dexamethasone or hydrocortisone at a concentration of 7.7 X 10(-6) M for 8 days in primary culture. The treated cultures displayed homogeneous population consisting of epithelial-like clear cells, while the untreated cultures displayed mixed population consisting of epithelial-like clear cells and fibroblast-like cells. The epithelial-like clear cells, which proliferated in the cultures treated with glucocorticoids for 8 days in primary culture, did not show any morphological changes following cultivation in glucocorticoid-free medium. After continuous glucocorticoid-treatment for more than 1 month, the treated cultures showed relatively low cell densities at confluence. The surface area of individual epithelial-like clear cells in the cultures treated with glucocorticoids for long periods of time was evidently greater than that in the cultures treated for only 8 days. The epithelial-like clear cells had glucose 6-phosphatase and tyrosine aminotransferase activities even though the levels of these enzyme-activities were very low compared with those in rat liver homogenates.
Serum alpha-fetoprotein (AFP) concentrations increased promptly 2 days following a single injection of DL-ethionine (ethionine) in adult female rats. Continuous elevation of serum AFP was also observed on feeding a diet containing 1% ethionine for at least 2-3 weeks. A rise of serum AFP was not found if the diet was supplemented with 2.8% methionine. Furthermore, in rats fed on 1% ethionine for 2 weeks, dietary change to the laboratory chow supplemented with and without 2.8% methionine produced a decrease of increased serum AFP levels.
The effect of 3' methyl-4-dimethylaminoazobenzene (3'-Me-DAB) in the induction of malignant transformation and of 8-azaguanine-resistant mutations and chromosomal aberrations was studied in a diploid strain derived from normal rat liver cells. The cells were malignantly transformed by treatment with 3'-Me-DAB 1.7 micrograms/ml for 130 to 221 d or 1.7 micrograms/ml for 53 d followed by 24.9 micrograms/ml for 27 to 77 d. The untreated control cells did not transform spontaneously until the 232nd d in culture. Some properties of the 3'-Me-DAB-treated cells were compared to those of untreated control cells but no reliable marker for predicting the tumorigenic potential of the cells was found. The single addition of 3'-Me-DAB caused little induction of 8-azaguanine-resistant mutations and chromosomal aberrations to the cells. However, mutations and chromosomal aberrations were significantly induced by N-acetoxy-4-methylaminoazobenzene, an active metabolite of 4-dimethylaminoazobenzene or 3'-Me-DAB in the presence of liver microsomes.
Erucic acid was incorporated into cardiac phosphatidylserine and hepatic and cardiac sphingomyelin of male Sprague-Dawley rat. The fatty acid compositions of mitochondrial and microsomal phospholipids were similar in both liver and heart. The effect of a low fat diet and a diet containing erucic acid on the fatty acid composition of mitochondrial and microsomal phospholipids was also similar, except for the effect on sphingomyelin. However, the diet containing erucic acid influenced the metabolism of phosphatidylcholine of the heart but not of the liver, indicating that the turnover of 1-stearoyl-2-arachidonoyl phosphatidylcholine in the heart was inhibited by the diet containing erucic acid. On the other hand, the proportion of erucic acid in the free fatty acid was higher in the heart than in the liver.
Bile acids in the spent medium for the cell culture were analyzed by gas-liquid chromatography and gas-liquid chromatography-mass spectrometry to determine whether human hepatoblastoma cell line could synthesize bile acids. Cholic, chenodeoxycholic, and lithocolic acids were found in the culture medium, and a portion of chenodeoxycholic acid and all of lithocholic acid were sulfated. Since the cells had been cultured in serum-free medium, it is clear that the bile acids were newly synthesized and sulfated by the cultured cells. Chenodeoxycholic acid was the main bile acid in the medium, suggesting that the cell line might predominantly synthesize chenodeoxycholic acid. On the other hand, the cells had fetal or hepatoma characters such as marked alpha-fetoprotein production. These results suggest that fetal or hepatoma type bile acid metabolism might occur in the cell line, and that the established cell line could be an useful in vitro model for the study of bile acid metabolism in hepatoma.
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A specific chromosome translocation, t(8q-; 14q+), was observed in a 43-year-old female with non-African Burkitt's lymphoma in which leukemic conversion had occurred. The chromosome studies used cells from ascites. The ascites was apparently the result of a primary tumor involving the ovaries and contained 68% of lymphoma cells. The frequent occurrence of abnormalities related to chromosomes 1, 8 and 14 in African and non-African Burkitt's lymphomas was emphasized.
The effects of steroid sex hormones on the established cell lines derived from human urinary bladder cancer, T24, and from human transitional cell cancer of the urinary tract, 253J, were examined using the colony formation method. Of the seven kinds of steroid hormones tested, estradiol-17 beta was intensively cytotoxic for both cells. The cytotoxic effect was depended on the dose and time of treatment. The combined effect of Adriamycin and estradiol-17 beta on T24 cells could be recognized at low concentrations of Adriamycin (less than or equal to 10(-3) micrograms/ml) after exposure for 24 h.
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A human hepatoma cell line, HuH-7, which was established from a hepatocellular carcinoma, was found to replicate continuously in a chemically defined medium when the medium was supplemented with Na2SeO3. The cells grew better in this medium than in serum-containing medium without any adaptation period. Other established human hepatoma and hepatoblastoma cell lines, HuH-6 cl-5, PLC/PRF/5, huH-1, and huH-4, also grew in the defined medium. Although HLEC-1 cells failed to proliferate continuously with Na2SeO3 alone, they grew if a cell-free conditioned medium from HuH-7 cells was added to the medium. These cell lines, except the HLEC-1 cell line, produced the following human plasma proteins among those examined: albumin, prealbumin, alpha 1-antitrypsin, ceruloplasmin, fibrinogen, fibronectin, haptoglobin, hemopexin, beta-lipoprotein, alpha 2-macroglobulin, beta 2-microglobulin, transferrin, lipoprotein, alpha 2-macroglobulin, beta 2-microglobulin, transferrin, Complement Components 3 and 4, and alpha 1-fetoprotein. Beside plasma proteins, the media from HuH-7, HuH-6 cl-5, PLC/PRF/5, and huH-1 contained anti-carcinoembryonic antigen-reactive proteins, and those from PLC/PRF/5, huH-1, and huH-4 medium contained hepatitis B surface antigen. These proteins were detected during periods of serial cultivation over 9 months under the above culture conditions. The hepatoma cell lines grown in the fully defined synthetic medium may provide a new approach for investigating the growth and metabolism of human hepatoma cells in vitro.