Gann
Print ISSN : 0016-450X
Volume 49, Issue 3
Displaying 1-8 of 8 articles from this issue
  • HIDEYA ENDO
    1958 Volume 49 Issue 3 Pages 157-166
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    6-(β-Indolyläthyl) aminopurin wurde dargestellt, dessen Wirkung auf normale Zellen (Hühnerfibroblasten) und Tumorzellen (Hela) an Gewebekulturen getestet und cytologisch untersucht.
    Es zeigte sich eine etwa gleichmässig starke Hemmung des Zellwachstums mit Auftreten pathologischer Mitoseformen und eine deutlich Anhäufung von zweiund mehrkernigen Zellen.
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  • HIDEYA ENDO, KAZUO NITTA
    1958 Volume 49 Issue 3 Pages 167-170_2
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    As the side path of the process in which nucleic acid is synthesized from nucleotide pool, a pathway from desoxyadenosin to kinetin is supposed. From this speculation tetrahydrokinetin was synthesized as a model of the hypothetical intermediate. This substance was found to markedly inhibit the growth of HeLa cells in tissue culture, although kinetin is known to have no effect.
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  • HIDEYUKI HOSHIZIMA
    1958 Volume 49 Issue 3 Pages 171-176
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    Toxohormone prepared by the method of Ono et al. (acetic acid-methanol extraction) induced a parallel depression of total ascorbic acid and catalase of mouse liver, and showed no effect on the level of liver riboflavin.
    Toxohormone prepared by the original method of Nakahara and Fukuoka (water extraction and alcohol precipitation) showed no effect on the level of liver ascorbic acid and riboflavin, but it depressed catalase activity and ferritin iron, although the extent of their depression was not in parallel.
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  • IZUMI KAWAKAMI
    1958 Volume 49 Issue 3 Pages 177-192
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    1. The inductive effects of nodules of the ascites hepatoma of the rat were tested, using the presumptive neuro-epidermis of Triturus gastrula as reactor.
    2. Two kinds of the ascites hepatoma, AH 7974 and AH 130, which have different morphological and pathological characteristies, were used.
    3. The experiments were done by the usual sandwich explantation method. A small piece of fresh or ethanol-fixed cancer tissue was sandwiched between pieces of presumptive ectoderm.
    4. In the control series the normal rat liver tissue induced solely neural tissue, especially archencephalic structures.
    5. The inductive capacity of fresh tissue of the nodule of each cancer was notably weak and the rate of induction was not over 15 per cent, against that of the normal hepatic tissue of 70 per cent.
    6. The cancer tissue fixed by ethanol for short periods (from 1 to 24hrs.) produced inductions in rather high percentage, but protracted ethanol treatment (from 3 to 8 days) reduced induction frequency to percentages as low as those in the fresh cancer tissue series. There were no detectable differences in the inductive action between AH 7974 and AH 130.
    7. The weak inductive effect of the cancer tisssue seems to depend upon a pathological change of the hepatic cell surface, since in a preliminary experiment the crude proteins extracted from nodules of ascites hepatoma showed a strong inductive effect.
    8. Some inductions by the fresh cancer tissue or cancer tissue fixed for short periods in ethanol showed spino-caudal characteristics and were occasionally accompanied by notochord differentiation. The mesoderm-inducing tendency seems to be due to a modification of the inductive capacity of the hepatic cells caused by their becoming neoplatic.
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  • NOBUYUKI ITO
    1958 Volume 49 Issue 3 Pages 193-198
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    The studies described in this paper are concerned with the effect of loading Kupffer cells on the destruction of DAB by rat liver slices. India ink, trypan blue, congo red, and carmine were used as agents to ′block′ the Kupffer cells.
    DAB-destroying ability by rat liver slices were generally depressed by loading of various kinds of dyes. However, the degree of depression varied according to the kinds of dyes or the intervals after the time of loading. The depression of DAB-destroying ability in congo red group was most remarkable and with least fluctuation. Histologically, Kupffer cells in the liver loaded with those dyes revealed various degrees of hypertrophy in each group and stage of loading. The DAB-destroying ability of rat liver slices showed different values according to the degree of loading in the Kupffer cells. The hepatic parenchymal cells revealed no marked change during 48 hours after injection.
    From these results it is presumed that Kupffer cells may play an important role in the destruction of DAB in the rat liver.
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  • TOYOZO SEKIGUCHI, TUTOMU WATARI, HIDEO ETO, HARUHISA YOSHIKAWA
    1958 Volume 49 Issue 3 Pages 199-208
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    1) The metabolism of DNA of rat tumor, and liver and spleen of the tumor bearing animals were studied with the use of 32P, the charcteristic time course of the specific activity of the DNA, prepared by the method of Mirsky and Pollister and purified by Wyatt′s procedure, was observed in each of the tissues.
    2) The DNase II activity was measured by the method of Allfrey and Mirsky, and a close correlation of the DNase II activity was observed with the metabolic rates of DNA of each tissue by the use of 32P, namely highest in tumor, and low activity in liver.
    3) Following whole body X-ray irradiation, the metabolic rates of DNA of each tissue was depressed conciderably, and on the contrary, the DNase II activity was enhanced after irradiation, namely the DNase II activity of the spleen was increased about two fold.
    4) On the mechanism of augmentation of DNase II activity caused by the X-ray irradiation some in vitro experiments were carried out, paticulary from the standpoint of the enzyme protein synthesis.
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  • ISAMU USUBUCHI, SHOCHI OBOSHI, RYOICHI TSUCHIDA, HIDEHARU TANABE
    1958 Volume 49 Issue 3 Pages 209-222
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    1) Mitomycin C showed a broad anti-tumor spectrum on ascitic forms of rat and mouse tumors 48 hours after intraperitoneal translantation, especially showing a maked effect on two strains of Hirosaki sarcoma and Ascites hepatoma 130.
    1) Mitomycin C showed a marked effect on solid forms of each strain of Hirosaki sarcoma 3-10 days after subcutaneous transplantation.
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  • I. OVERALL METABOLISM OF DIMETHYLAMINOAZOBENZENE AND CARCINOGENESIS
    HIROSHI TERAYAMA
    1958 Volume 49 Issue 3 Pages 223-232
    Published: September 30, 1958
    Released on J-STAGE: November 14, 2008
    JOURNAL FREE ACCESS
    1) A method to fractionate the metabolic intermediates of DAB after the dye was incubated with the fortified liver homogenate, has been established.
    2) It has been demonstrated that at least three metabolic pathways are available under the experimental conditions: demethylation, hydroxylation and reductive cleavage of the azo bond.
    3) The species specificity and the organ specificity concerning the DAB carcinogenesis was shown to be related to the metabolism of the dye. DAB was metabolized by rat liver with the highest speed but not by other animal′s liver or other organs of rats.
    4) A large dose of DAB administered with the aid of a stomach tube caused a remarkable decrease in the ability of rats liver to metablize DAB even three days after the administration. The administration of DAB, however, did not change the activity of mice liver much. Administration of MAB or AB seems to have no effect.
    5) The above observations do not contradict our working hypothesis that the carcinogenic aminoazo dye might be bound with one (or some) of the enzymes in microsomes responsible for metabolizing the dye administered.
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