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Biomedical subjects

D Mizuno

Publications and source records attributed to D Mizuno.

At least 145 records · Page 8Linked to original sources
PubMed1979

Conservation of ribosomal fidelity during ageing.

The function of ribosomes prepared from the liver of young (2--5 months old) and senescent (15--26 months old) mice were compared in vitro. The conclusions that can be drawn from the liver of senescent mice is 10 to 40% lower than that of young mice; (2) the fidelity of translation does not change grossly with age; (3) the thermosensitivity of translational activity of ribosomes and the activity of ribosome-associated ribonuclease do not change with age; (4) there is an age-dependent accumulation of free 40S ribosomal subunits in the cytoplasm of mouse liver. The relation of age-dependent changes in the structure and function of ribosomes is discussed.

Aging↗
PubMed1979

In vivo degradation of rat globin messenger RNA during maturation of reticulocytes.

The degradation of globin mRNA in rat reticulocytes maturing in the peripheral blood was investigated. Poly(A) and non poly(A) portions of mRNA molecules were determined quantitatively by hybridization with radioactive poly(U) and complementary DNA, respectively. During the degradation of mRNA in vivo, it was shown that (1) globin mRNA and the bulk of RNA decrease in parallel, (2) the average chain length of poly(A) segments in the mRNA does not change, (3) the percentage of poly(A) (-) globin mRNA in total globin mRNA does not change, and (4) fragments of large molecular weight do not accumulate. Possible mechanisms of degradation of globin mRNA in the reticulocytes are discussed on the basis of these observations.

Animals↗
PubMed1979

Inhibitory effects of nucleoside triphosphates on nucleolar RNA synthesis.

Studies on the effects of substrates on RNA polymerase I [EC 2.7.7.6] in vitro showed that nucleolar RNA synthesis was inhibited by an excess of substrate nucleoside triphosphates in the presence of Mg2+. GTP and UTP were more inhibitory than CTP and ATP. These compounds specfically inhibited nucleolar RNA synthesis and a concentration of GTP that strongly inhibited nucleolar RNA synthesis did not inhibit RNA synthesis by partially purified RNA polymerase I. The inhibition of nucleolar RNA synthesis disappeared at pH 9.0 without any change in the apparent Km for GTP or the Vmax of RNA synthesis.

Adenosine Triphosphate↗
PubMed1978

Increase in the ratio of 18S RNA to 28S RNA in the cytoplasm of mouse tissues during aging.

The possibility of alterations in cytoplasmic RNA in mouse liver, kidney and brain during aging was investigated. The cytoplasmic RNAs in these organs gave similar profiles of optical density at 260 nm with three major peaks at 28S, 18S and 4S on sucrose gradient centrifugation. However, the ratio of the amounts of 18S and 28S RNA increased significantly with age in the brain and liver. The polyacrylamide gel electrophoretic patterns of extracts of the three tissues under both native and denaturing conditions were nearly identical regardless of the age of the animals. Since most of the minor components separated on gels were probably in vivo degradation products of ribosomal RNA, these results suggest that the extent of apparent and hidden breaks in ribosomal RNA does not change during aging.

Aging↗
PubMed1978

Analysis of RNA synthesized in isolated nuclei of Ehrlich ascites tumor cells.

The molecular size and poly-A content of RNA synthesized in isolated nuclei of Ehrlich ascites tumor cells were measured. KCl was found to be essential for synthesis of high molecular weight RNA: when 0.4 M KCl was added to the reaction mixture, the average molecular size of the RNA formed was 14S; without KCl the average molecular size was 5S. A significant amount of poly-A sequences was found in RNA synthesized in the presence of alpha-amanitin, suggesting that RNA polymerase I and/or III may synthesized some RNA containing poly-A in isolated nuclei.

Amanitins↗
PubMed1978

Induced synthesis of immunoglobulin messenger RNA accompanies induction of immunoglobulin production in cultured mouse spleen cells.

Immunoglobulin kappa type light chain mRNA (Lkappa mRNA) accumulated in parallel with secretion of immunoglobulin M in cultured mouse spleen cells activated by lipopolysaccharide. Actinomycin D suppressed the accumulation of kappa chain mRNA completely without affecting the degradation rate of kappa chain mRNA. The half life of kappa chain mRNA was about 9 h. Available evidence indicates that lipopolysaccharide stimulates de novo synthesis of kappa chain mRNA. The accumulation of kappa chain mRNA was markedly suppressed by inhibitors of DNA or protein synthesis such as hydroxyurea, cytosine arabinoside and cycloheximide.

Animals↗
PubMed1978

In vitro induction of antibody-dependent cytotoxic macrophages by the local anesthetic lidocaine.

Normal macrophages were activated to antibody-dependent cytotoxic effector cells by in vitro treatment with the local anesthetic lidocaine. Experiments on the dose-response and time course of the effect oflidocaine showed that incubation of normal macrophages with 10 mM lidocaine for 10 min at 28 C was enough for induction of antibody-dependent cellular cytotoxicity. The activation by lidocaine was accompanied by enhanced phagocytosis of sheep red blood cells (SRBC) sensitized with anti-SRBC antiserum, but not enhanced ingestion of polystyrene latex particles (PLP). These findings suggest that lidocaine, which has various effects on cell membranes, induces some perturbation of macrophage membranes, resulting in activation of Fc receptor functions in antibody-dependent cytotoxicity and phagocytosis.

Animals↗
PubMed1978

Immune response of mice in immunotherapy of tumors with syngeneic antitumor serum plus lipopolysaccharide.

Humoral and cellular immune responses were investigated after combination therapy with syngeneic antitumor serum and bacterial lipopolysaccharide (LPS). The titer of antitumor antibody determined by using a macrophage-mediated system was very high in mice cured by the combination therapy, and this high titer lasted for a long time. In contrast, no significant titer was detected using an antibody-dependent lymphocyte-mediated system. Thus, antibody-dependent macrophage-mediated cytolysis was a more sensitive method for detecting antitumor antibody. The cellular immune response was measured as the delayed hypersensitivity reaction to tumor cells. In mice that had been cured by combination therapy, this reaction appeared at an early stage, before any antitumor antibody was detectable, but it soon decreased. On the other hand, tumor-bearing mice showed a low level of antibody and no significant delayed hypersensitivity reaction.

Animals↗
PubMed1978

Correlation of differences in antigenicity of four 3-methyl-cholanthrene-induced tumors in syngeneic mice with the susceptibility of tumors to an immunopotentiator, PS-K.

Eleven syngeneic tumors were induced by 3-methylcholanthrene in DDD mice. Their antigenicity in vivo was examined by measuring growth inhibition of transplanted tumors in mice immunized by implanting tumors into their tail and then cutting off the tail. Four tumors with different antigenicity were selected from them for study. The growth-suppressive effect of an immunotherapeutic agent, PS-K, on the four tumors was examined. The growth of highly antigenic tumors in mice was inhibited by PS-K, but that of weakly antigenic tumors was not, and a close correlation was found between the antigenicity of tumors and the antitumor activity of PS-K against them. No similar correlation was found between their antigenicity and their sensitivity to a mitotic poison, 6-mercaptopurine. These results suggest that the antitumor effect of an immunopotentiator depends greatly on the antigenicity of tumors.

Animals↗
PubMed1978

Antitumor immunity after surgical removal of 3-methylcholanthrene-induced murine tumors: correlation between resistance and delayed hypersensitivity reaction.

The relationship between tumor resistance and the antitumor delayed hypersensitivity reaction (TDHR) after resection of the tumor was studied by using the syngeneic 3-methylcholanthrene-induced murine tumor, MCA-DDD. MCA-DDD was inoculated subcutaneously into the tail of DDD mice and 4 weeks later the tumor-bearing tail was resected. The tumor resistances of the mice were then determined from the diameters of the tumor that developed 14 days after subcutaneous challenge of the mice with tumor cells in the flank. It was found that the mice showed a specific resistance to the tumor until 30 days after tumor resection. In parallel with tests on tumor resistance, TDHR of the mice after tumor resection was examined by the footpad test. The cell-free fraction of sonicated MCA-DDD tumor cells was used as the preparation of tumor antigens. TDHR of the mice appeared soon after tumor resection, reached a maximum on day 7, and then decreased slowly until day 29. Mice that acquired tumor resistance showed rapid increase of TDHR after challenge with fresh tumor cells. TDHR was high on day 4 after the challenge and its level was well correlated with tumor resistance of the mice.

Animals↗
PubMed1977

Protein which interacts with a stimulatory factor of RNA polymerase II of Ehrlich ascites tumor cells.

When partially purified Ehrlich ascites tumor RNA polymerase II was further purified on a column of phosphocellulose, stimulation of its catalysis of RNA synthesis by stimulatory factor S-II was greatly decreased. This decrease in sensitivity to the stimulatory factor was reversible: the enzyme eluted from phosphocellulose became sensitive to the factor when mixed with a protein fraction eluted from the phosphocellulose at high salt concentration. Evidence was obtained that this protein, named helper protein, binds, to the enzyme eluted from phosphocellulose, causing it to recover sensitivity to stimulatory factor S-II.

Animals↗