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Biomedical subjects

N Ishida

Publications and source records attributed to N Ishida.

At least 487 records · Page 27Linked to original sources
PubMed1980

Interaction between Sendai virus and the cell membranae I. Restricted number of Sendai virus particles engaged in fusion with chicken red cell membrane.

The interaction between Sendai virus (HVJ) and the cell membrane was studied from a quantitative point of view, using artificially induced haemolytic virus particles and chicken red blood cells (CRBC). It was shown that one artificially induced haemolytic virus particle can lyse one erythrocyte. A method to accurately enumerate the actual number of virus particles fused to one CRBC was established. The number of virus particles adsorbed on to the CRBC increased with increasing multiplicities of infection (moi). The highest number of virus particles fused with one CRBC was 20 and was obtained from an inoculation of about 100 virus particles per CRBC (moi 100).

Adsorption↗
PubMed1980

Interaction between Sendai virus and the cell membrane II. The role of Sendai virus neuraminidase in haemolysis.

When chicken erythrocytes (CRBC) were pretreated with non-haemolytic Sendai virions or isolated HANA spikes, they acquired a resistance to the haemolytic action of "second challenge" viruses. This resistance was dependent on the quantity of N-acetylneuraminic acid liberated from the surface of the CRBC by the initial virus, and not on the use of different viral sources. When exposed to Sendai virus, CRBC were more difficult to be lysed and easier liberated N-acetylneuraminic acid than human 0 erythrocytes. The restricted number of virions able to fuse CRBC was explained by such neuraminidase function of the HANA spike of the virion.

Animals↗
PubMed1980

Impaired induction of type II interferon in tumor-bearing mice.

The response of mice to type II interferon inducers such as purified protein derivative of tuberculin or OK-432 was significantly impaired after either the implantation of tumor cells or the injection of cell-free tumor ascitic fluids. Complete inhibition of type II interferon induction occurred in 3 to 5 days. This inhibitory effect persisted until the death of mice implanted with tumors or for 7 days after i.p. injection of 0.2 ml of tumor ascitic fluid. The inhibitory activity was seen even with 0.2 ml of the 10,000-fold dilution of the fluid and with its filtrate passed through a Diaflo UM-10 membrane (greater than 10,000-dalton exclusion), However, such tumor ascitic fluids did not affect the induction of type I interferon in mice by polyriboinosinic-polyribocytidylic acid or tilorone-HCl. Moreover, adjuvant-induced nontumorous ascitic fluid had no inhibitory activity. These results indicate that the in vivo induction of type II interferon is specifically impaired by tumor-mediated factor(s) with molecular weights of less than 10,000.

Animals↗
PubMed1980

Establishment of a cell line from a human fetal liver and its xenotransplantation to nude mice.

An epithelial cell line, NuE15-1, was established from the liver of a 24-week-old human fetus. The cells had round clear nuclei with clear (agranular) cytoplasm of polygonal shape and grew in a pavement-like manner. The karyotype was human and heteroploid. alpha-Fetoprotein and alpha 1-antitrypsin were detected in the concentrated culture medium but albumin was not. This may indicate the hepatocytic origin of the cell line. Malignant transformation was confirmed by xenotransplantability to nude mice. When inoculated intraperitoneally, the implanted cells caused lethal peritonitis carcinomatosa in 9 out of 10 mice within 3 weeks and liver metastasis was observed in one case. A possible role of alpha-fetoprotein-producing cells as precursors of tumor cells in hepatocarcinogenesis is discussed.

Animals↗
PubMed1980

Isolation of an inhibitor of type II interferon induction from tumor ascitic fluids.

A low-molecular-weight fraction (M.W. approximately 700) that specifically impairs the induction of type II interferon in mice by purified protein derivative of tuberculin or OK-432 was isolated from the cell-free ascitic fluid of mice bearing Ehrlich ascites carcinoma. Purification was achieved by ultrafiltration and gel filtration. The inhibitory activity of the isolated fraction was 10 times greater than that of the unfractionated starting material in the impairment of type II interferon induction. The significant inhibition was observed even when 0.2 ml of the 10,000-fold dilution of the fraction, which was previously adjusted to 0.25 A unit at 290 nm absorption, was once treated i.p. in normal mice 48 hr before challenge of type II interferon inducers. This fraction was stable to heating at 56 degrees for 60 min. The active component, however, did not affect the in vivo induction of type I interferon by polyriboinosinic-polyribocytidylic acid or tilorone-HCl. In parallel experiments, an identical low-molecular-weight fraction that impairs the type II interferon induction in mice was isolated from the ascitic fluids of rats bearing AH-100B ascites tumor and from a human hepatoma case with advanced cancer metastatic to the peritoneal cavity. However, nontumorous ascitic fluids obtained from adjuvant-stimulated mice and a human liver cirrhosis case did not contain any such inhibitory activity.

Animals↗
PubMed1980

Caffeine-induced recovery from G2 block caused by neocarzinostatin.

Caffeine was found to act as a stimulator of the recovery of HeLa-S3 cells from the G2 phase arrest induced by a cancer chemotherapeutic agent, neocarzinostatin (NCS). When the cells were incubated in the presence of caffeine after removal of NCS, the time required for the recovery of mitosis was dependent on the concentration of NCS and was markedly shortened by caffeine treatment in a concentration-dependent manner. When puromycin, a specific protein synthesis inhibitor, was added together with caffeine, a temporary recovery of mitosis was observed, followed by an irreversible arrest of mitosis, suggesting that the terminal point of action of NCS resides closer to the M phase than that of puromycin. These results indicate that the mechanism of NCS-induced G2 block is closely related to that of X-ray-induced G2 block.

Antibiotics, Antineoplastic↗
PubMed1980

Effects of caffeine on neocarzinostatin-induced inhibition of cell cycle traverse in HeLa-S3 cells.

Caffeine was found to suppress the cell cycle effects of the cancer chemotherapeutic agent neocarzinostatin (NCS). When caffeine was added together with NCS to the culture of HeLa-S3 cells, NCS-induced inhibition of DNA synthesis and of mitosis was markedly reduced in the presence of caffeine. Theophylline was also effective, but N6, O2'-dibutyryl cyclic adenosine 3':5'-monophosphate was not. The caffeine-caused reduction of cell cycle effects was also observed in several other cancer chemotherapeutic agents, including bleomycin and Adriamycin. In contrast, the single-strand scission of cellular DNA and the final cell lethality induced by NCS were not affected by caffeine. These results suggest that the mechanism by which NCS inhibits the cell cycle traverse involves a kind of cell damage which is repairable in a manner promoted by caffeine and hence is different from single-strand scission of DNA. Such a mechanism might be common to the cell cycle effects of X-irradiation and several cancer chemotherapeutic agents including NCS.

Antibiotics, Antineoplastic↗
PubMed1979

Systemic candidiasis from Candida albicans colonizing the gastrointestinal tract of mice.

Reproducible induction of systemic Candida infection was achieved by treating mice in which Candida colonization had been established in the gastrointestional tract by aminobenzylpenicillin treatment. Systemic candidiasis was induced in these mice by X-ray irradiation followed by immunosuppressive doses of dexamethasone or X-ray irradiation followed by immunosuppressive doses of trypan blue. Macrophages seem to play an important role in thie systemic infection.

Animals↗
PubMed1979

Selective modification of positive chemotaxis in the true slime mold Physarum polycephalum by ethylenediaminetetraacetic acid treatment.

The plasmodium of the true slime mold Physarum polycephalum was treated with EDTA or EGTA and the effect of the treatment on the chemotactic response was examined by measuring the chemotactic motive force with the double-chamber method. The results obtained were as follows: (1) The treatment of the plasmodium with 5 mM EDTA (pH 7.0, 20 min) did not give any significant effect on the protoplasmic streaming or motility. (2) The plasmodium treated with EDTA exhibited no chemotactic response to non-electrolyte attractants (D-glucose, D-galactose, D-mannose, and maltose) and negative chemotaxis to electrolyte attractants (cyclic AMP and NaH2PO4). (3) The EDTA treatment gave no effect on the chemotactic response to repellents (D-fructose, NaCl, CaCl2, MgCl2). (4) The EDTA-treated plasmodium exhibited changes in the membrane potential in response to both attractants and repellents as similar to the untreated plasmodium. (5) The treatment of the plasmodium with 5 mM EGTA (pH 7.0, 20 min) gave results similar to those obtained with the EDTA treatment. The results obtained suggested that EDTA (or EGTA) treatment did not affect the receptor sites but modified the transduction mechanism from reception into tactic movement.

Chemotaxis↗
PubMed1979

Korean haemorrhagic fever in staff in an animal laboratory.

In March, 1975, and January, 1978, there were outbreaks of Korean haemorrhagic fever (K.H.F.) among staff in the animal laboratory of the clinical research building of Tohoku University hospital. 13 doctors and 1 veterinarian had K.H.F., and all except 1 had a mild but typical clinical course. K.H.F. antibody titres were significantly raised in all 14 patients. 12 other doctors working in the same room had no symptoms and no K.H.F. antibody. K.H.F. antibody was also detected in 3 animal technicians who had not been ill, but who had worked in the same room. Antibody was not detected in any of the 4 technicians who worked in different animal rooms in another building. Epidemiological studies suggest that laboratory rats were the source of the infection. High titres of K.H.F. antibody were most common in rats reared in the animal laboratory associated with the outbreak.

Adult↗
PubMed1979

Inhibitory effect of cytokinins on PHA-induced human lymphocyte stimulation.

The inhibitory effect of various purine derivatives on PHA-induced human lymphocyte blast formation was studied. Two nucleoside cytokinins, N6-benzyladenosine and N6-isopentenyladenosine, inhibited blast formation at concentrations as low as 10(-6) M. However, the other cytokinins, which lacked the ribosyl residue at N9 position, had to be at the higher molar concentration of 10(-4) before they could induce the same inhibitory effect.

Adenosine↗