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Biomedical subjects

N Ishida

Publications and source records attributed to N Ishida.

At least 325 records · Page 18Linked to original sources
PubMed1986

Structure and function of the interleukin 2 receptor: affinity conversion model.

We cloned cDNAs of the human and mouse IL-2 receptors. Comparison of their structures allowed us to identify several conserved regions localized to exons 2 and 4, the cytoplasmic portion and the transmembrane portion. These regions might be important for the functions of the IL-2 receptor. The human IL-2 receptor, which was expressed on an IL-2-dependent murine T-cell line, CTLL-2, by cDNA transfection, was shown to be functionally active by blocking the endogenous mouse IL-2 receptor with monoclonal antibodies. On the other hand, the human IL-2 receptors expressed on non-lymphoid cells were functionally inactive. They were unable to mediate the growth signal, were of low affinity species and aberrant in internalization. We postulated that the dysfunction of the IL-2 receptors in non-lymphoid cells would be due to the absence of the putative converter protein which is expressed specifically in lymphoid cells. Since the human IL-2 receptor is active in the murine T cell, the converter may interact with the receptor at the portions conserved between man and mouse. We proposed the affinity conversion model that explained the high affinity state of the receptor by the ternary complex formation between IL-2, the IL-2 receptor and the converter.

Allosteric Regulation↗
PubMed1986

Selective elimination of anti-DNA antibody-producing cells by antiidiotypic antibody conjugated with neocarzinostatin.

A new strategy was shown for the manipulation of autoantibody production in humans. Antiidiotypic antibody to human anti-DNA autoantibody was conjugated with neocarzinostatin (NCS), a cytotoxic agent, by using N-succimidyl 3-(2-pyridyldithio) propionate as a coupling agent. Human B cell clones, which produce anti-DNA autoantibodies, were killed by in vitro treatment with antiidiotype (Id)-NCS conjugates, while clones expressing an Id with irrelevant specificity were unaffected. These results indicate that treatment with anti-Id-NCS conjugates can act as a potent and specific means of generating immunosuppression of autoantibody production. This approach will have a significant advantage in aborting clones that are not effectively suppressed for the autoantibodies by anti-Id antibodies alone, and will result in a potential therapeutic treatment for systemic lupus erythematosus.

Antibiotics, Antineoplastic↗
PubMed1986

A review of toxicology studies on cyanurate and its chlorinated derivatives.

Chlorinated cyanurates are added to swimming pools as disinfectants. In the presence of water, these materials hydrolyze to yield cyanurate and hypochlorous acid. To evaluate the safety of exposure to these materials, a comprehensive testing program was undertaken. This review summarizes the results of acute and subchronic tests on chlorinated isocyanurates. Findings from acute, subchronic, reproduction, metabolism, mutagenicity, and chronic/carcinogenicity tests on cyanurate are also summarized. Results from these tests indicate that chlorinated isocyanurates are safe for use in swimming pools.

Animals↗
PubMed1986

The effect of trypsin on the growth and infectivity of human rotavirus.

The effect of trypsin on the infectivity of human rotavirus (HRV) was examined using HRV strains that are cultivable only when treated with trypsin. Their infectivity in cell culture systems was enhanced in relation to enzyme concentration. The primary effect of trypsin appeared to be on the virus. Trypsin untreated HRV virions were capable of being adsorbed on the cell (MA104) but not of passing into it without trypsin. For multiple cycles of replication the presence of trypsin in the maintenance medium was required.

Adsorption↗
PubMed1986

Low molecular weight immunosuppressive factors found in elevated amounts in cancer ascitic fluids of mice. 1. Isolation, identification and immunosuppressive effects of uric acid and uracil.

A definite increase in two low molecular weight factors, G10-2 and G10-3 was found in Ehrlich ascitic fluids, parallel to tumor growth. The isolation and identification of the two factors were attempted through gel filtration and reversed phase column chromatography, using ascitic fluids obtained 13 days after intraperitoneal implantation of Ehrlich tumor cells. As a result, two highly purified factors were observed upon examination by high performance liquid chromatography. Additional analytical data, collected by UV spectrum, NMR spectrum and mass analysis, allowed us to identify G10-2 as uric acid and G10-3 as uracil. Detailed immunological analysis of uric acid and uracil revealed that the augmenting activities of mouse and human NK cells by mouse IFN alpha/beta or human rIFN alpha A/D were impaired in the presence of either compound at concentrations of 0.07 mM, the concentration detectable in the ascitic fluid of tumor bearing mice.

Animals↗
PubMed1986

Low molecular weight immunosuppressive factors found in elevated amounts in cancer ascitic fluids of mice. 2. 1-Methyladenosine isolated from cancer ascitic fluids enhances Listeria infection in mice.

The low molecular weight fraction (mol wt less than 1,000) of Ehrlich cancer ascitic fluid has been known to enhance Listeria infection in mice. Chemical characterization of the entities in this fraction revealed four purine and pyrimidine analogues, i.e. uric acid, uracil, pseudouridine and 1-methyladenosine (m1Ado). When the effect of each of these components was studied on Listeria infection in mice, only m1Ado markedly enhanced the infection and killed the mice within a short period. The optimal enhancement was obtained when m1Ado was given intravenously to mice 3-6 days before the infection at a concentration of between 1 and 100 micrograms/mouse. On the other hand, uric acid, uracil and pseudouridine failed to show such an enhancing effect. m1Ado inhibited macrophage accumulation in the peritoneal cavity of mice after an intraperitoneal injection of phytohemagglutinin. Although m1Ado did not show any inhibitory effect on the phagocytic and bactericidal activities of macrophages in vitro, peritoneal macrophages obtained from mice which received m1Ado 3 days ahead revealed impaired bactericidal activity, suggesting the migration of different cell populations from the bone marrow of m1Ado-receiving mice. The results may suggest that m1Ado is a major factor in tumor ascites causing, in small doses, an impairment of macrophage functioning as can be detected in tumor-bearing hosts.

Adenosine↗
PubMed1986

Unstability of neocarzinostatin-chromophore.

The unstability of neocarzinostatin (NCS), apo-NCS and NCS-chromophore (NCS-chr) has been investigated by using an extra-weak chemiluminescence (CL) analyzer. A significantly high emission intensity (10,840 counts/10 seconds) was detected from NCS under dark conditions at 20 degrees C, while no significant emission was observed in other antitumor antibiotics, such as, mitomycin C and pepleomycin. This high emission intensity of NCS was due to NCS-chr I (epoxide form) but not apo-NCS. The functional group generating the high extra-weak CL of NCS-chr I is probably the epoxide in the molecule, since the emission intensity of NCS-chr I (epoxide form) is much higher than that of NCS-chr II (hydrochloride adduct form). The extra-weak CL emission of NCS decreased under a nitrogen atmosphere and it was greatly enhanced under an oxygen atmosphere. The spectral analysis of NCS showed emission peaks around 460 and 570 nm. These observations strongly suggest that one of the emission species of NCS-chr may be due to singlet oxygen.

Antibiotics, Antineoplastic↗
PubMed1986

[The effects of neocarzinostatin on superoxide production by monocyte-derived macrophages].

Monocyte-derived macrophages (M phi) from cancer patients injected with low doses of Neocarzinostatin (NCS, 500 units/day, three times a week) 12 times produced significantly more superoxide (O2-) than controls. Lymphocyte functions, such as PHA response, surface marker and serum IAP, before and after NCS injections were the same. M phi from normal persons cultured with NCS (0.4 microgram/ml) for three days produced more O2- than controls, but those cultured with rINF gamma did not. These results suggest that the increased O2- production of M phi from patients taking low doses of NCS may be due to the direct action of NCS on the M phi.

Antibiotics, Antineoplastic↗
PubMed1986

Inhibition of intravascular mouse melanoma dissemination by recombinant human interferon alpha A/D.

The effects of pure recombinant human interferon alpha A/D (IFN alpha A/D) on natural killer (NK) activity and the experimental lung metastasis of B16-F10 melanoma were studied. Treatment of C57BL/6 mice with IFN alpha A/D augmented splenic NK activity and also inhibited the experimental lung metastasis of B16-F10 melanoma in a dose-dependent manner. The augmentation of NK activity and the inhibition of experimental lung metastasis by IFN alpha A/D were completely abolished in anti-asialo GM1-pretreated mice. These results suggested that the effector cells which inhibited melanoma metastasis in the present system were mainly NK cells, and that it was by activating NK cells that IFN alpha A/D had its effect. We next studied the timing of IFN alpha A/D administration for the most effective prevention of melanoma metastasis. The inhibitory effect of IFN alpha A/D was most pronounced when it was given 12 hr before or at the same time as melanoma inoculation. This suggested that melanoma cells were susceptible to NK cells only for a short period of time after intravascular invasion.

Animals↗
PubMed1986

Antitumor effect of recombinant human interferon alpha A/D on Meth-A sarcoma in mice.

Recombinant human interferon alpha A/D (IFN alpha A/D) is known to be as active on murine cells as on human cells. We studied the antitumor effect of pure IFN alpha A/D on Meth-A sarcoma subcutaneously transplanted into female syngeneic BALB/c mice. When administered systematically (intraperitoneally), IFN alpha A/D was only marginally (but significantly, P less than 0.05) effective in inhibiting tumor growth. With intralesional injection, however, IFN alpha A/D strongly suppressed the growth of Meth-A sarcoma, even leading to complete tumor regression and to subsequent immunity to Meth-A sarcoma cells in the host mice when the treatment was started early after tumor transplantation and with a high IFN alpha A/D dose. We also found that treatment of mice with IFN alpha A/D increased the level of serum alpha 1-acid glycoprotein, one of the acute-phase proteins.

Animals↗
PubMed1986

[The anti-tumor efficacy of lymphokine-activated killer (LAK) cells induced in vitro from peripheral blood lymphocytes of patients with malignant glioma].

We studied whether lymphokine-activated killer (LAK) cells were capable of being induced in vitro from peripheral blood lymphocytes (PBL) of patients with malignant glioma, by using recombinant IL-2 (rIL-2). We then investigated whether they possessed anti-tumor efficacy against malignant gliomas (ONS-12, -20, -44). Human LAK cells were generated by placing 5 X 10(6) PBL into each well of 24-well plates (Corning) containing 2 ml of complete medium (CM) with 10 units of rIL-2 (TGP-3, provided by TAKEDA Chemical Industries, Ltd.). The CM consisted of RPMI 1640 with 0.1 mM nonessential amino acids, 1 microM sodium pyruvate, 5 X 10(-5) M 2-mercaptoethanol, 50 micrograms/ml gentamicin sulfate, 0.03% glutamine and 1% heat-inactivated human AB serum. The plates were incubated horizontally at 37 degrees C in a 5% CO2 atmosphere for 72-96 hours. The LAK cells were then harvested, washed three times with Hanks balanced solution, and resuspended in RPMI 1640 with 1% heat-inactivated human AB serum for the in vitro cytotoxicity assays. The anti-tumor cytotoxic activity of LAK cells was estimated in triplicate by 4-hr 51Cr release assays. The cytotoxic activity of the LAK cells against autogeneic ONS-44 glioma cells and PHA blasts was approximately 30% and a few %, respectively. The Natural Killer (NK) activity of the patient with ONS-44 glioma cells was equivalent to that of healthy subject.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Neoplasms↗
PubMed1986

Variants of a human monocytic leukemia cell line (THP-1): induction of differentiation by retinoic acid, interferon-gamma, and T-lymphocyte-derived differentiation-inducing activity.

Induction of terminal differentiation of two variant sublines derived from the human monocytic leukemia cell line THP-1 by all-trans-beta-retinoic acid (RA) was studied. One of the variants was approximately 10 times more resistant to RA and the other, approximately 10 times more sensitive than the parent THP-1. Differentiation of the RA-resistant variant could be induced by immune interferon (IFN-gamma) and a T-lymphocyte-derived lymphokine of a differentiation-inducing activity (DIA), alone or in combination with 10 nM RA. These induced cells showed many of functional monocyte and/or macrophage characteristics, such as superoxide anion production, phagocytosis, and antibody-dependent cellular cytotoxicity. RA suppressed the expression of Fc receptors, phagocytosis, and 5'-nucleotidase activity of the resistant cells, although not the expression of the sensitive variant. These results indicate that RA-resistant cells can be fully induced to differentiate by the combination of RA and IFN-gamma or DIA.

Antibody-Dependent Cell Cytotoxicity↗