Search PubMed⌕ Search

Biomedical subjects

M Okada

Publications and source records attributed to M Okada.

At least 1,423 records · Page 79Linked to original sources
PubMed1986

Induction of Tac antigen and proliferation of myeloid leukemic cells by ATL-derived factor: comparison with other agents that promote differentiation of human myeloid or monocytic leukemic cells.

We studied seven cases of myeloid leukemia at various differentiation stages to investigate the response of leukemic cells to phorbol 12-myristate 13-acetate (PMA) and various biological factors. gamma-Interferon (gamma-IFN)-treated cells expressed higher amounts of Fc receptors on leukemic cells in five out of seven cases. Expression of HLA-DR antigen of gamma-IFN-treated leukemic cells was significantly enhanced in three cases. PMA did not induce Fc receptors or HLA-DR antigen on these cells. Induction of Tac antigen, a putative interleukin 2 (IL 2) receptor, was observed in two cases after cultivation with PMA or with a novel lymphokine, adult T cell leukemia-derived factor (ADF). Cells from one of these patients expressed Tac antigen immediately after cell separation, and expression of Tac antigen was augmented by PMA and ADF. Interleukin 1 (IL 1) or IL 2 did not induce Tac antigen. Leukemic cells from this patient also proliferated vigorously in the presence of ADF but not PMA, IL 1, or IL 2.

Aged↗
PubMed1986

Metabolic fate of N-nitrodibutylamine in the rat.

The metabolic fate of N-nitrodibutylamine (NO2DBA) and N-nitrobutylamine (NO2BA) was investigated in the rat. Eight N-nitramines, including glucuronides, were isolated and identified from urine of rats given NO2DBA. They were produced by omega, omega-1, omega-2 and alpha oxidations of the N-nitramine. The in vivo metabolic pattern of NO2DBA was similar to that of N-nitrosodibutylamine, except that the monodealkylated metabolite NO2BA was also isolated and characterized. When NO2BA was administered to rats, no N-nitramine other than a small amount of unchanged NO2BA was identified in the urine. Besides N-nitramines, N-acetyl-S-(butyl, 3-oxobutyl and 3-hydroxybutyl)-L-cysteines were isolated and identified (as their methyl esters) from the urine of rats given both NO2DBA and NO2BA. The relative ratio of these three L-cysteine derivatives obtained from NO2DBA was quite similar to that from NO2BA, indicating that NO2DBA produces in vivo a chemical species with butylating ability through NO2BA.

Alkylating Agents↗
PubMed1986

Cytotoxicity of interleukin 2-activated lymphocytes for leukemia and lymphoma cells.

Studies were undertaken to determine whether leukemia and lymphoma cells would be lysed by autologous and allogeneic lymphokine-activated killer (LAK) cells. Peripheral blood mononuclear cells (PBMC) from patients and normal donors were cultured for five days, 2 weeks, and 4 weeks with medium containing 2,500 units of recombinant interleukin 2 (IL-2) per mL, and their cytotoxicity was assayed by a five-hour 51Cr-release test. Of primary tumors isolated from patients with acute nonlymphoblastic leukemia, acute lymphoblastic leukemia, and non-Hodgkin's lymphoma, tumors of 37 out of 40 patients tested were shown to be susceptible to normal donors' LAK, and tumors of 18 of 20 patients tested were shown to be susceptible to autologous LAK. LAK cultured for longer periods showed a tendency to have lower cytotoxicity. LAK had also low, but significant, levels of cytotoxicity for nonmalignant target cells. Because PBMC expanded in IL-2-containing medium consisted mainly of OKT3-positive pan T cells, OKT8-positive suppressor/cytotoxic cells, and Leu-11-positive natural killer (NK) cells, and treatment with OKT3 and Leu-11 monoclonal antibodies (mAb) reduced LAK activity for autologous and allogeneic tumor cells, both T and NK cells appeared to be effector cells for LAK activity. Mechanisms of target-cell recognition in the LAK system seem to be different from those in alloreactive cytotoxic T lymphocytes (CTL) based on the results that, while cytotoxicity of alloreactive CTL was inhibited by the treatment of effector cells with mAb, OKT3, and OKT8, and by the treatment of target cells with a mAb that reacts with HLA class I antigen, LAK activity was not inhibited by the above treatment. When chromosomes of IL-2-expanded PBMC in nine patients and two normal individuals were analyzed, PBMC from one patient showed chromosomes of clonal abnormalities, and PBMC from five donors showed those of nonclonal abnormalities.

Antibodies, Monoclonal↗