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Biomedical subjects

J Yata

Publications and source records attributed to J Yata.

At least 127 records · Page 7Linked to original sources
PubMed1984

A neonatal mass-screening for congenital adrenal hyperplasia in Japan.

A pilot neonatal mass-screening for congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency (21-OHD) was performed in the western region of Shizuoka Prefecture, Japan, using a simplified radioimmunoassay method for 'Disc-17-hydroxyprogesterone (17-OHP) determination. The results obtained during a 30-month period indicated that 3 infants out of the 34314 neonates examined were proved to have 21-OHD, and the incidence of homozygotes and heterozygotes were estimated to be 1:11438 and 1:54, respectively. At the time of recall, the concentrations of plasma 17-OHP and 21-deoxycortisol and their urine metabolites as well as plasma sodium levels were quite applicable to diagnosis, while the clinical signs that may be manifest in 21-OHD were of little value in this connection. Prematurity and perinatal complications of neonates tended to give false-positive results, being secondary to the function of the residual foetal adrenal cortex and non-specific stimulatory effects of various stresses. Despite several technical and practical problems to be solved, the present study demonstrated the importance and validity of a neonatal mass-screening program for CAH.

17-alpha-Hydroxyprogesterone↗
PubMed1984

Natural killer activity of pediatric patients with acute lymphoblastic leukemia in remission.

We examined the natural killer (NK) activity of pediatric patients with acute lymphoblastic leukemia (ALL) in remission by using several methods, including a newly established single cell assay. HNK-1 antigen-positive cells, which are now considered to assume NK activity, were not decreased in the patients, although the NK activity of the patients was found to be depressed. Neither monocyte depletion nor the addition of interferon-alpha improved the decreased NK activity of the patients. According to the results of the single cell assay, conjugate-forming cells (effector cells that form conjugates with target cells), lytic conjugate-forming cells (fractions of conjugate-forming cells that actually go on to kill target cells) and the recycling activity of NK cells were all decreased in the patients. Thus, it is apparent that there were defects in several steps of NK activity in the patients. The NK activity of 19 patients was further studied successively to investigate the correlation between NK activity and clinical course. The longest observation period was 38 months. Six bone marrow relapses of leukemia occurred, but the NK activity of these patients at the time of relapse or at the previous test was not necessarily depressed as compared to that of the other patients.

Adolescent↗
PubMed1984

Low dose of deoxyguanosine increases IL-2 receptors of IL-2-dependent cultured T cells.

Deoxyguanosine ( dGuo ) is a purine nucleoside phosphorylase (PNP) substrate which has been shown to inhibit T lymphoblast growth, PHA-induced cell proliferation and suppressor T cell activity. Low dGuo concentrations (0.5-5 microM) increase interleukin-2 (IL-2) sensitivity of IL-2-dependent cultured T cells (CTC). dGuo alone has no direct mitogenic effect on CTC. The increased IL-2 sensitivity of CTC was more marked in the presence of low IL-2 concentrations than high ones. CTC incubated with dGuo at 37 degrees C for 24 hrs absorbed more exogenous IL-2 than control non-treated CTC. CTC incubated at 4 degrees in the presence of dGuo did not absorb any more IL-2 than control CTC. FACS analysis further showed increased Tac expression on CTC due to dGuo . These findings indicate that a 37 degrees incubation of CTC with dGuo increases the number of CTC IL-2 receptors. dGuo was not found to increase IL-2 production by PHA-stimulated PBM. Therefore, low dGuo concentrations selectively augment the sensitivity of cells responding to IL-2 by increasing IL-2 receptors.

Cells, Cultured↗
PubMed1983

Helper and suppressor T-cells regulating killer cells of EB virus infected cells.

Using an in-vitro human lymphocyte system, a study was performed to determine whether helper T-cells and suppressor T-cells control the generation of killer cells against autologous B-cells transformed by Epstein-Barr (EB) virus. When T-cells were treated with mitomycin C and reacted in the presence of macrophages with target cells bearing HLA-DR, helper T-cells were induced but suppressor T-cells were not. In contrast, when T-cells were reacted in the absence of macrophages to target cells lacking HLA-DR, suppressor T-cells but not helper T-cells were induced. The culture supernatant of the T-cells which showed suppressor activity also suppressed the generation of killer cells. The thus-induced suppressor T-cells also suppressed the HLA incompatible allogeneic killer cells which were directed against autologous B-cells transformed by EB virus and also autologous killer cells directed against allogeneic target cells. These observations indicated that there is no HLA restriction between the suppressor T-cells and the killer cells and the suppression is antigen nonspecific.

B-Lymphocytes↗
PubMed1983

Induction of suppressor T cells by anti-globoside antibodies in cancer sera.

T cells treated with cancer sera frequently suppressed immunoglobulin production by autologous lymphocytes stimulated with pokeweed mitogen. Sera from healthy individuals did not induce suppressor activity. This suppression is not caused by TG cells (T cells bearing receptors for the Fc portion of immunoglobulin G [IgG]) interacting with immune complexes, because we used T cells depleted of TG cells. The suppressor-inducing factors were separated into an IgG-containing fraction and a fraction with a smaller molecular weight. IgG fractions from all sera that were positive for anti-globoside antibody induced suppressor T cells, and elimination of the anti-globoside antibody from these IgG fractions reduced the ability to induce suppressor T cells. T cells treated with rabbit anti-globoside antiserum also activated suppressor T cells. These observations indicate that the antibodies directed to the globoside antigen on suppressor T cells stimulate the suppressor T cells, and that anti-globoside antibody in cancer sera may play a role in causing immunodeficiency in cancer patients.

Antibodies↗
PubMed1983

[Studies on the effect of lentinan on human immune system. II. In vivo effect on NK activity, MLR induced killer activity and PHA induced blastic response of lymphocytes in cancer patients].

Immunological activities of lymphocytes were studied in patients with cancer of digestive organs and mamma after administration of lentinan. When 11 cancer patients received lentinan i.v. 2 mg, NK activity of lymphocytes was increased in 4 patients on the following day. With the same condition, MLR induced killer activity against Raji cell of lymphocytes was increased in 3/7 patients and PHA response was also increased in 3/7 patients. These activities were returned to values before the administration of lentinan. Then each activity was examined after administration of lentinan twice a week. NK activity, MLR induced killer activity and PHA response were increased in 4/15, 8/12 and 5/11 patients, respectively.

Cytotoxicity, Immunologic↗
PubMed1982

[The relationship between the number of anti-thyroglobulin antibody forming cells from the cultured peripheral lymphocytes and the serum antibody titers in patients with chronic thyroiditis (author's transl)].

Anti-thyroglobulin antibody forming cells (AFC) were generated from the cultured peripheral lymphocytes of patients with chronic thyroiditis. In order to clarify whether this reflects the antibody formation in vivo, the number of antibody forming cells generated in the culture was related to the serum antibody titer in 121 cases. There was no case which produced more than 10 AFC from 2 x 10(5) B-cells in the group with the low serum antibody titer (less than 10(2)), while 29.4% produced more than 10 AFC in the patients with antibody titer of 20(2) and 20(4) and 65.2% in the group with titer of 80(2) approximately 640(2). The average number of AFC of the last group was 31.4 +/- 17.7 (SD). AFC and serum antibody titers were estimated on various occasions with the same patients. A good relationship was observed between these two parameters. There was no significant correlation between the numbers of AFC and serum antimicrosome antibody titers.

Adolescent↗