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J Yata

Publications and source records attributed to J Yata.

At least 109 records · Page 6Linked to original sources

[A reverse phase high performance liquid chromatography-UV spectrometry method for the analysis of several intrinsic adrenal delta 4-steroid concentrations].

Taking an advantage of the property of delta 4-steroid that have a maximum absorbance around 250 nm wave-length of ultraviolet, we devised an assay method for the determination of serum delta 4-steroids concentration using a reverse phase high performance liquid chromatography (HPLC)-UV spectrometry. The assay procedure was as follows: A mixed solvent containing methanol, acetonitrile and water in 55/3/42 by volume was used as a mobile phase, and which was pumped at a constant flow rate of 1.5 ml/min. The main column and precolumn used were ERC-ODS-1161 (phi 6 mm X 10 cm) and ERC-ODS-1652 (phi 6mm X 3 cm), respectively. Two liquid-liquid extraction methods were used. One was a conventional method using dichloromethane for an extraction solvent, and the other was a simplified method using Extrelut column and ethyl acetate. Before a practical assay we examined the retention time of each steroid determined and its ratio of peak height to that of the internal standard (dexamethasone). We found good correlations between the concentrations of cortisol (F), 17 alpha-hydroxyprogesterone (17-OHP) and 21-deoxycortisol (21-DOF) estimated by this HPLC method and those by highly specific radioimmunoassay method. The concentrations of cortisone (E) and F of eight umbilical venous blood specimens were 159.7 +/- 26.3 (Mean +/- SD) ng/ml and 93.3 +/- 58.9 ng/ml, respectively, and 17-OHP was detected 7 of them and its concentration was 17.4 +/- 12.4 ng/ml. On the other hand, 17-OHP and 21-DOF peaks could not be detected in 1 month old normal infants.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗

Immunoregulatory function and expression of OKT17 antigen of adult T-cell leukemia cells.

Research was carried out on neoplastic T-cells taken from 10 cases of Japanese adult T-cell leukemia (ATL) in regard to their immunoregulatory activity on pokeweed mitogen (PWM)-driven immunoglobulin (Ig) production and their differentiation antigens. ATL cells were reactive with OKT3, OKT4 and OKT11 in most cases; however, the ATL cells from one case did not react with OKT11 nor formed E-rosettes. ATL cells of three cases were reactive with OKT8 as well as OKT4. In six cases, the ATL cells were reactive with OKT17 and coincidentally displayed suppressor activity on Ig production. The cells of the remaining four cases did not have such reactivity with OKT17 or suppressor activity. Moreover, the OKT17(+) ATL cells from one case sorted by FACS 440 demonstrated suppressor activity, while the OKT17(-) ATL cells did not. These results indicated that ATL cells with suppressor activity had OKT3(+), OKT4(+), OKT17(+) phenotype.

Adult↗

Defect of suppressor cell induction in patients with juvenile rheumatoid arthritis.

We studied the suppressor cell activity induced by concanavalin A (Con A) in 9 patients with acute febrile juvenile rheumatoid arthritis (JRA). The suppressor activity of JRA patients was higher than that of normal controls. However, the activity was significantly reduced by treating Con A-activated cells with mitomycin C (MMC) (P less than 0.05). On the other hand, the suppressor activity of normal controls and systemic lupus erythematosus (SLE) patients was not affected by MMC treatment. Two of 5 SLE patients showed low activity even before MMC treatment. The addition of the culture supernatant of Con A-stimulated peripheral blood mononuclear cells from a normal donor restored the induction of suppressor activity of JRA which was decreased by MMC treatment. The results indicated that patients with acute febrile type of JRA had reduced MMC resistant suppressor cell activity and that this was due to a defect in the ability of the cells to produce soluble factors needed to induce MMC resistant suppressor cells.

Arthritis, Juvenile↗

Primary immunodeficiency diseases and malignancy in Japan.

Twenty-two cases out of a total of 683 patients (3.2%) with primary immunodeficiency diseases registered in the All-Japan Immunodeficiency Registry were reported to have developed malignant diseases. In the childhood patients with ataxia-telangiectasia the incidence of death due to malignancy was approximately 625 times higher than that of the normal Japanese childhood population. The incidence of lymphoproliferative disorders, such as malignant lymphoma, in Chediak-Higashi syndrome and the incidence of non-Hodgkin lymphoma and various carcinomas in ataxia-telangiectasia were both high, 37.5% and 13.7%, respectively. Only one case out of 45 with Wiskott-Aldrich syndrome was reported to have malignant lymphoma. The data obtained were compared with international statistics reported by the Immunodeficiency Cancer Registry.

Adolescent↗

[Age-related changes of serum 17 alpha-hydroxypregnenolone and 17 alpha-hydroxypregnenolone sulfate concentrations in infancy and childhood].

In order to clarify a part of the developmental processes of the human adrenal cortex or steroidgenesis in infancy and childhood, serum concentrations of 17 alpha-hydroxypregnenolone (17-OH-delta 5 P), 17 alpha-hydroxypregnenolone-3-sulfate (17-OH-delta 5 P-S) and 17 alpha-hydroxyprogesterone (17-OH-delta 4 P) were measured using a combined radioimmunoassay method previously reported, and age-related changes of these steroids were evaluated. In addition to the serum concentrations, a ratio of 17-OH-delta 5 P-S to 17-OH-delta 5 P (S/delta 5 P ratio) and that of 17-OH-delta 4 P to 17-OH-delta 5 P (delta 4 P/delta 5 P ratio) were also estimated as the indices of the activities of steroid sulfokinase (SK) and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), respectively. Serum 17-OH-delta 5 P, 17-OH-delta 5 P-S and 17-OH-delta 4 P concentrations in umbilical cord blood were 13.5 +/- 6.02 (Mean +/- SD) ng/ml, 965 +/- 363 ng/ml and 46.3 +/- 21.1 ng/ml, respectively. These values decreased consecutively to the nadirs which were 0.47 +/- 0.16 ng/ml in subjects 1 to 2 years old, 1.26 +/- 0.82 ng/ml in subjects 3 to 6 years old and 0.17 +/- 0.007 ng/ml in subjects 3 to 4 months old, respectively, and they were followed by gradual increases up to the adult levels. S/delta 5 P ratio also showed the same profile.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxypregnenolone↗

Immunoregulatory functions of neoplastic lymphoid cells and their humoral products.

The immunologic functions of neoplastic lymphoid cells from 57 cases of lymphocytic leukemia or malignant lymphoma were examined in vitro where cells from 16 cases demonstrated regulatory functions in immunoglobulin production: 4 with helper activity, 8 with suppressor activity, 1 with presuppressor activity, and 3 with helper-inducer activity. The neoplastic lymphoid cells with such functions did not necessarily form E-rosettes, but because of the presence of human T-cell antigens, most of them appeared to be of the T-cell lineage. These regulatory functions were proven to be mediated by the humoral factor, at least in some of the cases tested. Neoplastic lymphoid cells from all 6 cases with Fc receptors showed antibody-dependent cell-mediated cytotoxicity, but lacked natural killer activity. These studies should provide further insight into the origin of the neoplastic cells.

Adolescent↗

[A combined radioimmunoassay method for the determination of 17 alpha-hydroxypregnenolone, 17 alpha-hydroxypregnenolone sulfate and 17 alpha-hydroxyprogesterone in human blood].

It is well recognized that in the fetal adrenal cortex, 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity is lower and in fetal tissues, steroid sulfokinase (SK) is higher than in the adult. In order to clarify a part of the development processes of the adrenal cortex or steroidgenesis in humans, a combined radioimmunoassay (RIA) method to estimate serum 17 alpha-hydroxypregnenolone (17-OH-delta 5 P), 17 alpha-hydroxypregnenolone sulfate (17-OH-delta 5 P-S) and 17 alpha-hydroxyprogesterone (17-OH-delta 4P) was devised. The method consisted of the following procedures: 1) diethyl ether extraction and chromatographic separation of unconjugated steroids (17-OH-delta 5P and 17-OH-delta 4P), 2) enzymatic hydrolysis of 17-OH-delta 5P-S using the residue of diethyl ether extraction for a material, 3) diethyl ether extraction and chromatographic purification of hydrolyzed 17-OH-delta 5P-S, and 4) RIAs for 17-OH-delta 5-P to estimate 17-OH-delta 5P and 17-OH-delta 5P-S concentration, and for 17-OH-delta 4P. Extracted 17-OH-delta 5P was well separated from 17-OH-delta 4P by Sephadex LH-20 microcolumn chromatography, using a benzene/methanol = 95/5 (v/v) solvent as a mobile phase. Several procedures for hydrolysis or solvolysis of 17-OH-delta 5P-S were compared using available tritiated delta 5-3 beta-hydroxysteroids including dehydroepiandrosterone (DHA), DHA sulfate (DHA-S) and 17-OH-delta 5P, and it was found that the most suitable method was an enzymatic hydrolysis by arylsulfatase from Helix Pomatia in an appropriate condition in which the percent hydrolysis was 92.9 +/- 1.2 (mean +/- SEM)%. The final percent recoveries were 88.7 +/- 1.2% in 17-OH-delta 4P, 90.7 +/- 1.4% in 17-OH-delta 5P and 78.1 +/- 2.1% in 17-OH-delta 5P-S, respectively. A suitable antiserum and its final dilution titer for RIA of 17-OH-delta 5P (hydrolyzed 17-OH-delta 5P-S also) was 1:12,000 dilution of anti-17-OH-delta 5P-3-succinate-BSA serum. An anti-7-oxo-17-OH-delta 5P-7-carboxymethyloxime-BSA serum was considered to be unsuitable for the measurement of hydrolyzed 17-OH-delta 5-P-S, presumably because of a significant cross-reactivity with a large amount of unknown steroid sulfates simultaneously hydrolyzed.(ABSTRACT TRUNCATED AT 400 WORDS)

17-alpha-Hydroxypregnenolone↗

A rapid isolation technique of unmodified human T cells on a polystyrene resin column.

An easy and rapid isolation technique of human T cells on a polystyrene resin particle column has been developed. The cells of the effluent fraction contained more than 90% sheep erythrocyte (SRBC) rosette-forming cells and less than 1% of cells bearing surface immunoglobulin (Ig) or peroxidase. The T cell (SRBC rosette-forming cells) recovery rate was 80%. The distribution of OKT antigen T cell subsets was essentially the same as that of T cells separated by rosette sedimentation. Cell functions such as tritiated thymidine uptake by T cells and helper activity in Ig production were also the same as that of T cells separated by SRBC rosette sedimentation. Natural killer-like activity of the T cells isolated by the present method increased more than that of T cells obtained by the conventional method. Moreover, it was free from functional modification which tends to result from stimulation such as by the SRBC antigen in the SRBC centrifugation method. The combination of a T cell population offered by the present method and B cells depleted of SRBC-binding B cells minimized background plaque formation and enabled us to quantify the plaque-forming cell number in an antigen-specific plaque-forming assay. Furthermore, these populations produced relatively pure interleukin 2 (IL 2) by stimulation of an autologous mixed lymphocyte reaction without any absorption of IL 2 produced in the same culture. It seemed to be useful to evaluate the ability of lymphocytes from normal individuals and patients to produce IL 2.

Antigens, Surface↗

In-vitro analysis of defective IgA production in selective IgA deficiency in childhood.

IgA production from B cells can be driven by three signals (anti-Ig antibody, B cell growth factor and helper T cell factor). It was thought that this three signal system might be a way other than the mitogen-stimulated system, to access B cell differentiation into Ig-producing cells. Seven children with IgA deficiency were investigated by this method. In all cases B cell differentiation was defective when using this three signal system. In one case, IgA producing cells were generated in normal number from B cells when stimulated with pokeweed mitogen in the presence of normal T cells. Definite abnormality of regulatory T cells in the IgA production was observed in only one case. These observations suggested that the main cause of IgA deficiency in most cases is the defect of B cells to differentiate into IgA secreting cells.

B-Lymphocytes↗

A case report of T-cell lymphoma with suppressor phenotype and helper function for immunoglobulin synthesis.

A patient with T-cell lymphoma is presented. The morphologic features of a biopsied lymph node were consistent with adult T-cell lymphoma with hypergammaglobulinemia, and most of the lymph node cells were reactive with monoclonal antibody OKT8, which detects suppressor/cytotoxic T lymphocytes. However, in a pokeweed mitogen-driven test system in which the capability of T lymphocytes to help or suppress the differentiation of B lymphocytes is measured, the lymphoma cells induced immunoglobulin synthesis of B lymphocytes, thus providing helper function. As far as we know, this is the first report on T-cell lymphoma having suppressor phenotype and helper function for immunoglobulin synthesis.

Antibodies, Monoclonal↗

T-cell subsets regulating anti-acetylcholine-receptor-antibody formation in myasthenia gravis and characterization of suppressor T-cell factors involved.

The in vitro generation of anti-acetylcholine-receptor (AChR)-antibody-forming cells from B cells of myasthenia gravis (MG) patients occurred only in the presence of OKT4+ cells. Anti-AChR-antibody formation by lymphocytes from MG patients was suppressed by normal T cells, and the requirement of both OKT4+ and OKT8+ cells was suggested for this suppression. Culture supernatant from normal T cells stimulated with excess doses of AChR antigen, but not T cells from patients, suppressed anti-AChR-antibody formation by lymphocytes from patients. The fraction of the culture supernatant with molecular weight of 45,000 to 67,000 seemed to contain an AChR-antigen-specific and antigen-binding suppressor factor with some allogeneic barrier, while the fraction with a molecular weight of 10,000 to 28,000 contained the antigen-nonspecific factor.

Antibody Formation↗

Increased sensitivity of IL2-dependent cultured T cells and enhancement of in vitro IL2 production by human lymphocytes treated with Bestatin.

Bestatin is an inhibitor of leucine aminopeptidase and aminopeptidase B which potentiates various immune functions, such as delayed hypersensitivity and antibody formation, and inhibits tumor cell growth in animal models. Our study focuses on the effect of Bestatin on interleukin 2 (IL2) sensitivity of IL2-dependent cultured T cells (CTC) and on IL2 production by human peripheral blood mononuclear cells (PBM). Bestatin (0.01 - 10 micrograms/ml) increases CTC 3H-TdR incorporation in the presence of suboptimal (low) concentrations of exogenous IL2. Bestatin alone has no mitogenic effect on CTC. This phenomenon is due to increased CTC IL2-receptors after treatment with Bestatin. Bestatin (1 - 10 micrograms/ml) also increases (1.4 - 21 fold) IL2 production by PHA-stimulated PBM. Bestatin therefore increases both IL2 sensitivity and IL2 production. This may explain the various immunopotentiating effects of Bestatin previously described.

Adjuvants, Immunologic↗