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Biomedical subjects

Y Ichikawa

Publications and source records attributed to Y Ichikawa.

At least 811 records · Page 45Linked to original sources
PubMed1980

Production of a colony-stimulating factor following differentiation of leukemic myleoblasts to macrophages.

Leukemic cells in the myeloblastic stage from a murine myeloid leukemia cell line (M1) were induced to differentiate to macrophages by lipopolysaccharide (LPS) from Gram-negative bacteria. A granulocyte-macrophage colony-stimulating factor (CSF) was produced only during differentiation. After induction of differentiation, the continued presence of LPS was necessary to stimulate the macrophages to release CSF. In contrast, a macrophage cell line (Mm-1) derived from the M1 line produced CSF without LPS-stimulation, but CSF release was stimulated by the presence of LPS.

Animals↗
PubMed1980

Differentiation and production of colony-stimulating factor induced by immunostimulants in a leukemia cell line.

Immunostimulants from various microorganisms were tested on a myeloid leukemia cell line (M1) for the ability to induce production of CSF and to cause differentiation of these cells. Based on their activities, the compounds were divided into two general classes: those inducing extensive cellular differentiation and those devoid of this effect. The stimulants which were active in this regard always produced large quantities of CSF, whereas those devoid of a differentiating effect did not cause CSF production. Even the potent stimulants had no effect on the D subline, in which the differentiation was not inducible.

Adjuvants, Immunologic↗
PubMed1980

Changes in contractile proteins during differentiation of myeloid leukemia cells. I. Polymerization of actin.

Quantitative and qualitative changes in cellular actin were followed during differentiation of a myeloid leukemia cell line, namely Ml, which was inducible with conditioned medium (CM). During 3 d of incubation with CM, when the Ml cells differentiated to macrophages and lost their mitotic activity, the actin content, F-actin ratio in total actin, and the actin synthesis showed an increase. A greater difference before and after differentiation was found in the ability of G-actin to polymerize. Actin harvested from CM-treated cells showed a greater ability to polymerize, depending on the increased concentration of MgCl2 and/or KCl and proteins, as compared with the actin from untreated Ml cells. Actin harvested from the Mml cell line, a macrophage line, had a particularly high polymerizability with or without CM treatment. In contrast, the actin from the D- subline, which is insensitive to CM, showed almost no polymerization.

Actins↗
PubMed1980

Correlation between postsialographical changes of salivary isoamylase levels in serum and histopathological findings in sublingual glands in patients with Sjögren's syndrome.

Salivary isoamylase values in sera were evaluated before and after sialography in 14 patients with Sjögren's syndrome (SS) and were compared with those in non-SS patients. Non-SS patients consisted of cases of systemic lupus erythematosus, rheumatoid arthritis and ulcerative colitis. In non-SS patients, salivary isoamylase 3 to 6 hours after injection of Conray-400 increased to 2.3 +/- 0.5 fold higher than that prior to the injection and returned to the previous values after 48 hours. On the basis of increases in salivary isoamylase after injection of Conray-400, SS could be divided into three groups: the high response group, the group showing the same values as in non-SS patients and the low response group. The high response group was further classified into two subgroups. Salivary isoamylase before injection in the high response group was higher in patients who showed mild mononuclear cell infiltration histopathologically in their sublingual glands and was lower in patients whose sublingual glands showed diffuse infiltration of mononuclear cells. Mononuclear cells had infiltrated severely in the sublingual glands of patients in the low response group, although they showed salivary isoamylase values before injection within the same ranges as in non-SS patients. These data suggest that both salivary isoamylase before injection and maximum salivary isoamylase increased significantly in cases of mild sialadenitis, the former value decreased with increasing infiltration of mononuclear cells into the sublingual glands, and both values were lower in cases of severe sialadenitis.

Amylases↗
PubMed1980

Circulating immune complexes in Sjögren's syndrome.

Circulating immune complexes (IC) in patients with Sjögren's syndrome (SjS) were examined using the 125I-Clq binding method. IC were detected in 52% of the patients, and the highest incidences (80%) of IC were observed in SjS patients with systemic lupus erythematosus (SLE). IC were also demonstrated even in 40% of SjS patients without definite associated diseases. Several systemic manifestations suggesting participation of IC and hypocomplementemia were recognized in these IC-positive patients at the time of assay for IC. The levels of IC were positively correlated with both the erythrocyte sedimentation rate (ESR) and serum gammaglobulin in SjS patients. The incidences of IC increased in patients with severe sialographical changes in their parotid glands. The roles of circulating IC in advancement of the disease as well as in the occurrence of systemic manifestations in this syndrome were proven by the present results.

Age Factors↗
PubMed1980

Cellular immunity to secretory IgA (as a common duct antigen of exocrine glands) in Sjögren's syndrome.

Autoimmunity to salivary duct cells has been suggested in Sjögren's symdrome (SjS). We were interested in the secretory component (SC) of secretory IgA (s-IgA) as a common duct cell antigen of systemic exocrine glands because of the possible analogy between SC in SjS and thyroglobulin in Hashimoto's thyroiditis. Therefore, we isolated s-IgA as a source of SC from human milk and investigated lymphocyte responses to s-IgA in patients with SjS. Higher mitogenic indices against s-IgA were demonstrated in SjS than in rheumatoid arthritis, other autoimmune diseases and normal persons. In addition, mitogenic indices in patients with SjS alone were significantly higher than those in SjS patients with associated diseases. These results suggest both the role of SC as a common antigen of exocrine glands in the pathology of SjS, and the presence of an etiologically different subgroup in patients with SjS.

Humans↗
PubMed1980

Lymphocytotoxic antibody in Sjögren's syndrome.

The autoimmune mechanism in Sjögren's syndrome (SjS) and the close association of this syndrome with systemic lupus erythematosus (SLE) have been suggested in several reports. Although the pathological significances of lymphocytotoxic antibody is obscure, possible roles of this antibody in the pathogenesis of autoimmunity have been speculated. The purposes of the present study were to demonstrate lymphocytotoxic antibody in sera of patients with SjS, and then to analyse various correlations of this antibody with clinical parameters of SjS. We detected cold-reactive lymphocytotoxic antibody not only in most (86.4%) of the patients with SLE, but also in many patients with SjS (51.6%; excluding SjS patients with SLE), rheumatoid arthritis (RA; 31.6%) and myasthenia gravis (MG; 36,4%), which are considered to be autoimmune diseases. On the other hand, lymphocytotoxic antibody was detected in only one (5.6%) of eighteen healthy persons. We also confirmed that the cold-reactive lymphocytotoxic antibody detected in SLE is 2-mercaptoethanol sensitive and T-lymphocytotoxic antibody. Frequent demonstration (50%) of this antibody even in SjS patients without any associated diseases supports the immunological basis of SjS as well as virological participation in SjS. Although this antibody did not significantly correlate with most of the clinical parameters in SjS patients, this antibody may become a hallmark as one of immunological abnormalities in SjS, even though it was produced by non-specific lymphocyte activation.

Animals↗
PubMed1980

Antibody-dependent cell-mediated cytotoxicity by peripheral blood mononuclear cells from patients with Sjögren's syndrome, with special reference to differentiation from phagocytic activity.

Antibody-dependent cell-mediated cytotoxicity (ADCC) by peripheral blood mononuclear cells in patients with Sjögren's syndrome (SjS) was estimated with special reference to differentiation from phagocytic activity caused by phagocytes. There was no significant difference in ADCC activity of peripheral blood lymphocytes (phagocyte-depleted lymphocyte fraction) between patients with SjS and normal persons. Higher ADCC activity of the crude lymphocyte fraction (CLF), however, was demonstrated in patients with SjS than in normal persons. It was proved that increased ADCC activity of CLF in patients with SjS resulted from reduced erythro-phagocytic activity of contaminating monocytes in this fraction.

Adult↗
PubMed1979

Physicochemical properties of reduced nicotinamide adenine dinucleotide phosphate-cytochrome P-450 reductase from bovine adrenocortical microsomes.

Adrenocortical NADPH-cytochrome P-450 reductase (EC. 1.6.2.4) was purified from bovine adrenocortical microsomes by detergent solubilization and affinity chromatography. The purified cytochrome P-450 reductase was a single protein band in sodium dodecyl sulfate-polyacrylamide gel electrophoresis, being electrophoretically homogeneous and pure. The cytochrome P-450 reductase was optically a typical flavoprotein. The absorption peaks were at 274, 380 and 45 nm with shoulders at 290, 360 and 480 nm. The NADPH-cytochrome P-450 reductase was capable of reconstituting the 21-hydroxylase activity of 17 alpha-hydroxyprogesterone in the presence of cytochrome P-45021 of adrenocortical microsomes. The specific activity of the 21-hydroxylase of 17 alpha-hydroxyprogesterone in the reconstituted system using the excess concentration of the cytochrome P-450 reductase, was 15.8 nmol/min per nmol of cytochrome P-45021 at 37 degrees C. The NADPH-cytochrome P-450 reductase, like hepatic microsomal NADPH-cytochrome P-450 reductase, could directly reduce the cytochrome P-45021. The physicochemical properties of the NADPH-cytochrome P-450 reductase were investigated. Its molecular weight was estimated to be 80 000 +/- 1000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and analytical ultracentrifugation. The cytochrome P-450 reductase contained 1 mol each FAD and FMN as coenzymes. Iron, manganese, molybdenum and copper were not detected. The Km values of NADPH and NADH for the NADPH-cytochrome c reductase activity and those of cytochrome c for the activity of NADPH-cytochrome P-450 reductase were determined kinetically. They were 5.3 microM for NADPH, 1.1 mM for NADH, and 9-24 microM for cytochrome c. Chemical modification of the amino acid residues showed that a histidyl and cysteinyl residue are essential for the binding site of NADPH of NADPH-cytochrome P-450 reductase.

Adrenal Cortex↗
PubMed1979

Effect of sodium chloride on the respiratory function of Staphylococcus aureus.

Sodium chloride at concentrations below 0.5 M, enhanced the respiratory activity (O2-consumption) of Staphylococcus aureus under endogenous and sugar-supported conditions, but did not overcome the inhibitory action of sodium azide. Several sugars, including the glucose analogue alpha-methylglucoside, and their metabolites enhanced bacterial O2-consumption, but acetylmethylcarbinol was ineffective.

Azides↗
PubMed1979

Requirements for RNA and protein synthesis in the induction of several differentiation-markers in a myeloid leukemia cell line.

In a myeloid leukemia cell line, the inducibilities of the Fc receptor, phagocytosis and cell motility were compared. Thymidine analogues such as BUdR, BCdR and IUdR blocked the induction of phagocytosis and motility but not induction of the Fc receptor. This BUdR susceptibility in the induction of phagocytosis and motility was lost in a BUdR resistant line which was isolated for its growth capability in a high concentration of BUdR. Actinomycin D and puromycin brought about a marked decrease in the inducibility of phagocytosis but not in that of the Fc receptor. This led us to the following conclusion: There is a genetic control in the inducibility of phagocytosis and motility in this cell line, and the incorporation of BUdR into cellular DNA results in the DNA becoming unresponsive to a differentiation-stimulating factor. In contrast, gene activation does not seem to be necessary for induction of the Fc receptor. The order of induction of several differentiation markers was also discussed.

Animals↗