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Biomedical subjects

O Taniguchi

Publications and source records attributed to O Taniguchi.

At least 19 recordsLinked to original sources
PubMed2001

Flow cytometric analysis of hemetopoietic progenitor cells in peripheral blood stem cell harvest from patients with CD34 positive acute leukemia.

We analyzed CD34 positive cells in peripheral blood stem cell harvest (PBSCH) using flow cytometry. PBSCH from CD34 positive acute myelogeous leukemia (AML-M2) patient contained 1.87% CD34 positive cells, of which 1.21% was represented by MRD.PBSCH from CD34 positive acute lymphoblast leukemia (ALL) patient contained 3.14% CD34 positive cells, of which 0.11% was accounted for by minimal residual disease (MRD). If PBSCH from CD34 positive acute leukemia patient is analyzed for CD34 monoclonal antibody alone, the presence of CD34 positive MRD may escape attention so that CD34 positive hematopoietic progenitor cells may be overestimated. To avoid this risk, it is necessary to analyze PBSCH using both CD34 monoclonal antibody and characteristic markers of leukemia cells that were found pre-treatment.

Antigens, CD34↗
PubMed1995

Effect of dexamethasone and prednisolone on insulin-induced activation of protein kinase C in rat adipocytes and soleus muscles.

We examined the effect of glucocorticoids on [3H]2-deoxyglucose ([3H]2-DOG) uptake, [125I]insulin binding, tyrosine kinase activity, and protein kinase C (PKC) activity in rat adipocytes and soleus muscles. In adipocytes, insulin-stimulated [3H]2-DOG uptake was decreased by prior 60-minute treatment with dexamethasone (DEX) or prednisolone (PSL), whereas [125I]insulin binding, insulin (INS) receptor autophosphorylation, and tyrosine kinase activity, as measured using exogenous substrate of poly(Glu80-Tyr20), were not significantly changed. Cytosolic PKC activity decreased and membrane-associated PKC activity increased during a 60-minute treatment of adipocytes and soleus muscles with DEX or PSL, indicating that both DEX and PSL stimulate the translocation and activation of PKC. However, pretreatment of adipocytes and soleus muscles with glucocorticoids resulted in reduced INS-stimulated translocation of PKC from cytosol to membrane. INS-induced decreases in cytosolic PKC activity (50% +/- 7% v 10% +/- 8% and 20% +/- 7%, P < .05 to .01, for nonpretreated [control], DEX pretreated, and PSL pretreated cells) and increases in membrane PKC (100% +/- 10% v 50% +/- 9% and 20% +/- 9%, P < .01, for control, DEX pretreated, and PSL pretreated cells) were larger in nonpretreated adipocytes than in adipocytes pretreated with glucocorticoids. These results raise the possibility that glucocorticoids, namely, DEX and PSL, stimulate the translocation and subsequent degradative downregulation of PKC, and that this may be pertinent to their inhibitory effects on INS-stimulated glucose transport.

Adipose Tissue↗
PubMed1994

Phorbol ester and insulin stimulate protein kinase C isoforms in rat adipocytes.

We examined effect of insulin or 12-O-tetradecanoyl phorbol 13-acetate (TPA) on the subcellular redistribution of protein kinase C isoforms in rat adipocytes. Total Mono Q column-elutable novel PKCs (nPKCs) which are Ca(2+)-independent and phospholipid-dependent protein kinases, decreased in the cytosolic fraction and increased in the membrane fraction during treatment with insulin or phorbol ester for 10 min. Immunoblot analysis of novel PKCs, -epsilon, -delta and -zeta, showed that insulin stimulated the translocation of these PKC isoforms from cytosol to membrane, similar to the translocation of conventional Ca2+/phospholipid-dependent PKCs (cPKCs), -alpha, -beta, and -gamma. Phorbol esters stimulated the translocation of PKC-alpha, -beta, -gamma, -epsilon and -delta, but not PKC-zeta. These results suggest that (a) insulin and phorbol esters similarly stimulate the translocation of each PKC isoform except for PKC-zeta, and (b) the translocation of both nPKCs and cPKCs occurs during insulin and TPA actions in rat adipocytes.

Adipocytes↗
PubMed1994

Thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in NIDDM patients treated by diet, sulphonylurea or insulin.

We studied thrombin-induced metabolism of phosphoinositide, protein phosphorylation and platelet aggregation in platelets from 32 NIDDM patients and 12 control subjects. To clarify the effect of diet, sulphonylureas, or insulin treatment, the subjects were divided into three groups based on the type of treatment. Thrombin-induced platelet aggregation was measured with an aggregometer. Low-dose thrombin (0.25 U/ml)-stimulated platelet aggregation in diabetic patients was significantly increased compared with the control subjects. Platelet aggregation in the sulphonylurea and insulin groups was significantly lower than in the diet group. On the other hand, in platelets incubated with [32P]orthophosphate, thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) was significantly lower in the sulphonylurea and insulin groups than in the diet group. Thrombin-induced incorporation of [32P] radioactivity into phosphatidylinositol (PIP) for 10 s was significantly higher in the sulphonylurea group than in the diet group. There were no differences in thrombin-induced 47 kDa protein phosphorylation between platelets from the diet, sulphonylurea, or insulin groups. These results suggest that sulphonylureas and insulin induce suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP2 and production of PA, which leads to inhibition of platelet aggregation.

Adult↗
PubMed1994

ACTH and phorbol ester stimulated redistribution of protein kinase C in human cortisol-producing adrenal adenoma.

We studied the steroidogenetic action and concomitant subcellular redistribution of protein kinase C (PKC) in cortisol hypersecreting adrenal adenoma cells obtained from two patients with Cushing's syndrome. Isolated adenoma cells were treated with 10(-9) M and 10(-6) M 12-O-tetradecanoyl phorbol-13-acetate (TPA) or 10(-6) M ACTH. Treatment of the isolated adenoma cells with TPA resulted in cortisol secretion equivalent to that with ACTH-treatment. Immunoblot analysis of PKC during treatment with ACTH or TPA showed that PKC beta translocated from cytosol to membrane. A small amount of PKC alpha, but not membrane-associated PKC alpha, was detectable in the cytosolic fraction. It appeared that TPA-induced cortisol secretion mimicked ACTH-induced cortisol secretion, and that PKC beta translocated from cytosol to membrane on stimulation by both ACTH and TPA. We suggested that ACTH-induced cortisol secretion in human cortisol hypersecreting adrenal adenoma is mediated by PKC beta activation.

Adenoma↗
PubMed1992

Distribution and clinical significance of lupus anticoagulant and anticardiolipin antibody in 349 patients with systemic lupus erythematosus.

Samples from 349 patients with systemic lupus erythematosus (SLE) were tested simultaneously for lupus anticoagulant (LAC) and anticardiolipin antibodies (ACL). LAC was detected in 27.2% of 349 SLE patients by a modified mixing kaolin clotting time. ACL was detected in 34.7% by enzyme-linked immunosorbent assay. Only half of the patients who had LAC or ACL were positive for both of them. In addition, isotypes of ACL in these patients were studied. The IgG isotype was detected in 81.8% of 121 patients, and more than half had only the IgG isotype. When clinical features of patients with LAC or ACL were studied, the incidence of thrombosis, fetal loss, and thrombocytopenia were significantly higher in both groups compared with patients without LAC or ACL. In particular, the patients with both LAC and ACL showed the highest risk of fetal loss (89%) during pregnancy. These results indicate that LAC and ACL are detected in partly different groups of SLE patients, but both of these groups are clinically similar.

Antiphospholipid Syndrome↗
PubMed1991

Klinefelter's syndrome associated with progressive systemic sclerosis: report of a case and review of the literature.

A case of Klinefelter's syndrome associated with progressive systemic sclerosis (PSS) is described. The patient had been infertile for 20 years after marriage and was diagnosed as PSS with Klinefelter's syndrome at the age of 43. In reviewing the literature, we observed that five cases with PSS within the range of 41 to 61 years of age, and seventeen cases with systemic lupus erythematosus (SLE), but only few cases with other connective tissue diseases were reported in association with Klinefelter's syndrome. Possible involvement of male hypogonadism in the pathogenesis of PSS was suggested.

Connective Tissue Diseases↗
PubMed1989

An improved method for the detection of IgE antibody of defined specificity by ELISA using rat monoclonal anti-IgE antibody.

An improved method for the detection of IgE antibody of defined specificity by ELISA using rat monoclonal anti-IgE antibodies is described. The innovation consists of coating the plates first by a monoclonal rat anti-murine IgE antibody, adding the sera to this antibody-coated plates and then adding the biotin-conjugated antigen after the sera. The plates are then reacted with streptavidin-peroxidase and developed. This procedure eliminates possible competitions with other isotypes of the same specificity. The method is useful especially to quantitate IgE with defined specificity in the presence of high amounts of isotypes of the same specificity.

Animals↗
PubMed1989

[Evaluation of the 1987 revised ARA criteria for rheumatoid arthritis in Japan].

Three hundred and sixty two Japanese patients with rheumatoid arthritis (RA) and 455 patients with other rheumatic diseases (SLE 233, PSS 63, MCTD 51, PM-DM 41 Behcet's disease 33 and OA 33) were examined for the evaluation of the 1987 revised ARA criteria for RA. In our cases sensitivity was slightly decreased and specificity was markedly increased 5 out of 7 criterions compared with the results reported by ARA. In the investigation how many number of criterions at least which the patients with RA should satisfy, 4 out of 7 criterions in the 1987 criteria turned out the highest figure in the accuracy (the mean of sensitivity and specificity values). So the patients who satisfied at least 4 criterions were classified to have RA. Sensitivity of the 1987 criteria decreased to 90% although that of the 1958 ARA criteria was 93%. Specificity were markedly increased from 88% to 95% (the 1958 and 1987 criteria, respectively). These results might be based on the revision of the duration of "morning stiffness" (lasting at least 1 hour) and on the deletion of "joint pain or tenderness" which was relatively less specific for RA.

Arthritis, Rheumatoid↗
PubMed1988

Leu-1(CD5) B cell subpopulation in patients with various liver diseases--special reference to hepatitis B virus carrier and to changes caused by prednisolone therapy.

A human B cell subpopulation identifiable by the expression of the cell surface antigen Leu-1(CD5) was examined in peripheral blood lymphocytes obtained from patients with various liver diseases by dual two-color fluorescence flow cytometry. A significantly high level of Leu-1 B cells in chronic hepatitis and in liver cirrhosis especially in hepatitis B surface antigen (HBsAg)-positive patients (hepatitis B virus carriers) was observed. However, there was no significant difference between the percentage in controls and those in patients with acute hepatitis and primary biliary cirrhosis. Moreover, we could not demonstrate a correlation between the incidence of these cells and positive IgM class rheumatoid factor in patients with liver diseases. The percentage of Leu-1 B cells in patients who had been receiving prednisolone at the time of this study was lower than that in healthy controls. These results suggested that Leu-1 B cells might be associated with the continuation of the HBsAg-positive state and that the presence of the Leu-1 B cell population might be modified by prednisolone administration.

Adult↗
PubMed1988

Anti asialo GM1 antibody detected in the patients' sera from systemic lupus erythematosus and Behçet's diseases with neurological manifestations.

A high incidence of antibody to asialo GM1 was observed in the sera from the patients with Systemic Lupus Erythematosus (SLE) and Behçet's disease with neurological manifestations, using Enzyme Linked Immunosorbent Assay (ELISA), and Thin-layer Chromatography (TLC) immunostaining. The sera from 60 out of 102 cases of SLE with neurological disorders and 6 out of 10 patients with neuro Behçet's disease showed antibody activity against asialo GM1 but not against the asialo GM2, GM1 and galactocerebroside. In 7 out of 123 cases SLE having a history without neurological manifestations and 1 out of 19 Behçet's patients without neurological disorders, antiasialo GM1 antibody could be detectable. However, sera from the patients with other autoimmune diseases, such as RA (60 cases) and P S S (32 cases) or from normal subjects did not show any antibody activity against asialo GM1. Antiasialo GM1 antibody activity presents in both IgM and IgG immunoglobulin classes by class specific ELISA and TLC immunostaining. These studies suggest that detection of antiasialo GM1 antibody may be useful in clinical diagnosis and these autoantibody plays a important role in the pathogenesis of neurological manifestations accompanying SLE and Neuro-Behçet's disease.

Antigen-Antibody Complex↗
PubMed1988

Studies on murine IgE with monoclonal antibodies. I. Characterization of rat monoclonal anti-IgE antibodies and the use of these antibodies for determinations of serum IgE levels and for anaphylactic reactions.

Rat monoclonal antibodies were constructed by fusion of immunized rat spleen cells with a nonsecreting mouse myeloma cell. Two monoclonal antibodies (6HD5 and HMK-12) were selected for further study. Both reacted with various IgE molecules of different specificities and different allotypes, but did not react with immunoglobulins of other isotypes and with light chains. These antibodies were therefore anti-isotypic (IgE) and not anti-allotypic or anti-idiotypic. It was shown by competition studies that these antibodies recognize different epitopes on the FcR epsilon fragment. A sensitive ELISA for the quantitation of murine IgE was developed with these monoclonal antibodies; the sensitivity was between 2 and 250 ng/ml for detection of serum IgE levels. Good correlation was obtained with protein amounts as determined by enzyme-linked immunosorbent assay (ELISA) and passive cutaneous anaphylaxis (PCA) activities. Both monoclonal antibodies were used to study anaphylactic reactions elicited by IgE antibodies. Both could inhibit PCA reactions and both could elicit reverse PCA reactions.

Animals↗
PubMed1987

The Leu-1 B-cell subpopulation in patients with rheumatoid arthritis.

Ly-1-B cells have been shown to be elevated in autoimmune mice, especially NZB, and to secrete IgM autoantibody, suggesting that Ly-1 B cells may participate in autoimmune diseases. In this study, B-cell populations carrying Leu-1, a human T-cell surface molecule homologous to mouse Ly-1 (Leu-1 B), were examined by dual fluorescence flow cytometry, in peripheral blood lymphocytes taken from patients suffering from various autoimmune disease. These B cells were shown to be present at a significantly high percentage in rheumatoid arthritis (RA) patients. There was no significant correlation among the incidence of Leu-1 B cells, rheumatoid factor (RF) titers, and the amount of IgM production in vitro. There was, however, a significantly high incidence of Leu-1 B cells in RA patients with a high RF titer (greater than 5 X 2(13), suggesting that these B cells in RA may play an important role in IgM RF production in vivo.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1984

Fixation of complement by anti-F(ab')2 antibodies or ssDNA when added to systemic lupus erythematosus sera.

A solid phase total hemolytic complement assay was used to quantitatively determine the % complement fixation by anti-F(ab')2 antibodies or ssDNA when added to serum from patients with systemic lupus erythematosus (SLE). Both autologous and homologous anti-F(ab')2 antibodies with demonstrated anti-anti-ssDNA activity fixed complement when added to SLE sera and normal human complement. Furthermore, comparable amounts of anti-F(ab')2 antibodies with minimal anti-anti-ssDNA activity fixed zero or minimal amounts of complement when added to the same lupus sera. When measured by the same assay with the same sera, ssDNA fixed greater amounts of complement than did comparable amounts of any of the anti-F(ab')2 antibodies.

Antibodies, Anti-Idiotypic↗