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Biomedical subjects

N Taniguchi

Publications and source records attributed to N Taniguchi.

At least 667 records · Page 37Linked to original sources
PubMed1982

Studies of human T gamma cells: division of a T gamma subset in normal and leukemic cells by using anti-T gamma-CLL heteroantiserum.

A specific heteroantiserum was prepared against the leukemic cells from a patient with T-derived chronic lymphocytic leukemia (T-CLL). The anti-serum was absorbed with cells of a morphologically different type from another patient with T-CLL. Both the immunizing cells and absorbing cells had Fc receptor for IgG (Fc gamma R), so the former case was named T gamma-CLL type 1, and the latter T gamma-CLL type 2. This antiserum, termed anti-T gamma-1, reacted with 19% of normal peripheral blood T lymphocytes, but not with non-T lymphocytes or monocytes. The T lymphocytes in the blood that reacted to anti-T gamma-1 were 72% of the T gamma cells. Anti-T gamma-1 also reacted to 60-78% of the thymocytes. Except for T gamma-CLL type 1 cells, anti-T gamma-1 did not react with various types of leukemia cells from lymphoid malignancies, myelogenous leukemias and monocytic leukemias. Studies on the relation between anti-T gamma-1 and OKT8 monoclonal antibody revealed that anti-T gamma-1 reactive (anti-T gamma-1+) cells and OKT8+ cells largely overlapped, but they were different in part. More interestingly, OKT8 inhibited Fc gamma R binding, but anti-T gamma-1 did not. These results indicate that anti-T gamma-1 is useful for detecting a certain subset of T cells and for classifying lymphoproliferative disorders.

Antibodies, Monoclonal↗
PubMed1982

Expression of Ia-like antigens defined by monoclonal OKIal antibody of hemopoietic progenitor cells in cord blood: a comparison with human bone marrow.

Expression of Ia antigens on granulocyte/macrophage colony-forming cells (CFU-GM) in human cord blood was compared with that in bone marrow with the use of monoclonal OKIal antibody. Mononuclear cells prepared from cord blood and bone marrow were pretreated with OKIal antibody plus complement, and, thereafter, the ability of cord blood and bone marrow cells to form colonies of CFU-GM was assayed in semisolid agar culture. Consistent reduction in the number of CFU-GM in cord blood to 58.8% +/- 13.0% (mean +/- SD) of controls treated with complement alone was shown after elimination of Ia-antigen-bearing CFU-GM, but was significantly remarkable than that in bone marrow (18.0% +/- 5.6%). Although the reduction of both granulocyte (CFC-G) and macrophage colony (CFC-M) types of cord blood, characterized by the double staining for esterase activity, was shown following treatment with OKIal antibody plus complement, the relative inhibition of CFC-G weas significantly greater than that of CFC-M (p less than 0.02). These results suggest some differences in the characteristics of Ia-antigen-bearing CFU-GM between cord blood and bone marrow cells. Furthermore, it is suggested that Ia-dependent regulatory mechanisms might participate in the differentiation of CFU-GM to CFC-G and CFC-M.

Antibodies, Monoclonal↗
PubMed1982

Discrepancy in expression ability of Tac antigen and Ia determinants defined by monoclonal antibodies on activated or cultured cord blood T lymphocytes.

T lymphocytes from cord blood and adults stimulated with mitogens and alloantigen were analyzed using monoclonal antibodies that detect Ia and Tac antigens associated with lymphocyte activation. Less than 5% of T cells freshly isolated or cultured without stimuli expressed Ia and Tac antigens assessed by the indirect immunofluorescence method. When both T cells from cord blood and adults were cultured with phytohemagglutinin (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), or allogeneic cells, variable proportions of them expressed Tac antigen. The expression of Tac antigen on stimulated T cells increased in parallel with DNA synthesis, and was significantly correlated with the proliferative response of stimulated T cells. In contrast to Tac antigen, the expression of Ia antigens appeared to show some time lag behind the proliferative response. Although expression of Ia antigens was too weak to assess in PHA- or Con A-stimulated cultures, adult T cells were stimulated by PWM or allogeneic cells to express strongly Ia antigens in culture. However, the percentage of Ia+ cells in cord blood T cells stimulated with PWM or allogeneic cells was markedly lower as compared with that of adults. In addition, cord blood T cells grown in the presence of T cell growth factor showed the same degree of Tac antigen as adult ones did, whereas their expression of Ia antigens was negligible as compared with adult controls. These observations suggested that T cells in cord blood might be deficient by nature in their ability to express Ia antigens on activation. The inability to develop Ia+ T cells seemed to be characteristic of functional immaturity of T cells in early human ontogeny.

Adult↗
PubMed1982

Functional significance of Tac antigen expressed on activated human T lymphocytes: Tac antigen interacts with T cell growth factor in cellular proliferation.

Cultured human T cells (CTC), which are grown in conditioned medium containing T cell growth factor (TCGF), proliferate in response to TCGF. It has been shown that an antigen (Tac) defined by a monoclonal antibody, termed anti-Tac antibody, is expressed on human T cells activated by mitogens or antigens and CTC grown in the presence of TCGF. To elucidate the functional significance of Tac antigen expressed on activated T cells, we studied the effect of anti-Tac antibody on TCGF-dependent proliferation of CTC. The addition of anti-Tac antibody strongly inhibited the proliferation of CTC induced by TCGF. This inhibition was observed only when the antibody was added at the early phase of culture, but not when the addition of the antibody was delayed beyond 24 hr of culture. Seven-day-old PHA-induced T cell blasts, but not fresh peripheral blood lymphocytes, were able to absorb TCGF activity in conditioned medium, as assessed by the DNA synthesis of CTC. When PHA-induced blasts were treated with anti-Tac antibody before absorption, their capacity to absorb TCGF activity was almost completely eliminated. In contrast, absorption of TCGF by PHA-induced blasts was not significantly reduced even when they were pretreated with other monoclonal antibodies (anti-Ia, OKT9, or OKT10) with specificity for antigens expressed on activated T cells. Based on the view that TCGF interacts with activated T cells via specific membrane receptors, these observations suggested that anti-Tac antibody might specifically block the binding of TCGF to the corresponding membrane binding sites, resulting in the inhibition of TCGF-dependent proliferation of CTC. Tac antigen expressed on activated T cells seems to participate in responding process of activated T cells to TCGF.

Antigen-Antibody Reactions↗
PubMed1981

Low urinary excretion of heparan sulfate in three patients with Lowe's syndrome.

Urinary glycosaminoglycans were isolated with the cetylpyridinium chloride (CPC) precipitation method and the excretion of individual species of urinary glycosaminoglycans in three patients with Lowe's syndrome was compared with that of age-matched control children by means of electrophoresis on cellulose acetate membranes and by quantification of hexosamine contents. Total daily excretion of urinary glycosaminoglycans in the patients seemed to be normal, but the relative excretion of urinary heparan sulfate was significantly reduced and ranged from 26 to 46% of the age-matched control mean, when calculated on the basis of relative glucosamine content in urinary glycosaminoglycans. Although electrophoretograms of urines from patients with Lowe's syndrome suggested some excess of low sulfated chondroitin sulfate corresponding in mobility to dermatan sulfate, the enzymatic subunit assay employing chondroitinases did not disclose any significant differences in the excretion pattern or in the degree of sulfation of chondroitin sulfate isomers between lowe's syndrome and control children.

Adolescent↗
PubMed1981

Zinc deficiency states and carbonic anhydrase isozyme in experimental hemolytic and bleeding anemia of rabbits.

Zinc deficiency states were produced in rabbit erythrocytes by experimentally induced bleeding anemia and hemolytic anemia. Parallel decreases in total zinc levels and the contents for major zinc protein, carbonic anhydrase I and II isozymes were observed in the erythrocytes. During the process of the anemias the zinc status in the erythrocytes varied remarkably and the relative increase of zinc ions other than that derived from carbonic anhydrase was observed, suggesting that the former zinc ions play an important role in forming a zinc pool in the erythrocytes under the anemic conditions.

Anemia↗
PubMed1981

Echocardiographic visualization of ventricular septal defect in infants and assessment of hemodynamic status using a contrast technique. Comparison of M-mode and two-dimensional imaging.

Twenty-seven patients with ventricular septal defect (VSD), ages 2 months to 2 years, were evaluated by both M-mode and two-dimensional echocardiography (2-D echo) with the aid of a peripheral venous contrast technique. M-mode echocardiography was unreliable for imaging VSD. Using 2-D echo, defects in the interventricular septum were visualized in all patients examined; defects in the membranous portion (24 patients) were visualized by the subcostal frontal approach and defects in the supracristal portion (three patients) by the subcostal sagittal approach. The 2-D echo contrast study revealed negative contrast jets appearing through the defect in the right ventricle in 22 patients with a pulmonary-to-systemic blood flow ratio greater than 2.0, and positive contrast jets appearing through the defect in the left ventricle in 13 patients with a right-to-left ventricular peak pressure ratio greater than 0.71. We conclude that 2-D echo with peripheral contrast technique confirmed the anatomic location of VSD and indicated the approximate right-to-left ventricular peak pressure ratio, showing the contrast material shunting through the defect itself.

Cardiac Catheterization↗
PubMed1981

Effect of pyridoxal 5-phosphate on the activity of GOT isozyme in plasma from patients with Duchenne muscular dystrophy.

GOT isozyme (soluble GOT, s-GOT and mitochondrial GOT, m-GOT) activities with and without reactivation by the co-enzyme pyridoxal 5-phosphate (PALP) in plasma from 42 patients with Duchenne muscular dystrophy (DMD), and 11 normal controls were investigated. The magnitude of the enzyme activities in patients at the early stage of DMD greatly exceeded those of controls. As the disease progressed, the levels gradually declined, but late stage values were still higher than the control values except s-GOT with PALP. At the mid stage as well as the late stage, the increase in m-GOT activity was approximately to double the unstimulated activity, indicating that, in these patients, as much as half the m-GOT in the circulation was in the inactive apoenzyme form, whereas s-GOT showed negligible increase following PALP addition at any stage.

Adolescent↗