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Biomedical subjects

N Tamura

Publications and source records attributed to N Tamura.

At least 289 records · Page 16Linked to original sources
PubMed1986

Abnormal expression of complement receptor (CR1) in IgA nephritis: increase in erythrocytes and loss on glomeruli in patients with impaired renal function.

The number of complement receptor for C3b (CR1) molecules in erythrocytes from patients with renal diseases was measured by an immunoradiometric assay using monoclonal antibodies against CR1. IgA nephritis patients with high serum creatinine value (Scr) showed markedly elevated levels of CR1, whereas patients with normal Scr had normal CR1 levels. A similar increase in CR1 number was observed in membranoproliferative glomerular nephritis with high Scr. CR1 of these patients functioned normally as a cofactor of C3b inactivator in cleaving immune complex-bound C3b. In contrast, a high frequency (5/6) of negative staining of glomerular CR1 was observed in IgA nephritis patients with high Scr by immunofluorescence study. We postulate that the disease-associated, acquired factors at least in part contribute to the abnormal expression of CR1: elevated levels in erythrocytes and defective expression on glomeruli.

Anticoagulants↗
PubMed1986

Foreign bodies of dental origin in the air and food passages.

6 cases in which a reamer or a cast object was swallowed into the stomach or into the bronchus during dental treatment are described, with a review of the Japanese literature. The foreign bodies were removed by duodenotomy in one case, by endoscopic or bronchoscopic procedure in three cases; spontaneous evacuation in the stool occurred in two cases. The management of patients who swallowed a foreign body into the airway or into the alimentary canal is discussed.

Adult↗
PubMed1986

Flow cytometric analysis of lymphocyte subsets in the bronchoalveolar lavage fluid and peripheral blood of healthy volunteers.

The lymphocyte subsets in the bronchoalveolar lavage fluid (BALF) and the peripheral blood of 25 healthy volunteers were examined by analysis with a fluorescence-activated cell sorter. Comparison of the lymphocyte subsets in the BALF with those of the peripheral blood revealed much higher values for the ratios of each Leu 3a+ (CD4), Leu 3+8-, and Leu 2+15- cells, while the ratios of Leu 1+ (CD5), Leu 2a+ (CD8), Leu 7+, Leu 8+, Leu 10+, Leu 11a+ (CD16), Leu 12+, and Leu 2+15+ cells were low in the BALF. The above results indicate that the lymphocyte subsets in the BALF from healthy individuals are mainly composed of cells with surface phenotypes of helper T cells and cytotoxic T cells with virtual absence of cells carrying suppressor T and NK cell phenotypes, and with low B cell ratio. Therefore, it is assumed that the local immune mechanism of the lung is different from that of the peripheral blood.

Adult↗
PubMed1985

Characterization of functional properties of C4-binding protein by monoclonal antibodies.

We prepared mouse monoclonal antibodies to human C4-binding protein (C4-bp) by fusing spleen cells from mice immunized with purified C4-bp to the mouse myeloma line P3U1. Of four monoclonal antibodies that reacted with intact C4-bp, two were specific for a 48K fragment, one of the chymotryptic cleavage products of C4-bp, and one was specific for another fragment (160K). The fourth monoclonal antibody did not react with either fragment. One of the monoclonals that reacted with the 48K fragment blocked the binding of C4-bp to cell-bound C4b. This monoclonal antibody (TK3) also inhibited two other functions of C4-bp, serving as an essential cofactor for C3b/C4b inactivator (I) in the cleavage of fluid-phase C4b and accelerating the decay of C2a from the C4b,2a complex. The other monoclonals had little or no effect on these activities of C4-bp. In addition, we found that the 48K fragment lost the binding affinity for C4b. However, it can function as a cofactor for I and as a decay-accelerator, although its activities were about 200 times weaker than intact C4-bp on a molar basis. The monoclonal antibody TK3 completely inhibited these activities of the 48K fragment. On the basis of these findings, we conclude that the functionally active site of C4-bp is located on the 48K fragment. Probably, the cofactor and decay-accelerating activities of C4-bp result from the binding of C4-bp to C4b.

Animals↗
PubMed1985

Interaction of complement solubilized complexes with mouse peritoneal macrophages and their clearance and tissue uptake.

To clarify the biological activity of complement solubilized immune complexes, we studied their interaction with mouse peritoneal macrophages. The solubilized complexes lost their binding affinity for C3b receptor and Fc receptor but still bound to MPM mainly via the C3bi receptor (CR3). When solubilized immune complexes were injected into mice, they were more rapidly removed from the circulation than antigen excess soluble complexes and taken up by the liver Kupffer cells. Therefore, the solubilized complexes could be catabolized by the reticuloendothelial system, mainly in the liver. Probably, CR3 plays an important role in this process.

Animals↗
PubMed1984

Sexual dimorphism of the fifth component of mouse complement.

Sexual dimorphism of mouse complement component 5 (C5) was detected by isoelectric focusing of desialated ethylenediamine tetraacetic acid (EDTA)-plasma on agarose gel, followed by immunofixation with anti-mouse C5. Male plasma displayed two C5 bands, basic and acidic, while female plasma had only a basic C5 band. In all mouse strains tested except C5-deficient strains, the identical patterns of the dimorphism were obtained. The basic and acidic C5 were antigenically and hemolytically indistinguishable from each other. In the neonatal mice of both sexes, the basic C5 was observed at the same levels, but the acidic C5 was only slightly detected. Injection of testosterone into mice resulted in an appearance of the acidic C5 in females and its increase in males. By contrast, injection of estradiol decreased the acidic C5. These results indicate that the expression of the acidic C5 is under the control of testosterone.

Animals↗
PubMed1984

Pretreatment with antigen or adjuvant, and the preventability of allergic encephalomyelitis induced by basic protein with synthetic muramyl dipeptide in comparison with Freund's complete adjuvant.

Protection against experimental allergic encephalomyelitis (EAE) was examined by prior injection of following materials with Freund's incomplete adjuvant (FIA), Mycobacterium tuberculosis (Tbc), synthetic muramyl dipeptide (Mdp), polyinosinate-polycytidylate (poly IC), or myelin basic protein (BP). 26 days later, guinea pigs received encephalitogenic challenge in the form of 20 micrograms BP + 20 micrograms Tbc in FIA (BP + Tbc) or 20 micrograms BP + 10 micrograms Mdp in FIA (BP + Mdp). (1) Either pretreatment with Mdp, poly IC or FIA alone showed no protecting effects. (2) Tbc/FIA was not effective on challenge with BP + Mdp, but effective on challenge with BP + Tbc, and produced passive hemagglutinating (PH) antibodies of moderate titer and and complement fixing (CF) antibodies of higher titer. (3) BP/FIA was effective on both BP + Tbc and BP + Mdp challenges, and produced PH antibodies of higher titer than that of CF antibodies. (4) Clinicopathological survey revealed that the challenge with BP + Mdp was blocked perfectly by prior injection with BP/FIA whereas the challenge with BP + Tbc was incompletely blocked by either Tbc/FIA or BP/FIA pretreatment. (5) The finding was verified also by cerebrospinal fluid cell count at the termination of clinical observation. As compared with FCA, Mdp adjuvant itself has no antigenic component, which seems to explain the results in this study.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Interaction of C3 with antigen-antibody complexes in the process of solubilization of immune precipitates.

The binding properties of activated C3 to immune complexes were studied by using solubilization phenomenon as a model system. IgG or F(ab')2 immune precipitates were solubilized by the six isolated alternative pathway proteins, and the solubilized complexes were analyzed by SDS-PAGE. As a result of solubilization, we observed some high m.w. bands. Under reducing conditions, the bands with m.w. of 150,000 and 115,000 appeared in the case of IgG and F(ab')2 complexes, respectively. Two-dimensional SDS-PAGE revealed that hydroxylamine treatment resulted in the dissociation of the 150,000-m.w. polypeptide into the C3 alpha-65 and the heavy chain of IgG. Similarly, the 115,000-m.w. polypeptide was dissociated into the C3 alpha-65 and the Fd chain. Therefore, it is likely that iC3b binds covalently to the Fd region of the heavy chain of IgG via an ester bond. Under nonreducing conditions, iC3b-IgG and iC3b-F(ab')2 complexes had apparent m.w. of 340,000 and 270,000, respectively, corresponding to one iC3b molecule bound to one antibody molecule. In addition, a considerable amount of iC3b also binds to antigen molecules via an ester bond. The findings that C3 binds to the F(ab')2 molecules and bovine serum albumin, which contain only a small amount of carbohydrate, suggest that C3 may not bind to the carbohydrate moiety of antibody molecules. Indeed, various carbohydrate molecules did not inhibit the solubilization even at high concentrations. In contrast, acetyl tyrosine having an aromatic ring and a hydroxyl group produced the best inhibition of the solubilization. Furthermore, we demonstrated that generation of C3b in the presence of 3H-tyrosine resulted in covalent binding of the tyrosine specifically to the C3 alpha' chain, indicating that the inhibition of solubilization may be due to the competition between tyrosine and immune complexes for the covalent binding of C3. Thus, it could be concluded that C3 binds covalently to the amino acid residues of antigen and antibody molecules during solubilization.

Amines↗