PubMed Health⌕ Search

Biomedical subjects

Y Takekoshi

Publications and source records attributed to Y Takekoshi.

At least 37 records · Page 2Linked to original sources
PubMed1992

Inherited copper toxicity in Long-Evans cinnamon rats exhibiting spontaneous hepatitis: a model of Wilson's disease.

The copper concentrations in organs of developing Long-Evans Cinnamon (LEC) rats (2 d to 13 mo) were measured to elucidate the pathogenesis of their hereditary hepatitis. Hepatic copper contents of LEC rats were significantly higher than those of control rats (26 to 92 times higher). The subcellular distribution of hepatic copper indicated that the nuclear and large granular fractions had been saturated and the cytosol fraction contained about 70% of all the hepatic copper in LEC rats. The serum concentrations of copper and ceruloplasmin were significantly lower than those of control rats from the 4th wk (10-12% and 5-19%, respectively). Copper contents in kidney of LEC rats did not exhibit an increase over those of control rats until 12 wk, but then increased to nearly 40 times higher during fulminant hepatic failure. Accumulation of copper was not detected in the brain or small intestines of LEC rats until 13 mo. The hepatic copper concentration, its subcellular distribution, and serum copper concentration of F1 rats (LEC x Long-Evans Agouti) exhibited the same levels as those of Long-Evans Agouti rats. In addition to their similarity concerning inheritance of autosomal recessive means and clinical course, we found causality relating copper accumulation to the pathogenesis of the disease. We propose that LEC rats will be the most promising animal model for the study of Wilson's disease.

Age Factors↗
PubMed1992

Acute serum sickness in normal and C6 deficient rabbits: role of membrane attack complex.

Acute serum sickness was induced in New Zealand White (NZW) and in C6 deficient (C6D) rabbits, to compare the histology, immunofluorescence, especially distribution of poly C9 (MAC), and electron microscopic characteristics of the disease in each strain. Glomerulonephritis and albuminuria of comparable extent occurred in 13/17 NZW and 4/8 C6D rabbits. In NZW rabbits with albuminuria an early intense glomerular infiltration by mononuclear cells was associated with focal small fine granular glomerular basement membrane (GBM) deposits of IgG and BSA and more diffuse and larger deposits of C3 and MAC. After the disappearance of monocytes and decrease in mesangial cell proliferation, development of large subepithelial GBM deposits rich in all immune reactants was observed in NZB rabbits. In C6D rabbits with albuminuria a similar monocytic infiltrate occurred, but no association with IgG and C3 GBM immune deposits was noted. No deposits of MAC and no large subepithelial GBM 'humps' were observed in C6D rabbits. We conclude that the exudative (monocytic) phase of glomerular injury and albuminuria in acute serum sickness nephritis are not dependent upon terminal complement components, but the subsequent formation of large subepithelial GBM deposits does not occur in this model in the absence of MAC.

Albuminuria↗
PubMed1991

Urinary excretion of terminal complement complexes in glomerular disease.

To evaluate renal terminal complement activation in patients with glomerular diseases, we measured terminal complement complexes (TCCs) in plasma and urine with sandwich enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody against a C9 neoepitope expressed on TCC and a polyclonal antihuman C7 antibody. TCCs were detectable in plasma but not in urine in most of normal controls. In plasma, TCC levels were elevated in 4 of 22 patients with lupus nephritis and in 6 of 12 with membranoproliferative glomerulonephritis. However all patients with IgA nephritis, focal glomerulosclerosis, idiopathic membranous nephritis and idiopathic minimal change nephrotic syndrome (MC) showed normal values. In urine, TCCs were detectable in almost all patients with heavy proteinuria (greater than or equal to 100 mg/ml) except MC. The TCCs present in urine were partially purified by gel filtration using Sepharose 6B and were found to contain C5, C6, C7, C8, C9 and S protein by ELISA. Although the molecular weight of TCC is similar to that of IgM, the fractional excretion rate of TCC was about 100 times higher than that of IgM. These results suggest that TCCs detectable in urine contain SC5b-9 complexes and are mostly of renal origin.

Adolescent↗
PubMed1990

Using polymerized C9 to produce a monoclonal antibody against a neoantigen of the human terminal complement complex.

The terminal complement complex (TCC), consisting of C5b, C6, C7, C8, and C9, contains neoantigens that are absent from the individual native components. Neoantigens are present both in the membrane-bound (MAC) and the fluid-phase (SC5b-9) complex. The present study describes production of monoclonal antibodies (MoAbs) against neoantigens of both forms of the TCC using human C9 polymerized in Zn2+ as an immunogen. One of ten MoAbs obtained, MoAb 1B4, reacted with the tubular C9 polymer, but not with either the native or sodium dodecyl sulfate-denatured monomeric C9, as shown by enzyme-linked immunosorbent assay and Western blotting. Moreover, MoAb 1B4 cross-reacted both with MAC and SC5b-9. This suggests MoAb 1B4 recognized a neoantigen in the moiety of C9 polymer in the TCC. MoAb 1B4 will be of value for definitive identification of MAC and for quantitation of SC5b-9 in plasma and urine.

Antibodies, Monoclonal↗
PubMed1990

IgA nephritis in Behçet's disease: case report and review of the literature.

We describe a 13-year-old girl with the incomplete type of Behçet's disease who had recurrent oral and genital ulcers, folliculitis, proteinuria and hematuria. Renal biopsy specimens revealed diffuse proliferative glomerulonephritis with strongly positive IgA deposits in the glomerular mesangial area, which is histologically indistinguishable from primary IgA nephritis. Further studies of the IgA subclasses showed that IgA1 deposits were predominant in the glomerular mesangium. Primary IgA nephritis is thought to be associated with polymeric IgA1. So it appears that there may be a common underlying disease or mechanism involved in both primary IgA nephritis and the IgA nephritis in Behçet's disease.

Adolescent↗
PubMed1989

Glomerular deposition of C4 cleavage fragment (C4d) and C4-binding protein in idiopathic membranous glomerulonephritis.

Renal biopsies from 12 patients with idiopathic membranous glomerulonephritis (IMGN) were investigated by immunofluorescence microscopy for the localization of C4d and C4-binding protein (C4bp). Although Clq and C4 deposits were found in only 2 of 12 cases (16%), C4d and C4bp deposits were identified in 11 cases (92%) in close association with IgG deposits in the glomeruli. The results suggest that complement activation through the classical pathway usually occurs in IMGN. The detection of C4d and C4bp in the glomeruli appears to be a sensitive indicator of the classical pathway activation in IMGN.

Carrier Proteins↗
PubMed1979

Free "small" and IgG-associated "large" hepatitis B e antigen in the serum and glomerular capillary walls of two patients with membranous glomerulonephritis.

Nephrotic syndrome developed in two children who carried hepatitis B virus. Both their serums contained hepatitis B surface antigen and hepatitis B e antigen (HBeAg). Two physicochemically and immunologically different categories of HBeAg activity were identified in their serums--i.e., small molecular (free) and large molecular (associated with IgG). Their kidney-biopsy specimens disclosed pathologic changes typical of membranous glomerulonephritis. By a fluorescent-antibody technic, HBeAg was found to be deposited in diffuse granular fashion, along glomerular capillary walls together with IgG and beta1C, but no deposition of hepatitis B surface antigen was detected. The presence of HBeAg in association with IgG both in the serum and in the kidneys of these patients suggests that HBeAg caused membranous glomerulonephritis by inducing the formation and deposition of immune complexes.

Antigen-Antibody Complex↗