start-ver=1.4
cd-journal=joma
no-vol=30
cd-vols=
no-issue=1
article-no=
start-page=33
end-page=47
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=198801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=鶏胚中腎における基底膜の形成と糸球体毛細血管壁の選択的透過性に関する電顕的観察
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=徳山清之
kn-aut-sei=徳山
kn-aut-mei=清之
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=365
end-page=372
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=1990
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Assay of GBM antigen in urine and serum with an anti-human renal monoclonal antibody
kn-title=抗ヒト腎モノクローナル抗体を用いた尿中及び血中のGBM抗原の測定 第2編
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Using a monoclonal antibody (Mab-G3) recognizing glomerular basement membrane (GBM), we assayed GBM antigen (G3-Ag) in the urine and serum of renal disease patients by sandwich ELISA. The subjects included normal control (NOR), minimal change nephrotic syndrome (MCNS), IgA nephropathy (IgA), membranous nephropathy (MN), membranoproliferative glomerulonephritis (MPGN) and chronic renal failure (CRF). The urine and serum was used as the material. With urinary G3-Ag, there were no statistically significant differences among the NOR, MCNS, IgA, MN, MPGN and CRF groups. Although no correlation was observed with proteinuria, hematuria, serum creatinine, serum β2 microglobulin and urinary NAG, urinary G3-Ag showed a significant (p<0.05) increase in excretion in the group of progressive CRF patients with s-Cr more than 1.0 mg/dl/month as compared to the stationary CRF group with s-Cr<1.0 mg/dl/month. Serum G3-Ag showed lower values in almost all cases, and there were no significant differences among the renal disease groups. The above findings led us to believe that the assay of urinary G3-Ag was useful in determining the degree of GBM disorder. It was also presumed that assay of renal antigens in urine and serum with the respective anti-human renal monoclonal antibodies could be a new tool in diagnosing renal diseases.
en-copyright=
kn-copyright=

en-aut-name=MinoYasuaki
en-aut-sei=Mino
en-aut-mei=Yasuaki
kn-aut-name=味埜泰明
kn-aut-sei=味埜
kn-aut-mei=泰明
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学第三内科
en-keyword=monoclonal antibody
kn-keyword=monoclonal antibody
en-keyword=sandwich ELISA
kn-keyword=sandwich ELISA
en-keyword=GBM antigen
kn-keyword=GBM antigen
en-keyword=renal disease
kn-keyword=renal disease
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=353
end-page=364
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=1990
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Study on the change of glomerular antigenicity in various renal diseases with anti-human renal monoclonal antibodies
kn-title=抗ヒト腎モノクローナノレ抗体を用いた疾患腎における抗原性の変化の検討 第1編
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We produced 22 different kinds of monoclonal antibody (Mab) by immunizing mice with human GBM antigens. In these Mabs, Mab-G1 to G5 recognized only GBM in the glomerulas, Mab-E1 and E2 recognized only glomerular epithelial cells, and Mab-M1 to M4 recognized mainly mesangium. The reactions of these Mabs with known GBM antigens such as type IV collagen, fibronectin and laminin were negative by immunoblotting. Using Mab-G1, Mab-E1 and Mab-M1, changes in the antigenicity of antigens recognized by Mabs were examined on kidney sections from the patients with various renal diseases by the indirect immunofluorescence test. When Mab-G1 recognizing GBM was used, there was no particular change of anti-genicity in minimal change nephrotic syndrome (MCNS) and IgA nephropathy (IgA), whereas in membranous nephropathy (MN) thickened GBM was found to maintain anti-genicity and the region of deposits was observed as negative punched-out region. In type I and III of membranoproliferative glomerulonephritis (MPGN), GBM was observed only outside of subendothlial deposits without showing double contour. In type II MPGN, GBM showed a double linear pattern and antigenicity of GBM in regions of dense deposits was not detected. When Mab-E1 recognizing glomerular epithelial cells was used, there was no change of antigenicity in the renal diseases. Further, in crescentic glomerulone-phritis, the region of the cellular crescents was not stained, When Mab-M1 recognizing mesangium was used, extensive staining was observed in the increased mesangium in IgA, MPGN, and diabetic nephropathy. We feel that it is of significance in elucidating the pathogenesis of renal diseases to study the changes of glomerular antigenicity in diseased kidneys by using anti-human renal monoclonal antibodies.
en-copyright=
kn-copyright=

en-aut-name=MinoYasuaki
en-aut-sei=Mino
en-aut-mei=Yasuaki
kn-aut-name=味埜泰明
kn-aut-sei=味埜
kn-aut-mei=泰明
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学第三内科
en-keyword=monoclonal antibody
kn-keyword=monoclonal antibody
en-keyword=human kidney antigen
kn-keyword=human kidney antigen
en-keyword=GBM
kn-keyword=GBM
en-keyword=mesangium
kn-keyword=mesangium
en-keyword=glomerular epithelial cell
kn-keyword=glomerular epithelial cell
END