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Publications (7)0 Total impact

  • S Moteki, H Yoshida, T Nishimaki
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    ABSTRACT: Autoantibody to mitotic spindle associated antigen (MSA) was examined in sera from patients with positive mycoplasma pneumoniae particle agglutination (PA) test along with various autoimmune diseases and healthy subjects by means of indirect immunofluorescence (IF) using HEp-2 cells as substrates. Anti-MSA antibody was identified in 9 patients sera including 7 out of 180 sera with positive mycoplasma pneumoniae PA test, one with systemic lupus erythematosus (SLE) and one with scleroderma (PSS) respectively. Five of 9 sera with positive anti-MSA antibody contained anti-nuclear antibody (ANA) including 4 with speckled staining ANA and one with homogeneous + nucleolar staining ANA. Two collagen diseases sera positive for anti-MSA antibody showed negative mycoplasma pneumoniae PA test. In addition, there was no correlation between the presence of anti-MSA antibody and the titers of mycoplasma pneumoniae PA test. Our results indicated that anti-MSA antibody was not limited to such connective tissue diseases as previously described by other workers. It would be speculated that mycoplasma pneumoniae infection might induce anti-MSA antibody production.
    Rinsho byori. The Japanese journal of clinical pathology 01/1992; 39(12):1337-41.
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    ABSTRACT: Recently, tissue cultured cells including HEp-2 cell have widely been used as the substrates for detecting autoantibody to nuclear antigen (ANA) by indirect immunofluorescence method. In this study, sera from aged subjects ranging from 70 to 92 years of age were examined for the presence of anti-nuclear antibodies by the indirect immunofluorescence method. Positive reactions were obtained in 51 of 269(23.3%) aged subjects and positive fluorescent staining patterns of ANA were speckled in 40, homogeneous in one, speckled + homogeneous in 4, nucleolar in one and discrete speckled in two sera respectively. The titers of ANA were low ranging between 1:20 and 1:320, however two cases showed discrete speckled staining with high titers at 1:2,560. Antibody to extractable nuclear antigen (ENA) was not detected by precipitation test in aged subjects. The aged individuals with low ANA titers did not show any symptoms suggestive of collagen diseases. In two patients whose sera contained high titers of anti-centromere antibody (ACA), one was suspected to be accompanied by primary biliary cirrhosis (PBC), however the other showed neither any other abnormal symptoms nor abnormal laboratory data. Our results indicated that low titer ANA other than ACA might not be clinically significant in aged subjects.
    Rinsho byori. The Japanese journal of clinical pathology 04/1991; 39(3):273-7.
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    ABSTRACT: Anti-centromere antibody (ACA) has been believed to be specific to patients with CREST syndrome, a variant of scleroderma (PSS). This study was undertaken to clarify the distribution of ACA in various diseases and the significance of autoantibodies coexisting with it. The sera of patients with primary biliary cirrhosis (PBC) along with collagen diseases and aged subjects were examined for ACA by immunofluorescence method (IF) using cultured HEp-2 cells and chromosomes prepared from K 562 cells. ACA were found in sera of 10 patients with PBC, one with scleroderma, one with cerebral infarction and one with chronic renal failure respectively. ACA positive sera were examined for antibodies against other nuclear antigens including nRNP, Sm, Scl-70, SS-A and SS-B and cytoplasmic antigens by double immunodiffusion methods using rabbit thymus extract etc. as the antigens and by IF method using cryostat sections of rat kidney and stomach. In 13 sera with ACA, antimitochondrial antibody (AMA), anti-smooth muscle antibody (ASMA) and anti SS-A antibody were found in 10, 4 and one sera respectively. In 10 PBC patients with ACA, various collagen disease-related disorders were found to coexist; CREST syndrome in one, CRST syndrome in one, Raynaud's phenomenon in two and Sjögren's syndrome in 5. These results would indicate that ACA may be one of the common serological abnormalities among patients with PBC, CREST syndrome and Sjögren's syndrome.
    Rinsho byori. The Japanese journal of clinical pathology 09/1990; 38(8):888-94.
  • S Moteki, H Yoshida
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    ABSTRACT: In 1948, Hargraves described the phenomenon of the LE cells and equated it with systemic lupus erythematosus (SLE). Kunkel and his colleagues elucidated the immunochemical basis of this phenomenon, showing that it was related to the circulating autoantibodies to deoxyribonucleoprotein (DNP). Their pioneering studies led to the continuing discoveries of antinuclear antibodies (ANA) and today's considerable knowledge concerning the molecular identity of antigens and further consolidation of ANA. In addition to the role of diagnostic markers, spontaneously occurring autoantibodies, including anti-PCNA (proliferating cell nuclear antigen) antibody and anticentromere antibody (ACA), turned out to be useful as powerful probes for cell biology. In this study, the sera of patients with primary biliary cirrhosis (PBC) along with collagen diseases were examined for the presence of antinuclear antibodies. In using HEp-2 cells and chromosomes derived from K 562 as the substrates for the immunofluorescence method, the frequency of ANA and ACA in PBC sera were 84% and 44% respectively. Anti-DNA, antiSS-A and antiSS-B antibodies were found in one, 4 and one sera respectively. On the other hand, antibodies to nRNP, Sm and Scl-70 were not found in PBC sera. In some PBC patients with ACA, various complications related to collagen diseases were found to coexist. Our results indicated that there might be common serological abnormalities among patients with PBC, CREST syndrome and Sjögren's syndrome.
    Rinsho byori. The Japanese journal of clinical pathology 08/1990; 38(7):765-72.
  • S Moteki
    Nippon rinsho. Japanese journal of clinical medicine 03/1990; 48 Suppl:580-3.
  • Rinsho byori. The Japanese journal of clinical pathology 07/1989; 37(6):634-9.
  • Rinsho byori. The Japanese journal of clinical pathology 06/1989; 37(5):517-21.