Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
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Volume 39, Issue 4
Displaying 1-14 of 14 articles from this issue
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Contents
  • Evaluation of an immunological fecal occult blood test by diagnosis of colon diseases
    KOH MORICHIKA, HIDEKI TAIRA, KUNIAKI INAMI, KEIICHIRO KABUKI, TAKAO KU ...
    1994 Volume 39 Issue 4 Pages 469-473
    Published: February 15, 1994
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.39.469
    JOURNAL FREE ACCESS
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    Immunological fecal occult blood test was evaluated in a test positive group (A) and non-test group (B) between January in 1992 and May in 1993. Colon diseases were diagnosed 74 of 115 patients (64.3%) in group A and 159 of 334 patients (47.7%) in group B. Colon cancer was found 4 patients in group A and 3 in group B. The immunological fecal occult blood test was useful in both mass screening and clinical diagnosis.
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  • H-2z Homozygous New Zealand mice as a model for B-cell chronic lymphocytic leukemia
    elevated bcl-2 expression in CD5 B-cells at premalignant and at malignant stages.
    HIROSHI OKAMOTO, AYAKO SHINOZAKI, HIROYUKI NISHIMURA, HIROMITI TSURUI, ...
    1994 Volume 39 Issue 4 Pages 474-483
    Published: February 15, 1994
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.39.474
    JOURNAL FREE ACCESS
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    In New Zealand mice, the major histocompatibility complex (MHC) controls the development of both autoimmune disease and B cell chronic lymphocytic leukemia (B-CLL). While H-2d/H-2z heterozygosity acts as one major predisposing genetic element for autoimmune disease, H-2z/H-2z homozygosity acts as an elenent for B-CLL. In the H-2z/H-2z homozygotes, there was an age-dependent increase in the percentage of CD5 B cells in the blood and spleen, and such CD5 B cells were oligoclonal to monoclonal expansion, giving rise to B-CLL. B-CLL cell from these mice had surface phenotypes typical of the CD5 B lineage cells, and expressed ligh levels of proto-oncogene bcl-2 expression was also observed in the premalignant B cells in the aged mice, thereby suggesting that apoptosis-resistant, long surviving CD5 B cells with a self-renewal capacity form the basis of malignant transformation. This model is useful for analyzing multiple steps of genetic alterations involved in the generation of B-CLL, and for clarifying the relationship between B-CLL and autoimmune disease.
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  • Suppressive effect of anti-I-E monoclonal antibody treatment on autoimmunity in NZB×NZW F1 mice
    DANQING ZHANG, HIROYUKI OHMURO, SACHIKO HIROSE
    1994 Volume 39 Issue 4 Pages 484-493
    Published: February 15, 1994
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.39.484
    JOURNAL FREE ACCESS
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    NZB×NZW (NZB/W) F1 mice spontaneously develop an antoimmune disease resembling human systemic lupus erythematosus (SLE). The disease is characterized by the immune. complex-type severe lupus nephritis in association with the production of a variety of antoantibodies, including those to DNA. As the production of IgG anti-DNA antibodies in these mice is highly dependent on helper T cells and is strictly restricted by the major histocompatibiliy complex (MHC) heterozygosity of H-2d from NZB and H-2Z from NZW mice, the interplay between F1-unique mixed haplotype MHC class II molecules on B cells and a certain repertoire of T cell receptor may play an important role in this process. In the present studies, we treated NZB/W F1 mice with anti-MHC class II monoclonal antibodies (anti-I-E) for about 2 months before the onset of disease and examined the effect on the disease severity. The results demonstrated that anti-I-E treatment markedly prolonged the survival and reduced the severity of disease. The serum levels of anti-DNA antibodies were significantly decreased in the treated mice. The possible mechanisms of the effects were suggested by studies on a cellular basis. A notable finding on the B cells was the preferential reduction in the number of the CD5+ B1 cell subset which is known to be responsible for autoantibody production. Although the number of this B cell subset recovered gradually, the serum levels of anti-DNA antibodies, particularly of IgG class, did not reach the levels in the control, untreated mice. Together with the finding that the treatment prevented the generation of activated CD4+ cells in the blood, which normally increase with aging in untreated NZB/W F1 mice, these findings suggested that either central or peripheral self tolerance is at least partly induced in these mice by the treatment. Clarification of this mechanism may contribute to the future application of anti-HLA class II monoclonals for the therapy of human SLE.
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  • The expressions of DAF and CD59 in hematological malignant disorders
    KIYOSHI SAITO
    1994 Volume 39 Issue 4 Pages 494-503
    Published: February 15, 1994
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.39.494
    JOURNAL FREE ACCESS
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    The expressions of DAF and CD59 on the leukocytes were analyzed by FACStar in 20 patients with hemotological malignant disorders (MDS : 11 patients, AML : 3 patients, CML : 4 patients, T-LGLL : 1 patient, CLL : 1 patient). The expression of DAF decreased in four patients and increased in seven patients with MDS, whereas the expression of CD59 increased in 9 patients. The expression of CD59 on the peripheral blood cells and bone marrow cells was studied in a patient with MDS. The expession of CD59 varied among different bone marrow cells, whereas that on peripheral blood cells was high. These findings indicated that dishaemopoiesis was caused on bone marrow cells with low expression of CD59 in patients with MDS. The expressions of DAF and CD59 increased in a CML patient with marked leukocytosis, whereas those decreased in two patients whose WBC counts were well controlled by interferon in a case wihout treatment. The expressions of DAF and CD59 decreased on T lymphocytes from a patient with T-LGLL, particularly, decreased expression of DAF was striking. The expressions of DAF and CD59 on the lymphocytes seem to resemble that on NK cells, suggesting the importance of discussing the origin of T-cell and NK cell.
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