Ensho
Online ISSN : 1884-4006
Print ISSN : 0389-4290
ISSN-L : 0389-4290
Volume 2, Issue 1
Displaying 1-19 of 19 articles from this issue
  • Hideo Hayashi
    1982 Volume 2 Issue 1 Pages 1-2
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Masaru Yoshinaga, Shuji Nakamura, Shigeki Nakayama, Susumu Ohkawara
    1982 Volume 2 Issue 1 Pages 3-8
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    Inflammatory responses, which were induced in the peritoneal cavity of mice by a variety of stimuli, produced an enhanced immune response to sheep erythrocytes when the antigen was introduced at an early stage of the inflammatory responses. The enhancement could be reproduced when early peritoneal exudate cells, consisting mostly of neutrophils, were adaptively transferred at the same time as antigen. The neutrophils were shown to produce a lymphocyte-activating soluble factorin vivaandin vitro. The PMN-derived factor produced the enhancement of several lymphocyte functions, including T-cell proliferative response, primary plaque forming cell response and allo-reactive killer T cell response.
    The PMN factorper sewas non-mitogenic and exhibited maximum potentiation of T lymphocyte response when added within 3 hr of antigen or mitogen stimulation. Mitogen-stimulated, but not nonstimulated thymocytes absorbed PMN factor activity.125I-labelled factor binding to stimulated thymocytes was proved. Thus, it is suggested that an acceptor site for PMN factor may be generated on the thymocyte surface only after mitogen stimulation.
    The PMN factor was composed of two isoelectrophoretically distinct factors, a cationic (pI 9.8) and a neutral (pI 5.4) PMN factor. The two purified, 125I-labelled PMN factors were homogeneous on SDS-PAGE. Their molecular weights were calculated to be 19, 000 for cationic-and for 21, 000 neutral PMN factor by Svedberg equation.
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  • Toshio Shikata
    1982 Volume 2 Issue 1 Pages 9-13
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    Pathogenic mechanism of chronicity of viral hepatitis might be related with two quite different mechanisms. One of them is persistent infection of hepatitis B virus and non-A, non-B virus, which may be caused by incomplete immune reaction of the host to eliminate such viruses. Incomplete immune response against hepatitis virus is usually observed in newborn babies, young children and in patients receiving immunosuppressive drugs, leads to persistence of infection. Transition from acute hepatitis to chronic pattern or primary chronic hepatitis are more frequently observed in non-A non-B hepatitis than in hepatitis B. The second mechanism of chronicity of hepatitis may be related with autoimmune reaction against liver-cell membrane protein.
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  • Masami Hayashi, Juzo Matsuda, Tadatoshi Kinoshita, Takeshi Abe
    1982 Volume 2 Issue 1 Pages 17-22
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    Prostaglandin E1 (Prostandin, Ono Pharm. Co., Ltd.) was infused intravenously twice a day for 7 days into 10 patients of SLE, PSS and so called Raynaud's disease with Raynaud's phenomena, instead of conventional continuous infusion therapy through artery and/or vein. And its clinical effect was monitored by plethysmography, platelet aggregation test and beta-thromboglobulin concentration in plasma.
    In the course of PGE1treatment, amplitude of platelet aggregation induced with ADP and/or collagen and concentration of plasma beta-thromboglobulin were not changed so significantly during of and after the termination of PGE1infusion, but patterns of plethysmography were markedly improved during and even after PGEI infusion, being concordant with improvement of subjective symptolnes of Raynaud's phenomena.
    So it was suggested this intermittent infusion therapy of PGE1was worth trying for patients, having been suffering from inveterate thromboangitis obliterans, arteritis oblilterans, Raynaud's phenomena and so forth, who had not been able to endure the conventional continuous PGE1 infusion treatment through artery and/or vein.
    And our laboratory results suggest that the main effects of PGE1infusion on Raynaud's phenomena could be introduced not through inhibition of platelet functions but through distention of arteries, but more additional experiments might be required to clarify this hypothesis.
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  • Toshio Ozaki, Susumu Yasuoka, Tadashi Nakayama, Hisayasu Ishimi, Tomoh ...
    1982 Volume 2 Issue 1 Pages 23-29
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    In order to clarify the physiolosical and significance of glucocorticoid (GC) receptors in bronchoalveolar cell (BAC) fraction, we measured the content of GC receptors in BAC fraction obtained by segmental bronchoalveolar lavage from normal volunteers, control patients with localized lung cancer and pulmonary tuberculosis, and the patients with diffuse interstitial lung diseases such as idiopathic pulmonary fibrosis (IPF) and hypersensitivity pneumonitis (HP) . Segmental bronchoalveolar lavage was performed in a segment of right middle lobe or lingula, and was performed in the contralateral lung to the lesions in the control patients.
    In con'rol groups (normal volunteers and control patients), the BAC fraction consisted mainly of alveolar macrophages. The mean content of GC receptors in BAC fractions from normal volunteers was about 10, 000 sites per cell. This value might reflect that of alveolar macrophages and was significantly higher than those of monocytes, lymphocytes and polymorphonuclear leukocytes in peripheral blood.
    In the patient groups, the composition of BAG fraction was much changed compared with the control groups; increase of neutrophils in IPF and significant increase of lymphocytes in HP. In some patiets in this group, the contents of GC receptors in BAG fraction were decreased compared with control groups. The patients, who showed the same GC receptor content as control groups, responded well to glucocorticoids, but the patients, who showed lower GC receptor content, did not respond to glucocorticoids. These results suggested that the content of GC receptors in BAG fraction may be a parameter to glucocorticoid therapy in diffuse interstitial lung diseases.
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  • Mikio Zeniya, Yumiko Fujita, Hiroshi Takahashi, Masamichi Deura, Yoshi ...
    1982 Volume 2 Issue 1 Pages 30-34
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    Immune mechanism of hepatocytes-in july in chronic liver diseases was studied. Live specific lipoprotein (LSP, Meyer zum Bizschenfelde) may play an important role in the chronic liver diseases, and that in chronic active hepatitis, a LSP-mediated antibody dependent cell-mediated cytotoxicity (ADCC) may established itself, which would serve as an immunopathogenic cause of liver cell injury.
    The K-cell populatin of peripheral blood, the effector cell of ADCC, was significantly decreased compared with that in normal subjects even in patients with demonstrated serum ADCC activity to hepatocytes. This decrease of K-cell population showed that serum inhibitory factors of K-cell exsists beside the antibodies which induce ADCC in patients serum by an underlying experiments.
    Analysis by Sephadex G 100 gel filtration of supernates from cultures of LSP-sensiti-zed peripheral lymphocytes from patients revealed a factor, recovered as a forth fraction, which proved capable of increasing the K-cell population.
    The results have also demonstrated the presence of an immunopathogenic mechanism whereby hepatocellular injury due to ADCC in chronic liver diseases, particularly in chronic active hepatitis is controlle by K-cells, the effector cells.
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  • Kenichiro Tsuyama, Keiro Ono, Yukihiko Kitamura
    1982 Volume 2 Issue 1 Pages 35-38
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    Spleen cells of beige C57BL mice or those of normal C57BL mice were injected intravenously into sublethally irradiated F1 hybrid mice (C57BL×CBA) .Recipient receiving plecn cell of beige mice survived longer than those receiving splecn cells of normal mice. The present result suggests that in beige mice effetor cells of GVH reaction (mainly T-lymphocytes) may have functional impalrments, as do neutrophils, platclets, and natural killer cells.
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  • Kimimasa Nakabayashi, Toshihiko Nagasawa, Mituru Takada
    1982 Volume 2 Issue 1 Pages 39-44
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    One case of membranous glomerulonephritis (MGN) associated with primary diabetes mellitus has been followed for more than 5 years. Peripheral blood lymphocyte, lymphocytotoxins, immune complexes, and EB virus antibodies were serially assayed. These studies demonstrated that the patient had 50% of B cells (C3 receptor, Fc receptor and/or IF positive cell), 3% of Tγ cells, positive lymphocytotoxins, increased lymphocyte blastogenesis with decreased Ig secretion less than 50% of control lymphocytes, and VCA (IgG) 320×, VCA (IgM) <10×, EA. DR (IgG) 20×, and EBNA<10× that suggested latent EB virus infection. Renal histology was the typical MGN in addition to diffuse lesion of diabetic nephropathy diagnosed by LM, IF, and EM. However, no positive immunofluorescent findings for insulin, anti-insulin antibody, and EB virus antigens were found. During the long term observation, the nephrotic syndrome disappeared spontaneously and it was paralleled wih the association of Tγ cell increment to 17%, raised lymphocytotoxins to 50% accompanied by positive anti-Tγ cell antibody, and increased EB virus antibodies such as VCA (IgG) to 640×, VCA (IgM) to<10×, EA. DR (IgG) to 80×, and EBNA to 40×, which were considered as the reactivation of EB virus. The possibie pathogenetic relationships between diabetes mellitus, MGN, and EB virus infection were discussed.
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  • Hiroshi Nagura, Hideaki Hasegawa, Noriyuki Komatsu
    1982 Volume 2 Issue 1 Pages 49-58
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Yuichi Shiokawa
    1982 Volume 2 Issue 1 Pages 64-67
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Susumu Tsurufuji
    1982 Volume 2 Issue 1 Pages 68-70
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Kanji Shichikawa, Yoshitaka Takenaka
    1982 Volume 2 Issue 1 Pages 71-73
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Mitsuo Homma, Yoichi Ichikawa, Yoshifumi Abe
    1982 Volume 2 Issue 1 Pages 74-77
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Yutaka Mizushima
    1982 Volume 2 Issue 1 Pages 78-80
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
    Download PDF (318K)
  • Sachiko Oh-ishi
    1982 Volume 2 Issue 1 Pages 85
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Hajime Nasu
    1982 Volume 2 Issue 1 Pages 86
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • IIP still a syndrome
    Takehiro Tanaka
    1982 Volume 2 Issue 1 Pages 87
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Role of Langerhans's cell
    Michitoshi Murakami, Shigeo Nishiyama
    1982 Volume 2 Issue 1 Pages 88
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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  • Jutaro Yamagata, Satoru Katayama, Shun-ichi Shirai, Mahito Nagahama
    1982 Volume 2 Issue 1 Pages A1-A3
    Published: January 01, 1982
    Released on J-STAGE: April 12, 2010
    JOURNAL FREE ACCESS
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