Japanese Journal of Medical Science and Biology
Online ISSN : 1884-2828
Print ISSN : 0021-5112
ISSN-L : 0021-5112
Volume 41, Issue 4
Displaying 1-3 of 3 articles from this issue
  • Koomi KANAI, Surang DEJSIRILERT
    1988 Volume 41 Issue 4 Pages 123-157
    Published: 1988
    Released on J-STAGE: December 08, 2010
    JOURNAL FREE ACCESS
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  • Kikuko MIYAMURA, Kazuyo YAMASHITA, Naokazu TAKEDA, Toshio OGINO, Etsuk ...
    1988 Volume 41 Issue 4 Pages 159-174
    Published: 1988
    Released on J-STAGE: March 19, 2010
    JOURNAL FREE ACCESS
    Epidemics of acute hemorrhagic conjunctivitis due to a coxsackievirus A24 variant occurred in July-November, 1985 and August-October, 1986 in Okinawa Prefecture, Japan. This is the first report of an acute hemorrhagic conjunctivitis epidemic due to a coxsackievirus A24 variant in Japan. The epidemic involved most islands of the prefecture. The prefectural surveillance center was notified of 9, 952 cases in 1985 and 6, 096 cases in 1986 from three sentinel eye clinics. The neutralizing antibody-positive rate against the coxsackievirus A24 variant of the serum samples collected before and immediately after the 1985 epidemic rose from 1.0% to 8.5%. The coxsackievirus A24 variant was isolated from 48 out of 68 conjunctival swabs collected during the epidemics. The isolates were indistinguishable antigenically in the plaque reduction test from the prototype strain, EH24/70, but had a markedly distinct oligonucleotide pattern.
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  • Tosiki NISIZAWA, Manabu SAITO, Kazue NAKAYAMA, Tatsuji NISHIHARA, Susu ...
    1988 Volume 41 Issue 4 Pages 175-187
    Published: 1988
    Released on J-STAGE: March 19, 2010
    JOURNAL FREE ACCESS
    The effects of continuous exposure to nitrogen dioxide (NO2) on the pathologic and immunologic responses of ddY mice to the infection with Mycoplasma pulmonis were investigated. The organisms grew well in the trachea as early as 7days after infection but barely grew in the lung even after 28 days, causing slight pneumonic lesions in only a few of the infected mice exposed to 1 and 5 ppm NO2. When mice were exposed to 10 ppm NO2 at or after the infection, however, mycoplasmal growth in the lung, but not in the trachea, was greatly enhanced, and pneumonic lesions were evident in the lung of almost all the mice examined. The serum antibody titers to M. pulmonis increased with time after infection regardless of the concentration of NO2 exposed or the mycoplasmal number in the respiratory tract in the infected mice. The in vitro immune responses of the spleen cells of the infected mice were significantly depressed by exposure to 10 ppm NO2 in not only mitogenic resposne to LPS and ConA but also antibody production to SRBC, whereas uninfected healthy mice were apparently not modulated except for a slight decrease in Con A response.
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