Japanese Journal of Allergology
Online ISSN : 1347-7935
Print ISSN : 0021-4884
ISSN-L : 0021-4884
Volume 32, Issue 12
Displaying 1-15 of 15 articles from this issue
  • Article type: Cover
    1983 Volume 32 Issue 12 Pages Cover10-
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
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  • Article type: Cover
    1983 Volume 32 Issue 12 Pages Cover11-
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    Download PDF (105K)
  • Article type: Bibliography
    1983 Volume 32 Issue 12 Pages Misc4-
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
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  • Tsutomu Saji, Tetsuro Umezawa, Reiko Hashiguchi, Norio Matsuo
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1129-1133
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    Serum autoantibodies in Kawasaki disease(mucocutaneous lymphnode syndrome)were studied. Anti smooth muscle antibody(SMA)was positive in 9 of 25 cases(36.0%), and anti heart antibody in 1 of 28 cases(3.6%). Anti platelet antibody was negative in all of the 20 cases examined, and anti microzome antibody and anti mitochondria antibody were negative in 6 cases. Presence of coronary artery involvement was significantly more frequent in SMA positive patients than in SMA negative patients(22.0% vs 6.3%, p>0.05). Elevated serum GOT and GPT values were more frequent in SMA positive patients at admission(88.9% vs 37.5%)and during the course of treatment(66.7% vs 18.8%). In SMA positive patients, fever >37.0^〇 over 2 weeks, positive CRP and abnormal ESR over 30 days were significantly more frequent than SMA negative patients(p<0.05). These results indicated that the presence of serum SMA has some correlation with hepatic dysfunction, coronary artery involvement and severity of illness in Kawasaki disease.
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  • Hiroshi Sakakibara, Susumu Suetsugu, Hiromichi Umeda
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1134-1143
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    The β-adrenergic receptor of peripheral blood lymphocytes from bronchial asthmatics was studied by radioreceptor assay with ^5H-dihydroalprenolol(^5H-DHA)to determine whether abnormality of the β-adrenergic receptor contributes to the occurrence of bronchial hyperresponsiveness and bronchial asthma. The results were as follows:(1) Inactive asthmatics not taking medications did not differ from the control group in terms of Bmax and Kd of the β-adrenergic receptor of lymphocytes. However, this group of patients, although inactive, did show bronchial hyperresponsiveness. Therefore, if the lymphocyte β-adrenergic receptor reflects the nature of the receptor of bronchial smooth muscle, we must seek elsewhere for the cause of the bronchial hyperresponsiveness. (2) A remarkable decrease in the density of the β-adrenergic receptor(^5H-DHA binding at 2 nM)was observed among moderate and severe asthmatics not taking medications. This decrease appeared to be due to the effects of high circulating levels of endogenous catecholamines during asthma attacks, rather than to a primary defect in the pathogenesis of the bronchial hyperresponsiveness or asthma. (3) A significant decrease in the density of the β-adrenergic receptor was observed in the lymphocytes from asthmatics undergoing continuous administration of β-stimulants. (4) Glucocorticoids appeared to be effective to some extent in preventing decrease in the density of the β-adrenergic receptor of lymphocytes from patients during asthma attacks and/or receiving continuous administration of β-stimulants.
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  • Shunichi Mita, Mitsuru Adachi, Terumi Takahashi
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1144-1150
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    In order to investigate the relationship between airway hypersensitivity and β-adrenergic blockade, serum insulin was measured before and after administration of orciprenaline in 10 symptomatic asthmatics undergoing β-stimulant treatment, 7 asymptomatic asthmatics without treatment and 10 normal subjects. Although both symptomatic and asymptomatic asthmatics revealed the same level of airway hypersensitivity, as judged by methacholine inhalation test, symptomatic asthmatics showed significantly lower insulin response than normal subjects. There was no significant difference between asymptomatic asthmatics and normal subjects in insulin response. β-adrenergic blockade state of pancreas β-receptors was produced in normal subjects after 7-day administration of oral tulobuterol, a new selective β_2-stimulant.These results suggest that β-adrenergic blockade state of pancreas β-receptors in symptomatic asthmatics might be induced by long-term administration of β-stimulant. They also suggest that decrease of insulin response after administration of β-stimulant does not reflect airway hypersensitivity.
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  • Shoichi Ozaki, Hiroo Imura, Toshikazu Shirai, Yoshihiro Hamashima
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1151-1159
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    Incidences of anemia in New Zealand Black(NZB), C57BL/6, their F1 and F1×NZB backcross mice were 95, 0, 0 and 26%, respectively. This finding is in accordance with the assumption that a combined effect of one or more dominant predisposing NZB gene(s) and two dominant modifying C57BL/6 genes regulates the development of anemia. Present studies have suggested that one of the modifying genes is identical or closely linked to a modifying gene of anti-erythrocyte autoantibody production, Aem-1. We have also analyzed the genetic regulation of splenomegaly and found that the trait is controlled by a combined effect of one dominant predisposing NZB gene and one dominant modifying C57BL/6 gene, the latter of which is also suggested to be identical to Aem-1. Thus, the modifying gene of anti-erythrocyte autoantibody production also seems to regulate the development of both anemia and splenomegaly. The other modifying gene remains to be determined.
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  • Takeshi Fukuda, Shinji Motojima, Tomohiro Otsuka, Sohei Makino
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1160-1165
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    The mechanism by which glucocorticoids potentiate the bronchodilator effects of beta-adrenergic stimulants is poorly understood. In the preceding paper, we reported our study of the time course of the potentiating effects of dexamethasone on the relaxing activity of isoproterenol in guinea-pig tracheal smooth muscle. We found that potentiation occurs not only immediately after dexamethasone administration, but also again after an interval of 3 hours. We named the former "rapid-onset potentiation" and the latter "slow-onset potentiation". Glucocorticoids combine their receptors in the cells and induce the production of protein responsible for the mediation of the cellular responses. In our recent study, we examined the influence of cycloheximide, an inhibitor of protein synthesis, on this dually occurring dexamethasone-induced potentiation. Cycloheximide(10μg/ml)did not influence the rapid-onset potentiation induced by dexamethasone(1×10^<-4>M). However, the slow-onset potentiation was completely inhibited by cycloheximide. These observations show that protein synthesis is required in the slow-onset potentiation produced by dexamethasone, but not in the rapid-onset potentiation. It is considered to be highly possible that the dexamethasone-induced, slow-onset potentiation is a steroid receptor-mediated process.
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  • Kenzo Inoue, Tetsuzo Fujitani, Elliott Jr Middleton
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1166-1171
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    We have already reported that PHA-stimulated mononuclear cells produce the smooth muscle contraction augmenting factor(CAF)to histamine. In the present paper we report our studies which subsets of mononuclear cells produced CAF and what effect CAF had on the smooth muscle of trachea. For this purpose, mononuclear cells were separated into monocytes and lymphocytes using carbonic iron. T cells and B cells were obtained from the lymphocytes by the method of E-rosette formation. All of the purified cells produced a small amount of CAF but a mixed cell culture of monocytes and B cells produced the same amount of CAF as that the unpurified mononuclear cells produced. CAF also augmented the contractile responsive to acetylcholine of the smooth muscle of isolated cat and guinea pig trachea. These results indicate the CAF was produced by the cooperation of monocytes and B cells. CAF may not be one of the classical PGs but it may be other product of arachidonic cyclooxygenase pathway.
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  • Takashi Itoh
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1172-1179
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    We studied the correlation between bronchoconstriction and release of chemical mediators(SRS-A and histamine)in 15 atopic asthmatic patients. SRS release from polymorphonuclear cells(PMN)was measured by constriction of guinea-pig ileum and release of histamine from PMN was measured by fluorometric assay. The mean value of the extent of SRS release in the group with positive response to bronchial provocation test(BPT)was significantly higher than that in the negative group. On the time course study of BPT for the changes in levels of chemical mediators released from PMN induced by calcium ionophore A23187, histaimne release was the lowest at 10 min after antigen inhalation, while the extent of SRS release from PMN was the lowest at 20 min after antigen inhalation. These results may reflect the fact that SRS-A and histamine were released from PMN by antigen inhalation and that rest capacity of release of chemical mediators from PMN decreased when calcium ionophore A23187 was added.
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  • Machiko Kishimoto, Masahiko Katagiri, Shinpei Torii
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1180-1185
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    The ability of SRS release from human polymorphonucler leukocytes by incubation with autologous serum and zymosan was studied. And the behavior of SRS released from human PMN on HPLC was compared to that of synthetic leukotrienes(LTC4, LTD4, LTE4 mixture). The results obtained were as follows: 1. The stimulation of fresh autologous serum and zymosan was capable to release SRS from human PMN. This was also the case in incubation with zymosan activated serum and opsonized zymosan, but SRS release did not occur when heat-inactivated serum and zymosan were used. So, it seemed that complement activation was needed for the release of SRS from PMN. 2. SRS released from PMN was revealed to contain the components LTC4, LTD4 and LTE4 in comparison with synthetic LT on HPLC.
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  • [in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...
    Article type: Article
    1983 Volume 32 Issue 12 Pages 1186-1199
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
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  • Article type: Index
    1983 Volume 32 Issue 12 Pages 1200-1205
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
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  • Article type: Appendix
    1983 Volume 32 Issue 12 Pages 1206-1209
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
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  • Article type: Cover
    1983 Volume 32 Issue 12 Pages Cover12-
    Published: December 30, 1983
    Released on J-STAGE: February 10, 2017
    JOURNAL FREE ACCESS
    Download PDF (130K)
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