Beta-adrenergic effects of catecholamines include bronchodilation, glycogenolysis, eosinopenia and vasodilation. Patients with bronchial asthma show exaggerated responses of bronchoconstriction to various stimuli. Beta-adrenergic blockade theory of asthma (Szentivanyi) explains the hypersensitivity of the bronchi as follows: in asthma the reactivity or number of beta-adrenergic receptors of the bronchi diminishes and the homeostatic balance of the bronchi to keep them open is impaired. Consequently, any stimuli to cause bronchoconstriction results in exaggerated responses. Moreover, beta-adrenergic antagonists such as adrenaline and isoproterenol appear to cause diminished responses of hyperglycemia, hyperlactacidemia, eosinopenia and vasodilation in asthma, suggesting that in asthma the functions of beta-adrenergic receptors is impaired even in the organs other than the bronchi. The impaired function of the receptors can partly explain increased formation of antibody, eosinophilia, bronchodilating effect of theophylline and corticosteroids, and worsening of asthmatic symptoms after respiratory infections, which are commonly observed in asthma. Accumulating reports in this field have not established beta-adrenergic blockade as the etiology of asthma, but also have not ruled it out. One feels that it is worth while investigating the etiology of asthma by using beta-adrenergic blockade theory as a working hypothesis.

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In 1967, J. Porath et al described a method for coupling carbohydrates (Sephadex, Cellulose etc.) to proteins and peptides by activation of carbohydrates with CNBr. By the use of the procedure, it was tried in this paper to purify the nephrotoxic serum antigen. Gamma-globulin fraction of nephrotoxic serum was coupled to Sepharose 2B previously activated with CNBr. Thus, the stable immunosorbent was prepared. This highly stable immunosorbent was supended in Tris-HC1 buffer solution at pH8.2, and the antigenic substance (ultrasupernatant substance of tryptic digested rat glomerular basement membrane) was added to the suspension. The mixture was stirred for 24 hours at 4℃. The effective nephrotoxic serum antigen resulted to bind to the immunosorbent by a specific antigen antibody reaction. The free non-conjugated antigenic fraction was removed from Sepharose 2B on the glass filter with the Tris-HC1 buffer at pH8.2. The immune complex composed of nephrotoxic serum γ-globulin and its specific antigen was then dissociated with 0.5M acetic acid solution, yielding the purified nephrotoxic serum antigen in 10% of the starting material. Immunological and pathological studies on the purified antigen, indicated that the purified antigen thus obtained was about four times as potent as the starting material. These results seem to indicate that the effective nephrotoxic serum antigen can be highly purified by the use of the procedure described above.

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Second Report; Participation of food allergy, especially as a congenital factor, in the etiology of eczema in the brease-fed neonatal infant. Indirect elimination testing and indirect provocative testing of food allergens, such as, egg, milk and soybean was carried out on fifteen breast-fed neonates with eczema, By conducting elimination and trial ingestion diets to the mothers. As a result, the participation of food allergy in the etiology of eczema was demonstrated. At the same time the important role of congential factor in its etiology was assumed from the higher BDB haemagglutination titers against causative food allergens in most of the maternal amniotic fluid specimens, as well as positive provocative test on the infants in the weaning period persisting in spite of the use of elimination diets for several months.

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[in Japanese]

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There is some evidence to suggest that immunological factors are involved in the pathogenesis of certain gastric diseases. Autoantibodies against gastric mucosa have been detected in atrophic gastritis (A.G.) as well as in pernicious anemia. One of these autoantibodies is reported to be complement-fixing. To elucidate the autoimmune mechanism in A.G., serum complement titer and complement-fixing autoantibodies against gastric mucosa were investigated in 163 cases which included 12 normal subjects, 10 of superficial gastritis, 58 of A.G., 33 of fresh gastric ulcer (G.U.), 32 of chronic G.U. and 18 of gastric cancer. The diagnosis was made gastroscopically and also on histopathological examinations of specimens obtained by biopsy. 1) The antigastric antibody was obseved in A.G. in 35% and in chronic G.U. in 23% by the complement fixation test and the immuno-flurescent technique (indirect method). 2) Whole serum complement titer (CH_<50>) was estimated by Mayer's method. CH_<50> decreased in 20 of 58 cases with A.G. and in 12 of 32 cases with chronic G.U. The average titers were 39.8 U. in 12 normals, 32.0 U. in 10 cases of superficial gastritis, 31.6 U. in 57 cases of A.G., 41.1 U. in 33 cases of fresh G.U. and 31.7 U. in 32 cases of chronic G.U. respectively. Among the 18 cases of gastric cancer, 16 exhibited average level of 38.4 U. and two showed the level under 10 U. 3) The titer of components of complement made no difference in every group. 4) C1-biniding capacity of antibodies in gastric mucosa, evaluated by Nishioka's C1 transfer method, was increased in A.G. and chronic G.U. The average titers were 0.2 U./mg(CH_<63>) in 3 normals, 0.90U./mg in 35 cases of A.G., 0.63 U./mg in 19 cases of fresh G.U. and 0.85 U./mg in 21 cases of chronic G.U. 5) Using immunofluorescent method, β-c globulin (C3) was detected in cytoplasma of parietal cells of gastric mucosa. Positive staining was observed in 2 of 9 normals, 23 of 40 cases with A.G. and 11 of 26 cases with chronic G.U. In A.G., cases with positive staining showed higher titers of complement-fixing antibody and more increased C1-binding capacity than in negative cases. These findings suggest a participation of complement in antigen-antibody reaction is gastric mucosa.

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