We investigated the usefulness of a mask in reducing exercise-induced bronchoconstriction. Five normal children as control and eight asthmatic children were selected for this research. Ergometer exercise was performed and airway response was measured on two separate days in February, 1981. On one of the two days, subjects wore a mask. On the day on which masks were not worn, no change in pulmonary function was seen in the normal children after exercise, but significant decrease in pulmonary function was seen in the asthmatic children. On the day masks were worn, decrease in pulmonary function diminished significantly. Some 3rd day, we measured VO_2 during ergometer exercise. VO_2 during ergometer exercise was 36.6±4.5ml/kg/min(mean±SD), and this exercise proved suitable for testing of EIB. This study demonstrated the effectiveness of a mask in protecting asthmatic children against exercise-induced bronchoconstriction during outdoor sports.

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The in vitro effects of auranofin(oral gold compound) on lymphocyte proliferative response, auranofin-induced cell conculture assay system to autologus peripheral blood mononuclear cell proliferation, and auranofin-induced cell treated with indomethacin coculture assay system were studied, using peripheral blood mononuclear cells from twelve healthy individuals. In vitro T- and B-lymphocyte proliferative responses were suppressed at any dose of auranofin ranging from 0.1μg/ml to 10μg/ml in a dose-related manner. This suppressive effect of auranofin on lymphocyte proliferative reaponse was caused by generation of suppressor cell activity by auranofin, furthermore, auranofin-induced suppressor cell activity was diminished by the presence of indomethacin(1μg/ml) at its generating phase. In contrast, concanavalin A-activated suppressor cell exhibited indomethacin-resistent activity. In recent years, loss of suppressor cell activity has been demonstrated in patients with rheumatoid arthritis. Thesse results suggest that auranofin is useful in the management of patients with rheumatoid arthritis.

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T cell subsets defined by monoclonal antibodies were first examined for their capacity to proliferate in the normal autologous mixed lymphocyte reaction(AMLR).Treatment of T cells with OKT4 and complement (C')ablated their proliferative respnse in AMLR; treatment of T cells with OKT8+C' had no effect on the proliferation. This was true regardless of the time when treatment was performed before or after AMLR. Thus, a T4 cell subset appears to be the major responder T cells in AMLR. We have next investigated the role of T4 cells activted by AMLR in the immunoregulation of B cell differentiation. Here the T4 cells were obtained by C'-dependent lysis of AMLR-activated cells with OKT8. T4 cells activated for 3 days in AMLR acted as helper cells, while T4 cells activated for 6 days in AMLR could exert potent suppression.The data suggest that T4 cells activated in AMLR contain two functionally different subsets; helper and suppressor cells, and that AMLR may reflect a mechanism of feedback suppression.

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Treatment of human PMNs by trypsin resulted in reduced EAC rosette formation and increased EA rosette formation, suggesting selective removal of C3 receptors from PMN surface. The effect of the removal of C3 receptors by trypsin on phagocytosis and lysosomal enzyme release by PMNs was investigated with following results. 1. Phagocytosis and lysosomal enzyme release were enhanced by trypsin treatment. 2. There was no difference between EA(IgG) and EA(IgG)C in phagocytosis and lysosomal enzyme release. 3. EA(IgM)C was also phagocytosed and induced lysosomal enzyme release. However, these findings were not significant.

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We studied the effect of H_1 and H_2 histamine antagonists on bronchoconstriction induced by histamine and methacholine in monkeys. The bronchoconstriction was induced by aerosol challenge with histamine and methacholine. The histamine blockers were intravenously injected. Pretreatment with diphenhydramine(H_1 histamine antagonist) significantly suppressed increase in total respiratory resistance(Rrs.) due to histamine aerosol challenge, and it also suppressed that due to methacholine to a slight degree. Pretreatment with H_2 histamine antagonist, metiamide 73 mg and cimetidine 76 mg, had no effect on bronchoconstriction due to histamine or methacholine. The injection of H_1 blocker also reduced histamine-induced bronchoconstriction by 61.2% in total respiratory resistance(Rrs.), and the methacholine-induced by 43.5%. Howere, the injection of H_2 blocker did not produce uniformal change in the elevated Rrs. induced by histamine and methacholine.

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We have examined the influence of mitogens, lymphocyte subsets and other factors on T lymphocyte colony formation. Normal human peripheral blood mononuclear cells and lymphocyte subsets were cultured in 0.35% agar medium containing 10% fetal calf serum. 30μg/ml phytohaemagglutinin(PHA) and 0.8% sheep red blood cells. Colony formation required at least 2×10^5 mononuclear cells per milliliter, and optimal results were obtained at concentrations of 5×10^5 cells/ml. Peak production of colonies was shown after 7 days of incubation. Addition of 30μg/ml of concanavalin A (Con A) or 10μg/ml of pokeweed mitogen(PWM) also induced colony formation, but the frequency of formation was lower than with incubation by PHA. T lymphocyte subset alone formed colonies in agar with PHA identical with those of whole mononuclear cells, whereas culturing with Con A ro PWM required the presence of mononuclear cells for the production of colonies. IgG・Fc-receptor-positive T lymphocytes were found to have a very low colony-forming capacity, while IgG・Fc-receptor-negative lymphocytes produced normal numbers of colonies. On the other hand, the colony-forming cells themselves were T lymphocytes, all of them being IgG・Fc-receptor-negative and surface immunoglobulin negative cells. These results suggest that colony-forming cells are derived from a selective lymphocyte subset.

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To clarify the development of the complement system, the author measured the activity of the total hemolytic complement(CH50) and the levels of complement proteins in cord sera from 41 newborn infants. The subjects divided into preterm(28 to 37 weeks) and full-term, low birth weight(810 to 2500gm) and normal birth weight(NBW), and SFD abd AFD infants. The levels of Clq, Cls, C4, C3, C5, C9, factor B, ClINH and C36bINA in serum were measured by single radial immunodiffusion methods using monospecific antisera. The activity of total hemolytic complement was determined by Mayers' method. These values in newborn sera were compared with those of normal adults. 1. Preterm infants of 28 weeks to 37 weeks gestation had less whole complement activity and lower complement protein levels than full-term infants. 2. Infants weighing 810g to 2500g at birth had less whole complement activity and lower complement protein levels than infants of 2501g to 4000g. 3. The values of CH50 and complement proteins in SFD and AFD infants. a) At 33 weeks to 37 weeks gestation, the values of CH50 and complement proteins except for C9 were lower in SFD infants than in AFD infants. These differences were statistically significant(p<0.05-P<0.001). b) The levels of Clq, Cls, C3, C9, factor B and C3bINA in SFD infants of 33 weeks to 37 weeks gestation were lower than these levels in AFD infants of 28 weeks to 32 weeks gestation. c) The levels of Clq, Cls, C5, C9, factor B and ClINH in full-term SFD infants were lower than these levels in AFD infants of 33 weeks to 37 weeks gestation. d) At full-term, the values of CH50 and complement proteins were lower in SFD infants than in AFD infants. These differences were statistically significant (p<0.05-p<0.01). 4. Comparison of the values of CH50 and complement proteins in newborn sera between Japanese standards for intrautering growth and birth weight. a) The values of CH50 and complement proteins in full-term AFD infants and in infants of 2501g to 4000g weere not significantly different, and the ratios of these mean values to the adult mean values ranged from 10% to 75%. b) In full-term SFD infants the values of CH50 and complement proteins were significantly lower than these values in infants of 2501g to 4000g(p<0.05-p<0.001). c) The values of CH50, Clq and C3 in full-term SFD infants were lower than these values in infants of 2001g to 2500g. 5. There was a statistically significant correlation between increasing birth weight or gestational age and increasing serum values of CH50, Clq, Cls, C4, C3, C5 and ClINH. These results suggest that the complement system develops with increasing birth weight or gestational age during the perinatal period.

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A Study was undertaken to establish the normal values of peak flow rate using Wright peak flowmeter at several Japanese chest clinics and laboratories. The subjects were 417 healthy children aged 6 to 15 years. Prediction equations and regression lines are presented for each sex. The predicted values of the peak flow rate is calculated from standing height. The peak flow rate correlated well with forced vital capacity(FVC), forced expiratory volume one second (FEV_<1.0>) and maximum mid-expiratory flow(MMEF) in healthy children, but not in asthmatic children. The performance of Wright peak flowmeter is compared with that of the spirometer in the same subjects. There were differences in readings of the two instruments. The peak flowmeter readings are slightly lower than the spirometer readings for values under 200l/min and over 400l/min. These results can be considered to show the normal standard values of peak flow rate in our country.

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An experimental model of asthma in guinea pigs has been developed. A 10% TDI(toluene diisocyanate) solution dissolved in ethyl acetate was painted on the bilateral nasal cavities of guinea pigs with a thin cotton applicator once daily for five consecutive days. The amount of the TDI solution which was painted on the both sites each time was about 10mg in all. Three weeks later, the animals were challenged with a 5% TDI solution. Exertional breathing accompanied by the prolongation of expiratory phase was observed among the test animals. The number of animals which suffered from the attacks increased with the repetition of the provocation procedures. It was found that the attacks could be brought about by TDI in a concentration of 0.1% when the animals had become suffciently sensitive to TDI. Both eosinophilic infiltration in the lung and eosinophilia in the peripheral blood were found among the test animals. This experimental model was developed by the application of a simple chemical alone to the respiratory tract of guinea pigs. The model is considered useful not only for studies of asthma induced by TDI but also in various other research fields of asthma because of the simplicity of the experimental technique.

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