Pulmonary functions were measured in 53 patients with hepatic cirrhosis who had no clinical or radiographic evidence of pulmonary involvement. Spirometric tests such as TLC, VC, FRC, RV and FFV_1.0 were within a normal range in all subjects. Flow volume curve and closing volume tests, however, were abnormal in the majority. The maximal expiratory flow at 50 percent of forced vital capacity (V₂₅) was not altered but the maximal expiratory flow at 25 percent of forced vital capacity (V₅₀) was decreased significantly in patients with hepatic cirrhosis. The closing volume in patients with hepatic cirrhosis was also significantly increased. The abnormalities in flow volume curve and closing volume curve were demonstrated also in nonsmokers and at any age in cases of hepatic cirrhosis. These results suggest that the narrowing or closure in small airway may occur in patients with hepatic cirrhosis. We suspect that these changes may be due to be mechanical compression of small airways by interstitial pulmonary edema, although at present it is impossible to make any distinct conclusion concerning which factors in the lungs change in hepatic cirrhosis.

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Six adult male healthy volunteer subjects were exposed to 0.15ppm O₃ and 0.15ppm NO₂ alone and in combination, with intermittent light exercise for two hours. Three of the 6 subjects developed coughing during deep inspiration and one subject had chest pain or chest discomfort during exposure both to O₃ alone and to O₃ in combination with NO₂. Nobody had any symptom during exposure to NO₂ alone.
Significant decrease of specific airway conductance (Gaw/Vtg) was observed in 5 of 6 subjects during exposure to O₃ alone, in 3 subjects during exposure to NO₂ alone and in all six subjects during exposure to the O₃+NO₂ mixture in comparison with control measurements. Significant enhanced decrease of Gaw/Vtg after the O₃+ NO₂ mixture was observed in 3 subjects. These results suggested that the effect of the two gases at 0.15ppm was more than additive in some subjects when performing exercise.

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A field survey on farmer's lung was performed in a farming community located in northern Hokkaido. Of 262 dairy farmers, 13 showed typical findings such us micronodular or reticulo-nodular shadows, or shrinkage of the lung in routine chest roentgenograms and 18 showed ill defined micronodular shadows suggesting the disease, and 44 were positive in serum precipitin antibody tests to thermoactinomyces vulgaris (T. V.) and 67 to micropolyspora faeni (M. F.). Eleven patients showed not only the typical radiologic findings but also positive reaction to the precipitin antibody tests to T. V. and/or M. F. In respiratory function tests in 13 out of 31 patients who had radiologic findings, 4 showed decreased pulmonary difusing capacity, and 11 abnormal flow-volume curves, suggesting small airway disease. No certain correlation between the occurrence of farmer's lung and the working period, number of cows, area of grassland, working time in the cowshed, daily exposure time to hay, and smoking history were found statistically. After the cultivation of the dust from hays which were sampled from two patient's cowshed, 7 sorts of mold included T. V. and M. F. were detected.
These results may suggests that there is a considerable number of patients with farmer's lung in certain districts of Japan.

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In order to investigate the pathophysiological role of pulmonary alveolar macrophages (PAMs) in pulmonary diseases, we measured the biological and biochemical activities of PAMs obtained from normal volunteers and patients with pulmonary diseases with those of rat PAMs as control. In particular we examined the effect of smoking on the function of human PAMs.
PAMs were obtained from two groups; 11 normal volunteers aged 24±1 years (mean±SD) and 27 patients with well localized pulmonary disease aged 63±12 years, by segmental bronchoalveolar lavage. The lavaged site of the patient group was free of lesions. Only specimens in which percentage and viability of PAMs was over 75%, were used as test samples.
1) The number of PAMs was about 1.5 times larger in the smokers than in the nonsmokers, and their mean viability was about 85%, in both groups.
2) The O₂ consumption in cell level, protein content and acid phosphatase activity of PAMs from the smokers were significantly (1.5-3-fold) higher than those from the nonsmokers in both groups.
3) In the patient group, per cent adherence of PAMs from smokers was significantly lower than in non-smokers.
4) Phagocytic activity of PAMs from normal volunteers was measured with heterogeneous erythrocytes. The erythrophagocytic activity of PAMs from both smokers and nonsmokers were markedly higher with ORBC coated with anti-ORBC rabbit IgG than with that not coated with the IgG. When SRBC coated with both anti-SRBC rabbit IgM and human complement was used as erythrocyte, the erythrophagocytic activity was significantly lower in the smokers than in the nonsmokers.
5) Levels of O₂ consumption at the cell level of rat PAMs were similar to those of human PAMs from nonsmokers, but acid phosphatase and β-glucuronidase activities of rat PAMs were different from those of human PAMs.
These results indicate that the number and functions of PAMs are affected by smoking, and that the effect of smoking on the different functions of PAMs differs according to the individual.

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Host factors and clinical characteristics in five patients with respiratory mucor infection in the last five years were studied. From the point of host factors, the mechanism of mucor infection to the lung was classified into three groups as primary, secondary, and saprophytic infection. One out of the 5 was primary, 2 were saprophytic, and the remaining 2 were secondary mucor infections. The primary mucor mycosis case was an asymptomatic 52-year-old man without any predisposing factors and discovered by annual chest X-ray survey.
The 2 saprophytic mucor infection cases had previous cystic lung lesions from tuberculosis. Secondary mucor infection occurred in two leukemic patients with administration of large doses of steroids, anti-cancer drugs, and antimicrobs. We stressed in this paper the type and relatively good prognosis of saprophytic pulmonary mucor infection.

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Factors causing pulmonary mycotic infection in 31 patients over the last five years were studied. In terms of host factors, the mechanisms of fungal infection to the lung mere classified in three groups as primary, secondary, and saprophytic infection. Primary pulmonary mycosis was a fungal infection to the lung in asymptomatic patients with no obvious underlying diseases. Three patients with nodular lesions on chest X-ray detected by annual survey belonged to this group.
Secondary pulmonary mycosis was an opportunistic fungal infection in patients in deteriorated condition with severe underlying diseases and those treated with steroid hormones, antineoplastic drugs, and antimicrobials. Fungal infections in 13 patients belonging to this group were detected by microscopic examination of the autopsy specimen, which revealed candida sp., aspergillus sp., mucor sp., cryptococcus sp., or torulopsis graburata.
The important host factors in saprophytic mycosis were the existence of abnormal spaces in the lung, such as cavities, bullae, cysts, and bronchiectasis. Most of the 15 patients belonging to this group had fungus ball formation by aspergillus sp. in open negative cavities in pulmonary tuberculosis.

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A patient with Goodpasture's syndrome was maintained by chronic hemodialysis for over 37 months and the pulmonary hemorrhage was best controlled by corticosteroid therapy.
Circulating anti-glomerular basement membrane antibody (anti-GBM Ab) was detected by indirect immunofluorescent techniques.
The diagnostic value of demonstrating circulating anti-GBM Ab by indirect immunofluorescent techniques is discussed.

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