A clinical study of hypersensitivity pneumonitis in Japan was carried out, and 59 cases were studied. Nearly 75% cases occured from June to September and some of them had repeated episodes over several years in the same season. Causative antigens were immunologically determined in only nine cases of this study, and the rest were undetermined. It was suspected that there was a new mode of hypersensitivity pneumonitis—so-called “summer type hypersensitivity pneumonitis” in Japan the antigen of which was thought to be different from known ones but was not yet determined.
In these 59 cases, clinical symptoms of dyspnea, cough, fever, sputum and palpitations were noted. Rales were audible frequently and chest X-ray revealed diffuse scattered nodular shadows. Laboratory data showed elevated erythrocyte sedimentation rates, leukocytosis with neutrophilia, increased immunoglobulins, decreased vital capacity, DLco and PaO₂. Findings of biopsied lung specimens showed granulomatous pneumonitis. Prognoses of these cases were good, although some cases of “summer type hypersensitivity pneumonitis” showed repeated the episodes.

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An autopsy case of “respirator lung” occurring in a 56-year-old housewife with amyotrophic lateral sclerosis is presented. The patient was admitted because of dysarthria and muscular atrophy of the upper extremities. During the clinical course she suffered from pneumonia and was transferred to the Respiratory Care Unit. Her ventilation was assisted by a Bird respirator operating from an oxygen drive. She recovered from pneumonia after two weeks with medication, but the assisted ventilation with bugle oxgen concentration was continued for 70 days until the patient's death. Postmortem examination revealed gross and histological evidence of oxygen alveolopathy including intra-alveolar fibrin exudate, hyaline membranes along alveolar walls, interstitial edema and early fibrosis and diffuse hyperplasia of the alveolar lining cells with the formation of a cuboidal epithelial layer.

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A granulomatous response in the lungs was produced in BCG-vaccinated rabbits by intravenous injection of live or heat-killed BCG. Four days after a granulomatous response, alveolar macrophages (AM) and the lung lavage fluids (pulmonary washings from immune rabbits=I-PW) were harvested from the lungs by bronchial lavage with sterile physiological saline solution. The function of the AM from granulomatous lungs was enhanced markedly in comparison to those of normal or BCG-infected non-granulomatous lungs, with respect to chemokinesis to casein, phagocytosis, NBT reduction and superoxide production. The enhanced activity of AM functions was conferred on normal resident AM by AM activating factors in the I-PW. Two factors were found in the I-PW when the I-PW was separated by Sepharose 4B column chromatography, i. e., one was found in Fraction III (m. w. 300, 000 to 700, 000) and the other in Fraction IV (m. w. 50, 000 to 300, 000). The factor in Fraction IV was also found in the normal serum (N-serum), in the serum from the rabbits with granulomatous lungs (I-serum), and in the lung lavage fluids from normal rabbit lungs (N-PW). The factor in Fraction IV was thought to be lavage-procured IgG when determined by gel-immunodiffusion test using goat anti-rabbit IgG serum and by its molecular weight, as we previously reported. The factor in Fraction III, however, was found only in the I-PW, but not in Fraction III of N-PW, N-serum nor I-serum.
These results suggest that AM function in the inflamed lungs is enhanced markedly with respect to chemokinesis, phagocytosis and intracellular killing of bacteria, and the enhanced activity of AM functions is induced by an AM activating factor which may be produced in inflamed lung.

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Twenty-two patients with malignant pleural effusions were entered into this study, consisting of 14 patients with lung cancer and 8 patients with breast cancer.
The pleural fluid was evacuated through a trocar catheter under general anesthesia using a Carlens' double lumen intrabronchial catheter with selective inflation of the affected lung. Immediately after total removal of the fluid, anticancer-drugs were instilled either alone or in combination into the thoracic cavity. Evacuation was discontinued when marked decrease of the aspirated fluid was obtained.
Specimens aspirated for 6 consecutive days were microscopically examined daily until removal of the catheter.
Cancer cells in the fluid disappeared within almost 2 or 3 days after the instillation of the drugs. Even in less effective cases they showed markedly degenerative changes which were almost unidentifiable as of malignant origin. Some other floating cells in the fluid such as lymphocytes, macrophages, and granulocytes were also influenced by the anti-cancer drugs administered into the thoracic cavity. Lymphocytes in the pleural fluid initially decreased and then increased. This tendency was more frequently observed in lung cancer cases not responding to therapy. Macrophages remained almost within initial levels throughout this observation. Granulocytes increased markedly after instillation of the drugs, and then decreased rapidly. Lymphocytes and granulocytes in the peripheral blood showed a somewhat similar change.
In some pleural effusions a cancer cell-lymphocyte or -macrophage adherence phenomenon was observed but the exaet mechanism remains uncertain. T-lymphocytes, which were detected predominantly in the pleural fluid, may have a certain role against cancer cells in malignant pleural effusion.

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In order to study the role of gaseous diffusion and convective mixing within the pulmonary airways for pulmonary gas exchange, the steady state uptake of carbon monoxide was measured in healthy young subjects with normal pulmonary function by varying the physical properties of the inspired gases and patterns of breathing.
As ventilatory flow rate was increased there was an almost linear increase in CO uptake for 80%N₂+0.08% CO+20% O₂ gas mixture but it was greater when maintaining breathing frequency and altering tidal volume than when maintaining tidal volume and altering breathing frequency. Therefore, the effect of background gas N₂ and He on CO uptake was assessed only by varying breathing frequency at constant tidal volume.
The experimental results showed that CO uptake for 80% N₂+0.08% CO+20% O₂ gas mixture (N₂) was greater than that for 80% He+0.08% CO+20% O₂ (He) as ventilatory flow rate increased, while it tended to be greater for He than for N₂ as ventilatory flow rates decreased in some cases.
To explicate these observed results, a simultaneous washout curve of He and SF₆ at constant expiratory flow rate (350ml/sec) was measured after a single inspiration of 5% He+5% SF₆ (instead of N₂)+90% O₂ gas mixture (500ml) with an inspiratory flow rate of 500ml/sec and 250ml/sec, respectively. The ratio of He to SF₆ concentration (F_He/F_SF6) on the late portion of washout curve was higher with a lower inspiratory flow rate than with a higher inspiratory flow rate.
It was concluded from the relationship between CO uptake and the results of a single washout of SF₆ and He that the role of convective mixing for CO transport in the pulmonary airways was significant at higher ventilatory flow rates, while gaseous diffusion was more important at lower ventilatory flow rates.

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A 65 year-old man presented with fever and dyspnea in Dec. 1972. Chest X-ray examination revealed bilateral fine ground glass densities predominantly in both lower lung fields. His discomfort disappeared spontaneously, but he had fever again in Jan. 1974, which continued despite antibiotics therapy and subsided with glucocorticoid therapy. In. June, he experienced dyspnea on exertion, and in Jan. 1975, he was admitted complaining of fever and breathlessness. Cyanosis and finger clubbing were observed. His X-ray film revealed micro-nodular and reticular shadows in the bilateral lower fields, and bronchogram demonstrated bronchioloectasis and slight collapse of the lower lobes, and lung function studies showed constrictive failure and reduction of diffusing capasity.
Open lung biopsy was carried out. The microscopic finding was compatible with that of DIP characterized by large numbers of mononuclear cells in the distal air spaces with slight thickening of the alveolar walls. No necrosis nor hyaline membrane was found.
He was given prednisolone and had an uneventful course for 3 years but died suddenly, cause unknown. At autopsy, diffuse interstitial fibrosis and widespread pleural adhesion were found, but there were few intraalveolar desquamated cells noted in the initial biopsy.
We found 18 reported cases of biopsied DIP reexamined histopathologically after an interval of six months or more. In 2 cases the final histopathological findings were about the same as those of the first biopsies. and in 8 cases, diffuse interstitial fibrosis had advanced but some of the findings seen on initial biopsy could be recognized. In 9 cases autopsied lungs, the histopathological findings were diffuse interstitial fibrosis or UIP, and there was no remnant of DIP as seen on initial biopsy. We found that DIP can progress to diffuse interstitial fibrosis indistinguishable from UIP.

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61才, 男子, 右胸膜炎の型で発症し, 徐々に右肺の萎縮, 右全胸膜の肥厚が著明となり1年2カ月の経過で死亡した. 胸部X線上両側の横隔膜に小さな石灰化像を認め, 石綿暴露が示唆されたが, 剖検材料の鉱物学的検索で chrysotile 並びに amosite を証明した.

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