For years, the difference in cause of pulmonary hypertension between massive and miliary embolism has been discussed. It has been proposed by some investigators that miliary embolism causes pulmonary vasoconstriction superimposed on simple mechanical obstruction, although the effect of massive embolism is mainly due to its mechnical blockade of the pulmonary artery.
Studies on strict!y unilateral miliary pulmonary embolism, as reported by us before, showed that initial diminution of the unilateral blood flow was improved with time considerably rapidly, and no influence on the opposite pulmonary vascular tone was observed. As the result, the importance of local factors was stressed. This paper presents a supplementary data to the previous paper.
The left lower lobe of the adult dog was excised, and perfused with heparinized autologous blood. Ventilation was maintained by a positive pressure respirator with mixed gas of various O₂ concentration as needed. Embolization, single or recurrent, with lycopodium spores was carried out and effects of isoproterenol, propranolol or prostaglandin (PG) E₁ on pulmonary inflow pressure elevation induced by embolism were tested.
The pattern of inflow pressure elevation due to miliary embolism in the excised lung lobe was very similar to that observed in miliary pulmonary embolism in living animal, whereas neural pathways were cut off in the excised lung.
PG E₁, as well as isoproterenol, is known as a pulmonary vasodilator. In our experience, however, no evident vasodilative effect on the excised perfused lung was obtained with a comparable dose of PG E₁, unless any vasoconstrictive state existed. Accordingly, the fall by PG E₁ in the elevated inflow pressure in miliary embolism appeared to show subsidence of the vasoconstriction of affected vessels.
In conclusion, the pulmonary vasoconstriction superimposed on mechanical obstruction of pulmonary vessels in miliary pulmonary embolism has been verified, and it must be due to some local mechanism.

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A report of percutaneous lung biopsies performed in 247 cases including 150 cases of primary lung cancer with a fine needle (0.8 and 1.0mm outer diameter) was presented, and its complications and indication were discussed.
A diagnosis was established in 77.6% of the patients having primary bronchial carcinomas. Complications consisted of 25 cases of pneumothorax (10%), 10 instances of bloody sputum (4%) and others.
For the evaluation of needle biopsy, diagnostic procedures in 87 resected cases of lung cancer for the past three years were analyzed and the reasons for negative bronchial biopsies were clarified. There were 25 negative bronchial biopsies, of which 15 cases were anatomically difficult to obtain malignant cells through the bronchi. Ten cases of 25 negative brushings were applied for the needle biopsy and eight of them became positive by this methods. These results suggested that a percutaneous needle biopsy is the best methods in peripheral coin lesions or localized parenchymalnodules which can not be diagnosed by bronchial biopsies, sputum studies or other available procedures.

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There is well-established evidence for the role of immediate and Arthus-type reaction involving precipitating antibodies in allergic bronchopulmonary aspergillosis.
Pepys et al (1968) reported four cases with asthma and pulmonary eosinophilia who had evidence of Type I and Type III allergy to Candida albicans. Recently we have observed a patient whose clinical and immunological features might be attributable to the same mechanism. This report is believed to be the first case with the syndrome reported in Japan.
Patient Y. N., a 32-year-old female, gave a history of asthma for 2 years. She was admitted to our hospital in June 1973 for recurrent episodes of dyspnea and productive cough. Chest X-ray was negative. Bronchogram revealed no abnormality. The leukocyte count was 10, 500 with 8% eosinophils; sedimentation rate, 52mm/hr; smear of sputum revealed eosinophilia and cultures yielded growth of C. albicans.
She reacted on Intradermal testing to C. albicans and three other allergens, but did not to Aspergillus fumigatus. A “dual” response was obtained with crude extract and mannan from C. albicans group A, with appearance of wheal and flare at 30 minutes, followed at 5 hours by a diffuse edematous swelling. intradermal testing with the crude extract also gave induration and erythema at 24-72 hours. Agar-gel diffusion gave precipitation arcs to the crude extract and mannan A. She was underwent inhalation challenge with the crude extract (0.8mg). There was a moderate decrease in FVC and FEV _1.0 with dyspnea immediately after exposure. She developed progressive dyspnea, FEV _1.0 decreased to 47% of the pre-test level at 6 hours and 64% at 24 hours. Systemic reactions such as fever, malaise headache etc. were not remarkable, but accompanied by an increase at 24 hours in the white blood and eosiniphile count. Chest X-ray showed a definite infiltration in right upper lobe 24 and 48 hours after exposure, which disappeared by a week.
The inhalation test was repeated after 3 weeks with mannan A (3mg). The patient exhibited a “dual” asthmatic response, immediate followed by late type, reaching maximum severity at 6 hours, and the dyspnea gradually subsided and diasppeared by 24 hours.
During her stay in the hospital, chest X-ray Ead demonstrated fluctuating pulmonary infiltrations in right and left upper lobe, and bilateral lower lung fields accompanied by pleural effusion occasionally. She was placed on corticosteroids, bronchodilators and amphotericin B (by aerosol) with good response and discharged in April 1974.

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The patient, 32 year old male, visited the clinic with the complaint of cough, sputum and slight fever. By X-ray examinations of the chest the round shadow was found in the right lower lung field and was suspected the pulmonary benign tumor of the lung.
The results of operation revealed the liver herniation encapsulated with peritoneum and with parietal pleura into the thorax through the defect of the right side diaphragm.

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