We analysed lung sounds of 53 asbestos workers who had bilateral basal crackles by sound spectrograms with corresponding time expanded wave-forms to elucidate the basic features of crackles and to examine the relationship of crackle features to radiographic findings of asbestosis.
1) Fine crackles were classified into four patterns in terms of sound spectrograph and time expanded wave-form analysis. These four patterns were apparently correlated to stages in radiographic findings of asbestosis.
2) The number of crackles per inspiration significantly increased as radiographic abnormalities progressed.
3) Concerning results of wave form analysis by the zero crossing method, it was found that crackles both on inspiration and on expiration were fine; however, when radiographic changes showed honeycombing, inspiratory crackles changed from fine to medium.
Thus, we have shown that lung sound analysis is of value for monitoring asbestos workers.

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Twenty-one patients with clinically and histologically confirmed sarcoidosis were studied for precipitins against various antigens of hypersensitivity pneumonitis; Aspergillus fumigatus, Cephalosporium acremonium, pigeon droppings, Pullularia pullurans, Thermoactinomyces vulgaris, Trichoderma viridi, Cryptostroma corticale, Micropolyspora faeni, Pigeon serum, Sitophilus granarius. The serum precipitins against Sitophilus granarius, Micropolyspora faeni, and Thermaoactinomyces vulgaris were positive in 76%, 71%, 33% cases out of 21 patients with sarcoidosis, respectively, but in only 10% of 20 healthy controls.

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The anti-horseradish peroxidase antibody used as a tracer was prepared by immunizing intradermally a rat with 2mg of horseradish peroxidase in complete Freunds adjuvant, and pulmonary edema induced by alpha-naphtylthiourea in rats was observed by electron microscopy.
Anti-horseradish peroxidase antibody was seen in pinocytotic vesicles of endothelial and type I alveolar epithelial cells, between interendothelial junctions, within basement membrane and edematous interstitial space, but there was no staining of type II alveolar epithelial cells or interalveolar cell junctions. We concluded that protein containing edema fluid leaks through pinocytotic vesicles and intercellular junction in the capillary endothelium to interstitial space and is likely transported by means of pinocytotic vesicles across type I alveolar epithelial cells.

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An airway model (from trachea down to the fifth generation) was made using plastic tubes and joints. By appropriate damping the quality factor (Q) of the model was approximated to those of human lungs. Upward and downward transmission characteristics were studied by pulse waves and sinusoidal waves of 0.1 to 1kHz. In both situations the model behaved as a low-pass filter with a cut-off frequency of about 140-250Hz and an attenuation of about 15-24dB/octave. The results agreed with those of Buller who reported on downward transmission characteristics of human lungs. When the model was excited by a pulse wave, the output signals were different both in shape and timing depending on where they were recorded. By increasing the distance between the sound source and the microphone, the waveform of the output signals became more round (due to the attenuation of higher frequency components), smaller in amplitude and the delay became more prominent. When the input signals (pulse waves) were given from the periphery (fifth generation), the signals were transmitted at most to the neighboring branch but practically not at all beyond because of a large attenuation of 31-61dB/octave with a cut-off frequency of 170-500Hz. Our results were compatible with clinical observations made by Forgacs who pointed out that the pattern of crackles changes when the stethoscope is moved over a short distance. Our results also indicate that the filtering effect of the lung is primarily due to the geometrical structure of the airway. An equivalent electrical circuit of the airway is a tree system with filters connected in parallel and cascade.

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Hamartoangiomyomatosis, a rare disease, has been known to cause repeated spontaneous pneumothorax in women and patients rarely survive beyond the age of 50 because of bilateral penumothorax or progressing respiratory failure. The patient was a Japanese woman born in 1923, whose first episode of spontaneous pneumothorax was in 1964. She experienced spontaneous pneumothorax 4 times and was first admitted to our hospital in 1974. Chest rentogenogram revealed left spontaneous penumothorax and reticular and bullous shadows on both sides.
Partial resection was done for tension pneumothorax. At operation, mulitiple bullae were found and histologically hamartoangiomyomatosis was revealed. Thereafter, right spontaneous pneumothorax occured 3 times and Broncasma Berna was administered into the pleural cavity each time. However, bilateral partial pneumothorax occured once and Broncasma Berna was readministered. Since February 1978, she has had no episode of spontaneous pneumothorax.
She is now 57 years old, well and does not complain of dyspnea. This case suggests that pleurodesis using Broncasma Berna for spontaneous pneumothorax of the disease caused prolongation of life.

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A 33 year-old, female, taking predonin for the treatment of fever for about 5 months, developed scattered cutaneous lesions. Acid-fast bacilli were detected in sputum, urine, and pus from the subcutaneous abscesses several times. Cultures of the pus were positive for Mycobacterium kansasii. Right paratracheal lymphadenopathy and splenic abscess followed the development of pulmonary parenchymal lesions. Disseminated Mycobacterium kansasii infection has not been reported in Japan, and the complications of mediastinal lymphadenopathy and splenic abscess have rarely been described in the literature.

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A 42-year old man was admitted on 15 December 1981 because of swelling of the face and neck over the past 2 months. He had complained of recurrent oral ulcer and superficial thrombophlebitis of the right chest wall. There was no scrotal ulcer and the examination of the eyes by an ophthalmologist was negative. Needle reaction of the skin was positive. According to the above symptons, the patient was diagnosed as having Behcet's disease.
On admission the classical signs of superior vena caval obstraction, with prominent venous collaterals over the chest and abdomen, were present. A chest radiograph showed slight widening of the superior mediastinum. Superior vena cavagram revealed complete occlusion of the brachiocephalic veins. Collateral circulation was evident. Mediastinal biopsy by means of the right parasternal incision was normal, but thorombophlebitis of the superior vena cava was recognized. Biopsy of a nodule of the right chest wall showed non-specific granulomatous reaction with occluded veins.
Thorombophlebitis of the superior vena cava as a complication of Behçet's disease led to superior vena cava syndrome. The patient was treated with predonisone and diuretics. His chief complaint improved and he was discharged from hospital on 30 January 1982.

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