Newborn infants with congenital esophageal atresia associated with tracheoesophageal fistula often die of lung complications, so-called “retention lung”. The tracheal wall of these infants is devoid of ciliated cells and completely lined with squamous epitheliums and the alveoli are filled with many macrophages. The constant association of these two lesions in this disease suggests a cause-and-effect relationship. In 1971, Emery et al. suggested that these pulmonary lesions might have been due to extensive absence of ciliated cells of the tracheobronchial tree.
To test this hypothesis, we have done experiments on rats in which radiation to the trachea was used to destroy the ciliated cells, hopefully to impair the ciliary transport mechanism, thereby producing retention lung simulating the condition seen in the tracheoesophageal fistula of the infants. This report is concerned with the histological findings of this experiment.
Twenty male rats of Donryu strain weighing 210-270g were used. Each rat was subjected to lineac X-ray-irradiation exclusively of the trachea at a dose of 500 rads per day for 30 days. Rats were sacrified 35 days after the completion of radiation. The tracheal walls of the experimental rats were devoid of ciliated cells and lined with cells resembling squamous epitheliums. The alveoli of these rats were filled with large alveolar cells. We did not find any superimposed pneumonia in all sections studied.
Although such lesions are generally of focal nature in the present study, it is quite clear that we have produced in rat lungs a condition similar to that seen in the lungs of human infants dying of tracheoesophageal fistula.
The present findings provide an experimental basis for the better understanding of the pathogenesis of “retention lung”, the hallmark of the tracheoesophageal fistula of newborn infants.

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The present study was undertaken in order to (l) evaluate whether peripheral airway disorders as detected by frequency dependence of compliance was present in asymptomatic smokers whose routine pulmonary function tests are otherwise normal and to (2) evaluate the differences in the mechanics of breathing in young smokers and relatively aged smokers. We selected 29 healthy male subjects, who were classified in three groups.(l) Eight young students (age: 20±1) who had never smoked. (2) Twelve young students (age: 20±1) who had smoked more than 20 cigarettes a day for 1 to 3 years. (3) Nine middle-aged subjects (age: 39±6) who had smoked more than 20 cigarettes a day for more than 10 years.
Airway resistance, VC and TLC and FEV1.0 did not reveal any consistent difference between the smokers and the non-smokers. The static deflation P-V curves in young smokers and nonsmokers were identical, and those of middle aged smokers also remained within the normal limits.
Dynamic compliance was measured at several breathing frequencies up to 2Hz (120 breaths/minute), and was related to the slope of the inspiratory static P-V curve at the same lung volume range (about 1l), expressed as a Cdyn(l)/Cst(l) ratio. At and above 0.5Hz, the Cdyn(l)/Cst(l) ratio was significantly lower in both young and aged smokers.
The Cdyn(l)/Cst(l) ratio, measured at lower lung volumes (1l lower resting level) showed more frequency dependence in middle-aged smokers than in young smokers, presumably as a result of small airway closure increasing linearly with age.
We interpret the occurence of frequency dependent compliance in the presence of normal airway resistance and static compliance to mean that these are structural changes in peripheral airways of asymptomatic smokers even in a young college-age group.
Maximum expiratory flow at 10% of the vital capacity (V10) decreased significantly in smokers, and the decreased V10 was exaggerated in middle-aged smokers. Also the V50V25 ratio (Takishima et al. 1972), which expresses the shape at the end of the V-V curve, indicates a significant difference between smokers and non-smokers. MMF significantly decreased in middle-aged smokers.
The decrease of maximum flow at lower volumes of vital capacity also indicates that airways upstream from the flow limiting segment (peripheral airways) have increased resistance in smokers, since no changes in the elastic properties of the lung were demonstrated.

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Monosporium apiosperum (M. ap.) causes most commonly the lesion of skin and subcutaneous tissues of the foot and become clinically one of the causes of madura foot. Primary infection of this fungus in lung is extremely rare. Two cases of pulmonary Monosporiosis were found in the resected lungs postoperatively. The first case was reported in Japan J. Med. Mycol. in 1966 by the authors and Uetsuka and the second was found in 1972.
The first case was a 31-year-old farmer's housewife with complaints of frequent cough, spu tum and rapid onset of pulmonary symptoms. Progressive inflammation and marked saccular bronchiectasis with disseminated granules of M. ap. were observed from the distal end to the proximal portion of B⁵ in the resected left lung.
The second case was a 49-year-old single female with complaints of occasional bloody expectoration for the past 2 decades. The chest radiogram had revealed almost unchanged fungus ball 2.0cm in diameter in a cavity. Bronchiectatic cavity containing fungus ball of M. ap. was found in distal branch of B²_a of the resected right upper lobe.
Histological findings of the cases were similar to those of aspergillosis. For the detection of M. ap. from the foci, egg-media was more excellent than Sabouraud's agar media.

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An autopsy case of a 45-year-old male with Hand-Schüller-Christian's disease is reported. He had chief complaints of coughing, expectoration of sputa and general fatigability, accompanying incomplete diabetes insipidus. On chest X-ray films diffuse pulmonary fibrosis which progressed gradually was demonstrated. Biopsy specimen of the lung revealed diffuse interstitial fibrosis with occasional presence of histiocytes. At autopsy the pulmonary lesion was proved to be diffuse interstitial fibrosis with histiocytic infiltration which was a pulmonary manifestation of Hand-Schüller-Christian's disease. From the findings of the lung at biopsy and autopsy, the pulmonary lesion seemed to be a diffuse interstitial fibrosis even in the early phase.
Therefore, Hand-Shüller-Christian's disease should be included in the differential diagnosis of the diffuse interstitial pulmonary fibrosis.

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A 23 year old woman with acute leukemia had fever, non-productive cough and chest pain during the remission induction therapy. Chest X-ray film revealed hazy homogenous as well as patchy shadows. These shadows had disappeared almost completely following the antibiotic treatment. However a month later she developed high fever, cough and dyspnea. Chest X-ray film again revealed the same kind of infiltrates in the same distribution. She had gradually developed respiratory insufficiency and expired three weeks later. Autopsy findings of the lungs showed pulmonary alveolar proteinosis and pulmonary aspergillosis.

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