To investigate the relationship between diameter of airways and lung volume in various respiratory phases, serial bronchography and simultaneous spirography with records of X-ray exposures have been performed. Serial bronchograms have been taken at a speed of 3 films per second in resting respiration or forced expiration. 17 normal and 16 diseased cases were selected as subjects for this study. Diameters of airways were measured in about 10 bronchial divisions in each case.
The results obtained were as follows:
1) In most of normals, airway diameters in resting inspiratory phase was always larger than those in expiratory phase (Type I). The type I is considered as basic pattern of changes of airway calibre in normal resting respiration, particularly in airways smaller than lobar bronchi.
2) In forced expiration, in normals and in most of diseaseds, trend of reduction in each airway diameter was almost linear in the first one second. Diameter of bronchi in lower lobe reduced much more than those in upper lobe. This difference became larger in the last part of forced expiration (Fig. 4).
3) In forced expiration, 2 normals showed infolding of posterior membranous portion of the wall in large bronchi associated with remarkable reduction of diameters in most other airways. The appearance of tracheobronchial collapse syndrome would be related to the stage, where infolding phenomenon occurs.
4) In some patients with obstructive disturbance, most of airway diameters reduced remarkably soon after the beginning of forced expiration, and then enlarged at the end of first second (Fig. 6). In this consideration, one of reasons of obstructive disturbance seems to be this marked reduction of airway diameters at the early stage of forced expiration.
5) Airway diameters at 1.0 second in forced expiration had negative correlation with FEV 1.0%, and the degree of this correlation was higher in lobar bronchi than in other bronchi (Table 3).
6) Airway diameters at 2.5 seconds in forced expiration had also negative correlation with % VC, but the degree of this correlation was insignificantly small, particularly in trachea (Table 4).

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The Marfanoid Hypermobility Syndrome is a new entity of heritable disorder of connective tissue. This syndrome has both clinical features of the Marfan Syndrome and the Ehlers-Danlos Syndrome. The first case of this syndrome was reported by Walker et al, in 1969.
1972, we found a family with many cases of this syndrome and surveyed clinically all members of this family.
On this investigation we could first make clear that this syndrome was transmitted in autosomal dominant mode.
2 out of 19 members of this family had had spontaneous pneumothorax or many kinds of pulmonary diseases. In this paper, we mentioned that these intrathoracic diseases tightly combined with the Marfanoid Hypermobility Syndrome. And we concluded that this syndrome had both of the intrathoracic diseases of the Marfan Syndrome, such as spontaneous pneumothorax and multiple lung cysts, and those of the Ehlers-Danlos Syndrome, such as spontaneous pneumothorax, hemoptysis and megabronchus.

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A 42 years old female teacher who has not been in any tropical region was admitted to our hospital with a remittent high fever, night sweats, wheezing, cough, rather small amount of mucous sputum and moderate dyspnea with little cyanosis.
Her chest roentgenogram showed rather homogenous dense consolidations in the peripheral upper and middle regions of the right lung.
The white blood cell count revealed a prominent leucocytosis up to 22, 500 per cubic milimeter with 68 per cent eosinophils.
The tuberculin reaction, mycoplasma C. F., and all of the examined serum viral reactions were negative. Any causative agent including tubercle bacillus, fungi or malignant tumor cells in sputum and parasite or its egg in feces were not detected.
There was no signs or symtoms of periarteritis nodosa, Wegener's granulomatosis or other collagen diseases throughout the course of the disease.
Fever continued more than one month in spite of various antibiotic therapies, and progressive pulmonary shadows were persistent changing their features and locations rapidly.
The corticosteroid therapy showed a surprisingly excellent response. The fever remission occured immediately and pulmonary shadows decreased markedly within three or four days and completely disappeared within one month.
Eosinophilia, elevated gamma-globulin, IgG and ESR also returned to the normal level.
These findings are strictly compatible with the Carrington's “Chronic eosinophilic pneumonia” described in 1969, although the histological confirmation by the lung biopsy was not performed.

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