The tissue distribution on T-lymphocytes and histocytes in diffuse panbronchiolitis (DPB) and DPB-like bronchiolitis was studied by an immunohistochemical method.
Unlike the diseases principally involving the central airway such as chronic bronchitis, only a very small number of anti-S-100⁺ histiocytes (T-zone histiocytes) were found in the bronchiolar walls, although anti-lysozyme⁺ histocytes were seen there. In the immunosuppressed patients, anti-S-100⁺ histiocytes and anti-lysozyme⁺ histiocytes were rarely found in the bronchiolar walls.
In DPB and bronchiolitis, Leu 3⁺ (helper/inducer) lymphocytes always overwhelmed Leu 2⁺ (suppressor/cytotoxic) lymphocytes in number.
At the site of proliferation of lymphocytes in DPB, relatively large numbers of Leu 7⁺ lymphocytes were observed as compared with the lungs of other diseases. Anti-S-100⁺ histiocytes were also found at the site.
In DPB and similar diseases in which the lesion is highly localized, it seems important to clarify accurate distribution and characteristics of immune cells in order to elucidate the etiology of diseases.

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The present study was carried out in order to clarify the relationship between the incidence of mediastinal and subcutaneous emphysema complicating bronchial asthma and the concentration of NO₂ in the atomosphere. There were 96 cases of mediastinal and subcutaneous emphysema out of 67, 666 cases of moderate to severe asthmatic attack treated at our OPD, and the rewere 69 cases of such complications out of 4029 cases of severe asthmatic attacks living in 6 wards of Tokyo (Koto, Sumida, Taito, Adachi, Katushika and Edogawa) admitted during 1973 and 1984.
There was no relationship between the incidence of these complications and the concentrations of NO₂ and NOX. However there was a significant relationship between the incidence of these complications in relation to severe asthmatic attack and the number of the days when the concentration of NO₂ was higher than 0.02ppm and lower than 0.04ppm. No statistically proved correlation between the number of days when the concentration of NO₂ was higher than 0.02ppm and the incidence of mediastinal and subcutaneous emphysema complicating bronchial asthma was recognized.
The deleterious effects of NO₂ to alpha-1-antitrypsin and lung tissue have been reported. We reported that in children with bronchial asthma with attacks complicated by infection, the relatively low level of serum alpha-1-antitrypsin might be one of the causes of mediastinal and subcutaneous emphysema. The results of this study were compatible with these reports.
It was suggested that NO₂ in the atmosphere might be one of etiological factor related to mediastinal and subcutaneous emphysema complicating bronchial asthma.

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Right heart catheterization studies were performed in 5 patients (4 males and a female), who were admitted to Shinshu University Hospital (610-m altitude) with high altitude pulmonary edema. These were all climbers aged between 21 and 45 years. Three patients were studied while oxygen was administered and two while breathing room air.
Moderate pulmonary hypertension and increased pulmonary vascular resistance were observed in four patients, while pulmonary arterial wedge pressure and cardiac index were within the normal range. Within 30 hours, there was normalization of pulmonary arterial pressure and pulmonary vascular resistance with improvement in arterial oxygen tension and disappearance of chest x-ray infiltrates. Inhalation of oxygen, however, did not completely improve pulmonary hypertension in the acute phase.
These findings suggest that high altitude pulmonary edema is a noncardiogenic pulmonary edema and that pulmonary hypertension in patients with high altitude pulmonary edema may be caused partly by a mechanism other than hypoxic pulmonary vasoconstriction.

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The environmental nicotine concentration and the exposure level of nonsmokers to ambient nicotine was measured with a device to determine the amount of involuntary smoking occurring in the daily lives of nonsmokers. Nicotine samples were collected by drawing air through an acid-treated diatomite sampler tube, either by a portable or a personal sampler. Gas chromatography using a flame thermionic detector was used to measure nicotine after an internal standard was added. This study showed that room size, ventilation rate, and quantity of tobacco smoked during a given period of time strongly influence nicotine concentration in an indoor environment and that nicotine levels fluctuate widely from spot to spot and from time to time, even in respective space. The only way to control nicotine concentration in room air is to control smoking, when room size and ventilation rate are fixed in respective space. A clear difference was found between nicotine concentration in the smoking and nonsmoking seats of trains and airplanes. As for personal exposure to nicotine, it was clearly heavier for nonsmoking subjects living with a smoker in their family than subjects without the smoker. In one nonsmoking family, a woman and a six-year-old daughter were unable to escape from nicotine exposure from an unexpected source.
A question that remains to be answered is that of whether or not there is any correlation between concentration of nicotine as measured by the personal sampler and the physical and psychological response of respective individuals.

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High ACE activity is found in serum and in granuloma tissue of patients with sarcoidosis. This study was performed to clarify the role of ACE on granuloma formation. Experiments were performed as follows. Granulomas were produced by injection of a mixture of cord factor (purified from Nocardia rubra) and Freund's incomplete adjuvant into the lung directly through the chest wall. Experiments were divided into three groups. Group 1 (control group). The mixture of cord factor and Freund's incomplete adjuvant was used. Group 2 (captopril group): 10M of captopril was added to the control menu. Group 3 (ACE group): 1U of ACE (semipurified from rabbit kidney) was added to the control menu. 0.1ml of each mixture were injected to both lungs of the rabbit through the chest wall. Rabbits were sacrificed on the 14th day after the injection, when the granuloma formation was most marked.
In the control group, granulomas formed on the surface of the lungs in the shape of cords or islands. On the cross section of the lung, granulomas were located just beneath the pleura. In the captopril group, the findings of the lung were similar to those in the controll group. In contrast to this, the findings of the lung in the ACE group were completely different from the former. Lungs were markedly enlarged diffusely, and in the cross section small granulomas were distributed uniformly throughout the lung. These granulomas consisted mainly of epithelioid cells. There were no difference of histology between the control group and the ACE group.
In conclusion, ACE changed the distribution of experimental granulomas in rabbit lung, but did not change the cell component of the granuloma.

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We developed a murine model of hypersensitivity pneumonitis (HP) by repeated transnasal administration of Thermoactinomyces vulgaris (Tv) bacilli. After 3 weeks' exposure diffuse alveolitis with granulomatous lesions was demonstrated in C57Black/6 mice. Anti-Tv-IgG antibodies and delayed-type hypersensitivity against Tv were also detected. Bronchoalveolar lavage (BAL) revealed marked increases in the total cell, lymphocyte and macrophage numbers.
Strain variation in Tv-induced HP was studied by using 4 kinds of syngeneic strains. C57Black/6 mice were high responders; C3H/He and Balb/C mice were low responders and CBA strain was intermediate.
Studies on the technique of BAL revealed that sufficient viable cells could be obtained by washing with 1ml saline 4 times. Histological examination of the lungs before and after the BAL procedure suggested that inflammatory and immune effector cells within the alveolar walls could be obtained by BAL.
Since lung pathology of athymic nude mice of high responders (C57Black/6N-nu) treated with Tv showed only minimal changes, there is a strong suggestion that the T cell-dependent immune system plays an essential role in the development of this murine HP model. We conclude that this murine model of HP is a useful tool for the study of the pathogenesis of human HP.

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Recent studies have suggested that cyclooxygenase products such as thromboxane A₂ (TXA₂) might be involved in bronchoconstriction by leukotriene (LT) C₄ and D₄ in guinea pigs, and that cyclooxygenase products also might play an important role in the development of airway hyperresponsiveness to acetylcholine induced by ozone exposure in dogs.
To determine whether TXA₂ may be associated with airway hyperresponsiveness in bronchial asthma, we studied the effects of a selective inhibitor of thromboxane biosynthesis (OKY-046) on the airway responsiveness to LTD₄ and acetylcholine in asthmatic patients in remission. Seventeen asthmatic subjects, 6 males and 11 females 16 to 62 years (mean age, 41.0 years), were studied. The subjects inhaled aerosols of increasing concentrations of LTD₄ and acetylcholine solutions and airway responses to these agents were expressed as the provocative cumulative doses which caused a 20% fall in FEV₁ (PD₂₀). Baseline asessment of spirometry (FEV₁, FEV₁/FVC, FEF_25-75) and PD₂₀ measurements were also carried out before and after OKY-046 400mg/day oral administration for 2 weeks.
Bronchial hyperresponsiveness to both LTD₄ and acetylcholine were significantly reduced (p<0.025) after OKY-046 administration, although baseline pulmonary functions did not change significantly during this study.
These results suggest (1) that: LTD₄-induced bronchoconstriction can be partially associated with TXA₂ synthesis, and/or (2) that inhibitors of TXA₂ synthesis may suppress non-specific airway hyperreactivity in asthma.

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The relative usefulness of various initial findings concerning pulmonary function tests and pulmonary hemodynamics in predicting survival is reported for 96 symptomatic patients with chronic lung disease.
All patients underwent cardiac catheterization and were followed up for an average of 4.8 years. The 5-year survival rate of all patients was 50% and 58 patients died within the follow up period.
A multiple regression analysis indicated that age, patterns of respiratory impairment, forced expiratory volume in 1 second (FEV1.0) and pulmonary arterial pressure (PAP) were independently useful parameters in predicting prognosis.
The 5-year survival of the high PAP group (PAM≥30mmHg) was signif icantry lower compared with that of the lower PAP group.
Our results showed that pulmonary circulatory disturbance was one of the most important predictors of prognosis especially in the patient with restrictive ventilatory disorder.

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Receptor-mediated superoxide (O₂^-) release by alveolar macrophages (PAM), peripheral monocytes (Mo) and polymorphonuclear leukocytes (PMN) from smokers and nonsmokers was studied. When the cells were incubated with monomeric IgG or monomeric Fc (IgG) fragment, no cell O₂^- release was observed. However, when cytochalasin D (Cyt D) was subsequently added to the cell suspension, we observed a markedly enhanced O₂^- release. Neither Cyt D alone nor the double stimulation of following Cyt D with monomeric IgG induced O₂^- release. Concanavalin A (Con A) also had a priming effect on O₂^- release in combination with Cyt D. On the other hand, heat-aggregated IgG, N-formyl-methionyl-leucyl-phenylalanine (FMLP), or phorbol myristate acetate (PMA) induced O₂^- release without the addition of Cyt D. Thus, we observed two different mechanisms in the receptor-mediated O₂^- release by human phagocytes. The reactivities to stimulants differed greatly among PAM, Mo and PMNs PAM from smokers, which had a higher affinity and a larger number of monomeric IgG binding sites per cell than those from nonsmokers and Mo, were more reactive to the stimulation of IgG than other phagocytes. PMN were not reactive to the stimulation of IgG, but more reactive to that of Con A and Cyt D, PMA, or FMLP than PAM or Mo. We conclude that the regulation of receptor-mediated O₂^- release by PAM differs at least in part from that of Mo or PMN.

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The present study was carried out to investigate the isolation of MRSA from sputum and the clinical features of bronchopulmonary infections due to MRSA from January of 1981 to December of 1985 at the Chiba University Hospital. The frequency of MRSA in Staphylococcus aureus from sputum culture increased during the 5 years from 3.6% (one strain) in 1981 to 32.8% (22 strains) in 1985. All strains were typed as coagulase type IV in 1981 and 1982, but from 1983 type II strains increased. The MCI₈₀ of cloxacillin, minocycline, vancomycin, and rifampicin against MRSA were 2μg/ml, 1μg/ml, 1μg/ml, and ≤0.06μg/ml, respectively. Many strains of MRSA were resistant to gentamicin, erythromycin and fosfomycin. Most of MRSA strains were isolated from inpatients (98%) with significant underlying conditions. Sixty-five percent of the patients were over 51 years of age and 74% of them had been treated with antibiotics before isolation of MRSA. Sixteen cases of bronchopulmonary infection and 4 cases of pyothorax due to MRSA were found. The prognosis of bronchopulmonary infection was poor and mortality was 56%. Recovery was obtained in 7 out of 16 cases by treatment with vancomycin, cloxacillin or minocycline.

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The effects of β-lactamase on the concentration of Ampicillin (ABPC) in the bronchoalveolar spaces in rats was studied using a bronchoalveolar lavage (BAL) technique.
In the group with pneumonia due to non-β-lactamase-producing bacteria, the amount of ABPC recovered by BAL was greater than that in the normal group.
In the group with pneumonia due to β-lactamase-producing bacteria, the amount of ABPC recovered by BAL was less than that in the group with pneumonia due to non-β-lactamase-producing bacteria.
When K. oxytoca was used as the β-lactamase-producing bacteria and was present at a concentration of 10⁴ or more per ml in the BAL solution, the ABPC concentration found was below the limit of measurement.
Among the group with pneumonia due to K. oxytoca, the group with an intrapulmonary bacterial count of 6.1×10⁶/g had an amount of ABPC in lungs equal to approximately 10% of that in the group with a bacterial count of 5.0×10³/g.

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A 28 year-old woman felt shortness of breath on exertion and anterior chest discomfort. The chest roentgenogram on admission showed a decrease in the vascular markings of the left lung and a niveau in the bilateral upper lung fields. The computed tomography of the chest showed a giant bulla which occupied nearly the entire left thoracic cavity and expanded into the right upper thorax beyond the mediastinum. Vital capacity (VC) was 1220ml, %VC was 38.9%, forced expiratory volume in one second (EFV_1.0) was 1120ml and FEV_1.0% was 93.3%. The above data suggested restrictive ventilatory defects. Blood gas analysis was within normal limits. On a diagnosis of giant bulla, she underwent bullectomy and thoracoplasty. After the operation both her complaints and respiratory function were remarkably improved.

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A 42 year-old male was admitted for the second time to our hospital in 1985 with complaints of epistaxis, edema of legs and slight fever. Hepatic dysfunction had been pointed since 1979. Because of exertional dyspnea and an abnormal shadow on chest X-ray film, he was initially referred to our hospital in 1982. A diagnosis of idiopathic interstitial pneumonia was made after TBLB and other detailed examinatins. After discharge, his condition was closely observed without administering steroid therapy, however, six months prior to the second admission, he developed edema of the legs which had to be treated with diuretics. On the second admission, bleeding episodes developed due to platelet deficiency. ECG and UCG revealed severe right ventricular hypertrophy and dilatation which had markedly developed in a very short period. Cardiac catheterization showed a marked pulmonary hypertension (94/36mmHg) without any other cardiac abnormalities. After some weeks, he suffered from epistaxis again but this subsided gradually after administering cardiac glycosides, xanthines, and an increased amount of diuretics. The bleeding episodes caused by platelet deficiency were due to congestive hepatosplenomegaly caused by marked right ventricular failure. Judging from the medical literature available on these points, we suggest that combined chronic hepatitis and idiopathic interstitial pneumonia can cause severe pulmonary hypertension in a very short period.

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A 41 year-old-man suffering from coughing, wheezing, and shortness of breath was admitted to our hospital. After birth he frequently had respiratory infection. He was admitted to the hospital because of pneumonia at the age of 100 days, 30 and 39 years old. At the last hospitalization the presence of bronchiectasis was pointed out, and thereafter the symptoms became more severe.
Bronchograms on this admission demonstrated generalized bronchiectasis mainly in the right-middle and right-lower lobes, and showed ballooning and collapse of bronchi during inspiration and expiration of tidal breathing, respectively. An anomalous branch of the right upper bronchus was also revealed. The flow-volume curve showed the characteristic findings of Williams-Campbell syndrome i. e. remarkable decrease of the maximum flow in the low lung volume level.
This case was thought to be an adult case of generalized bronchiectasis probably due to a deficiency of bronchial cartilage (Williams-Campbell syndrome) by the characteristic clinical course, roentogenographic findings, and the pattern of the flow-volume curve.
This case may be a familial case because his father, elder son and the second younger daughter have past histories of recurrent respiratory infection. We will have to perform futher examinations when his children have grown.

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In a 53 year-old woman, who had been followed for multiple bullae and exertional dyspnea for 8 years, three coexisting pulmonary lesions were found: multiple nodular amyloidosis, multiple bullae and severe peribronchiolar infiltration of lymphocytes and plasma cells. In multiple nodular deposits, Congo red staining was positive and elctronmicrograph showed nonbranching paired fibrils, consistent with amyloid fibrils. Pottasium permanganateincubated sections polarized with green birefringence after Congo red staining. Immunoperoxidase staining with anti-kappa chain antibody was strongly positive in surrounding plasma cells, indicating amyloid of light chain type and the likelihood of localized monoclonal process. On the other hand, peribronchiolar aggregated plasma cells presented polyclonality by immunoperoxidase staining.
Serological tests were almost normal except for polyclonal hypergammaglobulinemia. Results from biopsies of the stomach, rectal mucosa, small salivary glands and bone marrow were free from amyloid deposits. The histological change of the small salivary gland was compatible with that of Sjögren's syndrome.
To our knowledge, this is the third case in the international literatures which presented the combination of the nodular pulmonary amyloidosis and Sjögren's syndrome. Severe bronchiolitis and multiple bullae, which might result from bronchial restriction, made the clinical features of the present case complicated.

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A 53-year-old male was admitted with fever, epigastralgia and an abnormal shadow on chest roentgenogram. He recognized a left shoulder mass about 14 months ago and biopsy showed metastatic adenocarcinoma. The primary lesion could not be detected. After radiation, local chemotherapy and partial resection of the left humerus, he came to our hospital for the purpose of systemic chemotherapy.
On admission, no episodes of periodical hypertension were found. Peripheral blood examination revealed severe anemia, leukocytosis and increased ESR. Other abnormal laboratory data were hypoalbuminemia and elevation of transaminases. Fever did not respond to antibiotics and he died on the 10th hospital day.
The following histopathological findings were observed on autopsy. A solid yellowish tumor originated from left adrenal gland was found invading the upper portion of left kidney. Microscopically, large argentaffilic tumor cells with pleomorphic nuclei showed a solid or an alveolar structure with fine vascular stroma, which were the chracteristics of pheochromocytoma cells.
Phenochromocytoma was difficult to diagnose and this case is very suggestive, emphasizing the value of this report.

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A 60-year-old man was admitted to this hospital because of high fever. His chest X-ray showed a mass shadow in the right upper lobe and diffuse micronodular shadows in the right lung. He had past histories of artheritis (RA?) and chronic hepatitis. After admission bacterial pneumonia was diagnosed and antibiotics were administered. But, his general condition was not improved. Then we performed bronchoscopic examinations (bronchial washing, TBLB, brushing, etc). As we observed normal bronchial mucosa and brown watery secretion, we condidered this was not a case of common bacterial pneumonia. As Legionellosis was suspected, erythromycin was administered immediately. However, his general condition was aggravated and he died. At autopsy, bacterial examination of the lungs was performed and L. bozemanii was discovered. This is the first case of L. bozemanii pneumonia in Japan. We considered the brochoscopic findings i. e. in normal bronchial mucosa with brown watery secretion, to be of great interest.

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A 56 year-old male patient visited with complaints of hemosputum, swelling of the neck and left shoulder, and hoarseness. Chest X-ray film showed a huge mediastinal tumor with several nodules in the left lung field. (Chest) CT scan disclosed massive calcification in the mediastinal tumor. Radiotherapy was administered to the mediastinal tumor, then symptoms due to the vena cava superior syndrome and extension of the tumor gradually improved. However, he showed a progressive deterioration and passed away three month after admission. Pathological findings of autopsy revealed the extraskeletal osteosarcoma arisen from the mediastinum. Extraskeletal osteosarsoma is an uncommon disease and rarely develops in the mediastinum. To our knowledge, this case is the third instance of extraskeletal osteosarcoma of the mediastinum.

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A coin lesion was pointed out on the chest X-ray film of a 76-year-old man with diabetes mellitus. It was suspected to be lung cancer, so he was admitted to our hospital.
Chronic necrotizing pulmonary aspergillosis was histologically diagnosed.

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