Incremental exercise tests on a bicycle ergometer were performed by twenty pneumoconiosis patients working in foundries in order to determine the anaerobic threshold (AT) by abrupt increase in arterial blood lactate.
The validity of their AT in the evaluation of their physical working capacity was studied in comparison with their maximum oxygen uptake (V_O2·max) and also in consideration of pulmonary gas exchange function during exercise.
1. The mean values of their AT and V_O2·max were 0.771±0.279L/min (13.1±4.4ml/kg/min) and 1.600±0.417L/min (27.4±7.0ml/kg/min) respectively, which were lower than those in healthy male subjects, reported by other workers. This suggested that the physical working capacity of these patients was generally low.
2. The AT of each individual patient (V_O2·AT) correlated well with their V_O2·max. The regression equation was
V_O2·max=1.3948 V_O2·AT+0.5252 (L/min)r=0.9336, p<0.01
or, V_O2·max=1.4142 V_O2·AT+8.8387 (ml/kg/min) r=0.9028, p<0.01.
Accordingly, their physical working capacity can be evaluated by their AT without determining their V_O2·max.
3. Pa_O2 and AaD_O2 in each individual patient at AT significantly correlated with those at maximum work load (r=0.6591 & 0.7684, p<0.01), suggesting that the pulmonary gas exchange disturbances at AT reflected those at maximum work load.
4. The decrease of physical working capacity for these patients was related to some extent to the reduction of MVV, %MVV or %DL_CO and the severity of chest X ray findings (profusion of small opacities).
Consequently, we concluded that AT can be regarded as a useful index in the evaluation of physical working capacity for pneumoconiosis patients.

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It is widely known that the dysbolism of lung connective tissue contributes to various pulmonary diseases. Elastase (ELA) is an enzyme involved in the metabolism of connective tissue and the activity is regulated by protease inhibitors. In the present study, changes in serum ELA-I, elastase-inhibition (ELA-Inh), α₁-Antitrypsin (α₁-AT) and α₂-Macroglobulin (α₂-MG) were investigated in patients with various pulmonary diseases and lung cancer undergoing conservative treatment.
1) In non-fibrotic pulmonary diseases ELA-I correlated well with ELA-Inh but in the fibrotic pulmonary diseases ELA-I did not correlate well with ELA-Inh. In IIP and pulmonary tubercrosis ELA-I was high in comparison to ELA-Inh, while in secondary pulmonary fibrosis, ELA-I was low in comparison to ELA-Inh.
2) There was a higher positive correlation between ELA-Inh and α₂-MG than between ELA-Inh and α₁-AT, and α₁-AT varied considerably on various pulmonary diseases.
3) In patients with lung cancer, radiation and Bleomycin tended to induce pneumonitis when α₁-AT increased during treatment.
It was suggested that analysis of serum ELA-I and protease inhibitor was useful to clarify the mechanism of the development of various pulmonary diseases.

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Bronchoalveolar lavage fluid (BALF) was studied in terms of the correlation between disease activity and changes on chest X-ray in 21 patients with sarcoidosis.
1) Lymphocytes, total protein, IgG, IgA, IgM, ACE and β₂-microglobulin in BALF were significantly elevated in active cases compared with inactive cases.
2) Lymphocytes, IgG, IgA, IgM, ACE and β₂-microglobulin in BALF were significantly decreased in improved sarcoid patients on chest X-ray, but were not significantly decreased in unchanged cases.
3) The levels of complement, fibrinogen and immuno complex in BALF of sarcoidosis patients were low in quantity, therefore they were not useful.
These results suggest that in sarcoidosis patients BALF studies reflect the disease activity.

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Pulmonary capillary blood flow (Qc) is measured by the body plethysmograph method, and the analysis of its pulsatility can be used as a means of obtaining the pulmonary circulatory hemodynamics.
Qc was measured on 40 mongrel dogs put under pentobarbital-pancuronium anesthesia. After creating a state of experimental pulmonary hypertension through continuous infusion of serotonin, the dogs were divided into three separate groups, and Qc max/Qc, V syst/SV and Qc max/SV were set as indices to investigate fluctuations in the pulsatility of Qc when phenoxybenzamine (POB, n=14), sodium nitroprusside (SNP, n=14) and nitroglycerin (GTN, n=12) were additionary administered to each of the respective groups. (Qc max: maximum Qc, Qc: mean Qc, V syst: blood flow during the systolic period of Qc, SV: stroke volume)
1) With continuous infusion of 50mcg/kg/min serotonin, increase was observed in both the pulmonary arterial pressure and Qs/Qt. At the same time, the pulsatility of Qc decreased due to precapillary vasoconstriction, and pulmonary circulatory impairment was observed.
2) Bolus injection of POB 2mg/kg administered during the infusion of serotonin had the effect of decreasing the pulmonary arterial pressure and the Qs/Qt, and increasing the pulsatility of Qc. These effects are antagonistic to those of serotonin, so it can be considered that one of the elements which cause pulmonary circulatory impairment during the infusion of serotonin are mediated by the α adrenoceptor in the pulmonary vasculature.
3) Continuous infusion of 20mcg/kg/min SNP on the one hand, as well as continuous infusion of 20mcg/kg/min GTN on the other hand were performed during the infusion of serotonin. In both cases, decrease was observed in the pulmonary arterial pressure, but not in the Qs/Qt, meaning that the effect did not antagonize that of serotonin. Further, pulsatility of Qc increased with SNP, whereas no changes were observed with GTN, which suggests that SNP and GTN affect different regions within the pulmonary vasculature.

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Pulmonary tissue and serum concentrations of ceftizozime (CZX) after injection of 2g were investigated in 19 thoracotomized patients. Pulmonary tissue and serum were obtained at 1 hour in 7 cases, 2 hours in 6 cases and 3 hours in 6 cases after injection. The highest tissue concentration was seen after 1 hour gradually decreasing with time.
Factors influencing the pulmonary tissue concentration of CZX were age, %VC, %FEV_1.0/FVC, FEV_1.0/pred. VC.
The correlation with age was positive, but that with ventilation parameters was negative. BUN, P_O2, did not correlate with the pulmonary tissue concentration.

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During the last 12 years, 56 cases of 1, 405 postmortem examinations were diagnosed as acute pancreatitis or pancreatic fat necrosis in the Department of Pathology of Kyorin University School of Medicine. In 22 cases out of 56, there were no pulmonary diseases, including primary and metastatic malignant tumors, or severe pneumonia. The pancreatic and pulmonary tissues from these cases were divided into two groups according to the value of serum amylase; 12 cases had higher and 10 cases lower titer than normal (151 Somogyi Units). In both groups, intra-alveolar edema and leukostasis occured in the pulmonary arterioles, capillaries and venules. Furthermore, fibrin and platelet thrombi were seen in these vessels accompanied with perivascular edema and lymphagiectasia. Hyaline membrane was formed in the alveolar spaces in the group with a high titer of serum amylase.
After intravenous injection of trypsin (4.5mg/kg), the morphological changes of the lungs from 6 Japanese white rabbits were studied at 4 and 24 hours. As seen in the histology of autopsied specimens, leukostasis and thrombus formation were demonstrated in the pulmonary small vessels, with perivascular edema. No intra-alveolar edema was seen, however. Four hours after trypsin injection a wide distribution of fibrin thrombi was observed electron microscopically in these small vessels. At 24 hours, however, platelet aggregates partially adhering to the subendothelial tissues, increased in number in place of fibrin thrombi, resulting in the detachment of endothelial cells.
Consequently, the pulmonary lesions complicating acute pancreatitis are morphologically compatible with those in shock lung syndrome. In the pathogenesis of the pulmonary changes in these disease, influx of pancreatic trypsin may play a key role of the activation for blood coagulation and complement systems. The authors reconfirmed that pulmonary thrombosis and leukostasis should be prevented since the pulmonary complications are difficult to avoid in acute pancreatitis.

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The arachidnate metabolism in alveolar macrophages (AM) was investigated in human AM. The AM was obtained by bronchoalveolar lavage (BAL) from normal volunteers (NV group) and from patients with a localized pulmonary disease (control patients, CP group). In the CP group, BAL was performed in the lung contralateral to that with the lesion. The NV group consisted of nonsmokers and smokers, and the CP group consisted only of smokers.
I Uptake of radiolobelled arachidonic acid by AM
In vitro uptake of ¹⁴C-arachidonic acid by AM from smokers was not significantly different from that from nonsmokers, in the NV group.
The pattern of incorporation of ¹⁴C-arachidonic acid into phospholipid and neutral lipid fraction of AM from smokers was also not significantly different from that from nonsmokers.
II In vitro release of arachidonate metabolites by zymosan-stimulated AM
The amount of thromboxane A₂ (TX A₂) released by AM was evaluated by two methods. In method I, the amount to TX B₂ (stable from of TX A₂) released was directly measured by radioimmunoassay. In method II, AM was prelabelled with ¹⁴C-arachidonic acid, and the amount of TX B₂ released was judged by the percentage of radioactivity in the TX B₂ from incubation medium comparison to total uptake by AM. There was a significant correlation between the value by methods I and II. Therefore the amounts of other arachidnate metabolites released was judged by the method II.
The amount of prostaglandin E₂ and a lipoxygenase product, as well as TX B₂ released by 10⁶ of AM, was decreased in the AM from smokers compared with that from nonsmokers, in the NV group.
The number of AM obtained by BAL was larger in the smokers of both the NV and CP groups than in the nonsmokers of the NV group. When the amount of TX B₂ released from 10⁶ of AM was measured by method I, it was also decreased in the AM from smokers of both groups compared with that from nonsmokers of the NV group. However, the amount of TX B₂ released by total AM obtained by BAL tended to be larger in smokers than in nonsmokers.
These results indicate that release of arachidnate metabolite of AM in response to a stimulus may be decreased in smokers compared with nonsmokers. It was also suggested that the number as well as function of AM must be kept in mind when physiological and pathophysiological roles of arachidnate metabolite released by AM are considered.

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Urinary concentration of pseudouridine, primarily a degradation product of transfer ribonucleic acid, was determined in 35 patients with lung cancer and 24 controls by high-performance liquid chromatography. Urinary pseudouridine concentrations of patients with lung cancer were significantly higher than those of controls, they were 37.3±15.7nmol/μmol creatinine and 23.4±5.1nmol/μmol, creatinine respectively (p<0.001). No significant difference was observed in urinary pseudouridine concentration with respect to each cell type. At two cut-off levels, 30nmol/μmol creatinine and 25nmol/μmol, creatinine sensitivity was 65.7% and 88.6%, and specificity was 83.3% and 66.7%, respectively. Sensitivity increased to 97.1% at a cut off level of 25nmol/μmol creatinine with combined use of serum CEA value. These results suggest that urinary pseudouridine concentration is a useful marker in patients with lung cancer.

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A case of bilateral diffuse malignant pleural mesothelioma diagnosed after autopsy was reported. A 39-year-old female with complaints of dyspnea on exertion and chest pain was admitted to our hospital. Physical examination and laboratory studies revealed no findings of malignancy. Chest X-ray film revealed bilateral pleural effusions and patchy, reticular shadows in both lung fieleds. Pleural fluid showed exudate on admission and there was no apparent malignancy except for atypical cells with cytoplasmic blebs behind the lymphocytic predominant inflammatory cells on cytologis. Though diagnosis treatment was initiated with chemotherapy for tuberculous pleuritis, the patient died of respiratory encephalopathy secondary to respiratory failure on the 59th day of illness from admission.
A very rare case of bilateral diffuse malignant pleural mesothelioma was confirmed by autopsy, which revealed direct invasion to the left diaphragm, pericardium and parenchyma of both lungs. Though the clinical diagnosis of this tumor was very difficult, the possibility of clinical diagnosis by chest X-ray film and cytology of the pleural fluid was discussed.

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We reported a case of sarcoidosis showing diffuse small nodular shadows on chest X-ray with chief complaints of dry cough, low-grade fever and exertional dyspnea. The chest X-ray taken one month previously showed no shadows on both lung fields except for bilateral hilar lymphadenopathy. This case was also complicated with right pleural involvement and infiltration of scar of sarcoidosis.
Histologically, non-caseous epithelioid cell granuloma was proved by transbronchial lung biopsy and skin biopsy from the right knee. Clinical symptoms, laboratory data and chest X-ray findings markedly improved after administration of prednisolone.

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An unusual case of Hodgkin's disease with prominent pulmonary involvement is presented. The patient was an 80 year-old female and admitted to our hospital because of bilateral pulmonary infiltrates on chest roentogenogram. The initial radiographic manifestations of lung involvement were fibronodular infiltrates without mediastinal lymph node enlargement. A definitive diagnosis of Hodgkin's disease (Mixed cellularity) was established by a biopsy of the left supraclavicular lymph nodes. The pulmonary involvement was diagnosed by the fact that the radiographic abnormality was unresponsive to treatment other than chemotherapy specific for Hodgkin's disease. The lesions in the lung disappeared during systemic combined chemotherapy (cyclophosphamide, vincristine, and prednisolone). Immunological studies showed decreased serum immunoglobulins. Skin test reactivity to purified protein derivative was negative. The in vitro responses of peripheral blood lymphocytes (PBL) to stimulation with both phytohemagglutinin (PHA) and pokeweed mitogen (PWM) were depressed compared with those of age-matched normal subjects. Furthermore, lymphocyte responsiveness to these agents was more impaired in the lymph nodes than in blood. The study of lymphocyte subpopulations using monoclonal anti-T-cell antibodies demonstrated T-cell predominance which comprised the majority of helper T-cell both in the blood and in the lymph nodes. PHA and PWM responses of PBL and serum IgG level became normal an remission. These findings suggest that immunological abnormalities of Hodgkin's disease are reversible and systemic chemotherapy for Hodgkin's disease is useful for improvement of these immunological abnormalities.

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A 33 year-old male was diagnosed as having Hermansky-Pudlak syndrome basd on the findings of oculocutaneous albinism, qualitative platelet defect and deposition of ceroid-like material in bronchial mucosa. Accompanying interstitial pneumonia was demonstrated by chest roentgenogram, restrictive pulmonary function impairment and pathological examination of the TBLB specimen. The storage of ceroid-like substance in lung was suggested to induce pulmonary interstitial pneumonia in two ways. First, lipid peroxidation, the process responsible for ceroid-like substance production, is associated with the formation of free radicals that can damage lung tissues. Second, lysosomal enzymes may also be released from ceroid-like substance-laden macrophages and induce inflammatory or fibrotic responses in lung.

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An asymptomatic 52-year-old man came to our outpatient clinic for evaluation of an abnormal lung shadow detected by a routine chest roentgenographic examination. He had no episode of serious trauma.
Posterior-anterior and lateral chest roentgenograms showed a well circumscribed homogeneous mass with a smooth, convex superior margin in the posterior-medial portion of the left lower lung field. Computed tomography performed with and without contrast medium demonstrated the intrathoracic location of the left kidney. Intravenous pyelograms demonstrated that the right kidney was normal and the left kidney was high in its position and had double pelves and ureters. The patient had neither symptoms nor renal dysfunction, so we decided against further examinations.
We reviewed and summarized 47 cases of thoracic kidney in the Japanese literature, including this case. There was no significantly high incidence in age. Distribution of ages ranged from neonates to 79 years, averaging 29.7 years. The anomaly occured slighthy more often in males than in females, 26 of 47 cases were male and 20 of 47 cases were female subjects (1 case was not described). It has been reported that males are affected three to four times more frequently than females, but in our review there was not so large a difference.
It has also been postulated that thoracic kidney occurs more commonly on the left side than on the right side. In our review 26 of 47 cases thoracic kidney occured on the right side, 20 of 47 cases on the left side (1 case was not described). Most cases were completely asymptomatic, and were diagnosed by screening or incidental chest roentgenograms.
Renal dysfunction was reported in only 8 of 47 cases. These dysfunctions were not particularly severe, and it is rather difficult to demonstrate that these dysfunctions were directly related to the thoracic kidneys.
The site of renal artery origin was normal in 17 cases, a high position was described in 4 cases and in the other cases it was not described.
The main diagnostic procedures were IVP, PRP, angiogram, operation and biopsy. Since 1979 this anomaly has been diagnosed easily by CT scanning.

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A 66-year-old male was admitted to hospital on April 23, 1981. The patient complained of shortness of breath on exertion. Physical examination revealed no abnormal signs. Chest X-ray showed radiolucent areas in the right upper and middle lung field. The patient was followed in the out-patient clinic with annual chest films. On June 1982, the chest X-ray revealed a well defined coin lesion in the right middle lung field. CT-scan was most suggestive of neoplasm, at the base of a giant bulla.
A right lower lobectomy was carried out. A giant bulla, with a nodular mass at to base, was found arising in the superior segment of the RLL. The hilar and mediastinal node were uninvolved. The histological diagnosis was poorly differentiated adenocarcinoma. The postoperative course was uneventful and the patient's condition is good two years after operation.

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