Nonspecific esterases of epithelioid cells in the sarcoid and tuberculous granuloma were studied histochemically. The materials used in this experiments were 8 scalene nodes biopsied from 8 cases of sarcoidosis and 2 cervical nodes from 2 cases of tuberculous lymphadenitis. A pulmonary tuberculous lesion obtained by operation was also studied. The materials were quickly frozen and cut in 8μ sections by a cryostat. The sections were placed on glass slides and dried quickly by an air jet. Nonspecific esterases were assayed with the following substrates: naphthol AS-D acetate (AS-D), naphthol AS-D chloroacetate (AS-D Chl), naphthol AS acetate (AS) and α-naphthyl acetate (α-N). Acid phosphatase, a lysosomal enzyme cf mononuclear phagocytes (MNs), was also assayed as a marker of MNs activation. Nonspecific esterases hydrolyzing AS-D, AS-D Chl and AS except for α-N showed less activities in epithelioid cells of sarcoid granulomas than tuberculous granulomas.
Nonspecific esterase hydrolyzing α-N and acid phosphatase of epithelioid cells showed marked activities in all cases of sarcoid and tuberculous granulomas. The most interesting finding was that lower or negative activity of nonspecific esterase hydrolyzing AS-D was found in the epithelioid cells of 6 out of 8 sarcoid cases. On the other hand, increased AS-D activity was found in all tuberculous epithelioid cells.

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Ultrastructural studies on murine and human lung were performed with special attention to the interstitial acid mucopolysaccharides by ruthenium red staining and several enzyme digestion tests with streptomyces hyaluronidase, testicular hyaluronidase, chondroitinase ABC, trypsin and collagenase.
Periodic lateral granules on the major cross bands or amorphous coats of the collagen fibers became visible by ruthenium red staining. The surfaces of elastic fibers, associated microfibrils and some fine fibrils of 10-20nm in diameter were stained. Ruthenium red also stained the surface areas of fibroblasts and the smooth muscle cells, the basement membrane and FLS. In interstructural space, granular substances of ca. 10-80nm in diameter and fine filaments of ca. 3-4nm in thickness which formed a fine reticular network were clearly observed. They were not visible on the usual thin section. The granular substances were located on the cross points of the fine filaments. They spread continuously and connected with each of cells and the extracellular structures in the pulmonary interstitium. The microfibrils of the elastic fiber were digested by trypsin, but were resistant to collagenase, hyaluronidase and chondroitinase ABC. The fine filaments of ca. 3-4nm in thickness with granular substances disappeared after treatment with streptomyces hyaluronidase. The periodic lateral granules and the amorphous coats around the collagen fibers were mostly digested by trypsin, chondroitinase ABC and testicular hyaluronidase, but they were not affected by streptomyces hyaluronidase. Fine fibrils of ca. 10-20nm in diameter were mostly digested by trypsin, but resistant to chondroitinase ABC, testicular hyaluronidase and streptomyces hyaluronidase.

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Based on the calculated attenuation numbers in computed tomograms (CT) of the chest, histographical analy of distributions in CT for 18 patients with cryptogenic fibrosing alveolitis was performed. For better clinical understanding, this histogram was correlated to the attenuation numbers of each type tissue and structure within the chest wall.
On histograms for normal subjects, four steep peaks were observed and the attenuation number of each peak ranged from -400 to -440 (peak A), -80 to -100 (peak B), -40 to -50 (peak C) and 10 and 20 (peak D) respectively (settled attenuation numbers of water and air, 0 and -500, respectively). Examination of the corresponding tissue or structure to each peak showed that lung parenchyma was included mostly in peak A, since attenuation numbers of lung parenchyma ranged from -360 to -470. Peak B was comparable to bean bags, peak C to fat tissue and peak D to soft tissues apart from fat. On the other hand, the pulmonary blood vessels distributed widely on histogram ranging from -40 to -360 and no corresponding peak was observed.
In patients with cryptogenic fibrosing alveolitis, the most characteristic change on histogram was found on peak A which tended to decrease in height and to shift widely to the range of higher attenuation numbers. In advanced cases, this shift was observed up to peak C range. These changes shown on histograms were attributed to a markedly high density area of the lung on CT, since the attenuation number for this area ranged from -200 to -100. Therefore, histographical presentation of attenuation numbers was considered to be clinically useful for quantitative evaluation of cryptogenic fibrosing alveolitis.

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It is well known that prostaglandin E₁ (PGE₁) and PGE₂ induce relaxation and PGF_2α contraction in the tracheo-bronchial systems of various mammals.
PGD₂ as well as PGF_2α, increase airway resistance and pulmonary arterial pressure in anesthetized dog, although their biological effects are not completely the same.
In the present investigation we compared the effects of PGD₂ and PGF_2α on guinea pig tracheal strips while modulating their tensions.
1) Controls of both PGF_2α and PGD₂ obtained contractile responses in guinea pig tracheal strips, and at the dose of 350ng/ml and 500ng/ml the latter showed larger contractile responses.
2) PGF_2α obtained relaxation responses and such responses became less dominant by increasing the dose under conditions in which the tonus of guinea pig tracheal strips was elevated. PGD₂ showed contractile responses dose-dependently.
The above results suggest that PGD₂ may play a very important role in pathological conditions such as bronchial asthma, in which the tonus of tracheobronchial smooth muscle is very high.

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To evaluate pulmonary involvement in polymyositis, 26 patients were studied roentgenologically, functionally and histologically. Chest X-ray findings on admission revealed diffuse interstitial patterns in 11 patients (42.3%), of which 6 showed signs of lung shrinkage. With steroid therapy, muscular weakness improved in 20 patients (76.9%). In contrast, the interstitial patterns on chest X-ray films appeared or progressed in 21 patients (80.8%) during the course of therapy. No cases of improved chest X-ray findings were observed. The interstitial patterns showed micronodular and linear shadows in many cases, and reticulonodular and ring-like shadows in a few cases. Pleural and pericardial effusions were found in 4 and 5 patients, respectively. These chest X-ray findings were frequently seen from 1 to 10 years after onset of polymyositis. Pulmonary fibrosis preceded polymyositis in 1 case, and pleural effusion preceded in an other case. Respiratory functions tested after improvement of muscular weakness showed a restrictive pattern, low diffusion capacity and hypoxemia in many cases with interstitial patterns on chest X-ray film. Histological findings by transbronchial lung biopsy in 2 patients revealed interstitial fibrosis without inflammatory cell infiltration.
These results suggest that interstitial lung disease occurs in polymyositis more frequently than previously reported, and that the lung disease progresses slowly even with steroid therapy.

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A rare case of a 12-year-old girl with acute cardiac tamponade caused by penetration of a mature mediastinal teratoma into the pericardium is presented. In October 1979 the patient began to suffer from, fever, and dyspnea of more than one month's duration, when an abnormal shadow in the chest X-ray was pointed out by her physician. On the fifth day after admission, she suddenly suffered from severe dyspnea, anterior chest pain, high fever and hypotension. A chest X-ray film at that time showed marked widening of the cardiac silhouette. By echocardiography, cardiac tamponade was detected. As an emergency procedure, pericardiotomy was performed. Over 250ml. of pericardial effusion was removed together with a yellowish necrotic mass, bacterial culture of which yielded staphylococcus aureus. After chemotherapy for one month, she underwent removal of an anterior mediastinal tumor mass by median sternotomy. The tumor mass was a mature teratoma embedded in xanthogranulomatous tissue which was penetrating into the pericardium as well as the left upper lobe of the lung. Microscopically, a certain amount of the pancreatic tissue was found in the teratoma, secretion of digestive juice which was considered to be accountable for the penetration into boths lung and pericardium and also for further infection resulting in cardiac tamponade

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