We investigated the effect of histamine and leukotrienes on the regulatory mechanism of chemical mediator release from passively sensitized guinea pig lung tissue by antigen challenge. Antigen-induced SRS-A release was markedly accelerated by preincubating lung tissue with histamine and degree of acceleration became more marked by increasing the dose of histamine (10-100ng/ml). On the other hand, antigen-induced histamine release was markedly inhibited by preincubating lung tissue with leukotriene C₄ D₄ and E₄, and the degree of inhibition became predominant by increasing the dose of leukotrienes. In the same way, antigen-induced histamine release was markedly inhibited by preincubating lung tissue with the same doses of leukotriene C₄ D₄ and E₄, and the same doses of leukotriene C₄ and E₄, leukotriene C₄ and D₄ and leukotriene E₄ and D₄.
The above results may suggest that histamine and SRS-A, the main chemical mediators, interact with each other and regulate the release of chemical mediators from guinea pig lung tissue.

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Twenty-one cases of hematologic disorder, consisting of 16 cases of leukemia, 2 of malignant lymphoma and 3 of aplastic anemia, complicated by fungal pneumonia, were studied in terms of symptoms, roentgenological findings and immunoserological findings.
The causative fungi in 17 of 21 cases were aspergillus, one of mucor and three were unclear. Eight of 21 cases had an antemortem diagnosis of fungal pneumonia; two were proved by transbronchial lung biopsy, and six, confirmed later by postmortem findings were strongly suspected from clinical findings at antemortem stage. Six of these patients were successfuly treated with amphotericin B, 5-fluorocytosine and ketoconazole although two cases died despite antifungal therapy. The major distinguishing factor was that recovery of hematologic symptoms was recognized in the former and not in the latter.
In terms of symptoms, all had fever refractory to antibiotic therapy, cough was seen in 15 of them, sputa in 10, bloody sputum in 10, chest pain 9, rale in 16 and dyspnea in 9. On chest x-ray film, 12 had pneumonia-like shadows, 3 had patchy infiltration, 3 diffuse fine reticulonodular shadows and there was 1 cyst-like shadow. Circulating antibodies and antigens to Aspergillus fumigatus were not detected in any of our cases.
As a whole, early diagnosis of fungal pneumonia based on careful observation of symptoms, chest x-ray films and an aggressive diagnostic approch, including transbronchial lung biopsy, are warranted for prompt antifungal therapy with resultant resolution of these potentially fatal infections.

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A comparative study of HCL-C level and factors affecting it was carried out in 42 patients with bronchial asthma and 20 normal subjects. The HDL-C level in patients with bronchial asthma was 60.0±16.1mg/dl (mean±Sd) which was significantly higher (p<0.001) than the level in normal subjects (45.1±10.9mg/dl), and it was also noted that the level of HDL-C was markedly high in the group of severe asthma cases (70.5±17.8mg/dl). The HDL-C levels in patients with bronchial asthma showed no significant Difference between the sexes. Regarding the subfractions of HDL, both the HDL₂-C level and the HDL₃-C level were high in patients with bronchial asthma, and particularly, HDL₂-C showed predominantly high levels. In patients with bronchial asthma the LCAT activity and PHLA tended to show high values compared with normal subjects. These data resembled the change of subfractions of HDL and the LPL activity found in athletes.
The mechanism of HDL increase in patients with bronchial asthma was not clear, but it was presumed that the chronic asthmatic attack itself constituted an exercise to increase the conversion of HDL₃ to HDL₂ by the effects of the LCAT and LPL activities, causing elevated HDL-C levels, especially HDL₂-C in patients with bronchial asthma. It seemed that the change of HDL-C was little affected by bronchodilators and corticosteroids.

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A case of congenital lymphedema with left chylothorax was presented. Congenital lymphedema is a very rare disease in Japan.
A 19-year-old male with congenital lymphedema of the left leg was admitted on a complaint of exertional dyspnea and dry cough in October 1983. Physical and roentgenographic examinations revealed massive left pleural effusion. He was treated with a low-fat, high-protein diet, diuretics, thoracocentesis and intrapleural injection of a drug to induce pleural adhesion. Pleural effusion disappeared and pleural thickening remained. The post-therapeutic course was uneventful.

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A 34-year-housewife admitted to our hospital in March 1983 with chest pain and cough had been suffering from myasthenia gravis since 1975.
The chest X-ray film revealed multiple 2-6cm nodular lesions in the right lung and the chest CT scan revealed mass lesions in the mediastinum and in contact with the pleura. Open lung biopsy showed that the lesions were occupied by mature and benign lymphocytes.
Because the lesion of this case was considered to be the result of chronic inflammation rather than indignant disease, this patient was treated with corticosteroid hormones only and a good response was obtained. The case was definitively diagnosed as pseudolymphoma originating in the thymic legion.

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A 25-year-old male was admitted for further evaluation of abnormal shadow on chest X-ray film. Chest X-ray film on admission revealed a mediastinal mass adjacent to the right hilar area and a small nodular shadow in the right middle lung field. The serum AFP was elevated to 320ng/ml. In addition, a slight increase of serum LH, FSH and estrogen were observed.
The patient died in six months in spite of aggressive chemotherapy and radiotherapy. The autopsy disclosed embryonal carcinoma, which primarily originated from the right antero-superior mediastinum.
This case suggested the possibility of secretion of AFP, although the radioimmunoassay of AFP in the tumor tissue was not performed.

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