We used our quantitative sputum culture method to investigate the significance and reliability of the basis for estimating pathogens in respiratory infections, by which solated organisms exceeding 10⁷/ml are considered pathogens.
1) We studied pathogenic organisms of respiratory infections in two institutes and obtained similar results i.e., the main pathogens were Hemophilus influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa, in order of frequency in isolation.
2) 3637 strains were isolated from 1369 sputum specimens in the period from 1975 to 1976. The significant isolated organisms more than 10⁷/ml of which was isolated from primarily purulent specimens were Streptococcus pneumoniae, Hemophilus influenzae and Pseudomonas aeruginosa. On the other hand, the main organisms isolated from specimens with less than 50% purulence were α-Streptococcus, γ-Streptococcus, Neisseria catarrhalis, Hemophilus hemolyticus, Klebsiella pneumoniae and Candida albicans.
3) In retrospective estimation, the causative organisms on the basis of quantitative sputum culture studies were shown to be accurate by clinical studies in 97% of pneumonia cases, 95.4% of chronic bronchitis, 99% of chronic bronchiolitis, 84% of respiratory infections with lung cancer and 82% of respiratory infections with chronic pulmonary emphysema.
4) When the sputum specimens were purulent or mucopurulent, Hemophilus influenzae, when isolated in quantities exceeding 10⁷/ml was found to be indeed the pathogen by clinical studies in 100% of respiratory infection cases, Pseudomonas aeruginosa 98%, Staphylococcus aureus 100%, Streptococcus pneumoniae 97% and klebsiella pneumoniae 60%.
The above studies show that pathogen estimation in respiratory infecion cases by our quantitative sputum culture method is highly reliable.

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High levels of angiotensin I-converting enzyme activity were found in sarcoid lymph nodes (897.7±106.1nmol/wet weight g/min) in contrast with non-sarcoid lymph nodes (48.5±36.5nmol/wet weight g/min). After gel filtration on Sephadex G-200, the characteristics of the enzyme in lymph nodes, in normal human serum and in the serum of sarcoidosis patients were compared. The molecular weight (290, 000daltons), optimal pH(8.3), Km, inhibition by bradykinin potentiating peptide B, were all identical. The mechanism of the elevation of the enzyme in serum of sarcoidosis patients is still unclear, it is possible that the elevation of the enzyme inserum of sarcoidosis patients originated from the sarcoid lymph node.

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The intracellular distribution of angiotensin I-converting enzyme (ACE) in sarcoid lymph nodes was examined to find out the mechanism of the elevation of serum ACE in sarcoidosis patients. Cell fractionation of sarcoid lymph nodes and normal human lung was performed. Tissue was homogenized with 0.25M succurose-phosphate buffer, and 78000×g centrifugation was performed for 90min. The supernatant of this step was described as the soluble fraction. The precipitate of this step was treated with trypsin to solubilize membrane-bound enzyme, and solubilized enzyme by this step was described as the membrane-bound enzyme. In sarcoid lymph nodes, 73% of the total ACE was found in the soluble fraction. This was in contrast to normal lung in which more than 75% of the activity was found in the membrane fraction. Characteristics such as optimal pH, molecular weight, inhibition by bradykinin ptentiating peptide and Km, of enzymes from normal serum, serum of a sarcoidosis patient, normal human lung, soluble fraction of sarcoid lymph nodes and membrane-bound enzyme of sarcoid lymph nodes were identical to each other except for the effect of temperatures. The enzyme from the soluble fraction in sarcoid lymph nodes was less stable than that from the membrane fraction at 50°C and 53°C and was similar to that in serum. It was suspected that the enzyme in sarcoid lymph node is easily liberated to the blood stream and causes the elevation of serum ACE in sarcoidosis patients.

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Allergo-immunologic investigations and examinations of the autonomic nerve system were performed in a case of bronchial asthma with myasthenia gravis. The results were as follows:
1) Asthma attacks and blephaloptosis were observed to tend to appear alternately.
2) The same trend was shown by administration of mecholyl or other anti-cholinergic drugs and when such drugs were given asthma attacks increased, although blephaloptosis improved.
3) Asthma attacks in this patient resembling those of many patients with bronchial asthma were observed mainly in the early morning.
4) Allergy examinations showed normal serum IgE level, negative skin reaction tests and no peripheral eosinophilia.
These results show that asthma attacks and symptoms of myasthenia gravis seemed to appear alternately in interaction of acetylcholine, showing a see-saw phenomenon and suggest that the autonomic nervous system participates in an induction mechanism or process in asthma.

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The present investigation was conducted in an effort to demonstrate the attenuating effect of an alpha-adrenergic blocking agent (phenoxybenzamine) on the contraction of guinea pig trachea (GPT) with various bronchoconstrictors.
Male guinea pigs weighing 250-300g, were killed. Guinea pig tracheas were removed, suspended in bioassay glass jackets and superfused with Krebs-Henseleit solution at 37°C saturated with oxygen and carbon dioxide (95:5, v/v). Contraction of guinea pig trachea was detected by an isotonic transducer and displayed on a polyrecorder.
1) The contractile responses of guinea pig trachea with acetylcholine and serotonin decreased with continuous infusion of phenoxybenzamine, and continued to decrease with increasing doses of phenoxybenzamine.
2) The dose-response curves of acetylcholine, histamine, serotonin, bradykinin and prostaglandin F_2α in guinea pig trachea were lowered with continuous infusion of phenoxybenzamine.
3) These results may suggest that an alpha-adrenergic blocking agent (phenoxybenzamine) has an attenuating effect on bronchoconstrictors, in addition to potentiating effect on bronchodilators.

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We present 3 cases of broncho-pulmonary diseases, lung cancer, bronchial asthma and pulmonary abscess, which revealed selectively deficient serum IgA. Serum levels of IgA in these cases were definitely below normal. IgA levels in bronchial washing, sputum and saliva decreased in one case, but there were no abnormalities in IgA levels in external secretions in two other cases. In the bronchial asthma, deficiency of IgA might be induced by glucocorticosteroid or gold salt treatment.
The precise mechanisms of IgA deficiency have not yet been determined and it may be that some immunological abnormalities exist in these cases. Several mechanisms of IgA deficiency were discussed.

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A unique case of 16-year-old boy with allergic granulomatous angiitis following repeated attacks of asthma and Löffler syndrome is presented. His family history has a strong tendency to atopic diathesis. Since January 1975, he has repeatedly had attacks of Löffler syndrome (eosinophils: 500-1, 200/cmm). Because of strong positive skin tests for house dust, Candida, and Soba, hyposensitization therapy was started. One week thereafter, however, there appeared marked eosinophilia (maximum, 33, 700/cmm), edema, fever, abdominal distress, subcutaneous nodules, myositis, multiple mononeuritis, arthritis and so on. While these manifestations did not respond to glucocorticoid therapy during the hyposensitization therapy, they did well respond just after the cessation of the therapy. Biopsy specimens of the subcutaneous nodules showed histologic patterns compatible with allergic granulomatous angiitis. In this present case, the hyposensitization therapy seems to have acted as a trigger for the development of angiitis. It seems probable that the local type I reaction advanced, through the hyposensitization therapy, to systemic type I reaction and, simultaneously, to systemic type III reaction.

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