[Anesthetic management of patients with cardiac pacemaker].
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Biomedical subjects
Publications and source records attributed to K Konno.
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Transplantable rat ascites hepatoma AH-66F was examined by an electron microscope. C-particles were numerously observed in the intercellular spaces and on the cell surface. The size of these particles varied from 90 to 200 nm in diameter. Small vesicles were also observed. These vesicles ranged from 40 to 50 nm in diameter. Most of them were located near the group of C-particles. Occasionally, small vesicles were observed in the form of a rosette around the C-particles.
Measurement of the incorporation of iron into liver cells and liver ferritin of the rat revealed that both incorporated less iron under tumor-bearing condition than in the normal state.
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1. Rabbit liver enolase (EC 4.2.1.11) was purified about 200-fold and the enzyme was distinguished from crystalline muscle enolase by column isoelectrofocusing. It was found that the pI of muscle enolase was at about pH 8.8 and the pI of liver enolase was at about pH 6.7. Liver enolase was more liable to heat than muscle enolase. Anti-muscle enolase antibody did not react with liver enolase in double diffusion and immunoprecipitation tests. No substantial difference seemed to exist between muscle and liver enolases in pH optima, kinetic constants, and gel filtration. 2. It was observed by electrofocusing that the pI of rat muscle enolase was pH 7.2 to 7.9 and that of liver enolase was about pH 5.9. The main component of muscle enolase was designated as type A enolase, and liver enolase as type B enolase. Type A enolase was present in skeletal muscle and heart muscle. Type B enolase was widely distributed and present in liver, kidney, spleen, brain, lung, small intestine, and heart muscle. More acidic isozyme than type B enolase coexisted in the brain, and more basic isozyme than type A enolase, coexisted in the small intestine. A prototype of enolase in the early stage of differentiation was found to be type B enolase and, as differentiation progressed, type B decreased in muscle, while type A increased. On the other hand, liver enolase was retained as type B during differentiation. The enolase in regenerating liver was the same as in normal liver.
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The tissue of a benign, localized, pleural mesothelioma was digested with protease, and the crude polysaccharide was fractionated by a column of Dowex-1 (Cl-form). The eluate from the column was electrophoresed and incubated with various mucopolysaccharide lysases. Based on the results of column chromatography, electrophoresis, and enzymatic digestion, it was found that hyaluronic acid was the major constituent of the glycosaminoglycans in pleural mesothelioma. The hyaluronic acid from pleural mesothelioma seemed to be identical in structure with that from human umbilical cord; however, the hyaluronic acid from mesothelioma was eluted before that from human umbilical cord when fractionated by the column of Sepharose 4B, suggesting a differnence in molecular size between the two. Also, evidence was obtained for the presence of dermatan sulfate and heparan sulfate.
Changes in the breathing sounds such as stridor and dry and wet rales in asthmatic patients were studied. The breathing sounds were recorded with the small transistor warp type microphone inserted through the nasal orifice into the trachea, main bronchi and segmental bronchi, and were analyzed with sound analyzer. The results were as follows: The whistling rales were caused by the resonance of the bronchial wall, when the vibrating frequency was coincident with its specific frequency. Snoring rales were explained as the sound caused by the air flow passing promptly through contracted bronchi with little secretion. Resonance of either bronchial wall or highly viscous sputum was considered to be responsible for the sonorous rales. Sibilant rales were audible when bronchi promptly repeated dilation and contraction. Stridor was picked up at the upper part of the air tract, from the main bronchus to the trachea, and noise was the main component on the sonogram, presumably caused by the air turbulence due to the narrowing and deformity of bronchial tube or to the sputum adhering to the inner surface of the air tract.
The contribution of the bronchial smooth muscles to asthmatic attack has been supposed by many studies such as measurement of the intrabronchial pressure and bronchographical studies, but electromyographical evidence has not been established yet. A new bipolar platinum-ring electrode fixed on polyethylene catheter was invented in order to record action potentials from the bronchial smooth muscle through the intrabronchial lead. Action potentials obtained by this electrode were compared with those obtained by the direct peribronchial needle electrode during either artificial or spontaneous respiration in dogs and a monkey. Electrophotographical analysis confirmed that action potentials obtained by our new electrode were similar in discharge pattern to those by the direct peribronchial needle electrode. The active contribution of the bronchial smooth muscle to the maintenance of the bronchial caliber during spontaneous respiration was observed by our new electrode. Accordingly, this electrode is applicable to electromyographical studies of the bronchial smooth muscle.
We succeeded in recording action potentials from the bronchial smooth muscles in 10 healthy males and 20 cases of bronchial asthma by means of the new electrode described by us in the preceding paper (Akasaka et al. 1975). From these electromyographic studies, we presented the direct evidence of spasm of the bronchial smooth muscles as one of the etiological factors responsible for the airway narrowing in asthmatic attack.
The effect of feeding and lighting on the regulation of aryl hydrocarbon hydroxylase activity in liver, small intestine, and lung from C3H/He, DBA/2, and Swiss albino mice was investigated. A circadian rhythm of aryl hydrocarbon hydroxylase activity in the liver from DBA/2 mice was observed under the controlled lighting conditions, showing higher activity at the end of the light period of a day and lower activity in the dark period. Contrasting to the change of the enzyme activity in mice fed freely in the continuous dark period, inconsistent and variable results of the enzyme activity and its induction by 3-methylcholanthrene were observed in the mice that were fed during the continuous light period, depending on the sex and strain of the mice used. Different responses in the induction of aryl hydrocarbon hydroxylase to different routes of 3-methylcholanthrene administration were found between the liver and small intestine of the mice, but not in the lung. The higher levels of the enzyme activity induced in the liver and small intestine were detected after the intraperitoneal and intragastric administration of 3-methylcholanthrene. The significance of controlled feeding schedules for obtaining reproducible experimental results in the regulation of aryl hydrocarbon hydroxylase activity in the mice was discussed.
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The effects of 3-methylcholanthrene and 5,6- and 7,8-benzoflavones on aryl hydrocarbon (benzo[a]pyrene) hydroxylase in the liver, small intestine, lung, and skin tissues from C3H/He and DBA/2 strains of mice under the controlled lighting conditions were examined. Apparent differences were observed in the inducibility of the hepatic enzyme by the inducers between the two strains of mice, showing that the enzyme in the C3H/He mice is inducible but not in the DBA/2 mice. Comparison of the results on the enzyme induction by 3-methylcholanthrene in the liver among the parent, intercrossed, and backcrossed mice suggested that the inducibility may be inherited as a single autosomal dominant trait. However, different genetic responses to 3-methylcholanthrene and benzoflavones in the enzyme of small intestine might be considered, because a discrepancy in the inducibility of the enzyme between the liver and the small intestine from the identical mice was demonstrated when the progeny of F2 and (DBA/2 times F1) backcross were used. On the other hand, no apparent difference was found in the inducibility of the enzyme in the lung and skin between the C3H/He and the DBA/2 mice. It is assumed that the genetic regulation of the induction of aryl hydrocarbon hydroxylase was separately controlled in the respective tissues from the identical mice. By the repeated topical applications of benzo[a]pyrene, the incidence of skin cancer was higher in the DBA/2 mice than in the C3H/He mice. The relationship between the induction of aryl hydrocarbon hydroxylase and carcinogenicity in the skin is briefly discussed.
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