[A case of familial idiopathic hyperaldosteronism (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Ito.
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The main physicochemical and enzymic properties of non-activated and activated human amniotic renin (EC 3.4.99.19) were studied in order to clarify the relationships between the two enzymes. Human amniotic renin was activated by dialysis against acidic buffer (pH 3.3), direct acidification or trypsin treatment. All procedures produced similar activation. The physicochemical characteristics of non-activated and activated renin were compared to those of human renal renin. Non-activated renin had a molecular weight of 45,500. A similar molecular weight was obtained by gel eluate activation and by acid treatment of renin prior to gel filtration. Similar isoelectric points were also found for non-activated and activated renin. One major renin peak focused at pH 6.6, whereas no similar renin peak was detected in extracts from normal human kidney. In addition, non-activated and activated renin forms were found to have the same optimal pH, the same Km and the same inhibiting pepstatin concentrations.
Protease-S was extracted from thermally injured rat skin, and partially purified by column chromatography using Sephadex G-50, CM-Sephadex (A-50), Sephadex G-75 gel filtration. The optimum pH of this enzyme was 8.6--8.8, and the molecular weight determined by Sephadex G-75 gel filtration was approximately 30 000. This enzyme is active on the N-acetyl-L-tyrosine ethyl ester, N-succinyl-L-phenylalanine-p-nitroanilide (of chymotrypsin substrate) but not N-tosyl-L-arginine methyl ester, N-benzoyl-L-arginine-p-nitroanilide. Also, protease-S was completely inhibited by diisopropylfluorophosphate (1 mM) or phenylmethylsulfonylfluoride (10 micrometer), and N-tosyl-L-phenylalanine chloromethylketone (1 mM). These results are very similar to those obtained with bovine chymotrypsin. But the enzyme is not identical with the chymotrypsin-like proteases in mast cells and leukocyte granules. When proteases-S was measured during the inflammatory reaction in vivo, maximal activity was found after 8 h, at the end of inflammation.
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6 BETA-Iodomethyl-19-norsitost-5(10)-en-3 beta-ol (V) was synthesized by homoallylic rearrangement of 19-iodositost-5-en-3 beta-ol (IV), which was obtained by the hydrolysis of 19-iodositost-5-en-3 beta-ol acetate (III) derived from the displacement of sitost-5-ene-3 beta, 19-diol 3-acetate 19-p-toluenesulfonate (I) with sodium iodide in isopropanol. The radioiodinated IV and V were prepared by isotope exchange with sodium iodide-I-131.
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The polysaccharide antigen produced by Eubacterium saburreum, strain O2, is composed of (1 leads to 6)-linked beta-D-glycero-D-galacto-heptopyranosyl residues, all of which are substituted with 6-deoxy-alpha-D-altro-heptofuranosyl groups at O-3.
The effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker was evaluated in 15 awake dogs with experimentally induced A-V junctional rhythm. The duration of asystole after overdrive (D.A.O.) in these dogs was prolonged significantly in accordance with increase in the drive rate, and the mean +/- SD of the D.A.O. reached 4.7 +/- 1.1 seconds (N = 15) after overdrive at 2.5 times the spontaneous heart rate. After administration of atropine (0.4 mg/kg; i.v.) to eight dogs, the mean +/- SD of the D.A.O. at the same rate decreased from 4.5 +/- 0.9 to 3.4 +/- 1.2 seconds. After administration of practolol (0.5 mg/kg; i.v.) to the seven other dogs, the mean +/- SD of the D.A.O. at the same rate increased remarkably from 4.9 +/- 1.3 to 9.4 +/- 3.0 seconds. Intravenous injection of practolol (0.5 mg/kg) had no effect upon the D.A.O. in the five dogs with sinus rhythm. Thus, it is suggested that (1) the sympathetic nerve might play a more important role in regulating the automaticity of the A-V junctional pacemaker than the vagus and (2) it physiologically might take over 5.0 seconds for the A-V junctional pacemaker to initiate an escape beat during longstanding sinus arrest, if a marked dysfunction of the A-V junctional pacemaker occurs due to a decrease in tension of the sympathetic nerve.
Since 1974 we have performed muscle flap transposition (myoplasty) for the treatment of a skin loss of the lower leg with associated exposure of the bone. In order that the operative treatment may be completed in one stage, mesh skin graft was done simultaneously with muscle transfer. Twelve cases so far have been treated successfully by this procedure, the mesh skin graft taking well on the muscle flap.
In an attempt to know whether the existing anticonvulsants act on epileptogenic focus, the effect on SA induced by freezing of the visual cortex was examined in gallamine-immobilized cats. The SA was localized in the neighbor or ipsilateral cortex of the freezing area; little epileptiform activity was produced in the contralateral anterior cortex, and ipsilateral thalamus and hippocampus. Spike frequency and its amplitude were stable over 8 hr. Diazepam suppressed SA and decreased spike frequency and its amplitude. Dipropylacetate and acetazolamide also suppressed SA. On the other hand, phenobarbital, carbamazepine, and a high dose of phenytoin enhanced SA and increased the spike frequency. Low doses of phenytoin and trimethadione were without effect in this aspect. Taurine suppressed SA and changed the spikes to wave-like forms. The EEG arousal response was depressed with phenobarbital, carbamazepine, diazepam, and a high dose of phenytoin, but not with the other drugs examined. From these results, it is suggested that diazepam, dipropylacetate, acetazolamide, and taurine depress the epileptogenic focus activity itself without relation to the activating system.
Several 8-substituted alkylthio and alkylamino cyclic adenosine 3',5'-monophosphate (cAMP) derivatives were tested for their ability to stimulate beta-galactosidase synthesis in Estherichia coli in vivo and in vitro and to inhibit the cAMP phosphodiesterase activity of E. coli. Stimulation of beta-galactosidease synthesis in vivo by cAMP derivatives decreased with increasing length of the unbranched carbon chain of the substituent. On the other hand, the stimulation in vitro was increased as the carbon chain elongated. The 8-decylthio- and 8-dodecylthio-cAMP compounds stimulated beta-galactosidase synthesis almost eight-fold compared with cAMP, whereas 8-undecyl-, 8-dodectyl-, and 8-tridecylamino-cAMP stimulated beta-galactosidase synthesis about threefold. However, in in vitro experiments with a phosphodiesterase-deficient strain of E. coli, the Crooks strain, the stimulatory effects of the derivatives disappeared, except for 8-dodecylthio cAMP which stimulated beta-galactosidase about 1.4- to 1.6-fold. All derivatives were quite resistant to hydrolysis by phosphodiesterase. Most derivatives competitively inhibited the hydrolysis of cAMP by phosphodiesterase.
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Abnormal ECG changes were found in some patients who were treated glucocorticoid during long term. In experimental animals, chronic administration of glucocorticoid resulted abnormal ST and T changes of ECG, increased duration of action potential and induced electron microscopical changes of mitochondria. No significant changes were found in serum and myocardial potassium content.
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We studied whether pulmonary arterial levels of plasma prostaglandin E rose following pressor effects of angiotensin II in the intact dogs. Furthermore, the modulation by indomethacin of the effect of angiotensin II, PGF2 alpha, and PGE1 on pulmonary circulation was evaluated. Pulmonary arterial plasma PGE levels rose significantly from 0.52 +/- 0.10 (SE) ng/ml to 0.85 +/- 0.07 by the infusion of angiotensin II. This increase was not observed when indomethacin was given. The rise in pulmonary arterial pressure and total pulmonary resistance by angiotensin II was augmented significantly with pretreatment of indomethacin. These results showed that there was an augmentation of the pulmonary vasoconstrictor action of angiotensin II as indomethacin blocked an increase of pulmonary arterial PGE level. Thus, it was suggested that prostaglandins (especially PGE) modulated the pulmonary vasoconstrictor effects of angiotensin II.
This paper presents our recent results of the Mustard procedure (intra-artrial baffle operation) for the complete transposition of the great arteries performed in 24 infants and children during the past 6 years at the Tohoku University Hospital. All intracardiac repairs were performed using "bypass hypothermia" (surface-induced deep hypothermia, circulatory arrest, and limited cardiopulmonary bypass). The hospital mortality rate was 8% in patients with simple transposition without pulmonary hypertension (Group I, one death in 12 patients), 50% in patients with ventricular septal defect (VSD) and pulmonary hypertension (Group II, 3 deaths in 6 patients), and 20% in patients with VSD and pulmonary stenosis (Group III, one death in 5 patients). Various types of longstanding dysrhythmia were found in 6 out of 18 long-term survivors, and subsequent pace-maker implantation was necessary in one infant. Postoperative pulmonary venous obstruction occurred in 3 infants, and surgical relief of the obstruction was successfully undertaken in 2 of them. Prevention of postoperative dysrhythmia, pulmonary venous obstruction, and possible brain damage are also discussed.