Membrane receptor mobility changes by Sendai virus.
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Biomedical subjects
Publications and source records attributed to S Toyama.
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A diagnosis of persistent atrial standstill was made in a patient with syncopal attacks, based on: (1) the lack of P waves both in the routine 12-lead electrocardiogram (ECG) and in the right atrial cavity lead; (2) the absence of "a waves in the right atrial pressure curve; and (3) the failure of the atria to respond to electrical stimulation. Compared with previously reported cases of persistent atrial standstill with a slow, regular escape rhythm of supraventricular origin, the present case was characterized by alternate periods of bradycardia and tachycardia, the latter being suggested as AV junctional tachycardia with exit block. Furthermore, the His bundle electrogram (HBE) showed either regular, high frequency deflictions or irregular, deformed potentials, suggesting flutter and fibrillation-like phenomena in the His bundle.
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The nature of the interaction between Sendai virus and Sil mutant cells was examined by measuring a change in ESR spectrum of spin-labeled phosphatidylcholine molecules on the viral envelope. When spin-labeled virus was incubated with the Sil cells that had a reduced ability to respond to virus-induced cell fusion, interchange of the phospholipid molecules between viral envelope and cell surface membrane occurred to a smaller extent than that observed with parental cells. Moreover, the degree of the interchanging correlated with the degree of the fusion capacity of the mutant lines. The results show that the mutant cells carry such a lesion(s) on their surface membranes that the viral envelopes can hardly fuse into them.
The activity of taurine: alpha-ketoglutarate aminotransferase (taurine: 2-oxoglutarate aminotransferase, EC 2.6.1.55) from Achromobacter superficialis is significantly diminished by treatment of the enzyme with (NH4)2SO4 in the course of purification, and recovered by incubation with pyridoxal phosphate at high temperatures such as 60 degrees C. The inactive form of enzyme absorbing at 280 and 345 nm contains 3 mol of pyridoxal phosphate per mol. The activated enzyme contains additional 1 mol of pyridoxal phosphate with a maximum at 430 nm. This peak is shifted to about 400 nm as a shoulder by dialysis of the enzyme, but the activity is not influenced. The inactive form is regarded as a partially resolved form, i.e. a semiapoenzyme. The enzyme catalyzes transamination of various omega-amino aicds with alpha-ketoglutarate, which is the exclusive amino acceptor. Hypotaurine, DL-beta-aminoisobutyrate, beta-alanine and taurine are the preferred amino donors. The apparent Michaelis constants are as follows; taurine 12 mM, hypotaurine 16 mM, DL-beta-aminoisobutyrate 11 mM, beta-alanine 17 mM, alpha ketoglutarate 11 mM and pyridoxal phosphate 5 micron.
In order to differentiate the vectorcardiogram (VCG) in high posterior infarction (HPI) from VCGs of normal subjects, right ventricular hypertrophy (RVH) and primary myocardial disease (PMD), the following criteria were presented; cases satisfying the criteria could be diagnosed as high posterior infarction. In cases with posterior component/anterior component (P/L) less than 1.0 (Group A); (1)--45 degrees vector/ab less than or equal to 0.25, (2) the maximal T vector in the horizontal plane greater than or equal to + 20 degrees, (3) I (inferior component)/L (left component) less than 1.0 and (4) no anterior convexity of the afferent limb of the left sagittal QRS loop. In cases with P/A greater than or equal to 1.0 (Group B);--45 degrees vector/ab less than or equal to 0.2, (2) the maximal T vector in the horizontal plane greater than or equal to + 20 degrees, (3) I/L less than 1.0 and (4) no anterior convexity of the affernt limb of the left sagittal QRS loop. Only one false negative case in HPI was found and only seven false positive cases in normal subjects, RVH and PMD. A correct diagnosis can be made with 97.4% accuracy. These criteria for differentiation were tested by reexamining the cases with selective coronary arteriography. Five cases satisfied the criteria of this method. Complete obstruction of the circumflex coronary artery was found in four of these cases, and severe stenosis (greater than or equal to 90%) in one case. Akinesis or hypokinesis of the posterobasal segment in the left ventricle was also observed in all five cases.
Scanning electron microscopic observations were made of mouse embryonic heart cells in culture to clarify the interrelationship between morphological damage and cardiac arrhythmias and fibrillation induced by changes of ion concentrations. They were studied with particular reference to the abnormalities in the heart cell and the intercellular connections. The cells exhibited arrhythmias with any alteration in ion concentration (MgSO4, CaCl2, KCl, NaCl) in the culture medium, and they developed fibrillation-like beating under certain conditions of lowered potassium, or sodium, and increased sodium with a reduction in calcium or potassium. The heart cells showing arrhythmias were revealed by scanning electron microscopy to have more or less fine morphological changes in their slender processes, and detached or raised cell edges. Fold-like undulations in the cell body and cell ledge were also numerous in cells exhibiting fibrillation-like beating. These cell body changes may, however, be characteristic of cells maintained in cultures with lowered potassium content, since only these cultures showed such changes. Changes of cell ledge were also demonstrable in cultures with altered MgSO4, CaCl2 content or increased KCl or NaCl content although the cells in these cultures did not develop fibrillation. It was noted that there was a tendency for the changes of cell body and cell edge to be conspicuous in cells exhibiting fibrillation. The results obtained indicated that fibrillation developed only in the presence of altered concentrations of certain ions, in association with subtle morphological changes in the cells and intercellular connections.
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