Biomedical subjects
Publications and source records attributed to S Nagata.
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Echocardiographic features of the false tendon in th left ventricle and its clinical significance were reported. The subjects consisted of 132 consecutive patients, in whom the left ventricle was satisfactorily examined from various aspects with two-dimensional echocardiography. In general, the false tendon was detected in the long axis view of the left ventricle from the apical approach. It was detected in 61 of 132 consecutive patients with echocardiography. The incidence did not seem to be related to the kinds of underlying conditions. The false tendon was usually a string, a few millimeters in width, crossing the ventricular cavity from the vicinity of the papillary muscles to the interventricular septum. In a few patients it looked as Y-figure and net like. Sometimes, several sticks of the false tendon were detected. It was observed to be stretched in diastole and relaxed in systole. On the M-mode echocardiogram the false tendon was displayed as a linear echo moving with heart beat. The false tendon revealed near the interventricular septum, exhibited a motion so similar to that of the interventricular septum that it should be carefully differentiated from the echo of the left ventricular surface of the septum. In 2 patients of valvular heart disease, it was observed to be fluttered in diastole. Echocardiography was more useful in detecting the false tendon than left ventriculography.
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The mechanism of the systolic anterior motion (SAM) of the mitral valve and the relationship between SAM and the intraventricular pressure gradient in hypertrophic cardiomyopathy were analyzed. The subjects were 15 cases, in which SAM was observed on the M-mode echocardiograms. Real-time two-dimensional echocardiography was performed at the time of cardiac catheterization and the measurement of left ventricular pressure was made with observing the spatial relationship between the tip of of the catheter and the surrounding intracardiac structures. There were two modes of the systolic anterior motion of the mitral valve in cases with SAM as follows: (1) The hypertrophied papillary muscle protruded into the left ventricular cavity in systole and it caused the displacement of the chordae tendineae, but also the tips of both anterior and posterior mitral leaflets were anterosuperiorly pulled up by the enlarged papillary muscles and the leaflets seemed apparently to intersect the left ventricular outflow tract (type II). These two types seem to make a continuous spectrum. Seven of the 15 cases examined exhibited type I and 8 cases exhibited type II or the intermediate condition. In the cases of type I, the pressure gradient was noted at the level of the tip of the papillary muscles. The inflow tract and the suprapapillary of the outflow tract exhibited a low pressure, while the apical cavity exhibited a high pressure. It is suggested that the enlarged papillary muscles make the ventricular cavity much more narrowly, resulting in the development of pressure gradient at their level. In the cases of type II, the pressure gradient was noted across the anterior and posterior mitral leaflets perpendicular to the outflow tract (subaortic area). The inflow tract exhibited a high pressure in contrast to that in the cases of type I. It is suggested that the anterosuperiorly pulled anterior and posterior leaflets dam up the ventricular cavity, resulting in the development of pressure gradient across them. Here, it should be emphasized that not only the anterior mitral leaflet, but also the posterior leaflet participates to yield the SAM and the intraventricular pressure gradient.
The detailed informations and clinical significance of the Eustachian valve have not yet been elucidated. Real-time two-dimensional echocardiography has enabled one to investigate the Eustachian valve non-invasively. The valve was usually very small. The larger valve was a few cm in length and moved with heart beat. Its motion was analyzed with M-mode echocardiography. In the cases with sinus rhythm, the valve opened gradually in systole, and opened further in rapid filling phase,. followed by the rapid closing at the time of atrial contraction. In the cases of atrial fibrillation with severe tricuspid regurgitation, the valve remained at the semi-closed position throughout systole and opened in rapid filling phase. In one case of tricuspid regurgitation the valve was observed to flutter in systole. After the surgical repair of the tricuspid valve, systolic opening of the valve was noted, though atrial fibrillation persisted.
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Blood flows in the main pulmonary artery, right pulmonary artery and right ventricular outflow tract were analyzed in 11 cases of valvular pulmonary stenosis and 10 healthy subjects by pulsed echo Doppler cardiography (two-dimensional) with the parasternal and suprasternal approaches. 1) The systolic flow in the right pulmonary artery was detected in 7 cases of valvular pulmonary stenosis, in which the flow of both right and main pulmonary arteries was detected in only one case. The flows seemed to be turbulent. These abnormal signals were never detected in healthy subjects and considered to be caused by the narrowing of the pulmonic orifice. 2) Abnormal flow signals were also detected in the right ventricular outflow tract in patients of pulmonary stenosis. Their features were as follows: (1) A systolic turbulent flow was detected in a case with severe hypertrophy of the wall and narrowing of the lumen of the right ventricular outflow tract. (2) A/S ratio, which is a ratio of the peak velocity in atrial contraction (A) to the peak velocity in systole (S), was larger in cases with pulmonary stenosis than in healthy subjects (p less than 0.05). It was considered that the atrial component in the right ventricular filling was augmented in pulmonary stenosis. (3) The PEP/ET (pre-ejection period/ejection time) of the right ventricle was smaller in cases with pulmonary stenosis than in healthy subjects (p less than 0.05). The ratio exhibited a reverse correlation with the pressure gradient between the right ventricle and pulmonary artery (r = 0.74, p less than 0.025). (4) Acceleration time index, a ratio of the time interval between the upstroke and the peak velocity of ejection flow to the ejection time, as a parameter indicating the time delay of the peak velocity exhibited a significant correlation with the pressure gradient between the right ventricle and pulmonary artery (r = 0.67, p less than 0.05). (5) No correspondence was revealed between the time interval of Q-peak velocity in systole and that of Q-peak intensity of the murmur during systole. It was remained to be clarified.
The 12 interferon (IFN)-related sequences detected in a human gene bank fall into not less than eight distinct classes, indicating that there are at least eight IFN-related genes. Most, if not all, of these direct the synthesis of an IFN in Escherichia coli. The sequence of one chromosomal gene and its flanking regions was identical to that deduced for the cDNA corresponding to IFN-alpha l mRNA. No evidence was found for the existence of an intron, in either the coding or the non-coding segments of the gene.
The sequence of a human leukocyte-derived complementary DNA (cDNA), Hif-2h, which directs the formation in Escherichia coli of a polypeptide, IFN-alpha 1, with interferon (IFN) activity has been described. A second IFN cDNA, Hif-SN206, which also elicits synthesis of a biologically active IFN, IFN-alpha 2, is described in this article. Whereas IFN-alpha 2 is twice as active on human as on bovine cells, IFN-alpha 1 is 10 to 20 times more active on bovine than on human cells. As deduced from the cDNA's, the messenger RNA's for the two IFN's differ in length and in 20 percent of the nucleotides; the mature IFN polypeptides differ in 17 percent of the amino acids. Both IFN-alpha 1 and IFN-alpha 2 differ from the lymphoblastoid IFN described by others. Therefore, at least three different IFN-alpha genes are expressed in man; studies on genomic DNA reveal the presence of at least eight IFN-related genes.
Interferon-alpha 1 from Escherichia coli transformed with a hybrid plasmid containing a human leukocyte complementary DNA insert, induces resistance to virus in appropriate target cells. It also shares the following properties with natural leukocyte interferon (IFN). (i) It enhances natural killing activity of human lymphocytes, (ii) it enhances antibody-dependent cell-mediated cytotoxicity, (iii) it suppresses antigen- and mitogen-induced leukocyte migration inhibition, (iv) it inhibits growth of IFN-sensitive Burkitt lymphoma cells. Since these activities are exhibited by a cloned protein species, they are due to IFN itself and not to other human proteins.
The coding sequences of the dDNAs of cloned human leukocyte interferon I and human fibroblast interferon show homologies of 45% at the nucleotide and 29% at the amino acid level. We conclude that the two genes were derived from a common ancestor.
Double-stranded cDNA prepared from the 12S fraction of poly(A) RNA from interferon (IF)-producing human leukocytes was cloned in Escherichia coli using the pBR322 vector. One of the resulting clones had a 910-base pair insert which could hybridise to IF mRNA and was responsible for the production of a polypeptide with biological IF activity. Up to 10,000 units IF activity per g of cells was obtained from some clones.
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A case of cold urticaria, thought to be due to IgM, is presented. Passive transfer (PT) activity was manifested in cryoglobulin-free serum and in up to 20-fold dilutions of fraction I, the IgM-containing fraction obtained by Sephadex G-200 column chromatography. PT test results were positive with serum absorbed with cold agglutinins, and with heat-treated (56 degrees C, 4 hr) serum. These results were negative with cryoglobulin and after absorbing the supernatant of fraction I with anti-IgM. Skin adhesion time was within 24 hr. The in vivo histamine release during cold stimulation was recorded and in this patient, antihistamine administration proved the best method to alleviate the symptoms.
Human interferon (IFN) prepared from virus-induced human leukocyte suspensions (leukocyte-derived interferon) was compared to the IFN extracted from Escherichia coli harboring a human interferon-alpha cDNA hybrid plasmid (Hif-SN35-AH-L6). E coli-derived IFN was 20 to 50 times more active than leukocyte-derived IFN on heterologous bovine, feline, murine and guinea pig cells, relative to the activity on human cells. After partial purification by affinity chromatography on an anti-human lymphoblastoid IFN antibody column, the IFN was analyzed by SDS-polyacrylamide gel electrophoresis. While leukocyte-derived IFN gave a heterogeneous pattern with major peaks of activity of 24000 and 19000 daltons, E. coli-derived IFN gave a heterogeneous peak of activity at about 17-18000 daltons. The leading edge of leukocyte-derived IFN in SDS-polyacrylamide gels was significantly more active on bovine cells than on human cells and coincided in mobility with E. coli-derived IFN, which was also much more active on bone than on human cells. After reduction with mercaptoethanol in SDS, the E. coli-derived IFN lost no activity, whereas the leukocyte-derived IFN lost about 90% of its activity. After reduction, E. coli-derived IFN migrated in SDS-polyacrylamide gels as a single peak at 24000 daltons, as did the residual activity of reduced leukocyte-derived interferon. Out data suggest that the interferon produced by the E. coli harboring the clone Hif-SN35-AH-L6 is analogous in size and cross-species activity to one of the molecular species of leukocyte-derived interferon.
We have determined the nucleotide sequence of the human leukocyte interferon cDNA carried in hybrid plasmid Z-pBR322(Pst)/HcIF-2h, which has been shown to direct the formation of a polypeptide with human leukocyte interferon activity (Nagata et al., 1980). The 910 base pair insert contains a 567 (or 543) base pair coding sequence, which determines a putative preinterferon polypeptide consisting of a signal peptide of 23 (or less likely 15) amino acids, followed by an interferon polypeptide of 166 amino acids (calculated molecular weight, 19 390). The coding sequence is preceded by a (most likely incomplete) 56 bp leader and followed by a 242 bp trailer and seven A residues from the poly(A) tail: A comparison of the sequence of 35 amino terminal amino acids of lymphoblastoid interferon (Zoon et al., 1980; M. Hunkapiller and L. Hood, personal communication) and the corresponding sequence deducted for leukocyte interferon revealed 9 differences. This suggests that these two interferons are encoded by two non-allelic genes.
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