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Biomedical subjects

S Nagata

Publications and source records attributed to S Nagata.

At least 721 records · Page 40Linked to original sources
PubMed1982

Structure and expression of human alpha-interferon genes.

cDNA was prepared from induced leukocyte poly(A) RNA and cloned in Escherichia coli. Interferon (IFN)-alpha cDNA clones were isolated by subculture cloning using a translation hybridization assay. Definitive identification of the clones was based on the production of an interferon-like protein by the transformed bacteria. Different IFN-alpha cDNAs, with characteristic target cell specificities, were identified. The cloned cDNAs typically encode a mature polypeptide of 166 (or, in the case of IFN-alpha 2, 165) amino acids and a signal sequence of 23 amino acids.

Amino Acid Sequence↗
PubMed1982

[Mitral regurgitation in hypertrophic cardiomyopathy: an analysis with two-dimensional ultrasonic Doppler echocardiography].

Intracardiac blood flow pattern in the left ventricle and left atrium was noninvasively studied by the ultrasonic pulsed Doppler flowmeter incorporated with a real-time, phased array two-dimensional echocardiography in 28 cases of hypertrophic cardiomyopathy. Emphasis was placed on the incidence and characteristic features of mitral regurgitation in this condition. The relationship of mitral regurgitation with an early systolic murmur was also studied. The results were as follows: 1) A mitral regurgitant signal by Doppler technique was noted in all cases of hypertrophic obstructive cardiomyopathy and in half of the cases of hypertrophic nonobstructive cardiomyopathy. 2) The Doppler signal of mitral regurgitation began immediately after the first heart sound. 3) The mitral regurgitant flow spread over the left atrium or directed toward the posterior half of the left atrium in the obstructive cases. However, it was localized in the vicinity of the mitral orifice in the nonobstructive cases. These findings were different from those in rheumatic mitral regurgitation or idiopathic mitral valve prolapse. 4) The findings on mitral regurgitation by the Doppler technique exhibited a satisfactory correspondence to those by left ventriculography. 5) The early part of the systolic murmur in hypertrophic cardiomyopathy was considered to be more closely related to mitral regurgitation than a turbulent forward flow due to outflow obstruction. Therefore, mitral regurgitation might have some contribution in causing a murmur in the latter period of systole.

Adult↗
PubMed1982

[Evaluation of left ventricular morphology and function by cardiac computed tomographic examination].

Usefulness of cardiac computed tomography (CT) in the evaluation of left ventricular (LV) morphology and function was studied in clinical practice. One hundred and forty-nine adult cases of various heart diseases were examined by GE scanner with ungated scans covering whole LV and ECG-gated scans. In gating examination, "long-axial" and "short-axial" slices were scanned and end-diastolic area (EDA), end-systolic area (ESA) and "mean" area (MA) were obtained in each slices. 1) With regard to LV morphology, wall thickening in HCM and wall thinning and mural thrombus in myocardial infarction were easily visualized. 2) LV "mean" volume (LVMV) was easily calculated from the sum of sliced LV volume of ungated scans. The LVMV was well correlated with end-diastolic volume (EDV) obtained by LV angiocardiography (LVG) (r = 0.91), though the former was somewhat smaller than the latter. EDV by CT obtained after the correction with MA/EDA from gating examination showed a better correlation (r = 0.95) and both EDV showed almost the same value. 3) LV ejection fraction (EF) was calculated by exchanging ESA/EDA to ESV/EDV in "long-axial" and "short-axial" gated slices, and "long-axial" EF, "short-axial" EF and mean of both were well correlated with LVEF of LVG (r = 0.73-0.79). 4) LVEF calculated from "long-axial" EDA and ESA by application of "area-length" method was also correlated with EF of LVG (r = 0.68), but these EDV and ESV were smaller than those of LVG due to shorter long-diameter of LV in CT. 5) LV muscle volume was calculated from sum of sliced muscle volumes of ungated scans covering LV, and LV mass was easily evaluated from LV muscle volume and specific gravity of LV muscle. This LV mass was well correlated with that of LVG (r = 0.90) and the absolute values were almost the same.

Adult↗
PubMed1982

[New echocardiographic criterion in the diagnosis of mitral valve prolapse].

Currently, echocardiographic diagnosis of mitral valve prolapse is made when the mitral leaflets protrude into the left atrium crossing the mitral ring. However, there remains the possibility that some mitral valve prolapse, particularly mild one, is overlooked by the currently used criterion. In the present study, new echocardiographic criterion in the diagnosis of mitral valve prolapse is proposed. The criterion includes the systolic dislocation of the mitral leaflets at its coaptation zone. The validity of the new criterion is supported by the following facts. (1) Dislocation of the mitral leaflets at the coaptation zone was never observed in healthy subjects. (2) Real-time two-dimensional echocardiograms from eight cases with a midsystolic click and a late systolic murmur, the characteristic phonocardiographic findings of mitral valve prolapse, invariably demonstrated the dislocation of either the anterior or posterior mitral leaflet at the coaptation zone leading to the diagnosis of mitral valve prolapse. Four of five cases with a midsystolic click and a holosystolic murmur were also diagnosed echocardiographically as mitral valve prolapse based on the proposed criterion. However, two of the former cases and one of the latter cases did not demonstrate the protrusion of the mitral leaflets into the left atrium crossing the mitral ring, indicating inability to diagnose mitral valve prolapse based on the commonly adopted criterion. (3) Based on the extent and degree of dislocation of the coaptation of the mitral leaflets, mitral valve prolapse could be classified into nine grades. It was found that the incidence of mitral regurgitation proved by phonocardiography or angiocardiography is higher as the grade of prolapse becomes greater.

Echocardiography↗
PubMed1981

Molecular analysis of the human interferon-alpha gene family.

Fifteen DNA clones containing sequences related to human interferon-alpha cDNA were isolated from a human chromosomal gene bank (Nagata et al., Nature 287 (1980) 401-408) and characterized by restriction mapping, R-loop and heteroduplex analysis. Nine distinct DNA segments hybridized strongly with interferon-alpha 1 cDNA and formed R-loops with poly(A) RNA from interferon-producing human leukocytes; most if not all of these segments represent functional interferon genes. Five segments hybridized weakly with the probe and did not form R-loops with the poly(A) RNA; one of these was characterized as an interferon-alpha pseudogene. Several DNA segments overlap and define a region of 36 kilobase pairs (kb) that contains three strongly and three weakly hybridizing sequences. From our data and those of Goeddel et al. (Nature 290 (1981) 20-25) we conclude that there exist at least 11 distinct genes of gene-like sequences of the interferon-alpha type in the human genome, of which most likely represents an allelic variant, and at least five pseudogenes distantly related to the interferon-alpha genes.

Chromosome Mapping↗
PubMed1981

Target cell specificity of two species of human interferon-alpha produced in Escherichia coli and of hybrid molecules derived from them.

Plasmids containing cDNAs for human interferon (IfN) alpha-1, IFN alpha-2, and several hybrids of the two cDNAs, all joined identically to an Escherichia coli lac promoter fragment gave rise, in E. coli, to fused interferons (fIFNs) that had very different target-cell specificities. fIFN alpha-1 had a lower specific activity on human WISH cells than on bovine MDBK cells, while fIFN alpha-2 showed the opposite behavior. fIFN hybrids with the NH2-proximal half of fIFN alpha-2 behaved qualitatively like fIFN alpha-1, and those with the NH2-proximal half of fIFN alpha-2, behaved like fIFN alpha-2. On mouse L929 cells, fIFN alpha-2 was almost inactive, while fIFN alpha-1 showed relatively high activity. In this case, the fIFN hybrids with the COOH-proximal half of IFN alpha-1 showed activity on mouse cells, while the reciprocal hybrid did not. In many cases, the activity spectrum of the hybrids was very different from that of either parent. We propose that the IFN molecule has either two binding sites or two regions constituting the binding site, one in the COOH- and the other in the NH2-proximal half. The experimental findings can be accounted for if the fits of the two sites to their receptor counterparts on different cell lines are independent of one another.

Animals↗
PubMed1981

Partial mapping of ten genes of the human interferon- alpha family.

HulFN-alpha genes form a family of not less than 9-10 distinct members, at least three of which are arranged in tandem. In one case, two variants, believed to be alleles of the same gene, could be identified by sequence analysis. The three gene sequenced so far are devoid in introns.

Alleles↗
PubMed1981

A study on the transmural conduction velocity of activation front in the left ventricle of RBBB patients.

To investigate the effect of ventricular hypertrophy on the conduction velocity, the transmural conduction velocity was obtained from the findings of echocardiographic, and body surface potential mapping examinations on 20 RBBB patients. The transmural conduction velocity was linearly correlated with the ventricular septal thickness and the greater the thickness, the faster was the conduction velocity. There was no statistically significant difference in the duration of the left ventricular activation obtained from the mapping examinations as well as in the time of onset of intrinsicoid deflection in V5 between the group of left ventricular hypertrophy and that of non-hypertrophy. There was a good linear correlation between the imaginary distance covered by the activation front which proceeded in the direction from endocardium to epicardium during the left ventricular activation and the ventricular septal thickness. These findings were explicable from the faster conduction velocity in the hypertrophied ventricle. The increase in the conduction velocity in the hypertrophy group would be due to cable characteristics of hypertrophied cardiac cells and also due to increase in the number of multiple intercalated discs in the hypertrophied ventricle. It was concluded that the conduction velocity would be an important information to interpret the ECGs in ventricular hypertrophy as well as to estimate the pathological state of the heart.

Bundle-Branch Block↗