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Biomedical subjects

S Ono

Publications and source records attributed to S Ono.

At least 631 records · Page 35Linked to original sources
PubMed1988

[Detection of mural thrombi and analysis of blood flow velocities in the left atrial appendage using transesophageal two-dimensional echocardiography and pulsed Doppler flowmetry].

To correlate blood flow velocities with thrombogenesis in the left atrium (LA) and left atrial appendage (LAA), we performed transesophageal two-dimensional echocardiography (Eso 2-D Echo) combined with pulsed Doppler flowmetry, which was developed in our laboratory. Thirty-eight patients were studied; 1) 15 who had sinus rhythm including four with mitral stenosis (MS) and 11 normal subjects, and 2) 23 with atrial fibrillation (Af). The patients with Af were classified as lone Af (nine cases); Af-CI: Af with cerebral infarction having no MS (four cases); and Af-MS: Af with MS (10 cases). In four of 10 patients with Af-MS, mural thrombi were detected in the LA or LAA by Eso 2-D Echo, but they were not visualized by conventional echocardiography. In lone Af and Af-CI, however, abnormal echoes in the LAA were not observed by Eso 2-D Echo. Thus, Eso 2-D Echo proved superior to conventional 2-D echocardiography in detecting mural thrombi in the LA or LAA. In sinus rhythm, a biphasic flow pattern followed the P wave on the ECG. It was observed in the vicinity of the junction between the LA and LAA. In Af a flow with a saw-tooth appearance was observed throughout the cardiac cycle. The peak flow velocity in the LAA was significantly less in Af than in sinus rhythm (p less than 0.05). Especially in Af-MS, the peak flow velocity was markedly decreased (1 +/- 4 cm/sec: mean +/- SD) compared with those of the other Af groups (p less than 0.01), and it was significantly less in Af-CI (11 +/- 5 cm/sec) than in patients with lone Af (21 +/- 9 cm/sec) (p less than 0.05). These results indicate that analysis of blood flow velocities in the LAA by Eso 2-D Echo is of great value in assessing thrombogenesis in the LAA, and the patients with Af, even without MS, who have markedly reduced peak flow velocities in the LAA, should be prophylactically anticoagulated, because stagnation of blood is strongly suspected.

Aged↗
PubMed1988

[Atrial septal defect diagnosed and quantitatively-evaluated by transesophageal two-dimensional Doppler echocardiography].

Transesophageal two-dimensional (2-D) echocardiography (TEE: horizontal sector scan) combined with the pulsed Doppler method was performed to determine the size of atrial septal defect (ASD) and to measure directly shunt flow signals through the defects in six ASD patients (32 +/- 16 yrs) confirmed by cardiac catheterization. The size of the defect in the horizontal dimension was measured by TEE; the vertical dimension of the defect was determined from the distance of the transesophageal probe positions of the rostral and caudal margins of the defect. The size of defect determined by TEE was compared with that observed at surgery. Shunt flow signals were recorded by the pulsed Doppler technique by setting the sample volume at the center of the defect. Left-to-right shunt flow was determined as follows: shunt flow volume (ml/min) = mean velocity (cm/s) x the area of a defect (cm2) x 60. The shunt flow was compared with that obtained by the Fick's method. In all patients, TEE accomplished unequivocal visualization of a defect. The defect sizes by TEE correlated well with measurements obtained at surgery (r = 0.66). A clear laminar shunt flow with its peak in late systole and atrial systole was observed. Significant correlations were obtained between shunt volumes by TEE and those by the Fick's method (r = 0.91, p less than 0.05). Thus, TEE proved a useful method for diagnosing ASD and for evaluating shunt flow volumes.

Adolescent↗
PubMed1988

[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction].

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.

Animals↗
PubMed1988

T-cell-derived factor B151-TRF1/IL-5 activates blastoid cells among unprimed B cells to induce a polyclonal differentiation into immunoglobulin M-secreting cells.

Two distinct murine B-cell differentiation factors, designated B151-TRF1 and B151-TRF2, were described originally as B151K12 T-cell hybridoma-derived lymphokines that induce immunoglobulin (Ig) secretion by antigen-activated B cells and unstimulated B cells, respectively. In the present study, we found that a highly purified B151-TRF1 fraction prepared by reversed-phase high-performance liquid chromatography (RP-HPLC) also has the ability to cause a polyclonal differentiation of unstimulated B cells into IgM-secreting cells in the apparent absence of co-stimulant. The activity of the B151-TRF1 fraction but not the B151-TRF2 fraction on unstimulated B cells was markedly inhibited by addition of a monoclonal antibody (mAb) specific for the B151-TRF1/IL-5 to the culture. To determine whether B151-TRF1/IL-5 and B151-TRF2 act on distinct populations among unstimulated B cells, the responsiveness of neonatal B cells and adult B cells that had been fractionated by Percoll density gradient centrifugation was assessed. B151-TRF1/IL-5 predominantly acted on lower density B cells, which appeared around 3 weeks after birth in the spleen. In contrast, B151-TRF2 could activate both lower and higher density B cells almost equally and B151-TRF2-responsive B cells were already present by 1 week of age. Thus, these results suggest that B151-TRF1/IL-5 and B151-TRF2 act on distinct subpopulations among antigen-unprimed normal B cells to induce IgM-secreting cells.

Animals↗