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Articles by K. i. Hirata
Total Records ( 3 ) for K. i. Hirata
  N Sasaki , T Yamashita , M Takeda , M Shinohara , K Nakajima , H Tawa , T Usui and K. i. Hirata

Background— Accumulating evidence suggests that several subsets of regulatory T cells that actively mediate immunologic tolerance play crucial roles in atherogenesis. Recently, orally administered anti-CD3 monoclonal antibody has been shown as an inducer of novel regulatory T cells expressing latency-associated peptide (LAP) on their surface, which potently prevents systemic autoimmunity. In the present study, we hypothesized that oral anti-CD3 antibody treatment may inhibit atherosclerosis in mice.

Methods and Results— Six-week-old apolipoprotein E–deficient mice on a standard diet were orally given anti-CD3 antibody or control immunoglobulin G on 5 consecutive days, and atherosclerosis was assessed at age 16 weeks. Oral administration of anti-CD3 antibody significantly reduced atherosclerotic lesion formation and accumulations of macrophages and CD4+ T cells in the plaques compared with controls. We observed a significant increase in LAP+ cells and CD25+Foxp3+ cells in the CD4+ T-cell population in anti-CD3–treated mice, in association with increased production of the antiinflammatory cytokine transforming growth factor-β and suppressed T-helper type 1 and type 2 immune responses. Neutralization of transforming growth factor-β in vivo abrogated the preventive effect of oral anti-CD3 antibody.

Conclusions— Our findings indicate the atheroprotective role of oral anti-CD3 antibody treatment in mice via induction of a regulatory T-cell response. These findings suggest that oral immune modulation may represent an attractive therapeutic approach to atherosclerosis.

  T Onishi , H Kawai , K Tatsumi , T Kataoka , D Sugiyama , H Tanaka , Y Okita and K. i. Hirata

Background— The best predictor for postoperative left ventricular (LV) systolic dysfunction in patients with chronic aortic regurgitation is still a matter of debate. The aim of this study was to assess the clinical significance of preoperative systolic radial strain rate (Ssr) derived from tissue Doppler echocardiography as a predictor of postoperative LV systolic dysfunction in patients with chronic aortic regurgitation.

Methods and Results— In 52 patients (mean age, 58 years; 13 women) with isolated chronic aortic regurgitation, we performed standard and tissue Doppler echocardiography before and after operation, obtained echocardiographic parameters such as LV dimensions and LV ejection fraction, and measured Ssr in 4 walls of the LV. Linear regression analysis determined correlations between preoperative parameters and postoperative LV ejection fraction. Receiver-operating characteristic curve analysis assessed the optimal cutoff values of parameters that predicted postoperative LV systolic dysfunction (ejection fraction <50%). The operation caused significant decreases in LV dimensions and volumes and significant increases in Ssr (1.94±0.64 to 2.39±0.83 per second; P<0.001) and ejection fraction (53.0±8.7 to 59.0±8.8%; P<0.001). Multiple regression analysis demonstrated that averaged Ssr was the only independent predictor of postoperative LV systolic dysfunction among the covariates examined (P<0.001). Using receiver-operating characteristic curve analysis, averaged Ssr yielded the greatest area under the curve among preoperative parameters (0.80) and was indicated to be a good predictor of postoperative LV dysfunction, with 90.9% sensitivity and 73.2% specificity (cutoff value, 1.82 per second).

Conclusions— Measurement of preoperative averaged Ssr is useful in predicting postoperative LV systolic dysfunction and optimizing surgical timing in patients with isolated chronic aortic regurgitation.

  K Tatsumi , H Kawai , D Sugiyama , K Norisada , T Kataoka , T Onishi , H Tanaka and K. i. Hirata

Left ventricular (LV) remodeling can increase tethering force to mitral valve and functional mitral regurgitation (FMR). Because the relationship between FMR and regional myocardial function has not been quantitatively evaluated, we conducted a quantitative investigation of this association.

Methods and Results—

The effective regurgitant orifice (ERO) of FMR in 51 patients with depressed LV ejection fraction (32±9%) secondary to ischemic or nonischemic cardiomyopathy was compared with mitral deformation (valve and annulus), global LV remodeling (volume indices, function, and sphericity), and regional myocardial contractile function, as assessed by longitudinal peak systolic strain rate (Ssr) in LV anterior, anteroseptal, inferoseptal, inferior, inferolateral, and anterolateral segments at rest. Low-dose dobutamine (10 µg/kg per minute)-induced changes in ERO were compared with changes in the variables. Multivariable analysis identified the predictors of ERO at rest as mitral valvular tenting (β=0.062; P<0.001), Ssr in the inferior segment (inferior Ssr) (β=–0.178; P<0.001), and LV sphericity (β=0.414; P=0.001) and the predictors of valvular tenting at rest as inferior Ssr (β=–1.680; P<0.001), LV end-systolic volume index (β=0.022; P=0.001), and LV sphericity (β=3.886; P=0.012). Furthermore, dobutamine-induced reduction in ERO was predicted by reduction in valvular tenting (β=0.087; P<0.001) and increase in inferior Ssr (β=–0.082; P<0.001), and dobutamine-induced reduction in valvular tenting was predicted by increase in inferior Ssr (β=–0.860; P<0.001).


Inferior regional myocardial dysfunction was quantitatively associated with mitral valvular tenting and FMR. Moreover, improvement with dobutamine of inferior myocardial contractile function attenuated valvular tenting and FMR. Inferior myocardial contractile function can affect the configuration of the mitral apparatus and predict FMR severity.

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