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Articles by T Kataoka
Total Records ( 5 ) for T Kataoka
  M Oka , H Edamatsu , M Kunisada , L Hu , N Takenaka , S Dien , M Sakaguchi , R Kitazawa , K Norose , T Kataoka and C. Nishigori
 

Phospholipase C (PLC) is a phosphoinositide-specific PLC regulated by small guanosine triphosphatases including Ras and Rap. Our previous studies revealed that PLC gene-knockout (PLC–/–) mice exhibit marked resistance to tumor formation in two-stage skin chemical carcinogenesis using 7,12-dimethylbenz(a)anthracene as an initiator and 12-O-tetradecanoylphorbol-13-acetate as a promoter. In this model, PLC functions in tumor promotion through augmentation of 12-O-tetradecanoylphorbol-13-acetate-induced inflammation. In this study, we have further assessed the role of PLC in tumorigenesis using a mouse model of ultraviolet (UV) B-induced skin tumor development. We irradiated PLC+/+, PLC+/– or PLC–/– mice with doses of UVB increasing from 1 to 10 kJ/m2 three times a week for a total of 25 weeks and observed tumor formation for up to 50 weeks. In sharp contrast to the results from the two-stage chemical carcinogenesis study, PLC–/– mice developed a large number of neoplasms including malignant tumors, whereas PLC+/+ and PLC+/– mice developed a relatively small number of benign tumors. However, UVB-induced skin inflammation was greatly suppressed in PLC–/– mice, as observed with 12-O-tetradecanoylphorbol-13-acetate-induced inflammation, implying that PLC’s role in the suppression of UVB-induced tumorigenesis is not mediated by inflammation. Studies of the tumor initiation stage revealed that UVB-induced cell death in the skin was markedly suppressed in PLC–/–mice. Our findings identify a novel function for PLC as a critical molecule regulating UVB-induced cell death and suggest that resistance to UVB-induced cell death conferred by the absence of PLC is closely related to the higher incidence of skin tumor formation.

  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
  Background—

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).

Conclusions—

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.

  B. K Koo , K Waseda , H. J Kang , H. S Kim , C. W Nam , S. H Hur , J. S Kim , D Choi , Y Jang , J. Y Hahn , H. C Gwon , M. H Yoon , S. J Tahk , W. Y Chung , Y. S Cho , D. J Choi , T Hasegawa , T Kataoka , S. J Oh , Y Honda , P. J Fitzgerald and W. F. Fearon
 

Background— We sought to investigate the mechanism of geometric changes after main branch (MB) stent implantation and to identify the predictors of functionally significant "jailed" side branch (SB) lesions.

Methods and Results— Seventy-seven patients with bifurcation lesions were prospectively enrolled from 8 centers. MB intravascular ultrasound was performed before and after MB stent implantation, and fractional flow reserve was measured in the jailed SB. The vessel volume index of both the proximal and distal MB was increased after stent implantation. The plaque volume index decreased in the proximal MB (9.1±3.0 to 8.4±2.4 mm3/mm, P=0.001), implicating plaque shift, but not in the distal MB (5.4±1.8 to 5.3±1.7 mm3/mm, P=0.227), implicating carina shifting to account for the change in vessel size (N=56). The mean SB fractional flow reserve was 0.71±0.20 (N=68) and 43% of the lesions were functionally significant. Binary logistic-regression analysis revealed that preintervention % diameter stenosis of the SB (odds ratio=1.05; 95% CI, 1.01 to 1.09) and the MB minimum lumen diameter located distal to the SB ostium (odds ratio=3.86; 95% CI, 1.03 to 14.43) were independent predictors of functionally significant SB jailing. In patients with ≥75% stenosis and Thrombolysis In Myocardial Infarction grade 3 flow in the SB, no difference in poststent angiographic and intravascular ultrasound parameters was found between SB lesions with and without functional significance.

Conclusions— Both plaque shift from the MB and carina shift contribute to the creation/aggravation of an SB ostial lesion after MB stent implantation. Anatomic evaluation does not reliably predict the functional significance of a jailed SB stenosis.

Clinical Trial Registration: http://www.clinicaltrials.gov. Unique Identifier: NCT00553670.

  M Sakaino , T Kataoka and S. Taketani
 

Ferrochelatase (FECH) catalyses the insertion of ferrous ions into protoporphyrin IX to produce haem at the haem-biosynthetic pathway. The present study characterized a variant mRNA of mouse FECH, which was generated by skipping exon II (FECH-v). FECH-v mRNA was expressed in various tissues, including the liver and kidney, of mice. The mRNA was also expressed in mouse and human non-erythroid and erythroid cells to a different extent but could not be translated into functional FECH. The ratio of FECH-v/FECH increased in hemin-treated Balb/3T3 cells, while it decreased after treatment with succinylacetone, an inhibitor of haem biosynthesis, strongly suggesting that FECH expression was decreased by increasing the level of intracellular haem. These results demonstrated the haem-dependent negative feedback regulation of the expression of FECH at a post-transcriptional level.

 
 
 
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