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Articles by T Okada
Total Records ( 5 ) for T Okada
  K Shimada , H Isoda , T Okada , T Kamae , S Arizono , Y Hirokawa and K. Togashi

OBJECTIVE. For this study, we aimed to selectively visualize the intrahepatic portal veins using 3D half-Fourier fast spin-echo (FSE) MR angiography (MRA) with a time-space labeling inversion pulse (T-SLIP) and to optimize the acquisition protocol.

SUBJECTS AND METHODS. Respiratory-triggered 3D half-Fourier FSE scans were obtained in 25 healthy adult subjects combined with two different T-SLIPs: one placed on the liver and the thorax to suppress signals of the liver parenchyma, hepatic veins, and abdominal arteries and the other on the lower abdomen to suppress the ascending signal of the inferior vena cava. One of the most important factors was the inversion time (TI) of the inversion pulse for the liver and thorax. Image quality was evaluated in terms of signal-to-noise ratio, contrast-to-noise ratio, and mean visualization scores at four different TIs: 800, 1,200, 1,600, and 2,000 milliseconds.

RESULTS. Selective visualization of the portal vein was successfully achieved in all volunteers, and anatomic variations were also seen in three subjects. A TI of 1,200 milliseconds was optimal in our protocol because it was sufficient for peripheral portal vein visualization and was most suitable for signal suppression of the hepatic veins and liver parenchyma.

CONCLUSION. Half-Fourier FSE scanning with T-SLIPs enabled selective visualization of the portal vein without an exogenous contrast agent.

  T Yamada , H Doppalapudi , H. T McElderry , T Okada , Y Murakami , Y Inden , Y Yoshida , N Yoshida , T Murohara , A. E Epstein , V. J Plumb , S. H Litovsky and G. N. Kay

Idiopathic ventricular arrhythmias (VAs) can originate from the left ventricular papillary muscles (PAMs). This study investigated the electrophysiological characteristics of these VAs and their relevance for the results of catheter ablation.

Methods and Results—

We studied 19 patients who underwent successful catheter ablation of idiopathic VAs originating from the anterior (n=7) and posterior PAMs (n=12). Although an excellent pace map was obtained at the first ablation site in 17 patients, radiofrequency ablation at that site failed to eliminate the VAs, and radiofrequency lesions in a relatively wide area around that site were required to completely eliminate the VAs in all patients. Radiofrequency current with an irrigated or nonirrigated 8-mm-tip ablation catheter was required to achieve a lasting ablation of the PAM VA origins. During 42% of the PAM VAs, a sharp ventricular prepotential was recorded at the successful ablation site. In 9 (47%) patients, PAM VAs exhibited multiple QRS morphologies, with subtle, but distinguishable differences occurring spontaneously and after the ablation. In 7 (78%) of those patients, radiofrequency lesions on both sides of the PAMs where pacing could reproduce an excellent match to the 2 different QRS morphologies of the VAs were required to completely eliminate the VAs.


Radiofrequency catheter ablation of idiopathic PAM VAs is challenging probably because the VA origin is located relatively deep beneath the endocardium of the PAMs. PAM VAs often exhibit multiple QRS morphologies, which may be caused by a single origin with preferential conduction resulting from the complex structure of the PAMs.

  H Ihara , S Hanashima , T Okada , R Ito , Y Yamaguchi , N Taniguchi and Y. Ikeda

FUT8, a eukaryotic 1,6-fucosyltransferase, catalyzes the transfer of a fucosyl residue from guanine nucleotide diphosphate-β-l-fucose to the innermost GlcNAc of an asparagine-linked oligosaccharide (N-glycan). The catalytic domain of FUT8 is structurally similar to that of NodZ, a bacterial 1,6-fucosyltransferase, which acts on a chitooligosaccharide in the synthesis of Nod factor. While the substrate specificities for the nucleotide sugar and the N-glycan have been determined, it is not known whether FUT8 is able to fucosylate other sugar chains such as chitooligosaccharides. The present study was conducted to investigate the action of FUT8 on chitooligosaccharides that are not generally thought to be a substrate in mammals, and the results indicate that FUT8 is able to fucosylate such structures in a manner comparable to NodZ. Surprisingly, structural analyses of the fucosylated products by high performance liquid chromatography, mass spectrometry and nuclear magnetic resonance indicated that FUT8 does not utilize the reducing terminal GlcNAc for fucose transfer but shows a preference for the third GlcNAc residue from the nonreducing terminus of the acceptor. These findings suggest that FUT8 catalyzes the fucosylation of chitooligosaccharide analogous to NodZ, but that a nonreducing terminal chitotriose structure is required for the reaction. The substrate recognition by which FUT8 selects the position to fucosylate might be distinct from that for NodZ and could be due to structural factor requirements which are inherent in FUT8.

  T Okada , H Ihara , R Ito , M Nakano , K Matsumoto , Y Yamaguchi , N Taniguchi and Y. Ikeda

The baculovirus–insect cell expression system is in widespread use for expressing post-translationally modified proteins. As a result, it is potentially applicable for the production of glycoproteins for therapeutic and diagnostic purposes. For practical use, however, remodeling of the biosynthetic pathway of host-cell N-glycosylation is required because insect cells produce paucimannosidic glycoforms, which are different from the typical mammalian glycoform, due to trimming of the non-reducing terminal β1,2-GlcNAc residue of the core structure by a specific β-N-acetylglucosaminidase. In order to establish a cell line which could be used as a host for the baculovirus-based production of glycoproteins with mammalian-type N-glycosylation, we prepared and characterized Spodoptera frugiperda Sf21 cells that had been transfected with the rat cDNA for β1,4-N-acetylglucosaminyltransferase III (GnT-III), which catalyzes the addition of a bisecting GlcNAc. As evidenced by structural analyses of N-glycans prepared from whole cells and the expressed recombinant glycoproteins, the introduction of GnT-III led to the production of bisected hybrid-type N-glycans in which the β1,2-GlcNAc residue at the 1,3-mannosyl branch is completely retained and which has the potential to be present in mammalian cells. These results and other related findings suggest that bisected oligosaccharides are highly resistant to β-N-acetylglucosaminidase activity of the S. frugiperda fused lobes gene product, or other related enzymes, which was confirmed in Sf21 cells. Our present study demonstrates that GnT-III transfection has the potential to be an effective approach in humanizing the N-glycosylation of lepidopteran insect cells, thereby providing a possible preliminary step for the generation of complex-type glycoforms if the presence of a bisecting GlcNAc can be tolerated.

  H Kimura , X Li , K Torii , T Okada , K Kamiyama , D Mikami , N Takahashi and H. Yoshida

Background. Long-term treatment with glucocorticoids (GCs) reportedly exaggerates renal fibrosis in chronic progressive inflammatory kidney disease. GCs induce the gene expression of plasminogen activator inhibitor-1 (PAI-1), a fibrosis enhancer in non-renal cells. Tumour necrosis factor-alpha (TNF-) reduces the gene expression of 11β-hydroxysteroid dehydrogenase (HSD) 2, an inactivator of GCs, and may enhance GC activity. However, the individual and collective effects of adrenal steroids, TNF- and HSD2 status on PAI-1 production are unknown in human proximal renal tubular epithelial cells (HPTECs).

Methods. Confluent HPTECs were treated with adrenal steroids (10 nM to 10 µM) or TNF- (10 ng/ml) for up to 48 h. The mRNA amounts of the target genes were determined by TaqMan quantitative PCR, and the PAI-1 protein amounts were measured by an immunoassay.

Results. Dexamethasone (DXA) maximally increased the amounts of PAI-1 mRNA and protein at 100 nM. Aldosterone (Ald) increased PAI-1 expression dose dependently, but the effect was over 100-fold weaker than that of DXA. The PAI-1-increasing effects of DXA and Ald were abolished completely by U-486, a specific inhibitor of the glucocorticoid receptor (GR) but not by spironolactone, a specific inhibitor of the mineralocorticoid receptor. The effect of DXA was also blocked partially by AG1478 and herbimycin A, tyrosine kinase inhibitors. DXA further increased TNF--stimulated PAI-1 expression via the GR. Although TNF- treatment caused an 80% reduction in the gene expression of HSD2, an inactivator of GCs, HSD2 inhibition did not enhance DXA-induced PAI-1 production.

Conclusions. DXA induces basal and TNF--stimulated PAI-1 expression via the GR pathway, regardless of HSD2 status in HPTECs. Excess GCs may serve as a pro-fibrotic factor in chronic inflammatory kidney diseases.

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