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Articles by Y Yoshida
Total Records ( 3 ) for Y Yoshida
  Y Inuzuka , J Okuda , T Kawashima , T Kato , S Niizuma , Y Tamaki , Y Iwanaga , Y Yoshida , R Kosugi , K Watanabe Maeda , Y Machida , S Tsuji , H Aburatani , T Izumi , T Kita and T. Shioi
 

Background— Heart failure is a typical age-associated disease. Although age-related changes of heart are likely to predispose aged people to heart failure, little is known about the molecular mechanism of cardiac aging.

Methods and Results— We analyzed age-associated changes in murine heart and the manner in which suppression of the p110 isoform of phosphoinositide 3-kinase activity modified cardiac aging. Cardiac function declined in old mice associated with the expression of senescence markers. Accumulation of ubiquitinated protein and lipofuscin, as well as comprehensive gene expression profiling, indicated that dysregulation of protein quality control was a characteristic of cardiac aging. Inhibition of phosphoinositide 3-kinase preserved cardiac function and attenuated expression of the senescence markers associated with enhanced autophagy. Suppression of target of rapamycin, a downstream effector of phosphoinositide 3-kinase, also prevented lipofuscin accumulation in the heart.

Conclusions— Suppression of phosphoinositide 3-kinase prevented many age-associated changes in the heart and preserved cardiac function of aged mice.

  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
  Background—

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.

Conclusions—

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.

  F Kano , S Yamauchi , Y Yoshida , M Watanabe Takahashi , K Nishikawa , N Nakamura and M. Murata
 

Yip1A, a mammalian homologue of yeast Yip1p, is a multi-spanning membrane protein that is considered to be involved in transport between the endoplasmic reticulum (ER) and the Golgi. However, the precise role of Yip1A in mammalian cells remains unclear. We show here that endogenous Yip1A is localized to the ER-Golgi intermediate compartment (ERGIC). Knockdown of Yip1A by RNAi did not induce morphological changes in the Golgi, ER, or ERGIC. By analyzing a number of intracellular transport pathways, we found that Yip1A knockdown delayed the transport of Shiga toxin from the Golgi to the ER, but did not affect the anterograde transport of VSVGts045. We also found that a recombinant protein that corresponded to the N-terminal domain of Yip1A inhibited the COPI-independent retrograde transport of GFP-tagged galactosyltransferase, GT-GFP, but not the COPI-dependent retrograde transport of p58/ERGIC53. Furthermore, we found that Yip1A knockdown resulted in the dissociation of Rab6 from the...

 
 
 
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