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Articles by T Yamada
Total Records ( 7 ) for T Yamada
  Y Kotake , T Yamada , H Nagata , T Suzuki and J. Takeda

BACKGROUND: We hypothesized that mixed venous hemoglobin oxygen saturation (SvO2) can be estimated by calculation from CO2 production, cardiac output, and arterial oxygen saturation measured using a noninvasive cardiac output (NICO) monitor (Novametrix-Respironics, Wallingford, CT).

METHODS: Twenty-three patients undergoing aortic aneurysm repair underwent SvO2 monitoring using a pulmonary artery catheter and cardiac output monitoring using a NICO monitor. The estimated SvO2 value calculated from NICO monitor-derived values was compared with the SvO2 value measured using a pulmonary artery catheter. The accuracy of this estimation was analyzed with Bland-Altman method. The ability of this estimation to track the change of SvO2 was also evaluated using correlation analysis to compare the changes of estimated SvO2 and measured SvO2.

RESULTS: The bias ± limits of agreement of the estimated SvO2 against measured SvO2 was –2.1% ± 11.2%. The change of estimated SvO2 was modestly correlated with the change of measured SvO2.

CONCLUSIONS: SvO2 derived from the values measured by the NICO monitor cannot be used interchangeably with the values measured spectrophotometrically using the pulmonary artery catheter. More refinement is required to obtain more reliable estimate of SvO2 less invasively. However, large changes of SvO2 may be detected with this method and can be used as a precautionary sign when the balance between oxygen supply and demand is compromised without inserting a central venous catheter.

  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.

  Y Chen , Y Yamaguchi , Y Tsugeno , J Yamamoto , T Yamada , M Nakamura , K Hisatake and H. Handa

Transcription elongation factor DSIF/Spt4–Spt5 is capable of promoting and inhibiting RNA polymerase II elongation and is involved in the expression of various genes. While it has been known for many years that DSIF inhibits elongation in collaboration with the negative elongation factor NELF, how DSIF promotes elongation is largely unknown. Here, an activity-based biochemical approach was taken to understand the mechanism of elongation activation by DSIF. We show that the Paf1 complex (Paf1C) and Tat-SF1, two factors implicated previously in elongation control, collaborate with DSIF to facilitate efficient elongation. In human cells, these factors are recruited to the FOS gene in a temporally coordinated manner and contribute to its high-level expression. We also show that elongation activation by these factors depends on P-TEFb-mediated phosphorylation of the Spt5 C-terminal region. A clear conclusion emerging from this study is that a set of elongation factors plays nonredundant, cooperative roles in elongation. This study also shows unambiguously that Paf1C, which is generally thought to have chromatin-related functions, is involve directlyd in elongation control.

  L de la Torre Ubieta , B Gaudilliere , Y Yang , Y Ikeuchi , T Yamada , S DiBacco , J Stegmuller , U Schuller , D. A Salih , D Rowitch , A Brunet and A. Bonni

Neuronal polarity is essential for normal brain development and function. However, cell-intrinsic mechanisms that govern the establishment of neuronal polarity remain to be identified. Here, we report that knockdown of endogenous FOXO proteins in hippocampal and cerebellar granule neurons, including in the rat cerebellar cortex in vivo, reveals a requirement for the FOXO transcription factors in the establishment of neuronal polarity. The FOXO transcription factors, including the brain-enriched protein FOXO6, play a critical role in axo–dendritic polarization of undifferentiated neurites, and hence in a switch from unpolarized to polarized neuronal morphology. We also identify the gene encoding the protein kinase Pak1, which acts locally in neuronal processes to induce polarity, as a critical direct target gene of the FOXO transcription factors. Knockdown of endogenous Pak1 phenocopies the effect of FOXO knockdown on neuronal polarity. Importantly, exogenous expression of Pak1 in the background of FOXO knockdown in both primary neurons and postnatal rat pups in vivo restores the polarized morphology of neurons. These findings define the FOXO proteins and Pak1 as components of a cell-intrinsic transcriptional pathway that orchestrates neuronal polarity, thus identifying a novel function for the FOXO transcription factors in a unique aspect of neural development.

  K Izumi , K Narimoto , K Sugimoto , Y Kobori , Y Maeda , A Mizokami , E Koh , T Yamada , S Yano and M. Namiki

The safety and accuracy of active percutaneous needle biopsy for small renal tumors have been reported. However, there have been few reports of passive biopsy for renal tumors without clear pretreatment histological characterization based on imaging studies due to the rarity of these tumors. In this study, we examined the background, accuracy, adverse events and patient prognosis associated with such biopsies.


Japanese patients with renal tumors histological characteristics of which were unclear on imaging prior to treatment were enrolled in this study and analyzed retrospectively. The study population consisted of 24 renal cell carcinoma patients and 13 non-renal cell carcinoma patients.


Although the percentage of hypervascularity was significantly higher in clear cell renal cell carcinoma compared with the other neoplasms (P < 0.001), there were no significant differences between renal cell carcinoma and non-renal cell carcinoma with regard to hypervascularity, hydronephrosis, venous thrombus, hematuria or metastasis. The histological results in eight of nine (89%) nephrectomy patients were in accordance with those of biopsies. The median survival time of all 37 patients was 21 months and the 5-year survival rate was 31.1%. The 5-year survival rates of nephrectomy patients and non-nephrectomy patients were 75 and 0%, respectively. The overall survival of nephrectomy patients was significantly better than that of non-nephrectomy patients (P = 0.003).


Biopsy of renal tumors is safe and accurate regardless of the type of guidance and nephrectomy after appropriate diagnosis by biopsy contributed to longer survival.

  T Kobayashi , T Inoue , Y Shimizu , N Terada , A Maeno , Y Kajita , T Yamasaki , T Kamba , Y Toda , Y Mikami , T Yamada , T Kamoto , O Ogawa and E. Nakamura

We and others previously showed that signaling through cSrc or atypical protein kinase C (aPKC) pathway regulates the proliferation of prostate cancer cells and is associated with their progression to castrate-resistance in vivo. However, the interrelation of these two kinases has been largely unexplored. In the present study, we show that androgen-induced activation of cSrc regulates the activity of aPKC through the small molecular weight G protein Rac1 in androgen-dependent LNCaP cells. Knockdown of cSrc in those cells reduces the phosphorylation of aPKC and the abundance of activated form of Rac1. Additionally, the treatment of those cells with Rac1 inhibitor repressed cell cycle progression at G1/S transition. In fact, forced expression of a constitutively active Rac1 mutant in LNCaP cells promoted cell proliferation under androgen-depleted conditions both in vitro and in vivo. Moreover, LNCaP C4-2 and AILNCaP cells, the syngeneic androgen-independent sublines from LNCaP cells, harbored abundant Rac1-GTP. Importantly, the inhibition of Rac1 suppressed cell proliferation and induced apoptotic cell death in all prostate cancer cell lines tested irrespective of their androgen-dependence. In immunohistochemical evaluation of tumor specimens from prostate cancer patients, Rac1 pathway appeared to be activated in the majority of castrate-resistant diseases. Collectively, our present results both in vitro and in vivo highly implicate that Rac1 can be a potential therapeutic target for patients with advanced prostate cancer, especially those with castrate-resistant status.

  C Shimono , R. i Manabe , T Yamada , S Fukuda , J Kawai , Y Furutani , K Tsutsui , K Ikenaka , Y Hayashizaki and K. Sekiguchi

The C1q family is characterized by the C-terminally conserved globular C1q (gC1q) domain. Although more than 30 C1q family proteins have been identified in mammals, many of them remain ill-defined with respect to their molecular and biological properties. Here, we report on a novel C1q family protein specifically expressed in the central nervous system (CNS), which we designated neural C1q-like protein (nCLP) 2. nCLP2 was secreted as disulphide-bonded multimers comprising trimeric units. The multimers were stabilized by interchain disulphide bonds involving the cysteine residues in the N-terminal variable region and the C-terminal gC1q domain. The expression of nCLP2 was restricted to several brain regions and retina, including regions associated with memory formation (i.e. hippocampus, entorhinal cortex, anterodorsal thalamic nucleus). Immunoelectron microscopy revealed that nCLP2 was localized in the mossy fibre axons of hippocampal granule cells and their synaptic boutons and clefts, implying that nCLP2 was anterogradely transported in mossy fibres and secreted from the presynaptic termini. These results suggest that nCLP2 plays roles in synaptic function and maintenance in the CNS.

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