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Articles by T Kubo
Total Records ( 5 ) for T Kubo
  T Kubo , Y Kuroda , H Shimizu , A Kokubu , N Okada , F Hosoda , Y Arai , Y Nakamura , H Taniguchi , K Yanagihara , I Imoto , J Inazawa , S Hirohashi and T. Shibata

The tyrosine kinase (TK) family is an important regulator of signaling pathways that control a variety of physiological and pathological conditions, and a substantial proportion of TK genes are genetically altered in cancer. To clarify the somatic mutation profile of TK genes and discover potential targets for gastric cancer (GC) therapy, we undertook a systematic screening of mutations in the kinase domains of all human TK genes (636 exons of 90 genes) in 17 GC cell lines and 52 microdissected primary GCs with poorly differentiated histology. We identified 26 non-synonymous alterations (22 genes in total) that included 11 sequence alterations in cell lines and 15 somatic mutations in primary tumors. Recurrent mutations were found in four genes including a known oncogene (NTRK3), the Src kinase family (LTK and CSK) and a potential Wnt signal activator (ROR2). In addition, we analyzed copy number alterations of all the TK gene loci in the same cohort samples by array-based comparative genomic hybridization analysis and identified 24 high-level amplifications and two homozygous deletions. Both sequence alteration and frequent copy number aberration were detected in two TK genes (HCK and ERBB2), strongly suggesting that they encode potential oncogenes in GC. Our focused and integrated analyses of systemic resequencing and gene copy number have revealed the novel onco-kinome profile of GC and pave the way to a comprehensive understanding of the GC genome.

  H Okura , K Asawa , T Kubo , H Taguchi , I Toda , M Yoshiyama , J Yoshikawa and K. Yoshida

Background— Plaque rupture may be present in the peripheral arteries of the patients at high risk for cardiovascular events and is possibly associated with vascular vulnerability.

Methods and Results— One hundred one iliofemoral arteries from 101 patients undergoing angioplasty were studied. Intravascular ultrasound imaging was performed before intervention. Plaque rupture was defined as presence of a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. Incidence, numbers, and location of the plaque rupture were investigated. Plaque rupture was found in 42 of 101 arteries (42%). Patients with plaque rupture had significantly higher prevalence of acute coronary syndrome than did patients without plaque rupture (42% vs 16%, P=0.01). By multivariable logistic regression analysis, acute coronary syndrome (P=0.004) and male sex (P=0.01) were independent clinical correlates of plaque rupture. During follow-up (median, 14.7 months), the incidence of major adverse cardiac or cerebrovascular events (death, myocardial infarction, and ischemic stroke) was similar between the 2 groups. The incidence of major adverse cardiac or cerebrovascular events plus peripheral vascular events (unplanned vascular intervention and amputation) was significantly higher in patients with plaque rupture than in patients without plaque rupture (46% vs 21%, P=0.008). By multivariable Cox regression analysis, plaque rupture (hazard ratio=2.80, 95% CI: 1.23 to 6.37, P=0.01) and Fontaine stage IV (hazard ratio=3.50, 95% CI: 1.58 to 7.71, P=0.002) were independent predictors of major adverse cardiac or cerebrovascular events plus peripheral vascular events.

Conclusions— Ruptured plaque of the iliofemoral arteries is a common finding. Patients with plaque rupture had a higher prevalence of history of acute coronary syndrome and lower major adverse cardiac or cerebrovascular events plus peripheral vascular event-free survival.

  C Oviedo , A Maehara , G. S Mintz , H Araki , S. Y Choi , K Tsujita , T Kubo , H Doi , B Templin , A. J Lansky , G Dangas , M. B Leon , R Mehran , S. J Tahk , G. W Stone , M Ochiai and J. W. Moses

Background— Angiographic classifications of the location and severity of disease in the main vessel and side branch of coronary artery bifurcations have been proposed and applied to distal left main coronary artery (LMCA) bifurcation.

Methods and Results— We reviewed 140 angiograms of distal LMCA and ostial left anterior descending (LAD) and left circumflex (LCX) artery lesions with preintervention intravascular ultrasound (IVUS) of both the LAD and LCX arteries as well as the LMCA. Of 140 patients, 92.9% had at least 1 cross section with ≥40% IVUS plaque burden versus 57.2% of patients with an angiographic diameter stenosis ≥50%. Contrary to angiographic classifications, IVUS showed that bifurcation disease was rarely focal and that both sides of the flow divider were always disease-free. Continuous plaque from the LMCA into the proximal LAD artery was seen in 90%, from the LMCA into the LCX artery in 66.4%, and from the LMCA into both the LAD and LCX arteries in 62%. Plaque localized to either the LAD or LCX ostium and not involving the distal LMCA was seen in only 9.3% of LAD arteries and 17.1% of LCX arteries. Plaque distribution was not influenced by the LAD/LCX angiographic angle, lesion severity, LMCA length, or remodeling. We proposed an IVUS classification for bifurcation lesions illustrating longitudinal and circumferential spatial plaque distribution.

Conclusions— Angiographic classification of LMCA bifurcation lesions is rarely accurate. IVUS shows that the carina is always spared and that the disease is diffuse rather than focal.

Clinical Trial Registration— URL: Unique identifier: NCT00180466.

  A Tanaka , T Imanishi , H Kitabata , T Kubo , S Takarada , T Tanimoto , A Kuroi , H Tsujioka , H Ikejima , K Komukai , H Kataiwa , K Okouchi , M Kashiwaghi , K Ishibashi , H Matsumoto , K Takemoto , N Nakamura , K Hirata , M Mizukoshi and T. Akasaka

Although some recent guidelines recommend an early invasive strategy for non-ST-segment elevation acute coronary syndrome (NSTEACS), several studies have failed to identify any benefit for very early intervention for NSTEACS. The no-reflow phenomenon may inhibit the expected benefit from very early recanalization for NSTEACS subjects. The aim of this study was to investigate whether optical coherence tomography (OCT) could predict no-reflow in patients with NSTEACS.

Methods and results

This study comprised 83 consecutive patients with NSTEACS who underwent OCT and successful emergent primary stenting. On the basis of post-stent TIMI flow, patients were divided into two groups: no-reflow group (n = 14) and reflow group (n = 69). Thin-cap fibroatheroma (TCFA) was defined as a plaque presenting lipid content for >90°, and with thinnest part of the fibrous cap measuring <70 µm. Thin-cap fibroatheroma were more frequently observed in the no-reflow group than in the reflow group (50% vs. 16%, P = 0.005). The frequency of the no-reflow phenomenon increases according to the size of the lipid arc in the culprit plaque. Final TIMI blush grade also deteriorated according to the increase in the lipid arc. A multivariable logistic regression model revealed that lipid arc alone was an independent predictor of no-reflow (odds ratio 1.018; CI 1.004–1.033; P = 0.01).


Optical coherence tomography can predict no-reflow after percutaneous coronary intervention (PCI) in NSTEACS. The lipid contents of a culprit plaque may play a key role in damage to the microcirculation after PCI for NSTEACS. From our results, it is found that OCT is useful tool for stratifying risk for PCI for NSTEACS.

  T Kubo , Y Uchida , Y Watanabe , M Abe , A Nakamura , M Ono , S Akira and T. Takai

Pathogens are sensed by Toll-like receptors (TLRs) expressed in leukocytes in the innate immune system. However, excess stimulation of TLR pathways is supposed to be connected with provocation of autoimmunity. We show that paired immunoglobulin (Ig)-like receptor B (PIR-B), an immunoreceptor tyrosine-based inhibitory motif–harboring receptor for major histocompatibility class I molecules, on relatively primitive B cells, B-1 cells, suppresses TLR9 signaling via Bruton's tyrosine kinase (Btk) dephosphorylation, which leads to attenuated activation of nuclear factor B p65RelA but not p38 or Erk, and blocks the production of natural IgM antibodies, including anti-IgG Fc autoantibodies, particularly rheumatoid factor. The autoantibody production in PIR-B–deficient (Pirb–/–) mice was further augmented in combination with the Faslpr mutation, which might be linked to the development of autoimmune glomerulonephritis. These results show the critical link between TLR9-mediated sensing and a simultaneously evoked, PIR-B–mediated inhibitory circuit with a Btk intersection in B-1 cells, and suggest a novel way toward preventing pathogenic natural autoantibody production.

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