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Articles by Y Ishikawa
Total Records ( 5 ) for Y Ishikawa
  S Yamamoto , S Kawakami , J Yonese , Y Fujii , T Tsukamoto , Y Ohkubo , Y Komai , Y Ishikawa and I. Fukui

The aim of this study was to assess the surgical outcome of high-grade prostate cancer (PCA) treated with antegrade radical prostatectomy with intended wide resection (aRP) and to establish the risk stratification.


A consecutive 77 Japanese patients with Gleason score 8–10 PCA were treated with aRP alone and excluding patients with persistently elevated prostate-specific antigen (PSA), prospectively observed without any treatment until PSA failure was confirmed. PSA failure-free, cancer-specific and overall survival curves were generated with Kaplan–Meier method and the difference between groups was assessed with log-rank test. Cox's proportional hazards model was used to elucidate predictors of PSA failure.


During a median follow-up of 6 years, PSA failure was observed in 41 (53%) of the 77 patients. Five- and 10-year PSA failure-free survival rates of the entire cohort were 44.6% and 40.1%, respectively. Both overall and cancer-specific survival rates of the entire cohort at 5 and 10 years were 96.8% and 87.9%, respectively. In a multivariate analysis, PSA (P = 0.008), specimen confinement (SC) (P = 0.006) and persistently elevated PSA after aRP were identified as significant and independent predictors of PSA failure. When stratifying patients into three risk groups according to PSA level and SC status, PSA failure-free survival rate in patients with PSA < 10 ng/ml and specimen-confined disease (SCD) was significantly better than that in those of any other groups.


Good prognosis can be expected in patients with high-grade PCA treated with aRP alone when PSA < 10 ng/ml and the tumor was removed as an SCD.

  K Abe , K Osakabe , Y Ishikawa , A Tagiri , H Yamanouchi , T Takyuu , T Yoshioka , T Ito , M Kobayashi , K Shinozaki , H Ichikawa and S. Toki

BRCA2 is a breast tumour susceptibility factor with functions in maintaining genome stability through ensuring efficient double-strand DNA break (DSB) repair via homologous recombination. Although best known in vertebrates, fungi, and higher plants also possess BRCA2-like genes. To investigate the role of Arabidopsis BRCA2 genes in DNA repair in somatic cells, transposon insertion mutants of the AtBRCA2a and AtBRCA2b genes were identified and characterized. atbrca2a-1 and atbrca2b-1 mutant plants showed hypersensitivity to genotoxic stresses compared to wild-type plants. An atbrca2a-1/atbrca2b-1 double mutant showed an additive increase in sensitivity to genotoxic stresses compared to each single mutant. In addition, it was found that atbrca2 mutant plants displayed fasciation and abnormal phyllotaxy phenotypes with low incidence, and that the ratio of plants exhibiting these phenotypes is increased by -irradiation. Interestingly, these phenotypes were also induced by -irradiation in wild-type plants. Moreover, it was found that shoot apical meristems of the atbrca2a-1/atbrca2b-1 double mutant show altered cell cycle progression. These data suggest that inefficient DSB repair in the atbrca2a-1/atbrca2b-1 mutant leads to disorganization of the programmed cell cycle of apical meristems.

  M. A Kheirbek , J. A Beeler , W Chi , Y Ishikawa and X. Zhuang

In appetitive Pavlovian learning, animals learn to associate discrete cues or environmental contexts with rewarding outcomes, and these cues and/or contexts can potentiate an ongoing instrumental response for reward. Although anatomical substrates underlying cued and contextual learning have been proposed, it remains unknown whether specific molecular signaling pathways within the striatum underlie one form of learning or the other. Here, we show that while the striatum-enriched isoform of adenylyl cyclase (AC5) is required for cued appetitive Pavlovian learning, it is not required for contextual appetitive learning. Mice lacking AC5 (AC5KO) could not learn an appetitive Pavlovian learning task in which a discrete signal light predicted reward delivery, yet they could form associations between context and either natural or drug reward, which could in turn elicit Pavlovian approach behavior. However, unlike wild-type (WT) mice, AC5KO mice could not use these Pavlovian conditioned stimuli to potentiate ongoing instrumental behavior in a Pavlovian-to-instrumental transfer paradigm. These data suggest that AC5 is specifically required for learning associations between discrete cues and outcomes in which the temporal relationship between conditioned stimulus (CS) and unconditioned stimulus (US) is essential, while alternative signaling mechanisms may underlie the formation of associations between context and reward. In addition, loss of AC5 compromises the ability of both contextual and discrete cues to modulate instrumental behavior.

  H Yanai , K Nakamura , S Hijioka , A Kamei , T Ikari , Y Ishikawa , E Shinozaki , N Mizunuma , K Hatake and A. Miyajima

Delta-like 1 protein (Dlk-1), also known as preadipocyte factor 1 (Pref-1), is a transmembrane and secreted protein with epidermal growth factor (EGF)-like repeats. Dlk-1 is known to be expressed in foetal liver, but absent in neonatal and adult liver in mice and rats. Dlk-1 is also expressed in a subpopulation of hepatic oval cells, which are considered as stem/progenitor cells in rat adult liver. In this study, we generated monoclonal antibodies against human Dlk-1 (hDlk-1) and investigated hDlk-1 expression in human liver and hepatocellular carcinoma (HCC). Like rodent livers, hDlk-1 was detected in foetal liver, but not in adult liver. In HCC, hDlk-1 was positive for 20.5% of the cases examined and was localized in both cytoplasm and cell membrane, whereas hDlk-1 was undetected in viral hepatitis, nodular cirrhosis. Interestingly, hDlk-1 positive HCC was found more frequently in younger patients and its expression was correlated with alpha-fetoprotein expression. Furthermore, hDlk-1 was also detected frequently in colon adenocarcinomas (58%), pancreatic islet carcinoma (50%), and small cell lung carcinoma (50%). Thus, hDlk-1 is a cell surface protein expressed in many carcinomas including HCC and may be a potential target for monoclonal antibody therapy for carcinomas.

  Y Ishikawa , J Wirz , J. A Vranka , K Nagata and H. P. Bachinger

The rough endoplasmic reticulum-resident protein complex consisting of prolyl 3-hydroxylase 1 (P3H1), cartilage-associated protein (CRTAP), and cyclophilin B (CypB) can be isolated from chick embryos on a gelatin-Sepharose column, indicating some involvement in the biosynthesis of procollagens. Prolyl 3-hydroxylase 1 modifies a single proline residue in the chains of type I, II, and III collagens to (3S)-hydroxyproline. The peptidyl-prolyl cis-trans isomerase activity of cyclophilin B was shown previously to catalyze the rate of triple helix formation. Here we show that cyclophilin B in the complex shows peptidyl-prolyl cis-trans isomerase activity and that the P3H1·CRTAP·CypB complex has another important function: it acts as a chaperone molecule when tested with two classical chaperone assays. The P3H1·CRTAP·CypB complex inhibited the thermal aggregation of citrate synthase and was active in the denatured rhodanese refolding and aggregation assay. The chaperone activity of the complex was higher than that of protein-disulfide isomerase, a well characterized chaperone. The P3H1·CRTAP·CypB complex also delayed the in vitro fibril formation of type I collagen, indicating that this complex is also able to interact with triple helical collagen and acts as a collagen chaperone.

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