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Articles by K Nishimura
Total Records ( 6 ) for K Nishimura
  C Xu , B. E Shmukler , K Nishimura , E Kaczmarek , S Rossetti , P. C Harris , A Wandinger Ness , R. L Bacallao and S. L. Alper

Flow-induced cytosolic Ca2+ Cai2+ signaling in renal tubular epithelial cells is mediated in part through P2 receptor (P2R) activation by locally released ATP. The ability of P2R to regulate salt and water reabsorption has suggested a possible contribution of ATP release and paracrine P2R activation to cystogenesis and/or enlargement in autosomal dominant polycystic kidney disease (ADPKD). We and others have demonstrated in human ADPKD cyst cells the absence of flow-induced Cai2+ signaling exhibited by normal renal epithelial cells. We now extend these findings to primary and telomerase-immortalized normal and ADPKD epithelial cells of different genotype and of both proximal and distal origins. Flow-induced elevation of Cai2+ concentration ([Ca2+]i) was absent from ADPKD cyst cells, but in normal cells was mediated by flow-sensitive ATP release and paracrine P2R activation, modulated by ecto-nucleotidase activity, and abrogated by P2R inhibition or extracellular ATP hydrolysis. In contrast to the elevated ATP release from ADPKD cells in static isotonic conditions or in hypotonic conditions, flow-induced ATP release from cyst cells was lower than from normal cells. Extracellular ATP rapidly reduced thapsigargin-elevated [Ca2+]i in both ADPKD cyst and normal cells, but cyst cells lacked the subsequent, slow, oxidized ATP-sensitive [Ca2+]i recovery present in normal cells. Telomerase-immortalized cyst cells also exhibited altered CD39 and P2X7 mRNA levels. Thus the loss of flow-induced, P2R-mediated Cai2+ signaling in human ADPKD cyst epithelial cells was accompanied by reduced flow-sensitive ATP release, altered purinergic regulation of store-operated Ca2+ entry, and altered expression of gene products controlling extracellular nucleotide signaling.

  T Adachi , M Nakanishi , Y Otsuka , K Nishimura , G Hirokawa , Y Goto , H Nonogi and N. Iwai

Background: MicroRNAs (miRNAs) are endogenous small RNAs 21–25 nucleotides in length. Recently, we reported that miRNA 208 (miR-208) is produced exclusively in the rat myocardium and that plasma miR-208 is a biomarker of myocardial injury in rats. In the present study, we assessed the hypothesis that plasma concentrations of myocardial-specific miRNAs can be used to diagnose myocardial injury in humans.

Methods: We used array analysis of miRNA production in various human tissues to identify heart-specific miRNAs. We assessed the plasma concentrations of miR-499 in 14 individuals with acute coronary syndromes, 15 individuals with congestive heart failure, and 10 individuals without cardiovascular diseases. Plasma miR-499 concentrations were measured with a real-time reverse-transcription PCR method that used an artificial small RNA as an internal calibrator.

Results: The miRNA array analysis of various human tissues indicated that miR-499 was produced almost exclusively in the heart. Plasma miR-499 concentrations were measurably increased in all individuals with acute myocardial infarction but were below the limit of detection for all individuals in the other patient groups.

Conclusions: The plasma concentration of miR-499 may be a useful biomarker of myocardial infarction in humans.

  Y Nakai , N Nonomura , A Kawashima , M Mukai , A Nagahara , M Nakayama , H Takayama , K Nishimura and A. Okuyama

Non-muscle-invasive high-grade (T1G3) bladder cancers have high potential for progression. The objective of this study is to clarify the clinicopathological factors affecting the outcome of T1G3 bladder cancer.


We retrospectively reviewed 60 cases of T1G3 bladder cancer between 1994 and 2006. The correlations of both intravesical recurrence and progression with prognostic factors, such as T stage, history of bladder cancer, multiplicity, concomitant carcinoma in situ, tumor size, intravesical instillation of bacillus Calmette–Guérin and intravesical chemotherapy, were evaluated by multivariate analysis with the Cox proportional hazards model.


Median follow-up period was 52 months (4–105 months). Thirty-seven cases of intravesical recurrence (61.7%) were observed during follow-up. Two- and 5-year recurrence-free survival rates were 44.1% and 36.1%, respectively. Tumor multiplicity and instillation of bacillus Calmette–Guérin were significantly correlated with intravesical recurrence on multivariate analysis. Ten cases of progression (16.7%) were observed during the follow-up period. Two- and 5-year progression-free survival rates were 87.7% and 83.4%, respectively. Only tumor multiplicity was significantly correlated with progression on multivariate analysis.


T1G3 cancers with multiple lesions showed high risks of intravesical recurrence and progression. Although bacillus Calmette–Guérin instillation reduced the risk of intravesical recurrence, no effect was observed on disease progression.

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