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   1 the apoptotic effect of sulindac sulfide and sulindac sulfone.                                       
     2 hypothesis, we studied the effect of dietary sulindac sulfone (500-2000 ppm), a metabolite of sulinda
     3 ide, a COX-1 and COX-2 inhibitor; exisulind (sulindac sulfone), a novel proapoptotic agent that does 
     4 support a specific chemopreventive effect of sulindac sulfone against mammary carcinogenesis and indi
     5  investigate the chemopreventive activity of sulindac sulfone against mammary carcinogenesis and to s
     6 e transformation assay, it was observed that sulindac sulfone also inhibited the formation of 7,12-di
  
     8 te, is required for the induction of SSAT by sulindac sulfone and is specifically bound by PPAR gamma
  
    10  of human colon cancer cells with exisulind (sulindac sulfone) and related compounds induces apoptosi
  
    12 is not required for the induction of SSAT by sulindac sulfone but can be bound by both PPAR delta and
    13 dac and its metabolites sulindac sulfide and sulindac sulfone can also inhibit the NF-kappaB pathway 
  
  
    16 e focused on a novel benzylamide analogue of sulindac sulfone, CP461, which is in clinical trials as 
    17  and mutational studies were done to map the sulindac sulfone-dependent response sequences in the SSA
    18 ic leukemia (CLL), we studied the effects of sulindac sulfone (exisulind), a non- cyclooxygenase-inhi
  
    20  investigate the chemopreventive efficacy of sulindac sulfone (exisulind), the sulfone metabolite of 
    21 uction of apoptosis in cancer cells, because sulindac sulfone (exisulind, Aptosyn) and certain deriva
    22 tment of SW480 human colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related der
    23 ves, or the cGMP phosphodiesterase inhibitor sulindac sulfone (exisulind, aptosyn, hereafter called e
  
    25 dac sulfide (a cyclooxygenase inhibitor) nor sulindac sulfone induced G(2)-M arrest, Bcl2 phosphoryla
  
  
    28 These data suggest that apoptosis induced by sulindac sulfone is mediated, in part, by the COX-indepe
  
  
  
    32  latency was also prolonged significantly by sulindac sulfone; the effect was particularly notable at
  
  
    35 anti-inflammatory drugs sulindac sulfide and sulindac sulfone, which attenuate beta-catenin transcrip
    36 ulindac sulfide or irreversible oxidation to sulindac sulfone, which lacks prostaglandin synthetase i
  
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