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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
7          Here, we demonstrate that sulindac, sulindac sulfone and indomethacin activate the NF-kappaB
8 te, is required for the induction of SSAT by sulindac sulfone and is specifically bound by PPAR gamma
9 were exposed to a range of concentrations of sulindac sulfone and sulfoxide.
10  of human colon cancer cells with exisulind (sulindac sulfone) and related compounds induces apoptosi
11                                              Sulindac sulfone at 600 mumol/L inhibited 14-3-3epsilon
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
14 c enzyme, was induced by clinically relevant sulindac sulfone concentrations.
15                           We used the NSAIDs sulindac sulfone (COX-2-independent) and NS-398 (a COX-2
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
19                                              Sulindac sulfone (exisulind), although a nonsteroidal an
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
24                               Interestingly, sulindac sulfone has been reported to have cancer chemop
25 dac sulfide (a cyclooxygenase inhibitor) nor sulindac sulfone induced G(2)-M arrest, Bcl2 phosphoryla
26                                              Sulindac sulfone inhibited COX-2 protein expression, whi
27                    Sulindac sulfide, but not sulindac sulfone, inhibits cyclooxygenase (COX) enzyme a
28 These data suggest that apoptosis induced by sulindac sulfone is mediated, in part, by the COX-indepe
29                     Moreover, the effects of sulindac sulfone on various enzymes responsible for regu
30                                              Sulindac sulfone reduced cellular polyamine contents in
31             However, the mechanisms by which sulindac sulfone suppresses cancer growth are not as def
32  latency was also prolonged significantly by sulindac sulfone; the effect was particularly notable at
33                                              Sulindac sulfone was incorporated into a purified diet a
34            Treatment of IL-10(-/-) mice with sulindac sulfone (which does not inhibit PG production)
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
37 flammatory drug sulindac and its metabolite, sulindac sulfone, which were readily distinguished.

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