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1 , or the nonsteroidal anti-inflammatory drug flufenamic acid.
2 ated nonselective cation conductance blocker flufenamic acid.
3 dependent nonspecific cation current blocker flufenamic acid.
4 SCC blockers gadolinium and SKF96365 but not flufenamic acid.
5 d by the nonsteroidal anti-inflammatory drug flufenamic acid.
6 alpha- or LPS-induced NFkappaB activation by flufenamic acid.
7 d a nonselective cation current inhibited by flufenamic acid.
8 adenosine diphosphate-ribose and blocked by flufenamic acid.
9 ckers of Ca(2+)-activated chloride channels, flufenamic acid (100 microM) and 9-anthracene chloride (
12 oride (200 microM), gentamicin (220 microM), flufenamic acid (40 microM), niflumic acid (100 microM),
13 ) with N-methyl-d-glucamine and inhibited by flufenamic acid (50-200 microm), which is compatible wit
14 ro is eliminated after blockade of ICAN with flufenamic acid, 9-phenanthrol, or intracellular BAPTA.
15 er of swelling-activated Cl- channels and by flufenamic acid, a blocker of Cl- and nonselective catio
16 d the effect of PGE2 on sigh activity, while flufenamic acid, a blocker of the calcium-activated non-
17 brane changes were also largely prevented by flufenamic acid, a blocker of transient receptor potenti
19 ll-known TTR inhibitors has shown that while flufenamic acid affinity for TTR was unchanged by haloge
21 lished the modulatory effect on sighs, while flufenamic acid, an antagonist for the calcium-activated
22 ic calcium for activation, and is blocked by flufenamic acid, an antagonist of a previously identifie
24 antagonists, VRG activity was eliminated by flufenamic acid and could not be reliably restored by ad
26 ctive at depolarized voltages, stimulated by flufenamic acid and inhibited by tetraethylammonium; a v
28 ting and membrane current were attenuated by flufenamic acid and SKF96365, agents known to antagonize
29 uggest that the anti-inflammatory effects of flufenamic acid and some other NSAIDs are due to their i
31 ng agents (carbenoxolone, octanol, heptanol, flufenamic acid, and 18alpha-glycyrrhetinic acid) with a
32 thoxyphenethyl]-1H-imidazole hydrochloride), flufenamic acid, and 2-APB (2-aminoethyl diphenylborinat
33 NS004 and NS1619, phloretin, niflumic acid, flufenamic acid, and 5-nitro-2-(3-phenylpropylamino)benz
34 junction and hemichannel inhibitors octanol, flufenamic acid, and carbenoxolone significantly blocked
35 blockers (heptanol, octanol, carbenoxolone, flufenamic acid, and mefloquine) are antagonists of the
36 NSAIDs, including fenoprofen, ibuprofen, and flufenamic acid, are also PPARgamma ligands and induce a
37 ve at hyperpolarized voltages, stimulated by flufenamic acid, blocked by Ba2+, and insensitive to dil
41 ndependent and blocked by 100 microm Cd2+ or flufenamic acid (FFA) (10-200 microm), which suggests th
43 ity Ca2+ chelator, and the I(CAN) antagonist flufenamic acid (FFA) decreased the magnitude of drive p
44 hanistic insight into the crystallization of flufenamic acid (FFA) in a confined environment of mesop
47 inution of PIP(2) reduced it; sensitivity to flufenamic acid (FFA) suggested that these effects of PI
49 n in the presence of bath-applied 100 microM flufenamic acid (FFA), which attenuates a Ca(2+)-activat
51 n of the nonsteroidal anti-inflammatory drug flufenamic acid (FFA; 2-{[3-(trifluoromethyl)phenyl]amin
55 (ursodeoxycholate) and synthetic inhibitors (flufenamic acid, ibuprofen, and naproxen) was also readi
59 4-methoxyphenyl)propoxy]ethyl-1H-imidazole), flufenamic acid, lanthanum, and gadolinium, consistent w
60 ructural and biophysical methods to evaluate flufenamic acid, meclofenamic acid, mefenamic acid, and
61 and UV-visible spectroscopy demonstrate that flufenamic acid, mefenamic acid, and tolfenamic acid are
62 mponent of substrate-selective inhibition by flufenamic acid, mefenamic acid, and tolfenamic acid.
63 y, we report that other fenamates, including flufenamic acid, mefenamic acid, tolfenamic acid, meclof
67 ckers 2-APB (2-aminoethyl diphenylborinate), flufenamic acid, SKF96365 (1-[beta-[3-(4-methoxyphenyl)p
69 he crystal structures of cocaine, flutamide, flufenamic acid, the K salt of penicillin G, and form 4
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