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1 and mimicked by the NO-releasing compound 3-morpholinosydnonimine.
2 by NO donors [sodium nitroprusside (SNP), 3-morpholinosydnonimine-1, and S-nitrosoglutathione] in P1
3 after treatment with hydrogen peroxide or 3-morpholinosydnonimine, a free radical-generating agent.
4 aminoguanidine or S-methylisothiourea; b) 3-morpholinosydnonimine, a NO donor; c) S-methylisothioure
5 xpress myelin basic protein, we found that 3-morpholinosydnonimine, a peroxynitrite generator, caused
6 n with peroxynitrite or by incubation with 3-morpholinosydnonimine, a peroxynitrite generator, for 2
7 fect in animals with low cNOS activity; e) 3-morpholinosydnonimine, alone or together with S-methylis
8 r of nitric oxide and superoxide radicals (3-morpholinosydnonimine), an inhibitor of glutathione synt
10 of NAD with NADH in the presence of SIN-1 (3-morpholinosydnonimine) and dithiothreitol increased modi
13 mine, a NO donor; c) S-methylisothiourea + 3-morpholinosydnonimine; and d) antineutrophil antibody (t
14 ryl trinitrate, sodium nitroprusside, and 3'-morpholinosydnonimine, at clinically attainable concentr
17 utant was more sensitive than wild type to 3-morpholinosydnonimine hydrochloride (SIN-1 , a peroxynit
18 of oxidants, hydrogen peroxide (H(2)O(2)), 3-morpholinosydnonimine hydrochloride (SIN-1), 4-nitroquin
20 ons were exposed to PN or to the PN donor, 3-morpholinosydnonimine hydrochloride (SIN-1), and then as
21 at both authentic peroxynitrite and SIN-1 (3-morpholinosydnonimine hydrochloride), a molecule that de
22 side, S-nitroso-N-acetyl-penicillamine, or 3-morpholinosydnonimine, increased heme oxygenase-I (HO-1)
23 ive effects against hydrogen peroxide- and 3-morpholinosydnonimine-induced neurotoxicity, induction o
25 were more sensitive to a superoxide donor, 3-morpholinosydnonimine N-ethylcarbamide, than were CX-1 c
26 gnificantly lower in the peroxynitrite- or 3-morpholinosydnonimine-nitrated IL-10 group than in the I
27 of nitric oxide (NO) and superoxide (e.g., 3-morpholinosydnonimine; NONOates plus xanthine oxidase/hy
28 SSG) glutathione, and NO/O(2) (released by 3-morpholinosydnonimine)) on RyR1 redox state and activity
29 effect of an exogenous NO donator, sin-1 (3-morpholinosydnonimine), on canine and human LTMCs and on
31 oline transporters (CHTs) are inhibited by 3-morpholinosydnonimine (SIN-1) [peroxynitrite (ONOO(-)) d
32 n the detectable amount of .NO released by 3-morpholinosydnonimine (SIN-1) and cultured endothelial c
33 y H2O2 and the ONOO(-)-generating compound 3-morpholinosydnonimine (SIN-1) compared to strain 2308, i
35 cytotoxic action of ONOO- was mimicked by 3-morpholinosydnonimine (SIN-1) which liberates both nitri
37 prusside (SNP), diethylamine sodium (DEA), 3-morpholinosydnonimine (SIN-1), and S-nitroso-N-acetyl-pe
38 f chondrocytes with peroxynitrite (ONOO-), 3-morpholinosydnonimine (SIN-1), and sodium nitroprusside
39 rite radical released from streptozotocin, 3-morpholinosydnonimine (SIN-1), and superoxide radical pr
40 -nitroso-N-acetyl-dl-penicillamine (SNAP), 3-morpholinosydnonimine (SIN-1), or sodium nitroprusside (
42 S-nitroso-N-acetylpenicillamine (SNAP) or 3-morpholinosydnonimine (SIN-1); the NO scavenger, hydroxo
44 ns of sodium nitroprusside (SNP, n = 8) or 3-morpholinosydnonimine (SIN-1, n = 6) in isolated guinea
45 moderate concentrations of peroxynitrite, 3-morpholinosydnonimine (SIN-1; a superoxide- and nitric o
46 4016, NCX 4040, and NCX 4050) compared with morpholinosydnonimine (SIN-1; an NO donor) and aspirin (
48 eryl trinitrate, sodium nitroprusside, or 3'-morpholinosydnonimine, the stable metabolite of molsidom
49 of N-methyl-N'-nitro-N-nitrosoguanidine or 3-morpholinosydnonimine to induce DNA damage and PARP-1 ac
50 trite or the .NO and O2.- generator SIN-1 (3-morpholinosydnonimine) was inhibited more effectively by
51 -inducing agent such as hydrogen peroxide, 3-morpholinosydnonimine, xanthine/xanthine oxidase or lipo
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