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1 bonds at rates that rival the hydrolysis of paraoxon.
2 laucoma drug echothiophate and the pesticide paraoxon.
3 rocatalytic activity toward the reduction of paraoxon.
4 ter inhibition by the organophosphorus agent paraoxon.
5 ampal kainate and systemic administration of paraoxon.
6 sing platform was developed for detection of paraoxon.
7 osarin, VX, and the OP pesticide metabolite, paraoxon.
8 agnitude lower than with its best substrate, paraoxon.
9 results in 340-fold enhanced reactivity for paraoxon.
10 the kinetic constants for the hydrolysis of paraoxon.
11 nsecticides such as the parathion metabolite paraoxon.
12 osphate pesticides and nerve agents, such as paraoxon.
13 ve to inhibition by organophosphates such as paraoxon.
14 sian blue nanoparticles for the detection of paraoxon.
15 -nitrophenyl acetate, and the organophospate paraoxon.
16 tants such as 1,2-dichloroethane (72 years), paraoxon (13 months), atrazine (5 months), and aziridine
17 ased device was applied for the detection of paraoxon, 2,4-dichlorophenoxyacetic acid, and atrazine a
18 paper-based platform was employed to detect paraoxon, 2,4-dichlorophenoxyacetic acid, and atrazine b
20 ies, obtaining satisfactory values (e.g. for paraoxon 90 +/- 1% and 88 +/- 2%, for 10 and 20 ppb, res
21 the identical experiment was performed with paraoxon, a "penetrating" AChE inhibitor, high K+ still
24 of achiral, chiral, and racemic mixtures of paraoxon analogues containing various combinations of me
27 limit was found to be ~0.5 for OP pesticide paraoxon and 1 muM for non-OP pesticide carbaryl, in a w
31 domonas diminuta catalyzes the hydrolysis of paraoxon and related acetylcholinesterase inhibitors wit
34 n explants with the organophosphate compound paraoxon and uncovered a unique mechanism of neurotoxici
36 d excess of diethyl 4-nitrophenyl phosphate (paraoxon) and subsequent dealkylation, the broad 16.1 pp
37 des like chlorpyrifos, malathion, parathion, paraoxon, and carbaryl which are present in food and env
39 conjugates formed by sarin, cyclosarin, VX, paraoxon, and tabun are enhanced severalfold in vitro.
41 terference from lead, cadmium, atrazine, and paraoxon, and without matrix effect in drinking, surface
46 araoxonase 1 (PON1) activity determined with paraoxon as substrate has been found to be associated wi
48 irreversibly inhibited by echothiophate and paraoxon, but G117H regained 100% activity within 2-3 mi
49 substitution enhances ySFGH reactivity with paraoxon by >1000-fold ( k i (W197I) = 16 +/- 2 mM (-1)
50 c activity of Dr-OPH toward ethyl and methyl paraoxon by 126- and 322-fold and raised the specificity
52 000-fold for hydrolysis of echothiophate and paraoxon by the G117H mutant compared to the nonenzymati
55 try and paraoxon as a model organophosphate, paraoxon concentrations as low as 8 x 10(-7) M could be
56 inear relationship with the logarithm of the paraoxon concentrations in the range of 0.05-50mugL(-1)
57 organophosphate (sarin, cyclosarin, VX, and paraoxon) conjugates of human acetylcholinesterase (hACh
58 ic/fluorescence approach was established for paraoxon detection with no interference from redox subst
60 d for all of the mutants with the substrates paraoxon, diethylphenylphosphate, acephate, and diisopro
61 exposure to lethal doses of soman, sarin, or paraoxon effectively and safely counteracted their toxic
63 s employed for the amperometric detection of paraoxon-ethyl, fenitrothion and chlorpyrifos ranging fr
68 anato-4-methylcoumarin) for the detection of paraoxon in aqueous solution, ranging from 10(-9) to 10(
69 easuring the hydrolysis of phenylacetate and paraoxon in serum samples of 87 patients with type 2 DM
70 roduction from hydrolysis of an insecticide, paraoxon, in a coupled assay involving phosphotriesteras
71 properties of the developed electrode toward paraoxon indicated that the nanocomposite possesses a pr
73 drolysis and oxidation of acetylcholine, and paraoxon-induced inhibition of acetylcholinesterase acti
80 VR inhibits H115W HuPON1 competitively when paraoxon is the substrate and noncompetitively when VX i
81 ncement of the rates of phosphorylation with paraoxon ( k i = 42 or 80 mM (-1) h (-1), respectively)
82 Km of (2.0 +/- 1.3) x 10(-1) M(-1)s(-1)) and paraoxon (kcat/Km of (4.6 +/- 0.8) x 10(3) M(-1)s(-1)),
84 2000 V, baseline resolution is observed for paraoxon, methyl parathion, fenitrothion, and ethyl para
86 optimized conditions, the biosensor measured paraoxon, parathion, and coumaphos pesticides with high
87 his set included analogues of the pesticides paraoxon, parathion, and dimefox, and the nerve agents D
88 ble microplate format with three substrates: paraoxon, phenyl acetate and the lactone dihydrocoumarin
89 ociation between PON1 substrate specificity (paraoxon/phenylacetate substrate activity ratios) and -9
91 d pesticide diethyl-4-nitrophenyl phosphate (Paraoxon) promoted by 1,2,4-triazole (TAZ) was investiga
92 The Arg192 (R192) PON1 isoform hydrolyses paraoxon rapidly, while the Gln192 (Q191) isoform hydrol
98 with IC50 = 10(-7) M for the organophosphate paraoxon, similar to mammalian cell culture-derived AChE
102 icate that low PON1 activity determined with paraoxon substrate is independently associated with SLE
103 ith findings in controls, PON1 activity with paraoxon substrate was reduced both in white lupus patie
104 ose proximity to the pro-S-ethoxy arm of the paraoxon substrate, was mutated to arginine, alanine, hi
106 ys catalytic constants for the hydrolysis of paraoxon that are essentially the same as those of the w
107 of the nerve agents soman and sarin, and of paraoxon, the active metabolite of the insecticide parat
108 he substrate and can range from 6000 s-1 for paraoxon to 0.03 s-1 for the slower substrates such as d
110 could efficiently catalyze the hydrolysis of paraoxon to yellow p-nitrophenol, which further reduced
111 d inhibitor 4-nitrophenyl diethyl phosphate (paraoxon) to the free enzyme at pH 7.5, and subsequent d
112 ly hydrolyse 4-methylumbelliferyl acetate in paraoxon-treated cells, while the native enzyme was foun
113 ilar antiepileptogenic effect was found when paraoxon-treated rats were exposed to isoflurane after S
115 cally toward the pesticides ethyl and methyl paraoxon, using structure-based and random approaches.
116 es for the mutant enzymes with the substrate paraoxon varied from near wild type values to a 4-order
117 H on the cell surface degraded parathion and paraoxon very effectively without any diffusional limita
121 plete protection against the lethal doses of paraoxon was observed with nano-OPH administered iv and
124 relation to neutral hydrolysis of DEDNPP and Paraoxon were observed, respectively, consistent with al
125 N1s are better able to promote hydrolysis of paraoxon, whereas HuPON1 is considerably better at catal
126 drolase (OPH), and to detect the presence of paraoxon, which is an organophosphorus compound, using t
128 F26G/C72I mutant catalyzed the hydrolysis of paraoxon with a kcat of 1.14 min-1, an increase of 16-fo
129 ound to catalyze the very slow hydrolysis of paraoxon with values of kcat and kcat/Km of 0.07 min-1 a
130 N male mice challenged with a lethal dose of paraoxon, with complete elimination of short-term clinic