ライフサイエンスコーパス: nerve agent

1 talytic activity against an authentic V-type nerve agent.

2 s of the o-alkyl identifier specific to each nerve agent.

3 lyze diisopropyl phosphofluoridate and other nerve agents.

4 unds, including fluorine-containing chemical nerve agents.

5 tic against the toxicity of chemical warfare nerve agents.

6 es not protect against parathion/paraoxon or nerve agents.

7 pyridostigmine bromide (PB), pesticides, and nerve agents.

8 ounds, including insecticide metabolites and nerve agents.

9 hosphonate (DMMP) that simulates phosphonate nerve agents.

10 ChEs inhibited by six different G and V type nerve agents.

11 rochemical biosensor device able to quantify nerve agents.

12 PTE) for the hydrolysis of organophosphonate nerve agents.

13 monitoring of organophosphate pesticides and nerve agents.

14 por-phase detection of organophosphorus (OP) nerve agents.

15 tor-free, membrane-free biosensor for V-type nerve agents.

16 ent of fluorescent biosensors for monitoring nerve agents.

17 variety of organophosphate insecticides and nerve agents.

18 r their ability to hydrolyze organophosphate nerve agents.

19 ding organophosphate pesticides and military nerve agents.

20 catalyzes the hydrolysis of organophosphate nerve agents.

21 ydrolysis of organophosphorus pesticides and nerve agents.

22 as insecticides and, unfortunately, also as nerve agents.

23 es for the detoxification of organophosphate nerve agents.

24 sterase (AChE) inhibited by organophosphorus nerve agents.

25 ed thus far for the detoxification of G-type nerve agents.

26 countermeasure against the organophosphorus nerve agents.

27 ocess, called "aging", which dealkylates the nerve agent adduct and results in a product that is high

28 erum as a means of identifying and measuring nerve agent adducts to human BuChE is presented here.

29 Analyte stability of nerve agent adducts was also evaluated, and the results

30 selected beads associated with hydrolysis of nerve agent analogs in assays performed in 100,000-well

31 We further use stereoselective nerve agent analogs to establish that hCE1 exhibits a 17

32 e kinetic constants obtained with the chiral nerve agent analogues accurately predict the improved ac

33 A series of enantiomerically pure chiral nerve agent analogues containing the relevant phosphoryl

34 cation of the more toxic S(P)-enantiomers of nerve agent analogues for GB, GD, GF, VX, and VR than th

35 mortality associated with organophosphorous nerve agent and pesticide exposure of animal subjects of

36 ed on the enzyme-catalyzed hydrolysis of the nerve agents and amperometric detection of the thiol-con

37 ent in countering weaponized organophosphate nerve agents and detecting commercially-used OP pesticid

38 rolysis of a wide variety of organophosphate nerve agents and insecticides.

39 However, parent nerve agents and known metabolites are generally rapidly

40 Toxicity from acute exposure to nerve agents and organophosphorus toxicants is due to ir

41 as well as to differentiate between the real nerve agents and other related compounds.

42 rs for prophylaxis against organophosphorous nerve agents and pesticides has progressed from the benc

43 Intoxication by organophosphate (OP) nerve agents and pesticides should be addressed by effic

44 icholinesterases including organophosphorous nerve agents and pesticides toward these BChE variants r

45 ring and diagnosis of potential exposures to nerve agents and pesticides.

46 ence sensitivity to specific insecticides or nerve agents and risk for cardiovascular disease.

47 m a field site known to have been exposed to nerve agents and subsequently cleaned up.

48 aordinarily effective for the degradation of nerve agents and their simulants.

49 y have been exposed to low gaseous levels of nerve agents and those unlikely to have been exposed.

50 Terrorist use of organophosphorus-based nerve agents and toxic industrial chemicals against civi

51 nerve agents (G-series, V-series, and "new" nerve agents), and blistering and incapacitating warfare

52 othioate) is a highly toxic organophosphorus nerve agent, and even low levels of contamination in wat

53 t is ideal for the catalytic deactivation of nerve agents, and it shows great promise as a new generi

54 odels that is frequently used for conducting nerve agent antidote evaluations.

55 ne and analyze prereaction conformers of the nerve agent antidote HI-6 in complex with Mus musculus A

56 Nerve agent antidotes are available in prepackaged autoi

57 Since the evaluation of nerve agent antidotes cannot be conducted in humans, res

58 The published evidence on the use of nerve agent antidotes consists of case reports, extrapol

59 examines the evidence supporting the use of nerve agent antidotes in children.

60 Nerve agents are discussed.

61 Pesticides and certain stereoisomers of nerve agents are expected to undergo aging by breaking t

62 Organophosphorus (OP) nerve agents are potent toxins that inhibit cholinestera

63 Organophosphorus acid anhydride (OP) "nerve agents" are rapid, stoichiometric, and essentially

64 agement of a mass casualty event caused by a nerve agent as shown in the social media.

65 catalyzes the hydrolysis of organophosphate nerve agents at rates approaching the diffusion-controll

66 cacious antidote delivery system following a nerve agent attack.

67 sure to organophosphorus (OP) pesticides and nerve agents based on a magnetic bead (MB) immunosensing

68 biosensor for organophosphate pesticides and nerve agents based on self-assembled acetylcholinesteras

69 Our results show that OP pesticides and nerve agents bind covalently to human albumin at Tyr411.

70 ariant versions of this enzyme with enhanced nerve agent binding and hydrolysis functions.

71 ) compounds, e.g., insecticides and chemical nerve agents, by directly detecting organophosphorylated

72 Alternatively, the enzyme-nerve agent complex can undergo a secondary process, cal

73 ting the neutral nitroaromatic explosive and nerve agent compounds, an operation without SDS leads to

74 of the total content of organic explosive or nerve agent compounds, as well as detailed micellar chro

75 parating and detecting toxic organophosphate nerve agent compounds, based on the coupling of a microm

76 the reactivation of human AChE inhibited by nerve agents containing bulky side chains GF, GD, and VR

77 d inexpensive tool for in situ assessment of nerve agent contamination.

78 ed measurements of the "total" explosives or nerve agent content.

79 ntly hydrolyze highly toxic organophosphorus nerve agents could potentially be used as medical counte

80 rystal structure of hCE1 in complex with the nerve agent cyclosarin.

81 y efficiencies for methyl phosphonate (MPA), nerve agent degradate, and ethylhydrogen dimethylphospho

82 as investigated for several chemical warfare nerve agent degradation analytes on indoor surfaces and

83 The persistence of chemical warfare nerve agent degradation analytes on surfaces is importan

84 We report the development of analyses for nerve agent degradation products or related species by t

85 detection of low-energy ionic explosives and nerve agent degradation products.

86 evice for the screening of organophosphonate nerve agent degradation products.

87 CE1 to act as protein-based therapeutics for nerve agent detoxification.

88 Here we report that for the first time, a nerve agent detoxifying enzyme, organophosphorus acid an

89 es paraoxon, parathion, and dimefox, and the nerve agents DFP, tabun, sarin, cyclosarin, soman, VX, a

90 Highly toxic OP nerve agents (e.g., sarin) are a significant current ter

91 onfirmed that the analogues mimic the parent nerve agents effectively.

92 l BuChE nonapeptides was calculated for each nerve agent-exposed serum sample using data collected in

93 MeP-P found in clinical samples suspected of nerve agent exposure and subjected to such post-sampling

94 nd the time postevent that a confirmation of nerve agent exposure can be made with confidence.

95 The current treatments for nerve agent exposure must be administered quickly to be

96 The data reveal region-specific effects of nerve agent exposure on intracellular signaling pathways

97 nience set of 96 serum samples with no known nerve agent exposure was screened and revealed no baseli

98 te the applicability of the method to verify nerve agent exposure well after the exposure event, rats

99 The procedure allows confirmation of nerve agent exposure within 30 min from receiving a samp

100 ic methods to protect at-risk personnel from nerve agent exposure, and protein-based approaches have

101 individualizing patient results following a nerve agent exposure.

102 hydrolase and protein-based therapeutic for nerve agent exposure.

103 suffering postwar morbidity from subclinical nerve agent exposure.

104 have been developed for the verification of nerve agent exposure.

105 nzyme inhibition for biomonitoring of OP and nerve agent exposures.

106 (breakdown products of Sarin, Soman, and VX nerve agents) followed by their sensitive contactless co

107 ibe geographic areas of low level, vaporized nerve agent for 4 days after the destruction.

108 l that hCE1 binds stereoselectively to these nerve agents; for example, hCE1 appears to react prefere

109 s 7-9 (OP), akin in size and shape to G-type nerve agents, form inclusion complexes with baskets 1-3

110 s products and/or precursors of highly toxic nerve agents (G-series, V-series, and "new" nerve agents

111 ation curves (R(2) = 0.99 or better) for the nerve agents GA, GB, and VX as well as the blister agent

112 In preventing the lethality of nerve agents, galantamine was far more effective than py

113 tralization with monoethanolamine/water, the nerve agent GB (isopropyl methylphosphonofluoridate, Sar

114 The nerve agent GD (pinacolyl methylphosphonofluoridate, Som

115 n of these mutants with the authentic G-type nerve agents has confirmed the expected improvements in

116 e smoke exposure or possible exposure to the nerve agent hazard areas.

117 e inhibited by racemic mixtures of bona fide nerve agents, hCE1 spontaneously reactivates in the pres

118 r was evaluated as a long-term repository of nerve agent hydrolysis products.

119 y shown to be among the fastest catalysts of nerve-agent hydrolysis in solution.

120 st multiple lethal doses of chemical warfare nerve agents in vivo.

121 l effort aimed at destroying the arsenals of nerve agents, including soman and sarin.

122 his approach identifies specific targets for nerve agents, including substrates for Cdk5 kinase, whic

123 The reactivation of nerve agent-inhibited acetylcholinesterase (AChE) by oxi

124 imarily depends on its ability to reactivate nerve agent-inhibited AChE.

125 ible inhibitors of AChE into reactivators of nerve agent-inhibited AChE.

126 If the in vitro oxime reactivation of nerve agent-inhibited animal AChE is similar to that of

127 d sarin, cyclohexylsarin, VX, and Russian VX nerve agent-inhibited BuChE were synthesized for use as

128 differences observed in the reactivation of nerve agent-inhibited guinea pig and human AChEs were no

129 ences were observed in the rates of aging of nerve agent-inhibited guinea pig and human AChEs.

130 ium oximes showed that oxime reactivation of nerve agent-inhibited human AChE in most cases was faste

131 Nerve agent-inhibited quality control serum pools were c

132 Organophosphorus nerve agents interfere with cholinergic signaling by cov

133 surprising result given that no pesticide or nerve agent is known to yield phosphorylated serine with

134 scavengers as a pretreatment for exposure to nerve agents is a challenging medical objective.

135 ol-containing degradation products of V-type nerve agents is described.

136 cused organized approach to the treatment of nerve agents is key to its successful management.

137 or rapid and sensitive quantification of the nerve agent metabolites ethyl, isopropyl, isobutyl, cycl

138 nel possibly exposed to subclinical doses of nerve agents might be at increased risk for hospitalizat

139 Demeton-S was used as a nerve agent mimic.

140 ct, rapid, and selective detection of V-type nerve agents' mimic demeton-S.

141 00% of the animals challenged with the sarin nerve agent model compound that caused lethality in 6/11

142 vivo for protection against the toxicity of nerve agent model compounds.

143 erans who were near Khamisiyah, Iraq, during nerve agent munition destruction in March 1991.

144 s important, from indicating the presence of nerve agent on a surface to guiding environmental restor

145 od capable of detecting all organophosphorus nerve agent (OPNA) adducts to human butyrylcholinesteras

146 drolysis of G- and V-series organophosphorus nerve agents (OPNAs) containing a phosphorus-methyl bond

147 diagnosing exposure to the organophosphorus nerve agents (OPNAs) sarin (GB), cyclohexylsarin (GF), V

148 multaneous detection of the organophosphorus nerve agents (OPNAs) tabun (GA), sarin (GB), soman (GD),

149 olinesterase (hBChE) inhibited covalently by nerve agent OPs, sarin, cyclosarin, VX, and the OP pesti

150 Exposure to nerve agents or organophosphorus (OP) pesticides can hav

151 Several methods for the bioanalysis of nerve agents or their metabolites have been developed fo

152 strategy for light-induced sequestration of nerve agents or, perhaps, other targeted compounds.

153 eens for the directed evolution of efficient nerve agent organophosphatases.

154 rophosphate (DDFP)], a close analogue of the nerve agent organophosphate substrate diisopropyl fluoro

155 Insecticide and nerve agent organophosphorus (OP) compounds are potent i

156 s (nitroaromatic explosives, organophosphate nerve agents, phenols).

157 idence that veterans possibly exposed to the nerve agent plumes experienced unusual postwar morbidity

158 Children symptomatic of nerve agent poisoning will likely need both supraphysiol

159 the most important step in the treatment of nerve agent poisoning.

160 nd function to the cholinesterase targets of nerve agent poisoning.

161 res for sample matching of ten stocks of the nerve-agent precursor known as methylphosphonic dichlori

162 Nerve agent purity can be determined with a precision an

163 Veterans possibly exposed to nerve agents released by the Khamisiyah demolition were

164 yl ethylphosphonate (DEEP, a simulant of the nerve agent sarin) of at least 5 times higher than a sim

165 us musculus AChE covalently inhibited by the nerve agent sarin.

166 ially hydrolyzes the R(P) enantiomers of the nerve agents sarin (GB) and cyclosarin (GF) and their ch

167 Uniquely, KGeNb facilitates hydrolysis of nerve agents Sarin (GB) and Soman (GD) (and their less r

168 in 50% of those exposed for 30 min) for the nerve agents sarin (methylphosphonofluoridic acid, 1-met

169 lity of wild-type hCE1 to process the G-type nerve agents sarin and cyclosarin has not been determine

170 amples when measuring BChE inhibition by the nerve agents sarin and VX.

171 the determination of purity for the military nerve agents sarin, soman, and VX has been developed.

172 oducts of the highly toxic organophosphonate nerve agents sarin, soman, GF, VX, and rVX.

173 The organophosphorus nerve agents sarin, soman, tabun, and VX exert their tox

174 honic acid (MPA), the degradation product of nerve agents sarin, soman, VX, etc., was achieved with p

175 genic probes is able to discriminate between nerve agents, sarin, soman, tabun, VX and their mimics,

176 during the hydrolysis of a chemical warfare nerve agent simulant over a polyoxometalate catalyst.

177 sensitivity to dimethyl methylphosphonate (a nerve agent simulant).

178 nditions, 1 catalyzes both hydrolysis of the nerve agent simulant, diethyl cyanophosphonate (DECP) an

179 Paraoxon, chosen as nerve agent simulant, is linearly detected down to 3micr

180 atalytically active in the methanolysis of a nerve agent simulant.

181 A nerve-agent simulant based on a phosphate ester is hydro

182 udy of the adsorption and decomposition of a nerve-agent simulant, dimethyl methylphosphonate (DMMP),

183 The location of protonation on the nerve agent simulants diisopropyl methylphosphonate (DIM

184 uated for performance in the presence of the nerve agent simulants dimethylmethylphosphonate (DMMP) a

185 thanolysis and hydrolysis of phosphate-based nerve agent simulants was examined.

186 d when the microbeads are subjected to other nerve agent simulants, a mustard gas simulant, and volat

187 Two nerve agent simulants, diisopropyl methylphosphonate (DI

188 s used for the real-time detection of liquid nerve agent simulants.

189 he half-lives of a CWA simulant compound and nerve agent soman (GD) are as short as 7.3 min and 2.3 m

190 tively measure the hydrolysis product of the nerve agent Soman in water.

191 ), the predominant hydrolytic product of the nerve agent soman.

192 om the acute toxicity of lethal doses of the nerve agents soman and sarin, and of paraoxon, the activ

193 ydrolysed by PON1, which also hydrolyses the nerve agents soman and sarin.

194 insecticides as well as the P-F bond of the nerve agents soman and sarin.

195 The nerve agents soman, sarin, VX, and tabun are deadly orga

196 ed to monitor organophosphate pesticides and nerve agents, such as paraoxon.

197 Nerve agents, such as sarin, soman, tabun, and VX exert

198 e ultratrace quantitation of a thiophosphate nerve agent surrogate.

199 atrace quantitation of a phosphoryl fluoride nerve agent surrogate.

200 libration plots were observed for the V-type nerve agent thiol degradation products, along with good

201 is being pursued with the goal of preventing nerve agent toxicity and protecting against the long-ter

202 and stereoselectivity against the authentic nerve agents used in this study.

203 ction of organophosphate (OP) pesticides and nerve agents using zirconia (ZrO(2)) nanoparticles as se

204 e of these microbeads make them suitable for nerve agent vapor detection and inclusion into microbead

205 d wearable wireless tattoo and textile-based nerve-agent vapor biosensor systems offer considerable p

206 id warning regarding personal exposure to OP nerve-agent vapors in variety of decentralized security

207 The nerve agent VR yielded no aged adduct, supporting crysta

208 size (241 A(3)) and polar characteristics to nerve agent VX (289 A(3)).

209 The direct detection of the nerve agent VX (methylphosphonothioic acid, S-[2-[bis(1-

210 chemical warfare agents, the extremely toxic nerve agent VX (O-ethyl S-2-(diisopropylamino)ethyl meth

211 A study of the volatilization rate of the nerve agent VX (O-ethyl S-2-(N,N-diisopropylamino)ethyl

212 adrillion by volume (ppqv) concentrations of nerve agent VX vapor actively sampled from ambient air.

213 The best mutant hydrolyzed the racemic nerve agent VX with a value of kcat/Km = 7 x 10(4) M(-1)

214 ects on the reactions of the extremely toxic nerve agent VX with KF/Al2O3 powder were explored.

215 ic and persistent degradation product of the nerve agent VX.

216 ornica acetylcholinesterase inhibited by the nerve agent VX.

217 atalysts ever reported for the hydrolysis of nerve agent VX.

218 was characterized using the organophosphorus nerve agent VX.

219 rably better at catalyzing the hydrolysis of nerve agents VX and VR.

220 Nerve agents VX, GB, and GD hydrolyze to yield surface-b

221 The V-type nerve agents (VX and VR) are among the most toxic substa

222 enzyme electrode for the detection of V-type nerve agents, VX (O-ethyl-S-2-diisopropylaminoethyl meth

223 rase with the same series of organophosphate nerve agents was also measured.

224 e direct measurement of organophosphate (OP) nerve agents was developed by modifying a pH electrode w

225 le for direct measurement of organophosphate nerve agents was developed.

226 lyze phenyl acetate, paraoxon, and V-type OP nerve agents were examined.

227 The nerve agents were perhydrolyzed to the respective nontox

228 rogen fluoride, a decomposition component of nerve agents, were detected using a SiO(2) microcantilev

229 hydrolysis of a variety of organophosphorus nerve agents with high efficiency.

230 t catalyze the hydrolysis of organophosphate nerve agents with high-rate enhancements and broad subst

231 ve fluorogenic analogues of organophosphorus nerve agents with the 3-chloro-7-oxy-4-methylcoumarin le