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 PTE) for the hydrolysis of organophosphonate nerve agents.

12 monitoring of organophosphate pesticides and nerve agents.

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

14 ent of fluorescent biosensors for monitoring nerve agents.

15 r their ability to hydrolyze organophosphate nerve agents.

16 ding organophosphate pesticides and military nerve agents.

17 catalyzes the hydrolysis of organophosphate nerve agents.

18 ydrolysis of organophosphorus pesticides and nerve agents.

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

20 strips for on-site vapor-phase detection of nerve agents.

21 ication of MOF-based protective gear against nerve agents.

22 rochemical biosensor device able to quantify nerve agents.

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

24 variety of organophosphate insecticides and nerve agents.

25 es for the detoxification of organophosphate nerve agents.

26 sterase (AChE) inhibited by organophosphorus nerve agents.

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

28 countermeasure against the organophosphorus nerve agents.

29 Organophosphorus nerve agents, a class of extremely toxic chemical warfar

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

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

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

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

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

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

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

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

38 Organophosphate (OP) intoxications from nerve agent and OP pesticide exposures are managed with

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

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

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

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

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

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

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

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

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

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

49 osphorus compounds, such as chemical warfare nerve agents and pesticides, are known to cause neurolog

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

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

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

53 d thus detoxifying, several organophosphorus nerve agents and their simulants.

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

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

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

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

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

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

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

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

62 Nerve agent antidotes are available in prepackaged autoi

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

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

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

66 nt events demonstrated that organophosphorus nerve agents are a serious threat for civilian and milit

67 Organophosphorus nerve agents are among the most toxic chemicals known an

68 Nerve agents are discussed.

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

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

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

72 a range of toxic chemicals, including sarin nerve agent, are a suspected root cause of GWI.

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

74 apply this method to screen VX, VM, and RVX nerve agents as well as methomyl, a carbamate pesticide,

75 anophosphate compounds (pesticides and sarin nerve agent) as the most likely cause(s) of GWI.

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

77 cacious antidote delivery system following a nerve agent attack.

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

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

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

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

82 st chemical warfare agents (organophosphorus nerve agents, blistering agents, and their simulants) an

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

84 osure to high doses, found in pesticides and nerve agents, can be lethal.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 (MOFs) are candidate materials for effective nerve agent detoxification due to their thermo- and wate

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

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

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

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

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

106 cid, first pass hydrolysis products from the nerve agents ethyl N-2-diisopropylaminoethyl methylphosp

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

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

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

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

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

112 and therapeutic strategies for survivors of nerve agent exposure or OP pesticide poisoning.

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

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

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

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

117 individualizing patient results following a nerve agent exposure.

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

119 suffering postwar morbidity from subclinical nerve agent exposure.

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

121 athy, chronic obstructive pulmonary disease, nerve agent exposures, and cognitive disorders.

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

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

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

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

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

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

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

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

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

131 The nerve agent GD (pinacolyl methylphosphonofluoridate, Som

132 ent in the protection against an ultra-toxic nerve agent (GD) in permeability studies as compared to

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

134 Nerve agents have experienced a resurgence in recent tim

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

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

137 e transdermal analysis of drugs of abuse and nerve agents holds promise for rapid countermeasures for

138 This places Ti-MFU-4l as one of the best nerve agent hydrolysis catalysts of any MOF reported to

139 anic framework (MOFs) are the most prevalent nerve agent hydrolysis catalysts, and relatively few rep

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

141 olyester fibers exhibit the highest rates of nerve agent hydrolysis.

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

143 Therefore, the transport of nerve agents in nanopores is an important factor in the

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

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

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

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

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

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

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

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

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

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

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

155 Nerve agent-inhibited quality control serum pools were c

156 Organophosphorus nerve agents interfere with cholinergic signaling by cov

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

158 The VX nerve agent is one of the deadliest chemical warfare age

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

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

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

162 dates for the benzylation of phosphonic acid nerve agent markers under neutral, basic, and slightly a

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

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

165 the discriminative detection of phosgene and nerve agent mimic diethyl chlorophosphate (DCP) in photo

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

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

168 o trace amounts of acids, bases, amines, and nerve agent mimics.

169 00% of the animals challenged with the sarin nerve agent model compound that caused lethality in 6/11

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

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

172 Rapid and robust sensing of nerve agent (NA) threats is necessary for real-time fiel

173 n) for the colorimetric determination of the nerve agent neostigmine, with excellent analytical perfo

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

175 ion of opioid (OPi) and organophosphate (OP) nerve agents on a single patch platform.

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

177 n provide a novel alternative to existing OP nerve agent (OPNA) quantification methods.

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

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

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

181 ted, and a clear and present danger posed by nerve agent OPs has become palpable in recent years.

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

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

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

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

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

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

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

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

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

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

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

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

194 hing between episodes of opioid overdose and nerve agent poisoning.

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

196 Nerve agent purity can be determined with a precision an

197 This study measured nerve agent-related neuropathology and determined whethe

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

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

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

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

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

203 0 for the detection of various CWAs, such as nerve agents sarin (GB), tabun (GA), soman (GD), and cyc

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

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

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

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

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

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

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

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

212 The concentration enhancement for the nerve agent simulant 4-methylumbelliferyl phosphate (15.

213 subsequent hydrolysis of an organophosphorus nerve agent simulant at Ti(IV)-based active sites in bas

214 tic performance toward the hydrolysis of the nerve agent simulant dimethyl (4-nitrophenyl)phosphate (

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

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

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

218 sport process and mechanism of a vapor-phase nerve agent simulant, dimethyl methyl phosphonate (DMMP)

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

220 nt catalytic hydrolysis performance toward a nerve agent simulant.

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

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

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

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

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

226 In addition, these nanomaterials can adsorb nerve agent simulants in solution and as a coating on fa

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

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

229 Two nerve agent simulants, diisopropyl methylphosphonate (DI

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

231 or the liquid- and solid-state hydrolysis of nerve agent simulants.

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

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

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

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

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

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

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

239 olytic degradation of extremely toxic G-type nerve agents, Soman (GD), and simulant diisopropylfluoro

240 However, addition of nerve agents such as diethyl chlorophosphate (DCP, sarin

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

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

243 Organophosphate (OP) nerve agents, such as soman (GD), pose great risk to neu

244 Organophosphonate-based nerve agents, such as VX, Sarin (GB), and Soman (GD), ar

245 xyl to hexyl gradient, the neutral ambipolar nerve agent surrogate diethyl (cyanomethyl)phosphonate (

246 followed by a single injection of the sarin nerve agent surrogate, diisopropyl fluorophosphate.

247 atrace quantitation of a phosphoryl fluoride nerve agent surrogate.

248 e ultratrace quantitation of a thiophosphate nerve agent surrogate.

249 ammetric (SWV) detection of the fentanyl and nerve agent targets, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 ornica acetylcholinesterase inhibited by the nerve agent VX.

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

268 was characterized using the organophosphorus nerve agent VX.

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

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

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

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

273 Detection of sarin nerve agent was verified.

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

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

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

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

278 The nerve agents were perhydrolyzed to the respective nontox

279 Organophosphorus (OP) nerve agents were used for chemical warfare, assassinati

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

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

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

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