ライフサイエンスコーパス: sarin

1 between Glu202 and the O-isopropyl moiety of sarin.

2 imulant and a precursor for the synthesis of Sarin.

3 t that is estimated to be less volatile than sarin.

4 nhibition with the more toxic P(S) isomer of sarin.

5 with diisopropylfluorophosphate, soman, and sarin.

6 hyl phosphonate, which serves as a mimic for sarin.

7 cide paraoxon and the chemical warfare agent sarin.

8 h also hydrolyses the nerve agents soman and sarin.

9 s the P-F bond of the nerve agents soman and sarin.

10 rsenals of nerve agents, including soman and sarin.

11 AChE covalently inhibited by the nerve agent sarin.

12 a complexed with TMTFA (2.66 +/- 0.28 A) and sarin (2.53 +/- 0.26 A) and at low pH (2.52 +/- 0.25 A).

13 s preceded by a conformational change in the sarin adduct itself.

14 nown substrates are considered, paraoxon and sarin, although their turnover rates vary about 100-fold

15 a 5-fold preference for the P(S) isomer of a sarin analog.

16 P) and R(P) enantiomers of the analogues for sarin and cyclosarin for the wild-type PTE and the G60A,

17 type hCE1 to process the G-type nerve agents sarin and cyclosarin has not been determined.

18 enantiomer of the chromophoric analogues of sarin and cyclosarin, whereas the H254G/H257W/L303T (GWT

19 ergy surfaces for the alkaline hydrolysis of sarin and O,S-dimethyl methylphosphonothiolate, a VX mod

20 A new method for detection of nerve gases, Sarin and Soman, was proposed on the basis of their cata

21 gradation of chemical warfare agents such as sarin and sulfur mustard using metal-organic frameworks.

22 ed mixtures of chemical weapon agents (CWAs) sarin and sulfur mustard.

23 sis; all four soman stereoisomers as well as sarin and VX were substrates.

24 y potencies similar to traditional CWAs like sarin and VX, and ii) bipyridinium-based oximes can reac

25 ChE) as its more potent counterparts such as sarin and VX, but has low toxicity, making it more pract

26 easuring BChE inhibition by the nerve agents sarin and VX.

27 yzed the hydrolysis of several OP, including sarin and VX.

28 hemical warfare related compounds, including sarin, and compared to secondary electrospray ionization

29 f lethal doses of the nerve agents soman and sarin, and of paraoxon, the active metabolite of the ins

30 s known in detail for the nerve gases soman, sarin, and tabun as well as the pesticide metabolite iso

31 composition of adsorbed sulfur mustard (HD), sarin, and VX was achieved at ambient temperatures withi

32 The P(S) stereoisomers of soman and sarin are known to be the more toxic stereoisomers, as t

33 Highly toxic OP nerve agents (e.g., sarin) are a significant current terrorist threat, as sh

34 est that the cleavage of the covalent enzyme-sarin bond is preceded by a conformational change in the

35 spontaneously reactivates in the presence of sarin but not soman or cyclosarin.

36 eport the structures of paraoxon, soman, and sarin complexes of group-VIII phospholipase A2 from bovi

37 orvos, diisopropylfluorophosphate (DFP), and sarin covalently bind to human albumin.

38 n digest products for uninhibited BuChE, and sarin, cyclohexylsarin, VX, and Russian VX nerve agent-i

39 nd dimefox, and the nerve agents DFP, tabun, sarin, cyclosarin, soman, VX, and Russian-VX.

40 de for reactivation of four organophosphate (sarin, cyclosarin, VX, and paraoxon) conjugates of human

41 hE) inhibited covalently by nerve agent OPs, sarin, cyclosarin, VX, and the OP pesticide metabolite,

42 tion rates for OP-hAChE conjugates formed by sarin, cyclosarin, VX, paraoxon, and tabun are enhanced

43 Four compounds were evaluated in vivo using sarin-exposed rats.

44 h sarin was confirmed by reaction of racemic sarin, followed by gas chromatography/mass spectrometry

45 zes the R(P) enantiomers of the nerve agents sarin (GB) and cyclosarin (GF) and their chromophoric an

46 KGeNb facilitates hydrolysis of nerve agents Sarin (GB) and Soman (GD) (and their less reactive simul

47 ation levels of, for instance, 29 ppt(v) for sarin (GB) within an averaging time of only 1 s.

48 ophosphonate-based nerve agents, such as VX, Sarin (GB), and Soman (GD), are among the most toxic che

49 to the organophosphorus nerve agents (OPNAs) sarin (GB), cyclohexylsarin (GF), VX, and Russian VX (RV

50 ophosphorus nerve agents (OPNAs) tabun (GA), sarin (GB), soman (GD), cyclosarin (GF), VR, VX, and VM

51 ection of various CWAs, such as nerve agents sarin (GB), tabun (GA), soman (GD), and cyclosarin (GF),

52 2-PAM, in vitro potency for reactivation of Sarin (GB)-inhibited AChE and BChE.

53 ent GB (isopropyl methylphosphonofluoridate, Sarin) gives isopropyl methylphosphonic acid (IMPA) and

54 reversible ligands, or formation of an S(P)-sarin-hAChE conjugate had no effect on homodimerization.

55 Aging of soman- and sarin-inhibited acetylcholinesterase occurs by C-O bond

56 reases the rate of reactivation of hCE1 from sarin inhibition by more than 60-fold but has no effect

57 ose exposed for 30 min) for the nerve agents sarin (methylphosphonofluoridic acid, 1-methylethyl este

58 agents such as diethyl chlorophosphate (DCP, sarin mimic) and diethyl cyanophosphate (DCNP, Tabun mim

59 otected 100% of the mice challenged with the sarin model compound.

60 bles quantification of the OPNA metabolites, Sarin (NATO designation "G-series, B", or GB) and Venomo

61 cted 100% of the animals challenged with the sarin nerve agent model compound that caused lethality i

62 tress, followed by a single injection of the sarin nerve agent surrogate, diisopropyl fluorophosphate

63 Detection of sarin nerve agent was verified.

64 ed organophosphate compounds (pesticides and sarin nerve agent) as the most likely cause(s) of GWI.

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

66 phonate (DEEP, a simulant of the nerve agent sarin) of at least 5 times higher than a similar sensor

67 ter acute exposure to lethal doses of soman, sarin, or paraoxon effectively and safely counteracted t

68 hylphosphonylation by the R(P) enantiomer of sarin promotes a 10-fold increase in homodimer dissociat

69 ensitivity for dimethyl methylphosphonate (a Sarin simulant) detection using a sensor containing inor

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

71 ethylphosphonic acids (breakdown products of Sarin, Soman, and VX nerve agents) followed by their sen

72 mes that may hydrolyze nerve poisons such as sarin, soman, and VX, monitoring the decontamination of

73 highly toxic organophosphonate nerve agents sarin, soman, GF, VX, and rVX.

74 The organophosphorus nerve agents sarin, soman, tabun, and VX exert their toxic effects by

75 Nerve agents, such as sarin, soman, tabun, and VX exert their toxicity by inhi

76 s able to discriminate between nerve agents, sarin, soman, tabun, VX and their mimics, in water or or

77 PA), the degradation product of nerve agents sarin, soman, VX, etc., was achieved with potentiometric

78 1881 and 1994 for DFP, and 1838 and 1938 for sarin; these masses fit a mechanism whereby OP bound cov

79 hydrolysis of diazoxon, soman and especially sarin, thus changing the view of which PON1 isoform is c

80 The nerve agents soman, sarin, VX, and tabun are deadly organophosphorus (OP) co

81 )C(S) isomer of soman and the P(S) isomer of sarin was also noted.

82 The P(S) stereoselectivity for reaction with sarin was confirmed by reaction of racemic sarin, follow

83 On the night of 21 August 2013, sarin was dispersed in the eastern outskirts of Damascus

84 lpy of activation for alkaline hydrolysis of sarin was found.

85 ylphosphonic acid, the hydrolysis product of sarin, was also detected in blow flies 14 days post expo

86 phosphonic acid (IMPA; hydrolysis product of sarin) were extracted from hair samples with N,N-dimethy