ライフサイエンスコーパス: soman

1 fic neurodegeneration 24 h after exposure to soman.

2 minant hydrolytic product of the nerve agent soman.

3 the analogue for the chemical warfare agent soman.

4 seizurogenic dose of the anticholinesterase, soman.

5 y in response to the seizurogenic actions of soman.

6 hour and 24 hours after a convulsive dose of soman.

7 Rats were injected with either soman (100 microg/kg SC; equivalent to 0.9 LD50) or sali

8 hronic effects of a single acute exposure to soman (132 ug/kg, s.c., 1.2 x LD(50)) on neuroinflammati

9 ), akin in size and polar characteristics to soman (186 A(3)), was also found to bind to dual-cavity

10 ate constants for inactivation with P(S)C(S)-soman 4.3-, 11.8-, and 263-fold and with P(S)C(R)-soman

11 e injected with a single, convulsive dose of soman (77.7 micrograms/kg, i.m.).

12 A targeted method identified the aged soman adduct on serine 203 in peptide FGESAGAAS.

13 the initiation of seizures and gliosis after soman administration, predominantly by the activation of

14 The results demonstrate that following soman administration: (1) there is a rapid increase in g

15 s express Fos within 30-45 minutes following soman administration; (3) between 1 and 4 hours, resting

16 rence for the P(R) enantiomers of analogs of soman and cyclosarin, respectively, and a 5-fold prefere

17 is reversed for the hydrolysis of diazoxon, soman and especially sarin, thus changing the view of wh

18 xpressed rHu BChE in mouse blood neutralized soman and O-ethyl S-2-N,N-diisopropylaminoethyl methylph

19 The P(S) stereoisomers of soman and sarin are known to be the more toxic stereoiso

20 toxicity of lethal doses of the nerve agents soman and sarin, and of paraoxon, the active metabolite

21 PON1, which also hydrolyses the nerve agents soman and sarin.

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

23 ying the arsenals of nerve agents, including soman and sarin.

24 rmediate complexes with the chemical weapons soman and tabun.

25 erence for binding of the P(S)C(S) isomer of soman and the P(S) isomer of sarin was also noted.

26 phosphonic acid (PMPA; hydrolysis product of soman) and isopropyl methylphosphonic acid (IMPA; hydrol

27 Here we report the structures of paraoxon, soman, and sarin complexes of group-VIII phospholipase A

28 are formed with diisopropylfluorophosphate, soman, and sarin.

29 purity for the military nerve agents sarin, soman, and VX has been developed.

30 osphonic acids (breakdown products of Sarin, Soman, and VX nerve agents) followed by their sensitive

31 t may hydrolyze nerve poisons such as sarin, soman, and VX, monitoring the decontamination of organop

32 Aging of soman- and sarin-inhibited acetylcholinesterase occurs b

33 ,3-dimethylbutyl) methylphosphonofluoridate (soman) are (92 +/- 7) x 10(6) M-1 min-1 and (13.7 +/- 0.

34 nd microglia in brain regions susceptible to soman become rapidly "reactive" in response to seizures.

35 osphonylation were additive for PSCR or PRCR soman, but were cooperative for the PSCS stereoisomer.

36 4.3-, 11.8-, and 263-fold and with P(S)C(R)-soman by 6.5-, 47.3-, and 685-fold, respectively.

37 tic reactivation and aging resistance of the soman conjugate.

38 Rats exposed to soman developed behavioral expression of electrographic

39 E202Q MoAChE inactivated with the soman diastereomers yielded pK3 = 5.5-5.8.

40 were performed with the mixture of the four soman diastereomers, all labeled with tritium in Calpha.

41 Soman-exposed animals developed epilepsy, confirmed by h

42 Behavioral deficits and EEG changes in soman-exposed animals further emphasize the long-term ne

43 PMPA was detected in 6 of the 7 (one of the soman-exposed hair samples was completely consumed in th

44 MPA was positively identified in 100% of the soman-exposed rats (N = 8) and was not detected in any o

45 dy identifies critical chronic biomarkers of soman exposure affecting the brain, serum, CSF, liver, a

46 At 18-24 h after soman exposure, significant increases in T(2), a possibl

47 g a 9.4 T MRI on rats prior to and following soman exposure.

48 n at least 24 h prior, 1 h and 18-24 h after soman exposure.

49 to discern the exact role TRH has following soman exposure.

50 yielding a quantity sufficient for detecting soman exposure.

51 vealed significant memory deficits following soman exposure.

52 By 90-120 min after soman, Fos and GFAP staining increased bilaterally in PC

53 es hydrolysis of nerve agents Sarin (GB) and Soman (GD) (and their less reactive simulants, dimethyl

54 s of a CWA simulant compound and nerve agent soman (GD) are as short as 7.3 min and 2.3 min, respecti

55 lphosphonothiolate (VX), cyclosarin (GF) and soman (GD) respectively.

56 such as nerve agents sarin (GB), tabun (GA), soman (GD), and cyclosarin (GF), as well as the blister

57 tion of extremely toxic G-type nerve agents, Soman (GD), and simulant diisopropylfluorophosphate (DIF

58 ed nerve agents, such as VX, Sarin (GB), and Soman (GD), are among the most toxic chemicals to humank

59 nerve agents (OPNAs) tabun (GA), sarin (GB), soman (GD), cyclosarin (GF), VR, VX, and VM adducts to t

60 Organophosphate (OP) nerve agents, such as soman (GD), pose great risk to neurological health by in

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

62 ter the exposure event, rats were exposed to soman, hair was collected after approximately 30 days, a

63 Only G117H/E197Q catalyzed soman hydrolysis; all four soman stereoisomers as well a

64 entrapment of the organophosphonate, akin to soman in size (186 A(3)), triggers the transformation of

65 re the hydrolysis product of the nerve agent Soman in water.

66 By 45-60 min after soman, increased Fos and GFAP staining in PC was evident

67 ne (TRH) in epileptogenic sites, we examined soman-induced convulsion effects on CNS TRH.

68 nvolved in the initiation and maintenance of soman-induced convulsions.

69 ochemical and behavioral consequences of the soman-induced increases in TRH, especially in the fronta

70 In the present study, we determined that soman-induced seizures also cause selective, rapid activ

71 nd norepinephrine triggers the production of soman-induced seizures initially in the piriform cortex

72 To investigate the role of ACh in soman-induced seizures, we lesioned cholinergic neurons

73 lnerable to the pathological consequences of soman-induced seizures.

74 The dealkylation in soman-inhibited AChE at pH 5.0 +/- 0.2 and 25 degrees C

75 oncluded that Hupresin can be used to enrich soman-inhibited AChE solubilized from 8 mL of frozen hum

76 Dealkylation in soman-inhibited AChEs is estimated to occur at >10(10) t

77 Dealkylation in soman-inhibited BChE is consistent with the participatio

78 t the push-pull mechanism of dealkylation in soman-inhibited cholinesterases proposed previously.

79 Product analysis of dealkylation in P(S)C(S)-soman-inhibited electric eel acetylcholinesterase (AChE)

80 The rate constants for diastereomers of soman-inhibited trypsin at 37.0 +/- 0.2 degrees C are pH

81 Nearly symmetric pH curves for soman-inhibited wild-type and E197D Hu BChE gave pK2 = 3

82 One hour following soman injection, staining was more intense in the pirifo

83 By 24 hours following soman injection, there is marked neuropathology in the p

84 pinacolyl methylphosphonofluoridate (soman); soman is among the most toxic synthetic poisons known.

85 Soman is an organophosphorus (OP) compound which irrever

86 This suggests that the inhibition of AChE by soman leads to increased acetylcholine (ACh) and neurona

87 honofluoridic acid, 1-methylethyl ester) and soman (methylphosphonofluoridic acid, 1,2,2-trimethylpro

88 used for 20 mL of RBC AChE inhibited with a soman model compound.

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

90 ent GD (pinacolyl methylphosphonofluoridate, Soman), [pinacolyl = 2-(3,3-dimethyl)butyl] produces pin

91 Soman (pinacolymethylphosphonofluoridate), a highly pote

92 Soman (pinacolymethylphosphonofluoridate), a highly pote

93 he 10(4)-fold more lethal PS stereoisomer of soman relative to the PR form.

94 Prior to NMR analysis, the Soman samples were hydrolyzed to the less toxic pinacoly

95 aging is known in detail for the nerve gases soman, sarin, and tabun as well as the pesticide metabol

96 soon after acute exposure to lethal doses of soman, sarin, or paraoxon effectively and safely counter

97 The nerve agents soman, sarin, VX, and tabun are deadly organophosphorus

98 ited by pinacolyl methylphosphonofluoridate (soman); soman is among the most toxic synthetic poisons

99 H/E197Q catalyzed soman hydrolysis; all four soman stereoisomers as well as sarin and VX were substra

100 d 0.128 min-1 for the PR/SCR, PSCS, and PRCS soman stereoisomers, respectively, at pH 7.5, 25 degrees

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

102 Nerve agents, such as sarin, soman, tabun, and VX exert their toxicity by inhibiting

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

104 nerve agents DFP, tabun, sarin, cyclosarin, soman, VX, and Russian-VX.

105 e degradation product of nerve agents sarin, soman, VX, etc., was achieved with potentiometric measur

106 ants inactivated with P(S)C(S)- and P(S)C(R)-soman was compared.

107 thod for detection of nerve gases, Sarin and Soman, was proposed on the basis of their catalyzed hydr

108 In this study, different batches of the CWA Soman were synthesized from three distinctive pinacolyl

109 ,3-dimethylbutyl) methylphosphonofluoridate (soman) were studied at 4.0 +/- 0.2 degrees C.