ライフサイエンスコーパス: cholinesterase

1 e protein RIC-3 (resistance to inhibitors of cholinesterase).

2 its through mechanisms other than inhibiting cholinesterase.

3 ere mixed-type reversible inhibitors of both cholinesterases.

4 n endoplasmic reticulum retention of the two cholinesterases.

5 neurotransmission through inhibition of the cholinesterases.

6 bind covalently to the active-site serine of cholinesterases.

7 role in determining substrate specificity in cholinesterases.

8 hree or four major oligosaccharides in other cholinesterases.

9 ornica acetylcholinesterase, and recombinant cholinesterases.

10 islet amyloid polypeptide, glucosidases, and cholinesterases.

11 esized and purified PIP exhibited binding to cholinesterases.

12 they can suppress hyperglycemia and inhibit cholinesterases.

13 ing for the complete amino acid sequences of cholinesterase 1 (ChE1) and cholinesterase 2 (ChE2) from

14 in) compared with tetrameric forms of plasma cholinesterases (1902-3206 min).

15 cid sequences of cholinesterase 1 (ChE1) and cholinesterase 2 (ChE2) from amphioxus.

16 have shown that resistance to inhibitors of cholinesterase 8 (Ric-8) proteins regulate an early step

17 model organisms, resistance to inhibitors of cholinesterase 8 (Ric-8), a G protein alpha (G alpha) su

18 e have identified resistant to inhibitors of cholinesterase 8 (Ric8) as a nonreceptor guanine nucleot

19 ric-8 (resistance to inhibitors of cholinesterase 8) genes have positive roles in variegate

20 Resistance to inhibitors of cholinesterase 8A (Ric-8A) is a highly evolutionarily co

21 Resistance to inhibitors of cholinesterase 8A (Ric8A) is an essential regulator of G

22 Resistance to inhibitors of cholinesterase 8A (Ric8A) protein is an important G prot

23 nist and Ric-8A (resistance to inhibitors of cholinesterase-8A).

24 Resistance to Inhibitors of Cholinesterase A (Ric-8A) is a 60-kDa cytosolic protein

25 ls in bedding, hepatitis A antibodies, serum cholinesterase (a marker of organophosphorus exposure),

26 The cholinesterases, acetylcholinesterase (AChE) and butyryl

27 mine oxidases (MAOs) and acetyl- and butyryl-cholinesterase (AChE and BChE) inhibitors.

28 Acetyl- and butyryl-cholinesterase (AChE and BuChE) activities were monitore

29 rally, based on inhibition of enzyme, acetyl cholinesterase (AChE), butyryl cholinesterase (BChE), ty

30 However, previous reports describe cholinesterase activities in several plant species and w

31 ed fruits exhibit anti-inflammatory and anti-cholinesterase activities.

32 Blood cholinesterase activity and insecticide concentration we

33 Thus, brain imaging of cholinesterase activity associated with Abeta plaques ha

34 Imaging cholinesterase activity associated with Abeta plaques in

35 The samples exhibited no in vitro anti-cholinesterase activity but presented strong antidiabeti

36 me can also be separated from the endogenous cholinesterase activity by its subcellular localization

37 However the presence of cholinesterase activity has been described also in non-m

38 Because cholinesterase activity is peculiar to each patient, the

39 several diseases, the antidiabetic and anti-cholinesterase activity of Spanish EVOO have not been as

40 Tissues were also stained for Abeta and cholinesterase activity to visualize Abeta plaque load f

41 Each retained cholinesterase activity with butyrylthiocholine as subst

42 a conductance change can be used to quantify cholinesterase activity, enabling assessment of acute/ch

43 f exposure and well after the restoration of cholinesterase activity.

44 AD brain tissues in which Abeta plaques had cholinesterase activity.

45 survival-forest analysis identified baseline cholinesterase and bilirubin as the most important varia

46 ealed a strong predictive value for baseline cholinesterase and bilirubin levels with a highly nonlin

47 New blood markers, such as serum cholinesterase and inflammatory cytokines, have been int

48 ethyl)prop-2-yn-1-amine (2, MBA236) as a new cholinesterase and monoamine oxidase dual inhibitor.

49 The extracts exerted weak cholinesterase and tyrosinase inhibition, and remarkable

50 tracellular domain with sequence homology to cholinesterases and include the neuroligins, synaptic ce

51 nerve agents are potent toxins that inhibit cholinesterases and produce a rapid and lethal cholinerg

52 olecules combining Ca(2+) channels blockade, cholinesterase, and H3 receptor inhibition were obtained

53 to the human liver CE, hCE1, or toward human cholinesterases, and have K(i) values as low as 14 nM.

54 alifornica acetylcholinesterase, recombinant cholinesterases, and monomeric fetal bovine serum acetyl

55 conversely mean aspartate aminotransferase, cholinesterases, and prothrombin time not differed in 2

56 fragment was selected for its inhibition of cholinesterases, and the flavonoid scaffold derived from

57 vel series of optically active inhibitors of cholinesterase: (-)- and (+)-O-carbamoyl phenols of tetr

58 The study aimed to evaluate anti-cholinesterase (anti-acetylcholinesterase and -butylchol

59 ndividual antioxidative, antibacterial, anti-cholinesterase, anti-diabetic, and estrogenic effects.

60 Cholinesterases are serine hydrolases that can potential

61 The successful application of serum-derived cholinesterases as bioscavengers stems from their relati

62 und herein described, (123)I-PIP, can detect cholinesterases associated with Abeta plaques and can di

63 ts also have Abeta plaques within the brain, cholinesterase-associated plaques are generally less abu

64 nzyme, acetyl cholinesterase (AChE), butyryl cholinesterase (BChE), tyrosinase and alkaline phosphata

65 dict individual risk from baseline values of cholinesterase, bilirubin, type of primary tumor, age at

66 is unmet need, synthesis and evaluation of a cholinesterase-binding ligand, phenyl 4-(123)I-iodopheny

67 The concept of using cholinesterase bioscavengers for prophylaxis against org

68 In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(

69 overall structure of NL2A resembles that of cholinesterases, but several structural features are uni

70 , a highly potent, irreversible inhibitor of cholinesterase, causes intense convulsions, neuropatholo

71 e cholinergic system (i.e., cerebrum, plasma cholinesterases; cerebrum muscarinic, nicotinic receptor

72 Cholinesterase (ChE) enzymes terminate action of the neu

73 d a series of 14 hybrid molecules out of the cholinesterase (ChE) inhibitor tacrine and a benzimidazo

74 the remaining intact cholinergic cells with cholinesterase (ChE) inhibitors.

75 activators of organophosphate (OP)-inhibited cholinesterases (ChE) was synthesized and tested in vitr

76 Cholinesterases (ChE), use a Glu-His-Ser catalytic triad

77 ity of a new series of oxime reactivators of cholinesterases (ChEs) that contain tertiary amine or im

78 present study, the interaction of E2020 with cholinesterases (ChEs) with known sequence differences,

79 r p 1 level, hepatitis A seropositivity, and cholinesterase concentration on risk of wheeze, and the

80 s unrelated to hepatitis A seropositivity or cholinesterase concentration.

81 Tissues containing a mixture of cholinesterases could be assayed for amount of G117H BCh

82 However, the circulatory stability of cholinesterases could not be correlated with the sialic

83 All studied cholinesterases displayed poor affinity for metaproteren

84 29 was the major metabolite and that plasma cholinesterases do not play the primary role in duration

85 ilar to the enzyme acetylcholinesterase, the cholinesterase domain lacks enzymatic activity and funct

86 ynaptic interactions via their extracellular cholinesterase domain with presynaptic neurexins (NRXs).

87 splice insertions (termed A and B) in the NL cholinesterase domain.

88 kpea showed the highest antioxidant and anti-cholinesterase effects, followed by kidney beans.

89 peutics such as oximes cannot reactivate the cholinesterase enzyme and relieve cholinergic inhibition

90 e action of tolserine (5) to favor a lack of cholinesterase enzyme subtype selectivity.

91 are able to inhibit in a reversible way the cholinesterase enzyme.

92 n situ hybridization histochemistry to study cholinesterase expression during embryogenesis.

93 SIB-1553A did not inhibit rat brain cholinesterase for up to 1 mM.

94 e, in part, for the multiphasic clearance of cholinesterases from the circulation of mice.

95 ies, including P450 monooxygenases, carboxyl/cholinesterases, glutathione-S-transferases, and ATP-bin

96 Radiolabeled ligands specific for cholinesterases have potential for use in neuroimaging A

97 of Alzheimer's disease were processed using cholinesterase histochemistry in the presence or absence

98 The glycans of tetrameric forms of plasma cholinesterases (human serum butyrylcholinesterase, feta

99 Activities of serum cholinesterase in fetal bovine serum and human serum wer

100 ic functions has also been demonstrated with cholinesterase in wet blood.

101 carbohydrate structure and the stability of cholinesterases in circulation, we determined the monosa

102 assays can be used to identify OP-resistant cholinesterases in culture medium and in animal tissues.

103 evelopmental and toxicological influences on cholinesterases in multiple microscopic regions of the r

104 Optimum staining for cholinesterases in neurons and axons was obtained at pH

105 se inhibitors tested, rivastigmine inhibited cholinesterases in normal and pathological structures wi

106 butyrylcholinesterase activities, to inhibit cholinesterases in plaques and tangles.

107 Cholinesterases in plaques, tangles and glia were staine

108 ific mechanistic cascade contributing to the cholinesterase-independent developmental neurotoxicant a

109 with verbal memory recall; and that central cholinesterase inhibition (ChI) would modulate this, imp

110 ystemic illness, such as that resulting from cholinesterase inhibition by organophosphate pesticides.

111 Since previous studies have shown that cholinesterase inhibition enhances visual extrastriate c

112 The clinical relevance of the benefits of cholinesterase inhibition remains controversial, and lon

113 Currently available cholinesterase inhibition therapy targets the cognitive

114 rine revealed no sign that carbamate-induced cholinesterase inhibition was readily reversed in vitro.

115 Additionally, significant potential for cholinesterase inhibition was revealed.

116 Cholinesterase inhibition with tacrine appears to reduce

117 ugh chlorpyrifos exerts some effects through cholinesterase inhibition, recent studies suggest additi

118 echanism for functional effects unrelated to cholinesterase inhibition.

119 rce the need to examine endpoints other than cholinesterase inhibition.

120 ide showed significant regional variation in cholinesterase inhibition.

121 pirically with a placebo-controlled study of cholinesterase inhibition.

122 Phenserine, a recently developed cholinesterase inhibitor (ChEI), has been reported to re

123 Therefore, use of a cholinesterase inhibitor (ChI) might improve cognitive f

124 Administration of a central cholinesterase inhibitor (ChI) partially restored the su

125 Cholinesterase inhibitor (ChI) therapy for mixed dementi

126 oman-6-ol (CR-6) with that of the lipophilic cholinesterase inhibitor 6-chlorotacrine results in comp

127 We show that a brief treatment with the cholinesterase inhibitor aldicarb induces a form of pres

128 Pharmacological assays using the cholinesterase inhibitor aldicarb suggest that VAs and G

129 d to determine the effects of galantamine, a cholinesterase inhibitor and a nicotinic allosteric pote

130 cluding a phenserine analogue as a potential cholinesterase inhibitor and constrained tryptamine deri

131 y measured the effects of treatment with the cholinesterase inhibitor and nicotinic receptor modulato

132 Short-term treatment with a cholinesterase inhibitor appears to enhance the activity

133 he brains of healthy human subjects with the cholinesterase inhibitor donepezil (trade name: Aricept)

134 zed by fusing the pharmacophoric features of cholinesterase inhibitor donepezil and diarylthiazole as

135 found that cholinergic enhancement with the cholinesterase inhibitor donepezil improved target detec

136 The cholinesterase inhibitor donepezil was administered to n

137 Cholinesterase inhibitor drugs improve cognition and neu

138 um samples from individuals asymptomatic for cholinesterase inhibitor exposure were analyzed using th

139 r a psychopharmacological challenge with the cholinesterase inhibitor galantamine (Reminyl).

140 trials of memantine in patients receiving a cholinesterase inhibitor have been performed.

141 The combination of the scaffolds of the cholinesterase inhibitor huprine Y and the antioxidant c

142 ver, a combination of an M2 antagonist and a cholinesterase inhibitor may reach the maximal disease-m

143 The cholinesterase inhibitor methyl paraoxon significantly d

144 with NAC in combination with the peripheral cholinesterase inhibitor neostigmine showed prolonged su

145 In the presence of the cholinesterase inhibitor neostigmine, EFS led to an addi

146 Central Register and/or by prescription of a cholinesterase inhibitor or memantine hydrochloride from

147 cision to initiate a trial of therapy with a cholinesterase inhibitor or memantine on individualized

148 However, the administration of neither the cholinesterase inhibitor physostigmine nor the benzodiaz

149 We studied the effect of the cholinesterase inhibitor physostigmine on subcomponents

150 ith age, and attenuation by the nonselective cholinesterase inhibitor physostigmine, but no attenuati

151 artially susceptible to improvement with the cholinesterase inhibitor physostigmine.

152 Whether a cholinesterase inhibitor should be used as augmentation

153 rophosphate (DCP), a model organophosphorous cholinesterase inhibitor simulant.

154 t dimethoxybenzilidene anabaseine (DMXB) and cholinesterase inhibitor tetrahydroaminoacridine (THA) w

155 We tested the premise that cholinesterase inhibitor therapy should target butyrylch

156 ia responds poorly to nonpharmacological and cholinesterase inhibitor therapy, and although corticost

157 of 91 participants, all receiving background cholinesterase inhibitor therapy, were randomized 1:1 be

158 es that provided a diagnosis, treatment with cholinesterase inhibitor together with physical and occu

159 Galantamine, a cholinesterase inhibitor used in Alzheimer's disease, si

160 ucted to assess the impact of galantamine, a cholinesterase inhibitor with nicotinic-receptor-modulat

161 Physostigmine (a centrally active cholinesterase inhibitor) also dose-dependently inhibite

162 while neostigmine (a peripherally restricted cholinesterase inhibitor) did not.

163 rior administration of muscarinic agonist or cholinesterase inhibitor) produced robust but transient

164 have an exaggerated paralytic response to a cholinesterase inhibitor, aldicarb.

165 The cholinesterase inhibitor, donepezil (Aricept), reverses

166 In contrast, a cholinesterase inhibitor, eserine, although significantl

167 ceptor (mAChR) agonist, oxotremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRP

168 te administration of rivastigmine, a central cholinesterase inhibitor, on patterns of brain activatio

169 from our laboratory have shown that a novel cholinesterase inhibitor, phenserine, reduces betaAPP le

170 Donepezil, a cholinesterase inhibitor, restored performance in animal

171 Rivastigmine, a cholinesterase inhibitor, was tested in a group of clini

172 effects of metrifonate, a second generation cholinesterase inhibitor, were examined on CA1 pyramidal

173 and were treated for at least 1 month with a cholinesterase inhibitor.

174 vention patients were more likely to receive cholinesterase inhibitors (79.8% vs 55.1%; P = .002) and

175 nd visual) were also affected in MCI and (2) cholinesterase inhibitors (ChEIs), one of the therapies

176 Known adverse events of cholinesterase inhibitors (nausea, vomiting, anorexia) w

177 lzheimer's dementia is commonly treated with cholinesterase inhibitors [4-7]; however, these are mode

178 tter addressed by multifunctional drugs than cholinesterase inhibitors alone.

179 mal limb muscles, response to treatment with cholinesterase inhibitors and 3,4-diaminopyridine, and t

180 er of direct acting muscarinic agonists, two cholinesterase inhibitors and a putative m1 agonist/musc

181 Cholinesterase inhibitors and corticosteroids have been

182 Cholinesterase inhibitors and memantine do not have regu

183 for randomised, placebo-controlled trials on cholinesterase inhibitors and memantine in patients with

184 sess the evidence for efficacy and safety of cholinesterase inhibitors and memantine in vascular deme

185 Cholinesterase inhibitors and memantine produce small be

186 Cholinesterase inhibitors and memantine slightly reduced

187 Cognitive enhancing drugs, such as cholinesterase inhibitors and methylphenidate, are used

188 ortant implications for the long-term use of cholinesterase inhibitors and other cholinomimetics in t

189 Evidence regarding the benefits of cholinesterase inhibitors and other therapeutic options

190 ning the interaction between carbamate-based cholinesterase inhibitors and their enzyme target.

191 cotinic cholinergic agonists are used, or if cholinesterase inhibitors are combined with other agents

192 Cholinesterase inhibitors are commonly used to improve c

193 results from randomized controlled trials of cholinesterase inhibitors are conflicting.

194 More effective treatments than cholinesterase inhibitors are needed for Alzheimer's dis

195 erate clinically detected Alzheimer disease, cholinesterase inhibitors are somewhat effective in slow

196 Cholinesterase inhibitors are the primary treatment for

197 , and fewer than 20% of patients stop taking cholinesterase inhibitors because of side effects.

198 ifos and diazinon are bioactivated to potent cholinesterase inhibitors by cytochrome P-450 systems.

199 results indicate that one mechanism by which cholinesterase inhibitors can improve memory is by enhan

200 In persons with MCI, cholinesterase inhibitors did not reduce dementia risk (

201 euptake inhibitors for psychiatric symptoms, cholinesterase inhibitors for cognition).

202 Clinical trials have shown the benefits of cholinesterase inhibitors for the treatment of mild-to-m

203 magnetic scavenging technique for extracting cholinesterase inhibitors from aqueous matrixes using bi

204 These results indicate that cholinesterase inhibitors have a modest beneficial impac

205 PSP, but trials of cholinergic agonists and cholinesterase inhibitors have failed to show improvemen

206 Cholinesterase inhibitors improve attention, as well as

207 Cholinesterase inhibitors improve cognitive outcomes in

208 ompared with placebo, patients randomized to cholinesterase inhibitors improved 0.1 SDs on ADL scales

209 ompared with placebo, patients randomized to cholinesterase inhibitors improved 1.72 points on the NP

210 treatment effects associated with the use of cholinesterase inhibitors in these populations.

211 Treatment with cholinesterase inhibitors is well tolerated by most pati

212 h cognitive and behavioral disturbances, and cholinesterase inhibitors may improve behavior in Alzhei

213 Our findings suggest that treatment with cholinesterase inhibitors may improve muscle function in

214 Cholinesterase inhibitors may improve symptoms of dement

215 Six to 12 months of treatment with cholinesterase inhibitors modestly slows the decline of

216 ny patients' preference to take memantine or cholinesterase inhibitors off-label rather than particip

217 Concomitant treatment with cholinesterase inhibitors or memantine was permitted.

218 The effect of cholinesterase inhibitors or other treatments on persons

219 Cholinesterase inhibitors positively affect cognition in

220 Cholinesterase inhibitors produce small improvements in

221 dence suggested that, compared with placebo, cholinesterase inhibitors produced small average improve

222 The cholinesterase inhibitors rivastigmine, donepezil, and m

223 ly reduced short-term cognitive decline, and cholinesterase inhibitors slightly reduced reported func

224 Unlike other cholinesterase inhibitors tested, rivastigmine inhibited

225 The use of cholinesterase inhibitors to correct the cholinergic def

226 ddition, we need to know when to switch from cholinesterase inhibitors to memantine or when to co-pre

227 blocking drugs and encapsulates them, making cholinesterase inhibitors unnecessary.

228 -inflammatory therapy, immune-modulators and cholinesterase inhibitors which could lead to new therap

229 preservation of the cholinergic system (via cholinesterase inhibitors) and hippocampal neurons (via

230 ong 82 patients with DLB and AD treated with cholinesterase inhibitors, 15% (n=12) showed symptomatic

231 organophosphorus compounds (OPs) are potent cholinesterase inhibitors, accounting for their use as i

232 Antipsychotics, cholinesterase inhibitors, and alpha-2 agonists are the

233 , diarrhoea, and insomnia) occurred with the cholinesterase inhibitors, but not with memantine.

234 Stable use of cholinesterase inhibitors, estrogen, low-dose aspirin, a

235 dults with moderate to severe CATD receiving cholinesterase inhibitors, low- to insufficient-strength

236 Alzheimer disease can be treated with cholinesterase inhibitors, memantine, and antiamyloid im

237 The cholinesterase inhibitors, tacrine and physostigmine, an

238 in locomotion behavior and responsiveness to cholinesterase inhibitors.

239 onsidered, concentrating upon studies of the cholinesterase inhibitors.

240 was no difference in efficacy among various cholinesterase inhibitors.

241 ntine or when to co-prescribe memantine with cholinesterase inhibitors.

242 orted by an improvement of these symptoms by cholinesterase inhibitors.

243 detection of organophosphates or exposure to cholinesterase inhibitors.

244 itiated memantine, 1820 (11.2%) discontinued cholinesterase inhibitors.

245 ly accessible both for the substrate and for cholinesterase inhibitors.

246 rase system, and achieve effective dual FAAH/cholinesterase inhibitors.

247 r is as a promising new tool for analysis of cholinesterase inhibitors.

248 erred both acetyl (AChE) and butyryl (BuChE) cholinesterase inhibitory activities at similar concentr

249 ric forms of each series demonstrated potent cholinesterase inhibitory activity (with IC(50) values a

250 In contrast to their potent cholinesterase inhibitory activity, all of the pyridophe

251 ing excellent antioxidant properties, strong cholinesterase inhibitory activity, less hepatotoxicity

252 e of five tissue-derived and two recombinant cholinesterases (injected intravenously in mice) with th

253 Moreover, their inhibition of cholinesterase is of interest regarding neurodegenerativ

254 RIC-3 (resistant to inhibitor of cholinesterase) is a transmembrane protein, found in inv

255 the continuous variables bilirubin level and cholinesterase level was determined.

256 Similarly, cholinesterase levels below 7.5 U predicted a strong inc

257 es a structural basis for design of improved cholinesterase ligands for treating Alzheimer's disease

258 shown by proton NMR that horse serum butyryl cholinesterase, like serine proteases, forms a short, st

259 roximately 720 residues), and the C-terminal cholinesterase-like (ChEL) domain ( approximately 570 re

260 sidues); regions II-III (~720 residues); and cholinesterase-like (ChEL) domain (~570 residues).

261 The carboxyl-terminal cholinesterase-like (ChEL) domain of thyroglobulin (Tg)

262 I, followed by the approximately 570 residue cholinesterase-like (ChEL) domain.

263 llectively as region I-II-III) followed by a cholinesterase-like (ChEL) domain.

264 ide new evidence that authentic AChE and the cholinesterase-like domain of Tg share a common tertiary

265 ociate with neuroligins (a related family of cholinesterase-like proteins), demonstrating potential f

266 we find that a Tg truncation, deleted of the cholinesterase-like region (but not a comparably sized d

267 atalytically inactive members of a family of cholinesterase-like transmembrane proteins that mediate

268 Concerning cholinesterases, LP was the most active, mainly due to l

269 recent histological studies using the acetyl cholinesterase method and also a more definitive techniq

270 They also inhibited the activity of enzymes (cholinesterases, monoaminoxidases A and B, and tyrosinas

271 choline acetyltransferase mRNA and decreased cholinesterase mRNAs.

272 arbolinium salts as potent inihitors of both cholinesterases, N-methyl-D-aspartate receptors, and mon

273 n mRNA levels of the related enzyme, butyryl-cholinesterase, nor of the high-affinity choline transpo

274 orous acid), and inhibitory activity against cholinesterase of the new blend were determined and comp

275 The effects of the anti-cholinesterase organophosphate pesticide chlorpyrifos (C

276 mechanism of dealkylation in soman-inhibited cholinesterases proposed previously.

277 symmetrization of meso-diacetate with acetyl cholinesterase, radical cyclization, and Lewis acid-cata

278 ar interstitial cells of Cajal (ICC-IMs) and cholinesterases restrict ACh accessibility to a select p

279 We suggest that the high catalytic power of cholinesterases results in part from the formation of a

280 Amino acid sequence alignments of cholinesterases revealed that 6 of 14 aromatic amino aci

281 1 genes, that are resistant to inhibitors of cholinesterase (Ric mutants).

282 Resistance to inhibitors of cholinesterase (Ric) 8A is a guanine nucleotide exchange

283 Resistance to inhibitors of cholinesterase (Ric-8)A and Ric-8B are essential genes t

284 erences in the pharmacokinetic parameters of cholinesterases seem to be due to the combined effect of

285 ed almost entirely by measurements of acetyl cholinesterase, size, and ploidy without concomitant ass

286 howed that the decrease in the percentage of cholinesterase-stained zones (CSZ) exhibiting nerve term

287 act with the synaptic basal lamina marked by cholinesterase staining even in the absence of the targe

288 e conclusions were later supported by acetyl cholinesterase staining using a method that appeared not

289 posed endocannabinoid system and the classic cholinesterase system, and achieve effective dual FAAH/c

290 similarity in structure and function to the cholinesterase targets of nerve agent poisoning.

291 c overactivity and NMJ Ca(2+) overload, anti-cholinesterase toxicity and the slow-channel myasthenic

292 Cholinesterases use a Glu-His-Ser catalytic triad to enh

293 The effect on the cholinesterases was not as strong as in previous reports

294 role of glycosylation in the circulation of cholinesterases, we compared the mean residence time of

295 Wild-type cholinesterases were completely inhibited by 0.1 mM echo

296 Mild effects on cholinesterases were observed with the certified samples

297 emporally regulated ganglionic expression of cholinesterases, which may be important in the developme

298 These pathological cholinesterases, with altered properties, are suggested

299 kely to result in inhibition of pathological cholinesterases, with the potential of interfering with

300 spatiotemporal change in expression of each cholinesterase within the DRG.