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1 ) provides the rationale for treatments with anticholinesterases.
2 ma is the likely target for schistosomicidal anticholinesterases.
3                      These were assessed for anticholinesterase action against freshly prepared human
4 were obtained by known procedures, and their anticholinesterase actions were similarly quantified aga
5                                 Finally, the anticholinesterase activities of intermediates N1, N8-bi
6                                          The anticholinesterase activities of N(8)-nor- and N(8)-subs
7 n for the development of new drugs that have anticholinesterase activity and may be used for the trea
8  activity and a steroidal glycoalkaloid with anticholinesterase activity and suggest spatial mutual e
9                        Both compounds lacked anticholinesterase activity in concentrations up to 30 m
10 e activation, nor was it associated with the anticholinesterase activity of the drug.
11                 An analysis of the structure/anticholinesterase activity relationship of the describe
12           To elucidate further the structure/anticholinesterase activity relationship of the describe
13 compounds possessed moderate but less potent anticholinesterase activity, with the same selectivity a
14 rred following administration of eserine, an anticholinesterase agent.
15    The compounds showed significant in vitro anticholinesterase (anti-ChE) activity, the most potent
16                                        These anticholinesterase compounds are classically considered
17 urotransmission in the OB by addition of the anticholinesterase drug neostigmine (20 mM) sharpened th
18 uine, the antifolate drug metoprine, and the anticholinesterase drug tacrine (an early drug for Alzhe
19 d Alzheimer's disease; four patients entered anticholinesterase drug trials.
20 arget is key for the development of improved anticholinesterase drugs and potentially a novel vaccine
21 e and fruit-methanol extracts exerted potent anticholinesterase effects (66.4 +/- 0.65% to 97.7 +/- 0
22 re more potent than, or similarly potent to, anticholinesterases in current clinical use, providing n
23           Recent studies have suggested that anticholinesterases including organophosphates and carba
24  We further compared the affinity of various anticholinesterases including organophosphorous nerve ag
25  were strongly ameliorated on treatment with anticholinesterase inhibitor in another patient.
26 h is the target of poisonous organophosphate anticholinesterase insecticides such as the parathion me
27 n cholinergic functions and is the target of anticholinesterase insecticides, whereas TcAce2 plays an
28 ion and increased larval susceptibilities to anticholinesterase insecticides.
29  dosing of neuromuscular blocking agents and anticholinesterases is often inappropriate and adequacy
30 Patients did not show long-term benefit from anticholinesterase medication and sometimes worsened, an
31 ffer in their sensitivity to the therapeutic anticholinesterase metrifonate.
32 ents to elucidate the mechanism of action of anticholinesterases on the nicotinic AChR in rat clonal
33 ither with a carbamate or an organophosphate anticholinesterase pesticide showed significant regional
34 ed a series of novel analogues of the potent anticholinesterases phenserine (2) and physostigmine (1)
35 and visual control tasks, using fMRI and the anticholinesterase physostigmine.
36  30-45 minutes of a seizurogenic dose of the anticholinesterase, soman.
37 and can be separated from alpha-tomatine, an anticholinesterase steroidal glycoalkaloid.
38 ns were not detected and patients respond to anticholinesterase treatments.

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