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1 ) provides the rationale for treatments with anticholinesterases.
2 ma is the likely target for schistosomicidal anticholinesterases.
4 were obtained by known procedures, and their anticholinesterase actions were similarly quantified aga
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
13 compounds possessed moderate but less potent anticholinesterase activity, with the same selectivity a
15 The compounds showed significant in vitro anticholinesterase (anti-ChE) activity, the most potent
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
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
24 We further compared the affinity of various anticholinesterases including organophosphorous nerve ag
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
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
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)
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