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1 ection of the acetylcholinesterase inhibitor neostigmine.
2  showing a higher affinity of the sensor for neostigmine.
3 reased by the acetylcholinesterase inhibitor neostigmine.
4 with acetylcholinesterase inhibitors such as neostigmine.
5 down with the acetylcholinesterase inhibitor neostigmine.
6 he breakdown of acetylcholine was blocked by neostigmine.
7 he decay phase of current was accelerated by neostigmine.
8 ection of the acetylcholinesterase inhibitor neostigmine.
9 ellular electrodes, often in the presence of neostigmine.
10  the MEPP was not reversed by 1 microgram/mL neostigmine.
11 antagonist scopolamine (40 mM) together with neostigmine (20 mM) attenuated the neostigmine-dependent
12 B by addition of the anticholinesterase drug neostigmine (20 mM) sharpened the ORF responses of mitra
13 usion) or the acetylcholinesterase inhibitor neostigmine (7.5-75 pmol per infusion) into the posterio
14 ivity in an atropine-sensitive manner, while neostigmine (a peripherally restricted cholinesterase in
15 wing lysolecithin injection, we administered neostigmine, a cholinesterase inhibitor, to artificially
16                Bath application of 10 microM neostigmine, a potent acetylcholinesterase inhibitor, pr
17 hout an initial response received open-label neostigmine; all had colonic decompression.
18 ing, samples were collected every 60 s while neostigmine, an acetylcholine esterase inhibitor, was in
19 ynamic changes elicited by microinjection of neostigmine, an inhibitor of acetylcholinesterase, that
20 ined from the fits were 3.8 x 10(3)M(-1) for neostigmine and 1.7 x 10(3)M(-1) for eserine, showing a
21 nists had minimal effects on ICC-IM, whereas neostigmine and carbachol increased Ca(2+) transients.
22                  These results indicate that neostigmine and carbaryl directly block the nicotinic AC
23                                              Neostigmine and carbaryl showed a biphasic effect; enhan
24 t duration were decreased in the presence of neostigmine and carbaryl.
25 nvolved in the analgesic effects of epidural neostigmine and could be more specifically targeted for
26                                         Both neostigmine and DFP applied after AChE inhibition by DFP
27 quent anesthetics during which they received neostigmine and glycopyrrolate for NMB reversal.
28   Neuromuscular blockade (NMB) reversal with neostigmine and glycopyrrolate has been reported to caus
29 , our experience would support the safety of neostigmine and glycopyrrolate in cardiac transplantatio
30 ore, the antiallodynic effect of intrathecal neostigmine and muscarine was largely eliminated by CGP5
31                                              Neostigmine and/or N-acetyl-cysteine (NAC) were applied
32 e first co-application with 10 or 100 microM neostigmine, and the current was eventually suppressed b
33  mice) the EPSCs resembled those observed in neostigmine but the steady inward current was much small
34  The pharmacological inactivation of AChE by neostigmine caused the appearance of an ultra-slow (seco
35 iously we showed that Ani (anisodamine)/Neo (neostigmine) combination produced anti-shock effect via
36 ther with neostigmine (20 mM) attenuated the neostigmine-dependent sharpening of ORFs.
37 enes are also envisioned due to the reliable neostigmine determination in unpretreated samples.
38 cologic acetylcholinesterase inhibition with neostigmine diminishes liver damage in acute liver failu
39                           In the presence of neostigmine, EFS increased pT38, pT853 and pS19.
40 the presence of the cholinesterase inhibitor neostigmine, EFS led to an additional increase in phosph
41  Neither the choice of sugammadex instead of neostigmine for reversal (OR(adj) 1.03, 95% CI 0.85-1.25
42 the placebo group and the one patient in the neostigmine group without an initial response received o
43          Ten of the 11 patients who received neostigmine had prompt colonic decompression, as compare
44 monstration of the method, we applied ACh or neostigmine in different spatial locations via the micro
45 llodynic actions of intrathecal muscarine or neostigmine in normal rats and in a rat model of diabeti
46 y attenuated the effect of both muscarine or neostigmine in normal rats.
47                              Side effects of neostigmine included abdominal pain, excess salivation,
48 VTA ACh levels (resulting from 10 microM VTA neostigmine infusion) increased VTA dopamine levels and
49        Injection of NLA into the mPRF before neostigmine injection also blocked the ability of neosti
50 lution of the acetylcholinesterase inhibitor neostigmine into the L7 level of the dorsal horn of anes
51 ke state (REM(Neo)) caused by microinjecting neostigmine into the PRF.
52 We randomly assigned 11 to receive 2.0 mg of neostigmine intravenously and 10 to receive intravenous
53                                              Neostigmine is an acetylcholinesterase inhibitor that am
54  used: as little as 0.015-0.025 mg kg(-1) of neostigmine is required at a train-of-four count of four
55     Uncontrolled studies have suggested that neostigmine, may be an effective treatment.
56                       Measured motility with neostigmine (mean, 0.39 au) was significantly higher tha
57 lation was manipulated by direct infusion of neostigmine, MLA, and scopolamine into the OB during olf
58        When the solution contained 10 microM neostigmine (NEO) 3000 stimuli reduced [integral]MEPCs b
59 otremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRPa of anaesthetized rats de
60 ensors were applied for the determination of neostigmine (Ns) ion in its bulk powder, different pharm
61 nd sensitive method for the determination of neostigmine (Ns) ion in its bulk powder, different pharm
62 ted by manipulation (using either drugs like neostigmine or genetic tools to inactivate neurotransmit
63 -controlled crossover study of either 0.5 mg neostigmine or saline (n = 11) or 20 mg intravenous buty
64 n a low-Mg(2+)-Ca2+ solution, sometimes with neostigmine present.
65 onse to conservative therapy, treatment with neostigmine rapidly decompresses the colon.
66  Two patients who had an initial response to neostigmine required colonoscopic decompression for recu
67 with the peripheral cholinesterase inhibitor neostigmine showed prolonged survival and improved outco
68        Intrathecal injection of muscarine or neostigmine significantly increased the withdrawal laten
69 njection were eligible to receive open-label neostigmine three hours later.
70 igmine injection also blocked the ability of neostigmine to decrease respiratory rate during the REM
71 nts such as opioids, clonidine, ketamine and neostigmine to potentiate the effects of local anestheti
72 g, IHG exercise increased sweat rate at both neostigmine-treated and untreated sites.
73  0.0086), APAP-alone-treated mice vs. APAP + neostigmine-treated mice) and histopathological signs of
74  0.0013), APAP-alone-treated mice vs. APAP + neostigmine-treated mice), inflammatory cytokine levels
75 ia, IHG exercise increased sweat rate at the neostigmine-treated site but not at the control site.
76                                              Neostigmine treatment led to significant reduction of se
77       The effect of intrathecal muscarine or neostigmine was examined through pretreatment with the s
78 y times (t1/2), regardless of whether or not neostigmine was present.
79 detection limits of 26 pM eserine and 0.3 nM neostigmine were achieved.
80 used with the acetylcholinesterase inhibitor neostigmine, while the other was perfused with the vehic
81 olorimetric determination of the nerve agent neostigmine, with excellent analytical performance in te