PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31893002-8 2020 Atropine combined with penehyclidine in OP patients also helped reduce the time to atropinization and AchE recovery, the rate of IMS and the rate of ADR. Atropine 0-8 acetylcholinesterase (Cartwright blood group) Homo sapiens 102-106 31893002-10 2020 CONCLUSION: Atropine combined with penehyclidine benefits OP patients by enhancing the cure rate, mortality rate, time to atropinization, AchE recovery, IMS rate, total ADR and duration of hospitalization. Atropine 12-20 acetylcholinesterase (Cartwright blood group) Homo sapiens 138-142 26368669-1 2015 Tabun-inhibited acetylcholinesterase (AChE) is rather resistant towards reactivation by oximes in vitro while in vivo experiments showed some protection of animals poisoned by this chemical warfare nerve agent after treatment with an oxime and atropine. Atropine 244-252 acetylcholinesterase (Cartwright blood group) Homo sapiens 16-36 30205495-1 2018 The acetylcholinesterase (AChE) reactivators (e.g., obidoxime, asoxime) became an essential part of organophosphorus (OP) poisoning treatment, together with atropine and diazepam. Atropine 157-165 acetylcholinesterase (Cartwright blood group) Homo sapiens 4-24 30205495-1 2018 The acetylcholinesterase (AChE) reactivators (e.g., obidoxime, asoxime) became an essential part of organophosphorus (OP) poisoning treatment, together with atropine and diazepam. Atropine 157-165 acetylcholinesterase (Cartwright blood group) Homo sapiens 26-30 27125761-2 2016 The need for an effective treatment of OP poisoning resulted in the implementation of a combination therapy with the muscarinic receptor antagonist atropine and an oxime for the reactivation of OP-inhibited acetylcholinesterase (AChE). Atropine 148-156 acetylcholinesterase (Cartwright blood group) Homo sapiens 229-233 26368669-1 2015 Tabun-inhibited acetylcholinesterase (AChE) is rather resistant towards reactivation by oximes in vitro while in vivo experiments showed some protection of animals poisoned by this chemical warfare nerve agent after treatment with an oxime and atropine. Atropine 244-252 acetylcholinesterase (Cartwright blood group) Homo sapiens 38-42 20807085-1 2011 The standard treatment of poisoning by organophosphorus compounds (OP) includes the reversible muscarine receptor antagonist atropine and oximes for the reactivation of OP-inhibited acetylcholinesterase (AChE). Atropine 125-133 acetylcholinesterase (Cartwright blood group) Homo sapiens 204-208 23959117-3 2013 Standard care involves the use of anticonvulsants (e.g., diazepam), parasympatolytics (e.g., atropine) and oximes that restore AChE activity. Atropine 93-101 acetylcholinesterase (Cartwright blood group) Homo sapiens 127-131 21761139-3 2012 These effects were abolished by muscarinic blocker atropine and therefore are caused by acetylcholine, which accumulates in the myocardium due to acetylcholinesterase inhibition even in the absence of vagal input. Atropine 51-59 acetylcholinesterase (Cartwright blood group) Homo sapiens 146-166 21771644-9 2011 Only when RBC-AChE was completely inhibited, therapy of cholinergic crisis required atropine doses up to 0.06 mg h-1 kg-1. Atropine 84-92 acetylcholinesterase (Cartwright blood group) Homo sapiens 14-18 24157926-2 2013 Standard treatment by administration of atropine and oximes, e.g., obidoxime or pralidoxime, focuses on antagonism of mAChRs and reactivation of AChE, whereas nicotinic malfunction is not directly treated. Atropine 40-48 acetylcholinesterase (Cartwright blood group) Homo sapiens 145-149 20105433-4 2010 Beside atropine as competitive antagonist of ACh at muscarinic ACh receptors oximes as reactivators of OP-inhibited AChE are a mainstay of standard antidotal treatment. Atropine 7-15 acetylcholinesterase (Cartwright blood group) Homo sapiens 116-120 21666889-1 2011 A conjugate of pyridine-4-aldoxime and atropine (ATR-4-OX) was synthesized and its antidotal efficiency was tested in vitro on tabun- or paraoxon-inhibited acetylcholinesterase (AChE) of human erythrocytes as well as in vivo using soman-, tabun- or paraoxon-poisoned mice. Atropine 39-47 acetylcholinesterase (Cartwright blood group) Homo sapiens 178-182 21787676-5 2011 Furthermore, the non-selective cholinergic antagonist atropine partially attenuated the paraoxon-induced N-AChE and c-Fos activations in both types of cells. Atropine 54-62 acetylcholinesterase (Cartwright blood group) Homo sapiens 105-111 19778190-8 2009 RBC-AChE activity mirrors the function of n-receptor- and m-receptor-mediated cholinergic signaling as measured by neuromuscular transmission and atropine requirements. Atropine 146-154 acetylcholinesterase (Cartwright blood group) Homo sapiens 4-8 19428953-3 2009 A mainstay of standard antidotal treatment is atropine for antagonizing effects mediated by over stimulation of muscarinic ACh-receptors and oxime to reactivate OP-inhibited AChE. Atropine 46-54 acetylcholinesterase (Cartwright blood group) Homo sapiens 174-178 19031285-7 2008 Atropine was given to about 30% of the individuals, including to some with no cholinergic symptoms or exposed to non-acetylcholinesterase inhibitors. Atropine 0-8 acetylcholinesterase (Cartwright blood group) Homo sapiens 117-137 15654704-2 2005 Standard treatment involves administration of intravenous atropine and oxime to counter acetylcholinesterase inhibition at the synapse. Atropine 58-66 acetylcholinesterase (Cartwright blood group) Homo sapiens 88-108 16293236-1 2005 Current antidotes for organophosphorus compounds (OP) poisoning consist of a combination of pretreatment with carbamates (pyridostigmine bromide), to protect acetylcholinesterase (AChE) from irreversible inhibition by OP compounds, and post-exposure therapy with anti-cholinergic drugs (atropine sulfate) to counteract the effects of excess acetylcholine and oximes (e.g., 2-PAM chloride) to reactivate OP-inhibited AChE. Atropine 287-303 acetylcholinesterase (Cartwright blood group) Homo sapiens 180-184 16518518-6 2006 Pretreatment with N-methyl D-aspartate (NMDA) receptor antagonist memantine, in combination with atropine sulfate, provides significant protection against inhibition of AChE, increases of ROS/RNS, and depletion of high-energy phosphates induced by DFP/carbofuran. Atropine 97-113 acetylcholinesterase (Cartwright blood group) Homo sapiens 169-173 4084346-0 1985 Influence of atropine upon ageing and reactivation of soman inhibited acetylcholinesterase from human erythrocytes. Atropine 13-21 acetylcholinesterase (Cartwright blood group) Homo sapiens 70-90 9726096-3 1998 A cholinergic syndrome resulting from the inhibition of acetylcholinesterase activity by irinotecan is frequently seen within the first 24 hours after irinotecan administration but is easily controlled with atropine. Atropine 207-215 acetylcholinesterase (Cartwright blood group) Homo sapiens 56-76 10445493-4 1999 Because of the reversibility of inhibition of acetylcholinesterase, the patients recovered after treatment with atropine and toxogonin. Atropine 112-120 acetylcholinesterase (Cartwright blood group) Homo sapiens 46-66 1729389-2 1992 Addition of either atropine or tubocurarine in the presence of the acetylcholinesterase inhibitor phospholine iodide enhanced acetylcholine release. Atropine 19-27 acetylcholinesterase (Cartwright blood group) Homo sapiens 67-87 4084346-7 1985 Reactivation of the non aged phosphonyl-AChE by several pyridinium oximes was enhanced by atropine with the ghost-bound enzyme; the reactivation of the phosphonylated solubilized enzyme, however, was not affected by atropine. Atropine 90-98 acetylcholinesterase (Cartwright blood group) Homo sapiens 40-44 4328180-1 1971 The binding of atropine and eserine to acetylcholinesterase. Atropine 15-23 acetylcholinesterase (Cartwright blood group) Homo sapiens 39-59 7256468-9 1981 Clinical recovery (the point at which atropine could safely be discontinued) generally correlated with a recovery of E-AChE activity to 30% or more of normal. Atropine 38-46 acetylcholinesterase (Cartwright blood group) Homo sapiens 119-123 6472626-7 1984 A rise in acetylcholinesterase concentration was obtained upon stimulation of the central ends of the sciatic nerves; this was inhibited by atropine but not by N-methylatropine, indicating that the rise was due to increased nervous activity and not to the circulatory effects of the stimulation, since the changes in blood pressure caused by the stimulation remained the same after atropine administration. Atropine 140-148 acetylcholinesterase (Cartwright blood group) Homo sapiens 10-30 497002-0 1979 Some adjuncts to oxime-atropine therapy for organophosphate intoxication--their effects on acetylcholinesterase. Atropine 23-31 acetylcholinesterase (Cartwright blood group) Homo sapiens 91-111 1151640-1 1975 NMR was used to study the binding of acetylcholine, atropine, and physostigmine to acetylcholinesterase. Atropine 52-60 acetylcholinesterase (Cartwright blood group) Homo sapiens 83-103 1151640-4 1975 The dissociation constant, KD and the linewidth of the acetylcholinesterase-inhibitor complex, increment v bound, for atropine and physostigmine can be estimated from the linewidth changes of the N-methyl and phenyl group resonances of atropine and from the N-methyl and C-methyl group resonances of physostigmine resulting from association with the enzyme. Atropine 118-126 acetylcholinesterase (Cartwright blood group) Homo sapiens 55-75 1151640-4 1975 The dissociation constant, KD and the linewidth of the acetylcholinesterase-inhibitor complex, increment v bound, for atropine and physostigmine can be estimated from the linewidth changes of the N-methyl and phenyl group resonances of atropine and from the N-methyl and C-methyl group resonances of physostigmine resulting from association with the enzyme. Atropine 236-244 acetylcholinesterase (Cartwright blood group) Homo sapiens 55-75 5083615-2 1972 A study by nuclear magnetic resonance of the acceleration of acetylcholinesterase by atropine and inhibition by eserine. Atropine 85-93 acetylcholinesterase (Cartwright blood group) Homo sapiens 61-81 33708959-10 2021 The effects were abolished by atropine and the selective M1 mAChR antagonist pirenzepine in OGD-induced PRNs suggesting an indirect M1 mAChR-mediated effect via inhibiting AChE activity to increase endogenous ACh level. Atropine 30-38 acetylcholinesterase (Cartwright blood group) Homo sapiens 172-176