PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 4181315-9 1969 The first involved reactivation of the phosphorylated AChase by pyridine-2-aldoxime methiodide (2-PAM), in conditions in which the reactivation of other enzymes would be insignificant. pralidoxime 64-94 acetylcholinesterase Mus musculus 54-60 5768869-4 1969 After being extensively washed, the enzyme acetylcholinesterase (AChase) was specifically reactivated by treatment with pyridine-2-aldoxime methiodide (2-PAM). pralidoxime 120-150 acetylcholinesterase Mus musculus 43-63 5768869-4 1969 After being extensively washed, the enzyme acetylcholinesterase (AChase) was specifically reactivated by treatment with pyridine-2-aldoxime methiodide (2-PAM). pralidoxime 120-150 acetylcholinesterase Mus musculus 65-71 34969248-1 2022 Maintaining a long-term continuous and stable reactivator blood concentration to treat organophosphorus nerve agent poisoning using acetylcholinesterase (AChE) reactivator pralidoxime chloride (2-PAM) is very important yet difficult. pralidoxime 172-192 acetylcholinesterase Mus musculus 132-152 34969248-1 2022 Maintaining a long-term continuous and stable reactivator blood concentration to treat organophosphorus nerve agent poisoning using acetylcholinesterase (AChE) reactivator pralidoxime chloride (2-PAM) is very important yet difficult. pralidoxime 172-192 acetylcholinesterase Mus musculus 154-158 34969248-1 2022 Maintaining a long-term continuous and stable reactivator blood concentration to treat organophosphorus nerve agent poisoning using acetylcholinesterase (AChE) reactivator pralidoxime chloride (2-PAM) is very important yet difficult. pralidoxime 194-199 acetylcholinesterase Mus musculus 132-152 34969248-1 2022 Maintaining a long-term continuous and stable reactivator blood concentration to treat organophosphorus nerve agent poisoning using acetylcholinesterase (AChE) reactivator pralidoxime chloride (2-PAM) is very important yet difficult. pralidoxime 194-199 acetylcholinesterase Mus musculus 154-158 34969248-8 2022 For mice after intragastric poisoning with sarin (a neurotoxic agent), an atropine-assisted 2-PAM@MIL-88B(Fe) treatment experiment revealed that 2-PAM@MIL-88B(Fe) continuously released 2-PAM for more than 72 h so that poisoned AChE was continuously and steadily reactivated. pralidoxime 92-97 acetylcholinesterase Mus musculus 227-231 34969248-8 2022 For mice after intragastric poisoning with sarin (a neurotoxic agent), an atropine-assisted 2-PAM@MIL-88B(Fe) treatment experiment revealed that 2-PAM@MIL-88B(Fe) continuously released 2-PAM for more than 72 h so that poisoned AChE was continuously and steadily reactivated. pralidoxime 145-150 acetylcholinesterase Mus musculus 227-231 34969248-8 2022 For mice after intragastric poisoning with sarin (a neurotoxic agent), an atropine-assisted 2-PAM@MIL-88B(Fe) treatment experiment revealed that 2-PAM@MIL-88B(Fe) continuously released 2-PAM for more than 72 h so that poisoned AChE was continuously and steadily reactivated. pralidoxime 185-190 acetylcholinesterase Mus musculus 227-231 3653568-4 1987 FBS-AChE, at a lower enzyme OP ratio, protected mice from 2 LD50s of the nerve agent methylphosphonofluoridic acid 1,2,2,-trimethylpropyl ester (soman) when used in conjunction with atropine and 2[(hydroxyimino)methyl]-1-methylpyridinium chloride. pralidoxime 195-246 acetylcholinesterase Mus musculus 4-8 20406208-2 2010 Human malathion poisoning has been treated with oximes (mainly pralidoxime) in an attempt to reactivate OP-inhibited acetylcholinesterase (AChE). pralidoxime 63-74 acetylcholinesterase Mus musculus 117-137 28849997-9 2017 Pralidoxime (PRAL) (600 microM), a classical AChE reactivator, significantly protected against MAL-induced AChE blockade; however, PRAL did not affect MAL-mediated fall in cellular viability, indicating that AChE inhibition is not necessarily correlated with insecticide-induced decrease in cell survival. pralidoxime 0-11 acetylcholinesterase Mus musculus 45-49 28849997-9 2017 Pralidoxime (PRAL) (600 microM), a classical AChE reactivator, significantly protected against MAL-induced AChE blockade; however, PRAL did not affect MAL-mediated fall in cellular viability, indicating that AChE inhibition is not necessarily correlated with insecticide-induced decrease in cell survival. pralidoxime 0-11 acetylcholinesterase Mus musculus 107-111 28849997-9 2017 Pralidoxime (PRAL) (600 microM), a classical AChE reactivator, significantly protected against MAL-induced AChE blockade; however, PRAL did not affect MAL-mediated fall in cellular viability, indicating that AChE inhibition is not necessarily correlated with insecticide-induced decrease in cell survival. pralidoxime 0-11 acetylcholinesterase Mus musculus 107-111 25346249-8 2014 Shift of DFP induced brain AChE IC50 curves to right was observed at 0.20 LD50 treatment dose of oximes with respect to 2-PAM. pralidoxime 120-125 acetylcholinesterase Mus musculus 27-31 21723318-0 2011 Effects of K074 and pralidoxime on antioxidant and acetylcholinesterase response in malathion-poisoned mice. pralidoxime 20-31 acetylcholinesterase Mus musculus 51-71 21723318-3 2011 In the present study, we investigated the potency of pralidoxime and K074 in reactivating AChE after acute exposure to malathion, as well as in preventing malathion-induced changes in oxidative-stress related parameters in mice. pralidoxime 53-64 acetylcholinesterase Mus musculus 90-94 21723318-5 2011 Oxime treatments (1/4 of LD(50), i.m., 6h after malathion poisoning) showed that pralidoxime significantly reversed malathion-induced blood AChE inhibition, although no significant effects were observed after K074 treatment. pralidoxime 81-92 acetylcholinesterase Mus musculus 140-144 21723318-10 2011 However, only pralidoxime significantly reversed the blood AChE inhibition induced by malathion poisoning. pralidoxime 14-25 acetylcholinesterase Mus musculus 59-63 10421446-2 1999 With DEPQ-inhibited wild-type mouse acetylcholinesterase (AChE), the reactivation kinetic profile demonstrated one-phase exponential association only when 2-[hydroxyimino methyl]-1-methylpyridinium chloride (2-PAM) and 1-(2-hydroxy-iminomethyl-1-pyridinium)-1-(4-carboxy-aminopyridi nium)-dimethyl ether hydrochloride (HI-6) were used as reactivators. pralidoxime 155-206 acetylcholinesterase Mus musculus 36-56 10421446-2 1999 With DEPQ-inhibited wild-type mouse acetylcholinesterase (AChE), the reactivation kinetic profile demonstrated one-phase exponential association only when 2-[hydroxyimino methyl]-1-methylpyridinium chloride (2-PAM) and 1-(2-hydroxy-iminomethyl-1-pyridinium)-1-(4-carboxy-aminopyridi nium)-dimethyl ether hydrochloride (HI-6) were used as reactivators. pralidoxime 155-206 acetylcholinesterase Mus musculus 58-62 20385200-2 2010 To alleviate peripheral respiratory failure oximes, e.g. obidoxime and pralidoxime, are used to reactivate inhibited acetylcholinesterase (AChE) with the intention to restore the disturbed neuromuscular function. pralidoxime 71-82 acetylcholinesterase Mus musculus 117-137 20385200-2 2010 To alleviate peripheral respiratory failure oximes, e.g. obidoxime and pralidoxime, are used to reactivate inhibited acetylcholinesterase (AChE) with the intention to restore the disturbed neuromuscular function. pralidoxime 71-82 acetylcholinesterase Mus musculus 139-143