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Paracetamol overdose results in more calls to poison control centers in the US than overdose of any other pharmacological substance, accounting for more than 100,000 calls, as well as 56,000 emergency room visits, 2,600 hospitalizations, and 458 deaths due to acute liver failure per year.[19] A recent study of cases of acute liver failure between November 2000 and October 2004 by the Centers for Disease Control and Prevention (US) found that paracetamol was the cause of 41% of all cases in adults, and 25% of cases in children.[20] At usual doses, the toxic metabolite NAPQI is quickly detoxified by combining irreversibly with the sulfhydryl groups of glutathione or administration of a sulfhydryl compound such as N-acetylcysteine, to produce a non-toxic conjugate that is eventually excreted by the kidneys.[17] Also, methionine has been recommended in some cases,[21] although recent studies show that N-acetylcysteine is a more effective antidote to paracetamol overdose.[22] Paracetamol, unlike other common analgesics such as aspirin and ibuprofen, has relatively little anti-inflammatory activity, and so it is not considered to be a non-steroidal anti-inflammatory drug (NSAID)

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While the dysregulation of EAAT3 has been associated with metabolic reprogramming and the progression of various solid tumors, the precise regulatory mechanisms governing EAAT3 remain insufficiently understood

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