https://www.selleckchem.com/products/tj-m2010-5.html After enrichment for pJNK by immunoprecipitation, we identified JNK2 as the only significantly hyperactivated JNK isoform, with expression of the 54 kDa pJNK2 variant elevated to a greater extent than the 46 kDa pJNK2 variant. Expression of the total amounts of both JNK2 variants (phosphorylated plus non-phosphorylated) was reduced in epilepsy, however, suggesting that activation of upstream phosphorylation pathways was responsible for JNK2 hyperactivation. Since our prior work demonstrated that pharmacological inhibition of JNK activation had an antiepileptic effect, JNK2 hyperactivation is therefore likely a pathological event that promotes seizure occurrences. This investigation provides evidence that JNK2 is selectively hyperactivated in epilepsy and thus may be a novel and selective antiepileptic target. © 2020 The Authors.Several studies have been conducted worldwide to develop effective and affordable methods to degrade pharmaceuticals and their metabolites/intermediates/oxidation products found in surface water, wastewater and drinking water. In this work, acetaminophen and its transformation products were successfully degraded in surface water by electrochemical oxidation using stainless steel electrodes. The effect of pH and current density on the oxidation process was assessed and the oxidation kinetics and mechanisms involved were described. Additionally, the results were compared with those obtained in acetaminophen synthetic solutions. It was found that conducting the electrochemical oxidation at 16.3 mA/cm2 and pH 5, good performance of the process was achieved and not only acetaminophen, but also its transformation products were totally degraded in only 7.5 min; furthermore, small number of transformation products were generated. On the other hand, degradation rates of acetaminophen and its transformation products in surface water were much faster (more than 2.5 times) and the reaction times much s