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Further, it revealed that PI3k inhibitors blocked the enhanced post-synaptic transmission, suggesting this effect might be dependent on PI3k activation [13]

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This suggests a delay between UA entry into the circulation and its arrival at target tissues, where it dissociates into the monomer to exert its effects

* Correspondence: Eva Liebau, [email protected] Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers

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