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http://dx.doi.org/10.1503/cmaj.210878 | DOI Listing |
Ther Adv Drug Saf
January 2025
Pharmacology Department, School of Medicine, University of Valladolid, Valladolid, Spain.
In 2019, intranasal esketamine gained approval as a promising therapy for those individuals grappling with treatment-resistant depression. Both clinical trials and real-world studies have underscored its efficacy in alleviating and remitting depressive symptoms, with sustained benefits observed for nearly 4.5 years.
View Article and Find Full Text PDFEur Neuropsychopharmacol
January 2025
National PTSD Research Centre at the Thompson Institute, University of the Sunshine Coast, Birtinya, QLD, 4575, Australia. Electronic address:
Neurocrit Care
January 2025
Division of Neurology, Children's National Hospital, Washington, DC, USA.
Background: The treatment of status epilepticus (SE) in children with cardiac disease is challenging given their often-tenuous hemodynamic state. We aim to determine whether ketamine is safe and effective in children with cardiac disease as the first-line continuous infusion for the treatment of refractory SE (RSE) and to compare ketamine to midazolam for the treatment of RSE in this population.
Methods: This is a single-center retrospective cohort study of pediatric patients with cardiac disease and RSE admitted to the cardiac intensive care unit at a tertiary children's hospital between January 1, 2017 and June 30, 2023.
Cell Biol Toxicol
January 2025
Laboratory of Neurobiology, Hebei Medical University, Shijiazhuang, 050017, China.
Esketamine, a newly developed antidepressant, is the subject of this research which seeks to explore its impact on depressive symptoms in neuropathic pain mice and the potential molecular mechanisms involved. Through transcriptome sequencing and bioinformatics analysis combined with in vivo studies, it was identified that esketamine markedly boosts the levels of the m6A methyltransferase METTL3 and the AMPA receptor GluA1 subunit. Esketamine activates METTL3, allowing it to bind with GluA1 mRNA, promoting m6A modification, thereby enhancing GluA1 expression at synapses.
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