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The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|April 16, 2010
Kv1.1 potassium channel deficiency reveals brain-driven cardiac dysfunction as a candidate mechanism for sudden unexplained death in epilepsyEdward Glasscock, Jong W Yoo, Tim T Chen, et al.
BMC Neuroscience|October 30, 2016
Severe respiratory changes at end stage in a FUS-induced disease state in adult ratsKasey L Jackson, Hemangini A Dhaibar, Robert D Dayton, et al.
Epilepsy Currents|March 3, 2026
Translational Research Symposium: Current State of SUDEP ResearchJustin M Ryan, Elizabeth J Donner, Quratulain Zulfiqar-Ali, et al.
Human Molecular Genetics|March 24, 2017
Scn2a deletion improves survival and brain-heart dynamics in the Kcna1-null mouse model of sudden unexpected death in epilepsy (SUDEP)Vikas Mishra, Bharat K Karumuri, Nicole M Gautier, et al.
Proceedings of the National Academy of Sciences of the United States of America|May 25, 2022
Kv1.1 preserves the neural stem cell pool and facilitates neuron maturation during adult hippocampal neurogenesisYuan-Hung Lin King, Chao Chen, John V Lin King, et al.
Plos One|January 23, 2016
Gradient Index Microlens Implanted in Prefrontal Cortex of Mouse Does Not Affect Behavioral Test Performance over TimeSeon A Lee, Kevin S Holly, Vladislav Voziyanov, et al.
Biorxiv : the Preprint Server for Biology|September 5, 2025
Cardiac-specific Kv1.1 deficiency alters cardiomyocyte electrophysiology without modifying overall cardiac function or arrhythmia susceptibilityKelsey Paulhus, Man Si, Krystle Trosclair, et al.
Journal of the American Heart Association|July 18, 2019
Deletion of the Cardiomyocyte Glucocorticoid Receptor Leads to Sexually Dimorphic Changes in Cardiac Gene Expression and Progression to Heart FailureDiana Cruz-Topete, Robert H Oakley, Natalie G Carroll, et al.
Physiological Reports|January 11, 2021
Kv1.1 potassium channel subunit deficiency alters ventricular arrhythmia susceptibility, contractility, and repolarizationKrystle Trosclair, Man Si, Megan Watts, et al.
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