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Author Spotlight: A Unique Mouse Model of Asphyxia-Induced Cardiac Arrest
Published on: April 14, 2023
Edilberto Amorim1, Wei-Long Zheng2, Jin Jing2
1From the Department of Neurology (E.A.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Neurology (E.A., W.-L.Z., J.J., M.B.W.), Massachusetts General Hospital, Boston; Department of Computer Science and Engineering (W.-L.Z.), Shanghai Jiao Tong University, China; Department of Neurology (J.J., T.P., M.B.W.), Beth Israel Deaconess Medical Center, Boston, MA; Department of Computer Science and Engineering (M.M.G.), Michigan State University, East Lansing; Department of Neurology (J.W.L.), Brigham and Women's Hospital; Athinoula A. Martinos Center for Biomedical Imaging (O.W.), Department of Radiology, Massachusetts General Hospital, Boston; Department of Neurology (S.T.H.), Barrow Neurological Institute Comprehensive Epilepsy Center, Phoenix, AZ; Department of Neurology (A.S., N.G., L.H.), Yale School of Medicine, New Haven, CT; Department of Neurology (N.G.), Universite Libre de Bruxelles, Belgium; Clinical Neurophysiology Group (B.J.R., M.C.T.-C., J.H., M.J.A.M.v.P.), University of Twente, Enschede; Department of Neurology (J.H.), Rijnstate Hospital, Arnhem; and Department of Neurology and Clinical Neurophysiology (M.J.A.M.v.P.), Medisch Spectrum Twente, Enschede, the Netherlands. edilbertoamorim@gmail.com amorim@ucsf.edu.
Transitions to high entropy neurophysiology states after cardiac arrest improve chances of good neurologic recovery. This indicates potential resilience mechanisms in the brain following hypoxic-ischemic injury.
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