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A conifer metabolite corrects episodic ataxia type 1 by voltage sensor-mediated ligand activation of Kv1.1.

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January 2025

Bioelectricity Laboratory, Department of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA 92697.

Loss-of-function sequence variants in , which encodes the voltage-gated potassium channel Kv1.1, cause Episodic Ataxia Type 1 (EA1) and epilepsy. Due to a paucity of drugs that directly rescue mutant Kv1.

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Bridging thrombolysis versus direct endovascular treatment in acute vertebrobasilar artery complex occlusion.

J Neurosurg

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1Department of Neurology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui.

Objective: Endovascular treatment (EVT) is an effective treatment for patients with acute vertebrobasilar artery complex occlusion (VBAO). However, the benefit of bridging thrombolysis prior to EVT remains controversial. The purpose of the present study is to explore the best treatment strategy between bridging treatment (BT) and direct EVT in patients with acute VBAO.

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Physical activity improves myocardial structure, function and resilience via complex, incompletely defined mechanisms. We explored effects of 1-2 wks swim training on cardiac and systemic phenotype in young male C57Bl/6 mice. Two wks forced swimming (90 min twice daily) resulted in cardiac hypertrophy (22% increase in heart:body weight, P<0.

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