Publication date: Available online 25 August 2020Source: Clinical NeurophysiologyAuthor(s): Elise Houdayer, Sae-Jin Lee, Mark Hallett
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New Findings What is the central question of this study ? Does fukutin deficiency in skeletal muscle cause mitochondrial dysfunction, and if so, can AMPK stimulation via AICAR attenuate this through regulation of mitochondrial biogenesis and autophagy? What is the main finding and its importance? Mitochondrial dysfunction is associated with fukutin deficiency and AMPK stimulation may benefit muscle contractility to a greater extent than mitochondrial function. Abstract Disruptions...
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Abstract The majority of individuals over an age of 60 have hypertension. Elevated blood pressure and older age are associated with very similar changes in brain structure and function. We review the parallel brain changes associated with increasing age and blood pressure. This review focuses on joint associations of aging and elevated blood pressure with neuropsychological function, regional cerebral blood flow responses to cognitive and metabolic challenges, white matter disruptions, grey matter...
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Key points By using a mechanically‐skinned fibre of rat, we investigated i) a transverse tubular‐system (T‐system) excitability after high‐intensity contractions, and ii) mechanisms undelying the fatigue‐induced alteration of the T‐system excitability. T‐system excitability estimated by using skinned fibre, which is highly regulated by T‐system Na+‐K+ ATPase, was decreased after muscle contractions, but it was fully restored by the treatment with dithiothreitol. The S‐glutathionylation of Na+‐K+...
Key points KV1.2 channels, encoded by the KCNA2 gene, regulate neuronal excitability by conducting K+ upon depolarization. A new KCNA2 missense variant was discovered in a patient with epilepsy, causing amino‐acid substitution F302L at helix S4, in the KV1.2 voltage‐sensing domain. Immunocytochemistry and flow cytometry showed that F302L does not impair KCNA2 subunit surface trafficking. Molecular dynamics simulations indicated that F302L alters the exposure of S4 residues to membrane lipids....
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