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These malfunctional astrocytes are characterised by a prominent functional asthenia and lose key homoeostatic proteins, such as glutamate transporters, K ir 4.1 channels, glutamine synthetase and gap junctional protein connexin 43, which results in an uncoupling of astrocytic syncytia

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The NAD+-dependent deacetylase SIRT2 attenuates oxidative stress and mitochondrial dysfunction and improves insulin sensitivity in hepatocytes

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