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https://www.selleckchem.com/products/nibr-ltsi.html Results Both aqueous and butanolic extracts were capable of reducing significantly the levels of glucose, cholesterol and triacylglycerol and thus demonstrating their hypolipidemic and hypoglycemiant effects. Furthermore, the extracts prevented the occurrence of hepatic complications during treatment. The phytochemical profile of the extracts was investigated, and the natural products detected were in agreement with those that had been previously described in the literature. Conclusion Based on the significant reductions in biochemical parameters and the histologic evidence for the absence of complications in the liver, pancreas of the treated animals, Equisetum giganteum can be a therapeutically relevant resource in the treatment of diabetes and hyperlipidemia.Timothy syndrome (TS) is a neurodevelopmental disorder caused by mutations in the pore-forming subunit α11.2 of the L-type voltage-gated Ca2+-channel Cav1.2, at positions G406R or G402S. Although both mutations cause cardiac arrhythmias, only Cav1.2G406R is associated with the autism-spectrum-disorder (ASD). We show that transcriptional activation by Cav1.2G406R and Cav1.2G402S is driven by membrane depolarization through the Ras/ERK/CREB pathway in a process called excitation-transcription (ET) coupling, as previously shown for wt Cav1.2. This process requires the presence of the intracellular β-subunit of the channel. We found that only the autism-associated mutant Cav1.2G406R, as opposed to the non-autistic mutated channel Cav1.2G402S, exhibits a depolarization-independent CREB phosphorylation, and spontaneous transcription of cFos and MeCP2. A leftward voltage-shift typical of Cav1.2G406R activation, increases channel opening at subthreshold potentials, resulting in an enhanced channel activity, as opposed to a rightward shift in Cav1.2G402S. We suggest that the enhanced spontaneous Cav1.2G406R activity accounts for the increase in basal transcriptional

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