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(3/20/18) mp3 #260 Jesse Sheidlower Time for a books & booze break

The effects of levocarnitine on body composition are modest, and it would be misleading to suggest otherwise

Key Points Friedreich ataxia is an autosomal-recessive disorder caused by mutations (usually GAA-repeat expansions) in the gene encoding the mitochondrial protein frataxin The mutations cause a dramatic reduction in the expression of frataxin Friedreich ataxia seems to be restricted to individuals from Europe, the Middle East, North Africa and India Well-established standards exist for the clinical and genetic diagnosis of Friedreich ataxia A phase II trial with the antioxidant and mitochondrial enhancer idebenone has shown concentration-dependent symptomatic benefits, as measured using neurological scales Other treatments that interfere with disease pathogenesis and progression are currently being developed, and preclinical data indicate that specific histone deacetylase inhibitors upregulate frataxin expression This is a preview of subscription content, access via your institution Access options Subscribe to this journal Receive 12 print issues and online access 186,36 per year only 15,53 per issue Buy this article Purchase on SpringerLink Instant access to the full article PDF

Endothelial-vasoprotective effects of high-density lipoprotein are impaired in patients with type 2 diabetes mellitus but are improved after extended-release niacin therapy