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The extant species-specific complement of AOX isoenzymes is the result of a complex evolutionary process consisting of a first phase characterized by a series of asynchronous gene duplications and a second phase where the pseudogenization and gene deletion events prevail

Malnutrition as a secondary diagnosis significantly impacts MS-DRG assignment and risk scores

Inhibition of ASAH2 led to increased p53 protein stability, upregulation of Hmox1 expression, suppression of ROS generation, and MDSC death via iron-dependent lipid peroxidation

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A loading phase of 4 to 6 weeks at the higher end of the range is common, followed by a maintenance dose of 1 mg/day three to five times per week