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It also improves endothelium-dependent vasodilation (Ellis et al., 2000), with effects partially independent of antioxidant actions, possibly involving NO-mediated vasodilation or inflammation regulation

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Regarding IFN-2, the symptomatic group had decreased levels in comparison to the asymptomatic group (respectively, 0.07286 0.07286 pg mg protein -1 and 0.9263 0.5807 pg mg protein -1

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Defects in upstream autophagy in neurodegenerative disease As strong genetic evidence implicates proteins of the autophagylysosome pathway and the broader ELA network in neurodegenerative disease pathogenesis, it is crucial to understand how this network maintains cell homeostasis and how its disruption may impact a wide range of neuronal and glial functions in disease and cause resulting phenotypes

51 As GSH is known to be present in CSF at very low concentrations (~0.2 mol/l in both healthy and PD subjects), 52 relative to brain tissue concentrations (~1 mmol/l), 7 LCModel-calculated Cr concentrations ( C measured ) were corrected ( C corrected ) using the following formula, which assumes negligible contribution of CSF GSH to the total GSH signal: Absolute GSH levels (IU) were calculated by multiplying GSH/Cr ratios by CSF-corrected absolute Cr concentrations (IU)