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Next, to assess whether the CSE induced defects in mitochondrial respiration were accompanied by changes in mtDNA genes, the expression of mitochondrial protein coding genes was determined for MT-CYB and MT-CO2 in cells exposed to gradually increasing concentrations of CSE, harvested at 3.5% (at 4 weeks) and 5% or 6% CSE (at 10 and 12 weeks)

Recent studies have shown that ULT made no difference in the occurrence of primary end-point events (composite of cardiovascular death, nonfatal MI, nonfatal stroke, or unstable angina with urgent revascularization)