Does resveratrol prevent the prohypertrophic effects of oxidative stress on LKB1?
Our data identify a molecular mechanism in the cardiomyocyte involving the oxidative stress-derived lipid peroxidation byproduct HNE and the LKB1/AMPK signaling pathway that contributes to the development of left ventricular hypertrophy. We also suggest that resveratrol may be a potential therapy for patients at risk for developing pathological cardiac hypertrophy by preventing this prohypertrophic process.
Preoperative manometric assessment of oesophageal motility does not correlate with postoperative outcome, and oesophageal dysmotility should not be regarded as a contraindication to laparoscopic Nissen fundoplication.