Heung M. Lee

TL;DR: The studies imply that the elevation in apelin expression during hypoxia and inflammation in the GI tract functions in part to stimulate epithelial cell proliferation.

TL;DR: The new rat model affords insight into the complex molecular pathophysiology of smoke inhalation in the brain, and microarray analysis revealed increased brain expression of nitric oxide synthase (NOS) and NOS ligand after inhalation of smoke.

TL;DR: It is shown that DNA adducts detectable by their ability to block PCR amplification form in the rat hippocampus after acute exposure to smoke, while mismatched bases emerged at the later recovery times, potentially due to an erroneous DNA repair process.

TL;DR: It is reported that a 30-minute exposure of awake rats to ambient wood combustion smoke induces protein nitration in the rat hippocampus and that mitochondrial proteins are a sensitive nitration target in this setting and may contribute to the reduction in mitochondrial respiratory capacity and underlie, in part, the brain pathophysiology after acute inhalation of combustion smoke.

TL;DR: It is suggested that prolonged inadequate oxygenation may trigger a compensatory increase in neuronal mitochondrial DNA content to partially mitigate compromised energy homeostasis and reduced energetic capacity in the developing hypoxic brain.