Timothy D Nelson, Tiffany D James, Jennifer Mize Nelson, Cara C Tomaso, Kimberly Andrews Espy
Executive control throughout elementary school: Factor structure and associations with early childhood executive control
Developmental psychology
pretreatment mice low hepatotoxic dose acetaminophen apap results resistance subsequent higher dose apap mouse model termed apap autoprotection used identify differentially expressed genes cellular pathways could contribute development resistance hepatotoxicity male c57bl6j mice pretreated apap 400mgkg challenged 48h later 600mg apapkg livers obtained 4 24h later total hepatic rna isolated hybridized affymetrix mouse genome mu4302 genechip statistically significant genes determined gene expression changes also interrogated using causal reasoning engine cre extensive literature review narrowed focus methionine adenosyl transferase1 alpha mat1a nuclear factor erythroidderived 2like 2 nrf2 flavincontaining monooxygenase 3 fmo3 galectin3 lgals3 downregulation mat1a could lead decreases sadenosylmethionine known protect apap toxicity nrf2 activation expected play role protective adaptation upregulation lgals3 one genes supporting nrf2 hypothesis lead suppression apoptosis reduced mitochondrial dysfunction fmo3 induction suggests involvement enzyme known metabolize apap development tolerance apap toxicity subsequent quantitative rtpcr immunochemical analysis confirmed differential expression genes apap autoprotection model conclusion genomics strategy identified cellular pathways might explain molecular basis apap autoprotection