James M. Vann

TL;DR: These findings suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals and suggest that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt 3.

TL;DR: It is shown that mammalian Sir2, SIRT1, represses repetitive DNA and a functionally diverse set of genes across the mouse genome and DNA damage-induced redistribution of SIRT 1 and other chromatin-modifying proteins may be a conserved mechanism of aging in eukaryotes.

TL;DR: Resveratrol, at doses that can be readily achieved in humans, fulfills the definition of a dietary compound that mimics some aspects of CR, andGene expression profiling suggests that both CR and resver atrol may retard some aspect of aging through alterations in chromatin structure and transcription.

TL;DR: Repression of neuronal gene expression is a prominent and recently evolved feature of brain aging in humans and rhesus macaques that may alter neural networks and contribute to age-related cognitive changes.

TL;DR: Aminoglycoside selection of staphylococcal menadione and hemin auxotrophs and subsequent persistence of these variants in the intracellular milieu may adapt S. aureus for evasion of host defenses and resistance to antimicrobial therapy.