Sox9 controls the determination of cartilage and muscle cell fate in muscle satellite cells, and may play important roles in regulating the process of fracture healing. As these factors are also involved in early embryonic cell fate determination, our work supports the notion that healing 
recapitulates development. Understanding these signaling events may eventually allow us to harness these mechanisms of chondrogenic differentiation to enhance fracture healing. Age-related cognitive deficits are highly prevalent and constitute an important health risk in the human population. They can presage development of neurodegenerative disease, and are a primary reason for elderly placement in assisted living facilities. Perturbations in sleep are also a common complaint among the elderly and include circadian advance, sleep fragmentation, and insomnia. Healthy young adults show some aging-like phenotypes when deprived of sleep, including daytime sleepiness, Chlorhexidine hydrochloride metabolic syndrome-like changes, and cognitive deficits. This is consistent with work suggesting that sleep promotes memory, possibly through slow wave influence on synapses and/or promotion of macro molecule synthesis. Further, numerous studies have pointed to the deleterious effects of stress and stress hormones on brain function and a major hypothesis of aging posits that continued exposure to stress and stress hormones over age is a fundamental cause of age-related deficits in various systems. Thus, dysregulated sleep and stress seen with age might contribute to age-related functional changes. Despite the seemingly similar effects of age, stress and sleep deprivation, and the high prevalence of sleep changes and new onset stress with age, relatively few studies have tested for a molecular relationship between the influences of SD, stress, and aging on brain tissue. Here, we hypothesized that an aged or stressed animal’s hippocampal transcriptional profile would be similar to that of a sleep-deprived subject. We tested a prediction of this hypothesis by sleep depriving young animals and statistically testing for aging- or stress-like transcriptional phenotypes in the hippocampus. Young F344 rats were sleep deprived for 24 or 72 hours using the modified multi-platform ‘flower pot’ method. Blood corticosterone levels, adrenal weights, body weights, and hippocampal CA1 gene expression profiles were measured. A second set of rats was exposed to novel environment stress for 24 or 72 hours to help control for non-specific stress effects of the environmental change necessitated by the sleep deprivation protocol. In a third set of animals, the SD protocol was applied and gene products were validated at the protein level using Western blots. Data were subjected to bioinformatic analysis and contrasted with results from prior transcriptional profiling studies as noted in Results. Transcriptional comparison suggests SD, stress and aging interact with a similar subset of genes within the hippocampal transcriptome. However, although there was strong directional agreement between SD and NES, notable disagreements between SD and aging were seen, including opposite inflammatory and glial expression changes. Our studies also identified SD-specific genes and gene profiles that may represent targets for therapeutic intervention. These include the previously identified Homer1 as a potential sleep regulation molecule, but also other novel Tulathromycin B candidate genes involved in pathways related to synaptic function, vesicular release and intercellular adhesion.