However, such inhibition is likely to be incomplete. In addition, Wnt/b-catenin signaling may exert distinct functions in a dose dependent manner. It is conceivable that the two functions of Wnt/b-catenin signaling are also dose-dependent: Strong Wnt/b-catenin signaling inhibits chondrocyte cell fate determination and maintenance whereas weaker Wnt/b-catenin signaling promotes chondrocyte hypertrophy by reducing PTHrP signaling activities. Our results suggest that Wnt/b-catenin signaling may also interact with PTHrP signaling indirectly through a secondary signaling pathway. To this end,GSK1120212 it will be interesting to further investigate genetically whether Gdf5/Bmp signaling control initiation chondrocyte hypertrophy by antago-nizing PTHrP signaling and whether Gdf5/Bmp signaling also mediates the role of Wnt/b-catenin signaling in hypertrophic chondrocyte maturation. It is well established that stress has a negative impact on reproductive processes in animals. Although the mechanisms are far from clear, the effects of stress are thought to be due to interactions of the hypothalamic-pituitary-adrenal axis with the HP-gonadal axis. For instance,ICG-001 corticotropin releasing factor, a key hypothalamic neurohormone that activates the HPA signaling cascade, also suppresses the release of hypotha-lamic gonadotropin-releasing hormone. While corticosteroid is essential in order for animals to recover from exposure to a stressor, this steroid also impacts the HPG axis at a number of sites, depending on the species, sex, and the magnitude and duration of this plasma hormonal response. For instance, cortisol inhibits GnRH pulsatility, and decreases gonadotropin release from the pituitary. In the testes, cortisol suppresses testosterone production by reducing LH responsiveness, including downregulation of LH receptors. In fish, cortisol decreased 11-keto testosterone production, but did not affect ovarian estradiol production in three species of fish. However, cortisol treatment decreased hepatic expression of estrogen receptors, vitelline envelope protein-b and vitellogenin.