We could then wonder why the major regulator of glucocorticoid metabolism, 11bHSD2, is not expressed? Could this lack of expression represent a temporal window necessary for glucocorticoid activity? The combined lack of renal 11bHSD2 activity and the absence of MR expression in the neonatal kidney leave glucocorticoids free to access and activate GR, which might have an important role in kidney development and maturation. It has been suggested that glucocorticoids are implicated in developmental programming. This hypothesis could be sustained by the fact that, at variance with the kidney, 11bHSD2 activity is detected in other organs in the newborn. It is particularly interesting to note that while it is barely expressed in the adult brain, a high 11bHSD2 activity is detected in the developping central nervous system in rats, mice and humans until the end of gestation. It has been postulated that 11bHSD2 during fetal and neonatal life is essential to protect the developing nervous system from deleterious consequences of glucocorticoid exposure. Therefore 11bHSD2 could have an organ specific pattern of expression in the neonatal period, protecting against or facilitating glucocorticoid actions. This developmental process could contribute to the increased short-term adverse outcome rate observed in extremely low birth weight infants with high cortisol concentrations. Moreover, this specific temporal window where the kidney appears to be particularly sensitive to glucocorticoid action could explain the deleterious effects of prenatal glucocorticoid overexposure on renal development or epigenetic modifications leading to the predisposition for adult hypertension. Finally, our study demonstrates the existence of Benzoylpaeoniflorin a physiological, temporal 11bHSD2 expression window specific to the kidney, which appears to be necessary for optimal fetal and neonatal development, but as a result could also represent a breach in the protective mechanisms against excess glucocorticoid exposure responsible for adverse short-term and long-term effects through fetal programming, with a higher predisposition to specific diseases in later life. Although menstruation is at least as old as the human species, knowledge of the underlying mechanisms is limited. Its physiology has rarely been studied, and this is partly due to a lack of appropriate animal models. Apart from humans very few species of Old World monkeys and apes experience a menstrual cycle. This includes the flushing out of endometrial tissue and blood from the uterus to the vagina, clearly visible as overt menstruation. Two menstruating species of non-primates have been described the elephant shrew and the bat. The estrous cycle is much more common in placental mammals than the menstrual cycle. The former is characterized by Ursolic-acid complete reabsorption of the endometrial lining, which is not externally visible. Both reproduction cycles involve proliferation of stromal cells and ovulation, followed by the formation of the progesteroneproducing corpus luteum in the ovary. However, in the menstrual cycle endometrial stromal cells differentiate into decidual cells in response to the rapidly increasing progesterone level despite the absence of a blastocyst. In contrast, in the estrous cycle decidualization occurs only after conception, e.g. in mice it starts on day 4 post coitum, when endometrial stromal cells surround the implanting blastocysts. The decidua provides a vascular network for nutrition and gas exchange for the developing embryo if implantation occurs before a functional placenta is established. In both the menstrual and the estrous cycle the absence of implantation induces the degeneration of the corpus luteum in the ovary and subsequently the progesterone level drops.