Does exogenous estradiol enhance apoptosis in regressing post-partum rat corpora lutea possibly mediated by prolactin?
We have established that estradiol accelerates apoptosis in the CL during post-partum luteal regression through a mechanism that possibly involves the secretion of pituitary prolactin. We have also shown that the post-partum rat CL express ERalpha and ERbeta mRNAs suggesting that they can be targeted by estrogen.
Hyperglycemia could be considered as a marker of brain injury and when present upon admission, could reflect extensive brain damage with frequently associated mortality and bad outcome. The inability to maintain normal blood glucose levels during the first 48 h could be a predictive factor of bad outcome. Avoiding hyperglycemia in the initial phase could be a major issue in children with severe TBI.