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aModel A, standard risk prediction model without estradiol.
In Table 3, we present the standard risk prediction model without estradiol and an enhanced model with imputed estradiol based on an average of five imputations.
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To assess the additional predictive power of serum estradiol, we computed age-specific (5-year age groups) deciles of the risk function without estradiol (model A) as well as including imputed estradiol (model B).
We used Fos-immunoreactivity (Fos-IR) to examine the activation of several subregions of the HPC and striatum in ovariectomized female rats with or without estradiol replacement 30 min after place or response learning.
However, after 3 weeks of ovariectomy with or without estradiol treatment, only Gpx3 gene expression was upregulated in response to the hormone.
The gene expression profile of human vascular cells treated with or without estradiol was assessed by using the Human Genome U133A plus 2.0 microarray technology from Affymetrix.
These six stably transfected LCLs were cultured with or without estradiol (E2), as described previously [ 6].
All CL cell lines were grown in 15% FBS in RPMI 1640 with 2 mM L-Glutamine for studies with and without estradiol (E2, 17β-estradiol) exposure.
Estradiol benzoate was diluted in 100% ethanol at 1 mg/ml, and an equivalent amount of ethanol (without estradiol) was added to control cultures.
The model for estradiol explained 19% of the variability in estradiol, while the model for progesterone explained 20% of the variability in progesterone.
In an immature rat uterine model, ethinyl estradiol increased the wet uterine weight after 3 days of treatment.
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