Also, in a study that examined the anti-glucocordicoid properties of the same dose of RU-486 as has been used in the current experiment, cortisol treatment given simultaneously with RU-486 was not able to prevent RU-486 from blocking P-facilitated behavior [29].
For experiments where cortisol alone was measured, cells were plated at a density of 0.5 1.0×106 cells/35 mm dish.
For experiments where cortisol was measured and RNA was isolated from cell lysates, cells were plated at a density of 5 7×106 cells/60 mm culture dish.
Also in this experiment, plasma cortisol levels were analysed in samples from the fish used for Ussing chamber experiments, but only in the the two extreme groups at day 36-38 but no differences could be revealed.
In this experiment plasma cortisol samples below limit of detection were removed in order not to violate the statistical analysis.
In Experiment I, salivary cortisol concentrations were additionally measured immediately before, during and after recognition testing to control for possible influences of circadian and awakening-related variations in glucocorticoid release known to influence memory function [34], [64].
Significant interactions, when present (i.e. plasma cortisol Experiment 2), was further analysed by Bonferroni corrected pair-wise comparisons.
In Experiment 1, water samples were collected at 00 00 on days 0, 3, 6, 14, 29 and 48; in Experiment 2, water cortisol samples were collected at 08 00 (prior to first feeding) on days 0, 1, 3, 7, 10, 15 and 28.
In addition, a gene array experiment demonstrated that cortisol modulates the expression of genes involved in DNA damage signaling, including the proto-oncogene Cdc25A (involved in cell cycle delay following DNA damage) and the genes coding for the DNA damage sensors Chk1, Rad53 and Rad9 [ 110].
In both experiments, furthermore, changes in cortisol concentrations from baseline were significantly greater among men who spoke with women relative to men in the control conditions.
