estrogen-induced

estrogen-induced

stimulated by high blood levels of estrogen.

estrogen-induced transdifferentation
a persistent high estrogen intake causes male behavior in ewes and secondary sex characters, e.g. mammary gland and teat hypertrophy, in wethers, and changes in the promotion of development of endometrial-type glands in the cervix.
estrogen-induced uroliths
diets high in estrogens thought to contribute to the development of uroliths by increasing the rate of epithelial desquamation in the urinary tract, thus facilitating the formation of a nidus around which concretion of salts can then develop.
References in periodicals archive ?
Co-transcriptional R-loops are the main cause of estrogen-induced DNA damage.
As mentioned above, estrogen did not increase the expression of ABCC4 and SLCO2A1 mRNAs in our previous study [8], but that observation has raised a question as to how PG movement is regulated in estrogen-induced pseudopregnant pigs.
1996) and that IGF-1 can stimulate LHRH secretion (Hiney and Dees 1991), suggesting that activation of the HPG axis leads to both sexual maturation and a growth spurt mediated through estrogen-induced stimulation of the GH/IGF-1 axis.
All of the women had had hysterectomies, so they did not need a progestin to protect their uterus from estrogen-induced cancers.
Use of lithium for treatment of estrogen-induced bone marrow hypoplasia in a dog.
This significant relationship between estrogen levels and HRV in the current study, and reports of estrogen-induced enhancement of vagal activity (Saleh & Connell et al (15), 2000) and reduction of sympathetic activity (Ettinger et al.
Sildenafil citrate increases uterine blood flow and potentiates estrogen-induced vasodilation (2).
The main reason for adding a progestin to estrogen therapy for vasomotor symptoms in postmenopausal women with a uterus is to prevent estrogen-induced development of endometrial polyps, hyperplasia, and cancer.
Visser found that Cyclopia extracts prevent the estrogen-induced growth of breast cancer cells by targeting and inhibiting estrogen receptor subtypes that promote the growth of these cells.
Our lab has shown a tight correlation of the estrogen-induced enhancement in memory to be highly dependent upon increases in NR2B -containing NMDARs because this enhancement is prevented when NR2Bs are pharmacologically blocked in hippocampus in vivo.

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