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1 eta-estradiol or diethylstilbestrol (DES), a synthetic estrogen.
2 estin) or a combination of a progestin and a synthetic estrogen.
3 The antidepressant fluoxetine (FLX) and the synthetic estrogen, 17 alpha-ethinylestradiol (EE2), are
4 ned the effects of tamoxifen (TAMOX) and the synthetic estrogen 17alpha-ethynylestradiol (EE) on estr
5 to show that Era(-/-) mice were resistant to synthetic estrogen 17alpha-ethynylestradiol (EE2)-induce
6 (Micropterus salmoides) exposed to a potent synthetic estrogen (17alpha-ethinylestradiol, EE2) at a
7 unction of beta-catenin to be induced by the synthetic estrogen, 4-hydroxytamoxifen, leading to regul
8 ently found that diethylstilbestrol (DES), a synthetic estrogen agonist, inhibits thrombin-induced Ca
16 ure to 17beta-estradiol and the nonsteroidal synthetic estrogen diethylstilbestrol (DES) disturbs the
17 es have shown that perinatal exposure to the synthetic estrogen diethylstilbestrol (DES) leads to fem
18 strated that perinatal administration of the synthetic estrogen diethylstilbestrol (DES) to mice and
19 Following 12 weeks of treatment with the synthetic estrogen diethylstilbestrol (DES), pituitary m
22 this model, neonatal exposure to the strong synthetic estrogen, diethylstilbestrol, downregulated ex
24 ies during development have used natural and synthetic estrogen dosages in the milligram to microgram
25 EN), and quercetin (QRC), were compared with synthetic estrogens, for example, bisphenol A (BPhA), no
26 those found when diethylstilbestrol (DES), a synthetic estrogen, is used, suggesting that the estroge
27 radiol (17beta-E2) and estrone (E1)] and two synthetic estrogen mimics [zeranol (alpha-ZAL) and zeara
28 hese receptors was activated or inhibited by synthetic estrogen or progesterone analogs that do not b
31 omoter or a promoter containing multimerized synthetic estrogen response elements were used to determ
32 of the vitellogenin B1 promoter as well as a synthetic estrogen responsive element (ERE)-containing p
34 naling, mediate the proliferative effects of synthetic estrogens such as tamoxifen, in promoting endo
35 adiol 3-sulfate (E2-3S), and two biochemical synthetic estrogen sulfates, 17 beta-estradiol 17-sulfat
38 n order to validate the applicability of the synthetic estrogens to immuno-recognition and to optimiz
39 ructural similarity to diethylstilbestrol, a synthetic estrogen, we examined whether resveratrol migh
40 erences and the effects of synthetic and non-synthetic estrogens were examined in a model of focal ce
41 at municipal wastewaters contain natural and synthetic estrogens, which interfere with development an
42 show that contraception can be achieved with synthetic estrogen, with progestin, and by combining the