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1 as gonadal steroid hormone replacement with estradiol benzoate.
2 eously with a behaviorally effective dose of estradiol benzoate.
5 itantly administered aromatase inhibitor and estradiol benzoate (2.0 mg/day each subcutaneously) serv
6 Ovariectomized rats were treated with 17beta-estradiol-benzoate (2 microg) and 26 hours later with oi
11 rats were hormonally primed with 0.5 microg estradiol benzoate and 500 microg progesterone to produc
12 mized rats, hormonally primed with 25 microg estradiol benzoate and 500 microg progesterone, received
13 ized rats, hormonally primed with 0.5 microg estradiol benzoate and 500 microg progesterone, were inf
16 pronounced differences were observed between estradiol benzoate and ovariectomized control groups in
21 osterone propionate (Testos; n = 10), 0.5 mg estradiol benzoate (E2; n = 10), or vehicle (control gro
23 Treatment of ovariectomized (OVX) rats with estradiol benzoate (EB) caused rapid and transient induc
24 r levels of lordosis behavior in response to estradiol benzoate (EB) compared with OVX females treate
26 variectomized (OVX) female rats treated with estradiol benzoate (EB) had a 30%-40% reduction in the l
27 /group) were treated with 0, 2, or 10 microg estradiol benzoate (EB) in sesame oil on 2 consecutive d
30 sed upon prior evidence that prepriming with estradiol benzoate (EB) reduced the ability of 8-OH-DPAT
31 r ovariectomy, and administration of 17-beta-estradiol benzoate (EB) restored this escalated anxiety-
32 rrets treated sequentially with TP, oil, and estradiol benzoate (EB) were given simultaneous access t
33 agonist MK-801, castrated males treated with estradiol benzoate (EB), and castrated males treated wit
36 ved daily injections of 10 microg of 17 beta-estradiol benzoate (EB), or 250 microg of testosterone p
37 omized and received replacement therapy with estradiol benzoate (EB), testosterone propionate (TP), o
38 ree weeks post-ovariectomy, animals received estradiol benzoate (EB, 0.03 mg or 0.3 mg kg(-1) day(-1)
39 ed (OVX) rats 24 h (but not 6 or 72 h) after estradiol benzoate (EB; 10 microg) administration had in
40 lectrophysiological recordings revealed that estradiol benzoate (EB; 25 microgram, s.c.) decreased th
41 ectomized (OVX) or OVX-estrogen-primed rats (estradiol benzoate, EB, 10 microg 48 and 24 h prior to e
42 amus (VMN), were injected with 0.5 microgram estradiol benzoate followed 48 h later with 500 microgra
43 f treatment, rats were primed with 10 microg estradiol benzoate followed 48 h later with 500 mug prog
44 tomized prairie voles that were treated with estradiol benzoate had a higher level of BDNF mRNA label
45 one acetate at counterpoising the effects of estradiol benzoate in the uterine wet weight assay using
46 d that treatment of ovariectomized rats with estradiol benzoate induced a rapid and reversible increa
47 ter treatment of gonadectomized animals with estradiol benzoate on P0, levels at all ages were simila
48 ized rats, primed subcutaneously (s.c.) with estradiol benzoate or estradiol benzoate plus progestero
49 ments animals were then injected with either estradiol benzoate or steroid suspension vehicle and the
51 mized (OVX) females treated with 5 microg of estradiol benzoate (OVX+E), OVX females, castrated (CAST
53 rmone primed with 2.5, 7.5, or 25 micrograms estradiol benzoate plus 500 micrograms progesterone.
56 cle cannulae were injected with 10 microg of estradiol benzoate s.c., followed 72 hr later by microin
57 ere was no effect of 2.5 microg or 25 microg estradiol benzoate (s.c.) on extracellular 5-HT; but the
59 naptic proteins altered by administration of estradiol benzoate, the ERalpha selective agonist PPT (1
61 nuclei showed a significant reduction in the estradiol benzoate versus control groups in areas of the
62 However, animals primed with 2.5 micrograms estradiol benzoate were significantly more affected by t
63 gression, nonpregnant pigs were treated with estradiol benzoate, which did not affect the SLA or beta
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