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1  as gonadal steroid hormone replacement with estradiol benzoate.
2 eously with a behaviorally effective dose of estradiol benzoate.
3 r one or two injections of E2 in the form of estradiol benzoate (1 microg).
4     In female rats primed with a low dose of estradiol benzoate (2 microg), but not with a higher dos
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
7                                         Both estradiol benzoate (20 microg/kg) and testosterone propi
8      Neither estrogen alone (2 x 2 microg of estradiol benzoate, 48 and 24 h prior to the experiment)
9 omized hamsters that had been primed with SC estradiol benzoate (5 or 10 microg).
10 DA receptor binding induced by injections of estradiol benzoate 72 and 48 hr before death.
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
14 (VMN), were hormonally primed with 10 microg estradiol benzoate and 500 microg progesterone.
15 ), were hormonally primed with 25 micrograms estradiol benzoate and 500 micrograms progesterone.
16 pronounced differences were observed between estradiol benzoate and ovariectomized control groups in
17 les with ovariectomized females treated with estradiol benzoate and P.
18 n ovariectomized rats hormonally primed with estradiol benzoate and progesterone.
19 itantly administered aromatase inhibitor and estradiol benzoate developed gingival overgrowth.
20 eatment cycles with vehicle (Oil) or 17-beta-estradiol benzoate (E).
21 osterone propionate (Testos; n = 10), 0.5 mg estradiol benzoate (E2; n = 10), or vehicle (control gro
22                 Short-term administration of estradiol benzoate (EB) by five injections of 15 or 40 m
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
25                               Treatment with estradiol benzoate (EB) for 3 days increased the density
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
28                                              Estradiol benzoate (EB) increases the satiating effect o
29 rats, and in ovariectomized (OVX) rats given estradiol benzoate (EB) or oil vehicle (OIL).
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
34               Rats were injected with either estradiol benzoate (EB), EB and progesterone, progestero
35               However, during treatment with estradiol benzoate (EB), GDX females, but not GDX males,
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
50  wildtype mice were gonadectomized and given estradiol benzoate or vehicle.
51 mized (OVX) females treated with 5 microg of estradiol benzoate (OVX+E), OVX females, castrated (CAST
52 al area in ovariectomized (ovx) and ovx plus estradiol benzoate (ovx+E)-treated female rats.
53 rmone primed with 2.5, 7.5, or 25 micrograms estradiol benzoate plus 500 micrograms progesterone.
54 utaneously (s.c.) with estradiol benzoate or estradiol benzoate plus progesterone were examined.
55  third cerebral ventricle of ovariectomized, estradiol benzoate-primed rats.
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
58 rols and three treated with 20 microg/day of estradiol benzoate subcutaneously for 14 days).
59 naptic proteins altered by administration of estradiol benzoate, the ERalpha selective agonist PPT (1
60                                On day 1, the estradiol benzoate-treated animals spent significantly l
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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