ライフサイエンスコーパス: estrogen

1 ha, and thrombin (positive control), but not estrogen.

2 onal corpora lutea through the production of estrogen.

3 erential response to EPO was associated with estrogen.

4 nt independently of and synergistically with estrogen.

5 ry insult, and this was further increased by estrogen.

6 tal liver and initially considered as a weak estrogen.

7 omen, perhaps owing to protective effects of estrogens.

8 vovaginal atrophy includes administration of estrogens.

9 Estrogen, 17beta-estradiol (E2), is a powerful therapeut

10 The cellular mechanisms by which estrogen acts on bone are still a matter of controversy.

11 Estrogen addition restored ERK phosphorylation in EVI1-s

12 TMBPF did not show estrogen-agonist or antagonist activity in the estrogen

13 on) The USPSTF recommends against the use of estrogen alone for the primary prevention of chronic con

14 Estrogen analytes were measured in serum or urine by liq

15 As protein expression levels of AROM, estrogen and androgen receptors did not differ between m

16 whose activity is repressed by the liganded estrogen and androgen receptors, and by the hypothalamic

17 l as receptors for the mammatrophic hormones estrogen and growth hormone.

18 n the pituitary, resulting in elevated serum estrogen and higher numbers of large ovarian follicles.

19 mmunohistochemical analysis was positive for estrogen and progesterone receptor expression and negati

20 95% confidence interval (CI), 0.94-1.39], by estrogen and progesterone receptor status, or by ages at

21 reast cancers (TNBC) that lack expression of estrogen and progesterone receptors (ER/PR), or amplific

22 Devoid of the estrogen and progesterone receptors, along with the rece

23 noma, tubular variant, strongly positive for estrogen and progesterone receptors.

24 inal epithelium does not respond properly to estrogen and progesterone signals and remains unreceptiv

25 enomenon is dependent on pregnancy hormones (estrogen and progesterone), delta-opioid receptors, and

26 eceiving MHT that contained a combination of estrogen and progestin (hazard ratio, 1.37; 95% CI, 1.10

27 SPSTF recommends against the use of combined estrogen and progestin for the primary prevention of chr

28 erstand the brain synthesis of steroids like estrogens and the implications for neurobiology and beha

29 The results show that testosterone, estrogen, and hydrocortisone did not alter basal CatSper

30 haride (LPS), in the presence and absence of estrogen, and the levels of IL6 expression evaluated.

31 rine immune system as a sensitive target for estrogens, and that oral exposures to BPA and EE can hav

32 Here, we analyzed 33 steroids, including estrogens, androgens, progestins, and glucocorticoids, i

33 ct of BPA was blocked by Fulvestrant, a full estrogen antagonist, while the effect of estradiol was n

34 The effects of estrogen are long-lasting; bone marrow-derived macrophag

35 Estrogens are synthesized in the periphery and in the br

36 the mammary gland where the direct action of estrogens can be tested during embryonic days (E)14 to 1

37 Although estrogens can enhance drug-seeking behavior, they do not

38 o incubated at male-producing temperature to estrogen causes it to develop ovaries.

39 , which in turn increases TAM-dependent anti-estrogen chemosensitivity in vitro and in vivo.

40 In females, estrogen concentrations fluctuate over the estrous/menst

41 antitative agreement between ER activity and estrogen concentrations, as well as the detection of AR

42 Potential triggers included estrogen-containing oral contraceptives (eOC), hormonal

43 one lining cells as important gatekeepers of estrogen-controlled bone resorption.

44 e potential impact of E1 as an environmental estrogen currently is underestimated.

45 ase in bone resorption observed in states of estrogen deficiency in mice is mainly caused by lack of

46 Age-related estrogen deficiency leads to accelerated bone resorption

47 r 1 y potently attenuated BMD loss caused by estrogen deficiency, improved bone turnover, promoted a

48 lavones may exert beneficial effects against estrogen-deficient bone loss.

49 t of IL-27 supplementation on ovariectomized estrogen-deficient mice on various immune and skeletal p

50 loss at the lumbar spine and femoral neck in estrogen-deficient women.

51 ar level, DUSP3 deletion was associated with estrogen-dependent decreased phosphorylation of ERK1/2 a

52 are attractive targets for the treatment of estrogen-dependent diseases like endometriosis and breas

53 o measured in female 129S6/SvEv mice bearing estrogen-dependent SSM3 mouse mammary tumors, male athym

54 ance imaging, we demonstrate here that acute estrogen depletion alters within minutes auditory proces

55 We report that acute estrogen depletion rapidly disrupts auditory processing

56 after acquisition of resistance to long-term-estrogen-deprivation (LTED) and subsequent resistance to

57 d at E14 and cultured for 5 days showed that estrogens directly altered fetal mammary gland developme

58 hasone (Dex)-induced trans-repression of the estrogen E2 program appears to depend on GR SUMOylation,

59 By contrast, under inflammatory conditions, estrogen effects depend upon strength of the partner mol

60 , female rats were ovariectomized to isolate estrogen effects on reinstatement.

61 However, in inflammatory conditions, estrogen effects were partially overwhelmed by pro-infla

62 We measured in vitro estrogen (ER), androgen (AR), and glucocorticoid recepto

63 In WTP influents, estrogens (estrone, 17beta-estradiol, and estriol), andr

64 ages from ovariectomized mice implanted with estrogen exhibited enhanced IL-4-induced M2 gene express

65 cer risk during adulthood has been linked to estrogen exposure during fetal life.

66 omboembolic risk, and lower-dose transdermal estrogen formulations are preferred over high-dose oral

67 e enriched for signaling pathways regulating estrogen, glucocorticoid, B-cell receptor signaling, and

68 In resting conditions, estrogens have strong regulatory effects on thymic epith

69 dentify a potential cellular source of local estrogen, here we examined the expression of aromatase,

70 210 DEGs are known to change in response to estrogen in the brain.

71 n the postmenopausal endometrium, similar to estrogen in the breast, we compared ERalpha sites in tam

72 The beneficial role of estrogen in the vascular system may be due, in part, thr

73 reflecting tumor evolution or acquisition of estrogen independence.

74 tion caused increased aromatase activity and estrogen-independent ERalpha binding to target genes, re

75 ies demonstrate that PTGER4 is essential for estrogen-independent growth.

76 nd male and female athymic nude mice bearing estrogen-independent MDA-MB-231 human breast cancer xeno

77 YBX1 to the estrogen receptor can promote an estrogen-independent phenotype that can be reverted by i

78 Several potential estrogen-induced paracrine-acting factors were identifie

79 pecialized nipple epidermis is maintained by estrogen-induced repression of TGFbeta signaling in the

80 To understand the molecular mechanisms of estrogen-induced uterine cell growth, we removed the est

81 stem for real-time imaging of a single-copy, estrogen-inducible transgene in human cells.

82 We found that supplementation of estrogen into ovariectomized female mice enhanced M2 pol

83 Estrogen is critical for skeletal homeostasis and regula

84 Estrogen is necessary for embryo transport in mammals; h

85 rt the hypothesis that early loss of ovarian estrogens is a risk factor for type 2 diabetes.

86 As preterm birth causes plasma estrogen level to drop 100-fold, the estrogen replacemen

87 BACKGROUND & AIMS: Low estrogen levels can contribute to development of fecal i

88 sis that individual variation in response to estrogen levels contributes to fear regulation and PTSD

89 regnant SERT (-/-) mice displayed normalized estrogen levels, markedly reduced fat accumulation, and

90 his may be mediated, in part, by circulating estrogen levels.

91 Low-dose vaginal estrogen, lidocaine, and dehydroepiandrosterone may also

92 ofile as radical scavengers, antimicrobials, estrogen-like activators and acetylcholinesterase/tyrosi

93 estradiol (EE) are synthetic chemicals with estrogen-like activities.

94 d that oral exposures to BPA and EE can have estrogen-like immunomodulatory affects in both sexes.

95 ypotheses for how metabolism of these parent estrogens may influence risk.

96 mammals; however, the mechanism involved in estrogen-mediated cellular function within the oviduct r

97 h the BRCA1 DNA repairing signalling and the Estrogen-mediated G1/S phase entry pathways were found u

98 improved bone turnover, promoted a favorable estrogen metabolite profile (2-OH:16alpha-OH), and stimu

99 atio, 1.37; 95% CI, 1.10-1.70) compared with estrogen monotherapy.

100 FSHD myoblasts) to investigate the effect of estrogens on muscle properties.

101 hormones, such as androgen, luteotropin, and estrogen, on corneal stroma bioenergetics.

102 Women using estrogen-only therapy compared with placebo had signific

103 us HCA risk factors, including imbalances in estrogen or androgen hormones.

104 pared with males, an effect tied to elevated estrogen phases of the ovarian hormone cycle.

105 Estrogen plays a critical role in many physiological pro

106 The beneficial versus detrimental roles of estrogen plus progesterone (E+P) in breast cancer remain

107 Women using estrogen plus progestin compared with placebo experience

108 ng menopausal estrogen therapy or menopausal estrogen plus progestogen therapy or raloxifene for the

109 Aromatase inhibitors (AIs) prevent estrogen production and inhibit ER signaling, resulting

110 Finally, we also show that estrogen production specifically modulates selectivity f

111 their promoters were relatively decreased in estrogen + progestin-treated tumors.

112 t or recent use of various oral combination (estrogen-progestin) contraceptives varied between 1.0 an

113 Estrogens protect against apoptosis of endothelial cells

114 The majority of breast cancers expresses the estrogen receptor (ER(+)) and is treated with anti-estro

115 e pathologic complete response (pCR) rate in estrogen receptor (ER) -positive primary breast cancer t

116 ed gene-expression profiles in patients with estrogen receptor (ER) -positive, early-stage breast can

117 ry effects of 17beta-estradiol (non-specific estrogen receptor (ER) agonist), PPT (ERalpha-specific a

118 ted greater expression of the IL-4Ralpha and estrogen receptor (ER) alpha compared with macrophages f

119 ted of altering estrogenic signaling through estrogen receptor (ER) alpha or beta (mERbeta1 in mice).

120 in the OV/MEPO and ARH were seen to express estrogen receptor (ER) alpha.

121 upregulation of NEMO, the gene that harbored estrogen receptor (ER) binding sites within its promoter

122 Studies of the estrogen receptor (ER) coactivator protein Mediator subu

123 rous/menstrual cycle, dynamically modulating estrogen receptor (ER) expression, activity, and traffic

124 The estrogen receptor (ER) is a target for endocrine therapy

125 tumors and was most strongly associated with estrogen receptor (ER) positivity (GRPR was high in 83.2

126 Estrogen receptor (ER) recruits steroid receptor coactiv

127 tabolites were significantly associated with estrogen receptor (ER)-positive (ER(+)) breast cancer (4

128 Greater than 50% of estrogen receptor (ER)-positive breast cancers coexpress

129 er risk and prognosis is well established in estrogen receptor (ER)-positive disease but less clear i

130 association studies (GWAS) of predominantly estrogen receptor (ER)-positive disease.

131 F2 induction and nuclear accumulation in the estrogen receptor (ER)-positive MCF7 breast cancer cells

132 y, particularly against tumors driven by the estrogen receptor (ER).

133 ice variant of the estrogen receptor, namely estrogen receptor (ERalpha-36), associated with a poor p

134 we showed that, in 3T3-L1 cells, E2 and the estrogen receptor 1 (ESR1) agonist PPT induced VEGFA exp

135 or 30 (GPR30), also called G protein-coupled estrogen receptor 1 (GPER1), is thought to play importan

136 ry breast cancer tissue and resected BrM (10 estrogen receptor [ER]-negative and 10 ER-positive) from

137 Bioavailable isoflavones with selective estrogen receptor affinity show potential to prevent and

138 The majority of human breast cancer is estrogen receptor alpha (ER) positive.

139 Approximately 75% of breast cancers express estrogen receptor alpha (ERalpha) and depend on estrogen

140 pid metabolism and body weight by repressing estrogen receptor alpha (ERalpha) expression.

141 ctions of glucocorticoid receptors (GRs) and estrogen receptor alpha (ERalpha) in breast cancer devel

142 Estrogen receptor alpha (ERalpha) is a critical prognost

143 Estrogen receptor alpha (ERalpha) is an important target

144 All compounds were high affinity estrogen receptor alpha (ERalpha) ligands but displayed

145 Estrogen receptor alpha (ERalpha) regulates gene transcr

146 The DNA-binding sites of estrogen receptor alpha (ERalpha) show great plasticity

147 lective loss- or gain-of-function mutants of estrogen receptor alpha (ERalpha) to define two distinct

148 Estradiol acts via estrogen receptor alpha (ERalpha)-expressing afferents o

149 Many estrogen receptor alpha (ERalpha)-positive breast cancer

150 Many estrogen receptor alpha (ERalpha)-positive breast cancer

151 fully applied for detection of the biomarker estrogen receptor alpha (ERalpha).

152 which can be eliminated by an antagonist of estrogen receptor alpha (ERalpha).

153 this effect was absent in mice lacking liver estrogen receptor alpha (Esr1) (LERKO mice).

154 -induced uterine cell growth, we removed the estrogen receptor alpha (Esr1) from mouse uterine stroma

155 uR1, depending on its activation by membrane estrogen receptor alpha (mERalpha; during diestrus) vers

156 s the estrogen receptor needed for feedback (estrogen receptor alpha [ERalpha]); kisspeptin neurons i

157 Estrogen receptor alpha is required for oviductal transp

158 rine ILC2s was observed in mice deficient in estrogen receptor alpha or estrogen receptor beta.

159 CD133(hi) CSCs that expressed low levels of estrogen receptor alpha.

160 different chemotherapeutic regimens based on estrogen receptor and human epidermal growth factor rece

161 athways, and with other receptors, including estrogen receptor and human epidermal growth factor rece

162 and in vitro models to determine the role of estrogen receptor beta (ER-beta) and its ligands on adip

163 Activation of estrogen receptor beta (ERbeta)-expressing neurons regul

164 ith sulforaphane and diarylpropionitrile, an estrogen receptor beta selective agonist, results in NRF

165 mice deficient in estrogen receptor alpha or estrogen receptor beta.

166 In contrast, estrogen receptor blocker did not affect BMP2 action.

167 CLM may attenuate signaling through the estrogen receptor by reducing levels of the estrogenic c

168 e transcription factors NFIB and YBX1 to the estrogen receptor can promote an estrogen-independent ph

169 as a potent ERalpha antagonist and selective estrogen receptor degrader (SERD), exhibiting good oral

170 coexposure with ICI 182780, demonstrating an estrogen receptor dependent mechanism.

171 sy indicated that the tumor was positive for estrogen receptor expression (50%), negative for progest

172 There is evidence that, through selective estrogen receptor modulation, isoflavones may exert bene

173 Resistance to the selective estrogen receptor modulator tamoxifen and to aromatase i

174 CNS-permeant PKC inhibitor is the selective estrogen receptor modulator tamoxifen.

175 eral FDA-approved drugs, including selective estrogen receptor modulators (SERMs), possess selective

176 GnRH neurons do not express the estrogen receptor needed for feedback (estrogen receptor

177 ganisations, cell proliferation, cell death, estrogen receptor pathways and phagocytic immune respons

178 In the population that was estrogen receptor positive or had unknown estrogen recep

179 ifen) at 10 years in the population that was estrogen receptor positive or had unknown estrogen recep

180 ctrometry of the EZH2-protein interactome in estrogen receptor positive, breast cancer-derived MCF7 c

181 with or without significant expansion, were estrogen receptor positive, which is consistent with bot

182 rent among women whose primary and CBCs were estrogen receptor positive.

183 those observed in patients and also identify estrogen receptor signaling as critical for protection i

184 cal stage (CS), final pathologic stage (PS), estrogen receptor status (E), and nuclear grade (G) (CPS

185 as estrogen receptor positive or had unknown estrogen receptor status was 2.1% (95% CI, -0.5% to 4.6%

186 as estrogen receptor positive or had unknown estrogen receptor status, 1,111 BCFS events were observe

187 Patients with positive margins, unknown estrogen receptor status, and comedo necrosis were more

188 ittle evidence of differential risk by tumor estrogen receptor status.

189 T3 correlated with worse clinical outcome in estrogen receptor+ (ER+) breast cancers.

190 gher proportions of positive family history, estrogen receptor+, progesterone receptor+, and/or human

191 e disruption of the binding affinity for the estrogen receptor, but oxidative stress and inflammation

192 e identified GPER/GPR30, a G-protein-coupled estrogen receptor, in goldfish (Carassius auratus) neura

193 naling regulation of a splice variant of the estrogen receptor, namely estrogen receptor (ERalpha-36)

194 ence of breast cancers that are negative for estrogen receptor, progesterone receptor, and ERBB2 (tri

195 No differences were detected in estrogen receptor, progesterone receptor, beta-catenin,

196 %) had ALND; ALND did not vary based on age, estrogen receptor, progesterone receptor, or HER2 status

197 m, h-Efp pathway and CARM1 and Regulation of Estrogen Receptor, which can be related to the metastasi

198 ar-old women with left-sided, T2N1, grade 3, estrogen receptor- and progesterone receptor-negative, h

199 ype is associated with higher percentages of estrogen receptor-, progesterone receptor-, or ki67-posi

200 p) on neutralizing epigenetic aberrations in estrogen receptor-alpha (ERalpha) leading to enhanced an

201 models that allow for selective deletion of estrogen receptor-alpha (ERalpha) or selective inhibitio

202 etic studies highlight the potential role of estrogen receptor-alpha (ESR1) mutations, which show inc

203 egree show a greater effect on the levels of estrogen receptor-alpha activity and nuclear factor eryt

204 get.Significance: These findings identify an estrogen receptor-binding protein as a critical mediator

205 In estrogen receptor-negative (ER(-)) and triple-negative b

206 both estrogen receptor-positive (ER(+)) and estrogen receptor-negative (ER(-)) breast carcinomas.

207 an women because of the higher prevalence of estrogen receptor-negative disease.

208 6 to 1.79; P for heterogeneity = .10) versus estrogen receptor-negative disease.

209 sterone receptor-positive cancer and 63% for estrogen receptor-negative progesterone- receptor-negati

210 s, we documented EVI1 overexpression in both estrogen receptor-positive (ER(+)) and estrogen receptor

211 itated by IL4 secreted by adipose tissue and estrogen receptor-positive and triple-negative breast ca

212 n mammary gland epithelial cells (HMECs) and estrogen receptor-positive breast cancer cell lines.

213 Tamoxifen therapy for estrogen receptor-positive breast cancer reduces the ris

214 east cancer recurrence risk in patients with estrogen receptor-positive breast cancer who underwent t

215 pproved for tamoxifen-resistant or relapsing estrogen receptor-positive breast cancer, these findings

216 approved (palbociclib) for treating advanced estrogen receptor-positive breast cancer, two major clin

217 Half of estrogen receptor-positive breast cancers contain a subp

218 CI, 1.14 to 1.66; mC, 0.55), but mainly for estrogen receptor-positive disease (IQ-OR, 1.44; 95% CI,

219 nt 3 CBCs per 100 women by 10 years after an estrogen receptor-positive first breast cancer, an absol

220 a key modifier of ribociclib sensitivity in estrogen receptor-positive MCF-7 breast cancer cells.

221 Eligibility included endocrine-refractory, estrogen receptor-positive metastatic breast cancer.

222 One patient-derived xenograft, the estrogen receptor-positive model T126, was chosen to gen

223 in of no ink on tumor to avoid reexcision in estrogen receptor-positive progesterone receptor-positiv

224 ary because the majority of the patients had estrogen receptor-positive tumors that may recur later i

225 C action in the transcriptional induction of estrogen receptor-related receptor alpha (ERRalpha), a n

226 trogen-agonist or antagonist activity in the estrogen receptor-transactivation assay.

227 ed variant in WNT4 alters the binding of the estrogen receptor.

228 d after treatment in women with early-stage, estrogen-receptor (ER)-positive breast cancer.

229 Isoflavones have an affinity for estrogen receptors (ERs) including beneficial affinity f

230 cancer, especially in the subtype expressing estrogen receptors (ERs), suggest tissue-specific procli

231 erived cells and the purported importance of estrogen receptors in BPH development and/or progression

232 iratory insufficiency suggests that membrane estrogen receptors may represent novel therapeutic targe

233 We tested the overall effects of estrogen receptors on the immune response by immunizatio

234 brane permeability, and no interference with estrogen receptors.

235 its relatively lower affinity for vertebrate estrogen receptors.

236 st/antagonist activity acting via endogenous estrogen receptors.

237 are likely mediated via membrane-associated estrogen receptors; however, the localization and distri

238 egulating CCND1, this enhancer regulates two estrogen-regulated long noncoding RNAs, CUPID1 and CUPID

239 om cardiac fibrosis in female rats can be an estrogen-related effect.

240 from glucose and dependent on the Drosophila estrogen-related receptor (dERR), which promotes L-2HG s

241 Here, we show how the estrogen-related receptor gamma (ERRgamma) negatively co

242 This increase was lost when estrogen-related receptor response element sites were mu

243 in kinase, sirtuin 1, PGC-1alpha, sirtuin 3, estrogen-related receptor-alpha, and Nrf-1; inhibition o

244 plasma estrogen level to drop 100-fold, the estrogen replacement in preterm infants is physiological

245 We speculate that estrogen replacement might partially restore neurogenesi

246 the recruitment of ERalpha and SRC-1 to the estrogen response element at the apoA-V promoter, implyi

247 ch were modified with DNA sequences known as estrogen response elements (DNA-ERE), where ERalpha bind

248 Because estrogen response elements are known to regulate genes o

249 ound that one novel combination, pairing the estrogen response modifier raloxifene with the c-Met/VEG

250 ys including apoptosis, DNA repair and early estrogen response that were differentially regulated bet

251 ulin signaling, reactive oxygen species, and estrogen response.

252 ted estrogen-stimulated transcription of the estrogen responsive genes pS2 and progesterone receptor.

253 e associated with decreased expression of an estrogen-responsive gene.

254 ptional activation by ER-alpha of endogenous estrogen-responsive genes.

255 ted amino acid residue, tyrosine 537, in the estrogen-responsive MCF7 breast cancer cell line.

256 PR-A, inducing invasiveness by counteracting estrogen's effects, particularly when cells are hypersen

257 ynthesized in the hypothalamus, is a part of estrogen's positive feedback loop.

258 ively, we will need to modify the concept of estrogen's positive feedback mechanism.

259 However, conceptus aromatase expression and estrogen secretion were decreased, indicating that IL1B2

260 The estrogen seems to restore neurogenesis by inhibiting the

261 polymeric coating increased proliferation of estrogen-sensitive MCF7 cells.

262 derstanding of the regulation of non-genomic estrogen signaling and open new avenues for personalized

263 In mice, loss of estrogen signaling contributes to oxidative damage cause

264 ed CYP19A1(amp) and promotes local autocrine estrogen signaling in AI-resistant metastatic patients.

265 males, and to identify a role for nongenomic estrogen signaling in any form of respiratory system neu

266 Over the past few years our understanding of estrogen signaling in the brain has expanded rapidly.

267 Previously, we reported that estrogen signaling in the stromal tumor microenvironment

268 We thus conclude that estrogen signaling is a major driver of female-biased ge

269 precise sequential molecular events of a new estrogen signaling network in an ERalpha-negative cell l

270 Ablation of estrogen signaling through ovariectomy produced nipples

271 The ability of nongenomic estrogen signaling within the cervical spinal cord to re

272 TGFbeta as a negatively regulated target of estrogen signaling.

273 affected by the cross-talk between TLRs and estrogen signalling.

274 rogen receptor alpha (ERalpha) and depend on estrogen signals for continued growth.

275 IL-1, TNF-alpha, and estrogen stimulate release of Hsp90 and augment activati

276 of either the N- or C-lobe of CaM abrogated estrogen-stimulated transcription of the estrogen respon

277 This sex difference may be regulated by estrogens, such as estradiol, that are synthesized in th

278 ance, and tumorigenicity, effects rescued by estrogen supplementation in ER(+) breast carcinoma cells

279 antagonist, produced partial to nearly full estrogen suppression in previous studies.

280 Together, these findings support that estrogen suppression is involved in SERT deficiency-indu

281 s in the cellular distribution of aromatase (estrogen synthase) in several species suggest that mecha

282 in the spatiotemporal increase in conceptus estrogen synthesis needed for the establishment of pregn

283 eptive circuits, whether it is through local estrogen synthesis or inhibitory neurotransmitter releas

284 Estetrol (E4) is a natural estrogen synthesized exclusively during pregnancy by the

285 e three new AEs suppressed proliferation and estrogen target gene expression in WT and mutant ER-cont

286 Apart from estrogens, the occurrence and ecotoxicity of steroids in

287 en receptor (ER(+)) and is treated with anti-estrogen therapies, particularly tamoxifen in premenopau

288 n 5: ACP recommends against using menopausal estrogen therapy or menopausal estrogen plus progestogen

289 length CaM slightly increased the ability of estrogen to enhance transcriptional activation by ER-alp

290 eins may decrease the level of adsorption of estrogen to SWCNTs by 5%.

291 rvical epithelium and stroma of untreated or estrogen-treated nontransgenic and HPV-transgenic mice.

292 We have now determined how HPV oncogenes and estrogen treatment affect genome-wide host gene expressi

293 Topical vaginal estrogen treatment increased (p < 0.001) BD2 concentrati

294 However, oral estrogen treatment is controversial because of its poten

295 nd that restoration of the hypoxic milieu or estrogen treatment might reverse interneuron generation.

296 However, estrogen treatment reduced the density of total and prol

297 c eminence (MGE) and, more importantly, that estrogen treatment reverses this perturbation in the pop

298 ges in the proximal stromal compartment, and estrogen treatment uniquely affected gene expression in

299 After estrogen treatment, ERalpha-36 rapidly associates with S

300 gly, the modulation of auditory responses by estrogens was much larger (both in amplitude and in topo