ライフサイエンスコーパス: estradiol

1 affinity similar to that of testosterone and estradiol.

2 IN lesions were treated with MPA plus 17beta-estradiol.

3 ion by the gonadal hormones testosterone and estradiol.

4 le to suppress conversion of testosterone to estradiol.

5 gulated during the reproductive cycle and by estradiol.

6 catalyzes the conversion of testosterone to estradiol.

7 gh levels of testosterone and its byproduct, estradiol.

8 inhibit its function, an effect mediated by estradiol.

9 mm, K20), in nociceptors incubated with beta-estradiol.

10 mmunodeficient mice supplemented with 17beta-estradiol.

11 n receptor alpha (ERalpha) to that of 17beta-estradiol.

12 SP11-knockdown (KD) cells in the presence of estradiol.

13 are activated by the steroid hormone 17beta-estradiol.

14 owth of xenografts in the presence of 17beta-Estradiol.

15 ts protective effect is stronger than 17beta-estradiol.

16 alpha5betaP), 3alpha5betaP sulfate, and beta-estradiol.

17 those from females and this was modulated by estradiol.

18 , 9 (38%) took spironolactone in addition to estradiol.

19 nductive polymer-coated electrodes to 17beta-estradiol.

20 levels of endogenous hormones; in this case, estradiol, 1 mg, and norethindrone acetate, 0.5 mg, once

21 C) monolayers were treated with 10(-8) mol/L estradiol +/- 10(-7) mol/L medroxyprogesterone acetate (

22 Interestingly, the endobiotic estradiol-17-glucuronide and the xenobiotic indomethacin

23 ogen glucuronides, estrone-3-glucuronide and estradiol-17-glucuronide, to estrone and estradiol, resp

24 rated that chronic exposure to low levels of estradiol-17beta (E2) increases mean arterial pressure (

25 Estradiol-17beta (E2) upregulates PF formation in develo

26 16alpha-(18)F-fluoro-17beta-estradiol ((18)F-FES) is a PET tracer for ER with relati

27 In the absence of exogenous estradiol, a TD by ACE interaction was observed on BOLD

28 ury, we demonstrated that both tamoxifen and estradiol accelerated endothelial healing, but only tamo

29 A switch of estradiol action from negative to positive feedback init

30 Estradiol acts via estrogen receptor alpha (ERalpha)-exp

31 ky choice), an effect that was attenuated by estradiol administration.

32 rts a stronger protective effect than 17beta-estradiol against kanic acid-induced hippocampal oxidati

33 Unlike control mice treated with 17beta-estradiol alone, cervical cancer was absent in the MPA-t

34 ll fraction, but inflammation, TGF-beta, and estradiol also prompted increased expression in human ad

35 bserved decrease in docosahexaenoic acid and estradiol, also occurring in response to BPA/BPS exposur

36 Ovarian estradiol alters both the intrinsic properties of gonado

37 USP11 expression was induced by estradiol, an effect that was blocked by tamoxifen and n

38 ith 115 of them predicted to be regulated by estradiol and 57 associated with female cancers.

39 PA2/B1-regulated miRNAs included response to estradiol and cell-substrate adhesion.

40 NS symptoms, as well as elevated hippocampal estradiol and compromised hippocampal physiology.

41 udy of serum levels of free testosterone and estradiol and current asthma in 7,615 adults (3,953 men

42 Endogenous estradiol and estrone are linked causally to increased r

43 Some phthalates mimic estradiol and may promote breast cancer.

44 e extent to which endogenous fluctuations in estradiol and progesterone alter functional cerebellar n

45 Modeling intra-individual fluctuations in estradiol and progesterone may provide unique insight in

46 Additionally, urinary estradiol and progesterone metabolites were measured dai

47 In addition, the differential effects of estradiol and progesterone on these uterine leiomyoma su

48 s an antiviral effect when mice receive both estradiol and progesterone, but not progesterone alone.

49 Chronic treatment with 17beta-estradiol and tamoxifen elicited differential gene expre

50 ta-HSD2 is thought to increase intracellular estradiol and testosterone in bone, thereby inhibiting b

51 To study the associations of endogenous estradiol and testosterone with carotid plaque compositi

52 To test the hypotheses that estradiol and time of day signals alter GnRH neuron resp

53 e conditions and following administration of estradiol and/or testosterone.

54 In WTP influents, estrogens (estrone, 17beta-estradiol, and estriol), androgens (androstenedione, and

55 regulation based on analysis of Doxorubicin, Estradiol, and TNFalpha combination treatment in MCF-7.

56 ortant upstream signaling regulator was beta-estradiol, and topical treatment with beta-estradiol con

57 agonist, leuprolide acetate; leuprolide plus estradiol; and leuprolide plus progesterone.

58 ted by reproductive hormones in women, where estradiol appears to promote vasodilation and heat dissi

59 We find that mice receiving estradiol are protected against intravaginal ZIKV infect

60 sex and reproductive hormones (particularly estradiol as an example) might contribute to affective i

61 siae estrogen biosensor capable of detecting estradiol, as well as ethinylestradiol, at concentration

62 erved with placebo treatment, treatment with estradiol attenuated the effects of ACE and TD such that

63 ngle injection of testosterone propionate or estradiol benzoate on the day of birth completely elimin

64 of research and monitoring have been 17beta-estradiol (beta-E2) and 17alpha-ethinylestradiol, due bo

65 xposure, indicating no change in regional ER estradiol binding, and (18)F-FDG uptake did not show a s

66 As observed for estradiol but not testosterone, IPI binding to SHBG was

67 UM-SCC-11A and UM-SCC-12 both produce 17beta-estradiol, but only UM-SCC-12, not UM-SCC-11A, xenograft

68 ntraceptives (COC) or etonorgesterol/ethinyl estradiol combined contraceptive vaginal ring (CCVR) for

69 As estradiol concentrations are important to eel aquacultur

70 y dysfunction against a milieu of decreasing estradiol concentrations during menopausal transition ma

71 Testosterone (total and free) and estradiol concentrations were comparable before and afte

72 eel serum samples to determine their 17beta-estradiol concentrations, which were found to be in the

73 a-estradiol, and topical treatment with beta-estradiol confirmed its function in corneal nerve regene

74 ts regarding the mechanisms by which loss of estradiol contributes to this vulnerability is lacking.

75 ne density only in mice stressed during high estradiol cycle phases.

76 human breast cancer cells, the acute 17beta-estradiol-dependent activation of functional enhancers r

77 Estradiol-dependent fibulin-2 interactions with SHBG sim

78 cutive function that are unmasked by loss of estradiol during menopause.

79 therefore undergo erythropoiesis after beta-estradiol (E(2)) addition.

80 We report that 17beta-estradiol (E(2)) decreased osteoclast number by promotin

81 r estrogenic candidates compared with 17beta-estradiol (E(2)) for the treatment of endocrine-resistan

82 G-1 mimics the beneficial effects of 17beta-estradiol (E(2)) on hippocampal CA1 spine density and me

83 e antiestrogen tamoxifen (Tam) as well as to estradiol (E(2)) withdrawal.

84 17beta-Estradiol (E(2))-mediated ER activation stabilized the D

85 t owing to a reduction in circulating 17beta-estradiol (E(2)).

86 different types of estrogens-planar [17beta-estradiol (E(2))] and angular triphenylethylene (TPE) de

87 thelium were treated with either 4 nM 17beta-estradiol (E) for seven days, 50 ng/ml E.coli flagellin

88 We report that 17beta-estradiol (E2) affects the behavior and the epigenome in

89 response of ovariectomized adults to 17beta-estradiol (E2) and artificial decidualization were measu

90 We studied the impact of estradiol (E2) and progesterone (P4), which impregnate t

91 The therapeutic benefits of estradiol (E2) and symptom-provoking effects of E2-withd

92 in bone is thought to increase intracellular estradiol (E2) and testosterone (T), which thereby inhib

93 ponse relationships describing plasma 17beta-estradiol (E2) as a function of plasma fadrozole, plasma

94 an inflammatory microenvironment and 17beta-Estradiol (E2) as an agonist of Estrogen Receptors, know

95 gs from the reference site were treated with estradiol (E2) during embryonic development prior to gon

96 Exposure of zebrafish embryos to 17beta-estradiol (E2) during liver development significantly de

97 ted by an immunospecific detection of 17beta-Estradiol (E2) following the competitive inhibition form

98 17beta-estradiol (E2) has broad tropism within the CNS, targeti

99 The hormone 17beta-estradiol (E2) has shown vascular protective effects in

100 Exposure to 17beta-estradiol (E2) increased proliferation of hepatocytes an

101 ChIP assay demonstrated estradiol (E2) induced ESR1 binding to Pck-1, G6Pase, Fa

102 Estradiol (E2) induced proliferation was blocked signifi

103 We found 17beta-estradiol (E2) inhibited hepatic gluconeogenic genes suc

104 Previously, we reported that 17beta-estradiol (E2) inhibits azoxymethane/dextran sulfate sod

105 by demonstrating that neuron-derived 17beta-estradiol (E2) is neuroprotective and critical for induc

106 17beta-Estradiol (E2) is produced from androgens via the action

107 The effect of 17beta-estradiol (E2) on IL-13-induced signaling pathways, gene

108 mixtures of clobetasol propionate (CLO) with estradiol (E2) or androstenedione (A4), each steroid exh

109 h-fat diet (HFD) that received either 17beta-Estradiol (E2) or vehicle implants.

110 models showed that pre-menopausal levels of estradiol (E2) promote TNBC-BM through incompletely unde

111 It is known that 17-beta estradiol (E2) regulates adipose tissue function and VEG

112 positive feedback effects of ovarian 17beta-estradiol (E2) regulating release of gonadotropin releas

113 Exposure to 0.1 pM, 10 pM, and 1 nM 17 beta-estradiol (E2) resulted in monotonic inhibition of mamma

114 chromatin structure across a time course of estradiol (E2) stimulation in human estrogen receptor al

115 Treatment with 17beta-estradiol (E2) synergized with DAC to reduce proliferati

116 Expression of the 17beta-estradiol (E2) synthesis enzyme aromatase is highly upre

117 We have previously reported that 17beta-estradiol (E2) treatment activates Notch signaling in EC

118 ts, and this reduction is reversed by 17beta-estradiol (E2) treatment in a model of human estrogen re

119 (5alpha-R) or to the active estrogen 17beta-estradiol (E2) via the aromatase enzyme.

120 2 weeks of exposure, levels of plasma 17beta-estradiol (E2) were significantly elevated in high PAH/h

121 ress the enzyme aromatase and produce 17beta-estradiol (E2), although the precise role of astrocyte-d

122 , DNA damage following treatment with 17beta-estradiol (E2), BP-3, and PP was determined by immunosta

123 e marmosets and reduced peripheral levels of estradiol (E2), but unexpectedly increased E2 levels in

124 the enzyme converting testosterone to 17beta-estradiol (E2), contributes to the regulation of this pl

125 25% of patients had persistent elevation in estradiol (E2), defined as E2 greater than 10 pg/mL (to

126 e in urinary estrone (E1) excretion, whereas estradiol (E2), estriol (E3), and 16ketoE2 excretion onl

127 ed female sex hormones, particularly 17-beta estradiol (E2), in the pathogenesis of these disorders.

128 y chemical neuromodulators, including 17beta-estradiol (E2), or patterns of synaptic activation, as i

129 ial cells (NHBE) were pretreated with 17beta-estradiol (E2), propyl-pyrazole-triol (PPT, ER-alpha ago

130 ed, recipients were supplemented with 17beta-estradiol (E2), tamoxifen, or left untreated.

131 tizaton dehyroepiandrosterone (DHEA), 17beta-estradiol (E2), testosterone (T), and their sulfates in

132 Ralpha KO mice have elevated levels of serum estradiol (E2), testosterone, and LH.

133 facilitate auditory consolidation is 17beta-estradiol (E2), which is associated with human speech-la

134 AF2ER is an AF-2 disrupted estradiol (E2)-insensitive mutant ERalpha, but AF-1-depe

135 ntly correlated with plasma levels of 17beta-estradiol (E2).

136 nsitivity for the endocrine disruptor 17beta-Estradiol (E2).

137 tase, which produces the neurosteroid 17beta-estradiol (E2).

138 ptor co-activator 6 (NCOA6) is essential for estradiol (E2)/ERalpha-activated GREB1 transcription.

139 activated receptor gamma agonist) and 17beta-estradiol (E2; an estrogen receptor alpha agonist) nearl

140 Elevations in estrogen (17beta-estradiol, E2) are associated with increased alcohol dri

141 ter exposure to two concentrations of 17beta-estradiol (E2beta; 2 ng/L and 50 ng/L) during four disti

142 17alpha-ethinyl estradiol (EE), a synthetic analog of 17beta-estradiol,

143 e bioavailability and bioactivity of ethinyl estradiol (EE2) sorbed onto SWCNTs in a fish gastrointes

144 o BPA, vehicle, or positive control [ethinyl estradiol (EE2)] by oral gavage beginning on gestational

145 tia, and childhood adversity further impacts estradiol effects on neural function.

146 Herein, we show that 17alpha-estradiol elicits similar genomic binding and transcript

147 The mechanisms by which 17alpha-estradiol elicits these benefits remain unresolved.

148 Furthermore, 17alpha-Estradiol enhanced experience-dependent plasticity in th

149 ronmental concentrations resulted in 17-beta-estradiol equivalency quotients ranging from 0.002 to 5.

150 tivities, with 13 surface waters with 17beta-estradiol-equivalent (E2Eq) activities greater than a 1-

151 WWTP replacement, in vitro ER (24 ng 17beta-estradiol equivalents/L)-, GR (60 ng dexamethasone equiv

152 Sex steroid hormones such as 17beta-estradiol (estradiol) regulate neuronal function by bind

153 ), and steroidal estrogens (estrone, 17-beta-estradiol, estriol, and 17-alpha-ethinylestradiol).

154 Signaling of 17beta-estradiol (estrogen) through its two nuclear receptors,

155 Prediagnostic concentrations of estradiol, estrone, and 13 metabolites were measured in

156 Estradiol, estrone, testosterone, luteinizing hormone (L

157 roles of ABAD is to maintain the balance of estradiol/estrone in neurons.

158 prisingly, females with higher physiological estradiol experienced stress-induced memory impairment a

159 and function programmed by testosterone and estradiol exposures in utero.

160 ctions between synaptic and active intrinsic estradiol feedback targets, dynamic clamp was used to si

161 h passive and active intrinsic properties by estradiol feedback thus renders arcuate kisspeptin neuro

162 amic arcuate nucleus help convey homeostatic estradiol feedback to central systems controlling fertil

163 NIFICANCE STATEMENT Kisspeptin neurons relay estradiol feedback to gonadotropin-releasing hormone neu

164 tropic glutamate receptors are important for estradiol feedback, but it is not known where they fit i

165 Estradiol had small effects on cAMP levels but G protein

166 Estradiol, however, decreased risky choice in both group

167 Consequently, neurofibromin depletion causes estradiol hypersensitivity and tamoxifen agonism, explai

168 ovariectomized mice bearing constant-release estradiol implants (OVX+E), GnRH neuron firing is suppre

169 17beta-Estradiol improved microcirculatory perfusion and reduce

170 Long-term cyclic administration of 17beta-estradiol improves working memory, and restores highly p

171 ces, we examined the acute effect of 17alpha-Estradiol in adult Long Evans rats following chronic mon

172 tive detection of the water pollutant 17beta-estradiol in buffer and tap water.

173 results support the idea that brain-derived estradiol in females may serve important functions in re

174 fen in the presence of physiologic levels of estradiol in human breast cancer in nude mice and in mur

175 lated bacteria, and those changes induced by estradiol in its signalling at the single cell level.

176 as it mimics the protective action of 17beta-estradiol in other tissues such as arteries.

177 gesterone in controls only, and decreased by estradiol in PMDD LCLs.

178 This study revealed that 17beta-estradiol in the brain mediated the physiological action

179 d calcium transients in the presence of beta-estradiol, in an IP3 receptor-dependent manner.

180 w that treating mice with estradiol to model estradiol increases during pregnancy induced HSC prolife

181 Estradiol increases membrane depolarization induced by G

182 ly depolarize arcuate kisspeptin neurons and estradiol increases this depolarization.

183 ic/transcriptional) demonstrated that 17beta-estradiol-induced acceleration of endothelial healing is

184 hypothesized that the mechanisms underlying estradiol-induced alterations in postsynaptic response t

185 To interrogate the role of the estradiol-induced changes in passive intrinsic propertie

186 dynamic clamp and mathematical modeling that estradiol-induced shifts in synaptic transmission alone

187 E6 and E7, short-term treatment with 17beta-estradiol induces CINs that progress to cervical cancer

188 Estradiol induces negative feedback on pulsatile GnRH/lu

189 network, and cellular levels, physiological estradiol influences the effects of stress on memory in

190 behavior in both males and females, and that estradiol is sufficient to promote risk aversion in both

191 estradiol (EE), a synthetic analog of 17beta-estradiol, is prescribed commonly and found in oral cont

192 17beta-estradiol led to a significant upregulation in pentose p

193 on to first assessment of centrally assessed estradiol level <= 2.72 pg/mL [<= 10 pmol/L] during neoa

194 were percent change from baseline in 17beta-estradiol levels (E2) and tricuspid annular plane systol

195 atics, PFASs were positively associated with estradiol levels and negatively associated with testoste

196 n was positively correlated with circulating estradiol levels and ovarian readiness.

197 ce, and suggest approaches to restore 17beta-estradiol levels as a novel treatment option for SERT de

198 he Grady Trauma Project and found that serum estradiol levels associates with DNA methylation across

199 d that DiNP exposure significantly decreased estradiol levels compared to control.

200 Plasma estradiol levels were equivalent between dominant and su

201 relate with any of these parameters, whereas estradiol levels were positively correlated with E-cadhe

202 a1 suppression, decreased circulating 17beta-estradiol levels, abnormal fat accumulation, and glucose

203 1) expression and reduced circulating 17beta-estradiol levels.

204 olism and energy expenditure, independent of estradiol levels.

205 les, was positively related to plasma 17beta-estradiol levels.

206 ively than tamoxifen even in the presence of estradiol, mainly by attenuation of the innate immune re

207 Indeed, estradiol may be associated with an increased ICC risk.

208 17beta-Estradiol-mediated enhancement of ethanol-induced excita

209 Estradiol-mediated stabilization of DAXX is necessary an

210 suggests that resilience may be explained by estradiol-mediated transactivation of beta1-integrins an

211 17beta-Estradiol mediates the sensitivity to pain and is involv

212 gions contained genes known to interact with estradiol metabolism and cancer.

213 differentially activated across high and low estradiol mice, and predicted memory impairment.

214 Thus, estradiol might be a treatment option to improve the qua

215 d, and then incubated in control medium with estradiol +/- MPA.

216 and OVX+estradiol (OVX+E) female mice during estradiol negative feedback revealed that estradiol redu

217 ed with vehicle or various concentrations of estradiol (nonspecific ER agonist) or genistein (ERbeta-

218 aromatase inhibitors that lower circulating estradiol occurs in up to 50% of patients, generally lea

219 n of dexamethasone or prednisolone or 17beta-estradiol on Charolais bulls.

220 r (GPER) activation mimics effects of 17beta-estradiol on hippocampal memory consolidation.

221 There was an interaction between Patch and estradiol on NA.

222 We attribute this to an inhibitory effect of estradiol on virus replication, which we were able to ob

223 ale sex and reproductive hormones (primarily estradiol) on mechanisms of cardiovascular control relev

224 There were no associations between serum estradiol or free testosterone concentrations and TFV-DP

225 nd Ki values was observed in the presence of estradiol or genistein.

226 atched wild-type (WT) mice were administered estradiol or vehicle in drinking water for 6 weeks.

227 for Q4 vs. Q1, 0.59; 95% CI, 0.37-0.91) and estradiol (OR for Q4 vs. Q1, 0.43; 95% CI, 0.23-0.78) le

228 ain slices from ovariectomized (OVX) and OVX+estradiol (OVX+E) female mice during estradiol negative

229 gnificantly associated with higher levels of estradiol (P = 0.02) and an increased risk of POPH (odds

230 t transmitted/founder viruses in vitro Thus, estradiol plays a key role in defining major differences

231 Thus, we conclude that estradiol plays a key role in shaping responses to early

232 .coli flagellin (F) for 12 h, or 4 nM 17beta-estradiol plus 50 ng/ml flagellin (E + F(12 h)).

233 New data reveal that estradiol potently alters inhibitory neurotransmission i

234 17beta-estradiol production by LSCC cell lines UM-SCC-11A and U

235 showed elevated basal oxytocin, lower ACTH, estradiol, progesterone and testosterone compared with n

236 xytocin, adrenocorticotropic hormone (ACTH), estradiol, progesterone and testosterone.

237 ptomatic) during the first month of combined estradiol/progesterone compared with the last month of l

238 The findings demonstrate that the change in estradiol/progesterone levels from low to high, and not

239 trual Tension scores in the second and third estradiol/progesterone months did not significantly diff

240 bo month, and the second and third months of estradiol/progesterone.

241 ancreatic carcinoma LM that is reversible by estradiol reconstitution.

242 Estradiol reduced both potassium current in the membrane

243 ng estradiol negative feedback revealed that estradiol reduced capacitance, reduced transient and sus

244 Consistent with these observations, estradiol reduced rheobase and action potential latency.

245 al cortex, and that a single dose of 17alpha-Estradiol reduced the expression of the calcium-binding

246 vations suggest that activational effects of estradiol regulate surge generation and maintain cyclici

247 x steroid hormones such as 17beta-estradiol (estradiol) regulate neuronal function by binding to estr

248 compendial shaking incubator method (for the estradiol-releasing ring Estring(R)) is described in the

249 patients, and its effects in the presence of estradiol remain undetermined.

250 uate its effects under physiologic levels of estradiol, representative of premenopausal patients.

251 x hormone therapy containing testosterone or estradiol (respectively) were enrolled in a 4-week study

252 and estradiol-17-glucuronide, to estrone and estradiol, respectively.

253 ures and xenografts were examined for 17beta-estradiol responsiveness in vivo.

254 The study provides evidence that 17beta-estradiol restores the tetramer-to-monomer ratio by auto

255 A structure of the ancestor with 17beta-estradiol revealed only one molecule in the active site,

256 men (P = .03) that inversely correlated with estradiol (rho = -0.79; P < .05).

257 arcuate kisspeptin neurons are regulated by estradiol-sensitive mechanisms including potassium condu

258 odel, we review our current understanding of estradiol signaling in the regulation of sexual receptiv

259 VI1-silenced cells, suggesting that EVI1 and estradiol signaling merge in MAPK activation.

260 This has an impact on the estradiol signaling required for proplatelet formation,

261 However, estradiol significantly decreased NF-kappaB transcriptio

262 EO-33 blocked 90% of tumor growth induced by estradiol sulfate, and no toxic effect was observed by a

263 izures, focusing on the regulation of 17beta-estradiol synthesis in the brain.

264 age without or with adult testosterone plus estradiol (T+E) to promote carcinogenesis.

265 sociated with the risk of T2D, whereas total estradiol (TE) was associated with increased risk of T2D

266 rence may be regulated by estrogens, such as estradiol, that are synthesized in the spinal cord and b

267 When treated with 17beta-estradiol, the lipid utilization in cancer cells jumped

268 alance and leads to a reduction in levels of estradiol, thus leading to an increase in reactive oxyge

269 the combination treatment with Doxorubicin + Estradiol + TNFalpha in comparison with single or double

270 Here we show that treating mice with estradiol to model estradiol increases during pregnancy

271 the late-stage C-H functionalization of beta-estradiol to rapidly prepare desired analogues that requ

272 tive intrinsic properties induced by in vivo estradiol treatment affect the response to synaptic inpu

273 To ask if estradiol treatment impacts structural and functional pl

274 17alpha-estradiol treatment improves metabolic parameters and sl

275 17beta-Estradiol treatment was associated with 2-fold increase

276 rine 214 (pS214-tau) are altered with age or estradiol treatment, and couple to working memory perfor

277 d young and aged monkeys received vehicle or estradiol treatment, and were tested on the delayed resp

278 arger in vivo in response to systemic 17beta-estradiol treatments.

279 hat AGO1 acts positively as a coactivator in estradiol-triggered transcription regulation by promotin

280 Here, we report a different role for AGO1 in estradiol-triggered transcriptional activation in human

281 is trial was to evaluate safety of IVT or an estradiol vaginal ring in patients with early-stage BC r

282 ous cell carcinoma (LSCC) responds to 17beta-estradiol via estrogen-receptor (ER, transcribed from ES

283 Removal of ethinyl estradiol was >40% for two of the three sealant fluids d

284 Removal of ethinyl estradiol was >=90% for all sealants in the increased hy

285 Examining histology, a doubling of estradiol was associated with a 40% increased risk of IC

286 Examining histology, a doubling of estradiol was associated with a 40% increased risk of IC

287 However with PBO, lower-than-usual estradiol was associated with greater decreases in NA.

288 asthma in obese women, and an elevated serum estradiol was associated with lower odds of current asth

289 ER binding, the gene expression response to estradiol was dampened for most genes.

290 17beta-Estradiol was effective in improving mesenteric perfusio

291 ynthesis in cancer cells treated with 17beta-estradiol was increased by 42%.

292 Estradiol was measured at baseline and weeks 4 and 12 us

293 s memory of mice stressed during estrus (low estradiol) was spared.

294 gen receptor through aromatase conversion to estradiol, we further examined how a potent non-aromatiz

295 In the past, estrogens such as estradiol were thought to be most important in the regul

296 sulfated or carboxylated steroids, and beta-estradiol, whereas many 5alpha-reduced steroids potentia

297 strous mice, characterized by high levels of estradiol, whereas memory of mice stressed during estrus

298 o guest molecules, dextromethorphan and beta-estradiol, which are widely found as pollutants in groun

299 rofound differences are influenced by 17beta-estradiol, which contributes both to T cell activation a

300 ronger among children with higher than lower estradiol, with odds ratios (OR) for asthma ranging from