ライフサイエンスコーパス: uterine

1 g exposure to different doses of BPA induced uterine abnormalities and molecular changes in a rat mod

2 rt cervix or short cervix this pregnancy; or uterine abnormality and/or current smoker of tobacco.

3 We also sought to determine the degree of uterine afferent innervation provided by the vagus nerve

4 that pregnant mice had lower frequencies of uterine Ag-experienced CD4 T cells and ZIKV-infected pre

5 ected pregnant mice had lower frequencies of uterine Ag-experienced CD8 T cells compared with ZIKV-in

6 s first-in-humans study of PLG in women with uterine and cervical cancer demonstrates its feasibility

7 Previously, we showed that the uterine and vaginal microbiome distinguishes patients wi

8 96 cell line RNA-seq profiles from ovarian, uterine, and basal breast cancers.

9 ated with higher odds of pancreatic, kidney, uterine, and cervical cancer and lower odds of esophagea

10 Danlos syndrome (vEDS), leading to arterial, uterine, and intestinal rupture and an average life expe

11 ival (5Y-OS) compared with breast, prostate, uterine, and ovarian cancer.

12 ivo vasoreactivity studies were conducted in uterine arteries (UtA) isolated from pregnant mice expos

13 e hypothesis that adipose tissue surrounding uterine arteries (uterine perivascular adipose tissue; P

14 presence of PVAT-conditioned media, isolated uterine arteries from both pregnant and non-pregnant rat

15 Uterine arteries from late pregnant wildtype and LOX-1 o

16 Pregnancy induces changes in uterine arteries that makes them responsive to uterine P

17 contractile and anti-dilatory effects on rat uterine arteries.

18 pro-contractile and anti-dilatory effects on uterine arteries.

19 .5, maternal nitrate/nitrite concentrations, uterine artery (UtA) blood flow and endothelial function

20 that hypoxia reduced AMPK activation in the uterine artery and placenta, and AICAR increased AMPK ac

21 riction (P < 0.01), due in part to increased uterine artery blood flow (P < 0.0001).

22 An increase in uterine artery blood flow (UtBF) is a common and necessa

23 ategy for improving fetal growth and raising uterine artery blood flow in pregnancy, which may be imp

24 rivascular adipose tissue (PVAT) potentiates uterine artery blood flow in pregnant rats, although not

25 vation vasodilates arteries and may increase uterine artery blood flow.

26 l growth restriction due, in part, to lesser uterine artery blood flow.

27 rug AICAR improved fetal growth and elevated uterine artery blood flow.

28 educed uterine artery diameter and increased uterine artery contractility in normoxic mice, providing

29 l inhibition of AMPK with Compound C reduced uterine artery diameter and increased uterine artery con

30 en" comprising fetal and placental size, and uterine artery Doppler.

31 PVAT) is a novel local mediator of UtBF and uterine artery tone during pregnancy.

32 least in part, as a result of its actions on uterine artery tone.

33 Uterine handling led to an acute increase in uterine artery vascular resistance, fetal peripheral vas

34 of total cardiac output flowing through the uterine artery was increased with AICAR in hypoxic mice

35 esponse to medical treatment, myomectomy and uterine-artery embolization are therapeutic options.

36 the myomectomy group and 80.0+/-22.0 in the uterine-artery embolization group (mean adjusted differe

37 hom 105 underwent myomectomy) and 127 to the uterine-artery embolization group (of whom 98 underwent

38 mectomy group and in 24% of the women in the uterine-artery embolization group.

39 ial to evaluate myomectomy, as compared with uterine-artery embolization, in women who had symptomati

40 of life at 2 years than those who underwent uterine-artery embolization.

41 One patient had grade 3 uterine bleeding (treatment unrelated).

42 inning, intraplacental T2-hypointense bands, uterine bulge, serosal hypervascularity, and signs of ex

43 e gene expression of metabolic adipokines in uterine but not in aortic PVAT.

44 st HRs for liver (3.31), pancreas (2.19) and uterine cancer (1.78).

45 Using an autochthonous mouse model of uterine cancer and the administration of respiratory hyp

46 nvasion and migration ability of ovarian and uterine cancer cells.

47 Critically important to reducing uterine cancer mortality is the development of more effe

48 5RHH-siAXL treatment reduces metastasis in a uterine cancer mouse xenograft model, without causing an

49 hows promise in the treatment of ovarian and uterine cancer patients.

50 (BC); however, its chronic use can increase uterine cancer risk and induce tamoxifen resistance.

51 ely affect prognosis of patients with occult uterine cancer, empirical evidence has been limited and

52 e involved in metastasis in both ovarian and uterine cancer.

53 ncreased mortality risk in women with occult uterine cancer.

54 Breast cancers, bladder cancers, and uterine cancers have spatial patterns that are particula

55 ultimately developed bulky endometrioid-type uterine cancers with 100% mortality by 8 months of age.

56 s including kidney, breast, lung, liver, and uterine cancers, but not in prostate cancer.

57 om most cancers, but are notably enriched in uterine cancers.

58 = 13), prostate adenocarcinoma (n = 5), and uterine carcinosarcoma (n = 4).

59 acing provided formal genetic proof that the uterine carcinosarcoma cell of origin is an endometrial

60 ic combination of driver events underpinning uterine carcinosarcoma have remained mysterious.

61 Uterine carcinosarcoma is an aggressive variant of endom

62 erestingly, an association was observed with uterine carcinosarcoma, (OR 9.24; 95% CI 2.08-37.17; p =

63 w7) as the critical combination underpinning uterine carcinosarcoma, and to Fbxw7 as a key driver of

64 cancers, including uterine serous cancer and uterine carcinosarcoma, which together account for over

65 cinomas eventually developed into definitive uterine carcinosarcomas with carcinomatous and sarcomato

66 by growth of endometrial tissue outside the uterine cavity and lacks adequate treatment.

67 and growth of endometrial tissue outside the uterine cavity in endometriosis patients are primarily d

68 The endometrial lining of the uterine cavity is a highly dynamic tissue that is under

69 Alterations to the epigenome of uterine cells may therefore contribute significantly to

70 Gynecology and Obstetrics staging system for uterine cervical cancer.

71 nd 0.93 (0.89, 0.97) for pancreatic, kidney, uterine, cervical, and esophageal cancer and melanoma, r

72 18)F-FDG is injected interstitially into the uterine cervix on the day of surgery, and its rapid tran

73 gens that commonly infect the oropharynx and uterine cervix.

74 ilator effect of AICAR was selective for the uterine circulation.

75 nges in the splanchnic, renal, cerebral, and uterine circulations in terms of endothelial and vascula

76 ve implications for understanding how embryo-uterine communication is key to determining an optimal i

77 tering, on the other hand, depends on embryo-uterine communication reliant on the LPAR3 signaling pat

78 Adiponectin links maternal metabolism to uterine contractility.

79 more efficient pharmaceutical treatments for uterine contraction disorders.

80 ain targets of pharmaceutical treatments for uterine contraction disorders.

81 s and calcium entry, which may contribute to uterine contraction.

82 METx (41 nM) had no effect on spontaneous uterine contractions and METx (100 nM) had no effect on

83 The onset of preterm uterine contractions is preceded by asymptomatic cervica

84 lular factors, targeted by drugs to regulate uterine contractions, and tissue level electromechanical

85 nd METx (100 nM) had no effect on OT induced uterine contractions.

86 Hysterectomy-corrected uterine corpus cancer incidence increased among non-Hisp

87 Hysterectomy-corrected age-standardized uterine corpus cancer incidence rates from 2000 to 2015

88 Uterine corpus cancer incidence rates have been projecte

89 years, and ranged from 0.37% (0.03-0.72) for uterine corpus cancer to 2.95% (2.74-3.16) for kidney ca

90 Hysterectomy-corrected incidence rates of uterine corpus cancer were similar among non-Hispanic wh

91 oral cavity/pharynx, colorectal, pancreatic, uterine corpus, and liver cancers constituted considerab

92 lated cancers (multiple myeloma, colorectal, uterine corpus, gallbladder, kidney, and pancreatic canc

93 res of manual removal of placenta (MROP) and uterine curettage, which are not universally available,

94 luminal and glandular epithelia, to maintain uterine cycling.

95 e implantation window and in first-trimester uterine decidua.

96 etrial responses and that disruption impairs uterine decidual development during pregnancy.

97 be caused by chromosomal errors, anatomical uterine defects, autoimmune disorders and endometrial dy

98 Conditional uterine deletion of Dicer1 and Pten in mice resulted in

99 We found that uterine deletion of Scrib by a Pgr-Cre driver leads to d

100 e uterine response to E2, and suggested that uterine-derived IGF1 is essential for reproductive succe

101 of uterine epithelial cells are critical for uterine development and function.

102 itical physical barrier, which permits extra-uterine development of the embryo.

103 e disrupts expression of genes important for uterine development, causing posteriorization and dimini

104 dysregulates paracrine signals necessary for uterine development, eventually resulting in apoptosis o

105 x17, as well as genes important for neonatal uterine differentiation (Wnt7a, Hoxa10, and Msx2), were

106 population also supports the regeneration of uterine endometrial epithelium post parturition.

107 Characterized by abnormal growth of uterine endometrial tissue in other body areas, endometr

108 thogenic mutation MRE11(G285C) identified in uterine endometrioid carcinoma exhibited a similar cellu

109 use models show a close resemblance to human uterine endometrioid carcinomas.

110 The uterine endometrium adopts multiple physiological states

111 transcriptional and proteomic changes in the uterine endometrium are required to facilitate receptivi

112 are common in neoplasms originating from the uterine endometrium.

113 However, its role in uterine epithelial cell function remains unknown.

114 Normal proliferation and differentiation of uterine epithelial cells are critical for uterine develo

115 ts suggest that EZH2 serves as a guardian of uterine epithelial integrity, partially via inhibiting t

116 The uterine epithelial stem cell population also supports th

117 These uterine epithelial stem cells provide a resident cellula

118 is tissue distribution allows these bipotent uterine epithelial stem cells to bidirectionally differe

119 Loss of EZH2 promoted stratification of uterine epithelium, an uncommon and detrimental event in

120 Rabbits underwent a subtotal uterine excision and were reconstructed with autologous

121 ential pharmacological target for modulating uterine excitability.

122 hey are a step forward towards understanding uterine excitation-contraction dynamics and developing s

123 The more reliable PTB induction and uniform uterine exposure provided by this new model will be usef

124 sses, BMT from WT donors leads to normalized uterine expression of numerous decidualization-related g

125 To determine the role of uterine EZH2, Ezh2 was conditionally deleted using proge

126 ld provide a treatment option for women with uterine factor infertility.

127 provide a regenerative medicine solution to uterine factor infertility.

128 x) aims at giving women affected by absolute uterine-factor infertility the possibility of carrying t

129 is now an established solution for absolute uterine-factor infertility.

130 health-related quality-of-life domain of the Uterine Fibroid Symptom and Quality of Life (UFS-QOL) qu

131 o-controlled, 6-month phase 3 trials (Elaris Uterine Fibroids 1 and 2 [UF-1 and UF-2]) to evaluate th

132 y embolization, in women who had symptomatic uterine fibroids and did not want to undergo hysterectom

133 Uterine fibroids are hormone-responsive neoplasms that a

134 The growth of uterine fibroids is sex hormone-dependent and commonly a

135 ose a unifying mechanism for pathogenesis of uterine fibroids mediated by H19 and identify a pathway

136 quence of AP-1 loss on gene transcription in uterine fibroids remains poorly understood.

137 ers and diseases (polycystic ovary syndrome, uterine fibroids, endometriosis) as well as contraceptio

138 Uterine fibroids, the most common type of tumor among wo

139 Among women with symptomatic uterine fibroids, those who underwent myomectomy had a b

140 ucing heavy menstrual bleeding in women with uterine fibroids.

141 ginal absorption and biodistribution via the uterine first-pass effect.

142 on that extracellular vesicles accumulate in uterine fluid during eggshell calcification and that the

143 We also demonstrate that EVs contain ACC in uterine fluid using spectroscopic analysis.

144 ansport to provide stabilized ACC in chicken uterine fluid where eggshell mineralization takes place.

145 nce of EDIL3 and MFGE8 proteins in eggshell, uterine fluid, and uterus.

146 Thus, uterine function over the reproductive lifespan of a mou

147 ms that regulate endometrial homeostasis and uterine function.

148 ith these SEs affected key estrogen-mediated uterine functions, including transforming growth factor

149 Mice were created lacking uterine Galpha(q) and Galpha(11); as a result, signaling

150 es revealed that a major mechanism via which uterine Galpha(q/11) signaling induces PR signaling is t

151 Uterine Galpha(q/11) signaling, in a progesterone-depend

152 nd Galpha(11); as a result, signaling by all uterine Galpha(q/11)-coupled receptors was disrupted.

153 ocated at a chromatin loop end and that most uterine genes in loop ends associated with these SEs are

154 oter proximal enrichment of Pol II occurs at uterine genes relevant to reproductive biology; thus, we

155 with other transcription factors and impact uterine gland development and function in a cycle phase-

156 In mice, FOXA2 is a critical regulator of uterine gland development in the neonate and gland funct

157 ck of LIF, a critical implantation factor of uterine gland origin.

158 ides novel evidence of crosstalk between the uterine glands and placenta.

159 hypothesis that FOXA2-regulated genes in the uterine glands impact development of the decidua, placen

160 Despite this, the role of uterine glands in first trimester human pregnancy is lit

161 ized sexually dimorphic effects of FOXA2 and uterine glands on fetoplacental development with potenti

162 es play a redundant role in the formation of uterine glands.

163 dations on follow-up for offspring born from uterine grafts, which includes specialty surveillance as

164 as accompanied by fertility defects, altered uterine growth and function, and the development of endo

165 fertility but did not impact the E2-induced uterine growth response.

166 of the enhancer did not affect fertility or uterine growth responses.

167 of pregnancy-related disorders such as intra uterine growth restriction, preeclampsia and preterm bir

168 ate, hemodynamic and hormonal changes, rapid uterine growth, changes associated with endothelial dama

169 e of a super enhancer in Igf1 regulation and uterine growth.

170 Therefore, the data support that uterine handling during abdominal surgery under general

171 This may be the consequence of uterine handling during abdominal surgery.

172 Uterine handling led to an acute increase in uterine art

173 cardiovascular and metabolic changes during uterine handling.

174 uid (ULF) in the most cranial portion of the uterine horn ipsilateral to the corpus luteum.

175 Anterogradely labeled axons innervated each uterine horn, these projected rostrally or caudally from

176 During infection, Il1a(-/-) oviducts and uterine horns exhibited reduced neutrophil infiltration,

177 s, likely due to the leakage of LPS from the uterine horns through the cervix.

178 After 7-9 days, uterine horns were stained to visualize traced nerve axo

179 resulting in apoptosis of the Misr2+ cells, uterine hypoplasia, and complete infertility in the adul

180 Deletion of uterine Igf1 in a PgrCre;Igf1f/f model decreased female

181 As a result, E2-mediated induction of mouse uterine Igf1 mRNA is completely eliminated, whereas hepa

182 rough E2 receptor alpha (ERalpha), increases uterine Igf1 mRNA levels.

183 Moreover, E2-dependent activation of uterine IGF1 signaling was not impaired by disrupting th

184 r region controls E2-responsive induction of uterine Igf1 transcripts.

185 infant formulas are infertile due in part to uterine implantation defects.

186 Finally, we demonstrate that uterine implantation sites in mice are neither random no

187 rsensitivity and pain unpleasantness, modify uterine innervation and restore cognitive function witho

188 n who were eligible for standard bolus intra-uterine insemination (IUI).

189 Regions of apoptosis at the decidual/uterine interface at e18.5 were observed in control anim

190 -based types (breast, colon, ovarian, renal, uterine), into ten proteome-based, pan-cancer subtypes t

191 significant overlap with several conditional uterine knockout mouse models, including Foxa2, Wnt4, an

192 rone and its receptor, PR, are essential for uterine leiomyoma (LM, a.k.a., fibroid) tumorigenesis, b

193 Uterine leiomyomas (fibroids) are a major source of gyne

194 Uterine leiomyomas or fibroids (UFs) are benign tumors c

195 ranscriptional dysregulation in MED12 mutant uterine leiomyomas.

196 re exploration of novel target therapies for uterine leiomyomas.

197 Uterine leiomyomata (UL) are associated with severe repr

198 Uterine leiomyomata (UL) are the most common neoplasms o

199 particularly bone and soft tissue sarcomas, uterine leiomyosarcoma, melanomas, and radiotherapy-rela

200 otes homing of circulating leukocytes to the uterine lumen to destroy most sperm.

201 guided by the number of embryos entering the uterine lumen.

202 is initiated when an embryo attaches to the uterine luminal epithelium and subsequently penetrates i

203 modulates the biochemical composition of the uterine luminal fluid (ULF) in the most cranial portion

204 regnant mice exhibited higher frequencies of uterine macrophages (CD68(+)) and CD11c(+) CD103(+) and

205 iology of the fetus or mother in response to uterine manipulation in otherwise healthy pregnancy.

206 tive study identified women with an atypical uterine mass at MRI between January 2000 and April 2017,

207 readers to confidently diagnose as benign a uterine mass demonstrating one or more of these signs (P

208 including proliferative germ-cell tumors and uterine masses that express neuronal and epidermal cell

209 rstanding embryo-initiated modulation of the uterine milieu.

210 m labor, but the influence of adiponectin on uterine myometrial physiology is unknown.

211 AdipoR agonist, AdipoRon, potently inhibited uterine myometrial strip contractions in physiologic org

212 This transition requires that the uterine (myometrial) smooth muscle cells increase their

213 Endometrial glands were observed embedded in uterine myometrium, indicating adenomyosis-like phenotyp

214 Uterine natural killer (uNK) cells, which are required f

215 gically classified as "simple-type." Rarely, uterine nerve cell bodies were labeled in nodose ganglia

216 identifier NCT02285192) in 23 patients with uterine or cervical cancer.

217 lelic TSC2 mutations, supporting a potential uterine origin for the LAM(CORE) cell.

218 breast, lung, prostate, colorectal, bladder, uterine, pancreatic, gastric cancer, or non-Hodgkin lymp

219 50 mug/kg BW/d altered the estrous cycle and uterine pathology with similarity to EE2.

220 ormal pregnant (NP) and preeclamptic reduced uterine perfusion pressure (RUPP) Sprague Dawley rats on

221 determined that the placenta in the reduced uterine perfusion pressure rat model of preeclampsia is

222 In vivo, uterine perivascular adipose tissue (PVAT) potentiates u

223 adipose tissue surrounding uterine arteries (uterine perivascular adipose tissue; PVAT) is a novel lo

224 In the anchor cell/ventral uterine precursor cell (AC/VU) fate decision during C. e

225 erine LPS-induced PTB mouse model, decreased uterine proinflammatory mRNA concentrations (IL-6, Cxcl1

226 xcluded if they had a third degree or higher uterine prolapse, if they were unable to walk or stand w

227 ovarian adipose tissue but had no effect on uterine PVAT adipocyte morphology.

228 s of ex vivo bioassays, we demonstrated that uterine PVAT had pro-contractile and anti-dilatory effec

229 In isolated preparations, uterine PVAT has pro-contractile and anti-dilatory effec

230 this is the first study to demonstrate that uterine PVAT plays a regulatory role in UtBF, at least i

231 Surgical removal of uterine PVAT reduced UtBF only in pregnant rats.

232 erine arteries that makes them responsive to uterine PVAT signalling.

233 myometrial contractility via AMPK to promote uterine quiescence in pregnancy.

234 ner, critically regulates the acquisition of uterine receptivity in the female mouse, and disruption

235 ner, critically regulates the acquisition of uterine receptivity in the female mouse.

236 tential FOXA2-regulated genes that influence uterine receptivity, blastocyst implantation, and stroma

237 /11)-coupled class of GPCRs as regulators of uterine receptivity.

238 sted for activity against the V2, V1a and OT uterine receptors and not tested against the V1b recepto

239 suggested that other growth mediators drive uterine response to E2, and suggested that uterine-deriv

240 Uterine response to the initial decidual stimulus of NEL

241 VBAC were significantly more likely to have uterine rupture (0.24%, n = 69 versus 0.04%, n = 17, adj

242 ometrial carcinoma and 334 women with occult uterine sarcoma who underwent a hysterectomy or myomecto

243 h higher mortality risk in women with occult uterine sarcoma, especially in those with occult leiomyo

244 Among women with occult uterine sarcoma, LSH/LM was associated with a higher ris

245 Background Improving the differentiation of uterine sarcomas from atypical leiomyomas remains a clin

246 hted MRI criteria to differentiate malignant uterine sarcomas from benign atypical leiomyomas.

247 rs (EOCs), cervical, endometrial tumors, and uterine sarcomas that are genomically and/or pharmacolog

248 ality ion images were obtained from a single uterine section.

249 or aggressive endometrial cancers, including uterine serous cancer and uterine carcinosarcoma, which

250 Ovarian and uterine serous cancers are extremely lethal diseases tha

251 e perform immunohistochemical analyses in 31 uterine serous tumors for ETV6 and 45 basal breast tumor

252 designed to investigate the effect of intra-uterine slow-release insemination (SRI) on pregnancy rat

253 This results in depolarization of the uterine smooth muscle cells and calcium entry, which may

254 signal-induced contraction in primary human uterine smooth muscle cells.

255 of the embryo and is regulated by adrenergic uterine smooth muscle contractions.

256 y, the excitability and contractility of the uterine smooth muscle layer, the myometrium, increase dr

257 1, a potassium channel previously unknown in uterine smooth muscle, as a potential significant contri

258 Uterine-specific deletion of Arid1a compromises gland de

259 Compared to other visceral organs, uterine spinal afferent endings displayed noticeably les

260 e-related peptide (CGRP)-immunoreactivity of uterine spinal afferent endings supplied by thoracolumba

261 While the origin of the cell bodies of uterine spinal afferents is clear, the identity of their

262 This potentially leads to insufficient uterine spiral artery remodeling and placental hypoperfu

263 T) play a key role in placental development, uterine spiral artery remodeling, and prevention of detr

264 ng of trophoblast cells may cause failure of uterine spiral artery remodeling, which may be related t

265 olds seeded with autologous cells to restore uterine structure and function in rabbits.

266 1:731 pregnancies, likely due to the rise in uterine surgeries (e.g., Cesarean sections).

267 atures (purulent vaginal discharge, pyrexia, uterine tenderness, and leukocytosis) or by the presence

268 PlGF levels were higher in the uterine than in the peripheral vein with a median differ

269 hat underlie hormonal regulation of genes in uterine tissue and optimal development of estrogen respo

270 Bioengineered uterine tissue could provide a treatment option for wome

271 to ERalpha in vivo within hormone-responsive uterine tissue in mice.

272 In this protocol, mouse uterine tissue is used as a model system to illustrate b

273 They are able to survive cyclical uterine tissue loss and persistently generate all endome

274 Uterine tissue remodeling by alpha-chymase (mast cell pr

275 with 100-um spatial resolution across mouse uterine tissue sections preparing for blastocyst implant

276 Decidua is a transient uterine tissue shared by mammals with hemochorial placen

277 served E. faecalis in vaginal, cervical, and uterine tissue.

278 xposed to GEN on postnatal days (PND)1-5 and uterine tissues collected on PND5, PND22-26, and during

279 and functional requirements within maternal uterine tissues during pregnancy.

280 ifferences in cell-signaling pathways in the uterine tissues of G12D and G12V mice were identified us

281 ) plasma exosomes derived from feto-maternal uterine tissues on parturition was determined.

282 ntly, the process of selecting an embryo for uterine transfer uses an ad hoc combination of morpholog

283 Mating elicited 5-fold increases in uterine Tregs accompanied by extensive Treg proliferatio

284 te the immunologic mechanism responsible for uterine tropism, we explored the role of regulatory T ce

285 Uterine tumor epithelium was associated with decreased e

286 structures, and about 90% of them developed uterine tumors with diverse histological features resemb

287 In particular, the abnormal spermatheca-uterine valve morphology of lin-28(lf) hermaphrodites tr

288 hese responses were mediated at the level of uterine vascular smooth muscle, whereas, in pregnant rat

289 ve extravillous trophoblasts, remodeling the uterine vasculature, or fuse into multinuclear syncytiot

290 stimated in 17 paired serum samples from the uterine vein (ipsilateral or contralateral to the placen

291 samples from the maternal radial artery and uterine vein and umbilical artery and vein were obtained

292 The difference when the sampled uterine vein was ipsilateral to the placenta was 54.8 (I

293 pump', by which the placenta and underlying uterine wall contract independently of the rest of the u

294 o and 96 genes required for infection of the uterine wall ex vivo.

295 n embryo following its implantation into the uterine wall is critical for the successful continuation

296 colonize the primate genital tract and cause uterine wall pathologic findings.

297 throughout multiple anatomical layers of the uterine wall.

298 GEN-exposed mice exhibited reduced uterine weight gain in response to E2 treatment or artif

299 EO-33 blocked the uterine weight stimulated by estrone sulfate in ovariect

300 Uterine weight was reduced by EC313 treatment compared t