ライフサイエンスコーパス: uterine

1 Regarding uterine development, multiple uterine abnormalities were noticeable at 4 weeks of age

2 Non-invasive measurement of uterine activity using electrohysterogram (EHG) surface

3 under-appreciated, impact of maternal age on uterine adaptability to pregnancy as major contributor t

4 entrality of regulated gene silencing in the uterine adaptation to pregnancy and suggest new areas in

5 Uterine ageing and labour dysfunction should be investig

6 In this study, we conditionally ablated uterine ALK5 using progesterone receptor-cre mice to def

7 uterine SAA3 transcripts, suggests that the uterine amyloid deposits were due to locally produced SA

8 ndant C-terminal peptides indicated that the uterine amyloid was largely composed of full-length SAA3

9 These results suggest that the intra-uterine and early life environments provided by older mo

10 Analyzing the uterine and embryo structure in 3D for different genetic

11 d in multiple cancer types including breast, uterine and glioblastoma, and TET1 activation is associa

12 ted with a worse overall survival in breast, uterine and ovarian cancers.

13 ons, we were able to distinguish between two uterine and two thyroid cancer subtypes.

14 In patients with uterine and vaginal abnormalities, a work-up for associa

15 impairs DNA replication and underlies intra-uterine (and postnatal) growth retardation, chronic neut

16 nd smooth muscle function were diminished in uterine (and tail) arteries from aged mice and post-meno

17 to explore the potential for alterations in uterine arterial flow as a contributing mechanism.

18 Measures of maternal uterine arterial flow, including resistance index and me

19 d inhibition of the BKCa channel activity in uterine arteries and new insights in understanding and a

20 phoblast (EVT) cells to remodel the maternal uterine arteries during the first and second trimesters

21 bundance and BKCa channel current density in uterine arteries from pregnant sheep exposed to high-alt

22 In uterine arteries of non-pregnant animals, hypoxia inhibi

23 Uterine arteries of pregnant sheep acclimatized to long-

24 In uterine arteries of pregnant sheep, hypoxia significantl

25 and inhibiting the BKCa channel activity in uterine arteries of pregnant sheep.

26 (14)C-MeAIB and (3)H-taurine was reduced and uterine arteries showed increased relaxation.

27 a in inhibiting the BKCa channel activity in uterine arteries via increased oxidative stress.

28 Under local anesthesia, both uterine arteries were embolized.

29 Uterine arteries were isolated from non-pregnant and nea

30 th profound structural alterations of murine uterine arteries, including the occurrence of outward hy

31 the production of reactive oxygen species in uterine arteries, which was blocked by N-acetylcysteine.

32 fects of hypoxia on BKCa channel currents in uterine arteries.

33 a-mediated, pregnancy-induced remodelling of uterine arteries.

34 (PRKAA1) have been implicated in the greater uterine artery (UtA) blood flow and relative protection

35 ient reduction and irregular fluctuations in uterine artery blood flow associated with cardiac arrhyt

36 High uterine artery Doppler resistance indexes (RIs) are pred

37 Tail cuff blood pressure and uterine artery Doppler ultrasound were measured on GD 15

38 reintervention (compared with myomectomy or uterine artery embolization [UAE]), but rates of more se

39 ate proliferation of pregnancy-derived ovine uterine artery endothelial cells (P-UAECs) through beta-

40 timulate pregnancy-specific proliferation of uterine artery endothelial cells derived from pregnant (

41 ough a well-characterized model of bilateral uterine artery ligation of the pregnant rat.

42 nant Sprague-Dawley dams underwent bilateral uterine artery ligation or anesthesia (control) at e19.5

43 ng and ultrasound/colour Doppler evidence of uterine AVM managed by abdominal hysterectomy, describin

44 type in HFD-fed atERalphaKO involving severe uterine bacterial infections likely resulting from a pre

45 s, ossifying jaw fibromas, renal tumours and uterine benign and malignant neoplasms.

46 The adjusted HR for all abnormal uterine bleeding (on vs off hormonal therapy) was 1.02 (

47 Abnormal uterine bleeding occurred more frequently with rivaroxab

48 the incidences of recurrent VTE and abnormal uterine bleeding with and without concomitant hormonal t

49 The observed increased risk of abnormal uterine bleeding with rivaroxaban needs further explorat

50 or the effects on recurrent VTE and abnormal uterine bleeding.

51 itate angiogenesis and ensure maintenance of uterine blood flow during pregnancy.

52 Sildenafil treatment also improved uterine blood flow, decreased uterine vascular resistanc

53 s, counteracted the NAI-induced reduction in uterine blood flow.

54 ction of the ovarian nerve, which innervates uterine blood vessels, counteracted the NAI-induced redu

55 and Relevance: Although the overall risk for uterine cancer after RRSO was not increased, the risk fo

56 Objective: To determine the risk for uterine cancer and distribution of specific histologic s

57 Censoring occurred at uterine cancer diagnosis, hysterectomy, last follow-up,

58 ortance: The link between BRCA mutations and uterine cancer is unclear.

59 database to identify women with stage I-III uterine cancer who underwent hysterectomy from 2006 to 2

60 rcoma, two clinically aggressive subtypes of uterine cancer with few therapeutic options.

61 efits of minimally invasive hysterectomy for uterine cancer, population-level data describing the pro

62 al cancer subtypes, including PTEN-deficient uterine cancer.

63 7878 due to pancreatic cancer; 209314 due to uterine cancer; 421628 due to kidney cancer; 487518 due

64 requently develops benign fibroid tumors but uterine cancers are relatively rare.

65 dian age 45.6 (IQR: 40.9 - 52.5), 8 incident uterine cancers were observed (4.3 expected; observed to

66 and KRAS, similar to endometrioid and serous uterine carcinomas.

67 HGSOC) patients and is a recurrent lesion in uterine carcinosarcoma and endometrial carcinoma.

68 Uterine carcinosarcomas (UCSs) are highly aggressive mal

69 riptomic, and proteomic characterizations of uterine carcinosarcomas (UCSs).

70 ctiveness of surgical correction of specific uterine cavity abnormalities before IVF is warranted.

71 IVF in women with a normal ultrasound of the uterine cavity and a history of unsuccessful IVF treatme

72 an 38 years who had normal ultrasound of the uterine cavity and history of two to four unsuccessful I

73 rtions were performed into the spine and the uterine cavity, in swine and pregnant ovine models in vi

74 indicating that stromal ESR1 is crucial for uterine cell growth and pregnancy.

75 Aberrant regulation of uterine cell growth can lead to endometrial cancer and i

76 the molecular mechanisms of estrogen-induced uterine cell growth, we removed the estrogen receptor al

77 The proposed approach resulted in targeting uterine cells in-vitro, inhibiting uterine contractions

78 lls in human papillomavirus (HPV)-associated uterine cervical SCC, the third-leading cause of death b

79 The uterine cervix is the boundary structure between the ute

80 Progesterone suppresses uterine contractility acting through its receptors (PRA/

81 xpectation, Cox-1 null mice displayed normal uterine contractility; therefore, this study sought to d

82 Uterine contraction is a central feature of PTB, so gain

83 ace electrodes has been attempted to monitor uterine contraction.

84 Prostaglandins stimulate uterine contractions and are clinically used for cervica

85 lished roles of oxytocin (OT) is in inducing uterine contractions and labor.

86 targeting uterine cells in-vitro, inhibiting uterine contractions ex-vivo, while doubling uterine dru

87 Treatment intended to reduce uterine contractions include tocolytic agents, such as i

88 Preterm labor caused by uterine contractions is a major contributor to neonatal

89 preterm labour, but their ability to repress uterine contractions lasts </= 48 h and their use does n

90 ceptor agonists that act via cAMP can reduce uterine contractions to delay preterm labour, but their

91 Main Outcomes and Measures: Incidence of uterine corpus cancer in BRCA+ women who underwent RRSO

92 o TCGA ovarian serous cystadenocarcinoma and uterine corpus endometrial carcinomas.

93 Human endometrial and mouse uterine cytokine/chemokine mRNA concentrations were sign

94 remarkable induction of GPR64 expression in uterine decidual cells points to its potential physiolog

95 Furthermore, we find that uterine decidual cells represent a cell-cell interaction

96 Uterine decidual NK (dNK) cells and macrophages infiltra

97 Uterine deletion of Vang-like protein 2, but not Vang-li

98 We recently found that mice with uterine deletion ofMsxgenes (Msx1(d/d)/Msx2(d/d)) are in

99 endent canonical microRNAs are essential for uterine development and physiological processes such as

100 on the DROSHA-DGCR8 complex are required for uterine development as well as female fertility in mice.

101 nt did not expand and became atrophic during uterine development in these mice.

102 have normal ovarian development, ovulation, uterine development, and uterine response to exogenous e

103 of the expression of KLF5, a gene linked to uterine development, is implicated in tumorigenesis.

104 eviously established roles of these genes in uterine development, maternal nutrition, and vascular co

105 Regarding uterine development, multiple uterine abnormalities were

106 n be physiologically supported in this extra-uterine device for up to 4 weeks.

107 Uterine DNA and RNA were examined by using methylated DN

108 uterine contractions ex-vivo, while doubling uterine drug concentration, decreasing fetal levels, and

109 Moreover, Alk3 cKO mice exhibit an elevated uterine E2 response and unopposed epithelial cell prolif

110 Glycosylation of uterine endometrial cells plays important roles to deter

111 deficits in sexual behavior, ovulation, and uterine endometrial differentiation.

112 signalling mechanisms involved in regulating uterine endothelial cell proliferation during pregnancy.

113 te, which is in direct contact with maternal uterine, endothelial, and immune cells; placental villi,

114 he inaccessibility of the fetal brain in the uterine environment and the challenge of disambiguating

115 During fetal development, the uterine environment can have effects on offspring bone a

116 Importantly, a young uterine environment can restore normal placental as well

117 e activation caused by ZIKV infection in the uterine environment could also interfere with fetal deve

118 survival of the mammalian embryo within the uterine environment depends on the placenta, a highly co

119 To mimic aspects of the uterine environment in normal pregnancy, we added PRL an

120 during implantation, the architecture of the uterine environment in which the early embryo develops i

121 oth genetic background (NOS3 deficiency) and uterine environment, becomes more evident with age (> 7

122 d preterm births are preceded by a stressful uterine environment, including multiple contributing fac

123 , via changes to gametes and the gestational uterine environment.

124 Embryo implantation requires a hospitable uterine environment.

125 stantially up-regulated inMsx1(d/d)/Msx2(d/d)uterine epithelia.

126 erone receptor (PR), is necessary to inhibit uterine epithelial cell proliferation, a key step for em

127 ogen receptor alpha (ERalpha) in oviduct and uterine epithelial cells have impaired fertilization due

128 el in which we specifically ablated Mig-6 in uterine epithelial cells using Sprr2f-cre mice (Sprr2f(c

129 r via inhibition of STAT3 phosphorylation in uterine epithelial cells, and the antitumor effects of P

130 We recently showed that E4 stimulates uterine epithelial proliferation through nuclear estroge

131 implantation is defined by the inhibition of uterine epithelial proliferation, structural epithelial

132 sophosphatidylcholine can be detected in the uterine epithelium and in pre-implantation-stage embryos

133 es occur via paracrine signaling between the uterine epithelium and stroma.

134 HB-) EGF and cyclooxygenase-2 (COX-2) in the uterine epithelium contributes to decidualization, a ser

135 are sterile and have defects in the luminal uterine epithelium, including increased microvilli densi

136 h its G-protein-coupled receptor LPA3 in the uterine epithelium.

137 cal innovation for the treatment of absolute uterine factor infertility.

138 or uterus transplantation as a treatment for uterine factor infertility.

139 with live donation to 9 women with absolute uterine factor infertility.

140 Is) have been hypothesized to play a role in uterine fibroid development.

141 egnancy rates after conventional and partial uterine fibroid embolization (UFE).

142 and illustrate the methodology by analyzing uterine fibroid gene expression data.

143 Our analysis of the uterine fibroid growth gene expression data suggests tha

144 sure has been shown in Eker rats to increase uterine fibroid incidence in adulthood.

145 ifically enriched according to the size of a uterine fibroid.

146 fant formula feeding and ultrasound-detected uterine fibroids among young African-American women with

147 59 women (mean age, 35.9 years +/- 4.8) with uterine fibroids and/or adenomyosis who were unable to c

148 E significantly improves symptoms related to uterine fibroids in 85%-90% of patients.

149 Uterine fibroids occur in approximately 50% of women ove

150 fective outpatient procedures for women with uterine fibroids who want to conceive.

151 o differences in breast fibrocystic disease, uterine fibroids, or endometrial lining thickness as ass

152 om normally cycling premenopausal women with uterine fibroids, who were not on hormonal treatment at

153 s regarding the molecular characteristics of uterine fibroids.

154 shows a modestly enlarged uterus with three uterine fibroids.

155 gesterone receptor-cre to study the roles of uterine Fst during pregnancy.

156 In the absence of uterine FST, activin B expression and signaling are up-r

157 Uterine Fst-cKO mice demonstrate severe fertility defect

158 gnized role for FOXA2 in regulation of adult uterine function and fertility and provide original evid

159 ed the global CpG methylation profile of the uterine genome and subsequent gene expression.

160 ed the global CpG methylation pattern of the uterine genome, subsequent gene expression, and estrogen

161 could be recovered from progesterone-induced uterine gland (PUGKO) but not wildtype (WT) mice on day

162 rus and is a critical regulator of postnatal uterine gland differentiation in mice.

163 tor (LIF), a critical implantation factor of uterine gland origin, was not expressed during early pre

164 rescued by LIF and was maintained to term in uterine gland-containing adult FOXA2-deleted mice, pregn

165 siological defects, including the absence of uterine glands and dysregulation of progesterone and est

166 We revealed 3D organization of uterine glands and found that they undergo a stereotypic

167 fertility and provide original evidence that uterine glands and, by inference, their secretions play

168 Uterine glands are essential for pregnancy in mice and l

169 These results support the ideas that uterine glands secrete factors that regulate ULF homeost

170 ay 10 in neonatal FOXA2-deleted mice lacking uterine glands.

171 Although total uterine glucose uptake determined by Fick's principle wa

172 sive and, in view of the current scarcity of uterine grafts and the anticipated future rise in demand

173 eripheral kisspeptin signaling in regulating uterine growth and adenogenesis.

174 n of Kiss1 or Kiss1r dramatically suppressed uterine growth and almost fully prevented adenogenesis.

175 Uterine growth and endometrial gland formation (adenogen

176 Thus, while uterine growth is largely dependent on ovarian E2-output

177 However, while uterine growth was fully rescued by E2 treatment of Kiss

178 ast to E2, ShERPAs did not cause significant uterine growth.

179 f hormone deficiency, including bone health, uterine health, and body composition in this rat model.

180 of cardiac function as well as systemic and uterine hemodynamics that reduces uteroplacental blood f

181 regnancy impairs cardiovascular function and uterine hemodynamics with consequential fetal ischemia.

182 Cyclic changes in vaginal cytology, uterine histology, serum hormone levels, and wheel runni

183 Screening 12 strains of mice for uterine horn dilation following C. muridarum infection r

184 The severity scores of uterine horn dilation observed macroscopically correlate

185 l relevance of nontubal pathologies, such as uterine horn dilation, developed in mice following chlam

186 ridarum into the mouse uterus increased both uterine horn/glandular duct dilation and hydrosalpinx.

187 Nevertheless, the chlamydial induction of uterine horn/glandular duct dilation may be used to eval

188 In all cases, one of the uterine horns revealed collection due to a hemivaginal s

189 Rates of uterine hyperstimulation were low in both the misoprosto

190 ur findings indicate that unlike lung IL2Cs, uterine ILC2s are regulated by female sex hormones, whic

191 Furthermore, uterine ILC2s highly expressed estrogen receptor alpha,

192 Likewise, a marked reduction in uterine ILC2s was observed in mice deficient in estrogen

193 Importantly, uterine ILC2s were nearly absent in ovariectomized mice

194 ptor alpha, and in vitro culture of isolated uterine ILC2s with 17beta-estradiol modified expression

195 IL-33 induced type 2 cytokine production in uterine ILC2s, suggesting that they respond to IL-33 in

196 hronic circadian disruption from the time of uterine implantation through weaning.

197 Uterine inactivation of muscle segment homeobox (Msx) ge

198 r to identify a mechanism of the exaggerated uterine infection in HFD-fed atERalphaKO mice, a marked

199 Uterine infections in dairy cows are common after calvin

200 onas aeruginosa strains isolated from equine uterine infections.

201 ic administration of PIBF1 mitigated PTL and uterine inflammation in B cell-deficient mice.

202 rvum colonized the amniotic fluid and caused uterine inflammation, but without overt chorioamnionitis

203 coordination of a dynamic sequence of embryo-uterine interactions.

204 ferentiate properly, contributing to shallow uterine invasion and deficient spiral artery remodeling.

205 Uterine lavage and paired blood samples were collected a

206 Given that a uterine lavage can be easily and quickly performed even

207 specific allele fraction were present in the uterine lavage DNA samples.

208 sequencing could detect somatic mutations in uterine lavage fluid obtained from women undergoing hyst

209 lar data from eyelid skin and peritoneal and uterine lavage fluid provide unprecedented opportunities

210 previously reported cfDNA fraction from the uterine lavage.

211 genomic studies have identified subtypes of uterine leiomyoma (LM) with distinctive genetic alterati

212 rospective trial performed in the context of uterine leiomyoma evaluation.

213 fects of estradiol and progesterone on these uterine leiomyoma subtypes emphasize the importance of s

214 al characteristics of the two most prevalent uterine leiomyoma subtypes, MED12-mutant (MED12-LM) and

215 aft assay was driven by progesterone in both uterine leiomyoma subtypes.

216 Approximately 90% of cells in HMGA2-uterine leiomyoma were smooth muscle cells (SMC) with HM

217 gning nonsurgical therapeutic strategies for uterine leiomyoma.

218 Uterine leiomyomas are common benign smooth muscle tumor

219 mangiomas, liver cysts, thyroid nodules, and uterine leiomyomas.

220 onance (MR) evaluation of known or suspected uterine leiomyomas.

221 ED12-LM) and HMGA2-overexpressing (HMGA2-LM) uterine leiomyomas.

222 a treatment-naive patient who has metastatic uterine leiomyosarcoma and has experienced complete tumo

223 Uterine leiomyosarcoma is the most common subtype of ute

224 cell deficiency in mice resulted in a lower uterine level of active progesterone-induced blocking fa

225 Exposure to maternal smoking during uterine life and low birth weight were independently ass

226 The inner uterine lining (endometrium) is a unique tissue going th

227 d possible unique aspects of soft tissue and uterine LMS.

228 Implantation occurs along the uterine longitudinal axis within specialized implantatio

229 In Fst-cKO mice, the uterine luminal epithelium does not respond properly to

230 Next, the uterus and uterine luminal fluid (ULF) were obtained from WT and PU

231 -fed atERalphaKO mice, a marked reduction of uterine M2-macrophages was detected, a cell type relevan

232 contributes to decidualization, a series of uterine morphological changes required for placental for

233 aging method to evaluate the endometrial and uterine morphology and fallopian tube patency.

234 striking peri-implantation abnormalities in uterine morphology that cannot be visualized by histolog

235 imaging findings can collectively delineate uterine morphology, indicate the absence of ipsilateral

236 Analysis of uterine mRNAs 24 h after administration of DHT identifie

237 induced effector T cells that rapidly seeded uterine mucosa with resident memory T cells (T(RM) cells

238 l extravillous trophoblasts (EVT) invade the uterine mucosa without being rejected by the maternal im

239 ld increased risk of high-grade serous extra-uterine Mullerian cancers (HGSEMC), otherwise referred t

240 ole of endothelin-1 as both a constrictor of uterine myometrial smooth muscle and a proinflammatory m

241 and cytokine expression in the placenta, and uterine myometrium and decidua, was also attenuated.

242 le Cdc73(+/-) mice, at 18 months of age, had uterine neoplasms comprising squamous metaplasia, adenof

243 hed mouse models for parathyroid tumours and uterine neoplasms that develop in the HPT-JT syndrome, p

244 Uterine neoplasms, myometria and jaw bones of Cdc73(+/-)

245 -A into AF at 17.5 days post coitum enhanced uterine NF-kappaB activation and contractile gene expres

246 KIR2DS4 is expressed by approximately 45% of uterine NK (uNK) cells.

247 In this article, we show that uterine NK cells are the key source of IL-10 that is req

248 all-cell lung, non-Hodgkin lymphoma, breast, uterine, or cervical) from 2010 to 2012 (N = 5,284) were

249 artifacts, and perceived ability to evaluate uterine, ovarian, and musculoskeletal structures.

250 ; nonmelanoma skin cancer; breast; cervical; uterine; ovarian; prostate; testicular; kidney; bladder;

251 rgeting TIM1 could suppress infection at the uterine-placental interface.

252 the endometrial stromal fibroblasts, during uterine preparation for pregnancy.

253 nal silencing of select gene targets ensured uterine quiescence by preventing the decidua from expres

254 ling and is implicated in the maintenance of uterine quiescence during pregnancy.

255 other cell types in the uterus to influence uterine receptivity and blastocyst implantation for the

256 pression of activin signaling by FST enables uterine receptivity by preserving critical BMP signaling

257 transport bioactive substances that regulate uterine receptivity for blastocyst implantation.

258 A number of known uterine receptivity genes and gland-specific genes were

259 est thatMsxgenes play important roles during uterine receptivity including modulation of epithelial j

260 standing the molecular mechanisms underlying uterine receptivity will enable the development of new i

261 Failure to attain uterine receptivity will impede blastocyst attachment an

262 mone signaling pathways in the regulation of uterine receptivity.

263 lopment, ovulation, uterine development, and uterine response to exogenous estrogen stimulation, but

264 carries a high risk of morbidity related to uterine rupture and extensive haemorrhage.

265 myloid in the uterus, together with elevated uterine SAA3 transcripts, suggests that the uterine amyl

266 e.g., Tb32 with IC50 = 12 pM against MES SA (uterine sarcoma) cell line and 2 pM against HEK 293T (hu

267 leiomyosarcoma is the most common subtype of uterine sarcoma.

268 e with a viable gestational sac in the lower uterine segment and elevated B-Hcg levels, the possibili

269 estational sac in the anterior part of lower uterine segment with a history of painless vaginal bleed

270 Due to a poor vascular supply to the lower uterine segment, caesarean scars may heal improperly pre

271 activation and causally linked to premature uterine senescence and preterm birth, results in aberran

272 dministration of chemotherapy in ovarian and uterine serous carcinoma patients by biodegradable nanop

273 Uterine serous carcinoma, one of the most aggressive typ

274 efficacy against i.p. chemotherapy-resistant uterine serous carcinoma-derived xenografts compared wit

275 Uterine smooth muscle cells remain quiescent throughout

276 1 signaling is increased in mice harboring a uterine-specific deletion of transformation-related prot

277 The uterine stroma of Fst-cKO mice also responds poorly to a

278 ineage, forming cell columns anchored to the uterine stroma.

279 icits in the decidualisation response of the uterine stroma.

280 Uterine stromal cell decidualization is an essential par

281 The decidualization of uterine stromal cells is a key event in implantation.

282 he estrogen receptor alpha (Esr1) from mouse uterine stromal cells, where the embryo is implanted dur

283 ntation is critical establishing an adequate uterine surface area for nutrient support during gestati

284 ntous threads within 1 h, which provides the uterine surface to support development and maintain func

285 g conceptus elongation and attachment to the uterine surface.

286 rity of levonorgestrel (LNG)-releasing intra-uterine systems for long-acting reversible contraception

287 C treatment also degraded ERalpha protein in uterine tissue and breast cancer cells, but not in bone

288 It was detected in uterine tissue by day 7 and induced mild inflammation an

289 in pathology, we selected small fresh frozen uterine tissue samples to investigate how the tissue pre

290 The systematic review demonstrates that uterine transplantation is a major surgical innovation f

291 Central Cochrane Library were used to locate uterine transplantation studies carried out in human or

292 Proof of concept for human uterine transplantation was demonstrated in 2014 with a

293 monstrate that conditional deletion of mouse uterine Trp53 (p53(d/d)), molecularly linked to mTORC1 a

294 assessed by clinical examination, mammogram, uterine ultrasound, or endometrial lining biopsy.

295 also improved uterine blood flow, decreased uterine vascular resistance, and improved fetal weights

296 oxide, which leads to vasodilatation of the uterine vessels and might improve fetal growth in utero.

297 ptual content could be projected through the uterine wall and perceived by the fetus, dependent on ho

298 l utilizing direct ZIKV inoculation into the uterine wall of pregnant, immunocompetent mice to evalua

299 ased on visual stimuli projected through the uterine wall with fetal participants is not currently kn

300 d to the uterus, where they implant onto the uterine wall.