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1,383 results for “Estrogen”
Effect of Vaginal Estrogen on Asymptomatic Microhematuria (AMH)
ClinicalTrials.gov study NCT02213757. IPD Sharing: NO. Countries: 1. Publications: 3.
Hydroxychloroquine, Palbociclib, and Letrozole Before Surgery in Treating Patients With Estrogen Receptor Positive, HER2 Negative Breast Cancer
ClinicalTrials.gov study NCT03774472. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Pembrolizumab, Endocrine Therapy, and Palbociclib in Treating Postmenopausal Patients With Newly Diagnosed Metastatic Stage IV Estrogen Receptor Positive Breast Cancer
ClinicalTrials.gov study NCT02778685. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Cetuximab + / - Carboplatin for Estrogen Receptor-Negative, Progesterone Receptor-Negative Metastatic Breast Cancer
ClinicalTrials.gov study NCT00232505. IPD Sharing: NO. Countries: 1. Publications: 2.
Estrogen Sensitivity and Ovulatory Dysfunction in Obesity
ClinicalTrials.gov study NCT01381016. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Ospemifene vs. Conjugated Estrogens in the Treatment of Postmenopausal Sexual Dysfunction
ClinicalTrials.gov study NCT03018106. IPD Sharing: NO. Countries: 1. Publications: 1.
Study of (1) Everolimus, (2) Estrogen Deprivation Therapy (EDT) With Leuprolide + Letrozole and (3) Everolimus + EDT in Patients With Unresectable Fibrolamellar Hepatocellular Carcinoma (FLL-HCC)
ClinicalTrials.gov study NCT01642186. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Alternative Dosing of Exemestane Before Surgery in Treating Postmenopausal Patients With Stage 0-II Estrogen Positive Breast Cancer
ClinicalTrials.gov study NCT02598557. IPD Sharing: Not stated. Countries: 2. Publications: 2.
Open-label, Phase II Study of Stomatitis Prevention With a Steroid-based Mouthwash in Post-menopausal Women With Estrogen-receptor-positive (ER+), Human Epidermal Growth Factor Receptor 2 (HER2)- Meta
ClinicalTrials.gov study NCT02069093. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Data from: Sex-specific thermoregulatory effects of estrogen signaling in <em>Reprimo</em> lineage cells
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Seasonal changes of vomeronasal responses to chemosensory cues associated with circulating estrogen in the female muskrats (Ondatra zibethicus)
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Concentrations of estrogenic chemicals in fish and shellfish tissues from Puget Sound, WA
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The Alginate Immobilization of Metabolic Enzymes (AIME) platform retrofits an estrogen receptor transactivation assay with metabolic competence
The U.S. EPA Endocrine Disruptor Screening Program utilizes data across the ToxCast/Tox21 high-throughput screening (HTS) programs to evaluate the biological effects of potential endocrine active substances (EAS). A potential limitation to the use of in vitro assay data in regulatory decision-making is the lack of coverage for xenobiotic metabolic processes. Both hepatic- and peripheral-tissue metabolism can yield metabolites that exhibit greater activity than the parent compound (bioactivation) or are inactive (bioinactivation) for a given biological target. Interpretation of biological effect data for both putative EAS, as well as other chemicals, screened in HTS assays may benefit from the addition of xenobiotic metabolic capabilities to decrease the uncertainty in predicting potential hazards to human health. The objective of this study was to develop an approach to retrofit existing HTS assays with hepatic metabolism. The Alginate Immobilization of Metabolic Enzymes (AIME) platform encapsulates hepatic S9 fractions in alginate microspheres attached to 96-well peg lids. Functional characterization across a panel of reference substrates for phase I cytochrome P450 enzymes revealed substrate depletion with expected metabolite accumulation. Performance of the AIME method in the VM7Luc estrogen receptor (ER) transactivation assay was evaluated across 15 reference chemicals and 48 test chemicals that yield metabolites previously identified as ER active or inactive. The results demonstrate the utility of applying the AIME method for identification of false positive and false negative target assay effects, reprioritization of hazard based on metabolism-dependent bioactivity, and enhanced in vivo concordance with the rodent uterotrophic bioassay. Integration of the AIME metabolism method may prove useful for future biochemical and cell-based HTS applications.
The Immp2l mutation causes ovarian aging through ROS-wnt/β-catenin-estrogen (cyp19a1) pathway: preventive effect of melatonin
<p>Mitochondria play important roles in ovarian follicle development. Mitochondrial dysfunction, including mitochondrial gene deficiency, impairs the ovarian development. Here, we explored the role and mechanism of mitochondrial inner membrane gene <i>Immp2l</i> in ovarian follicle growth and development. Our results revealed that the female Immp2l<sup>-/-</sup> mice were infertile, while the Immp2l<sup>+/- </sup>mice were normal. Body and ovarian weights were reduced in the female Immp2l<sup>-/- </sup>mice, ovarian follicle growth and development were stunted in the secondary follicle stage. Although a few ovarian follicles were ovulated, the oocytes were not fertilized due to mitochondrial dysfunction. Increased oxidative stress, decreased estrogen levels, and altered genes expression of Wnt/β-catenin and steroid hormone synthesis pathways were observed in 28-day-old Immp2l<sup>-/-</sup> mice. The Immp2l mutation accelerated ovarian aging process, as no ovarian follicles were detected in age of 5 months in Immp2l<sup>-/- </sup>mice. All the aforementioned changes in the Immp2l<sup>-/- </sup>mice were reversed by administration of antioxidant melatonin to the Immp2l<sup>-/-</sup> mice. Furthermore, our in vitro study using Immp2l knockdown granulosa cells confirmed that the Immp2l downregulation induced granulosa cell aging by enhancing ROS levels, suppressing <i>Wnt16</i>, increasing β-catenin and decreasing steroid hormone synthesis gene <i>cyp19a1</i> and estrogen levels, accompanied by an increase in the aging phenotype of granulosa cells. Melatonin treatment delayed granulosa cell aging progression. Taken together, Immp2l causes ovarian aging through the ROS-Wnt/β-catenin-estrogen (cyp19a1) pathway, which can be reversed by melatonin treatment.Mitochondria play important roles in ovarian follicle development. Mitochondrial dysfunction, including mitochondrial gene deficiency, impairs the ovarian development. Here, we explored the role and mechanism of mitochondrial inner membrane gene <i>Immp2l</i> in ovarian follicle growth and development. Our results revealed that the female Immp2l<sup>-/-</sup> mice were infertile, while the Immp2l<sup>+/- </sup>mice were normal. Body and ovarian weights were reduced in the female Immp2l<sup>-/- </sup>mice, ovarian follicle growth and development were stunted in the secondary follicle stage. Although a few ovarian follicles were ovulated, the oocytes were not fertilized due to mitochondrial dysfunction. Increased oxidative stress, decreased estrogen levels, and altered genes expression of Wnt/β-catenin and steroid hormone synthesis pathways were observed in 28-day-old Immp2l<sup>-/-</sup> mice. The Immp2l mutation accelerated ovarian aging process, as no ovarian follicles were detected in age of 5 months in Immp2l<sup>-/- </sup>mice. All the aforementioned changes in the Immp2l<sup>-/- </sup>mice were reversed by administration of antioxidant melatonin to the Immp2l<sup>-/-</sup> mice. Furthermore, our in vitro study using Immp2l knockdown granulosa cells confirmed that the Immp2l downregulation induced granulosa cell aging by enhancing ROS levels, suppressing <i>Wnt16</i>, increasing β-catenin and decreasing steroid hormone synthesis gene <i>cyp19a1</i> and estrogen levels, accompanied by an increase in the aging phenotype of granulosa cells. Melatonin treatment delayed granulosa cell aging progression. Taken together, Immp2l causes ovarian aging through the ROS-Wnt/β-catenin-estrogen (cyp19a1) pathway, which can be reversed by melatonin treatment.</p>
Data from: Relationship between maternal environment and DNA methylation patterns of estrogen receptor alpha in wild Eastern Bluebird (Sialia sialis) nestlings: a pilot study
There is mounting evidence that, across taxa, females breeding in competitive environments tend to allocate more testosterone to their offspring prenatally and these offspring typically have more aggressive and faster-growing phenotypes. To date, no study has determined the mechanisms mediating this maternal effect's influence on offspring phenotype. However, levels of estrogen receptor alpha (ERα) gene expression are linked to differences in early growth and aggression; thus, maternal hormones may alter gene regulation, perhaps via DNA methylation, of ERα in offspring during prenatal development. We performed a pilot study to examine natural variation in testosterone allocation to offspring through egg yolks in wild Eastern Bluebirds (Sialia sialis) in varying breeding densities and percent DNA methylation of CG dinucleotides in the ERα promoter in offspring brain regions associated with growth and behavior. We hypothesized that breeding density would be positively correlated with yolk testosterone, and prenatal exposure to maternal-derived yolk testosterone would be associated with greater offspring growth and decreased ERα promoter methylation. Yolk testosterone concentration was positively correlated with breeding density, nestling growth rate, and percent DNA methylation of one out of five investigated CpG sites (site 3) in the diencephalon ERα promoter, but none in the telencephalon (n = 10). Percent DNA methylation of diencephalon CpG site 3 was positively correlated with growth rate. These data suggest a possible role for epigenetics in mediating the effects of the maternal environment on offspring phenotype. Experimentally examining this mechanism with a larger sample size in future studies may help elucidate a prominent way in which animals respond to their environment. Further, by determining the mechanisms that mediate maternal effects, we can begin to understand the potential for the heritability of these mechanisms and the impact that maternal effects are capable of producing at an evolutionary scale.
Data from: The effects of synthetic estrogen exposure on pre-mating and post-mating episodes of selection in sex-role-reversed Gulf pipefish
Environmental estrogens have been shown to affect populations of aquatic organisms in devastating ways, including feminization of males, alterations in mating behaviors, and disruption of sexual selection. Studies have shown 17α-ethinylestradiol (EE2) exposure to induce female-like secondary sexual traits in male Gulf pipefish, changing how females perceive affected males. We aimed to understand the effects of EE2 exposure on the sex-role-reversed mating system and the strength of selection in Gulf pipefish. We used artificial Gulf pipefish breeding aggregations and microsatellite-based parentage analysis to determine maternity. We then calculated the opportunity for selection and selection differentials on body size for both sexes during three consecutive episodes of selection. Exposure to EE2 did not affect the strength of selection, likely due to the unusual sex-role-reversed mating system found in this species. With respect to multiply mated females, EE2 exposed females produced more eggs with higher embryo survivorship than non-exposed females. Thus, short-term exposure to low concentrations (2.0 ng/L) of EE2 in Gulf pipefish enhanced female reproductive success. However, higher EE2 concentrations (5.0 ng/L) caused complete reproductive failure in Gulf pipefish males. These results call for more work on the long-term effects of EE2 exposure in Gulf pipefish in artificial and natural populations.
Data from: Measuring fecal testosterone in females and fecal estrogens in males: comparison of RIA and LC/MS/MS methods for wild baboons (Papio cynocephalus).
The development of non-invasive methods, particularly fecal determination, has made possible the assessment of hormone concentrations in wild animal populations. However, measuring fecal metabolites needs careful validation for each species and for each sex. We investigated whether radioimmunoassays (RIAs) previously used to measure fecal testosterone (fT) in male baboons and fecal estrogens (fE) in female baboons were well suited to measure these hormones in the opposite sex. We compared fE and fT concentrations determined by RIA to those measured by liquid chromatography combined with triple quadropole mass spectrometry (LC/MS/MS), a highly specific method. Additionally, we conducted a biological validation to assure that the measurements of fecal concentrations reflected physiological levels of the hormone of interest. Several tests produced expected results that led us to conclude that our RIAs can reliably measure fT and fE in both sexes, and that within-sex comparisons of these measures are valid: (i) fTRIA were significantly correlated to fTLC/MS/MS for both sexes; (ii) fTRIA were higher in adult than in immature males; (iii) fTRIA were higher in pregnant than non-pregnant females; (iv) fERIA were correlated with 17β-estradiol (fE2) and with estrone (fE1) determined by LC/MS/MS in pregnant females; (v) fERIA were significantly correlated with fE2 in non-pregnant females and nearly significantly correlated in males; (vi) fERIA were higher in adult males than in immature males. fERIA were higher in females than in males, as predicted, but unexpectedly, fTRIA were higher in females than in males, suggesting a difference in steroid metabolism in the two sexes; consequently, we conclude that while within-sex comparisons are valid, fTRIA should not be used for intersexual comparisons. Our results should open the field to important additional studies, as to date the roles of testosterone in females and estrogens in males have been little investigated.
Chemical screening in an estrogen receptor transactivation assay with metabolic competence
<p>The U.S. EPA continues to utilize high-throughput screening data to evaluate potential biological effects of endocrine active substances without the use of animal testing. Determining the scope and need for <em>in vitro</em> metabolism in high-throughput assays requires the generation of larger data sets that assess the impact of xenobiotic transformations on toxicity-related endpoints. The objective of the current study was to screen a set of 768 ToxCast chemicals in the VM7Luc estrogen receptor transactivation assay (ERTA) using the Alginate Immobilization of Metabolic Enzymes (AIME) hepatic metabolism method. Chemicals were screened with or without metabolism to identify estrogenic effects and metabolism-dependent changes in bioactivity. Based on estrogenic hit calls, 85 chemicals were active in both assay modes, 16 chemicals were only active without metabolism, and 27 chemicals were only active with metabolism. Using a novel metabolism curve shift method that evaluates the shift in concentration-response curves, 29 of these estrogenic chemicals were identified as bioactivated and 59 were bioinactivated. Human biotransformation routes and associated metabolites were predicted <em>in silico </em>across the chemicals to mechanistically characterize possible transformation-related ERTA effects. Overall, the study profiled novel chemicals associated with metabolism-dependent changes in ERTA bioactivity, and suggested routes of biotransformation and putative metabolites responsible for the observed estrogenic effects. The data demonstrate a range of metabolism-dependent effects across a diverse chemical library and highlight the need to evaluate the role of intrinsic xenobiotic metabolism in endocrine and other toxicity-related health effects.</p>
Supplemental material for: The estrogen receptor α cistrome in human endometrium and epithelial organoids
<p>Endometrial health is impacted by molecular processes that underlie estrogen responses. We assessed estrogen regulation of endometrial function by integrating the estrogen receptor alpha (ESR1) cistromes and transcriptomes of endometrial biopsies taken from the proliferative and mid-secretory phases of the menstrual cycle together with hormonally stimulated endometrial epithelial organoids. The cycle stage specific ESR1 binding sites were determined by ChIPseq and then integrated with changes in gene expression from RNAseq data to infer candidate ESR1 targets in normal endometrium. Genes with ESR1 binding in whole endometrium were enriched for chromatin modification and regulation of cell proliferation. The distribution of ESR1 binding sites in organoids was more distal from gene promoters when compared to primary endometrium and was more similar to the proliferative than the mid-secretory phase ESR1 cistrome. Inferred organoid estrogen/ESR1 candidate target genes impacted formation of cellular protrusions, and chromatin modification. Comparison of signaling impacted by candidate ESR1 target genes in endometrium vs. organoids reveals enrichment of both overlapping and distinct responses. Our analysis of the ESR1 cistromes and transcriptomes from endometrium and organoids provides important resources for understanding how estrogen impacts endometrial health and function.</p>
Data from: Poor endometrial proliferation after clomiphene is associated with altered estrogen action
<p>Context: Suboptimal endometrial thickening is associated with lower pregnancy rates and occurs in some infertile women treated with clomiphene.</p> <p>Objective: To examine cellular and molecular differences in the endometrium of women with suboptimal versus optimal endometrial thickening following clomiphene.</p> <p>Design: Translational prospective cohort study from 2018-2020.</p> <p>Setting: University-affiliated clinic.</p> <p>Patients or Participants: Reproductive age women with unexplained infertility treated with 100mg of clomiphene cycle days 3-7 who developed optimal (≥8mm; n=6, controls) or suboptimal (<6mm; n=7, subjects) endometrial thickness.</p> <p>Interventions:<b> </b>Pre-ovulatory blood and endometrial sampling.</p> <p>Main outcome measures:<b> </b>Endometrial tissue architecture, abundance and location of specific proteins, RNA expression, ERa binding.</p> <p>Results: The endometrium of suboptimal subjects compared to optimal controls was characterized by a reduced volume of glandular epithelium (16% vs 24%, P=0.01), decreased immunostaining of markers of proliferation (PCNA, ki67) and angiogenesis (PECAM-1), increased immunostaining of pan-leukocyte marker CD45 and ERb, but decreased ERa immunostaining (all P<0.05). RNASeq identified 398 differentially expressed genes between groups. Pathway analysis of differentially expressed genes indicated reduced proliferation (Z-score= -2.2, P<0.01), decreased angiogenesis (Z-score = -2.87, P<0.001), increased inflammation (Z-score= +2.2, P<0.01), and ERb activation (Z-score= +1.6, P<0.001) in suboptimal subjects. ChIP-seq identified 6 genes bound by ERα that were differentially expressed between groups (P<0.01), some of which may play a role in implantation.</p> <p>Conclusions: Women with suboptimal endometrial thickness after clomiphene exhibit aberrant estrogen receptor expression patterns, architectural changes and altered gene and protein expression, suggesting reduced proliferation and angiogenesis in the setting of increased inflammation.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.