Relevant bibliographies by topics / Estrogen

Academic literature on the topic 'Estrogen'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Estrogen"

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Kumar, Anita, Antara Banerjee, Dipty Singh, Gargi Thakur, Nandini Kasarpalkar, Shubhangi Gavali, Sushama Gadkar, et al. "Estradiol: A Steroid with Multiple Facets." Hormone and Metabolic Research 50, no. 05 (March 22, 2018): 359–74. http://dx.doi.org/10.1055/s-0044-100920.

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AbstractSeventy-five glorious years have passed since estradiol was discovered by Edward Doisy. From discovery in the ovaries to delineation of diverse physiological effects, research on estrogens has covered a lot of ground. Estrogen receptors that mediate estrogenic effects, have been detected not only in reproductive organs, but also in other body organs. Estrogen receptors function either as conventional transcription factors or as rapid signal transducers. These different modes of action are opted by estrogens to elicit an array of reproductive and non-reproductive functions. It is well established that estrogens promote cell proliferation in various tissues and hence are also linked to carcinogenesis. Anti-estrogens are being used as adjunct therapies for cancers since several years. On the other hand, estrogen-based strategies are used to alleviate adverse effects of menopause. Apart from estrogens synthesized in various organs, exposure to environmental estrogens can also impact physiology. Thus, too much or too less of estrogens can tip the balance and lead to unfavorable consequences. Multiple estrogen receptors with their tissue- or cell type-specific expression eliciting dose-dependent effects make it perplexing to ‘unify’ estrogenic actions in diverse tissues/organs. This warrants more research on estrogen-mediated effects and their regulation in somatic and reproductive tissues. This review presents physiological and pathological aspects of estrogens thus highlighting the good, bad, and ugly facets of estrogens.
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Elger, W., A. Barth, A. Hedden, G. Reddersen, P. Ritter, B. Schneider, J. Züchner, et al. "Estrogen sulfamates: a new approach to oral estrogen therapy." Reproduction, Fertility and Development 13, no. 4 (2001): 297. http://dx.doi.org/10.1071/rd01029.

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Sulfamate substitution (-O-SO 2-NH 2) at carbon atom 3 of the steroid skeleton leads to orally active prodrugs of estrogens with much higher systemic, but lower hepatic, estrogenic activity than their parent steroids. This dissociation is achieved by first passage through the liver in erythrocytes, followed by systemic hydrolysis which releases the ‘parent’ estrogen. In the rat, orally administered tritiated estradiol sulfamate, unlike estradiol, appears in the circulation at high concentrations. At C max , approximately one third of the administered dose forms a depot in the circulation (98% in erythrocytes, 2% in plasma). Significant estradiol, estrone and estrone sulfate concentrations were recorded in plasma during depletion of the red blood cell pool. Estradiol sulfamate (J995) has no estrogen receptor affinity per se or estrogenic activity in vitro ( i.e. without hydrolysis). Its oral uterotropic activity in rats is approximately 100 times greater than that of estradiol, however, its hepatotropic activity is only marginally elevated. These functions include bile secretion, the secretion of angiotensinogen, lipoproteins (total and high-density lipoprotein cholesterol) and insulin-like growth factor I (IGF-I). Orally administred estradiol sulfamate led to systemic estrogenic effects without significant hepatic responses, whereas estradiol and other ‘conventional’ estrogens exerted parallel systemic and hepatic estrogenic effects. Sulfamate technology represents an approach to the use of natural estrogens for fertility control and hormone replacement therapy in both genders. In this context, reduced effects on hemostatic factors, angiotensinogen, bile and IGF-I secretion seem the most important aspects. In addition, blood concentrations of estrogens are less variable than with conventional estrogens.
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O’Leary, Emily, Connor Davis, Molly Mancheski, Peng Ma, and Thomas Wiese. "PMON14 Estrogen Activity of Supplements Targeted for Post-Menopausal Women." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A440—A441. http://dx.doi.org/10.1210/jendso/bvac150.916.

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Abstract A wide variety of dietary supplements are available for the treatment of post-menopausal symptoms in women. Many women choose these supplements to avoid the potential unwanted side effects and long-term complications associated with traditional hormone therapy. In this study, we evaluated the in vitro estrogen activity of extracts from eleven supplements targeted for post-menopausal women to test the hypothesis that some of these supplements will induce estrogen activity in human breast cancer cell bioassays. Ethanol extracts (1 g: 1 mL) were prepared from the supplements: Amberen, Nature's Bounty Black Cohosh, Nature's Bounty St. John's Wort, Swanson Chasteberry Fruit, Nature's Way Red Clover, Promensil Real Health, Estroven, Relizen, Remifemin, and Equelle. Black cohosh, St. John's Wort, Chasteberry fruit, and red clover are standalone products that are not sold under a brand name. Promensil, Estroven, and Equelle contain isoflavones that have been reported to be estrogenic. Estroven and Remifemin contain black cohosh. Relizen contains a purified Swedish flower pollen extract and Amberen contains succinates, amino acids, minerals, and vitamin E. The estrogen activity of each extract was measured using both the T47D-kb-Luc estrogen responsive reporter gene and MCF-7 E3 proliferation estrogen bio-assays. The extracts from Nature's Way Red Clover, Promensil Real Health, and Equelle induced full estrogen agonist efficacy in the MCF-7 proliferation assay and more than full efficacy in the T47D-kb-Luc assay compared to estradiol. The agonist activity of these extracts in both bio-assays was inhibited by fulvestrant. Extracts from Nature's Bounty Black Cohosh, Nature's Bounty St. John's Wort, Swanson Chasteberry Fruit and Relizen induced less than full agonist estrogen activity only in the MCF-7 proliferation assay that was not, or not completely inhibited by fulvestrant. Thus, some supplements in this study likely target the estrogen receptor as agonists while others may be only weak estrogens that may also activate other proliferative pathways. While estrogen therapy is known to provide relief of some post-menopausal symptoms, estrogen use is associated with increased breast cancer risk. Consumers may benefit from information about the estrogen activity of supplements targeted for post-menopausal women. The results of this study may allow women to make more informed decisions about the use of these supplements. This study may be a prototype for evaluating the estrogen activity of dietary supplements for the purpose of informing consumers. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.
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Matsui, S., H. Takigami, T. Matsuda, N. Taniguchi, J. Adachi, H. Kawami, and Y. Shimizu. "Estrogen and estrogen mimics contamination in water and the role of sewage treatment." Water Science and Technology 42, no. 12 (December 1, 2000): 173–79. http://dx.doi.org/10.2166/wst.2000.0265.

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The yeast estrogen screen was applied to sewage treatment process waters to identify the presence of estrogenic activity and to investigate the fate and behavior of estrogenic substances through treatment. Hydrophobic fractions in the water phase were extracted and concentrated using C18 cartridges for the effective extraction of 17β-estradiol (E2) and other estrogen mimics. Clear dose-dependent elevation in the synthesis of β-galactosidase in the yeast screen was observed with all the samples tested, demonstrating that these samples were estrogenic. However, estrogenic activity tended to reduce during the treatment, especiallyiin the biological process. Quantification results of the yeast estrogen screen in terms of E2 equivalent were compared with actual E2 concentrations measured by an ELISA. E2 occupied 34% of the whole estrogenicity in the raw sewage, while almost 100% in the final effluent. The analyses of the sewage treatment process waters revealed that human estrogens are major causative substances in terms of estrogenic activity in sewage and its treated effluent. Although findings of possible correlation of environmental estrogens with the real impact on human health and the ecosystem are still the focus of scientific debate and investigation, proper management should be established in the sewage treatment process which receives various environmental contaminants.
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Liang, Rubing, Jing Zhou, and Jianhua Liu. "Construction of a Bacterial Assay for Estrogen Detection Based on an Estrogen-Sensitive Intein." Applied and Environmental Microbiology 77, no. 7 (February 11, 2011): 2488–95. http://dx.doi.org/10.1128/aem.02336-10.

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ABSTRACTEscherichia colistrain DIER was constructed for estrogen detection by inserting an estrogen-sensitive intein (VMAERintein) into the specific site of the constitutively expressed chromosomallacZgene. This VMAERintein was generated by replacing the endonuclease region of theSaccharomyces cerevisiaeVMA intein with the estrogen binding region of the human estrogen receptor α (hERα). When there were estrogens or analogs, the splicing of the VMAERintein was induced to produce the mature LacZ protein, which was detected through a β-galactosidase colorimetric assay. Eight typical chemicals (17-β-estradiol, bisphenol A, chrysene, 6-OH-chrysene, benz[a]anthracene, pyrene, progesterone, and testosterone) were detected using this DIER strain, and the whole detection procedure was accomplished in 2 h. Their 50% effective concentrations (EC50), relative estrogenic activities, and estradiol equivalency factors were calculated and were quite consistent with those detected with the yeast estrogen screening (YES) system. Furthermore, the estrogenic activities of the synthetic musk samples extracted from the wastewater and waste sludge of a sewage treatment plant of Shanghai (China) were detected, and their results were comparable to those obtained from the YES system and gas chromatography-mass spectrometry (GC-MS). In conclusion, the DIER bioassay could fill a niche for the efficient, rapid, high-throughput screening of estrogenic compounds and has potential for the remote, near-real-time monitoring of environmental estrogens.
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O’Donnell, Liza, Kirsten M. Robertson, Margaret E. Jones, and Evan R. Simpson. "Estrogen and Spermatogenesis*." Endocrine Reviews 22, no. 3 (June 1, 2001): 289–318. http://dx.doi.org/10.1210/edrv.22.3.0431.

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Abstract Although it has been known for many years that estrogen administration has deleterious effects on male fertility, data from transgenic mice deficient in estrogen receptors or aromatase point to an essential physiological role for estrogen in male fertility. This review summarizes the current knowledge on the localization of estrogen receptors and aromatase in the testis in an effort to understand the likely sites of estrogen action. The review also discusses the many studies that have used models employing the administration of estrogenic substances to show that male fertility is responsive to estrogen, thus providing a mechanism by which inappropriate exposure to estrogenic substances may cause adverse effects on spermatogenesis and male fertility. The reproductive phenotypes of mice deficient in estrogen receptors α and/or β and aromatase are also compared to evaluate the physiological role of estrogen in male fertility. The review focuses on the effects of estrogen administration or deprivation, primarily in rodents, on the hypothalamo-pituitary-testis axis, testicular function (including Leydig cell, Sertoli cell, and germ cell development and function), and in the development and function of the efferent ductules and epididymis. The requirement for estrogen in normal male sexual behavior is also reviewed, along with the somewhat limited data on the fertility of men who lack either the capacity to produce or respond to estrogen. This review highlights the ability of exogenous estrogen exposure to perturb spermatogenesis and male fertility, as well as the emerging physiological role of estrogens in male fertility, suggesting that, in this local context, estrogenic substances should also be considered “male hormones.”
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Chmielewska, Małgorzata, Izabela Skibińska, and Małgorzata Kotwicka. "Mitochondria: Target organelles for estrogen action." Postępy Higieny i Medycyny Doświadczalnej 71, no. 1 (June 8, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.3828.

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Estrogens belong to a group of sex hormones, which have been shown to act in multidirectional way. Estrogenic effects are mediated by two types of intracellular receptors: estrogen receptor 1 (ESR1) and estrogen receptor 2 (ESR2). There are two basic mechanisms of estrogen action: 1) classical-genomic, in which the ligand-receptor complex acts as a transcriptional factor and 2) a nongenomic one, which is still not fully understood, but has been seen to lead to distinct biological effects, depending on tissue and ligand type. It is postulated that nongenomic effects may be associated with membrane signaling and the presence of classical nuclear receptors within the cell membrane. Estrogens act in a multidirectional way also within cell organelles. It is assumed that there is a mechanism which manages the migration of ESR into the mitochondrial membrane, wherein the exogenous estrogen affect the morphology of mitochondria. Estrogen, through its receptor, can directly modulate mitochondrial gene expression. Moreover, by regulating the level of reactive oxygen species, estrogens affect the biology of mitochondria. The considerations presented in this paper indicate the pleiotropic effects of estrogens, which represent a multidirectional pathway of signal transduction.
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Lee, Richard R., and Karen P. Phillips. "Role of Estrogen Receptors in Male Reproductive Physiology." Revue interdisciplinaire des sciences de la santé - Interdisciplinary Journal of Health Sciences 3, no. 1 (March 10, 2016): 40–45. http://dx.doi.org/10.18192/riss-ijhs.v3i1.1452.

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Canonical estrogen receptors (ER α/β) have a genomic mechanism of action, functioning as nuclear transcription factors for estrogen-dependent genes. Estrogen receptors are well established within the male reproductive tract with estrogen playing an essential role for male fertility. The recent characterization of novel G-protein coupled estrogen receptor GPR30 (alternatively known as GPER1), depending on non-genomic intracellular signaling pathways to transduce estrogenic signals, requires a re-examination of the roles of estrogen receptors in male reproduction. Further, the affinity of environmental estrogens (xenoestrogens) for estrogen receptor subtypes may provide additional understanding of the reproductive effects of these chemicals on male fertility. Here we review the structure and functions of each estrogen receptor within the context of male reproduction, with special consideration of the reproductive implications of xenoestrogen exposure.
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Hashimoto, T., K. Takahashi, and T. Murakami. "Characteristics of estrogen decomposition by ozonation." Water Science and Technology 54, no. 10 (November 1, 2006): 87–93. http://dx.doi.org/10.2166/wst.2006.806.

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Since the natural estrogens 17 β-estradiol (E2) and estron (E1), and the synthetic estrogen 17 α-ethynyl estradiol (EE2) have strong endocrine disrupting effects and the tendency to persist in effluent from wastewater treatment plants, effective measures are needed to remove them from wastewater. In this research, to gain an understanding of the characteristics of estrogen decomposition by ozonation, experiments were conducted using effluent from an actual wastewater treatment plant. In this experiment, estrogen was added to effluent at a concentration of 200 ng/l and 20 ng/l before the ozonation experiments. The results showed 90% or more of estrogen concentration and estrogenic activity of E2, E1 and EE2 to be removed at an ozone dose of 1 mg/l. At an ozone dose of 3 mg/l, the estrogen concentration and estrogenic activity of E2, E1 and EE2 in the treated water fell below the detection limit. The removal rate was not influenced by the kind of estrogen. No generation of byproducts with estrogenic activity was observed. The authors conclude that estrogen in secondary treated wastewater can be almost entirely removed at the practical ozone dose rate applied for the purpose of disinfection, which is up to about 5 mg/l.
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Chang, Minsun, Kuan-wei Peng, Irida Kastrati, Cassia R. Overk, Zhi-Hui Qin, Ping Yao, Judy L. Bolton, and Gregory R. J. Thatcher. "Activation of Estrogen Receptor-Mediated Gene Transcription by the Equine Estrogen Metabolite, 4-Methoxyequilenin, in Human Breast Cancer Cells." Endocrinology 148, no. 10 (October 1, 2007): 4793–802. http://dx.doi.org/10.1210/en.2006-1568.

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4-Methoxyequilenin (4-MeOEN) is an O-methylated metabolite in equine estrogen metabolism. O-methylation of catechol estrogens is considered as a protective mechanism; however, comparison of the properties of 4-MeOEN with estradiol (E2) in human breast cancer cells showed that 4-MeOEN is a proliferative, estrogenic agent that may contribute to carcinogenesis. 4-MeOEN results from O-methylation of 4-hydroxyequilenin, a major catechol metabolite of the equine estrogens present in hormone replacement therapeutics, which causes DNA damage via quinone formation, raising the possibility of synergistic hormonal and chemical carcinogenesis. 4-MeOEN induced cell proliferation with nanomolar potency and induced estrogen response element (ERE)-mediated gene transcription of an ERE-luciferase reporter and the endogenous estrogen-responsive genes pS2 and TGF-α. These estrogenic actions were blocked by the antiestrogen ICI 182,780. In the standard radioligand estrogen receptor (ER) binding assay, 4-MeOEN showed very weak binding. To test for alternate ligand-ER-independent mechanisms, the possibility of aryl hydrocarbon receptor (AhR) binding and ER-AhR cross talk was examined using a xenobiotic response element-luciferase reporter and using AhR small interfering RNA silencing in the ERE-luciferase reporter assay. The results negated the possibility of AhR-mediated estrogenic activity. Comparison of gene transcription time course, ER degradation, and rapid activation of MAPK/ERK in MCF-7 cells demonstrated that the actions of 4-MeOEN mirrored those of E2 with potency for classical and nonclassical estrogenic pathways bracketing that of E2. Methylation of 4-OHEN may not represent a detoxification pathway because 4-MeOEN is a full, potent estrogen agonist.
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Dissertations / Theses on the topic "Estrogen"

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Järvenpää, Paula. "Intestinal metabolism of estrogens including some studies on medroxiprogesterone acetate and megestrol acetate." Helsinki : Finnish Society of Sciences and Letters, 1991. http://books.google.com/books?id=ee5qAAAAMAAJ.

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Wade, Christian Bernard. "Mechanisms of estrogen rapid signaling /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6272.

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Nilsson, Ola. "The role of estrogen in growth plate chondrogenesis /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-410-0/.

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Lee, Isaish Chi Kin. "Measuring the binding kinetics of estrogen receptor alpha and dietary estrogens." HKBU Institutional Repository, 2014. https://repository.hkbu.edu.hk/etd_oa/28.

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Anti-estrogen drugs such as Tamoxifen and Raloxifene are widely prescribed for breast cancer patients. While they are effective, they also have serious side effects. Alternative drugs are therefore being developed. In the drug discovery process, the in vitro binding of estrogen receptors and lead compounds were studied. The binding strength was conventionally quantified in terms of equilibrium dissociation constants (K0 ). However, the binding kinetic rates and especially off-rates (k0 ff) were recently shown to be better indicators of drug potency. In this thesis, we identified a few dietary estrogens as candidate lead compounds. We studied the binding of full-length human recombinant ERa with these dietary estrogens. In particular, we measured for the first time their binding kinetics rate constants. We also measured the change in the receptor-ligand binding kinetics upon its recruitment of co-activators, as a means to gauge agonist/antagonist propensity ofthe ligand. Our results showed that the following dietary estrogens, a-Zearalenol, Zearalenone, and Coumestrol bind favorably to the estrogen receptor alpha.
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Zhang, Qiu-Xia. "Estrogen receptor gene alterations in human breast cancer." Lund : Jubileumsinstitutionen, Dept. of Oncology,Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39738537.html.

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Scherr, Frank. "Sorption, degradation and transport of estrogens and estrogen sulphates in agricultural soils." Diss., Lincoln University, 2009. http://hdl.handle.net/10182/1017.

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The fate and behaviour of estrogens in the environment are of concern due to the compounds’ endocrine disruption potential. Estrogens, namely 17β-estradiol (E2), estrone (E1), and estrogen sulphates, i.e. 17β-estradiol-3-sulphate (E2-3S) and estrone-3-sulphate (E1-3S) excreted by livestock constitute a potential source for estrogen contamination in the environment. A method was developed to separate and quantify the hormones by high-performance-liquid-chromatography (HPLC) and ultraviolet detection (UV). A combination of dichloromethane (DCM) and dicyclohexylamine hydrochloride (DCH·HCl) gave recoveries from 97.3 to 107% for E1-3S extraction from aqueous solutions. The recoveries from soil samples ranged from 80.9 to 95.2% (E2-3S), and from 86.3 to 91.7% (E1-3S), respectively. Results of batch sorption studies showed that Freundlich isotherms were nonlinear (N ≠ 1) with Kf values ranging from 34.2 to 57.2, and from 3.42 to 4.18 mg¹-N LN kg⁻¹ for E1, and E1-3S, respectively, indicating the sorption affinity of E1-3S was about an order of magnitude lower than that of E1. The hydrophilic sulphate group of E1-3S possibly shielded the compound from hydrophobic interactions with the soil organic matter and allophanic clay minerals that were proposed as sorbents for E1. Contraction of clay minerals, “salting out” and competitive sorption of artificial urine constituents were likely to have been responsible for observed changes in Freundlich parameters when artificial urine was used as mediator matrix. Plotting the effective distribution coefficient as a function of hypothetical exposure concentrations facilitated the comparison of the sorption behaviour of both compounds as influenced by the mediator solution. The results emphasized that using the CaCl₂ matrix might result in false inferences for the sorption behaviour of these compounds in a dairying environment. The four hormones rapidly degraded in the agricultural soils under aerobic conditions, and the majority of the compounds degraded > 50% within the first 24 hrs. Soil arylsulphatase activities were directly correlated with degradation rate constants of the estrogen sulphates. Estrone was identified as a metabolite of E2 and E1-3S, and these three compounds were observed as metabolites of E2-3S. Single-first order (SFO) and double first-order in parallel (DFOP) kinetics were used to model the degradation and metabolite formation data. The results showed that the DFOP model was in most cases better able to predict the parent compound degradation than the SFO model, and also enabled to estimate accurate degradation endpoints. ER-CALUX® analysis revealed the formation of estrogenicity during E2-3S degradation, which could partly be explained by the formation of the metabolites E2 and E1. Transport studies with E1-3S and E1 showed that the transport and retention of both compounds were significantly influenced by the mediator matrix. While no breakthrough curves (BTCs) were recorded during hormone application in CaCl₂ (10 mM) both hormones were detected in the leachate when applied in artificial urine. Rate-limited sorption processes were proposed for the delayed arrival of the hormone BTCs compared with a conservative bromide tracer. Intense colouration of the leachate during the artificial urine experiments suggested the hormones were likely to be moved by colloid-facilitated transport. Furthermore, the detection of residue hormone and metabolite concentrations implied that degradation of E1-3S and E1 was hampered by urine constituents such as glycine and urea.
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Graham, Lisa Anne. "Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor." Thesis, University of Canterbury. Chemistry, 2012. http://hdl.handle.net/10092/7173.

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Environmental xenoestrogens (EEs) are chemicals that when they enter the body, the body responds to them as it would to endogenous estrogens. Humans are exposed to these chemicals on a daily basis via natural components, additives and contaminants in food and water, through the use of pharmaceuticals and personal care products such as sunscreens, lotions and toothpaste. Exposure to EEs is thought to result in adverse effects on humans such as decreased fertility, increased susceptibility to hormone-sensitive cancers, deformities of the male genitalia and precocious puberty in females. The critical window of exposure is thought to be early fetal development, when tissues are rapidly differentiating under the control of endogenous estrogens. However, there is limited data in the literature on human fetal exposure to EEs. The first objective of this study was to assess human fetal exposure to a suite of 35 EEs by analysis of paired samples of amniotic fluid and maternal urine were collected from 32 New Zealand women between 14 and 20 weeks gestation. The analytical chemistry methods required for this study were developed and validated. The results demonstrate that fetal exposure is highly correlated with maternal exposure. This study is the first to report maternal urine levels of two UV filters and amniotic fluid levels of parabens, UV filters and triclosan. A model based on simple additivity of effect was developed that combined the measured concentrations with literature data on relative estrogenic potency to assess the magnitude of the estrogen signal that may be attributed to the EEs. This model suggests that the fetus may experience an estrogen signal due to the measured EEs that could be as large as the endogenous estrogen signal. A second objective was to use computational docking to study the interactions of the EEs with the human estrogen receptor (hER) protein. The docking studies show that the rigid endogenous ligand, 17β-estradiol (E2) interacts with the hER to produce a single, well-defined complex with the receptor and the flexible EEs produce multiple, distinct energy-equivalent complexes. EEs are not able to interact with the binding cavity to stabilise the rigid hER-E2-like topology of the complex. As a result, the hER-EE complexes can be thought of as more pliable or ‘floppy’ and thus able to respond to the cell context in multiple ways, leading to variations in gene expression in different target tissues. These multiple pathways may explain the range of physiological responses attributed to exposure that depend on the timing of exposure and the sex of the individual exposed.
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Lambert, K. Chad. "The effects of estrogen signaling in innate and adaptive immune cells /." Free to MU Campus, others may purchase, 2005. http://wwwlib.umi.com/cr/mo/fullcit?p3189934.

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Ansell, Peter James. "Regulation of the antioxidant response element by estrogens : a potential mechanism to help explain estrogen-induced cancer? /." free to MU campus, to others for purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3137674.

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Linford, Nancy J. "Effects of estrogenic compounds on neuronal apoptotic pathways /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/6289.

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Books on the topic "Estrogen"

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Rattner, Heilman Joan, ed. Estrogen. New York: HarperPerennial, 1991.

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Nachtigall, Lila. Estrogen. 2nd ed. New York: HarperPerennial, 1995.

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Nachtigall, Lila. Estrogen. 3rd ed. New York, NY: Harper Resource, 2000.

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Eyster, Kathleen M., ed. Estrogen Receptors. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1920-9.

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Eyster, Kathleen M., ed. Estrogen Receptors. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3127-9.

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D, Lindsay Robert Ph, Dempster David W, and Jordan V. Craig, eds. Estrogens and antiestrogens: Basic and clinical aspects. Philadelphia: Lippincott-Raven, 1997.

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Angerer, Erwin von. The estrogen receptor as a target for rational drug design. New York: Springer, 1995.

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Angerer, Erwin von. The estrogen receptor as a target for rational drug design. New York: Springer, 1995.

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Estrogen versus cancer. New York: Nova Science Publishers, 2009.

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The estrogen decision: A self-help program. Los Altos, Calif: Westchester Pub. Co., 1994.

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Book chapters on the topic "Estrogen"

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Lindsay, Robert. "Estrogens and Estrogen Agonists/Antagonists." In Osteoporosis, 351–58. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-459-9_15.

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Oladipo, A., and J. C. Stevenson. "Estrogen." In Management of Fractures in Severely Osteoporotic Bone, 411–21. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-3825-9_29.

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Cutolo, Maurizio. "Estrogen." In Encyclopedia of Behavioral Medicine, 790–91. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_249.

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LaCaille, Lara, Anna Maria Patino-Fernandez, Jane Monaco, Ding Ding, C. Renn Upchurch Sweeney, Colin D. Butler, Colin L. Soskolne, et al. "Estrogen." In Encyclopedia of Behavioral Medicine, 710–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_249.

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Cooley, Laura A., Daniel G. Bausch, Marija Stojkovic, Waldemar Hosch, Thomas Junghanss, Marija Stojkovic, Waldemar Hosch, et al. "Estrogen." In Encyclopedia of Intensive Care Medicine, 903. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1566.

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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "Estrogen." In Encyclopedia of Exercise Medicine in Health and Disease, 307. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2366.

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Leeth, Chris. "Estrogen." In Encyclopedia of Child Behavior and Development, 605. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_1032.

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Metzler, Marnie. "Estrogen." In Encyclopedia of Animal Cognition and Behavior, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_481-1.

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Metzler, Marnie. "Estrogen." In Encyclopedia of Animal Cognition and Behavior, 2433–36. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_481.

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Watts, Nelson B. "Estrogens, Estrogen Agonists/Antagonists, and Calcitonin." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 408–11. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch48.

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Conference papers on the topic "Estrogen"

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Islam, Nazmul. "Real-Time Detection of Estrogen by Microcantilever Sensor in Microfluidic Channel." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-68903.

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As the world becomes increasingly concerned with endocrine disruptor from estrogenic activity, and since the threat of estrogen can be substantially mitigated if detected early, the demand for real-time/on-site detection of estrogen is expanding quickly. However, current technology is expensive, technically complicated and not available for estrogen level determination at the contamination sites. The primary objective of this research is to develop and validate a robust, rapid lab-on-chip for detecting estrogen in environmental water samples. Anti-estrogen antibodies can be layered to the microcantilever (MC) surface through passive adsorption using a dilute solution of antibody. The estrogen in the water will bind/react with antibody, which will result in a strain in the cantilever. The strain of the cantilever can ultimately be measured as a resistance change in the microsystem. MC will be integrated with AC electokinetic to produce a lab-on-a-chip that can concentrate measure and differentiate viable estrogen.
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Ragaz, J., K. Wilson, G. Muraca, J. Budlovsky, and J. Froehlich. "Abstract P6-09-09: Dual Estrogen Effects on Breast Cancer: Endogenous Estrogen Stimulates, Exogenous Estrogen Protects. Further Investigation of Estrogen Chemoprevention Is Warranted." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p6-09-09.

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Prokić, Danijela, Marija Vukčević, Marina Maletić, Ana Kalijadis, Biljana Babić, Ivona Janković-Častvan, and Tatjana Đurkić. "Extraction of Estrogen Hormones from Water Using Carbon Cryogel as Sorbent." In 34th International Congress on Process Industry. SMEITS, 2021. http://dx.doi.org/10.24094/ptk.021.34.1.123.

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In this study, carbon cryogel was used as solid-phase extraction sorbent for the extraction of estrogenic hormones (estrone, 17β-estradiol, and 17α-ethinylestradiol) from water solution. The solid-phase extraction (SPE) method was optimized by choosing an appropriate mass of the sorbent, volume, and initial pH of estrogenic hormone water solution, as well as by choosing an appropriate organic solvent. The concentration of tested hormones after extraction was measured by liquid chromatography coupled with tandem mass spectrometry. Based on the obtained hormone recoveries, the following optimal conditions of the SPE procedure were chosen: 100 cm3 of hormone water solution at initial pH adjusted to 7, 20 mg of the sorbent, the methanol-dichloromethane mixture was used for hormone elution. Recoveries obtained under the optimal conditions ranged from 77 % for estrone, to 86 % for 17β-estradiol, with relative standard deviation from 7,4 to 18 %.
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Haddon, Lacey, Xiuying Hu, Hosna Jabbari, and Judith Hugh. "Abstract P6-05-05: The estrogen switch: Estrogen receptor alpha levels determine the proliferative response to estrogen." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p6-05-05.

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Zhao, Hong, John S. Coon, Robert T. Chatterton, Dolores Huberts, David Christopher Brooks, Francesco J. DeMayo, and Serdar E. Bulun. "Abstract 90: Estrogen accelerates the development of estrogen receptor-negative breast cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-90.

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Konings, Gonda, Niki Reynaert, Andrea Romano, Ken Bracke, Guy Brusselle, Emiel Wouters, and Juanita Vernooy. "Expression of estrogen receptors and estrogen metabolism genes in lungs of COPD patients." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3921.

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Sambucetti, L., C. Green, L. Rausch, W. Chao, S. Le Valley, N. Zaveri, and J. Mirsalis. "SR16157 Is a Potent Dual-Acting Inhibitor of Estrogen Biosynthesis and Estrogen Receptor." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5124.

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Fan, Ping, Fadeke A. Agboke, Amit Kumar Tyagi, and V. Craig Jordan. "Abstract 2863: Mechanisms underlying estrogen-induced inflammation in estrogen-deprived breast cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2863.

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Falk, Roni T., Gretchen L. Gierach, Xia Xu, Joanne F. Dorgan, Timothy D. Veenstra, and Louise A. Brinton. "Abstract A90: Relationship of serum estrogens and estrogen metabolites with postmenopausal breast cancer risk." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a90.

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Thornton, Gail M., Soraya J. Bailey, Xinxin Shao, Douglas Morck, David A. Hart, and Yamini Achari. "Influence of Early Ovariohysterectomy on the Mechanical Properties of Rabbit Medial Collateral Ligament." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176260.

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Female athletes have significantly higher incidence of anterior cruciate ligament (ACL) injuries than males participating in similar sports [1]. To date, no clear explanation has emerged for this disparity. However, hormonal differences may provide an explanation because some ACL injuries have been linked to physiologic fluctuations in estrogen levels over the menstrual cycle [2]. Receptors for estrogen have been identified in rabbit and human ACLs and medial collateral ligaments (MCLs) [3]. Increased estrogen levels caused decreased fibroblast proliferation and collagen synthesis in cell cultures from human and rabbit ACLs [4]. Since fibroblasts maintain collagen production and degradation in ligaments and collagen is the major load-bearing component of ligaments, estrogen may affect knee ligament mechanical properties.
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Reports on the topic "Estrogen"

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DeSombre, E. R., R. C. Mease, A. Hughes, P. V. Harper, O. T. DeJesus, and A. M. Friedman. Bromine-80m-labeled estrogens: Auger-electron emitting, estrogen receptor-directed ligands with potential for therapy of estrogen receptor positive cancers. Office of Scientific and Technical Information (OSTI), January 1988. http://dx.doi.org/10.2172/6347502.

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Bhat, Abhijit S. Analogs of Estrogen Metabolites as Probes of Estrogen-Induced Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada371246.

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Smith, Carolyn L. Activation of Estrogen Receptor-Beta-Dependent Transcription by Estrogen-Independent Pathways. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada400004.

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Smith, Carolyn L. Activation of Estrogen Receptor-Beta-Dependent Transcription by Estrogen-Independent Pathways. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada413466.

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Smith, Carolyn L. Activation of Estrogen Receptor-Beta-Dependent Transcription by Estrogen-Independent Pathways. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada393484.

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Smith, Carolyn L. Activation of Estrogen Receptor-Beta-Dependent Transcription by Estrogen-Independent Pathways. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada383071.

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Verdam, Mathilde, Jae-Yung Kwon, Lara Russel, Véronique Sébille, Mirjam Sprangers, and Rick Sawatzky. The impact of response shift on patient-reported outcome measures (PROMs): A systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0024.

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Review question / Objective: Are the serum levels of estrogens (estrone, estradiol, estriol), gonadotropins (FSH, LH), or other hormones altered after intravaginal application of estriol for the treatment of genitourinary syndrome of menopause? Condition being studied: The aim of this review is to study whether the vaginal application of estriol has any effects on the serum levels of different sex hormones, mainly estriol, estradiol, and FSH, as those have been previously used as proxies for the safety of similar estrogenic products. Study designs to be included: Included: RCTs, controlled studies, head-to-head comparisons, systematic reviews, meta-analyses, quasi-experimental studies (intervention/no control).
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Kolokythas, Argyrios, Petra Stute, Cornelia Betschart Meier, Dorothea Wunder, and Heidrun Janka. Effect of intravaginal administration of estriol on the serum levels of different estrogens, gonadotropins, and other hormones in postmenopausal women: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0023.

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Review question / Objective: Are the serum levels of estrogens (estrone, estradiol, estriol), gonadotropins (FSH, LH), or other hormones altered after intravaginal application of estriol for the treatment of genitourinary syndrome of menopause? Condition being studied: The aim of this review is to study whether the vaginal application of estriol has any effects on the serum levels of different sex hormones, mainly estriol, estradiol, and FSH, as those have been previously used as proxies for the safety of similar estrogenic products. Study designs to be included: Included: RCTs, controlled studies, head-to-head comparisons, systematic reviews, meta-analyses, quasi-experimental studies (intervention/no control).
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Russo, Jose. Estrogen and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428032.

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Berglund, J. Andrew. RNA Regulation of Estrogen. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada541794.

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