Relevant bibliographies by topics / Estrogeen

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Academic literature on the topic 'Estrogeen'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Estrogeen"

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Wang, Po-Hsiang, Yi-Lung Chen, Sean Ting-Shyang Wei, et al. "Retroconversion of estrogens into androgens by bacteria via a cobalamin-mediated methylation." Proceedings of the National Academy of Sciences 117, no. 3 (2019): 1395–403. http://dx.doi.org/10.1073/pnas.1914380117.

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Steroid estrogens modulate physiology and development of vertebrates. Conversion of C19 androgens into C18 estrogens is thought to be an irreversible reaction. Here, we report a denitrifying Denitratisoma sp. strain DHT3 capable of catabolizing estrogens or androgens anaerobically. Strain DHT3 genome contains a polycistronic gene cluster, emtABCD, differentially transcribed under estrogen-fed conditions and predicted to encode a cobalamin-dependent methyltransferase system conserved among estrogen-utilizing anaerobes; an emtA-disrupted DHT3 derivative could catabolize androgens but not estrogens. These data, along with the observed androgen production in estrogen-fed strain DHT3 cultures, suggested the occurrence of a cobalamin-dependent estrogen methylation to form androgens. Consistently, the estrogen conversion into androgens in strain DHT3 cell extracts requires methylcobalamin and is inhibited by propyl iodide, a specific inhibitor of cobalamin-dependent enzymes. The identification of the cobalamin-dependent estrogen methylation thus represents an unprecedented metabolic link between cobalamin and steroid metabolism and suggests that retroconversion of estrogens into androgens occurs in the biosphere.
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Lee, Heehyoung, and Wenlong Bai. "Regulation of Estrogen Receptor Nuclear Export by Ligand-Induced and p38-Mediated Receptor Phosphorylation." Molecular and Cellular Biology 22, no. 16 (2002): 5835–45. http://dx.doi.org/10.1128/mcb.22.16.5835-5845.2002.

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ABSTRACT Estrogen receptors are phosphoproteins which can be activated by ligands, kinase activators, or phosphatase inhibitors. Our previous study showed that p38 mitogen-activated protein kinase was involved in estrogen receptor activation by estrogens and MEKK1. Here, we report estrogen receptor-dependent p38 activation by estrogens in endometrial adenocarcinoma cells and in vitro and in vivo phosphorylation of the estrogen receptor α mediated through p38. The phosphorylation site was identified as threonine-311 (Thr311), located in helix 1 of the hormone-binding domain. The mutation of threonine-311 to alanine did not affect estrogen binding of the receptor but compromised its interaction with coactivators. Suppression of p38 activity or mutation of the site inhibited the estrogen-induced receptor nuclear localization as well as its transcriptional activation by estrogens and MEKK1. The inhibition of the p38 signal pathway by a specific chemical inhibitor blocked the biological activities of estrogens in regulating endogenous gene expression as well as endometrial cancer cell growth. Our studies demonstrate the role of estrogen receptor phosphorylation induced by the natural ligand in estrogen receptor's cellular distribution and its significant contribution to the growth-stimulating activity of estrogens in endometrial cancer cells.
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Kumar, Anita, Antara Banerjee, Dipty Singh, et al. "Estradiol: A Steroid with Multiple Facets." Hormone and Metabolic Research 50, no. 05 (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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Nwankudu, O. N. "Endocrine, Reproductive, Neurophysiologic and Extraneous Activities of Estrogen in Vertebrates." Nigerian Veterinary Journal 41, no. 2 (2021): 85–107. http://dx.doi.org/10.4314/nvj.v41i2.2.

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Estrogens are reproductive hormones synthesized in the gonads of both male and female vertebrates. This review is geared towards uncovering some endocrine, reproductive, neurophysiologic and extraneous activities of estrogen in vertebrates. The three most common naturally occurring estrogens are: Estrone (E1), estradiol (E2), and estriol (E3). In primates, estradiol is the most potent and predominant estrogen during reproductive years. Estrogens are synthesized primarily in the female ovaries and in small quantities in the male testes and the adrenal glands, brain, and fat of both sexes. Estrogens are steroid hormones. The adipose tissues are considered to be the major source of circulating estrogen after the gonads in both men and women. In essence, the presence of aromatase expression in a local tissue confirms extra-gonadal estrogen synthesis. In reproduction, estrogen promote secondary sexual characteristics in females and regulates maturation of sperm (spermiogenesis) in males. Neurophysiologically, estrogen promote glutamate activity in the central nervous system, facilitates dopaminergic neurotransmission but blocks gammaaminobutyric acid. Extraneously, estrogen decrease serum cholesterol and osteoporosis especially in menopausal females. However, acute estrogen droppostpartum leads to depressed mood experienced by most post parturient females. In this review, it is observed that, while serum estrogen decreases with age in females, in male it increases with age due to the extraneous synthesis of estrogen especially in the adipose tissue.
 Keywords: Estrogen, Female, Aromatase, Male, adipose tissue
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Birzniece, Vita, and Ken K. Y. Ho. "MECHANISMS IN ENDOCRINOLOGY: Paracrine and endocrine control of the growth hormone axis by estrogen." European Journal of Endocrinology 184, no. 6 (2021): R269—R278. http://dx.doi.org/10.1530/eje-21-0155.

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There is a strong biological link between the growth hormone (GH) and gonadal systems in growth, development and metabolism; however, regulatory interactions are poorly understood. Advances in estrogen biology and endocrine physiology have provided insights into mechanistic links between the two systems. Estrogens are synthesized from androgens by aromatase which is widely distributed in extragonadal tissues. Local generation of estrogens raise the possibility of paracrine control as an additional level to classical endocrine regulation of the GH system. To explore the mechanistic links, we review the pharmacology of estrogen, the effects of estrogen replacement, antagonism, and the impact of aromatase inhibition on the GH system as well as the metabolic sequelae. In men, estrogens derived from androgens drive the central secretion of GH, independent of the androgen receptor. In hypogonadal women, physiological replacement via a parenteral route evokes no effect while estrogen receptor antagonism and estrogen deprivation induce disparate effects, providing no consistent evidence that estrogens regulate the central secretion of GH via paracrine or endocrine mechanisms. However, delivery of estrogen by the oral route inhibits hepatic IGF-1 production, in turn increasing GH secretion via reduced feedback inhibition. This endocrine route-dependent effect of oral estrogen compounds on hepatic function induces detrimental metabolic effects on hypogonadal women. In conclusion, estrogens regulate the secretion and action of GH via complex paracrine and endocrine interactions and impart metabolic effects in a route- and gender-dependent manner. The metabolic sequelae of compounds mimicking, antagonizing, or depleting estrogens, should be considered in tailoring and optimizing their use.
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Henriksson, Peter, and Reinhard Stege. "Cost Comparison of Parenteral Estrogen and Conventional Hormonal Treatment in Patients With Prostatic Cancer." International Journal of Technology Assessment in Health Care 7, no. 2 (1991): 220–26. http://dx.doi.org/10.1017/s0266462300005110.

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AbstractThe present study compares the cost of antitumor therapy and adverse cardiovascular effects during the first year of treatment with oral estrogens, nonoral estrogens, or surgical castration in patients with prostatic cancer. We found a much higher cost for patients treated with orchidectomy and oral estrogens than for patients treated with nonoral estrogens. Twenty-five percent of the patients treated with oral estrogen suffered cardiovascular complications, compared to none of the patients treated by orchidectomy or nonoral estrogens. The initial cost of orchidectomy as compared to nonoral estrogen treatment was shown not to be balanced within the expected survival time of patients with advanced prostatic cancer. Furthermore, surgical castration causes psychological trauma to the patient. We recommend parenteral estrogen therapy as a low-cost therapeutic regimen in patients with prostatic cancer.
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Imai, Yuuki, Shino Kondoh, Alexander Kouzmenko та Shigeaki Kato. "Minireview: Osteoprotective Action of Estrogens Is Mediated by Osteoclastic Estrogen Receptor-α". Molecular Endocrinology 24, № 5 (2010): 877–85. http://dx.doi.org/10.1210/me.2009-0238.

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Abstract The osteoprotective action of estrogen in women has drawn considerable attention because estrogen deficiency-induced osteoporosis became one of the most widely spread diseases in developed countries. In men, the significance of estrogen action for bone health maintenance is also apparent from the osteoporotic phenotype seen in male patients with genetically impaired estrogen signaling. Severe bone loss and high bone turnover, including typical osteofeatures seen in postmenopausal women, can also be recapitulated in rodents after ovariectomy. However, the expected osteoporotic phenotype is not observed in female mice deficient in estrogen receptor (ER)-α or -β or both, even though the degenerative defects are clearly seen in other estrogen target tissues together with up-regulated levels of circulating testosterone. It has also been reported that estrogens may attenuate bone remodeling by cell autonomous suppressive effects on osteoblastogenesis and osteoclastogenesis. Hence, the effects of estrogens in bone appear to be complex, and the molecular role of bone estrogen receptors in osteoprotective estrogen action remains unclear. Instead, it has been proposed that estrogens indirectly control bone remodeling. For example, the enhanced production of cytokines under estrogen deficiency induces bone resorption through stimulation of osteoclastogenesis. However, the osteoporotic phenotype without systemic defects has been recapitulated in female (but not in male) mice by osteoclast-specific ablation of the ERα, proving that bone cells represent direct targets for estrogen action. An aberrant accumulation of mature osteoclasts in these female mutants indicates that in females, the inhibitory action of estrogens on bone resorption is mediated by the osteoclastic ERα through the shortened lifespan of osteoclasts.
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Kassi, E., and P. Moutsatsou. "Estrogen Receptor Signaling and Its Relationship to Cytokines in Systemic Lupus Erythematosus." Journal of Biomedicine and Biotechnology 2010 (2010): 1–14. http://dx.doi.org/10.1155/2010/317452.

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Dysregulation of cytokines is among the main abnormalities in Systemic Lupus Erythematosus (SLE). However, although, estrogens, which are known to be involved in lupus disease, influence cytokine production, the underlying molecular mechanisms remain poorly defined. Recent evidence demonstrates the presence of estrogen receptor in various cell types of the immune system, while divergent effects of estrogens on the cytokine regulation are thought to be implicated. In this paper, we provide an overview of the current knowledge as to how estrogen-induced modulation of cytokine production in SLE is mediated by the estrogen receptor while simultaneously clarifying various aspects of estrogen receptor signaling in this disease. The estrogen receptor subtypes, their structure, and the mode of action of estrogens by gene activation and via extranuclear effects are briefly presented. Results regarding the possible correlation between estrogen receptor gene polymorphisms and quantitative changes in the receptor protein to SLE pathology and cytokine production are reviewed.
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Lizcano, Fernando, and Guillermo Guzmán. "Estrogen Deficiency and the Origin of Obesity during Menopause." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/757461.

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Sex hormones strongly influence body fat distribution and adipocyte differentiation. Estrogens and testosterone differentially affect adipocyte physiology, but the importance of estrogens in the development of metabolic diseases during menopause is disputed. Estrogens and estrogen receptors regulate various aspects of glucose and lipid metabolism. Disturbances of this metabolic signal lead to the development of metabolic syndrome and a higher cardiovascular risk in women. The absence of estrogens is a clue factor in the onset of cardiovascular disease during the menopausal period, which is characterized by lipid profile variations and predominant abdominal fat accumulation. However, influence of the absence of these hormones and its relationship to higher obesity in women during menopause are not clear. This systematic review discusses of the role of estrogens and estrogen receptors in adipocyte differentiation, and its control by the central nervous systemn and the possible role of estrogen-like compounds and endocrine disruptors chemicals are discussed. Finally, the interaction between the decrease in estrogen secretion and the prevalence of obesity in menopausal women is examined. We will consider if the absence of estrogens have a significant effect of obesity in menopausal women.
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Liu, Jia Wei, Elisabeth Jeannin, and Didier Picard. "The Anti-Estrogen Hydroxytamoxifen Is a Potent Antagonist in a Novel Yeast System." Biological Chemistry 380, no. 11 (1999): 1341–45. http://dx.doi.org/10.1515/bc.1999.172.

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AbstractThe budding yeastSaccharomyces cerevisiaehas been used extensively as a biological ‘test tube’ to study the regulation of the human estrogen receptor (ER) α. However, anti-estrogens, which are of great importance as therapeutic agents and research tools, fail to antagonize the activation by estrogen in yeast. Here, we have surveyed the antagonistic potential of five different anti-estrogens of diverse chemical nature. While they all act as agonists for wild-type ERα we have established a novel yeast assay system for anti-estrogens, in which at least the commonly used anti-estrogen hydroxytamoxifen is a potent antagonist.
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Dissertations / Theses on the topic "Estrogeen"

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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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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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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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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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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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Van, Wyk Susan. "The effects of growth stimulants used at cattle feedlots, on reproductive health and thyroid function of Sprague-Dawley rats." Diss., University of Pretoria, 2011. http://hdl.handle.net/2263/24885.

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Reports of endocrine disrupting potential of common environmental chemicals and the effects on reproductive health are well documented in literature. It has been suggested that deteriorating male reproductive health could be due to in utero exposures to these chemicals. The effects mediated through endocrine disrupting chemicals (EDCs) are on the fetus and may therefore be trans-generational. Ultimately, these chemicals land up in aquatic systems and affect wildlife and humans. Humans are exposed to these chemicals through multiple routes including atmosphere, water, occupational, domestic and food consumption. South Africa (SA) is an important livestock producer with about 13.8 million cattle within the feedlot industry contributing up to 80% of the total beef production. Veterinary growth stimulants (VGS) are used by beef producers to enhance growth in cattle. In SA, the following five VGS have been approved for use in beef products under the Register Act 36 of 1947, estradiol, progesterone and testosterone (natural), α'-zearalanol and trenbolone (synthetic). These VGS and their metabolites are environmentally stable compounds. The excretions from the animals are not treated and land up in the local aquatic systems, indirectly posing a health risk. In SA no research has been done on VGS associated with feedlot activities. The aim of this study was to investigate the effects of a mixture of VGS, as possible EDCs on the reproductive health and thyroid function in male rats in utero, during lactation and life-time exposure. The (anti)estrogenic and (anti)androgenic activity in water from specific feedlots was determined by using a battery of screening bio-assays. Water samples were collected over a period of a year and assessed for EDC activity in the recombinant yeast screen (YES), the T47D-KBluc (estrogenic) and the MDA-Kb2 (androgenic) bioassays. The OECD (Organization for Economic Co-operation and Development) 415 protocol, (1983) for a one-generation reproduction toxicity study, was modified to accommodate one control and three experimental groups. The experimental groups were orally gavaged with mixtures of: zilpaterol, diethylstilbestrol (DES) and α-zearalanol (Group 2; estogenic); with β'-trenbolone and methyltestosterone (MT) (Group 3; androgenic); a combination of compounds (Group 4; estrogenic and androgenic) and the Control group received cottonseed oil only. The bio-assay results indicated that water samples analysed from selected feedlots contained compounds with estrogenic activity. The shorter anogenital distance (AGD) (Group 3), decreased seminal vesicle mass (Group 4), decreased prostate mass (Group 4), increased lumen diameter (Group 3 and 4), lowered sperm concentration (Group 3), and increased T4 (Group 2 and 3) differed significantly from the control. The body weight of the males in Group 2 in the F2 generation was significantly lower than the control. The F2 females in Group 2, 3 and 4 were also significantly lower than the control. The reduced AGD, decreased seminal vesicle and increased T4 (thyroxine) might be the result of an estrogenic effect. The reduced sperm concentration might be the result of in utero and lactation exposure to these VGS. The bio-assays confirmed estrogenic activity in the feedlot water sources. The reproductive toxicology study findings confirm the hypothesis that VGS can act as EDCs and could therefore be responsible for negative reproductive effects and thyroid function. More research is needed to investigate the effects of VGS mixtures at different concentrations on male reproductive health, thyroid function and their offspring. AFRIKAANS : Goed gedokumenteerde literatuur dui aan dat chemikalieë wat algemeen in die omgewing gevind word, die potensiaal het om die manlike voortplantingstelsel aan te tas. Dit word gespekuleer dat in utero blootstelling verantwoordelik kan wees vir hierdie agteruitgang. Die fetus en daarop- volgende geslagte se gesondheid kan ook beÏnvloed word deur chemikalieë. Hierdie chemikalieë het die potensiaal om die watersisteme te bereik en gevolglik dier en menslike gesondheid te beÏnvloed. Blootstelling kan plaasvind deur verskeie roetes wat die atmosfeer, water, werksomstandighede, huishoudelike produkte en gekontamineerde voedsel insluit. Suid-Afrika (SA) is 'n belangrike produsent van vleisprodukte met omtrent 13.8 miljoen beeste wat bydra tot 80% van die vleisproduksie. Veterinêre-groei-stimulante (VGS) word gebruik om die vleisproduksie te verbeter. Vyf groei stimulante naamlik estradiol, progesteroon, testosteroon (natuurlike), α-zearalanol en trenboloon (sinteties) is goedgekeur onder die Wet 36 van 1947, vir groei produksie van beeste. Hierdie VGS en hul metaboliete is stabiel in die natuur. Die fekale en urinere uitskeidingsprodukte van die diere word nie behandel nie en eindig op in ons waterstelsels. Geen navorsing is nog in SA gedoen om die potensiële bydraes wat voerkrale tot die besoedeling van water lewer, te bestudeer nie. Die doel van die studie was om die gesamentlike effekte van mengsels VGS as moontlike endokrien-ontwrigtende chemicalieë (EOC) op die manlike voortplantingstelsel en tiroïdhormone van mannetjiesrotte na in utero-, gedurende laktasie- en na 'n leeftyd-blootstelling te bepaal. Die (anti)estrogeniese en (anti)androgeniese aktiwiteit in water vanaf spesifieke voerkrale is met behulp van 'n reeks biologiese seltoetse bepaal. Watermonsters is geanaliseer met die gisseltoets (YES)(estrogenies), die T47D-KBluc (estrogenies) en die MDA-Kb2 (androgenies). Die OECD 415 protokol (1983) vir een generasie reproduktiewe toksologie toets was aangepas om een kontrole en drie eksperimentele groepe te huisves. Die eksperimentele groepe rotte is oraal gedoseer met 'n mengsel van zilpaterol, dietielstilbestrol (DES) en α-zearalanol (Groep 2); β-trenboloon en metieltestosteroon (Groep 3); 'n kombinasie van al bogenoemde (Groep 4); en 'n kontrole groep wat katoensaad olie VGS ontvang het nie. Estrogeniese aktiwiteit en sitotoksisiteit was teenwoordig in die water vanaf die voerkrale. Die verkorte anogenitale afstand (AGD) (Groep 3), kleiner seminale vesikel (SV) massa (Groep 4), kleiner prostaat massa (Groep 4), groter lumen deursneë (Groep 3 en 4), laer spermtelling (Groep 3), verhoogde T4 (Groep 2 en 3), het almal statisties-betekenisvol van die kontrole groep verskil. In die F2 generasie het die liggaamsmassas van die mannetjies in Groep 2 en liggaamsmassas van die wyfies in Groepe 2, 3 , 4, almal statisties-betekenisvol laer as die kontrole Groep. Die verkorte AGD, kleiner SV en verhoogde T4 kan moonlik wees as gevolg van 'n estrogeniese effek en die verlaagde sperm konsentrasie weens 'n in utero en laktasie blootstelling. Die biologiese seltoetse het die teenwoordigheid van estrogeniese aktiwiteit in voerkrale se water bevestig. Die gevolge van die blootstelling van EOC mengsels op voortplantings-parameters bevestig die moontlikheid van EOC effek geassosieer met VGS. Verdere navorsing is nodig om die dosisresponsverhoudings van verskillende VGS te ondersoek. Copyright<br>Dissertation (MSc)--University of Pretoria, 2011.<br>School of Health Systems and Public Health (SHSPH)<br>Unrestricted
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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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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 "Estrogeen"

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

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

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

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Rattner, Heilman Joan, ed. Estrogen. HarperPerennial, 1991.

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Nachtigall, Lila. Estrogen. 3rd ed. Harper Resource, 2000.

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Nachtigall, Lila. Estrogen. 2nd ed. HarperPerennial, 1995.

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

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

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International Congress on the Menopause (8th 1996 Sydney, N.S.W.). Progress in the management of the menopause: The proceedings of the 8th International Congress on the Menopause, Sydney, Australia, November 1996. Parthenon Pub. Group, 1997.

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Estrogen versus cancer. Nova Science Publishers, 2009.

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Book chapters on the topic "Estrogeen"

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

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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. John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch48.

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Bidlingmaier, M. "Estrogene." In Springer Reference Medizin. Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1051.

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Bidlingmaier, M. "Estrogene." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1051-1.

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Leeth, Chris. "Estrogen." In Encyclopedia of Child Behavior and Development. 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. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_481-1.

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Cooley, Laura A., Daniel G. Bausch, Marija Stojkovic, et al. "Estrogen." In Encyclopedia of Intensive Care Medicine. 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, et al. "Estrogen." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2366.

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LaCaille, Lara, Anna Maria Patino-Fernandez, Jane Monaco, et al. "Estrogen." In Encyclopedia of Behavioral Medicine. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_249.

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

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Conference papers on the topic "Estrogeen"

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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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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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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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Gu, Fangyi, Neil E. Caporaso, A. Heather Eliassen, Xia Xu, Susan E. Hankinson, and Regina G. Ziegler. "Abstract 3738: Associations between cigarette smoking and urinary estrogens/estrogen metabolites (EM) in premenopausal women." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3738.

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Liu, Aiping, and Naomi Chesler. "Effects of Estrogen on Pulmonary Vascular Remodeling in Pulmonary Artery Hypertension." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14736.

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Pulmonary artery hypertension (PAH) is a female dominant, fatal disease characterized by progressive increase of pulmonary vascular resistance and loss of compliance. The role of estrogen in these pulmonary vascular changes with PAH progression remains unclear. Our objective was to study the effects of estrogen on pulmonary arterial (PA) remodeling in a mouse model of progressive PAH, created via a combination of a VEGF inhibitor Sugen and chronic hypoxia (SuHx). To quantify PA hemodynamics, we measured in vivo pressure and flow simultaneously in live mice in order to obtain pulmonary vascular impedance, a comprehensive measure of RV afterload. Our results demonstrate that estrogen modifies the relationship between PA resistance and compliance by attenuating PA stiffening, which provides insight into sex differences in PAH progression.
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Cowden, Courtney, Naveen Chandrashekar, Javad Hashemi, Vaughan H. Lee, Daniel M. Hardy, and James R. Slauterbeck. "Effect of Estrogen on the Mechanical Properties of Prepubertal Rabbit ACL." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59986.

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Recent research suggests that estradiol affects the material properties of the Anterior Cruciate Ligament (ACL). Here we experimentally determine the cross-sectional area and tensile properties of ACLs from the groups of prepubertal rabbits: untreated control (C), estrogen treated (E) and estrogen and epidermal growth factor treated (E+EGF). Estradiol decreased the ultimate tensile strength and toughness of the ACL. Addition of EGF decreased the modulus of elasticity.
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Ciani, Cesare, Paula A. Ramirez Marin, Stephen B. Doty, and Susannah P. Fritton. "Estrogen Depletion Increases Osteocyte Canalicular Diameter in Cortical and Cancellous Bone of the Rat Proximal Tibia." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205382.

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Estrogen depletion has been shown to cause bone loss in the proximal metaphysis of the rat tibia [1,2]. A decrease in bone volume fraction is frequently reported, yet there is little analysis in the literature related to changes in microporosities during osteoporosis. Our recent work quantifying microporosity changes due to estrogen depletion has shown an increase in the lacunar-canalicular porosity surrounding osteocytes in the proximal metaphysis of the rat tibia [3].
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Dallal, Cher M., Louise A. Brinton, Charles E. Matthews, et al. "Abstract 2519: Is accelerometer-measured physical activity associated with urinary estrogens and estrogen metabolites among postmenopausal women?." 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.am2013-2519.

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Ferreri, Suzanne, and Yi-Xian Qin. "Alteration of Bone’s Nonlinear Elastic and Viscoelastic Nanomechanical Properties Is Triggered by Low Intensity Pulsed Ultrasound." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206711.

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Dynamic mechanotransduction, particularly under high frequency, low amplitude signals, has been proven effective in mediating bone loss and improving mechanical strength for tissues affected by estrogen deficient osteopenia. Ultrasound, which behaves as an alternating pressure wave in bone, may offer an effective, non-invasive technology for delivery of anabolic signals. In vitro, dynamic mechanical signals delivered using ultrasound have been shown to increase osteoblast proliferation [1], and in vivo studies have established ultrasound as an effective treatment for delayed and non-union fractures [2]. Previously, we showed that ultrasound signals similar to those currently used in a clinical setting for fracture healing were effective in mediating decreases in bone volume and mechanical strength at the millimeter length-scale in response to estrogen deficient osteopenia [3]. Due to bone’s inherent viscoelasticity and the dynamic nature of the applied ultrasound signals, it is particularly important to consider both elastic and viscous components of bone’s adaptive response to applied loads. In light of these findings, the goal of this study was to determine the role of therapeutic ultrasound signal intensity in modulating changes in bone’s nanoscale elastic and viscoelastic material properties associated with estrogen deficient osteopenia. We hypothesize that bone is sensitive to dynamic mechanical signals delivered via ultrasound and that bone’s tissue level nano-scale material properties, particularly nonlinear viscoelastic properties, are sensitive to ultrasound signal intensity.
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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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Reports on the topic "Estrogeen"

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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), 1988. http://dx.doi.org/10.2172/6347502.

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Wuttke, Deborah S. Breast Cancer Therapeutics, Environmental Estrogens, and the Estrogen Receptor (ER); Characterization of the Diverse Ligand Binding Properties of the ER. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada408777.

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Wuttke, Deborah S. Breast Cancer Therapeutics, Environmental Estrogens, and the Estrogen Receptor (ER); Characterization of the Diverse Ligand Binding Properties of the ER. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada420485.

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Bhat, Abhijit S. Analogs of Estrogen Metabolites as Probes of Estrogen-Induced Tumorigenesis. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada383071.

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

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

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Russo, Jose. Estrogen and Breast Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada428032.

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