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Departments of Obstetrics and Gynecology, Physiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan
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endometriosis ( Novembri et al . 2011 ). However, the regulatory mechanisms of Ucn2 expression in reproductive organs are not well understood. Estrogens regulate many physiological processes in both the reproductive system and the cardiovascular systems
EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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EMBRAPA-National Dairy Cattle Research Center, Juiz de Fora-MG, 36038-330, Brazil
Production Systems Research, US Meat Animal Research Center, Clay Center, Nebraska 68933, USA
Roslin Institute, Midlothian EH25 9PS, Scotland, UK
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can be restored by estrogen administration ( Wallace 1953 ). Studies in rodents have confirmed these observations and demonstrated that estrogens are required for growth and morphogenesis of mammary ducts. Classical endocrine ablation and hormone
Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Introduction Females have a significantly greater life expectancy than males, which in part may be due to the cardio-protective effects of the female sex hormone, estrogen, on vascular function ( Sader & Celermajer 2002 ). However
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Introduction Estrogen (17β-estradiol) is an important regulator of bone metabolism, which is illustrated by the low bone mass phenotype in a man carrying a mutation in estrogen receptor-α (ERα; Smith et al . 1994 ) and in individuals with a
Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Discipline of Pathology, University of Tasmania, Hobart, Tasmania 7000, Australia
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Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Discipline of Pathology, University of Tasmania, Hobart, Tasmania 7000, Australia
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Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Discipline of Pathology, University of Tasmania, Hobart, Tasmania 7000, Australia
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Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Discipline of Pathology, University of Tasmania, Hobart, Tasmania 7000, Australia
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Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Discipline of Pathology, University of Tasmania, Hobart, Tasmania 7000, Australia
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Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Discipline of Pathology, University of Tasmania, Hobart, Tasmania 7000, Australia
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this study, we have examined DTH responses in females that were intact, ovariectomized (OVX), or were OVX with estrogen (E2) replacement, and males to ask which local cytokines are implicated as important players in the hormonal regulation of the DTH
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Recent data indicate that the catechol estrogen, 2-hydroxyestrone (2-OHE(1)), has no effect on any target tissue including bone, whereas 16 alpha-hydroxyestrone (16 alpha-OHE(1)) exerts tissue-selective estrogen agonist activity. The effect of the catechol estrogen, 4-hydroxyestrone (4-OHE(1)), putatively associated with tumorigenesis, has not been studied in the skeleton. The purpose of this study was to assess the effect of 4-OHE(1) on tibia, uterine and mammary gland histology and blood cholesterol in ovariectomized (OVX'd) growing rats. Ten-week-old female Sprague-Dawley rats were injected subcutaneously with 200 microg/kg BW per day with 4-OHE(1), 17 beta-estradiol (E(2)) or vehicle for three weeks. OVX resulted in uterine atrophy, increased body weight, radial bone growth and cancellous bone turnover, and hypercholesterolemia. E(2) prevented these changes with the expected exception that the subcutaneous infusion of this high dose of estrogen did not prevent the hypercholesterolemia. 4-OHE(1) prevented the increase in blood cholesterol and the increase in body weight. 4-OHE(1) appeared to have partial estrogen activity in the uterus; uterine weight and epithelial cell height were significantly greater than the OVX rats but significantly less (twofold) than the E(2) animals. Analysis of variance indicated that 4-OHE(1) slightly decreased the periosteal mineral apposition rate (P<0.05) compared with vehicle-treated rats but had no effect on double-labeled perimeter or bone formation rate. Similarly, 4-OHE(1) was a partial estrogen agonist on cancellous bone turnover. The data suggest that the catechol estrogen, 4-OHE(1), unlike 2-OHE(1), has estrogen activity. Furthermore, the profile of activity differs from that of 16 alpha-OHE(1). Our results suggest that estrogen metabolites may selectively influence estrogen-target tissues and, concomitantly, modulate estrogen-associated disease risk.
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Introduction Two different genes coding for the estrogen receptor (ER) have been identified: the classical ERα ( Koike et al. 1987 ) and the more recently characterized ERβ ( Kuiper et al. 1996 ). 17-β Estradiol (E 2 ) binds ERα
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preventative and therapeutic approaches with minimal side effects. Epidemiologic studies have demonstrated a high correlation between circulating PRL and the risk of breast tumors that express estrogen receptor α (ERα also known as ESR1), which is independent
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this disease every year ( Ferlay et al. 2015 ). Approximately 70% of breast tumors are estrogen receptor α (ERα) positive, and tumor cell proliferation is thought to be dependent on the activity of this hormone-mediated transcription factor ( Hayashi
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-specific signaling may offer an alternative approach ( Petrangolini et al . 2006 ). Parafollicular C cells secrete a polypeptide hormone, calcitonin. Previously, it has been demonstrated that calcitonin gene expression is elevated in response to estrogen