Relevant bibliographies by topics / Hormones, Sex – Receptors

Academic literature on the topic 'Hormones, Sex – Receptors'

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Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Hormones, Sex – Receptors"

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Honma, Naoko, Yoko Matsuda, and Tetuo Mikami. "Carcinogenesis of Triple-Negative Breast Cancer and Sex Steroid Hormones." Cancers 13, no. 11 (May 25, 2021): 2588. http://dx.doi.org/10.3390/cancers13112588.

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Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor (ER), ER-α. Several sex steroid receptors other than ER-α: androgen receptor (AR), second ER, ER-β, and non-nuclear receptors represented by G-protein-coupled estrogen receptor (GPER), are frequently expressed in TNBC and their biological and clinical importance has been suggested by a large number of studies. Despite the structural similarity between each sex steroid hormone (androgens and estrogens) or each receptor (AR and ER-β), and similarity in the signaling mechanisms of these hormones, most studies or reviews focused on one of these receptors, and rarely reviewed them in a comprehensive way. Considering the coexistence of these hormones and their receptors in TNBC in a clinical setting, a comprehensive viewpoint would be important to correctly understand the association between the carcinogenic mechanism or pathobiology of TNBC and sex steroid hormones. In this review, the carcinogenic or pathobiological role of sex steroid hormones in TNBC is considered, focusing on the common and divergent features of the action of these hormones.
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Zarazúa, Abraham, Aliesha González-Arenas, Gabriela Ramírez-Vélez, Blanca Bazán-Perkins, Christian Guerra-Araiza, and María G. Campos-Lara. "Sexual Dimorphism in the Regulation of Estrogen, Progesterone, and Androgen Receptors by Sex Steroids in the Rat Airway Smooth Muscle Cells." International Journal of Endocrinology 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/8423192.

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The role of sex hormones in lung is known. The three main sex steroid receptors, estrogen, progesterone, and androgen, have not been sufficiently studied in airway smooth muscle cells (ASMC), and the sex hormone regulation on these receptors is unknown. We examined the presence and regulation of sex hormone receptors in female and male rat ASMC by Western blotting and flow cytometry. Gonadectomized rats were treated with 17β-estradiol, progesterone, 17β-estradiol + progesterone, or testosterone. ASMC were enzymatically isolated from tracheas and bronchi. The experiments were performed with double staining flow cytometry (anti-α-actin smooth muscle and antibodies to each hormone receptor). ERα, ERβ, tPR, and AR were detected in females or males. ERαwas upregulated by E2 and T and downregulated by P4 in females; in males, ERαwas downregulated by P4, E + P, and T. ERβwas downregulated by each treatment in females, and only by E + P and T in males. tPR was downregulated by P4, E + P, and T in females. No hormonal regulation was observed in male receptors. AR was downregulated in males treated with E + P and T. We have shown the occurrence of sex hormone receptors in ASMC and their regulation by the sex hormones in female and male rats.
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Baber, Rod. "Sex hormones, receptors and modulators." Australian and New Zealand Journal of Obstetrics and Gynaecology 57, no. 4 (August 2017): 391–92. http://dx.doi.org/10.1111/ajo.12666.

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Orshal, Julia M., and Raouf A. Khalil. "Gender, sex hormones, and vascular tone." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 2 (February 2004): R233—R249. http://dx.doi.org/10.1152/ajpregu.00338.2003.

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The greater incidence of hypertension and coronary artery disease in men and postmenopausal women compared with premenopausal women has been related, in part, to gender differences in vascular tone and possible vascular protective effects of the female sex hormones estrogen and progesterone. However, vascular effects of the male sex hormone testosterone have also been suggested. Estrogen, progesterone, and testosterone receptors have been identified in blood vessels of human and other mammals and have been localized in the plasmalemma, cytosol, and nuclear compartments of various vascular cells, including the endothelium and the smooth muscle. The interaction of sex hormones with cytosolic/nuclear receptors triggers long-term genomic effects that could stimulate endothelial cell growth while inhibiting smooth muscle proliferation. Activation of plasmalemmal sex hormone receptors may trigger acute nongenomic responses that could stimulate endothelium-dependent mechanisms of vascular relaxation such as the nitric oxide-cGMP, prostacyclin-cAMP, and hyperpolarization pathways. Additional endothelium-independent effects of sex hormones may involve inhibition of the signaling mechanisms of vascular smooth muscle contraction such as intracellular Ca2+ concentration and protein kinase C. The sex hormone-induced stimulation of the endothelium-dependent mechanisms of vascular relaxation and inhibition of the mechanisms of vascular smooth muscle contraction may contribute to the gender differences in vascular tone and may represent potential beneficial vascular effects of hormone replacement therapy during natural and surgically induced deficiencies of gonadal hormones.
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Fannon, Stacey A., Regina M. Vidaver, and Sherry A. Marts. "Historical Perspectives: An abridged history of sex steroid hormone receptor action." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1854–59. http://dx.doi.org/10.1152/jappl.2001.91.4.1854.

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The field of steroid hormone action is well established, although it is barely more than four decades old. Pivotal experiments in the late 1950s and 1960s showed that hormone-binding components exist within nuclei of target tissues and that steroid hormones act by regulating gene expression, rather than directly influencing enzymatic processes. The understanding that steroid hormone receptors interact with the general transcription machinery and alter chromatin structure came in the 1970s and 1980s, and details of this mechanism continue to be elucidated. In addition, the discovery of rapid cellular responses to steroid hormones has led to the identification of putative membrane-bound steroid receptors that act without affecting gene transcription. As noted in the recent Institute of Medicine report Exploring the Biological Contributions to Human Health: Does Sex Matter?, the effects of steroid hormones and defects in steroid hormone receptor action have a profound impact on human health and disease. Future research directives include the development of potent, selective steroid receptor modulators, the elucidation of nongenomic steroid hormone effects, and further exploration of hormone-genome interactions.
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Simão, Vinícius Augusto, Luiz Gustavo de Almeida Chuffa, and Isabel Cristina Cherici Camargo. "Ovarian sex steroid receptors and sex hormones in androgenized rats." Reproduction 152, no. 5 (November 2016): 545–59. http://dx.doi.org/10.1530/rep-16-0233.

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This study evaluated for the first time the effects of different doses of the anabolic steroid nandrolone decanoate (ND) on the expression of ovarian steroid receptors (AR, ER-α (ESR1) and ER-β (ESR2)) and related sex hormones after treatment and recovery periods in adult rats. The animals were injected subcutaneously with doses of ND (1.87, 3.75, 7.5 or 15 mg/kg b.w.) or mineral oil (control group) for 15 days, and the experimental groups were divided into three periods of evaluation: (a) ND treatment for 15 days, (b) ND treatment and recovery for a period of 30 days and (c) ND treatment and recovery for a period of 60 days. Estrous cycle was monitored daily. At the end of each period, rats were killed for collection of blood and ovaries. Persistent diestrus occurred in all rats during ND treatment and after 30-day recovery. The highest dose of ND was able to maintain all rats arrested at diestrus until 60-day recovery. The expression of steroid receptors varied in a dose- and period-dependent manner, having a more pronounced response with the dose of 15 mg ND/kg. ND treatment increased serum levels of testosterone, 17β-estradiol and dihydrotestosterone, especially at the highest doses of 7.5 and 15 mg ND/kg. No change was observed in the levels of follicle-stimulating hormone (FSH), whereas levels of the luteinizing hormone (LH) varied according to the dose and period. In conclusion, the ovarian sex steroid receptors and sex hormones were restored only at lower doses of ND and after a longer period of recovery.
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Bhatia, Aruna, Harmandeep Kaur Sekhon, and Gurpreet Kaur. "Sex Hormones and Immune Dimorphism." Scientific World Journal 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/159150.

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The functioning of the immune system of the body is regulated by many factors. The abnormal regulation of the immune system may result in some pathological conditions. Sex hormones of reproductive system are one of the major factors that regulate immune system due to the presence of hormone receptors on immune cells. The interaction of sex hormones and immune cells through the receptors on these cells effect the release of cytokines which determines the proliferation, differentiation, and maturation of different types of immunocytes and as a result the outcome of inflammatory or autoimmune diseases. The different regulations of sex hormones in both sexes result in immune dimorphism. In this review article the mechanism of regulation of immune system in different sexes and its impact are discussed.
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Simoncini, T., and AR Genazzani. "Non-genomic actions of sex steroid hormones." European Journal of Endocrinology 148, no. 3 (March 1, 2003): 281–92. http://dx.doi.org/10.1530/eje.0.1480281.

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Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.
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Higa, Gerald M., and Ryan G. Fell. "Sex Hormone Receptor Repertoire in Breast Cancer." International Journal of Breast Cancer 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/284036.

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Classification of breast cancer as endocrine sensitive, hormone dependent, or estrogen receptor (ER) positive refers singularly to ERα. One of the oldest recognized tumor targets, disruption of ERα-mediated signaling, is believed to be the mechanistic mode of action for all hormonal interventions used in treating this disease. Whereas ERαis widely accepted as the single most important predictive factor (for response to endocrine therapy), the presence of the receptor in tumor cells is also of prognostic value. Even though the clinical relevance of the two other sex hormone receptors, namely, ERβand the androgen receptor remains unclear, two discordant phenomena observed in hormone-dependent breast cancers could be causally related to ERβ-mediated effects and androgenic actions. Nonetheless, our understanding of regulatory molecules and resistance mechanisms remains incomplete, further compromising our ability to develop novel therapeutic strategies that could improve disease outcomes. This review focuses on the receptor-mediated actions of the sex hormones in breast cancer.
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Villablanca, Amparo C., Muthuvel Jayachandran, and Carole Banka. "Atherosclerosis and sex hormones: current concepts." Clinical Science 119, no. 12 (September 1, 2010): 493–513. http://dx.doi.org/10.1042/cs20100248.

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CVD (cardiovascular disease) is the leading cause of death for women. Considerable progress has been made in both our understanding of the complexities governing menopausal hormone therapy and our understanding of the cellular and molecular mechanisms underlying hormone and hormone receptor function. Understanding the interplay of atherosclerosis and sex steroid hormones and their cognate receptors at the level of the vessel wall has important ramifications for clinical practice. In the present review, we discuss the epidemiology of CVD in men and women, the clinical impact of sex hormones on CVD, and summarize our current understanding of the pathogenesis of atherosclerosis with a focus on gender differences in CVD, its clinical presentation and course, and pathobiology. The critical animal and human data that pertain to the role of oestrogens, androgens and progestins on the vessel wall is also reviewed, with particular attention to the actions of sex hormones on each of the three key cell types involved in atherogenesis: the endothelium, smooth muscle cells and macrophages. Where relevant, the systemic (metabolic) effects of sex hormones that influence atherogenesis, such as those involving vascular reactivity, inflammation and lipoprotein metabolism, are discussed. In addition, four key current concepts in the field are explored: (i) total hormone exposure time and coronary heart disease risk; (ii) the importance of tissue specificity of sex steroid hormones, critical timing and the stage of atherosclerosis in hormone action; (iii) biomarkers for atherosclerosis with regard to hormone therapy; and (iv) the complex role of sex steroids in inflammation. Future studies in this field will contribute to guiding clinical treatment recommendations for women and help define research priorities.
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Dissertations / Theses on the topic "Hormones, Sex – Receptors"

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ElBaradie, Khairat Bahgat. "Membrane effects of sex hormones on growth plate chondrocytes." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/45956.

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Understanding and studying the normal bone growth and development is causal. Bone and cartilage tissue provide in addition to their mechanical support, they provide a protection for vital organs such as heart, lung and brain. Longitudinal growth is regulated by the activity of chondrocytes in the epiphyseal growth plates of long bones. Many hormones and growth factors are involved in the regulation of this process. Among these, sex steroids are of crucial importance, especially during puberty. In long bones, endochondral bone formation occurs at the growth plate, a region of developing cartilage located between the epiphysis and the metaphysic. The process of endochondral ossification is regulated in part by sex steroid hormones. Androgens stimulate endochondral bone growth and elongation, while estrogen is known to suppress longitudinal bone growth and accelerate growth plate closure. Studies using rat costochondral growth plate chondrocytes as a model show that the effects of 17β-estradiol (E₂) on apoptosis are found in both male and female cells and the same mechanism is involved. In contrast, E₂ causes rapid activation of PKC in female cells but not in male cells. Dihydroxytestosterone (DHT) also has direct effects on growth plate chondrocytes, increasing matrix synthesis including sulfated glycosaminoglycan production, and enhancing cell maturation by increasing alkaline phosphatase enzymatic activity. Short stature and abnormally slow increase in height is one of the main reasons for referral to endocrinologist. Excessive growth and abnormally tall is also a problem, especially because it increase risk for the trunk abnormalities. Furthermore until now a few growth-promoting therapies are available for clinical use. Therefore future therapies for treating the growth disorders are essential. The overall goal of this project is to investigate the sexual-dimorphic effect of the sex steroid hormone in rat growth plate chondrocytes, the cellular signaling pathways mediating these actions, and their physiological role. The information gleaned from this study will provide new information about the role of sex steroid hormones in chondrogenesis and has implications in the development of new therapies for the treatment of bone fracture healing, and growth plate disorders. The central hypothesis was that sex steroid would play an important and sex-specific role in regulating chondrocytes as a main regulator of longitudinal bone growth.
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Isaksson, Friman Erika. "Hormonal treatments and the breast : effects on sex steroid receptor expression and proliferation /." Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-182-9/.

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Cluning, Carmel. "Steroid receptor-associated immunophilins : influence of targeted knockdown and altered expression on receptor signalling." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0215.

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[Truncated abstract] Steroid receptors belong to the superfamily of nuclear receptors, and include the androgen receptor (AR), estrogen receptors (ER[alpha] and ER[beta], glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and the progesterone receptors (PRA and PRB). Before binding ligand, the receptor undergoes biochemical and structural modifications through a series of interactions with molecular chaperones and cochaperones all within a receptor heterocomplex. The mature receptor complexes with the major chaperone Hsp90, the stabilising cochaperone p23, and one member of a group of cochaperones termed immunophilins. Steroid receptor-associated immunophilins include the cyclophilin, CyP40, two FK506-binding proteins, FKBP51 and FKBP52, and the protein phosphatase, PP5. Immunophilins are characterised by the presence of TPR domains which compete directly for the TPR-acceptor site within Hsp90. This leads to mutually exclusive, immunophilin-containing receptor complexes. While PP5 contains a C-terminal phosphatase domain, CyP40, FKBP51 and FKBP52 each contain an N-terminal peptidyl prolyl isomerase (PPIase) domain, which catalyses the cis/trans isomerisation of prolyl peptide bonds. FKBP52 has been demonstrated to potentiate the ligand-dependent activity of AR, GR and PR, but not ER[alpha]. Knowing that CyP40 is the preferred immunophilin associated with the ER[alpha] heterocomplex, it was hypothesised that this immunophilin plays a role in ER[alpha] function. ... As all mutants maintained this potentiating activity it was concluded that the five altered residues found within gpGR do not contribute to the altered interaction of FKBP52 and receptor. However, it cannot be discounted that FKBP51 is more competitive for gpGR. Immunophilins are hormonally regulated, with FKBP52 found to be essential for female fertility in mice. It was hypothesised that levels of immunophilins, associated with steroid receptors important in the menstrual cycle, would be regulated to reflect hormonal activity within cycling endometrium. Human pre-menopausal endometrial sections taken from different phases of the menstrual cycle were examined immunohistochemically for expression of CyP40, FKBP51, FKBP51 and PP5. Immunophilin levels peaked at the mid-secretory phase correlating with stromal decidualization, a process essential for eventual blastocyst implantation. The importance of immunophilins to steroid receptor action was therefore reinforced by the observation that immunophilins appear to be hormonally regulated in cycling pre-menopausal human endometrium. Further studies into the effects of immunophilin loss and knockdown on steroid receptor-mediated responses in specific mouse tissues, knockout-derived mouse embryo fibroblasts and cancer cell lines may contribute to our understanding of the receptor-selective and tissue-specific actions of the immunophilins. Elucidation of the mechanisms through which they modulate receptor function may provide opportunities for therapeutic intervention in steroid-related disease.
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Goold, Richard David. "Influence of endogenous female sex-steroids on mutagen metabolism." Thesis, Rhodes University, 1985. http://hdl.handle.net/10962/d1004919.

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Cytochrome P-450, the terminal oxidase of the metabolic mono-oxygenase system, is thought to exist in multiple forms, which have differing substrate specificities, and are variably inducible by different enzyme inducers. Many mutagens, themselves unreactive, require metabolic activation by one or more of these cytochrome P-450-dependent microsomal enzymes for mutagenic activity. Such mutagens may be detected in the Salmonella mutagenicity test only by the incorporation of an hepatic microsomal (59) fraction into the assay (as a first approximation to in vivo metabolism). Induction of the microsomal enzymes by different agents enhances the metabolic activation of mutagens; in fact, many mutagens are only detected when the 59 fraction has been induced by appropriate agents. Inducers of the phenobarbital-type are known to enhance microsomal steroid hydroxylation when administered at supraphysiological levels, inducers of several mono-oxygenase activities. In turn, the steroids, have been reported to be The inductive effects of the female sex-steroids and the combined effects of steroid and phenobarbital (PB) pretreatment on the metabolic activation of four mutagens have been investigated using the Salmonella assay. Female Sprague-Dawley rats were pret reated with 17a-oestradiol (E2) or progesterone (PRG) , at a level of either 1 mg/kg or 20 mg / kg daily for 14 days. A duplicate set of similarly pretreated groups were also induced with PB. Hepatic microsomal fractions were prepared from each group and incubated with each of the te st mutagens in the presence of a tester strain known to detect each particular type of mutagen. Induction of the hepatic metabolizing system by PB increased the activation of the mutagens significantly (as reflected by an increased number of revertant prototrophic S .typhimurium colonies). The administration of PRG also caused significant, and dose-dependent, induction of the activation of af l atoxin B1, benzo(a)pyrene, and dimethylnitrosamine. In general, E2 exhibited no inductive effect, but it did produce an increase in the activation of aflatoxin B1 (a reaction which is known to be catalysed by a mono-oxygenase prefe rentially inducible by PB). When use was made of a microsomal fraction that was prepared from animals which were both steroidpretreated and induced by PB, mutagenic activation was of the same order of magnitude as that observed when induction was brought about by PB alone. The absence of additive effect, taken together with the observations already mentioned, indicate that steroids induce the same cytochrome isozymes that are induced by PB. The implications of sex-hormonal regulation of the metabolic activation of mutagens are briefly discussed.
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Trout, Amanda L. "SEX DIFFERENCES IN CELL DEATH AND STEROID HORMONE RECEPTORS IN CORTICAL EXPLANTS." UKnowledge, 2013. http://uknowledge.uky.edu/physiology_etds/6.

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Estrogens, such as the biologically active 17-b estradiol (E2) have many actions in the male and female brain. Not only does E2 regulate reproductive behavior in adults, it organizes and activates the brains of younger animals in a sex-specific manner. In addition, many human studies have shown E2 to provide protection against a variety of neurological disorders, including stoke. These studies have been controversial and depend largely on the type and timing of hormone replacement. Animal studies are much less controversial and clearly demonstrate a neuroprotective role for E2 following ischemic brain injury. Because much of E2 neuroprotection requires sex steroid hormone receptors, it is essential to understand expression patterns of these receptors. For the current studies, I evaluated estrogen receptor alpha (ER α), estrogen receptor beta (ER β) and androgen receptor (AR) expression in the cortex. It is known that these receptors change in expression at several times in an animal’s life span including during early postnatal development and following ischemic brain injury. Here I used an in vitro cortical explant model to further examine how these receptors change both during development and following injury. This in vitro model is important because it provides a way to investigate changes in receptor expression pattern in the cortex without input from other brain regions. In addition to characterizing this model, I also evaluated the contribution of E2 to changes in receptor expression and on cell death following injury in the explants. To begin to decipher mechanisms for E2 mediated neuroprotection, I added antagonist for each of the receptors before and after injury. In each these experiments, I also examined potential sex differences by separating the female and male brains before I cultured the explants. Overall, these experiments showed that cortical explants are a good in vitro model. Here we found that E2 was protective in female, but not male cortical explants following injury. However, the exact mechanisms of E2-mediated neuroprotection are still to be deciphered.
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Williams, Maro R. I. 1974. "Dehydroepiandrosterone action in the cardiovascular system." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/7927.

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Tasende, Celia. "Pituitary and uterine sex steriod receptors in ewes : seasonal and postpartum anoestrus, oestrous cycle and experimentally induced subnormal luteal phases /." Uppsala : Dept. of Biomedical Sciences and Veterinary Public Health, Swedish University of Agricultural Sciences, 2005. http://epsilon.slu.se/200597.pdf.

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Meikle, Ana. "Reproductive endocrinology of prepubertal and anestrous ewes : regulation of uterine sex steroid receptors by ovarian hormones and effects of estradiol on gonadotropin secretion and follicular growth /." Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 2001. http://epsilon.slu.se/avh/2001/91-576-5915-X.pdf.

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Coulombe, Marie-andree. "Implication du sexe, des hormones gonadiques et de leurs métabolites dans la réponse nociceptive et la perception de la douleur." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ099/document.

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Plusieurs variables biologiques, psychologiques, ainsi que des différences culturelles, ont été mises en cause afin d'expliquer la différence de perception de la douleur existante entre les hommes et les femmes. Il est connu que les hormones gonadiques influencent la réponse nociceptive chez l’animal et chez l’humain. Le cerveau a aussi la capacité de synthétiser ses propres "hormones sexuelles", les neurostéroïdes. L'objectif de cette thèse était: 1) évaluer les facteurs physiologiques et psychologiques influençant de perception de la douleur chez les hommes et les femmes, 2) évaluer l'implication des androgènes et du cortisol sur les symptômes cliniques et la perception de la douleur chez des sujets atteints de fibromyalgie et sains, et 3) évaluer l'implication des hormones gonadiques et de leurs métabolites 3α5α-réduits dans la transmission et la modulation de la douleur chez animaux les mâles et les femelles par l'utilisation de modèles de douleur comportementaux
Several biological, psychological, and cultural differences can explain the difference in pain perception between men and women. It is known that gonadal hormones influence the nociceptive response in animals and humans. The brain also has the ability to synthesize its own "sex hormones", also named neurosteroids. The aims of this thesis were: 1) to assess the physiological and psychological factors influencing the difference in pain perception between men and women, 2) to relate the levels of androgens and cortisol with clinical symptoms and pain perception in healthy volunteers and patients with fibromyalgia, and 3) to evaluate the involvement of gonadal hormones and of their 3α5α-reduced metabolites in the transmission of pain and the effectiveness of descending pain modulation systems (DPMS) in males and females using behavioral pain model in rats and mice
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Pedroso, Luciana de Britto. "Avaliação da possível diferença na sensibilidade dolorosa de ratos machos e fêmeas e da resposta de cada sexo a crotalfina, um analgésico tipo opióide." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-23012012-114018/.

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Evidências clínicas e experimentais têm sugerido a existência de diferenças na sensação de dor e na resposta a fármacos analgésicos entre machos e fêmeas. A crotalfina (CRF), um peptídeo inicialmente isolado e caracterizado no veneno de serpentes Crotalus durissus terrificus, apresenta efeito antinociceptivo, quando avaliado em diferentes modelos experimentais de dor aguda e crônica. O efeito deste peptídeo é de longa duração e mediado pela ativação de receptores opióides periféricos do tipo k e d. Contudo, os estudos com a crotalfina foram sempre realizados utilizando roedores machos. Assim, o presente projeto de pesquisa teve por objetivo avaliar a diferença na sensibilidade dolorosa e no efeito antinociceptivo da crotalfina, entre ratos machos e fêmeas. Os resultados mostraram que fêmeas apresentam menor limiar nociceptivo e maior sensibilidade à dor. A crotalfina apresentou maior potência antinociceptiva em fêmeas. A diferença na sensibilidade dolorosa e na resposta a analgésicos pode ser decorrente da presença de hormônios esteroidais gonadais.
Several clinical and experimental evidence have suggested the existence of sex differences in pain sensation and in the analgesic effect of opioid drugs in human and rodents. Crotalphine (CRP), a peptide first characterized in the venom of the South American rattlesnake Crotalus durissus terrificus, displays potent and long-lasting opioid (peripheral k and d opioid receptors) analgesic activity in experimental models of acute and chronic pain. Due to its potent and long-lasting analgesic effect, pre-clinical trials with the synthetic peptide and analogues are now in progress. However, the experimental studies with CRP have always been developed in male animals. This study aims to evaluate the differences in pain sensation and in the analgesic response to CRP between male and female Wistar rats. Sex differences could be observed between male and female rats in relation to pain threshold. However, despite displaying opioid activity, the new analgesic peptide CRP is more effective in females than males. These differences could be related with sex hormones.
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Books on the topic "Hormones, Sex – Receptors"

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Gronemeyer, H., U. Fuhrmann, and K. Parczyk, eds. Molecular Basis of Sex Hormone Receptor Function. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03689-1.

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Sex steroid receptors: Handbook on receptor research. Rome: Field Educational Italia, Acta Medica, 1985.

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O'Malley, Bert. Receptors for Reproductive Hormones. Springer, 2012.

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Moudgil, Virinder K. Molecular Mechanism of Steroid Hormone Action: Recent Advances. Walter De Gruyter Inc, 1985.

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1945-, Moudgil V. K., ed. Molecular mechanism of steroid hormone action: Recent advances. Berlin: Walter de Gruyter, 1985.

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Moudgil, Virinder K. Molecular Mechanism of Steroid Hormone Action: Recent Advances. Walter de Gruyter, 1985.

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Chen, George G. Female Sex Hormones and Cancers. Nova Science Publishers, Incorporated, 2010.

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C, Spelsberg T., and Kumar Rajiv 1949-, eds. Steroid and sterol hormone action. Boston: Nijhoff, 1987.

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Cao, Zhiping. Chemical signaling in neural circuits that mediate sexual behaviors. 1994.

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H, Gronemeyer, Fuhrmann U. 1959-, and Parczyk K. 1960-, eds. Molecular basis of sex hormone receptor function: New targets for intervention. Berlin: Springer-Verlag, 1998.

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Book chapters on the topic "Hormones, Sex – Receptors"

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Migliaccio, Antimo, Gabriella Castoria, and Ferdinando Auricchio. "Non-Genomic Action of Sex Steroid Hormones." In Nuclear Receptors, 365–79. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3303-1_15.

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Callard, Ian P., and Gloria V. Callard. "Sex Steroid Receptors and Non-Receptor Binding Proteins." In Hormones and Reproduction in Fishes, Amphibians, and Reptiles, 355–84. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1869-9_12.

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Kovats, Susan, Esther Carreras, and Hemant Agrawal. "Sex Steroid Receptors in Immune Cells." In Sex Hormones and Immunity to Infection, 53–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02155-8_3.

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Döhler, K. D. "The special case of hormonal imprinting, the neonatal influence of sex." In Development of Hormone Receptors, 103–23. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9291-9_7.

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Thomas, Peter, Christopher Tubbs, Hakan Berg, and Gwen Dressing. "Sex steroid hormone receptors in fish ovaries." In The Fish Oocyte, 203–33. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6235-3_8.

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Spelsberg, Thomas C., Merry Jo Oursler, James P. Landers, Malayannam Subramaniam, Steven A. Harris, and B. Lawrence Riggs. "Human Bone Cells: Newly Discovered Target Cells for Sex Steroids." In Steroid Hormone Receptors: Basic and Clinical Aspects, 447–72. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-9849-7_18.

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Friend, Keith E., and Ian E. McCutcheon. "Estrogen Receptor Expression in the Pituitary Gland." In Sex-Steroid Interactions with Growth Hormone, 301–7. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1546-2_29.

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Pfaff, Donald, Elena Choleris, and Sonoko Ogawa. "Genes for sex hormone receptors controlling mouse aggression." In Novartis Foundation Symposia, 78–95. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470010703.ch6.

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Heine, M. J. S., and H. Gronemeyer. "Nuclear Receptors as Targets for Drug Design: New Options and Old Challenges." In Molecular Basis of Sex Hormone Receptor Function, 1–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03689-1_1.

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Giangrande, P., G. Pollio, and D. P. McDonnell. "Functional and Pharmacological Analysis of the A and B Forms of the Human Progesterone Receptor." In Molecular Basis of Sex Hormone Receptor Function, 179–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03689-1_10.

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Conference papers on the topic "Hormones, Sex – Receptors"

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Jönsson, Jenny-Maria, Nicolai Arildsen, Susanne Malander, Anna Måsbäck, Linda Werner Hartman, Mef Nilbert, and Ingrid Hedenfalk. "Abstract 1834: Sex hormone receptor expression affects ovarian cancer survival." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1834.

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Lin, H., H.-C. Fu, Y.-C. Ou, C.-H. Wu, and H.-Y. Kang. "P140 The roles of sex hormone receptors and chemosensitivity in ovarian cancer." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.202.

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Farhat, G., S. Cummings, N. Parimi, A. Huang, J. Cauley, T. Rohan, F. Hubbell, et al. "Sex Hormones and Risk of Estrogen Receptor (ER)-Positive and ER-Negative Breast Cancer." 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-09-907.

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Ferzel, Laura Ramos Silva, Kiara de Medeiros Braga Cruz Pessanha, Renata Magliano Marins, Meire Cardoso da Mota Bastos, and Isabelly dos Santos Belo. "Carcinoma metaplásico com diferenciação mesenquimal: relato de caso." In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130241.

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Introdução: Equivalendo a menos de 5% de todos os cânceres de mama, o carcinoma metaplásico representa um grupo morfologicamente heterogêneo das neoplasias malignas mamárias, que acomete, em sua maioria, mulheres na pós-menopausa. A principal manifestação clínica é nódulo palpável de crescimento progressivo e rápido. Histologicamente, é caracterizado por combinar componente epitelial e componente escamoso ou sarcomatoide. Manifesta-se tipicamente negativo para receptores hormonais e Human Epidermal growth factor Receptor-type 2 (HER2), independentemente do subtipo histológico. Objetivo: Relatar caso de carcinoma metaplásico que não foi diagnosticado em material de core biopsy. Método: Levantamento de dados clínicos, laboratoriais, exames de imagem e revisão bibliográfica pelas fontes PubMed, Literatura Latino-americana e do Caribe em Ciências da Saúde (LILACS) e Scientific Electronic Library Online (SciELO). Resultados: K.C.M.S.R., 35 anos, com queixa de nódulo palpável de crescimento progressivo em mama esquerda. Ultrassonografia (USG) de mamas: nódulo heterogêneo de contornos irregulares, em quadrante inferior lateral (QIL) da mama esquerda, medindo cerca de 4,5×4,1 cm, BIRADS 4. Laudo histopatológico de core biopsy: carcinoma invasivo SOE (padrão ductal — Organização Mundial da Saúde (OMS) 2012) grau histológico 3. Imuno-histoquímica: receptor de estrogênio e progesterona negativo, HER2 inconclusivo, FISH negativo e Ki 67 90% em mama esquerda. Indicada quimioterapia neoadjuvante, sem resposta e com progressão da lesão para aproximadamente 9 cm. Paciente então foi submetida à mastectomia com biópsia de linfonodo sentinela (BLS). Laudo anatomopatológico de peça cirúrgica constatou carcinoma metaplásico com componente de condrossarcoma. Conclusão: Apesar de triplo negativo, o carcinoma metaplásico não apresenta boa resposta à quimioterapia neoadjuvante. A cirurgia ainda é o principal tratamento em pacientes com tumores operáveis, independentemente do tamanho do tumor. Mais estudos são necessários para avaliação do comportamento biológico e da conduta terapêutica.
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Sakoda, Lori C., Noel S. Weiss, Matt Barnett, Gary E. Goodman, and Chu Chen. "Abstract 2858: Relation of androgen receptor polymorphisms and prostate cancer risk by level of sex steroid hormones." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2858.

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Noriega, Yamilet, Miguel Rivas, and Elizabeth Langley. "Abstract C56: Characterization of PinX1 as a coregulator of steroid hormone receptors." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c56.

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Jain, Raksha, Jennifer Ray, and Steven L. Brody. "Sex Hormone-Dependent Activation Of The Progesterone Receptor In Airway Epithelial Cells Inhibits Cilia Beat Frequency." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1226.

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Menamin, Una CMc, James Trainor, Helen G. Coleman, Damian T. McManus, Brian T. Johnston, and Richard Turkington. "PTH-117 Sex hormone receptor expression in oesophageal adenocarcinoma and recurrence and survival: a retrospective cohort study." In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.291.

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Novello, Silvia, Valentina Monica, Marina Longo, Sara Demichelis, Benedetta Crida, Matteo Giaj Levra, Simonetta G. Rapetti, and Enrica Capelletto. "Sex-Linked Hormone Receptor Expression In Lung Cancer Patients: Pilot Study In A Consecutive Group Of Patients With Advanced Lung Cancer." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5091.

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Spolador, Maria Eduarda Granucci, Maria Teresa Vasconcelos, Pedro Henrique Gunha Basílio, Samya Hamad Mehanna, and Victória Gayoso Neves Pereira. "TRATAMENTO DO CÂNCER DE MAMA TRIPLO NEGATIVO: O QUE DIZ A LITERATURA?" In I Congresso Nacional Multidisciplinar de Oncologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1581.

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Introdução: O câncer de mama triplo negativo (TNBC) caracteriza-se pela não expressão de receptores hormonais de estrogênio e progesterona, e negatividade do fator de crescimento epitelial humano 2 (HER2), correspondendo até 15% dos cânceres mamários. Este tipo molecular apresenta elevado índice proliferativo, sendo mais agressivo e capaz de produzir metástases e recidivas, apresentando pior prognóstico. O tratamento cirúrgico está indicado somado, principalmente, à quimioterapia. Objetivos: Identificar tratamentos atuais do TNBC e possíveis quimiorresistências. Material e métodos: Revisão bibliográfica de artigos da plataforma PubMed. Resultados: A quimioterapia neoadjuvante é usada para estágio inicial do TNBC, com altas taxas de resposta patológica completa (PCR). Entre os medicamentos utilizados, houve melhora na PCR das pacientes tratadas com paclitaxel semanalmente e quando adicionado carboplatina e/ou bevacizumabe houve acréscimo na taxa de PCR. Já para pacientes estágio II-III, o tratamento foi com paclitaxel semanalmente e doxorrubicina lipossomal não-peguilada, somado a bevacizumab ou trastuzumabe a cada 3 semanas, com/sem a adição semanal de carboplatina. A carboplatina adicional resulta em PCR mais frequentemente, porém há maior toxicidade. No tratamento adjuvante, recomendado para casos avançados ou metastáticos, relacionados à mutação BRCA ou resistência endócrina previamente tratados com antraciclina com/sem taxano, é indicado suplementar o regime com compostos de platina ou carboplatina, sendo que paclitaxel mostrou-se eficaz. Entre as justificativas para o subconjunto que apresenta resistência quimioterápica, correlaciona-se o efluxo de drogas mediado pelos transportadores de cassete de ligação de ATP (ABC), que utilizam ATP para efluir compostos através da membrana celular. Dentre os ABCs, destaque para proteína-1 multirresistente (ABCC1/MRP1) que teve sua expressão aumentada relacionada à neoadjuvância. Outros tratamentos incluem ainda imunoterapia e inibidores da enzima poliADP-ribose polimerase. Conclusão: Apesar dos avanços na terapêutica do TNBC, são necessárias pesquisas estabelecendo protocolos de tratamento otimizados, objetivando abordagens quimioterápicas personalizadas, resultando em melhores prognósticos aos pacientes.
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