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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Introduction Glucocorticoids are adrenal steroid hormones engaged in a myriad of functions including adaptation to stress, circadian function and immune regulation. Glucocorticoids also mediate quintessential processes in metabolic physiology
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Introduction Despite the introduction of a range of biological therapies aimed at specific aspects of the immune response, glucocorticoids are still widely used for their broad and potent therapeutic effects. Despite considerable efforts in
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matter ( Semenova et al. 2015 ). The driver mutations for NSCLC particularly have been well described, and mutation testing can be used for patient stratification and prescription of targeted therapy ( Pao & Girard 2011 ). The glucocorticoid
Medicine, Faculty of Life Sciences, Centre for Molecular
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Medicine, Faculty of Life Sciences, Centre for Molecular
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Introduction Glucocorticoid hormones exert a wide diversity of effects in target tissues. Their activity has been typically explored using a limited number of timed end points, both in vivo and in vitro , and using such approaches a variety of
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Introduction Endogenous glucocorticoids are steroid hormones secreted from the adrenal cortex under the influence of the hypothalamic–pituitary–adrenal (HPA) axis that constitutes an integral component of the response to stress. Corticosterone is
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themselves hormone-dependent, and are directly or indirectly controlled by factors such as growth hormone (GH), insulin-like growth factor 1 (IGF1), thyroid hormones and steroids; and in particular, the glucocorticoid hormones that govern hepatic
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adrenal medulla ( Wong 2006 ). This fast/acute response is trailed by an activation of the multi-step hypothalamus–pituitary–adrenal (HPA) axis and the release of glucocorticoids (GCs) – cortisol in humans and other primates, corticosterone in rodents
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Introduction Glucocorticoids, members of the steroid hormone superfamily, are secreted into the bloodstream by the adrenals in response to stress-induced activation of the hypothalamus–pituitary–adrenal axis. Through an interaction with their
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Centre for Discovery Brain Science, University of Edinburgh, Hugh Robson Building, Edinburgh, UK
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Clinical & Translational Research Institute, Newcastle University, International Centre for Life, Central Parkway, Newcastle upon Tyne, UK
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Mass Spectrometry Core Laboratory, Edinburgh Clinical Research Facility, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK
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Introduction 11β-Hydroxysteroid dehydrogenase 1 (11βHSD1) generates active 11-hydroxy glucocorticoids (cortisol (human), corticosterone (rodent and human)) from intrinsically inert 11-keto steroids (cortisone, 11-dehydrocorticosterone (11DHC
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Introduction Corticotropin-releasing hormone (CRH) neurons of the hypothalamic–pituitary–adrenal (HPA) axis integrate stress-dependent changes in neural input and direct negative feedback effects of glucocorticoids ( Dallman et al . 1987