Relevant bibliographies by topics / Glucocorticoids

Academic literature on the topic 'Glucocorticoids'

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Published: 4 June 2021
Last updated: 26 July 2024

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Journal articles on the topic "Glucocorticoids"

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Crowson, L., J. M. Davis, A. Hanson, E. Myasoedova, V. Kronzer, A. Makol, L. Peterson, D. Bekele, and C. S. Crowson. "POS0309 TIME TRENDS IN GLUCOCORTICOID USE IN RHEUMATOID ARTHRITIS DURING THE BIOLOGICS ERA: 1999-2018." Annals of the Rheumatic Diseases 82, Suppl 1 (May 30, 2023): 398–99. http://dx.doi.org/10.1136/annrheumdis-2023-eular.2025.

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BackgroundClinical guidelines recommend minimizing glucocorticoid use among patients with rheumatoid arthritis (RA) and many new therapeutic options in recent decades offer alternatives to glucocorticoids, but it is unknown whether glucocorticoid use has declined in patients with RA.ObjectivesTo examine time trends in glucocorticoid use among patients diagnosed with rheumatoid arthritis (RA) during the biologic era.MethodsA population-based inception cohort of RA patients diagnosed during 1999 - 2018 was followed longitudinally through their medical records until death, migration or 12/31/2020. All patients fulfilled 1987 and/or 2010 American College of Rheumatology classification criteria for RA. Glucocorticoid start and stop dates were collected along with dosages in prednisone equivalents. The cumulative incidence of glucocorticoid initiation and discontinuation adjusted for the competing risk of death was estimated. Cox models adjusted for age and sex were used to compare trends between time periods.ResultsThe study population was comprised of 399 patients (71% females) diagnosed in 1999 – 2008 and 430 patients (67% females) diagnosed in 2009 – 2018. Glucocorticoid use was initiated within 6 months of meeting RA criteria in 66.7% of patients in 1999-2008 and 70.9% of patients in 2009-2018, corresponding to a 29% increase in hazard for initiation of glucocorticoids in 2009-2018 (adjusted hazard ratio [HR]: 1.29; 95% confidence interval[CI]: 1.09-1.53). Among glucocorticoid users, similar rates of glucocorticoid discontinuation within 6 months after glucocorticoid initiation were observed in patients with RA incidence in 1999 – 2008 and 2009 – 2018 (39.1% versus 42.9%, respectively), with no significant association in adjusted Cox models (HR: 1.11; 95% CI: 0.93-1.31). Even in the 2009-2018 cohort, a large proportion of patients with RA (52%) remained on glucocorticoids beyond 3 months, and 30% were still on glucocorticoids after 2 years.Older patients with RA were more likely to initiate glucocorticoids (HR 1.06 per 10 year increase in age, 95% CI 1.00-1.13) and less likely to discontinue glucocorticoids (HR 0.91 per 10 year increase in age, 95% CI 0.86-0.96). There was no difference in the initiation of glucocorticoids by sex. Although females had a higher discontinuation rate within the first 12 months, afterwards discontinuation rates of glucocorticoids were similar in females and males. Smokers were less likely to discontinue glucocorticoids compared to non-smokers (HR 0.65; 95% CI: 0.51-0.82).ConclusionMore patients are initiating glucocorticoids early in their disease course now compared to previously despite the availability of biologics and other disease modifying antirheumatic drugs. The rates of glucocorticoid discontinuation are similar. A substantial proportion of patients remain on glucocorticoids for more than 3 months with a large proportion continuing use of glucocorticoidss even beyond 2 years. Real world use of glucocorticoids in patients with RA is not optimal or improving despite advances in RA therapy.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsLisa Crowson: None declared, John M Davis III Grant/research support from: Pfizer, Andrew Hanson: None declared, Elena Myasoedova: None declared, Vanessa Kronzer: None declared, Ashima Makol Consultant of: Boehringer Ingelheim, Lynne Peterson: None declared, Delamo Bekele: None declared, Cynthia S. Crowson: None declared.
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Washburn, Brian E., Joshua J. Millspaugh, John H. Schulz, Susan B. Jones, and Tony Mong. "Using Fecal Glucocorticoids for Stress Assessment in Mourning Doves." Condor 105, no. 4 (November 1, 2003): 696–706. http://dx.doi.org/10.1093/condor/105.4.696.

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Abstract Fecal glucocorticoid assays provide a potentially useful, noninvasive means to study physiological responses of wildlife to various stressors. The objective of our study was to validate a method for measuring glucocorticoid metabolites in Mourning Dove (Zenaida macroura) feces. We validated the assay using standard procedures (e.g., parallelism, recovery of exogenous corticosterone) to demonstrate that the assay accurately and precisely measured glucocorticoid metabolites in Mourning Dove fecal extracts. We conducted adrenocorticotropin (ACTH) challenge experiments to validate the assay's ability to determine biologically important changes in fecal glucocorticoids. Fecal glucocorticoid levels increased significantly approximately 2–3 hr after administration of ACTH at 50 IU per kg body mass to wild Mourning Doves held in captivity. In contrast, fecal glucocorticoid metabolites did not increase in control birds, birds that received saline injections, or a lower dose of ACTH (1 IU per kg body mass). Variation in overall fecal glucocorticoid metabolite levels may have been influenced by season and the length of time birds were held in captivity. Noninvasive fecal glucocorticoid metabolite analyses, in combination with demographic information, may have considerable utility for monitoring the effects of natural and anthropogenic disturbances on Mourning Dove populations. Uso de Glucocorticoides Fecales Para Evaluar el Estrés en Zenaida macroura Resumen. Las evaluaciones de glucocorticoides fecales representan un medio no invasor potencialmente útil para estudiar las respuestas fisiológicas de los animales silvestres ante agentes causantes de estrés. El objetivo de nuestro estudio fue validar un método para medir metabolitos glucocorticoides en heces de palomas Zenaida macroura. Validamos el método mediante procedimientos estándar (e.g., paralelismo, recuperación de corticosterona exógena) para demostrar que éste mide con exactitud y precisión los metabolitos glucocorticoides en extractos fecales de Z. macroura. Realizamos experimentos de desafío con adrenocorticotropina (ACTH) para validar la habilidad que tenía el método para determinar cambios biológicamente importantes en los glucocorticoides fecales. Los niveles de glucocorticoides fecales aumentaron de forma significativa aproximadamente 2–3 hr después de la administración de ACTH a 50 IU por kg de peso corporal a palomas silvestres mantenidas en cautiverio. En contraste, los metabolitos glucocorticoides fecales no aumentaron en aves control, ni en aves que recibieron inyecciones salinas o una menor dosis de ACTH (1 IU por kg de peso corporal). La variación en los niveles generales de metabolitos glucocorticoides fecales podría haber sido influenciada por la estación y la longitud del período de tiempo en que las aves fueron mantenidas en cautiverio. Los análisis no invasores de metabolitos glucocorticoides, en combinación con información demográfica, podrían ser de considerable utilidad para monitorear los efectos de los disturbios naturales y antropogénicos sobre las poblaciones de Z. macroura.
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Kajita, S., H. Iizuka, M. Hirokawa, M. Tsutsui, and T. Mizumoto. "Topical application of potent glucocorticoids augments epidermal beta-adrenergic adenylate cyclase response in vivo." Acta Dermato-Venereologica 66, no. 6 (November 1, 1986): 491–96. http://dx.doi.org/10.2340/0001555566491496.

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The effects of topical application of glucocorticoids on the epidermal beta-adrenergic adenylate cyclase response were investigated. A significant increase in this receptor response was observed 24 h following topical application of potent glucocorticoid ointments (0.12% betamethasone-17-valerate, 0.05% clobetasol-17-propionate). The application of a relatively weak glucocorticoid, hydrocortisone-17-butyrate, revealed no augmentation effect. There was no significant difference in other adenylate cyclase responses (adenosine-, and histamine-) between control and glucocorticoid-treated epidermis. UVB irradiation is known to augment the beta-adrenergic response of epidermis. Comparison of the effects revealed that topical glucocorticoid treatment had less effect than UVB irradiation, and when the UVB irradiation was combined with glucocorticoid treatment, the beta-adrenergic augmentation effect was not enhanced. Cyclic AMP phosphodiesterase activities were not significantly altered by the glucocorticoid-, UVB-, or combined treatments. Our data indicate that epidermal beta-adrenergic adenylate cyclase response is affected by topical application of ´potent´ glucocorticoids in vivo. Although the effect is weaker than that induced by UVB irradiation, we believe the system might be a useful tool for dissecting the glucocorticoidal potency of topical preparations using the epidermal keratinocyte response in vivo.
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Roberts, Jessica K., Chad D. Moore, Erin G. Romero, Robert M. Ward, Garold S. Yost, and Christopher A. Reilly. "Regulation of CYP3A genes by glucocorticoids in human lung cells." F1000Research 2 (August 13, 2013): 173. http://dx.doi.org/10.12688/f1000research.2-173.v1.

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Inhaled glucocorticoids are the first-line treatment for patients with persistent asthma. However, approximately thirty percent of patients exhibit glucocorticoid insensitivity, which may involve excess metabolic clearance of the glucocorticoids by CYP3A enzymes in the lung. CYP3A4, 3A5, and 3A7 enzymes metabolize glucocorticoids, which in turn induce CYP3A genes. However, the mechanism of CYP3A5 mRNA regulation by glucocorticoids in lung cells has not been determined. In hepatocytes, glucocorticoids bind to the glucocorticoid receptor (GR), which induces the expression of the constitutive androstane receptor or pregnane X receptor; both of which bind to the retinoid X receptor alpha, leading to the induction of CYP3A4, 3A5, and 3A7. There is also evidence to suggest a direct induction of CYP3A5 by GR activation in liver cells. In this study, these pathways were evaluated as the mechanism for CYP3A5 mRNA induction by glucocorticoids in freshly isolated primary tracheal epithelial, adenocarcinomic human alveolar basal epithelial (A549), immortalized bronchial epithelial (BEAS-2B), primary normal human bronchial/tracheal epithelial (NHBE), primary small airway epithelial (SAEC), and primary lobar epithelial lung cells. In A549 cells, beclomethasone 17-monopropionate ([M1]) induced CYP3A5 mRNA through the glucocorticoid receptor. CYP3A5 mRNA induction by five different glucocorticoids was attenuated by inhibiting the glucocorticoid receptor using ketoconazole, and for beclomethasone dipropionate, using siRNA-mediated knock-down of the glucocorticoid receptor. The constitutive androstane receptor was not expressed in lung cells. SAEC cells, a primary lung cell line, expressed CYP3A5, but CYP3A5 mRNA was not induced by glucocorticoid treatment despite evaluating a multitude of cell culture conditions. None of the other lung cells expressed CYP3A4, 3A5 or 3A7 mRNA. These studies demonstrate that CYP3A5 mRNA is induced by glucocorticoids in A549 cells via the glucocorticoid receptor, but that additional undefined regulatory processes exist in primary lung cells.
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Roberts, Jessica K., Chad D. Moore, Erin G. Romero, Robert M. Ward, Garold S. Yost, and Christopher A. Reilly. "Regulation of CYP3A genes by glucocorticoids in human lung cells." F1000Research 2 (October 8, 2013): 173. http://dx.doi.org/10.12688/f1000research.2-173.v2.

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Inhaled glucocorticoids are the first-line treatment for patients with persistent asthma. However, approximately thirty percent of patients exhibit glucocorticoid insensitivity, which may involve excess metabolic clearance of the glucocorticoids by CYP3A enzymes in the lung. CYP3A4, 3A5, and 3A7 enzymes metabolize glucocorticoids, which in turn induce CYP3A genes. However, the mechanism of CYP3A5 mRNA regulation by glucocorticoids in lung cells has not been determined. In hepatocytes, glucocorticoids bind to the glucocorticoid receptor (GR), which induces the expression of the constitutive androstane receptor or pregnane X receptor; both of which bind to the retinoid X receptor alpha, leading to the induction of CYP3A4, 3A5, and 3A7. There is also evidence to suggest a direct induction of CYP3A5 by GR activation in liver cells. In this study, these pathways were evaluated as the mechanism for CYP3A5 mRNA induction by glucocorticoids in freshly isolated primary tracheal epithelial, adenocarcinomic human alveolar basal epithelial (A549), immortalized bronchial epithelial (BEAS-2B), primary normal human bronchial/tracheal epithelial (NHBE), primary small airway epithelial (SAEC), and primary lobar epithelial lung cells. In A549 cells, beclomethasone 17-monopropionate ([M1]) induced CYP3A5 mRNA through the glucocorticoid receptor. CYP3A5 mRNA induction by five different glucocorticoids was attenuated by inhibiting the glucocorticoid receptor using ketoconazole, and for beclomethasone dipropionate, using siRNA-mediated knock-down of the glucocorticoid receptor. The constitutive androstane receptor was not expressed in lung cells. SAEC cells, a primary lung cell line, expressed CYP3A5, but CYP3A5 mRNA was not induced by glucocorticoid treatment despite evaluating a multitude of cell culture conditions. None of the other lung cells expressed CYP3A4, 3A5 or 3A7 mRNA. These studies demonstrate that CYP3A5 mRNA is induced by glucocorticoids in A549 cells via the glucocorticoid receptor, but that additional undefined regulatory processes exist in primary lung cells.
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Muhammad, Salam Abed. "Hydrocortisone as Antiallergic Drug." Journal for Research in Applied Sciences and Biotechnology 3, no. 1 (March 27, 2024): 305–14. http://dx.doi.org/10.55544/jrasb.3.1.50.

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Glucocorticoids are widely used for the suppression of inflammation in chronic inflammatory diseases such as asthma, rheumatoid arthritis, inflammatory bowel disease and autoimmune diseases, all of which are associated with increased expression of inflammatory genes. The molecular mechanisms involved in this anti-inflammatory action of glucocorticoids is discussed, particularly in asthma, which accounts for the highest clinical use of these agents. Glucocorticoids bind to glucocorticoid receptors in the cytoplasm which then dimerize and translocate to the nucleus, where they bind to glucocorticoid response elements (GRE) on glucocorticoid-responsive genes, resulting in increased transcription. Glucocorticoids may increase the transcription of genes coding for anti-inflammatory proteins, including lipocortin-1, interleukin-10, interleukin-1 receptor antagonist and neutral endopeptidase, but this is unlikely to account for all of the widespread anti-inflammatory actions of glucocorticoids.[3] The most striking effect of glucocorticoids is to inhibit the expression of multiple inflammatory genes.[3]
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CROXTALL, Jamie D., Mark PAUL-CLARK, and Peter Th W. van HAL. "Differential modulation of glucocorticoid action by FK506 in A549 cells." Biochemical Journal 376, no. 1 (November 15, 2003): 285–90. http://dx.doi.org/10.1042/bj20030821.

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Glucocorticoids inhibit the release of eicosanoid pro-inflammatory mediators. The immunosuppressant FK506 is known to enhance many aspects of glucocorticoid action. In the present study we show that FK506 (1 μM or 10 μM) inhibits the release of arachidonic acid and prostaglandin E2 from A549 cells and also inhibits their proliferation. Simultaneous treatment of FK506 together with the glucocorticoids dexamethasone, methyl-prednisolone, fluticasone or mometasone (10 nM) enhances the growth inhibitory effect of these steroids. Furthermore, the simultaneous use of FK506 and these glucocorticoids similarly results in enhanced inhibition of arachidonic acid release. When pretreated for 2 h, FK506 enhances glucocorticoid inhibition of COX2 (cyclo-oxygenase 2) expression. However, when administered simultaneously, FK506 blocks glucocorticoid inhibition of COX2 expression. Nuclear uptake of glucocorticoid receptors mediated by glucocorticoids is also blocked by the simultaneous administration of FK506. These results suggest that the effect of simultaneous treatment of FK506 with glucocorticoids differs significantly from that where pre-treatment of the immunosuppressant is used. Recently, immunophilin interchange has been identified as a first step in glucocorticoid receptor activation following ligand activation. We show here that the FKB51 (FK506-binding protein 51)–FKB52 switch is differentially regulated by glucocorticoid and FK506 treatment strategy.
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Walker, Brian R. "Glucocorticoids and Cardiovascular Disease." European Journal of Endocrinology 157, no. 5 (November 2007): 545–59. http://dx.doi.org/10.1530/eje-07-0455.

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AbstractChronic excessive activation of glucocorticoid receptors induces obesity, insulin resistance, glucose intolerance, dyslipidaemia and hypertension. Subtle abnormalities of the hypothalamic–pituitary–adrenal axis and/or of tissue sensitivity to glucocorticoids are also associated with these cardiovascular risk factors in patients with the metabolic syndrome. Furthermore, glucocorticoids have direct effects on the heart and blood vessels, mediated by both glucocorticoid and mineralocorticoid receptors and modified by local metabolism of glucocorticoids by the 11β-hydroxysteroid dehydrogenase enzymes. These effects influence vascular function, atherogenesis and vascular remodelling following intra-vascular injury or ischaemia. This article reviews the systemic and cardiovascular effects of glucocorticoids, and the evidence that glucocorticoids not only promote the incidence and progression of atherogenesis but also modify the recovery from occlusive vascular events and intravascular injury. The conclusion is that manipulation of glucocorticoid action within metabolic and cardiovascular tissues may provide novel therapeutic avenues to combat cardiovascular disease.
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Macfarlane, David P., Shareen Forbes, and Brian R. Walker. "Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome." Journal of Endocrinology 197, no. 2 (February 28, 2008): 189–204. http://dx.doi.org/10.1677/joe-08-0054.

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Glucocorticoid hormones constitute an integral component of the response to stress, and many of the manifestations of glucocorticoid excess (Cushing's syndrome) are predictable on the basis of their acute effects to raise blood pressure, induce insulin resistance, increase protein catabolism and elevate plasma glucose. However, it appears to be a paradox that the acute lipolytic effect of glucocorticoids is not manifest in long-term weight loss in humans. The effects of glucocorticoids on glucose metabolism are well characterised, involving impaired peripheral glucose uptake and hepatic insulin resistance, and there is mounting evidence that subtle abnormalities in glucocorticoid concentrations in the plasma and/or in tissue sensitivity to glucocorticoids are important in metabolic syndrome. The effects of glucocorticoids on fatty acid metabolism are less well understood than their influence on glucose metabolism. In this article, we review the literature describing the effects of glucocorticoids on fatty acid metabolism, with particular reference to in vivo human studies. We consider the implications for contrasting acute versus chronic effects of glucocorticoids on fat accumulation, effects in different adipose depots and the potential role of glucocorticoid signalling in the pathogenesis and therapy of metabolic syndrome.
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Ponticelli, Claudio, and Francesco Locatelli. "Glucocorticoids in the Treatment of Glomerular Diseases." Clinical Journal of the American Society of Nephrology 13, no. 5 (February 23, 2018): 815–22. http://dx.doi.org/10.2215/cjn.12991117.

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Glucocorticoids exert anti-inflammatory and immunosuppressive activities by genomic and nongenomic effects. The classic genomic effects are mediated by cytosolic glucocorticoid receptors that can upregulate the expression of anti-inflammatory proteins in the nucleus (transactivation) or repress the translocation of proinflammatory transcription factors from the cytosol into the nucleus (transrepression). The nongenomic effects are probably mediated by membrane glucocorticoid receptors. Glucocorticoid receptors are expressed also in podocytes and experimental data suggest that glucocorticoids may protect from podocyte injury. Glucocorticoids have a low therapeutic index and may exert a number of time-dependent and dose-dependent side effects. Measures to prevent or attenuate side effects include single-morning administration of short-acting glucocorticoids, dietetic counseling, increasing physical activity, frequent monitoring, and adapting the doses to the clinical conditions of the patient. Synthetic glucocorticoids, either given alone or in combination with other immunosuppressive drugs, are still the cornerstone therapy in multiple glomerular disorders. However, glucocorticoids are of little benefit in C3 glomerulopathy and may be potentially deleterious in patients with maladaptive focal glomerulosclerosis. Their efficacy depends not only on the type and severity of glomerular disease, but also on the timeliness of administration, the dosage, and the duration of treatment. Whereas an excessive use of glucocorticoids can be responsible for severe toxicity, too low a dosage and too short duration of glucocorticoid treatment can result in false steroid resistance.
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Dissertations / Theses on the topic "Glucocorticoids"

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Agnew, Emma Jane. "The effect of antenatal glucocorticoid treatment on fetal heart maturation in mice." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/29555.

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Glucocorticoids - cortisol and corticosterone - are steroid hormones synthesised in the adrenal gland that are important mediators of the stress response. Glucocorticoids are also vital in development to aid in organ maturation. Endogenous glucocorticoid levels rapidly rise before birth in all mammals to promote fetal organ maturation. Because preterm birth occurs before this natural rise in glucocorticoid levels, pregnant women at risk of preterm delivery are administered synthetic glucocorticoids to mature the fetal lung and aid neonatal survival. Mice that globally lack the glucocorticoid receptor (GR) die at birth, attributed to lung immaturity. Effects on tissues other than the lung remain less well characterised. Previous work has shown endogenous glucocorticoid action is also essential to mature the mouse fetal heart. Mice globally lacking GR have small, functionally and structurally immature hearts. Mice with tissue-specific deletion of GR in cardiomyocytes and vascular smooth muscle cells (SMGRKO mice; generated using Sm22α-Cre) also have an increased risk of death around the time of birth, suggesting that glucocorticoid maturation of the cardiovascular system is important for neonatal survival. GR expression within the fetal mouse heart initiates at E10.5 but GR in the myocardium is not activated and localised to the nucleus until E15.5. This suggests that mice can respond to glucocorticoid from E10.5. Here, it was hypothesised that antenatal glucocorticoid exposure, prior to the increase in endogenous glucocorticoid levels, would advance fetal heart maturation and this will depend on cardiovascular GR. To investigate the effects of antenatal glucocorticoid treatment on fetal heart maturation in mid-gestation and identify effects mediated by GR, mice with a conditional deletion of GR in cardiomyocytes and vascular smooth muscle cells were studied (SMGRKO mice). Pregnant mice received dexamethasone (dex) in the drinking water from E12.5-E15.5. Levels of Fkbp5 mRNA (a marker of glucocorticoid action) were unchanged between control and SMGRKO mice at E15.5 or following dex treatment. This suggested a lack of response to dex treatment. However, liquid chromatography mass spectrometry measurement confirmed the presence of dex and its active metabolite 6- hydroxydexamethasone (6OHDex) in livers of E15.5 fetuses from dex treated dams (fetal: Dex 0.46 ± 0.1 ng/g, 6OHDex 13.6 ± 0.35 ng/g; dam: Dex 7.96 ± 3.65 ng/g, 6OHDex 4.75 ± 1.2 ng/g). Livers of fetuses exposed to dex had lower levels of the naturally occurring active glucocorticoid, corticosterone, compared to vehicle treated fetuses. This suggests HPA axis suppression in dex exposed fetuses. Maternal liver showed no significant difference in corticosterone levels between dex and vehicle treated mice, suggesting that whilst dex suppressed the HPA axis in fetuses, it did not in the dams. To determine any persistent effects of early antenatal dex treatment on fetal heart, a later time point in gestation, E17.5, was also assessed. At E17.5, 2-days following cessation of dex treatment, dex and its metabolites were undetectable in the fetal and maternal liver. However, corticosterone levels remained reduced in fetal liver at E17.5 in dex exposed animals (vehicle treated: 4.31 ± 0.47 ng/g, Dex treated: 1.72 ± 0.42 ng/g, p < 0.01), whilst levels in the dam liver did not differ from vehicle treated controls. This suggests prolonged HPA axis suppression following dex treatment, which reduced the natural late-gestation rise in glucocorticoids required for fetal organ maturation. To determine whether early antenatal dex treatment could advance fetal heart function, Doppler imaging with a Vevo 770 high frequency ultrasound imager was used. Isovolumetric contraction time, isovolumetric relaxation time and ejection time of the left ventricle were unaltered by dex treatment. However, at E15.5 the mitral deceleration index (MDI), a measure of diastolic function that takes into account loading conditions, was 1.5 fold lower in vehicle treated SMGRKO mice than control (Cre-) littermates (p < 0.05). This reduction in SMGRKO mice suggests glucocorticoids are required within the fetal cardiomyocytes and/or vascular smooth muscle cells to mature the diastolic function of the fetal heart. Dex exposure had no effect on MDI in SMGRKO fetuses, but reduced the MDI by 1.5 fold in control mice to similar levels as in SMGRKO mice (p < 0.05). RNA analysis revealed a trend (p=0.09) for reduced levels of Nr3c1 mRNA (encoding GR) in hearts of E15.5 control (Cre-) fetuses following dex treatment. Although this requires confirmation at the level of GR protein, this finding together with the lack of induction of the GR target, Fkbp5, suggests dex may cause glucocorticoid resistance through down-regulation of GR. At E17.5, 2-days following cessation of dex there were no changes in systolic parameters and the reduction in MDI found at E15.5, following dex, had normalised. Litter size was reduced (close to a 50% reduction) at E17.5 in dex treated mice. This was similar between SMGRKO and control fetuses. The cause of death was not established, but potentially could be due to the reduction in the natural rise in glucocorticoids at E17.5, previously shown to be important for fetal heart maturation. It is therefore possible that mice with more immature hearts may die before reaching E17.5. RNA analysis was undertaken to determine any mechanistic alterations following dex treatment, which could support fetal heart functional alterations found at E15.5. In contrast to expectation, dex also decreased expression of mRNA encoding the calcium handling proteins SERCA2a, NCX1, and CaV1.2 in E15.5 fetal mouse hearts in both control and SMGRKO mice (p < 0.05), compared with the respective vehicle treated mice. These proteins had previously shown to be induced by glucocorticoid action in cardiomyocytes. However, the similar down-regulation in both genotypes indicates this effect is not dependent on GR in cardiomyocytes. Lowered SERCA2a activity following dex treatment could contribute to the changes in MDI observed in control mice. Similarly, Scnn1a and Kcnj12 mRNA levels, previously found to be induced by glucocorticoids in cardiomyocytes, were down-regulated in the E15.5 fetal heart in vivo following dex. Collectively, these data are consistent with glucocorticoid resistance or down-regulation of glucocorticoid action in E15.5 fetal hearts following dex administration. Mutations in KCNJ12 are associated with long QT syndrome, which is characterised by a delayed repolarisation of the heart following each contraction. An altered relaxation of the fetal heart found in control mice following dex could therefore be due to a prolongation of the cardiac action potential, particularly with a delayed repolarisation, because of lower Kcnj12 expression. At E17.5, there were no significant differences in expression of calcium handling genes or ion channel mRNAs between genotypes or following earlier dex exposure. Thus, effects of dex on mRNA expression level may not persist, which could account for the lack of functional changes observed 2-days following cessation of treatment. Because effects seen in vivo with dex treatment were contrary to those predicted, and to further investigate the effect of dex upon calcium content, an in vitro model of primary fetal E15.5 cardiomyocytes was used. Cardiomyocytes were treated with dex for 24 hours and effects on membrane potential voltage changes and calcium transients measured. Following dex, isolated fetal cardiomyocytes showed an elongated repolarisation phase of the action potential (untreated: 120.45 ± 13.81 ms, Dex: 142.34 ± 12.97 ms, p < 0.01), and duration of calcium transients (untreated: 103.31 ± 13.78 ms, Dex: 120.43 ± 23.36 ms, p < 0.05). This assessment of fetal cardiomyocytes was preliminary work to aid in the understanding of mechanisms of fetal heart functional alterations associated with glucocorticoid regulation. The results suggest glucocorticoids may be important in regulating calcium levels. In summary, dex treatment in mice from E12.5-E15.5 did not advance fetal heart maturation. It reduced litter size at E17.5, irrespective of whether GR was expressed in cardiomyocytes or not. The normal late-gestation increase in endogenous glucocorticoid levels in the fetus was reduced by dex, even after treatment finished.
The suppression of corticosterone levels following antenatal dex may reduce maturation of the heart at E15.5 and could be responsible for the reduction in litter size. Downregulation of GR in the fetal heart, may be a mechanism that results in glucocorticoid resistance following antenatal dex treatment, which could explain the lack of beneficial effects of antenatal dex upon fetal heart maturation in these experiments in mice.
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McInnes, Kerry J. "Hepatic 5α-reduced glucocorticoids : modulators of glucocorticoid receptor activation in obesity." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/24946.

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In obese versus lean Zucker rats, hepatic 5α-reductase type 1 mRNA expression and protein levels were increased. They also had increased activity of hepatic 5β-reductase activity. By contrast, 3α-hydroxysteroid dehydrogenase mRNA expression was unchanged in obesity. Greater inactivation of B by A-ring reductases in liver may decrease local corticosterone (B) concentrations in these sites, and increase the metabolic clearance rate of glucocorticoids, thus increasing drive to the hypothalamic-pituitary-adrenal axis (HPA). To investigate whether 5α-reduced metabolites of corticosterone are glucocorticoid receptor agonists, competition binding studies were carried out. In displacing tritiated dexamethasone from binding sites in hepatocytes from male lean Zucker rats, B and 5α-tetrahydrocorticosterone (5αTHB) had similar affinities which were greater than 5α-dihydrocorticosterone (5αDHB) and 5β-reduced metabolites. Binding of B and 5αDHB binding was impaired in obesity whereas 5αTHB binding was unaltered suggesting that 5αTHB may modulate GR activation in obesity. Activation of flucocorticoid receptors was assessed following transient transfection into HeLa cells with an MMTV-luciferase reporter. By comparison with corticosterone, 5αTHB was active and additive. 5β-Reduced metabolites did not activate glucocorticoid receptors. In addition, in H4IIe cells which express endogenous glucocorticoid receptors, 5αTHB induced tyrosine aminotransferase mRNA expression albeit to a lesser extent than corticosterone. 5αTHB was also found to possess glucocorticoid activity in vivo as suppression of plasma ACTH was demonstrated in adrenalectomised lean Zucker rats following i.p. administration of B or 5αTHB. We conclude that hepatic A-ring reduction is enhanced in the obese Zucker rat producing increased concentrations of 5αTHB. Transcription of glucocorticoid regulated genes in tissues which express 5α-reductases will thus be influenced by intracellular levels of both corticosterone and its 5α-reduced metabolites. Manipulation of this enzyme may prove to be a useful therapeutic target in obesity.
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Low, Lucinda. "Vascular lesion development : influence of endogenous and exogenous glucocorticoids." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5920.

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Atherosclerotic and restenotic lesions develop as a result of an excess inflammatory response to vascular injury. Glucocorticoid hormones have widely-recognised anti-inflammatory and anti-proliferative properties which appear to make them ideal candidates for inhibition of vascular lesion development. Indeed, administration of glucocorticoids to experimental animals does inhibit the growth of vascular lesions in some models. In addition, glucocorticoids are currently being trialled clinically as anti-restenotic agents. However, glucocorticoid excess in patients, either as a result of Cushing’s syndrome or chronic steroid therapy, is associated with enhanced CVD risk. Therefore, the effects of glucocorticoids on vascular lesion development remain imperfectly understood. The overall objective of these studies was to explore the influence of endogenous and exogenous glucocorticoids on vascular lesion development using murine models of atherosclerosis (ApoE-/- mice fed a “western” diet) and neointimal hyperplasia (wireinduced femoral artery injury). The work described in this thesis addresses the hypothesis that glucocorticoids are pro-atherogenic, yet anti-restenotic. Mice were bilaterally adrenalectomised to investigate the role of endogenous glucocorticoids on vascular lesion development. Removal of the adrenal glands had no influence on atherogenesis or neointima development. The influence of exogenous glucocorticoids on lesion development was assessed by orally administering dexamethasone (0.1 or 0.8mg/kg/day). Atherosclerotic lesion burden was augmented by dexamethasone administration. Conversely, fibro-proliferative neointimal proliferation was inhibited by dexamethasone. However, this effect was obscured by thrombotic lesion development. It was proposed that this thrombotic effect is attributable to increased plasminogen activator inhibitor-1 (PAI-1), which was tested using PAI-1 deficient mice. Although PAI-1 was found to mediate the systemic pro-thrombotic effect of dexamethasone, it is not required for the enhanced development of thrombotic lesions at the site of intra-luminal injury. These results suggest that physiological levels of endogenous glucocorticoids play a limited role in vascular lesion development. Conversely, although exogenous glucocorticoids inhibit fibro-proliferative intimal hyperplasia, they appear to have significant detrimental influences on lesion development, augmenting atherosclerosis and inducing thrombotic neointimal lesion formation following vascular injury. Further research is therefore required to improve the cardiovascular outcome of patients requiring glucocorticoid therapy and for the use of glucocorticoids as antirestenotic agents.
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Small, Gary R. "Glucocorticoids and angiogenesis." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29367.

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It was hypothesised that generation of endogenous glucocorticoids by 11βHSD1 within the vessel wall regulates angiogenesis. In vitro mouse aortic ring cultures established that physiologically-relevant concentrations of glucocorticoids inhibit angiogenesis in a glucocorticoid receptor-dependent manner.  In addition 11βHSD1 was found to modulate glucocorticoid-induced angiostasis, for 11dehydrocorticosterone (a substrate for 11βHSD1) although angiostatic in C57B16 aortae did not inhibit angiogenesis in llβHSD1 deficient animals. In vivo using subcutaneous sponge implants in mice, endogenous glucocorticoids were found to inhibit angiogenesis: sponges in adrenalectomised mice grew more vessels compared to sponges from sham-operated animals. 11βHSD1 regulated the angiostatic effects of glucocorticoids, for cortisone (the human equivalent of 11dehydrocorticosterone), although angiostatic in controls did not inhibit angiogenesis in 11βHSD1 deficient mice. In pathology in cutaneous wounds and infracted myocardium endogenous glucocorticoids were found to inhibit angiogenesis. RU38486, (a glucocorticoids receptor antagonist) in comparison to placebo enhanced angiogenesis in both tissues. In similar studies in C57B16 or llβHSD1 deficient mice, 11βHSD1 was found to tonically repress angiogenesis and impair left ventricular remodelling post infarction. Thus 11βHSD1 deficient mice had increased myocardial revascularisation and preserved left ventricular function. In conclusion, by using in vitro, in vivo, and pathological models, endogenous glucocorticoids were seen to inhibit angiogenesis. In addition, 11βHSD1 regeneration of glucocorticoids tonically repressed angiogenesis and influenced left ventricular remodelling post myocardial infarction. Thus 11βHSD1 appears to be an attractive therapeutic target for the management of tissue revascularisation.
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Thorsson, Lars. "Studies on the deposition, bioavailability and systemic activity of glucocorticoids in man." Lund, Sweden : Dept. of Clinical Pharmacology, Lund University Hospital, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57508512.html.

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Teelucksingh, S. "Glucocorticoids and the skin." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/27520.

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Glucocorticoids are the most effective anti-inflammatory agents currently available, but a variety of adverse effects limit their clinical usefulness. This work explores further two facets of the interaction between glucocorticoids and the skin, with the aim of identifying means of reducing glucocorticoid toxicity. (a) Metabolism of glucocorticoid by skin: Human skin is active in the terminal metabolism of cortisol to cortisone, but the biological implications of this process in skin are uncertain. Because there are technical difficulties in dealing with human skin, an animal model, the nude mouse, has been evaluated for its suitability to the study of the metabolism of corticosterone to 11β-dehydrocorticosterone (the homologous reaction in rodents of cortisol to cortisone conversion in man); a process mediated by 11β-hydroxysteroid dehydrogenase. In this model, skin 11β-hydroxysteroid dehydrogenase had an apparent Km for corticosterone of 37 uM. Skin 11β-hydroxysteroid dehydrogenase was up-regulated, in-vivo, by active glucocorticoids and was NADP dependent. By comparison, kidney 11β-hydroxysteroid dehydrogenase had a higher apparent Km (120 uM) for corticosterone, used NAD and NADP with equal facility and was not regulated in-vivo by glucocorticoids. These data suggest that the skin may possess an isoform distinct from that of the kidney. (b) Skin vasoconstrictor response (blanching) to topical glucocorticoids: Glucocorticoids applied topically to human skin produce vasoconstriction in dermal vessels, the degree of which correlates closely with the potency and clinical efficacy of these compounds. Although previous works had noted heterogeneity in blanching responses to glucocorticoids, this was never systematically studied. In qualitative studies, it was shown that skin blanching was inducible by RU-28362, a specific glucocorticoid receptor (type II) agonist and blocked by RU-38486, a glucocorticoid antagonist.
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Martin, Agnès. "Role of the glucocorticoid pathway in skeletal muscle wasting and hepatic metabolism rewiring during cancer cachexia in ApcMin/+ mice – Functional implication of myostatin gene invalidation." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSES034.

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La cachexie affecte environ la moitié des patients atteints d’un cancer et est caractérisée par une perte progressive de la masse corporelle résultant principalement d’une perte de masse musculaire squelettique. Cette perte de masse musculaire squelettique associée à une perte de force musculaire contribue fortement à réduire la qualité de vie des patients, l’efficacité des traitements et à terme, la survie des patients. Plusieurs facteurs sont connus pour être impliqués dans la régulation de la masse musculaire. Parmi eux, les glucocorticoïdes sont des hormones stéroïdiennes sécrétées sous le contrôle de l’axe hypothalamo-hypophysaire qui sont connues pour induire l’atrophie musculaire mais aussi pour avoir une action systémique via l’activation ou l’expression de gènes dans plusieurs tissus. Nous faisons l’hypothèse que la voie des glucocorticoïdes pourrait être activée pendant la cachexie associée au cancer dans les souris ApcMin/+, un model murin de cancer intestinal. Nous rapportons ici que l’activation du catabolisme musculaire était associée à une reprogrammation complète du métabolisme du foie. En outre, nous montrons une activation de l’axe hypothalamo-hypophysaire associée à une augmentation du niveau en corticostérone (le glucocorticoïde principal chez les rongeurs) dans le sérum, le muscle quadriceps et le foie des souris à un stade avancé de la cachexie associée au cancer. La signature transcriptionnelle dans le muscle quadriceps et le foie des souris à un stade avancé de la cachexie associée au cancer reflète celle observée dans des souris traitées avec de la dexaméthasone, un analogue des glucocorticoïdes. Il est important de souligner que l’inhibition de la cachexie associée au cancer par l’inactivation du gène de la myostatine dans les souris ApcMin/+ a restauré les niveaux en corticostérone et abolit la reprogrammation génique dans le muscle squelettique et le foie. Ensemble, ces données indiquent que les glucocorticoïdes induisent un programme transcriptionnel pour réguler de façon coordonnée la perte de masse musculaire et le remaniement du métabolisme hépatique. L’inhibition de cette réponse par l’invalidation du gène de la myostatine souligne l’existence d’un dialogue moléculaire entre le muscle squelettique et le foie
Cachexia affects about half of cancer patients and is characterized by a progressive body mass loss mainly resulting from skeletal muscle depletion. This loss of skeletal muscle mass together with a decrease in muscle force strongly contribute to reduce cancer patient quality of life, treatment efficiency and ultimately patient survival. Many factors are known to be involved in the regulation of skeletal muscle homeostasis. Among them, glucocorticoids are steroid hormones secreted under the control of the hypothalamic-pituitary axis that have been well described to promote skeletal muscle atrophy but also to exert systemic actions through activation or repression of gene expression in many tissues. We hypothesized that the glucocorticoid pathway could be activated during cancer cachexia in ApcMin/+ mice, a mouse model of intestinal cancer. Here, we reported that activation of skeletal muscle catabolism was associated with a complete reprogramming of liver metabolism. Moreover, we showed an activation of the hypothalamus-pituitary axis that was associated with an increase in the level of corticosterone (the main glucocorticoid in rodent) in serum, quadriceps muscle and liver of advanced cancer cachectic mice. The transcriptional signature in quadriceps muscle and liver of advanced cancer cachectic mice significantly mirrored that observed in mice treated with dexamethasone, an analog glucocorticoid. Importantly, the inhibition of cancer cachexia by myostatin gene invalidation in ApcMin/+ mice restored corticosterone levels and abolished skeletal muscle and liver gene reprogramming. Together, these data indicate that glucocorticoids drive a transcriptional program to coordinately regulate skeletal muscle mass loss and hepatic metabolism rewiring. The inhibition of this response by myostatin gene invalidation highlights the existence of a molecular dialog between skeletal muscle and liver
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Langley, Simon Cooke. "Central activity of glucocorticoids and glucocorticoid receptors in the genetically obese zucker rat (fa/fa)." Thesis, University of Southampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293839.

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Ayrout, Mohsen. "IMPACT DE L’HYPERCORTICISME SUR L’AXE GONADOTROPE FEMELLE." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS262/document.

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Le stress chronique apparait comme une cause importante de troubles de la fertilité chez la femelle. L’hypercorticisme (sécrétion excessive de glucocorticoïdes (GC) surrénaliens) induit par le stress agit sur l’axe de reproduction pour perturber le cycle œstrien et l’ovulation. Chez la femelle, l’axe de reproduction comprend 3 grandes structures : l’hypothalamus, l’hypophyse et l’ovaire. Pour bloquer l’activité de cet axe, les GC agissent via un récepteur spécifique (GR) pour induire une signalisation rapide non génomique et/ou une signalisation génomique tardive. Malgré de nombreuses recherches, les connaissances sur le mode d’action des GC sur cet axe restent fragmentaires. Au cours de ce travail de thèse, l’utilisation de différents modèles cellulaires et animaux nous a permis de mettre en évidence des mécanismes d’action des GC originaux sur l’axe hypothalamo-hypophysaire. Au niveau hypothalamique, nous avons décrit un nouveau dialogue entre les œstrogènes et les GC, qui favorise l’expression d’un neuropeptide hypothalamique inhibiteur, la dynorphine A. Ce neuropeptide pourrait ainsi participer au blocage des sécrétions pulsatiles de la GnRH (Gonadotropin-releasing Hormone) hypothalamique et des gonadotropines hypophysaires indispensables à l’ovulation. Au niveau hypophysaire, nous avons mis en évidence une action paradoxale des GC sur les cellules gonadotropes. En absence de GnRH, les GC stimulent une nouvelle voie de signalisation non génomique, initiée à la membrane plasmique par un GR palmitoylé. Cette signalisation rapide implique la calcium/calmoduline kinase II (CaMKII) ainsi qu’une de ses cibles, la synapsine-Ia. Néanmoins, en présence de GnRH, les GC bloquent la signalisation induite par la GnRH, en empêchant l’activation de la CaMKII, pouvant être à l’origine de l’inhibition de la sécrétion de la gonadotropine LH (Luteinizing Hormone).De nouvelles recherches sont à poursuivre pour approfondir nos connaissances sur les différents modes d’action des GC pouvant être spécifiquement mis en jeu au sein de chacune des cellules, et à l’origine des effets variés des GC au sein de l’organisme. Une meilleure compréhension des mécanismes moléculaires responsables de l’altération de la fertilité, en particulier durant un stress chronique, est essentielle pour envisager l’émergence de nouvelles cibles thérapeutiques innovantes
The chronic stress is an important cause of fertility disorders in female. Stress-induced hypercorticism (excessive secretion of glucocorticoids (GC)) acts on the reproductive axis to disrupt the estrous cycle and ovulation. In female, the reproductive axis comprises 3 structures: the hypothalamus, the pituitary and the ovary. To block the activity of this axis, GC act through a specific receptor (GR) to promote rapid non genomic and/or late genomic signaling. Despite extensive researches, knowledge on the mechanism of action of GC on this axis remains elusive. During my PhD, the use of different cellular and animal models allowed to highlight new mechanisms of GC actions on the hypothalamic-pituitary axis. At the hypothalamic level, we described a new genomic cross-talk between estrogen and GC to promote the expression of an inhibitory hypothalamic neuropeptide, dynorphin A. This neuropeptide could then participate in disrupting the pulsatile secretion of GnRH (Gonadotropin-releasing hormone) and pituitary gonadotropins which are essential for ovulation. At the pituitary level, we demonstrated a paradoxical action of GC on gonadotrope cells. In the absence of GnRH, GC stimulate a new non genomic pathway initiated at the plasma membrane through a palmitoylated GR. This rapid signaling involves calcium/calmodulin kinase II (CaMKII) as well as one of its targets, synapsin-Ia. Nevertheless, in the presence of GnRH, GC interfere with GnRH-induced signaling by preventing CaMKII activation, which may be responsible for the inhibition of LH (Luteinizing Hormone) release.Further researches are required to improve our knowledge on cell-specific mechanisms of action of GC that could explain the diversity of their activities. A better understanding of the molecular mechanisms responsible for fertility dysfunction, especially during chronic stress, is essential for the development of new and innovative therapeutic targets
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Leonelli, Carina. "Efeitos da corticoterapia pré-natal e durante a puberdade sobre a morfofisiologia do lobo ventral da próstata de ratos senis /." Botucatu, 2014. http://hdl.handle.net/11449/123262.

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Orientador: Sérgio Luiz Felisbino
Coorientador: Wellerson Rodrigo Scarano
Banca: Raquel Fantin Domeniconi
Banca: Luis Antonio Justulin Júnior
Banca: Renata Carolina Piffer
Banca: Glaura Scatamburio Alves Fernandes
Resumo: Estudos têm sugerido que o excesso de glicocorticoides (GCs) durante períodos críticos do desenvolvimento pode alterar a função reprodutiva. Apesar da função essencial da próstata no sucesso reprodutivo e de sua alta susceptibilidade ao desenvolvimento de lesões com o avançar da idade, o impacto tardio de corticoterapias precoces sobre a homeostase da glândula ainda é desconhecido. No presente estudo, investigamos os efeitos da corticoterapia prenatal (PRE), durante a instalação da puberdade (PU), e sua associação (PRE+PU=REE), sobre a morfofisiologia da próstata senescente. Ratas Wistar prenhes receberam betametasona (0.1mg/kg/dia, i.m.), ou salina, nos dias gestacionais 12, 13, 18 e 19. Os descendentes machos receberam doses de betametasona (7mg/kg/dia, gavage), ou salina, do dia pós-natal 35 ao 50 (PND35-50). Na idade senil (PND300), todos os animais foram eutanasiados, amostras de sangue foram coletadas para dosagens hormonais, e a próstata ventral (VP) foi dissecada e processada para a análise morfológica, bem como para quantificação e localização de proteínas (AR, GR, PAR-4 e PCNA). Reduzidos níveis de testosterona e insulina foram observados no grupo PRE, enquanto apenas a insulina mostrou-se reduzida no grupo PU, e nenhuma redução adicional foi observada em REE. Uma tendência de aumento no índice apoptótico e incidência de ácinos com epitélio metaplásico foi detectada dentre os grupos. A quantificação de proteínas revelou menor expressão de AR no grupo PRE, maior expressão do marcador de proliferação celular (PCNA) no grupo REE, porém, diferença significativa alguma foi observada na expressão do marcador de morte celular por apoptose (PAR-4). A análise da reação imunoistoquímica para o GR indicou uma maior expressão do receptor em células epiteliais dos grupos que receberam betametasona. Com base nos resultados, sugerimos que a corticoterapia com betametasona durante o final da ...
Abstract: Studies have suggested that glucocorticoids (GCs) excess during critical developmental time windows can alter reproductive parameters. Despite of the key function of the prostate in the reproductive success, and its high susceptibility to develop lesions in an age-dependent manner, the impact of early GCs excess on the gland homeostasis is still unknown. In the present study, we have investigated the effects of prenatal (PRE), peripubertal (PU) corticotherapy, and its combination (PRE+PU=REE), on aging prostate's morphophysiology. Pregnant Wistar rats received betamethasone (0.1mg/kg/day, i.m.), or saline, on the gestational days 12, 13, 18 and 19. Male descendents received betamethasone (7mg/kg/day, gavage), or saline, from 35th to 50th postnatal day (PND35-50). Late in life (PND300), all animals were euthanized, blood samples were taken for hormones levels estimation, and the ventral prostate (VP) was excised and processed for morphology evaluation, and for proteins (AR, GR, PAR-4 and PCNA) quantification and localization as well. Lower testosterone and insulin levels were detected in group PRE, while only insulin serum levels was reduced in group PU, and no additional decrease was seen in REE. An increasing trend in the apoptosis index and metaplastic epithelium acini incidence was observed along the treated groups. The protein quantifications showed a decreased AR expression in PRE, higher proliferation marker (PCNA) expression in REE, and no significant difference in the expression of the apoptosis marker PAR-4 was detected among the groups. The immunolocalization of GR indicated a higher receptor expression in epithelial cells of treated groups, when compared to NE. Based on these results, we suggest that the corticotherapy with betamethasone during late pregnancy can program fetal prostate, resulting in altered androgen and glucocorticoids signaling permanently. Peripubertal corticotherapy deflagrated cell ...
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Books on the topic "Glucocorticoids"

1

Goulding, Nicolas J., and Rod J. Flower, eds. Glucocorticoids. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1.

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Wolthers, Ole D. Exogenous glucocorticoids in paediatric asthma. Trivandrum: Transworld Research Network, 2007.

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Christian, Korting Hans, and Maibach Howard I, eds. Topical glucocorticoids with increased benefit/risk ratio. Basel: Karger, 1993.

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Pelt, Annemarie C. Glucocorticoids: Effects, action mechanisms, and therapeutic uses. Hauppauge, N.Y: Nova Science, 2011.

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Bujalska, Iwona. Glucocorticoids, 11 [beta]-hydroxysteroid dehydrogenase and obesity. Birmingham: University of Birmingham, 2000.

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Andrea, Giustina, Angeli Alberto, and Canalis Ernesto, eds. Glucocorticoid-induced osteoporosis. Basel: Karger, 2002.

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Society, Bone and Tooth. Glucocorticoid-induced osteoporosis: Guidelines for prevention and treatment. London: Royal College of Physicians, 2002.

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Fearon, Ursula. Factors involved in the regulation of human glucocorticoid and adrenal androgen production. Dublin: University College Dublin, 1996.

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Sternberg, Esther M., and Lewis L. Judd. Glucocorticoids and mood: Clinical manifestations, risk factors and molecular mechanisms. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2009.

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Erdeljan, Petar. Direct effects of glucocorticoids and serotonin on developing hippocampal cells. Ottawa: National Library of Canada, 2000.

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Book chapters on the topic "Glucocorticoids"

1

Goulding, Nicolas J., and Roderick J. Flower. "Glucocorticoid biology — a molecular maze and clinical challenge." In Glucocorticoids, 3–15. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_1.

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Toogood, John H. "Glucocorticoids and asthma." In Glucocorticoids, 161–73. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_10.

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Kirwan, John R. "Systemic glucocorticoids in chronic arthritis." In Glucocorticoids, 175–90. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_11.

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Baert, Filip J., and Paul R. Rutgeerts. "Glucocorticoids in the control of inflammatory bowel disease." In Glucocorticoids, 191–200. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_12.

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Munck, Allan. "Glucocorticoid biology — a historical perspective." In Glucocorticoids, 17–33. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_2.

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Parente, Luca. "The development of synthetic glucocorticoids." In Glucocorticoids, 35–51. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_3.

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Oakley, Robert H., and John A. Cidlowski. "The glucocorticoid receptor: expression, function, and regulation of glucocorticoid responsiveness." In Glucocorticoids, 55–80. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_4.

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Paliogianni, Fotini, and Dimitrios T. Boumpas. "Molecular and cellular aspects of cytokine regulation by glucocorticoids." In Glucocorticoids, 81–101. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_5.

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Pitzalis, Costantino, Niccoló Pipitone, and Mauro Perretti. "Glucocorticoids and leukocyte adhesion." In Glucocorticoids, 105–18. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_6.

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Croxtall, Jamie D. "Annexin I as a mediator of glucocorticoid action." In Glucocorticoids, 119–27. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8348-1_7.

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Conference papers on the topic "Glucocorticoids"

1

Adeel, Z., K. Kaczmarek, P. Ramos-Ramirez, and O. Tliba. "Non-Genomic Effects of Glucocorticoids Differentially Modulate Glucocorticoid Receptor Site-Specific Phosphorylation." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2375.

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Bansal, A., M. M. Mostafa, S. Shah, C. Kooi, R. Leigh, A. N. Gerber, and R. Newton. "Insights into Glucocorticoid Resistance: Synergy Between Glucocorticoids and Inflammatory Cytokines on TLR2 Expression." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7324.

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Djordjevic, Vera, Milena Despotovic, Ivana Stankovic, and Tatjana Jevtovic Stoimenov. "Association of ER22/23EK glucocorticoid receptor gene polymorphism with glucocorticoids dosage in COPD." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4400.

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Rider, Christopher F., Elizabeth M. King, S. L. Traves, Neil S. Holden, David Proud, Mark A. Giembycz, and Robert Newton. "Pro-Inflammatory Stimuli Reduce Glucocorticoid-Dependent Transcription: A Form Of Induced Resistance To Glucocorticoids." 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.a2129.

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Sekiyama, Akiko, Yasuhiro Gon, Masahiro Terakado, Ikuko Takeshita, Yutaka Kozu, Ken Matsumoto, and Shu Hashimoto. "Glucocorticoids Enhance Airway Epithelial Barrier Integrity." 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.a2818.

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Wang, G., X. Li, Z. Dou, W. Wang, and R. Liu. "AB0501 The association between glucocorticoids and damage accrual in patients with sle using glucocorticoid for long-term." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3931.

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Lehner, Eric, Arne Liebau, Karsten Mäder, and StefanK Plontke. "Intracochlear, biodegradable implants for controlled release of glucocorticoids." In 94th Annual Meeting German Society of Oto-Rhino-Laryngology, Head and Neck Surgery e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1767443.

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Fenton, C., C. Doig, S. Fareed, A. Naylor, C. Wehmeyer, C. Buckley, G. Lavery, M. Cooper, K. Raza, and R. Hardy. "OP0265 Local reactivation of glucocorticoids by 11Β-hydroxysteroid dehydrogenase type 1 mediates the development of glucocorticoid-induced bone loss." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3238.

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Safy, M., MJ De Hair, JW Jacobs, F. Buttgereit, MC Kraan, and JM van Laar. "AB0428 A systematic review on efficacy and safety of selective glucocorticoid receptor modulators in comparison to glucocorticoids in arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3254.

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Touma, Z., D. Gladman, J. Su, and M. Urowitz. "11 Development and initial validation of a novel lupus disease activity index to account for glucocorticoids: SLEDAI-2K glucocorticoids index (SGI)." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.11.

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Reports on the topic "Glucocorticoids"

1

Wang, Zuyi. Systems Biology of Glucocorticoids in Muscle Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada548681.

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Wang, Zuyi. CINRG: Systems Biology of Glucocorticoids in Muscle Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada575824.

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3

Mostov, Keith. Effects of FOS, JUN, TGF-B, Glucocorticoids on Polarized Membrane Traffic. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391573.

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4

zhang, yunkui, yuecheng yang, and jun zhang. Long-Term Outcomes after Use of Perioperative Glucocorticoids in Patients Undergoing Cancer Surgery. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2023. http://dx.doi.org/10.37766/inplasy2023.12.0015.

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Anheyer, Melanie, Holger Cramer, Thomas Ostermann, and Dennis Anheyer. Herbal medicine for atopic dermatitis – protocol of a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2023. http://dx.doi.org/10.37766/inplasy2023.4.0041.

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Abstract:
Review question / Objective: To evaluate the effectiveness of topical and systemic herbal medicine in patients with atopic dermatitis. Rationale: Atopic dermatitis is one of the most common skin diseases in both childhood and adulthood (1). Usually, the disease develops within the first year of life. In principle, all skin areas can be affected. However, there are age-dependent predilection sites (2). The diagnosis of atopic dermatitis is made clinically. Children and adults suffer primarily from the excruciating itching (1). As a result, atopic dermatitis not only affects quality of life, but also sleep, school, employment and social environment. The therapy includes a daily basic therapy with emollients. In acute episodes, topical glucocorticoids, in severe courses also systemically administered glucocorticoids or immunomodulators are used (1). Many parents and affected patients additionally use complementary and integrative medicine methods for various reasons (3, 4). Due to the increasing research in this field, an update of existing reviews is highly warranted. Therefore, this review aims to provide an overview of the current state of evidence in the overall field of both, topical and systemic herbal medicine.
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Wan, Yihong, and Steven K. Nordeen. The Identification of Genes Differentially Regulated by Progestins and Glucocorticoids in Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada406196.

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7

Maier, Steven F., and Matthew G. Frank. The Role of Glucocorticoids and Neuroinflammation in Mediating the Effects of Stress on Drug Abuse. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568600.

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Maier, Steven F., and Matthew Frank. The Role of Glucocorticoids and Neuroinflammation in Mediating the Effects of Stress on Drug Abuse. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada594247.

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Qiao, Wenxiao, Lihong Meng, Ye Zhang, Dian Li, Jingjing Chen, Jinyun Wang, Di Xie, and Xiaoming Xue. Safety and efficacy of glucocorticoids in the treatment of COVID-19: A meta-analysis of randomized control trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0074.

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10

Xu, Mingna, Zhaoqi Pan, Yunhai Tu, and Wencan Wu. Orbital Decompression versus Intravenous High-dose Glucocorticoids in Treatment for Dysthyroid Optic Neuropathy. A Systematic Review of the Literature. International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0005.

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