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Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Glucocorticoid resistance in Asthma"

1

Barnes, Peter J., Andrew P. Greening, and Graham K. Crompton. "Glucocorticoid Resistance in Asthma." American Journal of Respiratory and Critical Care Medicine 152, no. 6_pt_2 (December 1995): S125—S140. http://dx.doi.org/10.1164/ajrccm/152.6_pt_2.s125.

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2

Corrigan, Chris J., and Tak H. Lee. "Glucocorticoid Action and Resistance in Asthma." Allergology International 54, no. 2 (2005): 235–43. http://dx.doi.org/10.2332/allergolint.54.235.

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3

Keenan, Christine R., Michael J. Schuliga, and Alastair G. Stewart. "Pro-inflammatory mediators increase levels of the noncoding RNA GAS5 in airway smooth muscle and epithelial cells." Canadian Journal of Physiology and Pharmacology 93, no. 3 (March 2015): 203–6. http://dx.doi.org/10.1139/cjpp-2014-0391.

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The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway epithelial cells (AEC) play an important role in the pathogenesis and persistence of asthma and other chronic airways diseases. These airway structural cell types are also important cellular targets of the anti-inflammatory actions of glucocorticoids. In this study, we sought to examine the relevance of GAS5 to glucocorticoid sensitivity and resistance in ASM and AEC. We provide the first evidence that pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in AEC.
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4

Ito, Kazuhiro, Steve Getting, and Catherine Charron. "Mode of Glucocorticoid Actions in Airway Disease." Scientific World JOURNAL 6 (2006): 1750–69. http://dx.doi.org/10.1100/tsw.2006.274.

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Synthetic glucocorticoids are the most potent anti-inflammatory agents used to treat chronic inflammatory disease, such as asthma. However, a small number (<5%) of asthmatic patients and almost all patients with chronic obstructive pulmonary disease (COPD) do not respond well, or at all, to glucocorticoid therapy. If the molecular mechanism of glucocorticoid insensitivity is uncovered, it may in turn provide insight into the key mechanism of glucocorticoid action and allow a rational way to implement treatment regimens that restore glucocorticoid sensitivity. Glucocorticoids exert their effects by binding to a cytoplasmic glucocorticoid receptor (GR), which is subjected to post-translational modifications. Receptor phosphorylation, acetylation, nitrosylation, ubiquitinylation, and other modifications influence hormone binding, nuclear translocation, and protein half-life. Analysis of GR interactions to other molecules, such as coactivators or corepressors, may explain the genetic specificity of GR action. Priming with inflammatory cytokine or oxidative/nitrative stress is a mechanism for the glucocorticoid resistance observed in chronic inflammatory airway disease via reduction of corepressors or GR modification. Therapies targeting these aspects of the GR activation pathway may reverse glucocorticoid resistance in patients with glucocorticoid-insensitive airway disease and some patients with other inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease.
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5

Zein, Joe, Benjamin Gaston, Peter Bazeley, Mark D. DeBoer, Robert P. Igo, Eugene R. Bleecker, Deborah Meyers, et al. "HSD3B1 genotype identifies glucocorticoid responsiveness in severe asthma." Proceedings of the National Academy of Sciences 117, no. 4 (January 13, 2020): 2187–93. http://dx.doi.org/10.1073/pnas.1918819117.

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Asthma resistance to glucocorticoid treatment is a major health problem with unclear etiology. Glucocorticoids inhibit adrenal androgen production. However, androgens have potential benefits in asthma. HSD3B1 encodes for 3β-hydroxysteroid dehydrogenase-1 (3β-HSD1), which catalyzes peripheral conversion from adrenal dehydroepiandrosterone (DHEA) to potent androgens and has a germline missense-encoding polymorphism. The adrenal restrictive HSD3B1(1245A) allele limits conversion, whereas the adrenal permissive HSD3B1(1245C) allele increases DHEA metabolism to potent androgens. In the Severe Asthma Research Program (SARP) III cohort, we determined the association between DHEA-sulfate and percentage predicted forced expiratory volume in 1 s (FEV1PP). HSD3B1(1245) genotypes were assessed, and association between adrenal restrictive and adrenal permissive alleles and FEV1PP in patients with (GC) and without (noGC) daily oral glucocorticoid treatment was determined (n = 318). Validation was performed in a second cohort (SARP I&II; n = 184). DHEA-sulfate is associated with FEV1PP and is suppressed with GC treatment. GC patients homozygous for the adrenal restrictive genotype have lower FEV1PP compared with noGC patients (54.3% vs. 75.1%; P < 0.001). In patients with the homozygous adrenal permissive genotype, there was no FEV1PP difference in GC vs. noGC patients (73.4% vs. 78.9%; P = 0.39). Results were independently confirmed: FEV1PP for homozygous adrenal restrictive genotype in GC vs. noGC is 49.8 vs. 63.4 (P < 0.001), and for homozygous adrenal permissive genotype, it is 66.7 vs. 67.7 (P = 0.92). The adrenal restrictive HSD3B1(1245) genotype is associated with GC resistance. This effect appears to be driven by GC suppression of 3β-HSD1 substrate. Our results suggest opportunities for prediction of GC resistance and pharmacologic intervention.
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6

Wang, Alberta L., Ronald Panganiban, Weiliang Qiu, Alvin T. Kho, Geoffrey Chupp, Deborah A. Meyers, Eugene R. Bleecker, Scott T. Weiss, Quan Lu, and Kelan G. Tantisira. "Drug Repurposing to Treat Glucocorticoid Resistance in Asthma." Journal of Personalized Medicine 11, no. 3 (March 3, 2021): 175. http://dx.doi.org/10.3390/jpm11030175.

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Corticosteroid resistance causes significant morbidity in asthma, and drug repurposing may identify timely and cost-effective adjunctive treatments for corticosteroid resistance. In 95 subjects from the Childhood Asthma Management Program (CAMP) and 19 subjects from the Severe Asthma Research Program (SARP), corticosteroid response was measured by the change in percent predicted forced expiratory volume in one second (FEV1). In each cohort, differential gene expression analysis was performed comparing poor (resistant) responders, defined as those with zero to negative change in FEV1, to good responders, followed by Connectivity Map (CMap) analysis to identify inversely associated (i.e., negatively connected) drugs that reversed the gene expression profile of poor responders to resemble that of good responders. Mean connectivity scores weighted by sample size were calculated. The top five drug compound candidates underwent in vitro validation in NF-κB-based luciferase reporter A549 cells stimulated by IL-1β ± dexamethasone. In CAMP and SARP, 134 and 178 respective genes were differentially expressed in poor responders. CMap analysis identified 46 compounds in common across both cohorts with connectivity scores < −50. γ-linolenic acid, ampicillin, exemestane, brinzolamide, and INCA-6 were selected for functional validation. γ-linolenic acid, brinzolamide, and INCA-6 significantly reduced IL-1β induced luciferase activity and potentiated the anti-inflammatory effect of dexamethasone in A549/NF-κB-luc reporter cells. These results demonstrate how existing drugs, including γ-linolenic acid, brinzolamide, and INCA-6, may be repurposed to improve corticosteroid response in asthmatics.
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7

Ghiciuc, Cristina Mihaela, Andrei Gheorghe Vicovan, Celina Silvia Stafie, Sabina Antonela Antoniu, and Paraschiva Postolache. "Marine-Derived Compounds for the Potential Treatment of Glucocorticoid Resistance in Severe Asthma." Marine Drugs 19, no. 11 (October 20, 2021): 586. http://dx.doi.org/10.3390/md19110586.

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One of the challenges to the management of severe asthma is the poor therapeutic response to treatment with glucocorticosteroids. Compounds derived from marine sources have received increasing interest in recent years due to their prominent biologically active properties for biomedical applications, as well as their sustainability and safety for drug development. Based on the pathobiological features associated with glucocorticoid resistance in severe asthma, many studies have already described many glucocorticoid resistance mechanisms as potential therapeutic targets. On the other hand, in the last decade, many studies described the potentially anti-inflammatory effects of marine-derived biologically active compounds. Analyzing the underlying anti-inflammatory mechanisms of action for these marine-derived biologically active compounds, we observed some of the targeted pathogenic molecular mechanisms similar to those described in glucocorticoid (GC) resistant asthma. This article gathers the marine-derived compounds targeting pathogenic molecular mechanism involved in GC resistant asthma and provides a basis for the development of effective marine-derived drugs.
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8

Palumbo, María Laura, Andrés Prochnik, Miriam Ruth Wald, and Ana María Genaro. "Chronic Stress and Glucocorticoid Receptor Resistance in Asthma." Clinical Therapeutics 42, no. 6 (June 2020): 993–1006. http://dx.doi.org/10.1016/j.clinthera.2020.03.002.

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9

Matsumura, Yasuhiro. "Inflammation Induces Glucocorticoid Resistance in Patients with Bronchial Asthma." Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry 8, no. 4 (December 1, 2009): 377–86. http://dx.doi.org/10.2174/187152309789839055.

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10

Adcock, I. M., S. J. Lane, C. R. Brown, M. J. Peters, T. H. Lee, and P. J. Barnes. "Differences in binding of glucocorticoid receptor to DNA in steroid-resistant asthma." Journal of Immunology 154, no. 7 (April 1, 1995): 3500–3505. http://dx.doi.org/10.4049/jimmunol.154.7.3500.

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Abstract Although glucocorticosteroids are a very effective treatment for asthma and other chronic inflammatory diseases, a small proportion of patients are resistant to their therapeutic effects. The molecular mechanism for this steroid resistance is unclear. Steroid resistance cannot be explained by pharmacokinetic mechanisms, by a defect in the binding of steroids to glucocorticoid receptors, nor by defective nuclear translocation of this receptor, thereby suggesting that the molecular abnormality lies distal to nuclear translocation. We examined the ability of nuclear translocated glucocorticoid receptors to bind to their DNA binding sites (GRE) using electrophoretic mobility shift assays in PBMC from patients with steroid-sensitive and steroid-resistant asthma. The binding of the glucocorticoid receptor to DNA in these patients was also studied using Scatchard analysis. Dexamethasone induced a significant rapid and sustained twofold increase in GRE binding in PBMCs from steroid-sensitive asthmatic patients and nonasthmatic individuals, but this was markedly reduced in steroid-resistant asthmatic patients. Scatchard analysis of glucocorticoid receptor-GRE binding showed no change in binding affinity but did show a reduced number of receptors available for DNA binding in the steroid-resistant patients. These results suggest that the ability of the glucocorticoid receptor to bind to GRE is impaired in steroid-resistant patients because of a reduced number of receptors available for binding to DNA.
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Дисертації з теми "Glucocorticoid resistance in Asthma"

1

Matthews, John Graham. "The differential effects of glucocorticords in glucocorticoid-dependent asthma, glucocorticoid-resistant asthma and healthy subjects." Thesis, Imperial College London, 2006. http://hdl.handle.net/10044/1/8204.

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2

Lane, Stephen John. "Mechanism of glucocorticoid resistance in chronic bronchial asthma." Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300513.

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3

Loke, Tuck-Kay. "The cellular & molecular pathology of glucocorticoid resistant asthma." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430825.

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4

YAMAMOTO, MASAHIRO, YUTAKA OISO, MITSUYA MORIKAWA, SATOSHI KAKIYA, HISASHI YOKOI, ATSUSHI SUZUKI, and AKITOSHI KAWAKUBO. "A CASE OF PRIMARY GLUCOCORTICOID RESISTANCE." Nagoya University School of Medicine, 1995. http://hdl.handle.net/2237/16090.

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5

Hinds, Terry D. Jr. "Protein Phosphatase 5 and Glucocorticoid Receptor beta in Glucocorticoid Resistance and Lipogenesis." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1289929592.

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6

Jaffuel, Dany. "Corticothérapie et asthme : étude cellulaire de la transrépression du facteur de transcription AP-1 par le récepteur aux glucocorticoi͏̈des." Montpellier 1, 1997. http://www.theses.fr/1997MON11104.

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7

Gaffey, Kate. "Glucocorticoid resistance in COPD : the role of p38 MAPK." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-resistance-in-copd-the-role-of-p38-mapk(9c60954b-f891-4f8b-8004-825e6d173503).html.

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Chronic Obstructive Pulmonary Disease (COPD) is a chronic, inflammatory condition, characterised by airflow limitation. The use of glucocorticoids (GC) as an anti-inflammatory treatment in COPD has limited clinical benefits, and as such, new treatments are needed. Identifying key pathways involved in the inflammatory response in COPD may enable the development of novel treatments. The aims of this thesis were to examine the steroid sensitivity of an in vitro mixed sputum culture cell model, comparing COPD cells to smoking and non-smoking controls, examine expression of the intracellular signalling molecule p38 Mitogen Activated Protein Kinase (MAPK) in COPD lungs compared with controls, examine the GC and p38 MAPK inhibitor and dual therapy sensitivity of a bronchial epithelial cell line and finally, to understand the mechanisms by which a p38 MAPK inhibitor in combination with a GC synergistically inhibit pro-inflammatory mediator production in a bronchial epithelial cell line. Dexamethasone inhibits mixed sputum cell pro-inflammatory mediator release, with no differences in sensitivity observed between COPD and control cells. Isolated sputum neutrophils demonstrate modest sensitivity to dexamethasone, which is in contrast to blood neutrophils. There are increased numbers of cells positive for activated p38 MAPK in COPD lungs compared with controls, specifically localised to follicular B and CD8+ T cells, bronchial epithelial cells and alveolar and sputum macrophages. Lung and sputum neutrophils are devoid of activated p38 MAPK, and a pharmacological p38 MAPK inhibitor has no effect on pro-inflammatory mediator production from these cells. This is in contrast to blood neutrophils, whereby p38 MAPK activation can be induced following LPS stimulation and in vitro cell culture, and pro-inflammatory mediator release is inhibited by a p38 MAPK inhibitor. Dexamethasone and birb 796 inhibit stimulated pro-inflammatory mediator release from a bronchial epithelial cell line in a dose-dependent manner. Sensitivity to either drug is dependent on stimuli and the pro-inflammatory mediator analysed. There is additive and synergistic inhibition of pro-inflammatory mediator production when combination therapy comprising dexamethasone and birb 796 is used compared with either drug alone. This may be due to Birb 796 enhancing dexamethasone-mediated nuclear translocation of the glucocorticoid receptor, which may enhance the GC-mediated anti-inflammatory effects. Combination therapy may therefore be a useful therapeutic in the treatment of COPD.
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8

Kmyta, V. "Bcli polymorphism of glucocorticoid receptor gene in patients with bronchial asthma and obesity." Thesis, Sumy State University, 2015. http://essuir.sumdu.edu.ua/handle/123456789/40552.

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Certain investigations showed that genetic factors of bronchial asthma (BA) and obesity overlap each other, this indicates that they have common genetic predisposition. Thus, BA and obesity are associated with the genes, which encode β-adrenergic receptor, insulin-like growth factor, IL-1α, leukotriene A4 hydroxylase, glucocorticoid receptor (GR), uncoupling protein, etc.
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9

Butler, C. A. "Mechanisms of steroid resistance in therapy resistant asthma." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546017.

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10

Nixon, Mark. "Interactions between glucocorticoid metabolism and inflammation in obesity and insulin resistance." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5593.

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Inflammation plays a key role in the underlying pathogenesis of obesity and its associated health risks, with increased markers of inflammation evident in both liver and adipose tissue. In parallel, there is dysregulation of glucocorticoid metabolism in obesity, with increased adipose levels of the glucocorticoid-regenerating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) and increased hepatic levels of 5α-reductase type 1 (5αR1), which catalyses the reduction of glucocorticoids. Both the mechanisms and consequences of this glucocorticoid metabolism dysregulation remain unclear, however, there is evidence that it may be related to inflammation. In vitro studies have demonstrated that pro-inflammatory markers upregulate 11βHSD1 expression in adipocytes, potentially explaining increased expression of this enzyme in obesity. Previous work has also demonstrated that the glucocorticoid metabolites produced by 5αR1 lack the metabolic effects of the parent glucocorticoid, but retain its anti-inflammatory properties, indicating that increased expression of hepatic 5αR1 may serve to dampen down inflammation in the liver. The hypotheses addressed in this thesis are that in obesity, inflammation regulates adipose glucocorticoid metabolism through 11βHSD1, and that hepatic glucocorticoid metabolism regulates the inflammatory state of the liver through 5αR1. The role of inflammation in the regulation of 11βHSD1 was assessed in vivo in mice treated with the anti-inflammatory compound sodium salicylate (salicylate). In diet-induced obese mice, salicylate downregulated 11βHSD1 expression and activity selectively in visceral adipose tissue, alongside improved glucose tolerance, reduced plasma non-esterified fatty acids, and changes in adipose lipid metabolism. 11βHSD1-deficient mice fed a high-fat diet were resistant to the insulin sensitising effects of salicylate treatment. These results indicate a novel role for 11βHSD1 down-regulation in mediating the insulin sensitising effect of anti-inflammatory treatment. The mechanisms underpinning the anti-inflammatory properties of 5α-reduced glucocorticoids were explored in vitro and in vivo. In lipopolysaccharide-stimulated murine macrophages, both 5α-reduced glucocorticoid metabolites tested, namely 5α-dihydrocorticosterone (5αDHB) and 5α-tetrahydrocorticosterone (5αTHB), suppressed tumor necrosis factor-α (TNFα) and interleukin-6 (IL-6) release, although to a lesser extent than corticosterone (B). Similar to B, both 5αDHB and 5α THB suppressed phosphorylation of intra-cellular inflammatory signalling mitogen-activated protein kinases (MAPK) proteins c-Jun N-terminal kinase (JNK) and p38, as well as increasing protein expression of MAPK phosphatase-1 (MKP-1). Treatment of phorbol ester-stimulated HEK293 kidney cells with these 5α-metabolites revealed that 5αDHB suppressed nuclear factor κB (NFκB) and activator protein-1 (AP-1) activation to a similar extent to that of B, whilst 5αTHB increased activation of these pro-inflammatory transcription factors, indicating cell-specific effects of 5αTHB. In conclusion, reduced intra-adipose glucocorticoid regeneration by 11βHSD1 mediates the insulin sensitising effects of salicylate, suggesting that altered glucocorticoid metabolism may reflect altered intra-adipose inflammation in obesity. Furthermore, these data support the concept that this enzyme provides a therapeutic target in obesity-related metabolic disorders. 5α-reduced metabolites of glucocorticoids have similar anti-inflammatory properties to the parent glucocorticoid, indicating that the elevated hepatic levels of 5α-reductase in obesity may be a protective mechanism to limit the adverse metabolic effects of glucocorticoids upon the liver, but maintain the beneficial anti-inflammatory properties. These 5α-reduced glucocorticoid metabolites may provide a potential therapeutic treatment as selective glucocorticoid receptor modulators for inflammatory conditions.
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Книги з теми "Glucocorticoid resistance in Asthma"

1

Berger, William E. Allergy & asthma relief: Featuring the breathe easy plan : seven steps to allergen resistance. Pleasantville, N.Y: Reader's Digest Association, 2004.

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2

Stone, Doctor Daniel. Prednisone: The Glucocorticoid Medication Used to Decrease Inflammation in Conditions Such As Asthma, COPD and Rheumatologic Diseases. Independently Published, 2019.

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3

A, Kaliner Michael, and Barnes Peter J. 1946-, eds. The Airways, neural control in health and disease. New York: Dekker, 1988.

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4

Sentissi, Kinza, and Stephanie Yacoubian. Physiologic Airflow Disruption. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0017.

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Airflow disruption can be triggered through multiple mechanisms. The obstruction can stem from within the airway lumen, airway walls, or the tissues surrounding it. This section focuses on airflow disruption initiated by bronchospasm, obstructive lung disease, asthma and status asthmaticus. Bronchospasm presents with increased airway resistance secondary to airway hyperreactivity or anaphylaxis. Asthma and chronic obstructive pulmonary disease (COPD) are obstructive and inflammatory lung pathologies. Airflow disruption in asthma is reversible between exacerbations. The airway obstruction in COPD is not fully reversible. Status asthmaticus is the most severe presentation of asthma and can be life threatening. Poorly controlled obstructive lung disease can result in perioperative complications. Patients should therefore be medically optimized before undergoing operative procedures.
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5

Jayne, David. Treatment of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132.

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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Additional therapy with intravenous methylprednisolone and plasma exchange is employed in severe presentations with failing vital organ function. Drug toxicity contributes to comorbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem, with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn. Disease relapse occurs in 50% and requires early detection at a stage when it will not adversely affect outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator. Outcomes of vasculitis depend heavily on the level of tissue damage at diagnosis, especially renal dysfunction, but are also influenced by patient age, ANCA subtype, disease extent, and response to therapy. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)is treated along similar principles to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis but the persistence of steroid-dependent asthma in over one-third and differences in pathogenesis has suggested alternative treatment approaches. Chronic morbidity results from tissue damage and is especially common in the upper and lower respiratory tract and kidneys. Tracheobronchial disease is a severe late complication of GPA, while deafness, nasal obstruction, and chronic sinusitis are sequelae of nasal and ear vasculitis. Chronic infection of damaged epithelial surfaces acts as a drive for vasculitic activity and adequate infection control is necessary for stable remission. Chronic kidney disease can stabilize for many years but the risks of endstage renal disease (ESRD) are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful, with similar outcomes to other causes of ESRD.
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6

Prout, Jeremy, Tanya Jones, and Daniel Martin. Respiratory system. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0002.

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This chapter includes a summary of respiratory physiology, respiratory mechanics (pressure-volume relationships and compliance, airway resistance and the work of breathing) and the pulmonary circulation (pulmonary vascular resistance, shunt and lung zones). Measurement of respiratory flow, lung volumes and diffusion capacity is summarized, as well as measurement and interpretation of arterial blood gases. The physics behind capnography and pulse oximetry are explained with abnormalities related to clinical contexts. The common clinical scenarios of respiratory failure and asthma are discussed with initial management and resuscitation.
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7

Kreit, John W. Severe Obstructive Lung Disease. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0013.

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Although chronic obstructive lung disease, asthma, bronchiectasis, and bronchiolitis have very different causes, clinical features, and therapies, they share the same underlying pathophysiology. They are referred to as obstructive lung diseases because airway narrowing causes increased resistance and slowing of expiratory gas flow. Mechanical ventilation of patients with severe obstructive lung disease often produces two problems that must be recognized and effectively managed: over-ventilation and dynamic hyperinflation. Severe Obstructive Lung Disease reviews these two major adverse consequences of mechanical ventilation in patients with severe air flow obstruction. The chapter explains how to detect and correct both of these problems and provides guidelines for managing patients with respiratory failure caused by severe obstructive lung disease.
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8

Armstrong, Neil, and Willem van Mechelen, eds. Oxford Textbook of Children's Sport and Exercise Medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.001.0001.

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Comprehensive and up to date, this textbook on children’s sport and exercise medicine features research and practical experience of internationally recognized scientists and clinicians that informs and challenges readers. Four sections—Exercise Science, Exercise Medicine, Sport Science, and Sport Medicine—provide a critical, balanced, and thorough examination of each subject, and each chapter provides cross-references, bulleted summaries, and extensive reference lists. Exercise Science covers growth, biological maturation and development, and examines physiological responses to exercise in relation to chronological age, biological maturation, and sex. It analyses kinetic responses at exercise onset, scrutinizes responses to exercise during thermal stress, and evaluates how the sensations arising from exercise are detected and interpreted during youth. Exercise Medicine explores physical activity and fitness and critically reviews their role in young people’s health. It discusses assessment, promotion, and genetics of physical activity, and physical activity in relation to cardiovascular health, bone health, health behaviours, diabetes, asthma, congenital conditions, and physical/mental disability. Sport Science analyses youth sport, identifies challenges facing the young athlete, and discusses the physiological monitoring of the elite young athlete. It explores molecular exercise physiology and the potential role of genetics. It examines the evidence underpinning aerobic, high-intensity, resistance, speed, and agility training programmes, as well as effects of intensive or over-training during growth and maturation. Sport Medicine reviews the epidemiology, prevention, diagnosis, and management of injuries in physical education, contact sports, and non-contact sports. It also covers disordered eating, eating disorders, dietary supplementation, performance-enhancing drugs, and the protection of young athletes.
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Частини книг з теми "Glucocorticoid resistance in Asthma"

1

Wenzel, Sally E. "Glucocorticoid Insensitive Asthma." In Allergy Frontiers: Therapy and Prevention, 133–44. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-99362-9_8.

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2

van Rossum, Elisabeth F. C., and Steven W. J. Lamberts. "Glucocorticoid Resistance." In Cushing's Syndrome, 235–48. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-449-4_19.

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3

Nicolaides, Nicolas C., and Evangelia Charmandari. "Glucocorticoid Resistance." In Experientia Supplementum, 85–102. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-25905-1_6.

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4

Nicolaides, Nicolas C., and Evangelia Charmandari. "Glucocorticoid Resistance." In Practical Clinical Endocrinology, 367–71. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62011-0_36.

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5

Spahn, Joseph D., and Stanley J. Szefler. "Glucocorticoid Therapy in Asthma." In Allergic Diseases, 385–404. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-007-0_23.

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6

Barnes, P. J. "Glucocorticoids and Asthma." In Recent Advances in Glucocorticoid Receptor Action, 1–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04660-9_1.

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7

Malerba, M., G. Romanelli, and V. Grassi. "Glucocorticoid-Induced Osteoporosis in Asthma and Respiratory Diseases." In Glucocorticoid-Induced Osteoporosis, 86–93. Basel: KARGER, 2002. http://dx.doi.org/10.1159/000061075.

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8

Franchimont, Denis P., and George P. Chrousos. "Glucocorticoid Resistance and Hypersensitivity." In Hormone Resistance Syndromes, 259–71. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-698-0_14.

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9

Huizenga, Nannette A. T. M., and Steven W. J. Steven. "Syndromes of Glucocorticoid Resistance." In The Acth Axis: Pathogenesis, Diagnosis and Treatment, 307–27. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0501-3_15.

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10

Fukunaga, Koichi. "Corticosteroid Resistance in Asthma." In Advances in Asthma, 53–61. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2790-2_5.

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Тези доповідей конференцій з теми "Glucocorticoid resistance in Asthma"

1

Martins, MA, E. Vallota, PM Silva, RS Cordeiro, and MF Serra. "A Short-Term Murine Model of Asthma Marked by Resistance to Glucocorticoid Therapy." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4274.

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2

Butler, Claire A., Stephen McQuaid, Timothy Warke, Gregorz Skibinski, Michael Stevenson, Lorcan McGarvey, and Liam G. Heaney. "Glucocorticoid Receptor Beta And Histone Deacetylase 2 Airway Expression Are Increased In Therapy Resistant Asthma." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2751.

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3

Mori, Akio, Satoshi Kouyama, Miyako Yamaguchi, Chiemi Kumitani, Akemi Ohtomo-Abe, Yuto Nakamura, Yasuhiro Tomita, et al. "CTLA4-Ig enhanced glucocorticoid effect on murine asthma." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1148.

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4

Zijlstra, Jan, Fatemeh Fattahi, Dennie Rozeveld, Nick ten Hacken, Machteld N. Hylkema, Antoon van Oosterhout, and Irene H. Heijink. "Glucocorticoid-Induced CCL20 Production By Airway Epithelium; Role In Glucocorticoid Insensitive Neutrophilic Inflammation In Asthma?" In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1408.

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5

Gaston, B. M., N. Sharifi, P. Bazeley, M. Deboer, E. R. Bleecker, D. A. Meyers, S. A. A. Comhair, et al. "Androgen Metabolism and Severe Asthma: HSD3B1 Genotype Identifies Glucocorticoid Responsiveness." 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.a7393.

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6

Kan, M., C. Koziol-White, M. Shumyatcher, M. Johnson, W. Jester, R. A. Panettieri, and B. E. Himes. "Airway Smooth Muscle-Specific Transcriptomic Signatures of Glucocorticoid Exposure in Asthma and Non-Asthma Donors." 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.a2959.

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7

Dalin, Simona, Boyang Zhao, and Michael T. Hemann. "Abstract 35: Evolution of resistance to glucocorticoid receptor agonists." In Abstracts: AACR Precision Medicine Series: Integrating Clinical Genomics and Cancer Therapy; June 13-16, 2015; Salt Lake City, UT. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.pmsclingen15-35.

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8

Chen, Zhihong, Jin Bi, Zhihui Min, and Chunling Du. "PI3K inhibitor add-on strategy improve glucocorticoid insensitivity in severe asthma." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2906.

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9

Bantulà Fonts, Marina, Jordi Roca-Ferrer, César Picado, Irina Bobolea, Antonio Valero, Joaquim Mullol, Joan Bartra, and Ebymar Arismendi. "Asthma and severe obesity: glucocorticoid sensitivity before and after bariatric surgery." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2364.

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10

Jackson, David, Cris Roxas, Louise Thompson, Mariana Fernandes, Linda Green, Joanne Kavanagh, Alexandra Nanzer-Kelly, Grainne D’Ancona, and Brian Kent. "Real-world oral glucocorticoid-sparing effect of benralizumab in severe asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2527.

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