Relevant bibliographies by topics / Glucocorticoids inhibitors

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Glucocorticoids inhibitors'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Glucocorticoids inhibitors"

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Mann, Cynthia L., and John A. Cidlowski. "Glucocorticoids Regulate Plasma Membrane Potential During Rat Thymocyte Apoptosis in Vivo and in Vitro." Endocrinology 142, no. 1 (2001): 421–29. http://dx.doi.org/10.1210/endo.142.1.7904.

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Abstract Glucocorticoids induce a series of profound biochemical changes in thymocytes that initiate apoptosis; however, the pathways beyond receptor transactivation that lead to this form of cell death are not fully understood. In this study, we report a novel site of action for glucocorticoids at the site of the plasma membrane. Specifically, we find that glucocorticoids induce the loss of plasma membrane potential both in vivo and in vitro. The glucocorticoid-induced loss of plasma membrane potential in cultured primary isolated rat thymocytes was both dose and time dependent. Other steroid
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Hulleman, Esther, Karin M. Kazemier, Amy Holleman, et al. "Inhibition of glycolysis modulates prednisolone resistance in acute lymphoblastic leukemia cells." Blood 113, no. 9 (2009): 2014–21. http://dx.doi.org/10.1182/blood-2008-05-157842.

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Treatment failure in pediatric acute lymphoblastic leukemia (ALL) is related to cellular resistance to glucocorticoids (eg, prednisolone). Recently, we demonstrated that genes associated with glucose metabolism are differentially expressed between prednisolone-sensitive and prednisolone-resistant precursor B-lineage leukemic patients. Here, we show that prednisolone resistance is associated with increased glucose consumption and that inhibition of glycolysis sensitizes prednisolone-resistant ALL cell lines to glucocorticoids. Treatment of prednisolone-resistant Jurkat and Molt4 cells with 2-de
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Shah, O. Jameel, Scot R. Kimball, and Leonard S. Jefferson. "Glucocorticoids abate p70S6k and eIF4E function in L6 skeletal myoblasts." American Journal of Physiology-Endocrinology and Metabolism 279, no. 1 (2000): E74—E82. http://dx.doi.org/10.1152/ajpendo.2000.279.1.e74.

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The catabolic properties of glucocorticoid hormones are largely attributable to dual regulation of protein degradation and synthesis. With regard to the latter, glucocorticoids modulate the translational machinery, namely that component functional in translation initiation. This investigation revealed that in L6 myoblasts, dexamethasone, a synthetic glucocorticoid, deactivated the ribosomal protein S6 kinase (p70S6k) within 4 h, as evidenced by diminished phosphorylation of its physiological substrate, the 40S ribosomal protein S6. This deactivation correlated with dephosphorylation of p70S6k
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Diaz-Jimenez, David, Maria Grazia Petrillo, Jonathan T. Busada, Marcela A. Hermoso, and John A. Cidlowski. "Glucocorticoids mobilize macrophages by transcriptionally up-regulating the exopeptidase DPP4." Journal of Biological Chemistry 295, no. 10 (2020): 3213–27. http://dx.doi.org/10.1074/jbc.ra119.010894.

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Glucocorticoids are potent endogenous anti-inflammatory molecules, and their cognate receptor, glucocorticoid receptor (GR), is expressed in nearly all immune cells. Macrophages are heterogeneous immune cells having a central role in both tissue homeostasis and inflammation and also play a role in the pathogenesis of some inflammatory diseases. Paradoxically, glucocorticoids have only a limited efficacy in controlling the resolution of these macrophage-related diseases. Here, we report that the transcriptomes of monocyte-like THP-1 cells and macrophage-like THP-1 cells (THP1-MΦ) have largely c
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Nuralieva, N. F., M. Yu Yukina, and E. A. Troshina. "Secondary Adrenal Insufficiency: New Aspects of Diagnosis and Therapy." Doctor.Ru 20, no. 2 (2021): 51–59. http://dx.doi.org/10.31550/1727-2378-2021-20-2-51-59.

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Objective of the Review: To discuss the current idea of the aetiology, diagnosis and management of secondary adrenal insufficiency (SAI). Key Points. The article describes key causes of the disease, including iatrogenic causes, discusses the widely studied effect of adrenocorticotropic hormone suppression by glucocorticoids and a lesser studied autoimmune hypophysitis induced by check point inhibitors. Special aspects of SAI diagnosis, principles of replacement therapy and cases of unjustified glucocorticoids prescription are given in detail. Risk classification for disease development if gluc
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Stebbing, Justin, and Volker M. Lauschke. "JAK Inhibitors — More Than Just Glucocorticoids." New England Journal of Medicine 385, no. 5 (2021): 463–65. http://dx.doi.org/10.1056/nejme2108667.

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Schlis, Krysta D., Matthew Stubbs, Daniel J. DeAngelo, et al. "A Pilot Trial of Rapamycin with Glucocorticoids In Children and Adults with Relapsed ALL." Blood 116, no. 21 (2010): 3244. http://dx.doi.org/10.1182/blood.v116.21.3244.3244.

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Abstract Abstract 3244 Background: The mammalian target of rapamycin (mTOR) has been identified as a potential therapeutic target in acute lymphoblastic leukemia (ALL). Of particular interest is the potential for mTOR inhibitors to reverse lymphoblast resistance to glucocorticoids. Multiple studies have demonstrated that resistance of lymphoblasts to glucocorticoids, both in vitro and in vivo, predicts a poor clinical outcome in ALL. We have previously demonstrated that rapamycin can reverse glucocorticoid resistance in vitro via suppression of the anti-apoptotic protein MCL-1. Based on this p
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Chadwick, Jessica A., Sayak Bhattacharya, Jeovanna Lowe, Noah Weisleder, and Jill A. Rafael-Fortney. "Renin-angiotensin-aldosterone system inhibitors improve membrane stability and change gene-expression profiles in dystrophic skeletal muscles." American Journal of Physiology-Cell Physiology 312, no. 2 (2017): C155—C168. http://dx.doi.org/10.1152/ajpcell.00269.2016.

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Angiotensin-converting enzyme inhibitors (ACEi) and mineralocorticoid receptor (MR) antagonists are FDA-approved drugs that inhibit the renin-angiotensin-aldosterone system (RAAS) and are used to treat heart failure. Combined treatment with the ACEi lisinopril and the nonspecific MR antagonist spironolactone surprisingly improves skeletal muscle, in addition to heart function and pathology in a Duchenne muscular dystrophy (DMD) mouse model. We recently demonstrated that MR is present in all limb and respiratory muscles and functions as a steroid hormone receptor in differentiated normal human
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Lerner, Adam, John A. Meyers, Josephine A. Taverna, and Anthony Makkinje. "PDE4 Inhibitors Augment Glucocorticoid Receptor Levels in B-CLL Cells but Not in T Cells, B Cells, Monocytes or Neutrophils." Blood 108, no. 11 (2006): 2608. http://dx.doi.org/10.1182/blood.v108.11.2608.2608.

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Abstract cAMP analogues have long been known to induce apoptosis in specific lymphoid subsets and to augment the apoptotic effect of glucocorticoids. However, a clinically feasible means by which to take advantage of these effects for the treatment of lymphoid malignancies has not previously been identified. Inhibition of type 4 cAMP phosphodiesterases (PDE4) activates cAMP-mediated signaling in many cell types and several PDE4 inhibitors are currently in clinical trials for inflammatory illnesses such as asthma, COPD and psoriasis. We have previously reported that PDE4 inhibitors induce apopt
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Mao, Xinliang, A. Keith Stewart, Rose Hurren, et al. "A Chemical Biology Screen Identifies Glucocorticoids as Inhibitors of C-Maf and C-Maf-Dependent Transactivation of Cyclin D2." Blood 108, no. 11 (2006): 368. http://dx.doi.org/10.1182/blood.v108.11.368.368.

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Abstract The oncogene c-maf is frequently over-expressed in multiple myeloma cell lines and patient samples and contributes to increased cellular proliferation in part by inducing cyclin D2 expression. Therefore, small molecules that inhibit c-maf and its targets could be useful chemical probes to better understand the role and regulation of this protein. We developed a high throughput chemical screen in NIH 3T3 cells stably over-expressing the promoter of the c-maf target cyclin D2 driving firefly luciferase. From a screen of 2400 off-patent drugs and chemicals, we identified 32 compounds tha
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Dissertations / Theses on the topic "Glucocorticoids inhibitors"

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Varis, Tiina. "Studies on drug interactions between CYP3A4 inhibitors and glucocorticoids." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/varis/.

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Crocker, Irene Caroline Evenbly. "Studies on the modulation of phosphodiesterase activity in human T lymphocytes." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284579.

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Golding, Lauren Ashley. "Regulation of SGK1 Gene Promoter Activity by Glucocorticoids and Histone Deacetylase Inhibitors." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144357.

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Edwall, Dan. "Insulin-like growth factor-I in tissue regeneration and growth control." Stockholm : Karolinska Institute, 1993. http://catalog.hathitrust.org/api/volumes/oclc/28296811.html.

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RAMBAL, ANILA. "ROLE OF BCL-2 FAMILY MEMBERS TO PROMOTE GLUCOCORTICOID –INDUCED APOPTOSIS BY MEK INHIBITORS IN LEUKEMIC CELLS." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1790.

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Glucocorticoids (GC) are common components of many chemotherapeutic regimens for lymphoid malignancies. GC-induced apoptosis involves an intrinsic BCL-2 family-regulated pathway. It has been shown that BIM (BCL-2 interacting mediator of cell death), a BH3-only pro-apoptotic protein, is up-regulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia (ALL) cells. Furthermore, BIM is inactivated by extracellular signal-regulated kinase (ERK)-mediated phosphorylation. We therefore hypothesized co-treatment with Dex and MEK/ERK inhibitors would promote apoptosis in ALL cells throu
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Gagne, Didier. "Antiglucocorticoi͏̈des purs et partiels : mécanisme d'action, paramètres impliqués dans la réponse glucocorticoi͏̈de." Montpellier 2, 1988. http://www.theses.fr/1988MON20111.

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Malouitre, Sylvanie Désirée Marie. "Glucocorticoid receptor function, interactions with oestrogen receptors and a steroid inhibitor." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413737.

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Scheimann, Jessie R. "Sex Differences in the Role of Glucocorticoid Receptors in Excitatory vs Inhibitory Neurons." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1554213356486937.

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Samuelsson, Magnus. "p57Kip2, a glucocorticoid-induced CDK inhibitor, involved in cell proliferation, apoptosis and differentiation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-382-1/.

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Powell, Nicole Damico. "Immunomodulation of experimental autoimmune encephalomyelitis targeting the autoreactive T cell and the cytokine macrophage migration inhibitory factor /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141052089.

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Books on the topic "Glucocorticoids inhibitors"

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Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: hormone and cytokine treatments. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0007.

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The antidepressant and neuroprotective effects of oestradiol are described. Psychiatric consequences of oophorectomy, and treatment with tamoxifen and aromatase inhibitors, are then discussed. Androgen-deprivation therapy has temporary effects on cognitive function and mood that reflect the distribution of androgen receptors in the brain. The rapid-onset adverse psychiatric effects of high-dose glucocorticoids are presented (including ‘steroid psychosis’) and a novel, non-genomic molecular mechanism highlighted. In contrast, the depressive effect of chronic glucocorticoid use is then considere
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Shepherd, Angela J., and Juliet M. Mckee. Osteoporosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0015.

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Osteoporotic fractures are major causes of suffering and death. Dual-energy x-ray absorptiometry (DEXA) is the standard of care for diagnosis (T-score ≤ –2.5) of osteoporosis. Prevention of fractures requires addressing bone and muscle strength and balance. Physical exercise, good nutrition (fruits, vegetables, adequate calcium), adequate vitamin intake (C, D, and K), tobacco cessation, and no more than moderate alcohol intake enhance bone health and decrease fracture risk. Long-term treatment with glucocorticoids, certain drugs used in breast or prostate cancer treatment, and proton pump inhi
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McCulloh, Russell J., and Steven M. Opal. Drug-induced depression of immunity in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0290.

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Immunosuppressive drugs are among the fastest-growing category of drugs in medicine today, both in terms of new medication development and in terms of use. Glucocorticoids, calcineurin inhibitors, and biological agents, among others, are used in a variety of diseases. . Although often of great benefit to patients, immunosuppressive agents also pose significant long-term risks for opportunistic infection. These drugs can also blunt normal host responses to infection, and patients receiving immunosuppressive medications are at high risk for severe illness, sepsis, and death from opportunistic in
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Lahita, Robert, J. W. J. Bijlsma, Alfonse Masi, and Rainer Straub. Basic and Clinical Aspects of Neuroendocrine Immunology in Rheumatic Diseases (Annals of the New York Academy of Sciences). Blackwell Publishing Limited, 2006.

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M, Cutolo, and New York Academy of Sciences., eds. Basic and clinical aspects of neuroendocrine immunology in rheumatic diseases. Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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Herman, James P. Limbic Pathways to Stress Control. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0008.

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Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala
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Book chapters on the topic "Glucocorticoids inhibitors"

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Chuah, Sai Yee, and Boon Kee Goh. "Topical Glucocorticoids, Topical Calcineurin Inhibitors, and Topical Vitamin D3 Analogs." In Vitiligo. John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781118937303.ch16.

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Di Rosa, Massimo. "The Role of Glucocorticoid-Induced Phospholipase Inhibitory Proteins." In Drugs Affecting Leukotrienes and Other Eicosanoid Pathways. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-7841-9_25.

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Ito, Kodo, Kenichi Yamada, Setsuko Yoshida, Keiji Hasunuma, Yasushi Tamura, and Sho Yoshida. "Endogenous Kallikrein Inhibitor in Rat Kidney Cortex-Effect of Glucocorticoid Administration." In Kinins IV. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5143-6_49.

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Lukić, M. L., S. Stošić-Grujičić, Dj Lalošević, and S. Vukmanović. "Immunoregulation in Epidermis: Glucocorticoids Induced Epidermal Cell Derived Inhibitor of Interleukin 1 Activity." In Advances in Experimental Medicine and Biology. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5535-9_124.

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Østensen, Monika, and Ian Giles. "Adjustment of therapy before/during pregnancy and lactation." In Practical management of the pregnant patient with rheumatic disease, edited by Karen Schreiber, Eliza Chakravarty, and Monika Østensen. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198845096.003.0007.

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Treatment with medications during pregnancy and lactation is a challenge and needs to balance the risk of untreated maternal disease against any possible harm to the foetus or child. Indications for treatment are control of disease activity and ensuring a healthy pregnancy and healthy child outcomes. Administration of the following drugs is compatible with pregnancy: non-steroidal anti-inflammatory drugs (non-selective COX inhibitors until gestational week 32), glucocorticoids (preferentially at low dose), antimalarials, sulfasalazine, azathioprine (AZA), cyclosporine, tacrolimus, colchicine, and intravenous immunoglobulin. Methotrexate, mycophenolate mofetil, and cyclophosphamide require discontinuation before conception due to proven teratogenicity. Among biologics tumour necrosis factor (TNF) inhibitors are best studied and appear reasonably safe preconceptionally, during pregnancy, and lactation; for other biologics foetal safety has not yet been established. The pregnancy compatibility of medications administered for comorbidities must be assessed. Except for cyclophosphamide other immunosuppressives are compatible with fatherhood.
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Clerkin, Kevin J., and Maryjane A. Farr. "Orthotopic Heart Transplant Rejection and Immunosuppression." In Cardiothoracic Critical Care. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190082482.003.0026.

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This chapter focuses on orthotopic heart transplant rejection. Hyperacute rejection is a catastrophic complication that occurs early post-transplantation. This type of rejection is most often due to pre-formed donor-specific anti–human leukocyte antigen antibodies or an ABO blood type mismatch and is rarely seen in the current era because pre-transplant virtual and prospective crossmatch has become routine practice. Meanwhile, immune activation of recipient T cells against the cardiac allograft causes acute cellular rejection (ACR). Treatment of ACR will vary depending on the grade of rejection, symptoms, and hemodynamic significance. On the other hand, antibody-mediated rejection (AMR), previously known as humoral or vascular rejection, is primarily mediated by antibodies and not T cells, as in ACR. AMR is difficult to treat because it may persist or be recurrent and is associated with an increased risk of cardiac allograft vasculopathy and mortality. The chapter then discusses the management of acute rejection. Induction therapy is augmented immunosuppression in the early period following heart transplantation, when the recipient is at the greatest risk of rejection. Maintenance immunosuppression includes calcineurin inhibitors, anti-metabolites, glucocorticoids, and proliferation signal inhibitors.
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Baker, Kenneth F., and John D. Isaacs. "Rheumatoid arthritis." In Oxford Textbook of Medicine, edited by Richard A. Watts. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0446.

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Rheumatoid arthritis is a common autoimmune disease characterized by both synovial and systemic inflammation. Synovitis classically presents as a symmetrical destructive polyarthritis affecting the hands and feet typified by episodic pain, stiffness, and swelling. Systemic inflammation leads to a range of extra-articular manifestations including organ involvement (e.g. interstitial lung disease, scleritis), constitutional features (e.g. fatigue, depression) and other complications (e.g. accelerated atherosclerosis, nerve and spinal cord compression). Rheumatoid arthritis is a clinical diagnosis based largely upon history and examination, supported by a limited range of investigation findings including elevated acute-phase reactants, autoantibodies (rheumatoid factor and anti-citrullinated peptide antibody), and imaging (e.g. musculoskeletal ultrasound). If left untreated, patients can rapidly develop irreversible joint damage leading to chronic pain, deformity, disability, and premature mortality. However, with early initiation of disease-modifying anti-rheumatic drugs (DMARDs) in treat-to-target strategies, disease remission is now achievable for many patients. Conventional synthetic DMARDs are the anchor of rheumatoid arthritis therapy, with methotrexate the recommended first choice. Biological DMARDs (monoclonal antibodies and soluble receptors) and targeted synthetic DMARDs (Janus kinase inhibitors) are reserved as second-line agents. Glucocorticoids are helpful as bridging therapy, though their considerable side effect profile prohibits their use as maintenance therapy. Non-steroidal anti-inflammatory drugs (NSAIDs) are effective in relieving arthritis pain, but long-term use is limited by their potential cardiovascular, renal, and gastrointestinal toxicities. With optimal care from a multidisciplinary team, many patients achieve and retain disease remission with maintenance of employment and quality of life.
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Wahbi, Karim. "The heart in neuromuscular disease: Duchenne and limb girdle muscular dystrophies." In ESC CardioMed. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0371.

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Duchenne muscular dystrophy (DMD), the most common muscular disease, is caused by out-of-frame mutations in the dystrophin gene. Dilated cardiomyopathy is the most frequent cardiac presentation of the disease, with a prevalence increasing with age—it is uncommon before the age of 10 years and present in up to 80% after 18 years. Heart failure represents nowadays the leading cause of death in DMD. Electrocardiography and echocardiography are recommended at diagnosis and then every 2 years until 10 years of age and yearly after. Angiotensin-converting enzyme inhibitors are widely prescribed before left ventricular dysfunction is detected, generally before 10 years of age, with an indication supported by the results of a randomized trial showing a benefit in terms of prevention of systolic dysfunction and survival. Beta-adrenergic blockers and eplerenone are also promising medications for this indication, but additional studies are warranted to determine their benefit. Glucocorticoids, which are currently recommended in patients with DMD who are 5 years of age or older to protect muscular and pulmonary function, could also improve left ventricular function and long-term cardiac prognosis. An implantable cardioverter defibrillator and mechanical circulatory support can be indicated in selected patients. The term limb girdle muscular dystrophy encompasses a heterogeneous group of muscular dystrophies involving more than 30 genes and various prevalence and severity of cardiac disease, mostly dilated cardiomyopathy. Electrocardiography and echocardiography are recommended at diagnosis and thereafter according to initial findings and genetic diagnosis. Heart failure management should follow the same criteria as for the other forms of dilated cardiomyopathy.
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Liu, Y., A. Kiss, R. MacGregor, and G. Aguilera. "Differential Inhibitory Effects of Glucocorticoids on CRH and POMC Transcription." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p13.p1-619.

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Litwack, Gerald, Noreen M. Robertson, Andrew B. Maksymowych, and Mahmut Celiker. "Vitamin B6 and Other Inhibitors of Glucocorticoid Receptor Function and Cell Death of B16 Melanoma Cells." In Vitamins and Minerals in the Prevention and Treatment of Cancer. CRC Press, 2018. http://dx.doi.org/10.1201/9781351077590-2.

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Conference papers on the topic "Glucocorticoids inhibitors"

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Hafthorsdottir, R., AL Gunnarsdottir, TJ Love, G. Gerdur та B. Gudbjornsson. "NP-009 The impact of TNFα inhibitors on glucocorticoids use among patients with arthridis". У 25th EAHP Congress, 25th–27th March 2020, Gothenburg, Sweden. British Medical Journal Publishing Group, 2020. http://dx.doi.org/10.1136/ejhpharm-2020-eahpconf.467.

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Gebru, Melat Tsegaye, Hong-Gang Wang, and Jennifer Xavier. "Abstract 637: Glucocorticoids act synergistically with FLT3 inhibitors to enhance cell death in FLT3 mutant acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-637.

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Andreasen, P. A., A. Riccio, L. R. Lund, K. G. Welinder, F. Blasi, and K. Danø. "PLASMINOGEN ACTIVATOR INHIBITOR TYPE 1: STUDIES ON STRUCTURE AND REGULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642810.

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Human plasminogen activator inhibitor type-1 is an Mr∼54,000 protein which specifically inhibits urokinase-type (u-PA) and tissue-type (t-PA) plasminogen activators. During inhibition, u-PA and t-PA convert PAI-1 to an inactive form with Mr∼50,000. We have determined the amino-terminal amino acid sequence of native and converted PAI-1, and isolated and partly sequenced PAI-1 cDNA. The data show that the conversion of PAI-1 consists of cleavage of an Arg-Met bond 33 residues from the carboxy-terminus, thus localizing the reactive center of the inhibitor to that position, and identifying PAI-1 a
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Medcalf, R. L., E. van den Berg, and W.-D. Schleuning. "THE INFLUENCE OF GLUCOCORTICOID HORMONES ON THE GENE TRANSCRIPTION OF POUR COMPONENTS OF THE FIBRINOLYTIC SYSTEM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644611.

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The hormonal regulation of plasminogen activator (urokinase type (u-PA) and tissue-type (t-PA)) biosynthesis plays an important role in fibrinolysis and extracellular matrix turnover during invasive growth and cell migration. Recently, two genetically distinct inhibitors of both PA's (PA inhibitor 1 (PAI-1) and PA inhibitor 2 (PAI-2)) have been described which may contribute to the modulation of matrix stability. We have employed cloned cDNA probes to study the regulation of biosynthesis of these proteins in the human fibrosarcoma line HT1080. These cells constitutively express high levels of
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Gu, Wenwen, Bongsu Kim, and Yi Zhao. "Exploring Electrical Impedance Spectroscopy as an Innovative Tool for On-Chip Analysis of Human Trabecular Meshwork." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-40785.

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This work reports the investigation of in vitro cultured human trabecular meshwork (TM) using electric impedance spectroscopy. The outflow facility of aqueous humor contains a three-dimensional network composed of TM endothelial cells and the extracellular matrix (ECM). The network is a critical determinant of intraocular pressure (IOP), the increase of which is the main cause of primary open angle glaucoma (POAG). Electric impedance spectroscopy was chosen over other technologies for on-chip TM cell study because of its non-invasive and label-free natures as well as the ease of on-chip integr
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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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Kadushkin, Aliaksei, Anatoli Tahanovich, Anastasiya Arabey, Liudmila Shishlo, Andrei Savchanka, and Liudmila Movchan. "Prognosis of glucocorticoid response in patients with acute exacerbation of COPD using macrophage migration inhibitory factor." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp105.

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Matsukura, Satoshi, Masatsugu Kurokawa, Tetsuya Homma, Mio Kawaguchi, and Mitsuru Adachi. "Mechanisms Of Glucocorticoid's Inhibitory Effects On The Expression Of Inflammatory Chemokines Induced By DsRNA In Airway Epithelial Cells." 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.a2130.

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Lim, WonChung, and YoungJoo Lee. "Abstract B29: GILZ mediates glucocorticoid action and inhibits hypoxia-induced COX-2 expression in A549 cells." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b29.

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Pankov, Aleksandr, Haiying Zhou, Shravani Barkund, et al. "Abstract 4120: ORIC-101 comprehensively inhibits glucocorticoid pathways to overcome therapeutic resistance in pan-cancer models." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4120.

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