Log in

Relevant bibliographies by topics / Glucocorticoids inhibitors / Journal articles

To see the other types of publications on this topic, follow the link: Glucocorticoids inhibitors.

Journal articles on the topic 'Glucocorticoids inhibitors'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Glucocorticoids inhibitors.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

8

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

10

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

11

Mao, Xinliang, A. Keith Stewart, Alessandro Datti, and Aaron D. Schimmer. "A High Throughput Seeking Myeloma Therapeutics Identifies Glucocorticoids as Inhibitors of c-Maf-Dependent Transactivation of Cyclin D2." Blood 106, no. 11 (2005): 3384. http://dx.doi.org/10.1182/blood.v106.11.3384.3384.

Full text

Abstract:

Abstract c-Maf is a transcription factor that regulates expression of several genes including cyclin D2. c-Maf and cyclin D2 are frequently over expressed in multiple myeloma and associated with chemoresistance and poor clinical outcome. Therefore, molecules that inhibit c-Maf-dependent transactivation of cyclin D2 may be important biological tools to understand the pathogenesis of myeloma and could be therapeutically useful. To identify such compounds, we devised a high throughput screen in NIH3T3 cells. NIH3T3 cells over expressing c-Maf and the cyclin D2 promoter-driving luciferase were tre

APA, Harvard, Vancouver, ISO, and other styles

12

Walker, Brian R. "Extra-adrenal regeneration of glucocorticoids by 11β-hydroxysteroid dehydrogenase type 1: physiological regulator and pharmacological target for energy partitioning". Proceedings of the Nutrition Society 66, № 1 (2007): 1–8. http://dx.doi.org/10.1017/s002966510700523x.

Full text

Abstract:

The major glucocorticoid in man, cortisol, plays important roles in regulating fuel metabolism, energy partitioning and body fat distribution. In addition to the control of cortisol levels in blood by the hypothalamic–pituitary–adrenal axis, intracellular cortisol levels within target tissues can be controlled by local enzymes. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the regeneration of active cortisol from inert cortisone, thereby amplifying cortisol levels and glucocorticoid receptor activation in adipose tissue, liver and other tissues. 11β-HSD1 is under complex tissue-

APA, Harvard, Vancouver, ISO, and other styles

13

Verrière, Valia A., Darina Hynes, Sheila Faherty, et al. "Rapid Effects of Dexamethasone on Intracellular pH and Na+/H+ Exchanger Activity in Human Bronchial Epithelial Cells." Journal of Biological Chemistry 280, no. 43 (2005): 35807–14. http://dx.doi.org/10.1074/jbc.m506584200.

Full text

Abstract:

Glucocorticoids have been shown to produce rapid nongenomic responses in airway epithelia. By using an intracellular pH (pHi) spectrofluorescence imaging system and the NH4 Cl acid-loading technique, we have shown that the synthetic glucocorticoid,dexamethasone, accelerated intracellular pH recovery after an acid load in a human bronchial epithelial cell line (16HBE14o– cells). Exposure to NH4Cl (20 mm) elicited an intracellular acidification, followed by a pHi recovery. Inhibition of the Na+/H+ exchanger decreased the steady-state pHi and antagonized the dexamethasone stimulation of pHi regul

APA, Harvard, Vancouver, ISO, and other styles

14

Alheim, K., J. Corness, MK Samuelsson, et al. "Identification of a functional glucocorticoid response element in the promoter of the cyclin-dependent kinase inhibitor p57Kip2." Journal of Molecular Endocrinology 30, no. 3 (2003): 359–68. http://dx.doi.org/10.1677/jme.0.0300359.

Full text

Abstract:

Glucocorticoids are known regulators of the cell cycle, normally exerting an anti-proliferative effect. We have previously shown that glucocorticoids stimulate expression of p57(Kip2), a member of the Cip/Kip family of cyclin-dependent kinase inhibitors which, in some cell types, may account for the anti-proliferative responses seen after glucocorticoid treatment. The induction of p57(Kip2) involves primary transcriptional effects where no de novo protein synthesis is necessary, suggesting a direct interaction of the glucocorticoid receptor with the p57(Kip2) gene. In this study we have identi

APA, Harvard, Vancouver, ISO, and other styles

15

Dulaney, David T., Wassem Juakiem, Katherine Cebe, and Angelo H. Paredes. "A case of intestinal Behcet’s disease under Adalimumab." Case Reports in Internal Medicine 4, no. 3 (2017): 62. http://dx.doi.org/10.5430/crim.v4n3p62.

Full text

Abstract:

Behcet’s disease (BD) is a multisystem mucocutaneous inflammatory condition characterized by recurrent genital and oral ulcers, ocular inflammation, and can involve the gastrointestinal tract. Treatment involves the usage of immunosuppressive agents to control the disease with glucocorticoids utilized for treatment of flares. Tumor necrosis factor inhibitors are frequently used to control the disease as well. We present the case of a 40 years old African American female presenting with intestinal BD that was refractory to adalimumab therapy. In conjunction with glucocorticoids, the patient’s i

APA, Harvard, Vancouver, ISO, and other styles

16

Zakar, Tamas, Jane E. Mijovic, Damyanti Bhardwaj, and David M. Olson. "Tyrosine kinase inhibitors block the glucocorticoid stimulation of prostaglandin endoperoxide H synthase expression in amnion cells." Canadian Journal of Physiology and Pharmacology 77, no. 2 (1999): 138–42. http://dx.doi.org/10.1139/y98-148.

Full text

Abstract:

Human amnion cells in primary culture respond to glucocorticoids in a characteristic fashion by the increased expression of the inducible prostaglandin endoperoxide H synthase isoenzyme, PGHS-2. Since PGHS-2 induction by agonists generally involves tyrosine kinases, we examined the possibility that the glucocorticoid stimulation of PGHS-2 in the amnion cells is tyrosine kinase dependent. PGHS-2 expression was stimulated in confluent, serum-starved amnion cells with dexamethasone, and the effect of the tyrosine kinase inhibitors herbimycin A and tyrphostins AG126, AG1288, and A1 on enzyme activ

APA, Harvard, Vancouver, ISO, and other styles

17

Pitha, J., and R. Anand. "Alpha-Cyclodextrin Sulphate, an anti-HIV Agent, Retains its Antiviral Effect in the Presence of Hydrocortisol Phosphate." Antiviral Chemistry and Chemotherapy 4, no. 1 (1993): 65–66. http://dx.doi.org/10.1177/095632029300400108.

Full text

Abstract:

Cyclodextrin sulphates alpha (a) and beta (b) were found to be inhibitors of replication of human immunodeficiency virus (HIV-1) in phytohaemagglutinin (PHA)-stimulated human peripheral blood mononuclear cells (PBMC); the same cells were also stimulated to proliferate (Anand et al., 1990). B-Cyclodextrin sulphate was also found to stimulate another, more complex, cell proliferation-neovascularization process in rabbit cornea (Folkman et al., 1989). Since the process of neovascularization is generally associated with progression of tumour growth and other pathologies, it is obvious that its sti

APA, Harvard, Vancouver, ISO, and other styles

18

Kupczyk, Daria, Renata Studzińska, Rafał Bilski та Alina Woźniak. "Application of ELISA Technique and Human Microsomes in the Search for 11β-Hydroxysteroid Dehydrogenase Inhibitors". BioMed Research International 2019 (12 травня 2019): 1–8. http://dx.doi.org/10.1155/2019/5747436.

Full text

Abstract:

The metabolic syndrome is defined by impaired carbohydrate metabolism and lipid disorders and often accompanied by hypertension, all of which will lead to obesity and insulin resistance. Glucocorticoids play a regulatory role in the metabolism of proteins, lipids, and carbohydrates. There is growing evidence for a role of glucocorticoids in the development of the metabolic syndrome. The most important factor that regulates the access of endogenous glucocorticoids to receptors after release of glucocorticoids and their diffusion into the cytoplasm of target cells is the steroid metabolism invol

APA, Harvard, Vancouver, ISO, and other styles

19

Wang, Liu, Tae Gyu Oh, Jason Magida, et al. "Bromodomain containing 9 (BRD9) regulates macrophage inflammatory responses by potentiating glucocorticoid receptor activity." Proceedings of the National Academy of Sciences 118, no. 35 (2021): e2109517118. http://dx.doi.org/10.1073/pnas.2109517118.

Full text

Abstract:

In macrophages, homeostatic and immune signals induce distinct sets of transcriptional responses, defining cellular identity and functional states. The activity of lineage-specific and signal-induced transcription factors are regulated by chromatin accessibility and other epigenetic modulators. Glucocorticoids are potent antiinflammatory drugs; however, the mechanisms by which they selectively attenuate inflammatory genes are not yet understood. Acting through the glucocorticoid receptor (GR), glucocorticoids directly repress inflammatory responses at transcriptional and epigenetic levels in m

APA, Harvard, Vancouver, ISO, and other styles

20

Sooy, Karen, June Noble, Andrew McBride та ін. "Cognitive and Disease-Modifying Effects of 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition in Male Tg2576 Mice, a Model of Alzheimer's Disease". Endocrinology 156, № 12 (2015): 4592–603. http://dx.doi.org/10.1210/en.2015-1395.

Full text

Abstract:

Chronic exposure to elevated levels of glucocorticoids has been linked to age-related cognitive decline and may play a role in Alzheimer's disease. In the brain, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) amplifies intracellular glucocorticoid levels. We show that short-term treatment of aged, cognitively impaired C57BL/6 mice with the potent and selective 11β-HSD1 inhibitor UE2316 improves memory, including after intracerebroventricular drug administration to the central nervous system alone. In the Tg2576 mouse model of Alzheimer's disease, UE2316 treatment of mice aged 14 months for

APA, Harvard, Vancouver, ISO, and other styles

21

Riley, Thomas R., and Michael D. George. "Risk for infections with glucocorticoids and DMARDs in patients with rheumatoid arthritis." RMD Open 7, no. 1 (2021): e001235. http://dx.doi.org/10.1136/rmdopen-2020-001235.

Full text

Abstract:

Immunomodulatory therapy for rheumatoid arthritis (RA) carries risk for infectious complications. Understanding the risks of different therapeutic options is essential for making treatment decisions and appropriately monitoring patients. This review examines data on the risks for serious infections and other key infections of interest for the major classes of agents in use for RA: glucocorticoids, conventional synthetic disease-modifying antirheumatic drugs (DMARDs), biologics and Janus kinase (JAK) inhibitors. Conventional synthetic DMARDs have an excellent safety profile with recent data ava

APA, Harvard, Vancouver, ISO, and other styles

22

Farrell, RJ, and D. Kelleher. "Glucocorticoid resistance in inflammatory bowel disease." Journal of Endocrinology 178, no. 3 (2003): 339–46. http://dx.doi.org/10.1677/joe.0.1780339.

Full text

Abstract:

Glucocorticoids are potent inhibitors of T cell activation and proinflammatory cytokines and are highly effective treatment for active inflammatory bowel disease (IBD). However, failure to respond, acutely or chronically, to glucocorticoid therapy is a common indication for surgery in IBD, with as many as 50% of patients with Crohn's disease (CD) and approximately 20% of patients with ulcerative colitis (UC) requiring surgery in their lifetime as a result of poor response to glucocorticoids. Studies report that approximately one-third of patients with CD are steroid dependent and one-fifth are

APA, Harvard, Vancouver, ISO, and other styles

23

Chapman, Karen, Megan Holmes та Jonathan Seckl. "11β-Hydroxysteroid Dehydrogenases: Intracellular Gate-Keepers of Tissue Glucocorticoid Action". Physiological Reviews 93, № 3 (2013): 1139–206. http://dx.doi.org/10.1152/physrev.00020.2012.

Full text

Abstract:

Glucocorticoid action on target tissues is determined by the density of “nuclear” receptors and intracellular metabolism by the two isozymes of 11β-hydroxysteroid dehydrogenase (11β-HSD) which catalyze interconversion of active cortisol and corticosterone with inert cortisone and 11-dehydrocorticosterone. 11β-HSD type 1, a predominant reductase in most intact cells, catalyzes the regeneration of active glucocorticoids, thus amplifying cellular action. 11β-HSD1 is widely expressed in liver, adipose tissue, muscle, pancreatic islets, adult brain, inflammatory cells, and gonads. 11β-HSD1 is selec

APA, Harvard, Vancouver, ISO, and other styles

24

Piovan, Erich, Jiyang Yu, Pedro Real, Gawinowicz Mary Ann, Andrea Califano, and Adolfo Ferrando. "Oncogenic AKT Signaling Negatively Regulates Glucocorticoid Receptor Function to Promote Glucocorticoid Resistance In T Cell Acute Lymphoblastic Leukemia." Blood 116, no. 21 (2010): 11. http://dx.doi.org/10.1182/blood.v116.21.11.11.

Full text

Abstract:

Abstract Abstract 11 Glucocorticoids (GC) play a fundamental role in the treatment of all lymphoid tumors because of their capacity to induce apoptosis in lymphoid progenitor cells. The importance of GC therapy in lymphoid malignancies is underscored by the strong association of GC response with prognosis in childhood acute lymphoblastic leukemia (ALL). Thus, resistance to glucocorticoids is a well recognized feature of poor prognosis in the treatment of childhood ALL. A number of different mechanisms contributing to GC resistance in T-ALL have been proposed including increased expression of a

APA, Harvard, Vancouver, ISO, and other styles

25

Ogawa, Ryosuke, Michael B. Streiff, Artem Bugayenko, and Gregory J. Kato. "Inhibition of PDE4 phosphodiesterase activity induces growth suppression, apoptosis, glucocorticoid sensitivity, p53, and p21WAF1/CIP1 proteins in human acute lymphoblastic leukemia cells." Blood 99, no. 9 (2002): 3390–97. http://dx.doi.org/10.1182/blood.v99.9.3390.

Full text

Abstract:

Abstract Glucocorticoids are integral to successful treatment of childhood acute lymphoblastic leukemia (ALL) and other lymphoid malignancies. A large body of data indicates that in various model systems, elevation of cyclic adenosine monophosphate (cAMP) can potentiate glucocorticoid response, although this has not been well evaluated as a potential leukemia treatment. Although cAMP analogs have been studied, little data exist regarding the potential toxicity to leukemia cells of pharmacologic elevation of cAMP levels in leukemic blasts. Using MTT assays of cell proliferation on CEM ALL cells

APA, Harvard, Vancouver, ISO, and other styles

26

DE LOS PINOS, Elisabet, Silvia FERNÁNDEZ DE MATTOS, Manel JOAQUIN, and Albert TAULER. "Insulin inhibits glucocorticoid-stimulated L-type 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase gene expression by activation of the c-Jun N-terminal kinase pathway." Biochemical Journal 353, no. 2 (2001): 267–73. http://dx.doi.org/10.1042/bj3530267.

Full text

Abstract:

The hepatic isoform of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PF2K/Fru-2,6-BPase) is transcriptionally stimulated by glucocorticoids, whereas insulin blocks this stimulatory effect. Although this inhibitory effect has been extensively reported, nothing is known about the signalling pathway responsible. We have used well-characterized inhibitors for proteins involved in different signalling cascades to assess the involvement of these pathways on the transcriptional regulation of glucocorticoid-stimulated PF2K/Fru-2,6-BPase by insulin. Our results demonstrate that the phosphoinosi

APA, Harvard, Vancouver, ISO, and other styles

27

DU CAJU, Marc V. L., and Raoul P. ROOMAN. "Effect of steroids on cartilage metabolism "in vitro"." Acta Endocrinologica 113, no. 4_Suppl (1986): S35—S40. http://dx.doi.org/10.1530/acta.0.112s035.

Full text

Abstract:

ABSTRACT Conditions characterized by high levels of glucocorticoids are associated with poor growth. Serum somatomedin or insulin-like growth factor activity measured by cartilage bioassay systems is low, but is generally not accompanied by a fall in somatomedin concentration. Hydrocortisone and a synthetic analogue, dexamethasone, impaired the serum stimulated "in vitro" 35S sulphate and 3H-thymidine incorporation in porcine rib cartilage at physiological concentrations. Hydrocortisone added at a concentration of 0,1 μg/ml decreased the potency of normal serum to 50 % of controls. Dexamethaso

APA, Harvard, Vancouver, ISO, and other styles

28

Real, Pedro J., Valeria Tosello, Walden Ai, et al. "Inhibition of NOTCH1 Signaling Reverses Glucocorticoid Resistance in T-ALL." Blood 110, no. 11 (2007): 151. http://dx.doi.org/10.1182/blood.v110.11.151.151.

Full text

Abstract:

Abstract Gamma-secretase inhibitors (GSIs), which block the activation of the NOTCH1 receptor, are currently being tested in the treatment of T-cell lymphoblastic leukemias (T-ALL) with activating mutations in the NOTCH1 gene. However, inhibition of NOTCH1 signaling induces only a delayed cytostatic antileukemic effect with little or no apoptosis and GSI treatment is associated with severe gastrointestinal toxicity, which limits the clinical application of these molecularly targeted drugs. Here we show that combination therapy with GSIs plus glucocorticoids reverses glucocorticoid resistance a

APA, Harvard, Vancouver, ISO, and other styles

29

Landwehr, Laura-Sophie, Barbara Altieri, Jochen Schreiner, et al. "Interplay between glucocorticoids and tumor-infiltrating lymphocytes on the prognosis of adrenocortical carcinoma." Journal for ImmunoTherapy of Cancer 8, no. 1 (2020): e000469. http://dx.doi.org/10.1136/jitc-2019-000469.

Full text

Abstract:

BackgroundAdrenocortical carcinoma (ACC) is a rare endocrine malignancy. Tumor-related glucocorticoid excess is present in ~60% of patients and associated with particularly poor prognosis. Results of first clinical trials using immune checkpoint inhibitors were heterogeneous. Here we characterize tumor-infiltrating T lymphocytes (TILs) in ACC in association with glucocorticoids as potential explanation for resistance to immunotherapy.MethodsWe performed immunofluorescence analysis to visualize tumor-infiltrating T cells (CD3+), T helper cells (CD3+CD4+), cytotoxic T cells (CD3+CD8+) and regula

APA, Harvard, Vancouver, ISO, and other styles

30

Laurin, Louis-Philippe, Adil M. Gasim, Caroline J. Poulton, et al. "Treatment with Glucocorticoids or Calcineurin Inhibitors in Primary FSGS." Clinical Journal of the American Society of Nephrology 11, no. 3 (2016): 386–94. http://dx.doi.org/10.2215/cjn.07110615.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

WEHRENBERG, W. B., B. A. JANOWSKI, A. W. PIERING, F. CULLER, and K. L. JONES. "Glucocorticoids: Potent Inhibitors and Stimulators of Growth Hormone Secretion*." Endocrinology 126, no. 6 (1990): 3200–3203. http://dx.doi.org/10.1210/endo-126-6-3200.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Berard, E., T. Barnetche, L. Rouxel, et al. "SAT0540 ONE-YEAR OUTCOMES AFTER RHEUMATIC IMMUNE-RELATED ADVERSE EVENTS FROM CHECKPOINT INHIBITORS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1227.2–1227. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4366.

Full text

Abstract:

Background:Description and initial management of rheumatic immune-related adverse-events (irAEs) from cancer immunotherapies have been reported by several groups but to date, few studies have evaluated the long-term outcomes and management of rheumatic irAEs (1).Objectives:To describe the long-term management and assess the one-year outcomes of patients who experienced rheumatic immune-related adverse events (irAEs) due to immune checkpoint inhibitors (ICI).Methods:This was a single-centre prospective observational study including patients referred for musculoskeletal symptoms while treated wi

APA, Harvard, Vancouver, ISO, and other styles

33

Al Mushref, Mazen, Paul A. Guido, Frances A. Collichio, Dominic T. Moore, and David R. Clemmons. "THYROID DYSFUNCTION, RECOVERY, AND PROGNOSIS IN MELANOMA PATIENTS TREATED WITH IMMUNE CHECKPOINT INHIBITORS: A RETROSPECTIVE REVIEW." Endocrine Practice 26, no. 1 (2020): 36–42. http://dx.doi.org/10.4158/ep-2019-0244.

Full text

Abstract:

Objective: To describe thyroid dysfunction, factors associated with thyroid recovery, and survival in melanoma patients treated with immune checkpoint inhibitors that developed thyroid immune-related adverse events (irAEs). Methods: This was a retrospective study in a tertiary center from 2010–2017. We reviewed the charts of patients with melanoma that developed thyroid dysfunction after checkpoint inhibitor therapy. Cases with thyroid irAEs were grouped by recovery of thyroid function at 1 year. We collected a timeline of thyroid function tests, medication exposure, and survival and compared

APA, Harvard, Vancouver, ISO, and other styles

34

Picca, Alberto, Giulia Berzero, Kevin Bihan, et al. "Longitudinally Extensive Myelitis Associated With Immune Checkpoint Inhibitors." Neurology - Neuroimmunology Neuroinflammation 8, no. 3 (2021): e967. http://dx.doi.org/10.1212/nxi.0000000000000967.

Full text

Abstract:

ObjectiveTo define the characteristics and the outcome of myelitis associated with immune checkpoint inhibitors (ICIs).MethodsWe performed a retrospective research in the databases of the French Pharmacovigilance Agency and the OncoNeuroTox network for patients who developed myelitis following treatment with ICIs (2011–2020). A systematic review of the literature was performed to identify similar cases.ResultsWe identified 7 patients who developed myelitis after treatment with ICIs (anti-PD1 [n = 6], anti-PD1 + anti-CTLA4 [n = 1]). Neurologic symptoms included paraparesis (100%), sphincter dys

APA, Harvard, Vancouver, ISO, and other styles

35

Forsyth, Kevin D., and Vivienne Talbot. "Role of glucocorticoids in neutrophil and endothelial adhesion molecule expression and function." Mediators of Inflammation 1, no. 2 (1992): 101–6. http://dx.doi.org/10.1155/s0962935192000176.

Full text

Abstract:

Glucocorticoids are very effective inhibitors of both the acute and chronic inflammatory response. In this study the hypothesis that glucocorticoids inhibit an early component of the inflammatory response, neutrophil adhesion to endothelium, by down-regulation of adhesion molecules on neutrophils or endothelium was examined. No effect of dexamethasone on neutrophil adhesion to endothelium or of antigen expression by neutrophils or endothelium was found. The mechanism of action of glucocorticoids in the inflammatory response is probably not mediated by alterations in adhesion molecules.

APA, Harvard, Vancouver, ISO, and other styles

36

Fürst, Robert, Stefan Zahler, and Angelika M. Vollmar. "Dexamethasone-Induced Expression of Endothelial Mitogen-Activated Protein Kinase Phosphatase-1 Involves Activation of the Transcription Factors Activator Protein-1 and 3′,5′-Cyclic Adenosine 5′-Monophosphate Response Element-Binding Protein and the Generation of Reactive Oxygen Species." Endocrinology 149, no. 7 (2008): 3635–42. http://dx.doi.org/10.1210/en.2007-1524.

Full text

Abstract:

We have recently identified the MAPK phosphatase (MKP)-1 as a novel mediator of the antiinflammatory properties of glucocorticoids (dexamethasone) in the human endothelium. However, nothing is as yet known about the signaling pathways responsible for the up-regulation of MKP-1 by dexamethasone in endothelial cells. Knowledge of the molecular basis of this new alternative way of glucocorticoid action could facilitate the identification of new antiinflammatory drug targets. Thus, the aim of our study was to elucidate the underlying molecular mechanisms. Using Western blot analysis, we found that

APA, Harvard, Vancouver, ISO, and other styles

37

Real, Pedro Jose, Valeria Tosello, Teresa Palomero, et al. "Inhibition of NOTCH1 Signaling and Glucocorticoid Therapy in T-ALL." Blood 112, no. 11 (2008): 298. http://dx.doi.org/10.1182/blood.v112.11.298.298.

Full text

Abstract:

Abstract Activating mutations in NOTCH1 are present in over 50% of T-cell acute lymphoblastic leukemias (T-ALL). Consequently, inhibition of NOTCH1 signaling with small molecule γ-secretase inhibitors (GSIs) has been proposed as a targeted therapy for this disease. However, GSIs fail to induce robust apoptosis in T-ALL cells and their clinical application has been limited by the development of severe gastrointestinal toxicity (mucous diarrhea and goblet cell metaplasia) resulting from systemic inhibition of NOTCH signaling. Here we show that combination therapy with GSIs plus glucocorticoids c

APA, Harvard, Vancouver, ISO, and other styles

38

Low, Candice, and Richard Conway. "Current advances in the treatment of giant cell arteritis: the role of biologics." Therapeutic Advances in Musculoskeletal Disease 11 (January 2019): 1759720X1982722. http://dx.doi.org/10.1177/1759720x19827222.

Full text

Abstract:

Giant cell arteritis (GCA) is the most common form of systemic vasculitis. It is a potentially severe disease with 25% of patients suffering vision loss or stroke. Our treatment paradigm is based on glucocorticoids. Glucocorticoids are required in high doses for prolonged periods and subsequently are associated with a significant amount of treatment-related morbidity. Alternative treatment options are urgently needed to minimize these glucocorticoid adverse events. Many other agents, such as methotrexate and tumour necrosis factor alpha inhibitors have been used in GCA, with limited or no evid

APA, Harvard, Vancouver, ISO, and other styles

39

Morgan, Stuart A., Zaki K. Hassan-Smith, Craig L. Doig, Mark Sherlock, Paul M. Stewart та Gareth G. Lavery. "Glucocorticoids and 11β-HSD1 are major regulators of intramyocellular protein metabolism". Journal of Endocrinology 229, № 3 (2016): 277–86. http://dx.doi.org/10.1530/joe-16-0011.

Full text

Abstract:

The adverse metabolic effects of prescribed and endogenous glucocorticoid excess, ‘Cushing’s syndrome’, create a significant health burden. While skeletal muscle atrophy and resultant myopathy is a clinical feature, the molecular mechanisms underpinning these changes are not fully defined. We have characterized the impact of glucocorticoids upon key metabolic pathways and processes regulating muscle size and mass including: protein synthesis, protein degradation, and myoblast proliferation in both murine C2C12 and human primary myotube cultures. Furthermore, we have investigated the role of pr

APA, Harvard, Vancouver, ISO, and other styles

40

Szabó, Melinda Zsuzsanna, and Emese Kiss. "Nagyérvasculitisek korszerű kezelése." Orvosi Hetilap 158, no. 1 (2017): 5–12. http://dx.doi.org/10.1556/650.2017.30630.

Full text

Abstract:

Abstract: Giant cell arteritis and Takayasu arteritis classified to large vessel vasculitides have similar histopathology in the vascular wall proposing that these entities can be different phenotypes on a spectrum of a single disorder. Glucocorticoids are the mainstay of therapy combined with cyclophosphamide, azatioprine and mycofenolate mofetil, when it is required. However, a significant proportion of patients are glucocorticoid-dependent despite of the conventional disease-modifying antirheumatic drugs and suffer from serious side effects of the steroids, therefore alternate options for m

APA, Harvard, Vancouver, ISO, and other styles

41

Xia, Lijun, Junliang Pan, Longbiao Yao, and Rodger P. McEver. "A Proteasome Inhibitor, an Antioxidant, or a Salicylate, but not a Glucocorticoid, Blocks Constitutive and Cytokine-Inducible Expression of P-Selectin in Human Endothelial Cells." Blood 91, no. 5 (1998): 1625–32. http://dx.doi.org/10.1182/blood.v91.5.1625.

Full text

Abstract:

Abstract Proteasome inhibitors, antioxidants, salicylates, or glucocorticoids block the cytokine-induced expression of the endothelial cell adhesion molecules E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1. These pharmacological agents have been assumed to inhibit the expression of adhesion molecules primarily by blocking activation of the transcription factor NF-κB. We found that the proteasome inhibitor ALLN, the antioxidant PDTC, or sodium salicylate, but not the glucocorticoid dexamethasone, inhibited both the constitutive and the interleukin-4– or onc

APA, Harvard, Vancouver, ISO, and other styles

42

Xia, Lijun, Junliang Pan, Longbiao Yao, and Rodger P. McEver. "A Proteasome Inhibitor, an Antioxidant, or a Salicylate, but not a Glucocorticoid, Blocks Constitutive and Cytokine-Inducible Expression of P-Selectin in Human Endothelial Cells." Blood 91, no. 5 (1998): 1625–32. http://dx.doi.org/10.1182/blood.v91.5.1625.1625_1625_1632.

Full text

Abstract:

Proteasome inhibitors, antioxidants, salicylates, or glucocorticoids block the cytokine-induced expression of the endothelial cell adhesion molecules E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1. These pharmacological agents have been assumed to inhibit the expression of adhesion molecules primarily by blocking activation of the transcription factor NF-κB. We found that the proteasome inhibitor ALLN, the antioxidant PDTC, or sodium salicylate, but not the glucocorticoid dexamethasone, inhibited both the constitutive and the interleukin-4– or oncostatin M

APA, Harvard, Vancouver, ISO, and other styles

43

Rogatsky, Inez, Adam B. Hittelman, David Pearce, and Michael J. Garabedian. "Distinct Glucocorticoid Receptor Transcriptional Regulatory Surfaces Mediate the Cytotoxic and Cytostatic Effects of Glucocorticoids." Molecular and Cellular Biology 19, no. 7 (1999): 5036–49. http://dx.doi.org/10.1128/mcb.19.7.5036.

Full text

Abstract:

ABSTRACT Glucocorticoids act through the glucocorticoid receptor (GR), which can function as a transcriptional activator or repressor, to elicit cytostatic and cytotoxic effects in a variety of cells. The molecular mechanisms regulating these events and the target genes affected by the activated receptor remain largely undefined. Using cultured human osteosarcoma cells as a model for the GR antiproliferative effect, we demonstrate that in U20S cells, GR activation leads to irreversible growth inhibition, apoptosis, and repression of Bcl2. This cytotoxic effect is mediated by GR’s transcription

APA, Harvard, Vancouver, ISO, and other styles

44

Karateev, D. E., and E. L. Luchikhina. "Immunomodulatory drug therapy for the disease caused by SARS-CoV-2 infection (COVID-19)." Almanac of Clinical Medicine 48 (September 19, 2020): 51–67. http://dx.doi.org/10.18786/2072-0505-2020-48-036.

Full text

Abstract:

This systematic review focuses on the state-of-the-art pharmacotherapy of immune disorders in the novel coronavirus infection (COVID-19), leading to a cytokine storm and uncontrolled inflammatory response that causes severe tissue damage and multiple organ failure. A lot of theoretical, experimental and clinical data support the need for immunomodulatory (immunosuppressive) therapy for this disease. It should be emphasized that all immunomodulatory drugs for COVID-19 are prescribed off label, and the evidence base of the results of randomized trials is just being accumulated. We review the imm

APA, Harvard, Vancouver, ISO, and other styles

45

Gebru, Melat T., Jennifer M. Atkinson, Megan M. Young, et al. "Glucocorticoids enhance the antileukemic activity of FLT3 inhibitors in FLT3-mutant acute myeloid leukemia." Blood 136, no. 9 (2020): 1067–79. http://dx.doi.org/10.1182/blood.2019003124.

Full text

Abstract:

Abstract FLT3 is a frequently mutated gene that is highly associated with a poor prognosis in acute myeloid leukemia (AML). Despite initially responding to FLT3 inhibitors, most patients eventually relapse with drug resistance. The mechanism by which resistance arises and the initial response to drug treatment that promotes cell survival is unknown. Recent studies show that a transiently maintained subpopulation of drug-sensitive cells, so-called drug-tolerant "persisters" (DTPs), can survive cytotoxic drug exposure despite lacking resistance-conferring mutations. Using RNA sequencing and drug

APA, Harvard, Vancouver, ISO, and other styles

46

Lerner, Adam, Hongli Dong, Lewis Weintraub, Paul M. Epstein, and Sanjay Tiwari. "PDE4 Inhibitors Augment Glucocorticoid-Mediated Apoptosis in B-CLL Cells in the Absence of Exogenous Adenylyl Cyclase Stimulation." Blood 104, no. 11 (2004): 4793. http://dx.doi.org/10.1182/blood.v104.11.4793.4793.

Full text

Abstract:

Abstract cAMP-mediated signaling potentiates glucocorticoid-mediated apoptosis in lymphoid cells, but an effective means by which to take advantage of this observation in the treatment of lymphoid malignancies has not been identified. The PDE4 enzyme family regulates the catabolism of cAMP to AMP in a wide range of tissues. PDE4 inhibitors have recently been submitted for approval for use in asthma and COPD. In leukemic samples from 11 B-CLL patients, rolipram and RO20-1724, two structurally unrelated PDE4 inhibitors, synergized with either hydrocortisone or dexamethasone in inducing B-CLL but

APA, Harvard, Vancouver, ISO, and other styles

47

Chapagain, Ananda, Paul W. Caton, Julius Kieswich та ін. "Elevated hepatic 11β-hydroxysteroid dehydrogenase type 1 induces insulin resistance in uremia". Proceedings of the National Academy of Sciences 111, № 10 (2014): 3817–22. http://dx.doi.org/10.1073/pnas.1312436111.

Full text

Abstract:

Insulin resistance and associated metabolic sequelae are common in chronic kidney disease (CKD) and are positively and independently associated with increased cardiovascular mortality. However, the pathogenesis has yet to be fully elucidated. 11β-Hydroxysteroid dehydrogenase type 1 (11βHSD1) catalyzes intracellular regeneration of active glucocorticoids, promoting insulin resistance in liver and other metabolic tissues. Using two experimental rat models of CKD (subtotal nephrectomy and adenine diet) which show early insulin resistance, we found that 11βHSD1 mRNA and protein increase in hepatic

APA, Harvard, Vancouver, ISO, and other styles

48

Bénit, Christa P., and Charles J. Vecht. "Seizures and cancer: drug interactions of anticonvulsants with chemotherapeutic agents, tyrosine kinase inhibitors and glucocorticoids." Neuro-Oncology Practice 3, no. 4 (2015): 245–60. http://dx.doi.org/10.1093/nop/npv038.

Full text

Abstract:

Abstract Patients with cancer commonly experience seizures. Combined therapy with anticonvulsant drugs (AEDs) and chemotherapeutic drugs or tyrosine kinase inhibitors carries inherent risks on drug-drug interactions (DDIs). In this review, pharmacokinetic studies of AEDs with chemotherapeutic drugs, tyrosine kinase inhibitors, and glucocorticoids are discussed, including data on maximum tolerated dose, drug clearance, elimination half-life, and organ exposure. Enzyme-inducing AEDs (EIAEDs) cause about a 2-fold to 3-fold faster clearance of concurrent chemotherapeutic drugs metabolized along th

APA, Harvard, Vancouver, ISO, and other styles

49

Mao, Xinliang, A. Keith Stewart, Rose Hurren, et al. "A chemical biology screen identifies glucocorticoids that regulate c-maf expression by increasing its proteasomal degradation through up-regulation of ubiquitin." Blood 110, no. 12 (2007): 4047–54. http://dx.doi.org/10.1182/blood-2007-05-088666.

Full text

Abstract:

AbstractThe oncogene c-maf is frequently overexpressed in multiple myeloma cell lines and patient samples and contributes to increased cellular proliferation in part by inducing cyclin D2 expression. To identify regulators of c-maf, we developed a chemical screen in NIH3T3 cells stably overexpressing c-maf and the cyclin D2 promoter driving luciferase. From a screen of 2400 off-patent drugs and chemicals, we identified glucocorticoids as c-maf–dependent inhibitors of cyclin D2 transactivation. In multiple myeloma cell lines, glucocorticoids reduced levels of c-maf protein without influencing c

APA, Harvard, Vancouver, ISO, and other styles

50

Wang, Gui-Min, Ren-Shan Ge, Syed A. Latif, David J. Morris та Matthew P. Hardy. "Expression of 11β-Hydroxylase in Rat Leydig Cells". Endocrinology 143, № 2 (2002): 621–26. http://dx.doi.org/10.1210/endo.143.2.8638.

Full text

Abstract:

Abstract 11β-Hydroxy (11β-OH) derivatives of certain steroids function as inhibitors of 11β-hydroxysteroid dehydrogenase isoform 1 (11βHSD1), an enzyme expressed in Leydig cells that catalyzes the reversible oxidation of biologically active glucocorticoids to inactive 11-dehydro metabolites. 11β-Hydroxylase is an adrenal enzyme responsible for glucocorticoid biosynthesis, catalyzing 11β-hydroxylation of steroids and thus producing 11β-OH-steroid derivatives. The aims of the present study were 1) to examine whether 11β-hydroxylase is expressed in testis, 2) to define the biochemical characteris

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!