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nasal polyps/hypoxia
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 33 Αποτελέσματα
The effect of hypoxia and cycloxygenase inhibitors on nasal polyp derived fibroblasts.
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Σύνδεση εγγραφή
OBJECTIVE
The pathogenesis of chronic rhinosinusitis with nasal polyposis is unknown. Chronic inflammation along with local tissue hypoxia may effect polyp's growth. Activation of Cycloxygenases may also be involved. COX-2 up-regulates in response to different stimuli including hypoxia. Its
[Expression of hypoxia-inducible factor-1alpha in nasal polyps and its correlation with vascular endothelial growth factor and inducible nitric oxide synthase].
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Σύνδεση εγγραφή
OBJECTIVE
To detect the expression and distribution of hypoxia-inducible factor-1alpha (HIF-1alpha) in nasal polyps, to explore the relationship of HIF-1alpha with vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS), and to investigate the role of HIF-1alpha in the
Hypoxia regulates IL-17A secretion from nasal polyp epithelial cells.
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Σύνδεση εγγραφή
Hypoxia creates a microenvironment conducive to polypogenesis by regulating immune responses of the nasal polyp (NP) epithelium. We explored the immunocompetence of NP and control epithelial cells in response to hypoxia, to investigate potential relationships with polypogenesis. Three groups of
[Hypoxia effects on vascular endothelial growth factor derived epithelial cells of nasal polyps].
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OBJECTIVE
To understand the role of nasal mucous epithelial cells to hypoxia in early stage of nasal polyps(NP) formation.
METHODS
Epithelial cells of NP and inferior turbinate (IT) were cultured without serum under normal oxygen and hypoxia, and stimulus of inflammatory cytokines. Erythropoietin
Expression of hypoxia-inducible factor 1alpha in the nasal polyps by real-time RT-PCR and immunohistochemistry.
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OBJECTIVE
Hypoxia may result in increased recruitment of inflammatory cells and release of various inflammatory cytokines. Local hypoxia within the sinus is believed to aggravate sinus inflammation. In this study, we tried to investigate the correlation of hypoxia-inducible factor, which is
Hypoxia stimulates inflammatory and fibrotic responses from nasal-polyp derived fibroblasts.
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OBJECTIVE
Chronic sinusitis is primarily an inflammatory disorder characterized by hyperplasia of immune cells and sinus tissue. Nasal mucosal swelling or polyps can occlude the sinus ostia, decreasing the level of oxygen available to the sinus tissue. Hypoxia in many diseases results in increased
Overexpression of hypoxia-inducible factor 1α is associated with neutrophilic inflammation in chronic rhinosinusitis with nasal polyps.
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Hypoxia induces cysteine-rich 61, vascular endothelial growth factor, and interleukin-8 expressions in human nasal polyp fibroblasts: An implication of neutrophils in the pathogenesis of nasal polyposis.
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BACKGROUND
The purpose of this article was to elucidate the roles of neutrophils and angiogenesis factors in the pathogenesis of nasal polyposis. The effect of hypoxia on the expressions of angiogenesis factors as cysteine-rich 61 (Cyr61) and vascular endothelial growth factor (VEGF) and neutrophil
Hypoxia-stimulated vascular endothelial growth factor production in human nasal polyp fibroblasts: effect of epigallocatechin-3-gallate on hypoxia-inducible factor-1 alpha synthesis.
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OBJECTIVE
To verify the inhibitory effects of epigallocatechin-3-gallate (EGCG) on the synthesis of hypoxia-induced vascular endothelial growth factor (VEGF) in nasal polyp fibroblasts (NPFs).
METHODS
Eight primary cultures of NPFs were established from nasal polyps. Effects of EGCG on the
Increased expression of hypoxia-inducible factor 1alpha in the nasal polyps.
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OBJECTIVE
The etiology and mechanism of nasal polyps are still not well known. A newly discovered transcriptional factor, hypoxia-inducible factor (HIF), is a DNA-binding protein. Hypoxia-inducible factor is demonstrated to associate with various neoplasms. We investigate the expression of
Nox4 mediates hypoxia-stimulated myofibroblast differentiation in nasal polyp-derived fibroblasts.
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BACKGROUND
Chronic hypoxia is associated with remodeling in various organs. Reactive oxygen species (ROS) derived from NADPH oxidases (Nox), and transforming growth factor-β(1) (TGF-β(1)) have been implicated in the pathogenesis of hypoxia-induced remodeling. The aims of this study were to determine
Local tissue hypoxia and formation of nasal polyps.
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OBJECTIVE
To explore the response of nasal mucosa epithelial cells to hypoxia in terms of formation of nasal polyps (NP).
METHODS
Epithelial cells of NP and inferior turbinate (IT) were cultured serum-free under normal oxygen and hypoxic circumstances with stimulation of IL-1 beta and TNF alpha. The
Sirtuin 6 modulates hypoxia-induced autophagy in nasal polyp fibroblasts via inhibition of glycolysis.
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BACKGROUND
To elucidate the interaction between hypoxia-induced autophagy and glycolysis in nasal polyp fibroblasts, and the regulatory role of Sirtuin 6 (SIRT6) in the pathogenesis of nasal polyp.
OBJECTIVE
Through examining the expressions of lactate dehydrogenase (LDH), microtubule-associated
Vγ1⁺ γδT Cells Are Correlated With Increasing Expression of Eosinophil Cationic Protein and Metalloproteinase-7 in Chronic Rhinosinusitis With Nasal Polyps Inducing the Formation of Edema.
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OBJECTIVE
We have found that expression of γδT cells is increased in pathological mucosa of chronic rhinosinusitis with nasal polyps (CRSwNP) compared with normal nasal mucosa. This increase is correlated with the infiltration of eosinophils in CRSwNP. Here, we investigated the expression of γδT
Role of hypoxia-inducible factor-1α expression in regulatory T cells on nasal polypogenesis.
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OBJECTIVE
Hypoxia-inducible factor-1α (HIF-1α) is considered as a key molecule in regulating Th17:regulatory T-cells (Tregs) balance. The aims of this study were to investigate whether HIF-1α is associated with the RORγ (RAR-related orphan receptor gamma) expression of Tregs in nasal polyps and to
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