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nasal polyps/tyrosine
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12 hasil
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
Protein-tyrosine kinase Syk expressed in human nasal fibroblasts and its effect on RANTES production.
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Fibroblasts, a rich source of chemokines, interact with eosinophils and play a key role in the pathogenesis of airway disease. RANTES is produced by fibroblasts to attract and activate eosinophils. LPS is known to induce RANTES and cause protein tyrosine phosphorylation. Nonreceptor protein tyrosine
Syk-kinase inhibition prevents mast cell activation in nasal polyps.
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BACKGROUND
Mast cells are crucial effector cells in the allergic cascade. The cross-linking of the high affinity IgE receptor (FcεRI) activates mast cells and basophils. Spleen tyrosine kinase (Syk) is positioned upstream of the IgE receptor signal transducing pathway and may represent an important
Decreased expression of VE-cadherin and claudin-5 and increased phosphorylation of VE-cadherin in vascular endothelium in nasal polyps.
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VE-cadherin and claudin-5 are major components of adherens and tight junctions of vascular endothelial cells and a decrease in their expression and an increase in the tyrosine-phosphorylation of VE-cadherin are associated with an increase in endothelial paracellular permeability. To clarify the
Identification of key genes and pathways in chronic rhinosinusitis with nasal polyps using bioinformatics analysis.
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Expression of Syk is associated with nasal polyp in patients with allergic rhinitis.
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OBJECTIVE
Numerous signalings are involved in allergic inflammation. The non-receptor protein tyrosine kinase, Syk, is widely expressed in immune-potentiated cells and plays critical roles in initiating signal transduction in response to the activation of cytokine, chemokine and other types of
Cathepsin D activity in nasal polyps.
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OBJECTIVE
The aim of the study was to assess the activity of cathepsin D in polyps removed during first-time FESS surgery and in recurrent polyps removed during successive FESS surgeries.
METHODS
The study examined 24 polyps: 11 polyps were removed during first-time surgical procedures (termed
Mechanisms of aspirin desensitization.
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Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1. The mechanisms behind
Expression of vascular permeability factor (VPF/VEGF) messenger RNA by plasma cells: possible involvement in the development of edema in chronic inflammation.
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Edema occurs in some types of chronic inflammation such as nasal polyps, uterine cervical polyps and gastric hyperplastic polyps. However, the factors or cellular components involved in the development of edema in chronic inflammation remain to be clarified. Recently, the gene encoding vascular
Tissue transglutaminase activation modulates inflammation in cystic fibrosis via PPARgamma down-regulation.
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Cystic fibrosis (CF), the most common life-threatening inherited disease in Caucasians, is due to mutations in the CF transmembrane conductance regulator (CFTR) gene and is characterized by airways chronic inflammation and pulmonary infections. The inflammatory response is not secondary to the
Current molecular profile of juvenile nasopharyngeal angiofibroma: First comprehensive study from India.
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An attempt is made to analyze the molecular behavior of juvenile nasopharyngeal angiofibroma (JNA).
Case Series METHODS: Quantification of mRNAs expression was undertaken through real-time polymerase chain reaction in JNA (9-24) samples for VEGF-A, basic fibroblast growth factor (b-FGF),
Expression and functions of the vascular endothelial growth factors and their receptors in human basophils.
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Angiogenesis is a multistep complex phenomenon critical for several inflammatory and neoplastic disorders. Basophils, normally confined to peripheral blood, can infiltrate the sites of chronic inflammation. In an attempt to obtain insights into the mechanism(s) underlying human basophil chemotaxis
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