bronchiolitis/tyrosine

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Leathanach 1 ó 21 torthaí

Inhibition of obliterative bronchiolitis by platelet-derived growth factor receptor protein-tyrosine kinase inhibitor.

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Logáil Isteach / Cláraigh

Blockade of PDGF receptor protein-tyrosine kinase activity effectively inhibits development of rat CMV infection enhanced experimental obliterative bronchiolitis.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú

Logáil Isteach / Cláraigh

Spleen Tyrosine Kinase Modulates Fibrous Airway Obliteration and Associated Lymphoid Neogenesis After Transplantation.

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Logáil Isteach / Cláraigh

Chronic lung allograft dysfunction, the major cause of death following lung transplantation, usually manifests as irreversible airflow obstruction associated with obliterative bronchiolitis (OB), a lesion characterized by chronic inflammation, lymphoid neogenesis, fibroproliferation and small airway

Role of platelet-derived growth factor in obliterative bronchiolitis (chronic rejection) in the rat.

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Logáil Isteach / Cláraigh

The role of platelet-derived growth factor (PDGF) in the development of obliterative bronchiolitis (OB) as a manifestation of chronic rejection was investigated in the heterotopic rat tracheal allograft model. An increase in intragraft PDGF-Ralpha and -Rbeta mRNA expression, and in PDGF-AA and

Anti-HLA antibody binding to hla class I molecules induces proliferation of airway epithelial cells: a potential mechanism for bronchiolitis obliterans syndrome.

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Logáil Isteach / Cláraigh

OBJECTIVE Development of anti-HLA antibodies is associated with development of bronchiolitis obliterans syndrome after lung transplantation. We sought to determine the mechanism by which anti-HLA antibodies affect the development of bronchiolitis obliterans syndrome. We postulated that anti-HLA

Activation of human airway epithelial cells by non-HLA antibodies developed after lung transplantation: a potential etiological factor for bronchiolitis obliterans syndrome.

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Logáil Isteach / Cláraigh

BACKGROUND The main cause of morbidity and mortality after lung transplantation (LT) is bronchiolitis obliterans syndrome (BOS). Anti-HLA antibodies development after LT has been shown to play an important role in BOS pathogenesis. However, the nature of non-HLA antibodies developed after LT and

Synergism of imatinib mesylate and everolimus in attenuation of bronchiolitis obliterans after rat LTX.

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Logáil Isteach / Cláraigh

Bronchiolitis obliterans (BO) is a progressive and fatal disease after lung transplantation (LTX). Dysregulated growth factor-induced proliferation of myofibroblasts seems to be responsible for the development of BO. The aim was to confirm the efficacy of both inhibitors of receptor tyrosine kinases

An autopsy case of bronchiolitis obliterans as a previously unrecognized adverse event of afatinib treatment.

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Logáil Isteach / Cláraigh

Interstitial lung disease is a well-known pulmonary adverse event that occurs during epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy and results in restrictive ventilatory dysfunction. However, obstructive changes such as those associated with bronchiolitis obliterans

Platelet-derived growth factor regulates cytomegalovirus infection-enhanced obliterative bronchiolitis in rat tracheal allografts.

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Logáil Isteach / Cláraigh

BACKGROUND Cytomegalovirus (CMV) infection is a risk factor for the development of obliterative bronchiolitis (OB) after lung transplantation. METHODS In the rat tracheal allograft model, rat CMV (RCMV) infection is associated with accelerated OB through enhanced alloimmune activation and increased

IL-17 induces type V collagen overexpression and EMT via TGF-β-dependent pathways in obliterative bronchiolitis.

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Logáil Isteach / Cláraigh

Obliterative bronchiolitis (OB), a fibrotic airway lesion, is the leading cause of death after lung transplantation. Type V collagen [col(V)] overexpression and IL-17-mediated anti-col(V) immunity are key contributors to OB pathogenesis. Here, we report a previously undefined role of IL-17 in

Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation.

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Logáil Isteach / Cláraigh

BACKGROUND Imatinib, a tyrosine kinase inhibitor, has been proposed as a potential anti-fibrotic agent for fibroproliferative diseases, including bronchiolitis obliterans (BO). However, the underlying anti-fibrotic mechanisms of the agent remain unclear. We evaluated whether bone (BM)-derived

Personalized Transcriptomics Reveals Heterogeneous Immunophenotypes in Children with Viral Bronchiolitis.

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Logáil Isteach / Cláraigh

Rationale: A subset of infants are hypersusceptible to severe/acute viral bronchiolitis (AVB), for reasons incompletely understood. Objectives: To characterize the cellular/molecular mechanisms underlying infant AVB in circulating cells/local airway tissues. Methods: Peripheral

Pulmonary toxicities from targeted therapies: a review.

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Logáil Isteach / Cláraigh

Pulmonary toxicity is rarely seen with most commonly used targeted therapies. The endothelial growth factor receptor (EGFR) small-molecule tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib can cause interstitial lung disease (ILD). BCR-ABL tyrosine kinase inhibitors imatinib and dasatinib

Independent review of interstitial lung disease associated with death in TRIBUTE (paclitaxel and carboplatin with or without concurrent erlotinib) in advanced non-small cell lung cancer.

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Logáil Isteach / Cláraigh

BACKGROUND A rare but serious complication of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy is a lung injury syndrome commonly referred to as a drug-induced interstitial lung disease (ILD). It has a typical clinical presentation of rapidly progressive acute or

Role of platelet-derived growth factor and vascular endothelial growth factor in obliterative airway disease.

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Logáil Isteach / Cláraigh

BACKGROUND Platelet-derived growth factor (PDGF) is an important smooth muscle cell mitogen, and vascular endothelial growth factor (VEGF) is a known angiogenic and proinflammatory growth factor. We hypothesized that specific therapy aimed at these growth factors might inhibit the development of

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