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Reclassification of the overlap syndrome of Behçet's disease and antineutrophil cytoplasmic antibody-associated vasculitis in patients with Behçet's disease.
Korean J Intern Med
January 2025
Division of Rheumatology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Background/aims: This study applied the 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology (ACR/EULAR) criteria for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) to patients with Behçet's disease (BD) to investigate the proportion and clinical implications of the reclassification to the overlap syndrome of BD and AAV (OS-BD-AAV).
Methods: We included 280 BD patients presenting with ANCA positivity but without medical conditions mimicking AAV at diagnosis. Demographic data, items from the 2014 revised International Criteria for BD and 2022 American College of Rheumatology and European Alliance of Associations for Rheumatology criteria for AAV, ANCA positivity, and laboratory results were recorded as clinical data at diagnosis.
Longitudinal association between nailfold capillaroscopy and incident interstitial lung disease: A EUSTAR database analysis.
J Scleroderma Relat Disord
January 2025
Department of Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands.
Objectives: To evaluate (1) the association between nailfold capillaroscopy pattern and 5-year risk for incident interstitial lung disease and (2) the association between transition in nailfold capillaroscopy pattern and risk of incident interstitial lung disease.
Methods: Data of adult patients from the EUSTAR database fulfilling the ACR-EULAR criteria with a disease duration ⩽5 years, having a scleroderma pattern at nailfold capillaroscopy with high-resolution computed tomography confirmed absence of interstitial lung disease (i.e.
How macrophage heterogeneity affects tuberculosis disease and therapy.
Nat Rev Immunol
January 2025
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Macrophages are the primary host cell type for infection by Mycobacterium tuberculosis in vivo. Macrophages are also key immune effector cells that mediate the control of bacterial growth. However, the specific macrophage phenotypes that are required for optimal immune control of M.
View Article and Find Full Text PDFHypoxia-inducible factor 2 regulates alveolar regeneration after repetitive injury in three-dimensional cellular and in vivo models.
Sci Transl Med
January 2025
Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease in which repetitive epithelial injury and incomplete alveolar repair result in accumulation of profibrotic intermediate/transitional "aberrant" epithelial cell states. The mechanisms leading to the emergence and persistence of aberrant epithelial populations in the distal lung remain incompletely understood. By interrogating single-cell RNA sequencing (scRNA-seq) data from patients with IPF and a mouse model of repeated lung epithelial injury, we identified persistent activation of hypoxia-inducible factor (HIF) signaling in these aberrant epithelial cells.
View Article and Find Full Text PDFGenetic Risk Factors in Idiopathic and Non-Idiopathic Interstitial Lung Disease: Similarities and Differences.
Medicina (Kaunas)
November 2024
Respiratory Disease Unit, University Hospital of Modena, 41124 Modena, Italy.
Recent advances in genetics and epigenetics have provided critical insights into the pathogenesis of both idiopathic and non-idiopathic interstitial lung diseases (ILDs). Mutations in telomere-related genes and surfactant proteins have been linked to familial pulmonary fibrosis, while variants in MUC5B and TOLLIP increase the risk of ILD, including idiopathic pulmonary fibrosis and rheumatoid arthritis-associated ILD. Epigenetic mechanisms, such as DNA methylation, histone modifications, and non-coding RNAs such as miR-21 and miR-29, regulate fibrotic pathways, influencing disease onset and progression.
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