Results 191 to 200 of about 204,387 (261)

TWEAK/Fn14 Signaling Drives Oxidative Cardiac Injury in Systemic Lupus Erythematosus: Evidence From Patient Biomarker Studies, Lupus Mouse Models, and Cardiomyocyte Assays

open access: yesArthritis &Rheumatology, EarlyView.
Objective Cardiac involvement is a major cause of morbidity in systemic lupus erythematosus (SLE). Tumor necrosis factor–like weak inducer of apoptosis (TWEAK) is elevated in SLE, but its contribution to lupus‐associated cardiac injury is unclear. We investigated the role of TWEAK/fibroblast growth factor–inducible 14 (Fn14) signaling in SLE‐related ...
Yale Liu   +12 more
wiley   +1 more source

Fundus Photograph-Derived Computational Features Predict Risk of Cardiovascular Events in the Chronic Renal Insufficiency Cohort Clinical Observational Study. [PDF]

open access: yesKidney360
Dhamdhere R   +8 more
europepmc   +1 more source

Biologic and Targeted Synthetic Disease‐Modifying Antirheumatic Drugs Do Not Arrest Bone Loss in Patients With Rheumatoid Arthritis: A Long‐Term Multicenter Observational Study

open access: yesArthritis &Rheumatology, EarlyView.
Objective Osteoporosis causes fractures that further increase the disease burden of rheumatoid arthritis (RA); however, osteoporosis treatment rates remain low. Although several studies have reported that biologic or targeted synthetic disease‐modifying antirheumatic drugs (b/tsDMARDs) can prevent or improve osteoporosis in RA, our large‐scale, real ...
Takafumi Aritomi   +30 more
wiley   +1 more source

Identifying Systemic Lupus Erythematosus From Serum Proteomic Profiles Using Machine Learning and Genetic Risk Stratification

open access: yesArthritis &Rheumatology, EarlyView.
Objective Proteome‐wide risk models for lupus remain underexplored. We developed classification models to identify lupus from serum proteomic profiles. Methods Patients with lupus and individuals with other autoimmune diseases in the UK Biobank were included.
Mehmet Hocaoǧlu   +2 more
wiley   +1 more source

Higher Complement C4 Gene Copy Number Constitutes a Shared Genetic Risk Factor for Giant Cell Arteritis and IgA Vasculitis

open access: yesArthritis &Rheumatology, EarlyView.
Objective Low copy number (CN) of complement C4 isoforms and high CN of retroviral HERV‐K elements are known risk factors for many immune‐mediated inflammatory diseases (IMIDs), often showing sex‐biased effects. Here, we assessed whether CN variation within the C4 gene contributes to giant cell arteritis (GCA) and IgA vasculitis (IgAV), two complex ...
Laura Martínez‐Gutiérrez   +295 more
wiley   +1 more source

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