In patients with simultaneous systemic and arthritic components of systemic juvenile idiopathic arthritis (SJIA), these components appear to be related mechanistically. Moreover, the inflammatory pathways of SJIA appear to be distinct from those seen in polyarticular JIA.
BU’s New ENACT Arthritis Research Training and Outreach Program Off to Successful Start
A new research training program at the Boston University is making a profound impact on the Greater Boston arthritis community.
Therapies Aimed at Immune Cell Progenitors May Be Key to Reducing Post Myocardial Infarction Risk
Researchers have identified hematopoietic stem and progenitor cells that are liberated from bone marrow niches by a myocardial infarction.
Gadolinium Compounds Provide Insights into Pathogenesis of Fibrosing Diseases
Toll-like receptors appear to play an important role in the pathogenesis of fibrotic disorders including nephrogenic systemic fibrosis and systemic sclerosis.
Rheumatologists Seek Public Vote for Research Grant Award
Brigham and Women’s docs compete for BRIght Futures Prize for personalized medicine research
South Korea Okays First Officially Approved Monoclonal Antibody for RA
11 Products Looking for U.S. Marketing Nod
Neutralizing IL-23 and Its Targets May Improve Ankylosing Spondylitis
Researchers have identified a unique population of entheseal resident cells that can be activated by interleukin 23 (IL-23). This finding may be key to understanding how dysregulation of IL-23 results in precise inflammation of the entheses.
Newly Discovered Molecule Modulates Cartilage Repair
Chondrocytes play an important role in cartilage repair as well as symptom relief. Research published in Science provides insights into the role of stem cell–based therapies in the promotion of chondrogenesis and cartilage repair.
ACA Upheld: What Does This Mean for Rheumatology?
What does the Supreme Court decision to uphold the Affordable Care Act mean for rheumatologists?
Gene Mutation Could Cause Gut Microbe Changes that Lead to RA
A new study suggests that a small abnormality in an immunity gene can alter the gut flora in a way that induces development of rheumatoid arthritis.
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