Results 41 to 50 of about 118,558 (284)

Scotland Registry for Ankylosing Spondylitis (SIRAS) – Protocol [PDF]

open access: yes, 2016
Funding SIRAS was funded by unrestricted grants from Pfizer and AbbVie. The project was reviewed by both companies, during the award process, for Scientific merit, to ensure that the design did not compromise patient safety, and to assess the global ...
Dean, Linda E   +10 more
core   +1 more source

Association of Secukinumab Treatment With Tuberculosis Reactivation in Patients With Psoriasis, Psoriatic Arthritis, or Ankylosing Spondylitis

open access: yesJAMA dermatology, 2020
This pooled cohort study evaluates the safety of newer biological agents for the treatment of tuberculosis infection and activation in patients with psoriasis, psoriatic arthritis, and ankylosing spondylitis.
B. Elewski   +13 more
semanticscholar   +1 more source

Common MIR146A Polymorphisms in Chinese Ankylosing Spondylitis Subjects and Controls. [PDF]

open access: yesPLoS ONE, 2015
Common polymorphisms of microRNA gene MIR146A were reported as associated with different autoimmune diseases, include systemic lupus erythematosus, psoriatic arthritis, asthma and ankylosing spondylitis.
Zhenmin Niu   +5 more
doaj   +1 more source

HMG-Coenzyme A Reductase as a Drug Target for the Prevention of Ankylosing Spondylitis

open access: yesFrontiers in Cell and Developmental Biology, 2021
Statins are an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). Growing evidence indicates that statins may have an anti-inflammatory effect.
Zhenyu Zhong   +8 more
doaj   +1 more source

Ankylosing Spondylitis: a trade Off of HLA-B27, ERAP, and pathogen interconnections? Focus on Sardinia [PDF]

open access: yes, 2019
The frequency of HLA-B27 in patients with Ankylosing Spondylitis (AS) is over 85%. There are more than 170 recognized HLA-B27 alleles but the majority of them is not sufficiently represented for genetic association studies.
Cauli, A   +5 more
core   +2 more sources

Expression analysis of HLA-E and NKG2A and NKG2C receptors points at a role for natural killer function in ankylosing spondylitis [PDF]

open access: yes, 2018
Background. Ankylosing Spondylitis (AS) is a complex chronic inflammatory disease strongly associated with the majority of HLA-B27 alleles. HLA-E are non-classical MHC class I molecules that specifically interact with the natural killer receptors NKG2A ...
Angioni, Mm   +12 more
core   +1 more source

Birth Outcomes and Disease Activity During Pregnancy in a Prospective Cohort of Women With Psoriatic Arthritis and Ankylosing Spondylitis

open access: yesArthritis care & research, 2020
To add to data on adverse birth outcomes accounting for disease activity in women with psoriatic arthritis (PsA) and ankylosing spondylitis (AS).
Chelsey J. F. Smith   +3 more
semanticscholar   +1 more source

Conformational Plasticity of HLA-B27 Molecules Correlates Inversely With Efficiency of Negative T Cell Selection [PDF]

open access: yes, 2020
The development of autoimmune disorders is incompletely understood. Inefficient thymic T cell selection against self-peptides presented by major histocompatibility antigens (HLA in humans) may contribute to the emergence of auto-reactive effector cells ...
Loll, Bernhard   +3 more
core   +1 more source

Neutrophil/lymphocyte and platelet/lymphocyte ratios as potential markers of disease activity in patients with Ankylosing spondylitis: a case-control study

open access: yesAdvances in Rheumatology, 2020
Background The neutrophil/ lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) have the potential to be inflammatory markers that reflect the activity of many inflammatory diseases.
M. H. Al-Osami   +3 more
semanticscholar   +1 more source

Tumor necrosis factor inhibitors in psoriatic arthritis. [PDF]

open access: yes, 2017
INTRODUCTION: Psoriatic arthritis (PsA) is a chronic inflammatory disease that can result in significant disability. With the emergence of tumor necrosis factor inhibitors (TNFi), therapeutic outcomes in PsA have improved substantially.
Kraft, Walter K.   +2 more
core   +2 more sources

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