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Puslapis 1 nuo 56 rezultatus
Synovitis causes hypoxia and acidity in synovial fluid and subchondral bone.
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The purpose of the present study was to evaluate the environmental changes in synovial fluid and subchondral bone during synovitis in rabbits in which the knee joint on one side was subjected to a procedure causing instability; a traumatic synovitis rapidly developed. Three weeks following the
A hypothesis on the pathogenesis of rheumatoid and other non-specific synovitides. IV A. The possible intermediate role of local hypoxia and metabolic alterations.
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According to the original hypothesis, synovial tissue (ST) oedema and synovial fluid (SF) volume increase contribute to local hypoxia and metabolic alterations and to inflammation (A 1). Studies on biochemical mechanisms (A 2) in synovitides show that the SF volume correlates to SF hypoxia that
The contribution of hypoxia-reperfusion injury to inflammatory synovitis: the influence of reactive oxygen intermediates on the transcriptional control of inflammation.
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The Contribution of Hypoxia-Reperfusion Injury to Inflammatory Synovitis: The Influence of Reactive Oxygen Intermediates on the Transcriptional Control of Inflammation.
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Influence of hypoxia in inflammatory synovitis.
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Hypoxia and inflammatory synovitis: observations and speculation.
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Hypoxia, oxidative stress and rheumatoid arthritis.
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The synovial cavity has a negative pressure in health. When the joint is exercised, vascular patency is maintained, allowing for nutrition of the avascular cartilage. In rheumatoid synovitis, the situation is altered. The cavity pressure is raised and upon movement this pressure exceeds the
A hypothesis on the pathogenesis of rheumatoid and other non-specific synovitides based on a combination of observations often overlooked.
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In early synovitides the tissue inflammatory cell reaction is often weak and sometimes absent, many alterations being consistent with nonvasculitic exudation (I). Increased permeability to protein may require little, if any, endothelial damage. In rheumatoid arthritis (RA) increased transfer of
[Expression of hypoxia-inducible factor-1α and vascular endothelial growth factor in the synovium of patients with osteoarthritis].
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OBJECTIVE
To detect the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in patients with osteoarthritis and investigate their roles in the synovial lesions of osteoarthritis.
METHODS
The expressions of HIF-1α and VEGF in the synovium were detected by
Hypoxia upregulates angiogenesis and synovial cell migration in rheumatoid arthritis.
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BACKGROUND
Rheumatoid arthritis (RA) is characterised by invasion of cartilage, bone and tendon by inflamed synovium. Previous studies in our laboratory have shown that hypoxia is a feature of RA synovitis. In the present study, we investigated the consequences of hypoxia on angiogenesis and
Therapeutic effect of intra-articular injection of ribbon-type decoy oligonucleotides for hypoxia inducible factor-1 on joint contracture in an immobilized knee animal model.
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BACKGROUND
Limited range of motion (ROM) as a result of joint contracture in treatment associated with joint immobilization or motor paralysis is a critical issue. However, its molecular mechanism has not been fully clarified and a therapeutic approach is not yet established.
METHODS
In the present
[Role of hypoxia-inducible factor in the pathogenesis of rheumatoid arthritis].
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Rheumatoid arthritis (RA) is a destructive chronic autoimmune disease characterized by synovium inflammation, cartilage destruction, bone erosion and the presence of autoantibodies. Hypoxia is a prominent micro-environmental feature in a range of disorders including RA. A combination of increased
Downregulation of Hypoxia-Inducible Factor-1α by RNA Interference Alleviates the Development of Collagen-Induced Arthritis in Rats.
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Rheumatoid arthritis (RA) is the most common type of autoimmune arthritis. Hypoxia-inducible factor-1α (HIF-1α) as a transcription factor in response to hypoxia suggests that it could be a potential therapeutic target for the treatment of RA. In this study, we assessed whether the HIF pathway
Nitric oxide-driven hypoxia initiates synovial angiogenesis, hyperplasia and inflammatory lesions in mice.
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BACKGROUND
Rheumatoid arthritis (RA) is an inflammatory articular disease with cartilage and bone damage due to hyperplasic synoviocyte invasion and subsequent matrix protease digestion. Although monoclonal antibodies against tumor necrosis factor alpha (TNFα) have been approved for clinical use in
Angiogenesis inhibition as a therapeutic approach for inflammatory synovitis.
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Angiogenesis inhibition, long studied in the treatment of malignancies, has begun to emerge as a potential therapeutic approach in managing inflammatory arthritis, particularly rheumatoid arthritis. The growth of new vessels is required for the development of the rheumatoid pannus, which then leads
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