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Seite 1 von 31 Ergebnisse
[Mechanisms of gout inflammation].
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Gout inflammation is an acute and self-resolving reaction. MSU crystals can stimulate cells through either crystal-cell membrane interaction or after their phagocytosis. The onset of gout inflammation relies on non-hematopoietic resident cells whereas the amplification of the reaction is driven by
Expression of Caspase-1 Gene Transcript Variant mRNA in Peripheral Blood Mononuclear Cells of Patients with Primary Gout in Different TCM Syndromes.
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A large number of studies have shown that cysteinyl aspartate specific protease-1 (CASP1) played an important role in the inflammatory response of primary gout, but the decreased expression of different CASP1 transcript variant could inhibit the activation of IL-1β. Our study mainly analyzed the
[New aspects of the pathogenesis of gout. Danger signals, autoinflammation and beyond].
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Gout is caused by monosodium urate (MSU) crystal-induced inflammation of the joints and periarticular tissues. MSU crystals activate the NOD-like receptor (NLR) NALP3, which functions as a pattern recognition receptor (PRR). Activated NALP3 mediates interleukin-1b (IL-1b) generation from its
Is ritonavir boosting associated with gout?
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Asymptomatic hyperuricaemia is associated with ritonavir therapy, but gout has rarely been reported. We present a retrospective cohort study of 1825 HIV-positive patients seen at one inner London HIV clinic over a two-year period. In all, 18 patients had gout, of whom 15 were receiving
Neutral protease, collagenase and elastase activities in synovial fluids from arthritic patients.
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Neutral protease, collagenase and elastase activities were high in synovial fluids from inflammatory arthritic diseases such as gout, active rheumatoid arthritis and ankylosing spondylitis. The activities correlated well with biochemical parameters such as CRP, ESR and total protein. Values were
How neutrophil extracellular traps orchestrate the local immune response in gout.
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Neutrophil granulocytes possess a large arsenal of pro-inflammatory substances and mechanisms that empower them to drive local acute immune reactions to invading microorganisms or endogenous inflammatory triggers. The use of this armory needs to be tightly controlled to avoid chronic inflammation
Synovial tissue protease gene expression and joint erosions in early rheumatoid arthritis.
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OBJECTIVE
To relate the expression of proteases in the lining and sublining layers of the synovial membrane to the rate of joint damage during 1 year in patients with early inflammatory arthritis.
METHODS
Samples of synovial membrane were obtained by closed-needle biopsy or needle arthroscopy from
Inflammasome activators induce interleukin-1α secretion via distinct pathways with differential requirement for the protease function of caspase-1.
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Through their capacity to sense danger signals and to generate active interleukin-1β (IL-1β), inflammasomes occupy a central role in the inflammatory response. In contrast to IL-1β, little is known about how IL-1α is regulated. We found that all inflammasome activators also induced the secretion of
Tophaceous gout: an unusual cause of multiple fractures.
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OBJECTIVE
Fractures occurring at the site of a tophus have rarely been described in gout. In this paper we review the occurrence, clinical features, and outcome of fractures in tophaceous gout.
METHODS
A PubMed search was conducted to identify the relevant literature, following our experience with
Schistosoma mansoni SmKI-1 serine protease inhibitor binds to elastase and impairs neutrophil function and inflammation.
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Protease inhibitors have important function during homeostasis, inflammation and tissue injury. In this study, we described the role of Schistosoma mansoni SmKI-1 serine protease inhibitor in parasite development and as a molecule capable of regulating different models of inflammatory diseases.
Spatial Confined Synergistic Enzymes with Enhanced Uricolytic Performance and Reduced Toxicity for Effective Gout Treatment.
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Confinement of urate oxidase with detoxifying enzymes into multienzyme architecture is an appealing approach for gout treatment due to its capability to decompose serum uric acid without generation of H2 O2 . However, most of these strategies involve chemical modifications to the enzymes and barely
Structure-based design of a hyperthermostable AgUricase for hyperuricemia and gout therapy.
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Arthrobacter globiformis Uricase (AgUricase) is a homotetrameric uricase with the potential for therapeutic use in treating hyperuricemia-related diseases. To achieve sufficient therapeutic effects, it is essential for this enzyme to have high thermostability and long half-life in physiological
C-reactive protein (CRP) recognizes uric acid crystals and recruits proteases C1 and MASP1.
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Gout is caused by crystallization of uric acid in the form of monosodium urate (MSU) crystals, which induce a sterile inflammatory response that is hardly distinguishable from microbe-induced inflammatory responses. It is unclear, if MSU crystals (like microbes) are recognized by specific pattern
Mechanisms of unconventional secretion of IL-1 family cytokines.
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One of the most poorly understood processes in cell biology is the peculiar ability of specific leaderless proteins to be secreted via ER/Golgi-independent mechanisms ('unconventional protein secretion'). One such leaderless protein is the major immune-activating cytokine, interleukin-1β (IL-1β).
[Value and significance of the immunologic determination of various serum sialoglycoproteins in rheumatic diseases of inflammatory nature].
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A statistical method was used in the evaluation of alpha-1-antitrypsin, acid alpha-1-glycoprotein, and haptoglobin in patients with rheumatic fever, rheumatoid arthritis, gout, periarthritis, arthrosis with inflammation, and primary arthrosis. A highly significant increase was noted in rheumatic
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