spondylitis/protease

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Lack of correlation between clinical disease activity and erythrocyte sedimentation rate, acute phase proteins or protease inhibitors in ankylosing spondylitis.

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Disease activity was assessed clinically and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), orosomucoid, alpha 1-antitrypsin (alpha 1AT) and alpha 2-macroglobulin (alpha 2M) were measured in 65 patients with ankylosing spondylitis (AS). Positive correlations were found between ESR

Alpha-1-antitrypsin phenotypes in patients with ankylosing spondylitis.

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Alpha-1-antitrypsin (A1AT) is the most important plasma inhibitor of serine proteases present in numerous polymorphic varieties. It is suggested that phenotypes may be found more frequently in the connective tissue diseases. The purpose of our study was to determine individually the A1AT phenotype

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

Impaired proteolysis by SPPL2a causes CD74 fragment accumulation that can be recognized by anti-CD74 autoantibodies in human ankylosing spondylitis.

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Ankylosing spondylitis (AS) is associated with autoantibody production to Class II MHC-associated invariant chain peptide, CD74/CLIP. In this study, we considered that anti-CD74/CLIP autoantibodies present in sera from AS might recognize CD74 degradation products that accumulate upon deficiency of

The role of alpha 1 protease inhibitor (alpha 1 antitrypsin) in the regulation of immunologic and inflammatory reactions.

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Twenty-six different alleles have been identified for alpha 1 protease inhibitor (alpha 1 antitrypsin), each designated by a letter of the alphabet. In any individual two alleles codominantly determine the characteristics of alpha 1 protease inhibitor (Pi), including mobility on electrophoresis,

Functional autoantibodies against serpin E2 in rheumatoid arthritis.

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OBJECTIVE To search for novel autoantibodies in patients with rheumatoid arthritis (RA) in an effort to better understand the processes of joint destruction in this disease. METHODS Using a modified SEREX technique and complementary DNA derived from RA synovium, serpin E2 was identified as a novel

Alpha 1-antitrypsin in acute anterior uveitis and rheumatic diseases.

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To test the pathogenetic role of the phenotype MZ of alpha 1-antitrypsin/alpha 1-protease inhibitor (PI) in acute anterior uveitis (AAU) and in different rheumatic diseases we examined 360 unrelated patients including 93 with AAU alone, 24 patients with AAU and ankylosing spondylitis (AS), 21

Collagenase, cathepsin B and cathepsin L gene expression in the synovial membrane of patients with early inflammatory arthritis.

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OBJECTIVE To examine the expression of the matrix metalloproteinase, MMP-1, and the cysteine proteases, cathepsin B (CB) and cathepsin L (CL), in the synovial membrane (SM) of patients with early inflammatory arthritis. METHODS Samples of SM were obtained by blind needle biopsy or needle arthroscopy

Mapping of arthritogenic/autoimmune epitopes of cartilage aggrecans in proteoglycan-induced arthritis.

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Immunization of BALB/c mice with chondroitin sulfate-depleted proteoglycan (aggrecan) of fetal human cartilage produces progressive polyarthritis and ankylosing spondylitis. The development of the disease in genetically susceptible BALB/c mice is dependent upon the expression of both cell-mediated

LiverTox: Clinical and Research Information on Drug-Induced Liver Injury

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Monoclonal antibodies are antibodies that have a high degree of specificity (mono-specificity) for an antigen or epitope. Monoclonal antibodies are typically derived from a clonal expansion of antibody producing malignant human plasma cells. The initial monoclonal antibodies were created by fusing

Crystal structures of the endoplasmic reticulum aminopeptidase-1 (ERAP1) reveal the molecular basis for N-terminal peptide trimming.

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Endoplasmatic reticulum aminopeptidase 1 (ERAP1) is a multifunctional enzyme involved in trimming of peptides to an optimal length for presentation by major histocompatibility complex (MHC) class I molecules. Polymorphisms in ERAP1 have been associated with chronic inflammatory diseases, including

Clinical pharmacokinetics and use of infliximab.

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Tumor necrosis factor-alpha (TNFalpha) is a key proinflammatory cytokine involved in chronic inflammatory diseases. Infliximab, a chimeric (human-murine) monoclonal IgG1 anti-TNFalpha antibody, is used in the treatment of Crohn's disease (including fistulising disease) and rheumatoid arthritis (in

Periodontal Disease as a Risk Factor for Rheumatoid Arthritis: A Systematic Review.

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UNASSIGNED The objective of this systematic review is to identify and synthesise the best available evidence to examine whether periodontal disease is a risk factor for rheumatoid arthritis. BACKGROUND Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology and has a complex

Inhibitors of TACE and Caspase-1 as anti-inflammatory drugs.

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TNF-alpha neutralising agents such as Infliximab (Remicade), Etanercept (Enbrel) and the IL-1 receptor antagonist Anakinra (Kineret), are currently used clinically for the treatment of many inflammatory diseases such as Crohn's disease, rheumatoid arthritis, ankylosing spondylitis, juvenile

Coexpression and interaction of CXCL10 and CD26 in mesenchymal cells by synergising inflammatory cytokines: CXCL8 and CXCL10 are discriminative markers for autoimmune arthropathies.

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Leukocyte infiltration during acute and chronic inflammation is regulated by exogenous and endogenous factors, including cytokines, chemokines and proteases. Stimulation of fibroblasts and human microvascular endothelial cells with the inflammatory cytokines interleukin-1beta (IL-1beta) or tumour

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