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Puslapis 1 nuo 954 rezultatus
In vivo effects of antirheumatic drugs on neutral collagenolytic proteases in human rheumatoid arthritis cartilage and synovium.
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The destruction of joints in rheumatoid arthritis (RA) is thought to be related in part to an increased synthesis of proteolytic enzymes. We have determined neutral collagenolytic protease activity levels in human RA synovia and articular cartilage and examined the in vivo effects of various
Human rheumatoid arthritic cartilage and its neutral proteoglycan-degrading proteases. The effects of antirheumatic drugs.
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Measurements were made of the neutral proteoglycan-digesting protease activity in the cartilage matrix breakdown observed in the rheumatoid arthritic process. Normal knee (tibial plateau) cartilage specimens were obtained from 7 fresh cadavers and 29 cartilage specimens were obtained from 23
Nafamostat mesylate, a serine protease inhibitor, demonstrates novel antimicrobial properties and effectiveness in Chlamydia-induced arthritis.
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BACKGROUND
Effective treatment of reactive arthritis would ideally achieve both control of inflammation and eradication of persisting arthritogenic pathogens. We use a model of experimental Chlamydia trachomatis-induced arthritis (CtIA) to evaluate the effectiveness of nafamostat mesilate (NM), a
Cytochemical detection of proteases in synovial fluid of arthritic joints.
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A cytochemical method can be used to detect neutral proteases in polymorphonuclear leukocytes (PMN cells) in synovial fluid smears obtained from arthritic joints. Using this method, incubation of fixed smears in NaCl-borate buffer causes release of neutral PMN proteases, the enzymatic activity of
Elimination of protease-inhibitor complexes from the arthritic joint.
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In the rheumatic joint, destructive proteolytic enzymes are released and counteracted by complexation to the predominant inhibitors alpha 2-macroglobulin and alpha 1-antitrypsin. The articular elimination of these complexes is thought to be of decisive importance in the protease-inhibitor interplay
Impact of staphylococcal protease expression on the outcome of infectious arthritis.
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The exoproteases of Staphylococcus aureus have been proposed as virulence factors during S. aureus infections. To investigate this, we used the wild-type S. aureus strain 8325-4 and its mutants devoid of aureolysin, serine protease, and cysteine protease, respectively, in a well-established model of
Cysteine protease activity is up-regulated in inflamed ankle joints of rats with adjuvant-induced arthritis and decreases with in vivo administration of a vinyl sulfone cysteine protease inhibitor.
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OBJECTIVE
Cysteine proteases are postulated to play a role in tissue destruction in the joints of animals with arthritis. The purpose of the present study was to confirm the concept that cysteine proteases are enzymes involved in the pathology of rheumatoid arthritis (RA).
METHODS
Arthritis was
Increased frequency of the MZ phenotype of alpha-1-protease inhibitor in juvenile chronic polyarthritis.
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Pi phenotypes of alpha-1-protease inhibitor were determined by isoelectric focusing and print immunofixation in 96 English children suffering from juvenile chronic polyarthritis. A significantly increased frequency of the MZ phenotype (10.41%) was found in comparison with a geographically matched
Perturbation of protease inhibitors and substrates in inflammatory arthritis.
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Defective systemic fibrinolysis and articular persistence of fibrinlike material are well recognized in RA. Perturbation of the major plasma protease inhibitors, A1AT, A2MG, and AT III, was explored in RA, psoriatic arthritis, and Reiter's syndrome. Experimental evidence is presented and assessed
Detection of alpha 2-macroglobulin-associated proteases in the plasma of patients with rheumatoid arthritis.
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In previous work a polyclonal B cell activator has been detected in the serum of patients with rheumatoid arthritis (RA). This activator is associated with alpha 2-macroglobulin (alpha 2M) and its activity is blocked by low-Mr trypsin inhibitors, which suggests that it may be a protease-alpha 2M
[The protease-antiprotease system in pathogenesis of transient arthritis of a single joint in children].
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In 35 patients with transient arthritis of a single joint, levels of alpha-1-antitrypsin were determined in the serum in the acute stage of the disease, the recovery period, and the control group. The results were compared. Determination was that the results of examination have indicated a markedly
Serum cysteine proteases and their inhibitors in rheumatoid arthritis: relation to disease activity and radiographic progression.
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This study aims to investigate the serum levels of cysteine proteases cathepsins B and H and their inhibitors stefin A, stefin B, and cystatin C, as well as traditional inflammatory markers such as C-reactive protein in patients with rheumatoid arthritis and to correlate these markers with scores of
Matrix-degrading protease ADAMTS-5 cleaves inter-α-inhibitor and release active heavy chain 2 in synovial fluids from arthritic patients.
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Destruction of the cartilage matrix in joints is an important feature of arthritis. Proteolytic degradation of cartilage glycoproteins can contribute to the loss of matrix integrity. Human inter-α-inhibitor (IαI), which stabilizes the extracellular matrix, is composed of the light chain serine
Essential role of complement mannose-binding lectin-associated serine proteases-1/3 in the murine collagen antibody-induced model of inflammatory arthritis.
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Gene-targeted mice deficient in the complement mannose-binding lectin-associated serine protease-1 and -3 (MASP1/3(-/-)) express only the zymogen of factor D (pro-factor D [pro-Df]), a necessary component of the alternative pathway (AP). We used the murine collagen Ab-induced arthritis (CAIA) model,
Association of HLA-DR4, protease inhibitor phenotypes and keratoconjunctivitis sicca with pulmonary abnormalities in rheumatoid arthritis.
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One-hundred rheumatoid arthritis (RA) patients were assessed for the association of HLA-DR4, protease inhibitor (Pi) phenotype and keratoconjunctivitis sicca (KCS) with a variety of clinical features, airflow obstruction and bronchial reactivity. Spirometry, lung volume and gas transfer factor
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