Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An antiserum was raised in rabbits against human plasmin-antiplasmin complex and rendered specific for neoantigens of this complex by absorption with purified plasminogen and plasma. Polystyrene particles were coated with the specific antibodies and used in an agglutination test for the determination of plasmin-antiplasmin complex in the plasma from various patients. Purified plasmin-antiplasma complex at a concentration of 0.1-0.2 mg/l was found to cause a clear agglutination of the particles. Activation of fresh human plasma with urokinase caused progressive generation of agglutinating activity up to a plasma dilution of 1/480. Intravenous infusion of streptokinase into patients resulted in an increase of the plasmin-antiplasmin titre of at least 1/240. Sera from patients with rheumatoid factor also agglutinated the particles but this activity could be removed by absorbing rheumatoid factor on insolubilized human IgG. Out of 101 male and twenty-three female control subjects, only three men had a plasmin-antiplasmin titre above 1/16. Of 230 hospitalized patients, plasmin-antiplasmin titres of 1/40 or more were detected in twenty-five patients. Most of these patients had diseases which are frequently associated with in vivo coagulation or fibrinolysis, but among them there was only one who showed diffuse intravascular coagulation detectable by classical methods. In the absence of an increased plasmin-antiplasmin titre none of the haemostasis analyses were indicative of in vivo coagulation or fibrinolysis. Seven out of eight patients with diffuse intravascular coagulation of various origin had plasmin-antiplasmin titres of 1/80 or 1/160. Thus, the present latex agglutination test, owing to its simplicity and sensitivity, appears to be a practical routine screening test for detecting fibrinolytic activation in plasma.
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PMID:A latex agglutination test for rapid quantitative estimation of the plasmin-antipalsmin complex in human plasma. 13 93

An ideal immunoglobulin (Ig) preparation intended for clinical use should be safe and efficacious. Efficacy depends on suitable levels of protective antibodies against pathogens and the functional integrity of the Ig molecule. In the present paper, the functional integrity of the Ig molecule was investigated in eight intravenous Ig preparations commercially available in our country and compared to an intramuscular preparation. The experimental approach included protein A and rheumatoid factor binding, complement activation and opsonic activity. Ultracentrifugation profiles were obtained for all Ig preparations in order to ascertain the presence of components other than the expected 7S monomeric IgG. Immune complexes were investigated with C1q solid phase and conglutinin assays. Results show that chemical treatments such as sulfonation or reduction-alkylation, and enzymatic treatment such as plasmin digestion, variably but consistently impair Fc-mediated functions. The present data emphasize the use of in vitro tests for assessing the suitability of Ig preparations for intravenous administration.
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PMID:Intravenous immunoglobulin preparations: a comparative in vitro study of Fc mediated functions. 263 5

1. This investigation was designed to re-examine the possibility that anti-inflammatory steroids interfere with the kinin-forming system.2. We conclude that the anti-inflammatory action of corticosteroids cannot be explained by the inhibition of kinin formation. This view is based on the following findings.3. Neither hydrocortisone nor prednisolone nor dexamethasone inhibited the activation or activity of intrinsic plasma kinin forming enzymes resulting from dilution, incubation with kininase inhibitors, or exposure to glass, monosodium urate microcrystals or to precipitated complexes of rheumatoid factor and aggregated human gamma-globulin.4. Hydrocortisone did not inhibit the action of the active kinin-forming enzymes, human salivary or urinary kallikrein, or plasmin on purified kininogen.5. Hydrocortisone, prednisolone and dexamethasone did not inhibit the hydrolysis of benzoyl-arginine-ethyl ester by human plasmin, plasma kallikrein or hog pancreatic kallikrein.6. Kinin formation occurred normally in plasma taken from two patients receiving betamethasone and one receiving prednisone.
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PMID:Kinins and anti-inflammatory steroids. 417 57

Mouse spleen cells were cultured for 4 days in RPMI 1640 medium with 5% fetal calf serum. The neutral proteinases trypsin and plasmin, and bacterial lipopolysaccharide LPS, all polyclonal B lymphocyte activators, stimulated the development of immunoglobulin producing cells as detected by the protein A plaque assay. At the same time, direct plaque forming cells reacting with mouse, human and rabbit IgG and the Fc fragment of human IgG were induced by the stimulants. The plaques could be inhibited by free IgG or Fc fragment. In the culture supernatants, IgM and IgM anti-IgG antibodies were detected by enzyme linked immunosorbent assays. Both general IgM and IgM anti-IgG antibodies increased under the influence of the proteinases and of LPS. The results are discussed in relation to rheumatoid factor production during inflammatory diseases.
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PMID:Neutral proteinases induce rheumatoid factor production in mouse spleen cell cultures. 622 74

Clinical manifestations and laboratory findings in 40 patients with thrombotic thrombocytopenic purpura (TTP) in Japan are reviewed. The most common clinical features were central neurological sings. jaundice, fever, hemorrhagic tendency, and renal abnormalities. Laboratory tests showed anemia, thrombocytopenia, hyperbilirubinemia, high serum LDH levels, and low serum haptoglobin levels. BUN and serum creatinine levels were elevated only in about 15% of the patients, although microscopic hematuria and proteinuria were observed more frequently (about 70%). Autoantibodies, such as antinuclear antibody and rheumatoid factor, were also observed in 4% to 9% of the patients. Coagulation and fibrinolysis studies showed normal values in the majority of the patients, suggesting intravascular generation of thrombin and plasmin was minimal in TTP.
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PMID:[Clinical manifestations and laboratory findings of thrombotic thrombocytopenic purpura]. 843 12

Mast cell tryptase (MCT) is a key diagnostic test for mastocytosis and anaphylaxis. High serum tryptase levels are also one of the risk factors for adverse reaction in venom immunotherapy, yet occasional patients are seen with raised levels in the absence of either diagnosis. False positive results can be due to assay interference by heterophilic antibodies such as rheumatoid factor (RF) and human anti-mouse antibodies (HAMA). We therefore investigated heterophilic antibody interference by rheumatoid factor activity and HAMA as a cause of raised MCT results in the Phadia tryptase assay. Serum samples from 83 patients were assayed for MCT and rheumatoid factor before and after the use of heterophilic antibody blocking tubes (HBT). Samples with more than 17% reduction in MCT with detectable RF were then assayed for HAMA. Fourteen (17%) of the 83 samples with positive RF showed a >17% decrease in mast cell tryptase after HBT blocking. Post-HBT, eight of 14 (57%) reverted from elevated to normal range values with falls of up to 98%. RF levels were also decreased significantly (up to 75%). Only one of the 83 tested was apparently affected by HAMA in the absence of detectable IgM RF. In conclusion, any suspicious MCT result should be checked for heterophilic antibodies to evaluate possible interference. False positive MCT levels can be caused by rheumatoid factor. We suggest a strategy for identifying assay interference, and show that it is essential to incorporate this caveat into guidance for interpretation of MCT results.
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PMID:Raised tryptase without anaphylaxis or mastocytosis: heterophilic antibody interference in the serum tryptase assay. 2130 61

Autoimmune processes have been implicated in the development of rheumatoid arthritis (RA); however, specific autoantigens that play a role in the aetiology of RA have been lacking. In this study, we found that sera from RA patients were particularly immunoreactive against the protein tryptase. Compared with osteoarthritis (OA) patients and healthy controls, RA patients had relatively higher levels of tryptase and concomitant anti-tryptase antibodies in their synovial tissues and sera. Similarly, synovial fluid from RA patients, but not from OA patients, contained antibodies that recognized tryptase in vitro. In addition, serum tryptase levels in both early and late RA patients significantly correlated with clinical indices usually used to diagnose RA, such as rheumatoid factor, Disease Activity Score using 28 joint counts and autoantibodies against cyclic citrullinated peptide. Our results identify tryptase as a candidate autoantigen involved in the pathogenesis of RA and monitoring its levels may have diagnostic and prognostic value.
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PMID:Tryptase is a candidate autoantigen in rheumatoid arthritis. 2443 28

Phenomenon and mechanism of non-immune binding of immunoglobulins G and A by various emm-genotypes of group A streptococcus and in particular M-family proteins--main factors of pathogenicity of this causative agent of widespread human diseases are examined. The role of these receptor proteins in pathogenesis of post-streptococcal damage of kidneys (glomerules) and heart (myocarditis) are proved. Results of long-term studies that confirm hypothesis of initiating function of Fc-receptor M proteins in genesis of immune inflammation in organ tissues that precede development of glomerulonephritis and myocarditis are provided. According to the basic position, Fc-binding of an immunoglobulin by M proteins initiates production of anti-IgG, immune complexes of various composition and complement activation, deposition of those in tissues results in lymphocyte infiltration and production of pro-inflammatory cytokines. Literature data on the role of Fc-binding proteins in genesis of IgA-nephropathies and rheumatoid factor is also examined. An important role of other factors of the microbe is discussed such as cross-reacting antigens, erythrogenic toxin B, system of streptokinase-plasmin receptor or endostreptosin in post-streptococcal processes in kidneys. Their participation in the process must be mediated by an inflammation reaction in the tissue that is initiated by interaction of immunoglobulins with Fc-binding proteins of the microbe. A novel approach to understanding the nature of this pathology allowed to establish the ability of Fc-fragments of immunoglobulin G to suppress the development of the process.
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PMID:[Fc-receptor proteins of Streptococcus pyogenes and pathogenesis of post-infection complications]. 2528 15