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)

Plasmin activity in the tear fluid of the rabbit eye was examined during the wearing of soft contact lenses (SCL) and compared with the occurrence of corneal disturbances assessed in cryostat sections. Plasmin activity was determined with a semiquantitative method using dry punches of filter paper previously soaked in 0.1 M Tris-HCl buffer solution containing mmol/l D-Val-Leu-Lys-FCA (trifluoromethylaminocoumarine), pH 7.2. Punches were applied to the corneal surface for 5 s (tear collection) and incubated in wet chamber. The time of appearance of the bright yellow fluorescence in UV light was recorded and taken as a measure of plasmin activity. For calibration punches soaked in solutions containing plasmin in various concentrations, and processed in the same manner were used. Changes in the cornea were examined histochemically using methods of choice for acid glycosidases, proteases, dehydrogenases, and Na(+)-K(+)-ATPase. SCL with high and low water content were worn in rabbits in 1, 2, 4, 7, 14, 21 and 28 days. Decreased activity of Na(+)-K(+)-ATPase, GGT, and SDH in the corneal endothelium and epithelium were not accompanied by detectable plasmin activity in the tear fluid. Pronounced damage of the corneal epithelium (increased activities of acid glycosidases, acid proteases, LDH, markedly decreased activity of SDH) was accompanied by low concentration of plasmin (0.4-1.0 micrograms/ml) in the tear fluid. Middle activity of plasmin (1.0-2.0 micrograms/ml) was detectable when PMNs were present in the corneal stroma. High plasmin activity (2.0-3.0 micrograms/ml) correlated with corneal ulceration and vascularization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histochemical changes in the rabbit cornea and plasmin activity in the tear fluid during contact lens wear. Favourable influence of protease inhibitors (aprotinin, PC5, elastatinal). 137 62

The objective of this study was to determine the clinical significance of fibrinogenolysis in patients with isolated closed head injury. We correlated indices of fibrinolytic activity, fibrinogen degradation products (FgDP), and fibrin degradation products (FbDP) with outcome in order to accomplish this. This study consisted of 40 patients with isolated closed head trauma in whom blood sampling could be initiated within 3 h after injury. Patients were divided into two groups according to Glasgow Outcome Scale status at 3 months after injury, characterized as good recovery or moderate disability (group 1, n = 21); and severe disability, vegetative, or death (group 2, n = 19). The plasma fibrinogen concentration correlated with the Glasgow Coma Scale score on admission (r2 = 0.201, p < 0.01), and plasma fibrinogen concentrations in group 2 were lower than in group 1 (p < 0.05). Plasma concentrations of fibrin/fibrinogen degradation products (FDP) and plasmin-alpha2-plasmin inhibitor complex (PIC), molecular markers of activation of fibrinolysis, were higher in group 2 than in group 1 (p < 0.001), and both FgDP and FbDP concentrations in group 2 also were higher than in group 1 (p < 0.001). Both the FgDP and FbDP concentrations correlated with the PIC concentration. Moreover, the plasma FgDP concentrations correlated inversely with alpha2-plasmin inhibitor activity, a potent inhibitor of the fibrinolytic sysytem, as did the FbDP concentration. This study reveals that both fibrinolysis and fibrinogenolysis are involved in the coagulopathy that develops during the acute phase of head injury and correlate with fibrinolytic activity. Decreased activity of alpha2-plasmin inhibitor may contribute to fibrinogenolysis.
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PMID:Implications of fibrinogenolysis in patients with closed head injury. 1286 15

The accumulation of Abeta (amyloid beta-protein) peptides in the brain is a pathological hallmark of all forms of AD (Alzheimer's disease) and reducing Abeta levels can prevent or reverse cognitive deficits in mouse models of the disease. Abeta is produced continuously and its concentration is determined in part by the activities of several degradative enzymes, including NEP (neprilysin), IDE (insulin-degrading enzyme), ECE-1 (endothelin-converting enzyme 1) and ECE-2, and probably plasmin. Decreased activity of any of these enzymes due to genetic mutation, or age- or disease-related alterations in gene expression or proteolytic activity, may increase the risk for AD. Conversely, increased expression of these enzymes may confer a protective effect. Increasing Abeta degradation through gene therapy, transcriptional activation or even pharmacological activation of the Abeta-degrading enzymes represents a novel therapeutic strategy for the treatment of AD that is currently being evaluated in cell-culture and animal models. In this paper, we will review the roles of NEP, IDE, ECE and plasmin in determining endogenous Abeta concentration, highlighting recent results concerning the regulation of these enzymes and their potential as therapeutic targets.
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PMID:Abeta-degrading enzymes: modulators of Alzheimer's disease pathogenesis and targets for therapeutic intervention. 1624 55