Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.4.21.7 (plasmin)
9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three patients with chronic uremia on regular hemodialysis treatment (RDT) have been studied to determine whether coagulation and fibrinolysis are enhanced or not. We examined predialysis values of coagulation and fibrinolysis parameters including alpha-2-plasmin inhibitor-plasmin complex (alpha 2PIC), a good index of in vivo plasmin production, and cross-linked fibrin degradation products (XL-FDP), an index of fibrinolysis secondary to coagulation. Fibrinogen was significantly higher (p less than 0.001) in RDT patients than in normal controls. ATIII activity was significantly lower in RDT patients than in normal controls (p less than 0.001). Plasminogen activity and alpha-2-plasmin inhibitor (alpha 2PI) activity were significantly lower (p less than 0.001) in RDT patients than in normal controls. Alpha 2PIC and XL-FDP were both significantly higher (p less than 0.001) in RDT patients than in normal controls. XL-FDP was inversely correlated with alpha 2PI (r = -0.486, p less than 0.01) and positively correlated with alpha 2PIC (r = 0.646, p less than 0.001). These results suggest that coagulation and fibrinolysis are enhanced in RDT patients and that the enhanced fibrinolysis is mainly due to fibrinolysis secondary to coagulation.
...
PMID:Enhanced coagulation-fibrinolysis in patients on regular hemodialysis treatment. 183 Sep 34

Studies of blood fibrinolytic activity in 112 patients with repeated acute myocardial infarction or injury to the myocardium have revealed reduced fibrinolytic activity on non-heated fibrin plates, decreased plasmin activity and euglobulin+ fraction lysis, lowered levels of plasminogen activator, total nonenzymic fibrinolysis, antithrombin III, ++FFDP, and elevated soluble complexes of fibrin-monomer level. Complications of myocardial infarction presenting as thromboembolism; ciliary arrhythmia, chronic aneurysm with thrombosis are associated with still more marked disorders of the fibrinolysis system.
...
PMID:[The fibrinolysis system in recurrent myocardial infarction]. 183 32

Plasma levels of molecular markers of hemostatic activation were investigated in 205 samples from patients with haematopoietic malignancies. These markers included thrombin/antithrombin III complex (TAT), D-dimer, plasmin/alpha 2plasmin inhibitor complex (PIC) and thrombomodulin (TM), and were assayed by EIA methods. Samples were divided into 4 groups according to the level of FDP: group A; FDP 10 greater than, group B; 10 less than or equal to less than 20 group C; 20 less than or equal to less than 40, and group D; less than 40. The mean level of each marker except TM increased in the order of group A, B, C and D. However, in many samples belonging to group A the plasma TAT or PIC levels and both were increased in spite of low FDP level. Furthermore, levels of TAT and PIC in several samples belonging to groups C and D were within the normal range. Also, the mean levels of each marker except TM increased in the order of 2, 3, 4, 5 and over 6 points in DIC score according to the criteria of DIC diagnosis by the research committee on DIC of the Ministry of Health and Welfare in Japan. Eight of the 11 samples (72.7%) obtained from cases with a DIC score of 3 points had high plasma levels of TAT, PIC and D-dimer. Plasma levels of these markers were increased after chemotherapy. These findings lead to the following conclusions: 1) FDP reflexed activation of coagulation and fibrinolysis, but 2) FDP was not more sensitive than TAT and PIC, and 3) the increase of FDP rarely resulted from fibrinogenolysis or non-plasmin mediated fibrinolysis. Furthermore, 4) TAT, D-dimer and PIC may serve as sensitive parameters of hemostatic activation in circulating blood and be valuable markers for early diagnosis of DIC.
...
PMID:[Clinical application of laboratory diagnosis: leukemia and DIC]. 183 71

It has been shown that lipoprotein(a) (Lp[a]) may interfere with the fibrinolytic system and that the Lp(a) level in an individual remains constant. To evaluate the effects of Lp(a) on the fibrinolytic system in patients with unstable angina, we measured plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, and the thrombin-antithrombin III complex. The latter is a marker of thrombin generation, and the alpha 2-plasmin inhibitor-plasmin complex is an indicator of plasminogen activation. Venous plasma samples were taken from 18 patients with unstable angina and 18 patients with stable exertional angina who had been matched for clinical variables. On admission, plasma levels of Lp(a) were significantly higher in patients with unstable angina than in those with stable exertional angina (319 +/- 193 mg/l versus 191 +/- 141 mg/l, respectively; p less than 0.05). On admission, plasma levels of the alpha 2-plasmin inhibitor-plasmin complex and of the thrombin-antithrombin III complex were also significantly higher in patients with unstable angina than in those with stable exertional angina (0.78 +/- 0.42 micrograms/ml and 3.6 +/- 1.3 ng/ml versus 0.41 +/- 0.13 micrograms/ml and 1.9 +/- 0.5 ng/ml, respectively; p less than 0.01). In nine of the 18 patients with unstable angina, serial changes of plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, the thrombin-antithrombin III complex, and the acute-phase proteins C-reactive protein and alpha 1-antitrypsin were examined for 3 weeks after admission.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Transient increase of plasma lipoprotein(a) in patients with unstable angina pectoris. Does lipoprotein(a) alter fibrinolysis? 183 67

Plasma concentration of fibrinogen (Fbg), plasminogen (PLG), antithrombin III (AT III), alpha 2-plasmin inhibitor (alpha 2-PI), thrombin antithrombin III complex (TAT) and plasmin alpha 2-plasmin inhibitor complex (PIC) were evaluated in 23 nephrotic patients with proteinuria more than 3.5 g/day, including 4 cases with clinical evidence of thromboembolism. Among patients without thromboembolism, concentration of PLG and AT III was in the normal range but that of Fbg and alpha 2-PI was significantly elevated (p less than 0.01 for Fbg and p less than 0.001 for alpha 2-PI respectively). Also there was a positive relationship between AT III and serum albumin (p less than 0.05). Two fifth of these patients had an had an increased level of TAT, and also had a higher level of PIC compared with normal control (p less than 0.01). There was a positive relationship between TAT and PIC, TAT and Fbg (p less than 0.05), PIC and Fbg (p less than 0.01). TAT and PIC levels were markedly elevated in the patients with thromboembolism. From aforementioned data, it was suggested that patients with nephrotic syndrome would be in the prethrombotic state and the increased level of Fbg is one of the major risk factors of thromboembolic complications in these patients. Furthermore measurement of TAT and PIC are the useful means for the diagnosis of these complications.
...
PMID:[Concentration of thrombin antithrombin III complex and plasmin alpha 2-plasmin inhibitor complex in nephrotic syndrome]. 183 41

The functional operation of the cell surface pro-u-PA and plasminogen activating system has previously been shown to depend on the assembly of u-PA receptors, plasminogen binding sites, and their respective ligands at the focal adhesions of cell extensions. We now show that additional factors operate that affect the persistence of functional activity and that evidently involve charge interactions mediated by polyanions, such as those found in the cell surface proteoglycans. Heparin-like compounds and protamine were identified as fast-acting stimulators of cell surface plasminogen activation. Heparin stabilized surface u-PA activity during plasminogen activation, and we propose that a heparin binding site exists in the kringle structure of u-PA. Heparin at 40 micrograms/ml could reduce u-PA loss to only 20% compared with 60% on control cells activating plasminogen. Protamine (25 micrograms/ml) exerted a strong stimulatory effect on the level of generated bound plasmin and notably prolonged the persistence of this activity, so that 100 minutes after addition of plasminogen the level of plasmin on protamine-treated cells was five times higher than on control-treated cells. The effect of protamine on plasmin clearance suggests that an unknown plasmin inhibitor may be produced by rhabdomyosarcoma cells, whose action is accelerated by endogenous polyanions, in an analogous manner to thrombin inactivation by antithrombin III and protease nexin on endothelial cells and fibroblasts, respectively. The stimulatory effects of heparin and protamine do not affect the inactivation of cell surface u-PA by recombinant PAI-2.
...
PMID:Stimulation of cell surface plasminogen activation by heparin and related polyionic substances. 183 80

Thirty-six patients with chronic myeloproliferative disorders (CMPD) were studied as regards blood coagulation and fibrinolysis. These studies revealed various mild abnormalities: activated thromboplastin time (APTT) tended to prolong and the level of factor V decreased significantly. In several cases, the levels of D-dimer, thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex were elevated compared to normal. These results suggest that abnormal coagulation system in the patients with CMPD is related to low grade disseminated intravascular coagulation. Many coagulation factors did not correlate with peripheral blood cell counts. Two patients with polycythemia vera were evaluated for several abnormalities of the coagulation system before and during treatment. Coagulation abnormalities persisted after hematologic control had been achieved. Our results suggest that patients with CMPD have a chronic state of abnormal blood coagulation system even after normalization of blood cell counts.
...
PMID:[Abnormal blood coagulation and fibrinolysis in chronic myeloproliferative disorders]. 187 Feb 70

New trends in tests for coagulation and fibrinolysis and advances in diagnosis for the hypercoagulable state and utilization of immunological techniques such as various polyclonal and monoclonal antibodies are reported. We discussed (1) the new markers for hypercoagulable states, (2) differential diagnosis of disseminated intravascular coagulation (DIC) and abnormalities of coagulation in liver cirrhosis (LC), and (3) new markers for fibrinolysis and vascular function. Thrombin-antithrombin III complex (TAT) levels were higher in thrombotic diseases than in healthy controls. Therefore, TAT should be a good marker for hypercoagulation as fibrinopeptide A (FPA) and soluble fibrin monomer complex (SFMC). Measurement of TAT, plasma-alpha 2 plasmin inhibitor complex (PIC), and D dimer were useful for differential diagnosis of DIC and liver cirrhosis. t-PA-PAI complex correlated well with t-PA, but not with fibrinolytic parameters such as PIC. The t-PA-PAI complex may be a good marker for the function of the vascular endothelium.
...
PMID:[A new advance in theory of blood coagulation and fibrinolysis and its practical application]. 190 12

We evaluated a new enzyme immunoassay for determination of t-PA-PAI-1 complex (PAI-C) and studied the clinical utility of measuring PAI-C. This assay was performed by the capture/tag antibody technique using polystylene beads, in which the beads were coated with monoclonal antibody against PAI-1 and anti-t-PA polyclonal antibody was tagged (TDC-88, TEIJIN-LIMITED, Japan). The assay gave an excellent sensitivity with a detection limit of 0.1 ng/ml, and we were able to detect a trace amount of PAI-C in normal plasma. PAI-C in 6 volunteers showed significant daytime fluctuations. The normal value of PAI-C in plasma was below 13.8 ng/ml (n = 40). PAI-C levels in patients with accelerated fibrinolysis (n = 31) ranged from 2.9 to 66.4 ng/ml and 15 of them were outside the normal range. However, all of patients with DIC (n = 10) showed abnormally high PAI-C levels. In patients with accelerated fibrinolysis, PAI-C values correlated with t-PA antigen (r = 0.838), PAI-1 antigen (r = 0.519), ATIII activity (r = -0.669) (p less than 0.01) and D dimer levels (r = 0.391, p less than 0.05). However, PAI-C values did not correlate with plasminogen and alpha 2PI activity, alpha 2PI-plasmin complex or the FDP-E level in these patients. Our data suggests that PAI-C may be a new molecular marker that reflects t-PA release from endothelial cells and a useful indicator to study hypercoagulable states.
...
PMID:[Evaluation of a new enzyme immunoassay method for determination of t-PA-PAI-1 complex]. 190 14

To evaluate the activation of the extrinsic pathway of coagulation in disseminated intravascular coagulation (DIC), plasma factor VII coagulant activity (FVIIc) and antigen levels (FVIIag) were measured in 81 blood samples obtained from the 56 patients with DIC together with various hemostatic parameters. Plasma FVIIc (77 +/- 40%, range: 11-200%) and FVIIag (76 +/- 43%, range: 16-175%) were significantly lower in DIC subjects than in age-matched controls (FVIIc: 128 +/- 28%, FVII: 128 +/- 31%, p less than 0.01) and correlated significantly with both the antithrombin III and plasminogen activities (p less than 0.001). These results indicated that a decrease in factor VII levels is due to the consumption. However, there were several exceptions which showed elevated factor VII levels. This seems to be due to enhanced liver synthesis of factor VII compensating for the consumption. The level of tPA-PAI-I complex, a marker of pathologic endothelial stimulation, was negatively correlated with FVIIag (r = 0.45, p less than 0.05). Thus, the more the endothelium is pathologically stimulated, the more the extrinsic pathway is activated in DIC. The FVIIc/FVIIag ratio, an index of activation of factor VII zymogen, correlated with FDP and fibrin monomer levels (p less than 0.01). There were no correlations between the thrombin-antithrombin III complex. D-dimer, and alpha 2 antiplasmin-plasmin complex levels and factor VII levels. Considering the underlying diseases. the FVIIc and FVIIag levels were markedly lower in liver cirrhosis, but not significantly different in other diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Plasma factor VII levels in disseminated intravascular coagulation]. 192 Aug 59


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---