Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Continuous loss of bile in rats with a bile reservoir applied to the common bile duct caused an increase in specific activity of malic dehydrogenase, lactic dehydrogenase, glutamic dehydrogenase, glucose-6-phosphoric dehydrogenase, alkaline and acid phosphatase, urokinase and histidinase in the liver homogenates by the 7th day; the specific activity decreased by the 10th day. Disruption of innervation of the liver caused a sharp decrease of the ATP content and the abovementioned specifc activity in this organ. In continuous loss of bile there were revealed oscillations in the activity of the above-mentioned enzymes and sorbitol dehydrogenase in bile from the 1st to the 10th day of the experiment. Marked changes in the oscillations in the dysinnervated liver were in favour of the fact that those oscillations coursed under the control of the nervous system.
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PMID:[Enzyme activity of the bile and liver after disruption of its innervation and bile loss]. 18 5

A method is described in which the extent of myocardial infarction in man is assessed by mathematical analysis of the rise in plasma enzyme levels after infarction. Five enzymes are used in this study: lactate dehydrogenase (LDH); alpha-hydroxybutyrate dehydrogenase (alpha-HBDH); aspartate aminotransferase (GOT); creatine phosphokinase (CPK); and phosphohexoseisomerase (PHI). It is shown that a reasonable assessment of the total enzyme release, reflecting the extent of the infarcted area, can be made when a sufficient number of blood samples are taken after infarction. This could provide a method by which to judge therapeutic effects of intervention in the course of a myocardial infarction, as demonstrated in this study by the assessment of the effect of urokinase on the enzyme release after an infarct.
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PMID:Quantitation of infarct size in man by means of plasma enzyme levels. 119 41

Creatine kinase(CK), aspartate aminotransferase (AST), alpha-hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LD) and LD isoenzymes, CK-MB isoenzymes and CK-MM isoforms were measured in 17 acute myocardial infarction (AMI) patients treated with thrombolysis resulting in reperfusion and 2 not resulting in reperfusion as well as 71 treated conventionally to assess reperfusion. The results showed that the peak of the ratio of MM3 to MM1 was attained significantly earlier in patients with reperfusion than in those conventionally treated and those without reperfusion, and this ratio is considered to be a good indicator to assess reperfusion. The results were similar to those of previous reports. The peak in all the 17 patients with confirmed reperfusion was attained within 9 hours after onset of AMI, while only 9 of the 73 patients in the group without reperfusion had their peaks within 9 hours. The diagnostic efficiency was 94%. The authors suggested a new indicator for assess reperfusion. An increase of CK-MM3 over 10% from the first to the second hour after treatment with urokinase was found in 15 of the 17 urokinase-treated patients with reperfusion. The diagnostic efficiency was also 94%. We consider that it is an indicator as good as the peak of ratio of MM3/MM1. Furthermore, with this indicator, it is possible to assess reperfusion in two hours after treatment with urokinase.
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PMID:[Determination of serum creatinine kinase MM isoforms in assessing reperfusion after acute myocardial infarction]. 131 15

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pleural diseases. 157 32

A 33-year-old previously completely healthy man developed severe, at first colicky then persisting, pain in the left flank. The blood pressure was 190/110 mm Hg and he had pain over the left kidney on percussion. There was a mild leucocytosis (10,300/microliters), serum creatinine of 1.5 mg/dl and a rise in lactate dehydrogenase level to 395 U/l, while the urine was unremarkable. The pyelogram demonstrated on the left the upper calyceal system only and this very weakly. Colour Doppler ultrasound showed a massively reduced blood flow in the left renal vein while the artery was not visible. Digital subtraction angiography demonstrated eccentric narrowing of the left renal artery by an intravascular thrombus, providing the diagnosis of spontaneous renal artery dissection with thrombosis. Complete recanalization occurred after local thrombolysis with 500,000 IU urokinase over 7 hours, and subsequent administration of four times 40 mg tissue plasminogen activator over 4 hours. But the scintigram still demonstrated impaired renal function with decrease in clearance to 10% of total. The patient was still symptom-free on re-examination 16 months later, serum creatinine concentration was stable at 1.3 mg/dl and the blood pressure was normal.
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PMID:[The local lysis therapy of spontaneous renal artery dissection with arterial thrombosis]. 142 91

Serum kinetics of total creatine kinase (CK), CK-MB isoenzyme, aspartate aminotransferase (AST), lactate dehydrogenase (LD) and alpha-hydroxybutyrate dehydrogenase (HBD) activities were studied in twenty patients with acute myocardial infarction randomly assigned to receive either intracoronary urokinase (group A) or conventional (control) therapy (group B). The temporal characteristics of enzyme changes described were the time lag from onset of chest pain until maximum catalytic concentration value, the rate at which enzymes are released into blood, the peak value of the serum enzyme curves and (d) the fractional disappearance rate (Kd) for each enzyme considered. Thrombolytic treatment induced earlier peak times in group A: for CK, 10.8 vs 27.0 h, for CK-MB, 10.4 vs 23.1, for AST, 13.9 vs 31.3, for LD, 24.4 vs 49.1, and for HBD, 20.5 vs 48.5 (for all enzymes, p less than 0.001). The maximal rate of release for the enzymes was at least twofold greater in group A. Enzyme peak activities and Kd were not significantly different between the groups. The most significant discrimination between the two groups was obtained with AST peak time (Hartz overlap index (Oi) = 0.11) and CK-MB peak time (Oi = 0.12).
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PMID:Serum enzymes in acute myocardial infarction after intracoronary thrombolysis. 376 94

Human tear fluid has plasminogen activator activity. The type of plasminogen activator activity in unstimulated and stimulated tears was determined, using antibodies that specifically neutralize tissue plasminogen activator or urokinase. All plasminogen activator activity was tissue plasminogen activator-related in both types of tears. Correlations between activities of beta-hexosaminidase, lysozyme and lactate dehydrogenase with tissue plasminogen activator activity indicate that the contribution to plasminogen activator activity of conjunctival and corneal epithelium is more important in unstimulated tears than stimulated tears. In stimulated tears the tissue plasminogen activator activity originates mainly from the lacrimal gland. It is suggested that a constant concentration of plasminogen activator is released from the lacrimal gland and that this concentration is independent of the secretion rate of tear fluid and that the release from the conjunctiva is due to desquamation of cells.
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PMID:Immunological characterization and possible origin of plasminogen activator in human tear fluid. 668 45

The lung plasminogen activator (PA) response was examined in four different models of particle-induced pulmonary lesions in NMRI mice (single intratracheal administration, 0.75 to 5 mg/mouse). Sequential changes in cellular (total and differential counts) and biochemical markers of alveolitis (lactate dehydrogenase [LDH], total proteins) were monitored in bronchoalveolar fluid (BALF) and the fibrotic lung response was assessed histologically. An intense but spontaneously resolving alveolitis was produced by manganese dioxide (MnO2) and a fibrosing alveolitis was elicited by crystalline silica (DQ12). Minimal and noninflammatory responses were obtained after instillation of titanium dioxide (TiO2) and tungsten carbide (WC), respectively. The comparison between the resolving and the fibrosing alveolitis model was especially taken into consideration in an attempt to identify fibrinolytic changes associated with the development of fibrosis. At the alveolitis stage, similarly increased BALF PA activities were measured in both the resolving and the fibrosing alveolitis models whereas only slight and no PA modifications were noted after administration of TiO2 and WC, respectively. Persistently (up to 120 d) increased BALF PA activity was selectively associated with the progression to fibrosis (DQ12), suggesting that PA is involved in the fibrotic process. ELISA measurements demonstrated that the changes in BALF PA activity were exclusively related to changes in urokinase (uPA), not tissue-type PA. A rapid and persisting (up to Day 30) upregulation of cell-associated PA activity occurred after DQ12, MnO2, and TiO2 treatment only. Cellular PA activity was however significantly higher in fibrogenic inflammatory cells recovered from DQ12 than from MnO2-treated mice suggesting that the intensity of cellular PA upregulation may represent an early indicator of the progression to fibrosis. The implication of urokinase in the pathogenesis of silica-induced fibrosis was demonstrated by the use of a uPA knockout mice. The acceleration of the fibrotic process in uPA-deficient compared with the wild type animals demonstrated the contribution of uPA to limit the fibrotic process.
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PMID:Role of urokinase in the fibrogenic response of the lung to mineral particles. 947 81

Diagnosis of pleural effusion is difficult in children. The etiologies are numerous; however, infectious agents are more frequent. Thoracocentesis proves to be the first-line diagnostic tool. Light's criteria are the best for distinguishing whether the effusion is a transudate or an exudate. If the patient has an exudative pleural effusion, other tests are indicated to determine the etiology and in some cases the treatment: macroscopic appearance, cytology and differential white cell count (level of glucose, lactate dehydrogenase, adenosine deaminase, pH, bacterial cultures). Others investigations--biopsy of pleura by thoracoscopy or video-assisted thoracoscopy, bronchofibroscopy, CT scan--are sometimes useful. Intrapleural instillation of urokinase appears to be useful and safe. Evaluation is necessary for video-assisted thoracoscopy used early.
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PMID:[Pleurisy: diagnostic and therapeutic management]. 1079 45

Affinity adsorbents based on immobilized triazine dyes offer important advantages circumventing many of the problems associated with biological ligands. The main drawback of dyes is their moderate selectivity for proteins. Rational attempts to tackle this problem are realized through the biomimetic dye concept according to which new dyes, the biomimetic dyes, are designed to mimic natural ligands. Biomimetic dyes are expected to exhibit increased affinity and purifying ability for the targeted proteins. Biocomputing offers a powerful approach to biomimetic ligand design. The successful exploitation of contemporary computational techniques in molecular design requires the knowledge of the three-dimensional structure of the target protein, or at least, the amino acid sequence of the target protein and the three-dimensional structure of a highly homologous protein. From such information one can then design, on a graphics workstation, the model of the protein and also a number of suitable synthetic ligands which mimic natural biological ligands of the protein. There are several examples of enzyme purifications (trypsin, urokinase, kallikrein, alkaline phosphatase, malate dehydrogenase, formate dehydrogenase, oxaloacetate decarboxylase and lactate dehydrogenase) where synthetic biomimetic dyes have been used successfully as affinity chromatography tools.
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PMID:Biomimetic dyes as affinity chromatography tools in enzyme purification. 1099 23


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