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)

We report on the complication rates in 660 consecutive coronary angioplasties (725 lesions) performed using four procedures that differed with respect to catheter technology and adjuvant medication. After the PTCA regimen in our laboratory had been changed from conventional steerable systems to the monorail technique, we observed a significant increase in the incidence of transient vessel occlusions from 2.6% to 7.7%, of permanent occlusions from 3.6% to 8.8%, and of intracoronary thrombus-formation from 2.6% to 5.5%. This was associated with the frequent observation of thrombotic material on the partially Teflon-coated guidewires. Coronary perfusion with urokinase (1,670-6,670 U/min) lead to a further increase in the complication rates (10.4%/10.3%/6.5%). Our present percutaneous transluminal coronary angioplasty (PTCA)-regimen (monorail technique with P.E.T. balloons, fully silicon-coated guidewires, no urokinase) shows an incidence of 3.8% for intermittent and recurrent coronary occlusions and 1.9% for permanent occlusions. Urokinase did not prevent intracoronary thrombus formation with the monorail technique. Furthermore, we suspect that in the case of PTCA-induced regional intimal dissection, fibrinolysis can prevent reestablishment of intima adherence to the vessel wall. Because five procedural deaths were observed in the 212 patients treated with i.c. urokinase as opposed to three deaths in the 448 procedures without urokinase, we feel that i.c. urokinase in PTCA is a potentially harmful regimen. We suggest that the monorail technique should be performed with fully silicon-coated guidewires and without urokinase.
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PMID:Influence of catheter technology and adjuvant medication on acute complications in percutaneous coronary angioplasty. 222 38

We report on the complication rates in 660 consecutive coronary angioplasties (725 lesions) performed using four procedures that differed with respect to catheter technology and adjuvant medication. After the PTCA regimen in our laboratory had been changed from conventional steerable systems to the monorail-technique, we observed an increase in the incidence of intermittent and recurrent vessel occlusions from 2.6% to 7.7%, of permanent occlusions from 3.6% to 8.8%, and of intracoronary thrombus-formation from 2.6% to 5.5%. This was associated with the frequent observation of thrombotic material on the guide wires. Coronary perfusion with urokinase (1670-6670 U/min) lead to a further increase in the complication rates (10.4%/10.3%/6.5%). Our present PTCA-regimen (monorail-technique with PET balloons, silicon-coated guide wires, no urokinase) shows an incidence of 3.8% for intermittent and recurrent coronary occlusions, and of 1.9% for permanent occlusions. We suspect that in case of PTCA-induced regional intimal dissection, fibrinolysis prevents reestablishment of intima-adherence to the vessel wall. We conclude that i.c. urokinase in PTCA is a potentially harmful regimen and that the monorail-technique should be performed with silicon-coated guide wires.
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PMID:[Acute complications in coronary angioplasty: dependence on catheter material and adjuvant medication]. 237 61

Eight of 92 consecutive silastic central venous catheters used for home parenteral nutrition occluded. Six of the eight had patency restored by the instillation of urokinase or streptokinase into the catheter. The thrombus in one of the two catheters that was not reopened with thrombolytic agents was studied in detail by electron microscopy, x-ray dispersive analysis, solubility in isopropyl alcohol-diethyl ether (1:1, v:v), and thin-layer chromatography of extracted lipids. Electron microscopy found the clot to be an amorphous mass without features to suggest crystalline properties. The x-ray dispersive analysis showed that the only elements which were significantly increased were chloride and silicon and the silicon detected was likely from the underlying catheter. Treatment with isopropyl alcohol-diethyl ether left an insoluble, flaky residue that resembled protein from a thrombus. Thin-layer chromatography detected a lipid profile suggestive of circulating endogenous fat instead of the fat that was infused through the catheter.
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PMID:Analytical assessment of Broviac catheter occlusion. 392 75

Silica is the major component of airborne dust generated by wind, manufacturing and/or demolition. Chronic occupational inhalation of silica dust containing crystalline quartz is by far the predominant form of silicosis in humans. Silicosis is a progressive lung disease that typically arises after a very long latency and is a major occupational concern with no known effective treatment. The mechanism of silicosis is not clearly understood. However, silicosis is associated with increased cell death, expression of redox enzymes and pro-fibrotic cytokines and chemokines. Since alveolar epithelial cell (AEC) death and disruption of alveolar fibrinolysis is often associated with both acute and chronic lung injuries, we explored whether p53-mediated changes in the urokinase-type plasminogen activator (uPA) system contributes to silica-induced lung injury. We further sought to determine whether caveolin-1 scaffolding domain peptide (CSP), which inhibits p53 expression, mitigates lung injury associated with exposure to silica. Lung tissues and AECs isolated from wild-type (WT) mice exposed to silica exhibit increased apoptosis, p53 and PAI-1, and suppression of uPA expression. Treatment of WT mice with CSP inhibits PAI-1, restores uPA expression and prevents AEC apoptosis by suppressing p53, which is otherwise induced in mice exposed to silica. The process involves CSP-mediated inhibition of serine-15 phosphorylation of p53 by inhibition of protein phosphatase 2A-C (PP2A-C) interaction with silica-induced caveolin-1 in AECs. These observations suggest that changes in the p53-uPA fibrinolytic system cross-talk contribute to lung injury caused by inhalation of silica dust containing crystalline quartz and is protected by CSP by targeting this pathway.
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PMID:Role of p53-fibrinolytic system cross-talk in the regulation of quartz-induced lung injury. 2559 29