The Experts below are selected from a list of 45 Experts worldwide ranked by ideXlab platform
Paul M. Ford - One of the best experts on this subject based on the ideXlab platform.
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Effects of cupric chloride on coagulation in human plasma: role of fibrinogen
Journal of Thrombosis and Thrombolysis, 2018Co-Authors: Vance G. Nielsen, Timothy D. Ward, Paul M. FordAbstract:Introduction Copper poisoning is associated with severe multiorgan injury and potentially death if chelation therapy is not administered. Of interest, while important gastrointestinal and Urinary Tract Hemorrhage is associated with copper poisoning, very little is known concerning the nature of copper induced coagulopathy. Methods Using thrombelastography, we assessed changes in coagulation kinetics in human plasma following exposure to copper concentrations encountered during poisoning. Results While time to commence coagulation was not compromised, both velocity of thrombus growth and final strength were diminished. This result was duplicated with one concentration of copper in factor XIII deficient plasma. This pattern of coagulation kinetic response was interpreted as copper mediated fibrinogen dysfunction, perhaps via oxidation of key fibrinogen disulfide bridges. Lastly, experiments wherein glutathione was added implicated copper generated radical oxygen species as one of the mechanisms responsible for compromised coagulation kinetics. Conclusions While chelation therapy is the key to survival following copper poisoning, perhaps this and future investigations of how copper affects coagulation may provide insight into effective supportive therapy for patients with active bleeding.
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Effects of cupric chloride on coagulation in human plasma: role of fibrinogen.
Journal of Thrombosis and Thrombolysis, 2018Co-Authors: Vance G. Nielsen, Timothy D. Ward, Paul M. FordAbstract:Copper poisoning is associated with severe multiorgan injury and potentially death if chelation therapy is not administered. Of interest, while important gastrointestinal and Urinary Tract Hemorrhage is associated with copper poisoning, very little is known concerning the nature of copper induced coagulopathy. Using thrombelastography, we assessed changes in coagulation kinetics in human plasma following exposure to copper concentrations encountered during poisoning. While time to commence coagulation was not compromised, both velocity of thrombus growth and final strength were diminished. This result was duplicated with one concentration of copper in factor XIII deficient plasma. This pattern of coagulation kinetic response was interpreted as copper mediated fibrinogen dysfunction, perhaps via oxidation of key fibrinogen disulfide bridges. Lastly, experiments wherein glutathione was added implicated copper generated radical oxygen species as one of the mechanisms responsible for compromised coagulation kinetics. While chelation therapy is the key to survival following copper poisoning, perhaps this and future investigations of how copper affects coagulation may provide insight into effective supportive therapy for patients with active bleeding.
Vance G. Nielsen - One of the best experts on this subject based on the ideXlab platform.
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Effects of cupric chloride on coagulation in human plasma: role of fibrinogen
Journal of Thrombosis and Thrombolysis, 2018Co-Authors: Vance G. Nielsen, Timothy D. Ward, Paul M. FordAbstract:Introduction Copper poisoning is associated with severe multiorgan injury and potentially death if chelation therapy is not administered. Of interest, while important gastrointestinal and Urinary Tract Hemorrhage is associated with copper poisoning, very little is known concerning the nature of copper induced coagulopathy. Methods Using thrombelastography, we assessed changes in coagulation kinetics in human plasma following exposure to copper concentrations encountered during poisoning. Results While time to commence coagulation was not compromised, both velocity of thrombus growth and final strength were diminished. This result was duplicated with one concentration of copper in factor XIII deficient plasma. This pattern of coagulation kinetic response was interpreted as copper mediated fibrinogen dysfunction, perhaps via oxidation of key fibrinogen disulfide bridges. Lastly, experiments wherein glutathione was added implicated copper generated radical oxygen species as one of the mechanisms responsible for compromised coagulation kinetics. Conclusions While chelation therapy is the key to survival following copper poisoning, perhaps this and future investigations of how copper affects coagulation may provide insight into effective supportive therapy for patients with active bleeding.
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Effects of cupric chloride on coagulation in human plasma: role of fibrinogen.
Journal of Thrombosis and Thrombolysis, 2018Co-Authors: Vance G. Nielsen, Timothy D. Ward, Paul M. FordAbstract:Copper poisoning is associated with severe multiorgan injury and potentially death if chelation therapy is not administered. Of interest, while important gastrointestinal and Urinary Tract Hemorrhage is associated with copper poisoning, very little is known concerning the nature of copper induced coagulopathy. Using thrombelastography, we assessed changes in coagulation kinetics in human plasma following exposure to copper concentrations encountered during poisoning. While time to commence coagulation was not compromised, both velocity of thrombus growth and final strength were diminished. This result was duplicated with one concentration of copper in factor XIII deficient plasma. This pattern of coagulation kinetic response was interpreted as copper mediated fibrinogen dysfunction, perhaps via oxidation of key fibrinogen disulfide bridges. Lastly, experiments wherein glutathione was added implicated copper generated radical oxygen species as one of the mechanisms responsible for compromised coagulation kinetics. While chelation therapy is the key to survival following copper poisoning, perhaps this and future investigations of how copper affects coagulation may provide insight into effective supportive therapy for patients with active bleeding.
Melvin E Clouse - One of the best experts on this subject based on the ideXlab platform.
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embolotherapy for lower Urinary Tract Hemorrhage
Journal of Vascular and Interventional Radiology, 2009Co-Authors: Vikash Prasad, Barry Sacks, Stanley Kraus, Melvin E ClouseAbstract:The patient characteristics, techniques used, and outcomes of 11 patients with lower Urinary Tract Hemorrhage treated with embolotherapy are described. The authors focus on bilateral superselective embolization of the arterial supply to the bladder and techniques to embolize multiple small vessels supplying the bladder when the vascular anatomy is complicated and superselective catheterization is not possible. The immediate success rate was 100%, with three later recurrences. One procedure was complicated by asymptomatic occlusion of the posterior division of the internal iliac artery. Embolotherapy can provide at least short-term success adequate to improve quality of life for palliation with few complications.
Barry Sacks - One of the best experts on this subject based on the ideXlab platform.
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embolotherapy for lower Urinary Tract Hemorrhage
Journal of Vascular and Interventional Radiology, 2009Co-Authors: Vikash Prasad, Barry Sacks, Stanley Kraus, Melvin E ClouseAbstract:The patient characteristics, techniques used, and outcomes of 11 patients with lower Urinary Tract Hemorrhage treated with embolotherapy are described. The authors focus on bilateral superselective embolization of the arterial supply to the bladder and techniques to embolize multiple small vessels supplying the bladder when the vascular anatomy is complicated and superselective catheterization is not possible. The immediate success rate was 100%, with three later recurrences. One procedure was complicated by asymptomatic occlusion of the posterior division of the internal iliac artery. Embolotherapy can provide at least short-term success adequate to improve quality of life for palliation with few complications.
Timothy D. Ward - One of the best experts on this subject based on the ideXlab platform.
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Effects of cupric chloride on coagulation in human plasma: role of fibrinogen
Journal of Thrombosis and Thrombolysis, 2018Co-Authors: Vance G. Nielsen, Timothy D. Ward, Paul M. FordAbstract:Introduction Copper poisoning is associated with severe multiorgan injury and potentially death if chelation therapy is not administered. Of interest, while important gastrointestinal and Urinary Tract Hemorrhage is associated with copper poisoning, very little is known concerning the nature of copper induced coagulopathy. Methods Using thrombelastography, we assessed changes in coagulation kinetics in human plasma following exposure to copper concentrations encountered during poisoning. Results While time to commence coagulation was not compromised, both velocity of thrombus growth and final strength were diminished. This result was duplicated with one concentration of copper in factor XIII deficient plasma. This pattern of coagulation kinetic response was interpreted as copper mediated fibrinogen dysfunction, perhaps via oxidation of key fibrinogen disulfide bridges. Lastly, experiments wherein glutathione was added implicated copper generated radical oxygen species as one of the mechanisms responsible for compromised coagulation kinetics. Conclusions While chelation therapy is the key to survival following copper poisoning, perhaps this and future investigations of how copper affects coagulation may provide insight into effective supportive therapy for patients with active bleeding.
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Effects of cupric chloride on coagulation in human plasma: role of fibrinogen.
Journal of Thrombosis and Thrombolysis, 2018Co-Authors: Vance G. Nielsen, Timothy D. Ward, Paul M. FordAbstract:Copper poisoning is associated with severe multiorgan injury and potentially death if chelation therapy is not administered. Of interest, while important gastrointestinal and Urinary Tract Hemorrhage is associated with copper poisoning, very little is known concerning the nature of copper induced coagulopathy. Using thrombelastography, we assessed changes in coagulation kinetics in human plasma following exposure to copper concentrations encountered during poisoning. While time to commence coagulation was not compromised, both velocity of thrombus growth and final strength were diminished. This result was duplicated with one concentration of copper in factor XIII deficient plasma. This pattern of coagulation kinetic response was interpreted as copper mediated fibrinogen dysfunction, perhaps via oxidation of key fibrinogen disulfide bridges. Lastly, experiments wherein glutathione was added implicated copper generated radical oxygen species as one of the mechanisms responsible for compromised coagulation kinetics. While chelation therapy is the key to survival following copper poisoning, perhaps this and future investigations of how copper affects coagulation may provide insight into effective supportive therapy for patients with active bleeding.
