Daniel Swarovski Forschungslabor
Group: Mechanisms of ischemia/reperfusion (IR)- associated organ damage
Stefan Schneeberger, MD
Gerald Brandacher, MD
Members of the group: Felix Aigner, MD; Manuel Maglione, MD; Oliver Renz, MD; Kienzl Katrin; Stefan Scheidl; Otto Steinmassl; Thomas Michael; Dominik Wiedemann; Patrizia Grundinger; Herbert Maier; Bernhard Holzknecht;
The following topics are worked on in the area of "Mechanisms of ischemia/reperfusion (IR)- associated organ damage"
Topics:
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One major subject of our research is ischemia/reperfusion (I/R) injury. Early as well as late consequences of cold ischemia in organ transplantation have been investigated. Profiling gene expression after I/R allowed for detection of novel genes involved in this setting. These data now serve as the basis for developing novel therapeutic strategies for prevention/treatment of I/R injury.
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Definition of the role of Secretory Leukocyte Protease Inhibitor in I/R injury in cardiac transplantation. Effect of endogenous as well as exogenous SLPI in a mouse heart transplant model.
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To draw a comprehensive picture of intracellular signal propagation as well as of cellular events caused by I/R using the established heterotopic heart transplant model in the mouse and isolated cardiomyocytes as model systems. This work will provide the groundwork required for the identification of suitable candidates for the targeted interference with the events leading to I/R- induced organ damage.
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Elucidation of the immunosuppressive action of 4-amino tetrahydrobiopterin, a novel pterin based iNOS inhibitor. Pathogenetic mechanisms of iNOS in ischemia and reperfusion injury with a special interest on the influence on mitochondrial function following cardiac as well as islet cell ischemia reperfusion injury.
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To establish possible strategies for tolerance induction via modulation of tryptophan catabolism in dendritic cells and CD4+CD25+ T-regulatory cells by costimulatry blockade and conventional immunosuppressive agents.
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Assessment of the pathophysiologic significance of IDO mediated tryptophan catabolism following human solid organ transplantation.
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