Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Anne Wiesinger"'
Autor:
Anne Wiesinger, Wladimir Peters, Daniel Chappell, Dominik Kentrup, Stefan Reuter, Hermann Pavenstädt, Hans Oberleithner, Philipp Kümpers
Publikováno v:
PLoS ONE, Vol 8, Iss 11, p e80905 (2013)
The endothelial glycocalyx (eGC), a carbohydrate-rich layer lining the luminal side of the endothelium, regulates vascular adhesiveness and permeability. Although central to the pathophysiology of vascular barrier dysfunction in sepsis, glycocalyx da
Externí odkaz:
https://doaj.org/article/adcbc038534842fa9a6a4efe36e7b1d5
Autor:
Martin Hausberg, Uta Hillebrand, Susanne Amler, Hans Oberleithner, Marcus Brand, Manfred Fobker, Gabriele Köhler, Stefan Reuter, Hermann Pavenstädt, Giovana Seno Di Marco, Philipp Kümpers, Detlef Lang, Anne Wiesinger, Christian Stock, Maximilian König, Friedrich Buck, Stefanie Reiermann
Publikováno v:
Kidney International. 83(2):213-222
Hyperphosphatemia is associated with increased cardiovascular risk in patients with renal disease and in healthy individuals. Here we tested whether high phosphate has a role in the pathophysiology of cardiovascular events by interfering with endothe
Autor:
Philipp Kümpers, Anne Wiesinger, Jan Sören Padberg, Stefan Reuter, Hermann Pavenstädt, Giovana Seno Di Marco, Alexander Lukasz, Marcus Brand, Hans Oberleithner, Dominik Kentrup, Alexander Grabner
Publikováno v:
Atherosclerosis. 234(2)
The endothelial glycocalyx (eGC), a mesh of anionic biopolymers covering the luminal surface of endothelial cells, is considered as an intravascular compartment that protects the vessel wall against pathogenic insults in cardiovascular disease. We hy
Publikováno v:
The Journal of trauma. 71(5)
Autor:
Wladimir Peters, Stefanie Korte, Kristina Kusche-Vihrog, Anne Wiesinger, Alexandra S. Straeter, Hans Oberleithner
Publikováno v:
Pflugers Archiv : European journal of physiology. 463(2)
Plasma sodium, slightly above normal and in presence of aldosterone, stiffens vascular endothelium and reduces nitric oxide release with the consequence of endothelial dysfunction. This process is mediated by epithelial sodium channels (ENaC) and, mo