C
Charles F. Moldow
Researcher at University of Minnesota
Publications - 30
Citations - 3466
Charles F. Moldow is an academic researcher from University of Minnesota. The author has contributed to research in topics: Endothelium & Endothelial stem cell. The author has an hindex of 19, co-authored 30 publications receiving 3421 citations. Previous affiliations of Charles F. Moldow include University of Mississippi.
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Journal ArticleDOI
Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.
TL;DR: An in vitro model of granulocyte-induced cytotoxicity was constructed utilizing 51Cr-labeled human umbilical vein endothelial cell cultures, suggesting that close approximation of the granulocytes and endothelial cells is necessary for maximal cell injury.
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Complement-induced granulocyte aggregation: an unsuspected mechanism of disease.
TL;DR: The capacity of blood cells to aggregate, best exemplified by the response of platelets to vascular injury, is generally thought to be beneficial, however, if aggregation occurs inappropriately—particularly if it involves large numbers of cells—it can be harmful.
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Abnormal Adherence of Sickle Erythrocytes to Cultured Vascular Endothelium: POSSIBLE MECHANISM FOR MICROVASCULAR OCCLUSION IN SICKLE CELL DISEASE
TL;DR: It is concluded that sickle RBC adhere to vascular endothelial cells in vitro, perhaps caused by a calcium-induced aberration of membrane topography, which may be a pathogenetic factor in the microvascular occlusions characteristic of sickle cell disease.
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Protection against lethal hyperoxia by tracheal insufflation of erythrocytes: role of red cell glutathione
B. Sweder van Asbeck,John R. Hoidal,John R. Hoidal,Gregory M. Vercellotti,Bruce A. Schwartz,Charles F. Moldow,Harry S. Jacob +6 more
TL;DR: Results suggest that insufflated erythrocytes, through their recyclable glutathione, protect rats from toxic oxygen species engendered by hyperoxia.
Journal Article
Bacterial adherence to fibronectin and endothelial cells: a possible mechanism for bacterial tissue tropism.
Gregory M. Vercellotti,Daniel Lussenhop,Phillip K. Peterson,Leo T. Furcht,James B. McCarthy,Harry S. Jacob,Charles F. Moldow +6 more
TL;DR: Bacteria specifically attach to endothelial cells and to fibronectin-coated surfaces, which suggests that the ability of a bacterium to attach to these substrates may reflect the propensity to invade and colonize vascular tissues such as cardiac valves.