Thromboinflammatory diseases result from the interactions of vascular endothelial cells, inflammatory cells, and platelets with cellular adhesion molecules, plasma proteins, and lipids. Tipping the balance toward a prothrombotic, proinflammatory phenotype results from multicellular activation signals. In this issue of the
Gregory M. Vercellotti, John D. Belcher
Histology of a venule in the dorsal skin of transgenic sickle mice after 1 hour of hypoxia and 1 hour of reoxygenation.