Affiliation: Mount Sinai School of Medicine
- Reduction of neutrophil activity decreases early microvascular injury after subarachnoid haemorrhageVictor Friedrich
Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA
J Neuroinflammation 8:103. 2011..SAH was induced by endovascular perforation. Neutrophil infiltration and the integrity of vascular endothelium and basement membrane were assessed immunohistochemically. Vascular collagenase activity was assessed by in situ zymography...
- Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodiesE I B Peerschke
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York 10029, USA
Lupus 18:530-8. 2009..039). Sera from patients with aPL possess an enhanced capacity for in-situ complement fixation on platelets. This capacity may influence arterial thrombosis risk in patients with SLE...
- Complement activation on platelets correlates with a decrease in circulating immature platelets in patients with immune thrombocytopenic purpuraEllinor I B Peerschke
Weill Cornell Medical College of Cornell University, New York, NY, USA
Br J Haematol 148:638-45. 2010..063). Thus, complement fixation may contribute to the thrombocytopenia of ITP by enhancing clearance of opsonized platelets from the circulation, and/or directly damaging platelets and megakaryocytes...
- Complement activation on platelets: implications for vascular inflammation and thrombosisEllinor I Peerschke
Department of Pathology, Mount Sinai School of Medicine, New York, NY 10029, USA
Mol Immunol 47:2170-5. 2010..Taken together, these data support a role for platelet mediated complement activation in vascular inflammation and thrombosis...
- Blood platelets activate the classical pathway of human complementE I B Peerschke
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY, USA
J Thromb Haemost 4:2035-42. 2006..As platelets also posses binding sites for C1q, the recognition unit of the classical complement pathway, the present study examined classical pathway activation on platelets...
- gClqR/p33 in S. Aureus Endovascular PathogenesisEllinor Peerschke; Fiscal Year: 2005..Results from these studies will define a novel mechanism for S. aureus interactions at sites of endovascular damage, and may identify novel targets for therapeutic intervention. ..