Research Topics
| E I B PeerschkeSummaryAffiliation: Cornell University Country: USA Publications
| Collaborators
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Detail Information
Publications
The laboratory evaluation of platelet dysfunctionEllinor I B Peerschke
Department of Pathology, New York Presbyterian Hospital, Weill Medical College, Cornell University, 525 East 68th Street, Room F 715, New York, NY 10021, USA
Clin Lab Med 22:405-20. 2002..It remains to be seen whether such screening tests will better predict clinical bleeding or thrombotic risk...- Proposed research training guidelines for residents in laboratory medicineEllinor I B Peerschke
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA
Clin Lab Med 27:241-53; abstract v-vi. 2007..The proposed curricula are purposely unstructured to allow maximum flexibility for training programs to meet the needs and career goals of individual residents... - Human blood platelet gC1qR/p33E I Peerschke
Department of Pathology, Weill Medical College of Cornell University, New York, USA
Immunol Rev 180:56-64. 2001..Here we focus on the structure and function of platelet gC1qR and its emerging role in modulating platelet function at sites of vascular injury and inflammation... 
The contribution of gC1qR/p33 in infection and inflammationEllinor I B Peerschke
Department of Pathology, Weill Medical College of Cornell University, New York Presbyterian Hospital, 525 East 68th Street, Room F715, NY 10021, USA
Immunobiology 212:333-42. 2007....- 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... - gC1qR/p33 blockade reduces Staphylococcus aureus colonization of target tissues in an animal model of infective endocarditisEllinor I B Peerschke
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York, USA
Infect Immun 74:4418-23. 2006..aureus binding to fibrinogen. Such impacts may include direct modulation of complement (MAb 60.11) and kinin cascades (MAb 74.5.2) and/or activation of immune and inflammatory responses via localized immune complex formation... - Tissue factor pathway inhibitor-2 (TFPI-2) recognizes the complement and kininogen binding protein gC1qR/p33 (gC1qR): implications for vascular inflammationEllinor I B Peerschke
New York Presbyterian Hospital, Weill Cornell Center, 525 East 68th Street, Room F715, New York 10021, USA
Thromb Haemost 92:811-9. 2004..Taken together, these data suggest that gC1qR may participate in tissue remodeling and inflammation by localizing TFPI-2 to the pericellular environment to modulate local protease activity and regulate HK activation... - Ex vivo evaluation of erythrocytosis-enhanced platelet thrombus formation using the cone and plate(let) analyzer: effect of platelet antagonistsEllinor I B Peerschke
Department of Pathology, Weill Medical College of Cornell University, New York, NY, USA
Br J Haematol 127:195-203. 2004..These findings support the use of CPA for ex vivo evaluation of the contribution of RBC to platelet function and its inhibition under physiological shear conditions... - Activation-dependent surface expression of gC1qR/p33 on human blood plateletsEllinor I B Peerschke
Department of Pathology, Weill Medical College of Cornell University, New York, New York 10021, USA
Thromb Haemost 89:331-9. 2003..aureus protein A, supports the hypothesis that gC1qR expressed on activated platelets may contribute directly to thrombosis, inflammation, and endovascular infections... - 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... - Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesionsEllinor I B Peerschke
Department of Pathology, Weill Medical College of Cornell University, 525 East 68th Street, Room F715, New York, NY 10021, USA
Mol Immunol 41:759-66. 2004.... - Expression of complement components and inhibitors on platelet microparticlesWei Yin
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY, USA
Platelets 19:225-33. 2008..Complement activation contributes to a variety of vascular and inflammatory disease states including atherosclerosis and ischemia/reperfusion injury... - Platelet mediated complement activationEllinor I B Peerschke
Department of Pathology, The Mount Sinai School of Medicine, New York, NY 10029, USA
Adv Exp Med Biol 632:81-91. 2008..2007; Niculescu et al. 2004)... - Evidence that a C1q/C1qR system regulates monocyte-derived dendritic cell differentiation at the interface of innate and acquired immunityKinga K Hosszu
Department of Medicine, Stony Brook University, Stony Brook, New York, USA
Innate Immun 16:115-27. 2010..Thus, specific C1q/C1q receptor (R) interactions may control the transition from the monocyte state (innate immunity) toward the professional antigen-presenting cell state (adaptive immunity)... 
2008 ACLPS panel discussion on resident education in clinical pathologyEline T Luning Prak
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Am J Clin Pathol 131:618-22. 2009..Recommendations of the panel include the incorporation of active learning, clinical consultation, and competency assessment into CP resident training. A summary of the panel discussion is presented herein...- 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... - Laboratory assessment of factor VIII inhibitor titer: the North American Specialized Coagulation Laboratory Association experienceEllinor I B Peerschke
Department of Pathology, The Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Clin Pathol 131:552-8. 2009..These data provide information for the development of consensus guidelines to improve FVIII inhibitor quantification... - Lupus anticoagulant testing: performance and practices by north american clinical laboratoriesFrancine R Dembitzer
Center for Clinical Laboratories, 1425 Madison Ave, Room 8 02 A, New York, NY 10029, USA
Am J Clin Pathol 134:764-73. 2010..These data provide new insights into LAC testing in North America and identify opportunities for standardization... - Protein S assays: an analysis of North American Specialized Coagulation Laboratory Association proficiency testingElizabeth M Van Cott
Division of Clinical Laboratories, Department of Pathology, Massachusetts General Hospital, Boston 02114, USA
Am J Clin Pathol 123:778-85. 2005..Many total protein S antigen assays do not add to the diagnosis and can be unreliable for protein S deficiency subtyping. Better standardization of functional and antigenic assays is needed... - Receptor for the globular heads of C1q (gC1q-R, p33, hyaluronan-binding protein) is preferentially expressed by adenocarcinoma cellsDaniel B Rubinstein
Section of Hematology Oncology, Boston University School of Medicine, Boston, MA 02118, USA
Int J Cancer 110:741-50. 2004.... - cC1q-R (calreticulin) and gC1q-R/p33: ubiquitously expressed multi-ligand binding cellular proteins involved in inflammation and infectionBerhane Ghebrehiwet
Department of Medicine, State University of New York, Health Sciences Center, T 16040 State University of New York, Stony Brook, NY 11794 8161, USA
Mol Immunol 41:173-83. 2004.... - gC1q-R/p33: structure-function predictions from the crystal structureBerhane Ghebrehiwet
Department of Medicine, State University of New York, Stony Brook 11794 8161, USA
Immunobiology 205:421-32. 2002.... - Cooperation of C1q receptors and integrins in C1q-mediated endothelial cell adhesion and spreadingXiaodong Feng
Department of Dermatology, State University of New York, Health Sciences Center T 16 040, Stony Brook, NY 11794, USA
J Immunol 168:2441-8. 2002..Taken together these results suggest that endothelial cell adhesion and spreading require the cooperation of both C1qRs and beta(1) integrins and possibly other membrane-spanning molecules... - gC1qR/p33 serves as a molecular bridge between the complement and contact activation systems and is an important catalyst in inflammationBerhane Ghebrehiwet
Department of Medicine, SUNY at Stony Brook, Stony Brook, NY 11794, USA
Adv Exp Med Biol 586:95-105. 2006.... - Zinc induces exposure of hydrophobic sites in the C-terminal domain of gC1q-R/p33Rajeev Kumar
Department of Medicine, State University of New York, Stony Brook, NY 11794 8161, USA
Mol Immunol 39:69-75. 2002..Taken together, our data suggest that zinc can induce the exposure of hydrophobic sites in the C-terminal domain of gC1q-R involved in binding to HK/FXII... - Complement component C1q induces endothelial cell adhesion and spreading through a docking/signaling partnership of C1q receptors and integrinsBerhane Ghebrehiwet
Department of Medicine, Health Sciences Center, Division of Rheumatology, State University of New York, Stony Brook, NY 11794, USA
Int Immunopharmacol 3:299-310. 2003..5.2 and HK... - Rituximab in the treatment of acquired factor VIII inhibitorsAdrian Wiestner
Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
Blood 100:3426-8. 2002..Responses continue off treatment from more than 7 to more than 12 months. This report adds to the growing evidence that rituximab has efficacy in immune disorders resulting from autoantibody formation... - Regulated complement deposition on the surface of human endothelial cells: effect of tobacco smoke and shear stressWei Yin
Department of Pathology and Laboratory of Medicine, Weill Medical College of Cornell University, New York, New York, USA
Thromb Res 122:221-8. 2008..These results suggest that a balance between complement activation and regulation exists at the EC surface, and may impact vascular injury leading to thrombosis, arteriosclerosis, and atherogenesis...