E I B Peerschke

Summary

Affiliation: Cornell University
Country: USA

Publications

  1. ncbi The laboratory evaluation of platelet dysfunction
    Ellinor 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
  2. ncbi Proposed research training guidelines for residents in laboratory medicine
    Ellinor 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
  3. ncbi Human blood platelet gC1qR/p33
    E I Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, USA
    Immunol Rev 180:56-64. 2001
  4. pmc The contribution of gC1qR/p33 in infection and inflammation
    Ellinor 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
  5. ncbi Blood platelets activate the classical pathway of human complement
    E 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
  6. pmc gC1qR/p33 blockade reduces Staphylococcus aureus colonization of target tissues in an animal model of infective endocarditis
    Ellinor 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
  7. ncbi Tissue factor pathway inhibitor-2 (TFPI-2) recognizes the complement and kininogen binding protein gC1qR/p33 (gC1qR): implications for vascular inflammation
    Ellinor 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
  8. ncbi Ex vivo evaluation of erythrocytosis-enhanced platelet thrombus formation using the cone and plate(let) analyzer: effect of platelet antagonists
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, NY, USA
    Br J Haematol 127:195-203. 2004
  9. ncbi Activation-dependent surface expression of gC1qR/p33 on human blood platelets
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, New York 10021, USA
    Thromb Haemost 89:331-9. 2003
  10. pmc Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies
    E 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

Collaborators

Detail Information

Publications28

  1. ncbi The laboratory evaluation of platelet dysfunction
    Ellinor 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...
  2. ncbi Proposed research training guidelines for residents in laboratory medicine
    Ellinor 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...
  3. ncbi Human blood platelet gC1qR/p33
    E 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...
  4. pmc The contribution of gC1qR/p33 in infection and inflammation
    Ellinor 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
    ....
  5. ncbi Blood platelets activate the classical pathway of human complement
    E 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...
  6. pmc gC1qR/p33 blockade reduces Staphylococcus aureus colonization of target tissues in an animal model of infective endocarditis
    Ellinor 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...
  7. ncbi Tissue factor pathway inhibitor-2 (TFPI-2) recognizes the complement and kininogen binding protein gC1qR/p33 (gC1qR): implications for vascular inflammation
    Ellinor 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...
  8. ncbi Ex vivo evaluation of erythrocytosis-enhanced platelet thrombus formation using the cone and plate(let) analyzer: effect of platelet antagonists
    Ellinor 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...
  9. ncbi Activation-dependent surface expression of gC1qR/p33 on human blood platelets
    Ellinor 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...
  10. pmc Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies
    E 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...
  11. ncbi Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions
    Ellinor 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
    ....
  12. pmc Expression of complement components and inhibitors on platelet microparticles
    Wei 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...
  13. pmc Platelet mediated complement activation
    Ellinor 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)...
  14. pmc Evidence that a C1q/C1qR system regulates monocyte-derived dendritic cell differentiation at the interface of innate and acquired immunity
    Kinga 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)...
  15. doi 2008 ACLPS panel discussion on resident education in clinical pathology
    Eline 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...
  16. doi Complement activation on platelets correlates with a decrease in circulating immature platelets in patients with immune thrombocytopenic purpura
    Ellinor 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...
  17. doi Laboratory assessment of factor VIII inhibitor titer: the North American Specialized Coagulation Laboratory Association experience
    Ellinor 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...
  18. doi Lupus anticoagulant testing: performance and practices by north american clinical laboratories
    Francine 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...
  19. ncbi Protein S assays: an analysis of North American Specialized Coagulation Laboratory Association proficiency testing
    Elizabeth 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...
  20. ncbi Receptor for the globular heads of C1q (gC1q-R, p33, hyaluronan-binding protein) is preferentially expressed by adenocarcinoma cells
    Daniel B Rubinstein
    Section of Hematology Oncology, Boston University School of Medicine, Boston, MA 02118, USA
    Int J Cancer 110:741-50. 2004
    ....
  21. ncbi cC1q-R (calreticulin) and gC1q-R/p33: ubiquitously expressed multi-ligand binding cellular proteins involved in inflammation and infection
    Berhane 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
    ....
  22. ncbi gC1q-R/p33: structure-function predictions from the crystal structure
    Berhane Ghebrehiwet
    Department of Medicine, State University of New York, Stony Brook 11794 8161, USA
    Immunobiology 205:421-32. 2002
    ....
  23. ncbi Cooperation of C1q receptors and integrins in C1q-mediated endothelial cell adhesion and spreading
    Xiaodong 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...
  24. ncbi gC1qR/p33 serves as a molecular bridge between the complement and contact activation systems and is an important catalyst in inflammation
    Berhane Ghebrehiwet
    Department of Medicine, SUNY at Stony Brook, Stony Brook, NY 11794, USA
    Adv Exp Med Biol 586:95-105. 2006
    ....
  25. ncbi Zinc induces exposure of hydrophobic sites in the C-terminal domain of gC1q-R/p33
    Rajeev 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...
  26. ncbi Complement component C1q induces endothelial cell adhesion and spreading through a docking/signaling partnership of C1q receptors and integrins
    Berhane 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...
  27. ncbi Rituximab in the treatment of acquired factor VIII inhibitors
    Adrian 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...
  28. pmc Regulated complement deposition on the surface of human endothelial cells: effect of tobacco smoke and shear stress
    Wei 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...