Deborah Stearns-Kurosawa, PhD

Assistant Professor, Boston University School of Medicine

Associate Professor, adjunct, Oklahoma State University Center for Veterinary Health Sciences

 

Contact Information

 

Department of Pathology and Laboratory Medicine

670 Albany Street

Boston, MA  02118

Office: 617-414-7092

E-mail:  dstearns@bu.edu

 

Education

BS in biochemistry, Pennsylvania State University, University Park, PA

PhD in chemistry, Cleveland State University, Cleveland, OH

 

Research Interests

 

So why is it that some people get a bacterial infection, feel lousy for a few days, take antibiotics and then forget about it when they go back to class or work, but other people get the same infection and die in two weeks in the intensive care unit? It’s all about how our bodies respond to the infection.  It’s a highly orchestrated response that requires input from our immune, coagulation, neurologic, and inflammatory pathways.  And this in turn requires coordinated responses from cells and molecules in each of these pathways.  If the response is too much, too little, too short, too long, too soon, too late, too fast, then the disintegration begins leading to multiple organ failure, shock and death.  We have multiple projects in the laboratory to identify contributions at the cellular, molecular and genetic level that contribute to different responses to infection.  We want to identify the point where this disintegration process remains irreversible, so that patients can be identified earlier with better prognosis and less morbidity.  

 

Publications

 

 

  • Kinasewitz G, Stearns-Kurosawa DJ, Kurosawa S.  Soluble Thrombomodulin: a sign of bad times.  Critical Care Medicine, in press, 2008.
  • Reiner, AP, Carty CL, Jenny NS, Nievergelt C, Cushman M, Stearns-Kurosawa DJ, Kurosawa S, Kuller LH, Lange LA.  PROC, PROCR and PROS1 polymorphisms, plasma anticoagulant phenotypes, and risk of cardiovascular disease and mortality in older adults: the Cardiovascular Health Study, J Thromb Haemost, in press 2008.
  • Ireland H, Konstantoulas CJ, Cooper JA, Hawe E, Humphries SE, Mather H, Goodall AH, Hogwood J, Juhan-Vague I, Yudkin JS, di Minno G, Margaglione M, Hamsten A, Miller GJ, Bauer KA, Kim YT, Stearns-Kurosawa DJ, Kurosawa S. EPCR Ser219Gly:  Elevated sEPCR, prothrombin F1 + 2, risk for coronary heart disease, and increased sEPCR shedding in vitro. Atherosclerosis, 183:283-292, 2005.
  • Matsumoto T, Kaneko T, Wada H, Kobayashi T,  Abe Y, Nobori T, Shiku H, Stearns-Kurosawa DJ, Kurosawa S. Proteinase 3 expression on neutrophil membranes from patients with infectious disease. Shock, 26:128-133, 2006.
  • Stearns-Kurosawa DJ, Lupu F, Taylor FB Jr, Kinasewitz G, Kurosawa S. Sepsis and pathophysiology of anthrax in a non-human primate model.  Am J Pathol, 169:433-444, 2006.
  • Kaneko T, Stearns-Kurosawa DJ, Taylor, Jr. F, Twigg M, Osaki K, Kinasewitz GT, Peer G, Kurosawa S.  Down-modulation of neutrophil CD10 expression in non-human primates and humans after in vivo septic challenge.  SHOCK 20:130-137, 2003.
  • Stearns-Kurosawa DJ, Swindle K, D’Angelo A, Della Valle P, Fattorini A, Caron N, Grimaux M, Woodhams B, Kurosawa S.  Plasma levels of endothelial protein C receptor respond to anticoagulant treatment.  Blood, 99:526-530, 2002.
  • Boomsma MM, Stearns-Kurosawa DJ, Stegeman CA, Raschi E, Meroni PL, Kurosawa S, Cohen Tervaert JW.   Plasma levels of soluble endothelial cell protein C receptor in patients with Wegener’s granulomatosis.  Clin Exp Immunol, 128:187-194, 2002
  • Taylor FB Jr, Stearns-Kurosawa DJ, Kurosawa S, Ferrell G, Chang AC, Laszik Z, Kosanke S, Peer G, Esmon CT: The endothelial cell protein C receptor aids in host defense against Escherichia coli sepsis.  Blood 95:1680-1686, 2000.
  • Kurosawa S, Esmon CT, DJ Stearns-Kurosawa: The soluble endothelial protein C receptor binds to activated neutrophils: involvement of proteinase-3 and CD11b/CD18. J. Immunol, 165:4697-4703, 2000.
Primary teaching affiliate
of BU School of Medicine