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Mathew Parker Sharron, MD

The Center for Hospital-based Specialties

Departments
Critical Care Medicine

Programs
Pediatric Intensive Care Unit (PICU)


Board CertificationsAmerican Board of Pediatrics
American Board of Pediatrics/Critical Care
National Provider Identifier1134323900
E-Mail
Biography

Dr Sharron is an attending Physician in the Division of Critical Care Medicine and an Assistant Professor in the Departments of Pediatrics at the George Washington University School of Medicine and Health Sciences in Washington, DC. His research program focuses on platelets as cytotoxic mediators of apoptosis and multiple organ dysfunction in sepsis.
Education
TypeSchoolLocationDegreeField of StudyYears
Medical School Temple University School of Medicine Philadelphia, PADoctor of Medicine 2000 -2004

Training
TypeInstitutionLocationPositionSpecialtyYears
Internship Program St. Christopher's Hospital for Children Philadelphia, PAIntern Pediatrics 2004 - 2005
Residency Program St. Christopher's Hospital for Children Philadelphia, PAResident Pediatrics 2005 - 2007
Fellowship Program Children's National Medical Center Washington, DCFellow Pediatric Critical Care 2007 - 2010
National & International Recognitions
AwardInstitutionEventYear
Young Investigator Travel AwardPediatric Academic Society Meeting2010

Affiliations and Memberships
TitleInstitutionCommittee / SectionYears
MemberAmerican Academy of Pediatrics2004
MemberSociety for Critical Care Medicine2007
MemberAmerican Thoracic Society2009
Publications
Journal Article, 2 - Freishtat RJ, Natale J, Benton AS, Cohen J, Sharron M, Wiles AA, Ngor WM, Mojgani B, Bradbury M, Degnan A, Sachdeva R, Debiase LM, Ghimbovschi S, Chow M, Bunag C, Kristosturyan E, and Hoffman EP (2009), Sepsis alters the megakaryocyte-platelet transcriptional axis resulting in granzyme b-mediated lymphotoxicity, Am J Respir Crit Care Med , 179, 467-473.

Journal Article, Sharron M, Wiles AA, Hoptay C, Geha M, Benton AS, Nagaraju K, Freishtat RJ, Sepsis-Related Platelet-Induced End Organ Apoptosis Is Inhibited By GPIIb/IIIa Blockade.



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