Samir Mukund Parikh, M.D.
|Title||Assistant Professor of Medicine|
|Institution||Beth Israel Deaconess Medical Center|
|Address||Beth Israel Deaconess Med Ctr|
Research North 280C
330 Brookline Ave
Boston MA 02215
Available: 07/18/12, Expires: 07/17/14
The host immune response to severe infections has evolved in concert with exposure to microbial pathogens. The result is a multi-tiered, highly coordinated, redundant inflammatory and immune attack against invasive organisms. In sepsis, the host response is severe enough to injure its own organs, often culminating in death from shock and multi-organ failure. Yet, efforts to therapeutically manipulate the immune response in sepsis have uniformly failed.
Our laboratory studies another approach to sepsis--namely, limiting the bystander damage. In particular, we study molecular mechanisms in the vascular endothelium that prevent the profound leakiness of blood vessels that contributes to lung injury, hypoxia, and shock in sepsis. Applying a combination of human, animal, and cellular studies, we have found across-the-board evidence implicating one such pathway as a critical mediator of vascular leak and inflammation in sepsis, the Angiopoietin-Tie2 axis. We have proposed that Angiopoietin-2 may be an early prognostic biomarker of adverse outcomes in severe sepsis, and we have found that novel methods of stimulating Tie-2 prevent leakage and death of septic animals.
Defined student role: The interested student will perform laboratory-based research to study molecular mechanisms of Angiopoietin action in cellular models of sepsis and animal tissues. The project will utilize cloning, eukaryotic cell culture, PCR, Western analysis, confocal microscopy, and/or ELISA. This setting will provide an opportunity to perform translational research on a medically important topic, the results of which may have a lasting impact on the field.
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