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Li-Ke
He, M.D. |
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Research
Assistant Professor, Department of Surgery
Doctor of Medicine, The Third Military Medical University,
Shanghai, China
Interest:
Myelopoiesis following burn injury and sepsis
Despite
advances in critical care and anti-infective therapy, sepsis
after severe thermal injury remains a major cause of mortality.
The production and release, as well as the functional activity
of granulocytes and macrophages, which are key components
of the host defense system, are significantly altered following
burn injury and sepsis. The previous studies done by Dr. He
and the research team he is working with have shown with a
murine model that burn injury and sepsis resulted in a reduction
in the proliferative capacity of the bone marrow granulocyte-macrophage
progenitor cells (GM-CFC). This reduction is closely related
to the increased production of prostaglandin E2 (PGE2) in
bone marrow after burn and sepsis. The major source of PGE2
is most likely hyper-activated macrophage itself. Furthermore,
the bone marrow milieu seems to become conducive to monocytopoiesis.
The highly increased production of G-CSF in hematopoietic
tissues cannot correct sepsis-induced neutropenia. It may
be explained by the reduced expression of G-CSF receptors
in bone marrow resulted from sepsis. The production and function
of cyclooxygenase 1 and 2 (COX-1 and 2) have been dysregulated
following burn sepsis, and the administration of selective
COX-2 inhibitor significantly improved the suppression of
GM-CFC growth, neutropenia and survival. His future work is
to understand the mechanisms by which all observations they
have made will be extended, connected to each other, and fitted
in the complicated network of myelopoiesis in response to
injury and sepsis, eventually contributed to the treatment
strategy of burn patients.
Representative
Publications
View a partial list of
Dr.
He's publications through the National
Library of Medicine's PubMed online database.
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