Does blockade of Thrombopoietin reduce Organ Damage in Experimental Endotoxemia and Polymicrobial Sepsis?
Our results demonstrate that TPO participates in the development of organ damage induced by experimental endotoxemia or polymicrobial sepsis via a mechanism involving increased platelet-leukocyte adhesion, but not cytokine release, and suggest that blocking TPO may be useful in preventing organ damage in patients affected by systemic inflammatory response or sepsis.
This is the first description of an intragenic duplication of EHMT1 resulting in Kleefstra syndrome.