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Sepsis is a response to infection that can lead to a massive and dysregulated systemic inflammatory response resulting in multiple organ dysfunction and death. Although treatment with antibiotics treats the underlying infection, it does not reverse the cascade of signaling events activating the inflammatory responses. There are few interventional trials demonstrating clinical benefit in patients with sepsis. The Kaplan Laboratory is dedicated to understanding and treating the inflammatory responses in sepsis by using a basic, translational and clinical research approach.
Our research focuses on three main areas:
Kaplan JM, Denenberg A, Monaco M, Nowell M, Wong H, Zingarelli B. Changes in peroxisome proliferator-activated receptor-gamma activity in children with septic shock. Intensive Care Med. 2010 Jan;36(1):123-30.
Kaplan JM, Hake PW, Denenberg A, Mangeshkaar P, Piraino G, Zingarelli B. Phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 Is associated with the downregulation of peroxisome proliferator-activated receptor (PPAR)-γ during polymicrobial sepsis. Mol Med. 2010 Nov-Dec; 16(11-12):491-7.
Kaplan J, Cook J, O’Connor M, Zingarelli B. Peroxisome proliferator-activated receptor gamma is required for the inhibitory effect of ciglitazone but not 15-deoxy-Delta 12,14-prostaglandin J2 on the NFkappaB pathway in human endothelial cells. Shock. 2007 Dec; 28(6): 722-726.
Kaplan JM, Cook JA, Hake PW, O’Connor M, Burroughs TJ, Zingarelli B. 15-Deoxy-delta(12,14)-prostaglandin J(2) (15D-PGJ(2)), a peroxisome proliferator activated receptor gamma ligand, reduces tissue leukosequestration and mortality in endotoxic shock. Shock. 2005 July; 24(1): 59-65.
Jennifer M. Kaplan, MD, MSDivision of Critical Care MedicineCincinnati Children’s Hospital Medical Center
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