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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:
Wong HR, Cvijanovich N, Allen G, Thomas N, Freishtat R, Anas N, Meyer K, Checchia P, Lin R, Shanley T, Bigham M, Wheeler DS, Doughty LA, Tegtmeyer K, Poynter SE, Kaplan JM, Chima RS, Stalets E, Basu RK, Varisco B, Barr F. Validation of a gene expression-based subclassification strategy for pediatric septic shock. Critical Care Medicine. Nov; 39:2511-2517. 2011.
Sherwin CMT, Ding L, Kaplan J, Spigarelli MG, Vinks AA. Optimal design for a single dose, sparse sampling, pharmacokinetic study in pediatrics subpopulations: A proposed study of pioglitazone in septic pediatric patients. Journal of Pharmacokinetics and Pharmacodynamics. 38: 433-447. 2011.
Kaplan JM, Zingarelli B. Novel therapeutic agents in pediatric sepsis: peroxisome proliferator receptor gamma (PPAR gamma). The Open Inflammation Journal. 4:120-124. 2011.
Kaplan JM, Wong HR. Biomarker discovery and development in pediatric critical care medicine. Pediatric Critical Care Medicine. 12:165-173. 2011.
Kaplan JM, Hake PW, Denenberg A, Mangeshkaar P, Piraino G, Zingarelli B. Phosphorylation of ERK 1/2 is associated with downregulation of PPARg during polymicrobial sepsis. Molecular Medicine. Nov-Dec; 16(11-12):491-7. 2010.
Wong HR, Wheeler DS, Tegtmeyer K, Poynter SE, Kaplan JM, Chima RS, Stalets E, Basu RK and Doughty LA. Toward a clinically feasible gene expression-based sub-classification strategy for pediatric septic shock; initial proof-of-concept. Critical Care Medicine. Oct; 38:1955-1961. 2010.
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 Medicine. Jan; 36:123-130. 2010.
Kaplan J, Cook J, O’Connor M, Zingarelli B. Peroxisome Proliferator Activated Receptor-γ is Required for the Inhibitory Effect of Ciglitazone but not 15-Deoxy-Δ12,14-Prostaglandin J2 on the NF-κB Pathway in Human Endothelial Cells. SHOCK. Dec; 28(6): 722-726. 2007.
Kaplan JM, Cook JA, Hake PW, O’Connor M, Burroughs TJ, Zingarelli B. 15-Deoxy-Δ12,14-Prostaglandin J2 (15d-PGJ2), A Peroxisome Proliferator Activated Receptor-γ Ligand, Reduces Tissue Leukosequestration and Mortality in Endotoxic Shock. SHOCK. July; 24(1): 59-65. 2005.
Jennifer M. Kaplan, MD, MSDivision of Critical Care MedicineCincinnati Children’s Hospital Medical CenterMLC 20053333 Burnet AvenueCincinnati, Ohio 45229
Phone: 513-636-4259Fax: 513-636-4267Jennifer.Kaplan@cchmc.org
Administrative assistant:Shawn Brockert
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026 | 1-513-636-4200 | 1-800-344-2462 | TTY:1-513-636-4900
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