I am a child at heart. I love kids, and most of my jobs growing up dealt with kids. But I love science, too, and I wanted to pursue laboratory-based research.
As I advanced in my studies and spent increasing amounts of time in the lab, I missed human interaction. I decided then that being a pediatrician would allow me to pursue my scientific interests while also applying them in a meaningful way as I cared for sick children and their families.
I chose pediatric critical care because I'm a tinkerer. I love to know how things work, and I love fixing them when they don't. Human physiology is intricate and amazing, but when it goes wrong, kids can get very sick. I love having the knowledge and tools to understand and fix that physiology in real-time in the intensive care unit (ICU) to help kids get better from life-threatening diseases.
Currently, I study sepsis and sepsis-induced organ failure, specifically how cellular metabolism changes in sepsis-associated heart and kidney failure. My research interests stem from a medical school rotation in the pediatric ICU. There, I helped care for two unrelated boys admitted to the hospital within 24 hours of each other, each with severe septic shock. Though their clinical presentations were very similar, one unfortunately succumbed to sepsis while the other recovered. I was intrigued, and I wanted to know why.
Since then, I have studied the fundamental mechanisms of sepsis to better understand how it works and what we, as doctors, can do to fix it. I want to do everything possible to prevent negative outcomes for children when they get sick.
My research focuses on the downstream effects of the inflammatory signals released by the immune system in response to significant infection. Sepsis causes the release of high levels of these inflammatory signals, which then influence cells to change how they function. In response, cells adapt their metabolism and alter what they do. Sepsis-associated organ failure is caused by cells that stop performing their normal functions.
My expectation is that, when we understand how inflammation changes cellular metabolism and function, we can design more targeted, effective treatments to reverse the pathological cellular changes and restore organ function.
MD: University of Rochester School of Medicine, Rochester, NY, 2005.
Residency: General Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, 2008.
Fellowship: Pediatric Critical Care, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2011.
Pediatric Intensive Care Unit PICU
Detrimental effects of PCSK9 loss-of-function in the pediatric host response to sepsis are mediated through independent influence on Angiopoietin-1. 2023.
First-Time Use of the Seraph® 100 Microbind® Affinity Blood Filter in an Adolescent Patient with Severe COVID-19 Disease: A Case Report. Case Reports in Nephrology and Dialysis. 2023; 13:1-6.
Choline supplementation attenuates experimental sepsis-associated acute kidney injury. American Journal of Physiology - Renal Physiology. 2022; 323:F255-F271.
Candidate Biomarkers for Sepsis-Associated Acute Kidney Injury Mechanistic Studies. Shock. 2022; 57:687-693.
Multi-Organ Transcriptome Dynamics in a Mouse Model of Cecal Ligation and Puncture-Induced Polymicrobial Sepsis. Journal of Inflammation Research. 2021; 14:2377-2388.
The application of omic technologies to research in sepsis-associated acute kidney injury. Pediatric Nephrology. 2021; 36:1075-1086.
NMR-based serum and urine metabolomic profile reveals suppression of mitochondrial pathways in experimental sepsis-associated acute kidney injury. American Journal of Physiology - Renal Physiology. 2021; 320:F984-F1000.
PPARα contributes to protection against metabolic and inflammatory derangements associated with acute kidney injury in experimental sepsis. Physiological Reports. 2019; 7.
Steve Standage, MD, Ming Tan, PhD ...5/26/2020
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