The UPMC Children’s Hospital Foundation (CHPF) is a nonprofit organization dedicated to supporting the world-class research and clinical efforts at UPMC Children’s Hospital of Pittsburgh. As the sole fundraising arm for Children’s Hospital, the Foundation brings in support from the Pittsburgh community to further their vision of being a world leader in pediatric health care, education, and discovery.
And every year, as part of their support of research and discovery at Children’s and at the Department of Pediatrics, the CHPF pools some of its charitable resources to directly support the research efforts of the most promising faculty and clinical staff in their clinical, translational, and basic science endeavors. By supporting this early stage research, the CHPF ensures that groundbreaking science can continue to impact the lives of children here in Pittsburgh and around the world.
This year, the CHPF Trust is proud to announce two grants to clinician/researchers Megan Freeman, MD, PhD, and Aidan Porter, MD.
Freeman is an Assistant Professor of Pediatrics in the Division of Infectious Disease and works closely with our i4Kids organization. Her research primarily focuses on studying picornaviruses with central nervous system tropism using human tissue models (organoids) of relevant sites derived from induced, pluripotent stem cells. The current focus is on how enterovirus D68 (EV-D68) mediates acute flaccid myelitis (AFM), a polio-like illness, by using a novel human spinal cord organoid model.
Porter completed his fellowship in our Division of Nephrology, where his research focused on acute kidney injury and in medical education, with an effort to create an interactive, multidisciplinary curriculum to train ICU and nephrology fellows in the use of continuous renal replacement therapy (CRRT). Porter’s laboratory research focused on the Unfolded Protein Response (UPR), an intracellular “quality control” process governing the recycling of aberrant proteins. Porter studied how loss of a particular molecular chaperone impairs waste excretion and salt and water homeostasis in the renal tubules leading to acute kidney injury.
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