Degrees:

Janet L. Rossi, MD

Assistant Professor of Pediatrics
Section of Critical Care

Children's Hospital
200 Henry Clay Avenue
New Orleans, LA 70118

Phone: (504) 894-5428
Fax: (504) 894-5389

E-mail: jross5@lsuhsc.edu
 

 
MD – 1997
Louisiana State University School of Medicine

 

Biography:



Pediatric Residency – Louisiana State University Health Sciences Center, New Orleans, LA, 1997-2000

Fellow, Pediatric Critical Care Medicine
Children's Memorial Hospital, Chicago, IL 2000-2003

 Board Certification:
American Board of Pediatrics

 

Research/
Clinical
Interests

 

Tissue barrier dysfunction related to injury

Cerebral Edema is a common complication of many different diseases in the Pediatric Intensive Care Unit. Multiple different pathways are involved in the development of cerebral edema for example immunology, neuroendocrine, metabolic, cardiovascular, neurologic, signal transduction, cytoskeletal organization, DNA replication and repair are just a few of the pathways that contribute to the development of cerebral edema with different levels of contributions depending on the underlying cause of the cerebral edema. Traumatic Brain Injury (TB) is one disease process that develops cerebral edema in children but begins with all systems in homeostasis before the injury. The injury then sets in motion alterations in every pathway, culminating in the development of cerebral edema resulting in neurological decline and life long deficits. Using a closed head mouse model of pediatric TBI we are investigating the stimulus leading to the disruption of pathways leading to cerebral edema. Understanding the stimulus that disrupts multiple pathways will lead to identifying potential targets for repair.