The Robert Wise Lab conducts clinical trials to study chronic obstructive lung diseases (COPD). We investigate inhaled corticosteroids in patients with mild to moderate COPD and the effectiveness of anti-inflammatories in allowing lung growth in mild to moderate asthmatic children. Our research includes exploring the efficacy of various treatments for asthmatic women who are pregnant and of lung-volume reduction surgery for emphysema patients. We also conduct studies of the clinical epidemiology, pathobiology and treatment of interstitial lung disease in patients with scleroderma.

Dr. Raul Chavez-Valdez is an assistant professor in the Department of Pediatrics with great interest in the mechanisms of delayed injury and repair/regeneration in the developing neonatal brain following injury, specifically following hypoxic-ischemic encephalopathy (birth asphyxia). He collaborates with Dr. Frances Northington (Pediatrics) and Dr. Lee Martin (Pathology/Neuroscience) in unveiling the importance of programmed necrosis in the setting of brain injury induced by birth asphyxia. He is especially interested in the role of brain derived neurotrophic factor and neurotrophin-4 following birth asphyxia and the changes that may explain the suspected excitatory/ inhibitory (E/I) imbalance particularly in the hippocampus. His work is highly translational since delayed hippocampal injury due to E/I imbalance may explain memory deficits observed despite therapeutic hypothermia in neonates suffering birth asphyxia. All of these aspects of developmental neuroplasticity are the base of his Career Development Award (NIH/NINDS-K08 award) and applications to other agencies. Additionally, he is part of multiple clinical efforts as part of the Neuroscience Intensive Care Nursery (NICN). He has been a Sutland-Pakula Endowed Fellow of Neonatal Research since September 2013.

Work in the Rachel Damico Lab explores topics within the fields of vascular biology and pulmonary medicine, with a focus on acute lung injury and apoptosis in lung diseases. Our studies have included examining idiopathic and scleroderma-associated pulmonary arterial hypertension, vascular receptor autoantibodies, and the link between inflammation and the Warburg phenomenon in patients with pulmonary arterial hypertension. We have also researched the inhibitory factor of macrophage migration and its governing of endothelial cell sensitivity to LPS-induced apoptosis.