The Systems Biology Lab applies methods of multiscale modeling to problems of cancer and cardiovascular disease, and examines the systems biology of angiogenesis, breast cancer and peripheral artery disease (PAD). Using coordinated computational and experimental approaches, the lab studies the mechanisms of breast cancer tumor growth and metastasis to find ways to inhibit those processes. We use bioinformatics to discover novel agents that affect angiogenesis and perform in vitro and in vivo experiments to test these predictions. In addition we study protein networks that determine processes of angiogenesis, arteriogenesis and inflammation in PAD. The lab also investigates drug repurposing for potential applications as stimulators of therapeutic angiogenesis, examines signal transduction pathways and builds 3D models of angiogenesis. The lab has discovered over a hundred novel anti-angiogenic peptides, and has undertaken in vitro and in vivo studies testing their activity under different conditions. We have investigated structure-activity relationship (SAR) doing point mutations and amino acid substitutions and constructed biomimetic peptides derived from their endogenous progenitors. They have demonstrated the efficacy of selected peptides in mouse models of breast, lung and brain cancers, and in age-related macular degeneration.

Chronic rhinosinusitis (CRS) is a leading cause of morbidity globally and is the single most common self-reported chronic health condition and accounts for billions of dollars in health care costs and lost work days annually. Exposure to air pollutants is thought to be a critical modifier of CRS susceptibility. Despite marked reductions in air pollution levels in the United States, the fine particulate component of air pollution (PM2.5) and ultrafine pollutants secondary to traffic continue to remain a recalcitrant issue globally and in the United States. The Ramanathan Lab focuses on studying the role of air pollution (PM2.5) in CRS. In collaboration with scientists at the Bloomberg School of Public Health, we have utilized a state of the art air pollution exposure system to develop a novel mouse model of air pollution induced rhinosinusitis that mimics many of the features of CRS in humans. Our lab uses transgenic mouse models and novel immunologic/genomic techniques to study the mechanisms by which PM2.5 causes eosinophilic inflammation and sinonasal epithelial barrier dysfunction. We are also interested in the role of the antioxidant transcription factor, Nrf2, which has shown to stabilize the epithelial barrier and reduce eosinophilia in PM induced rhinosinusitis as a potential therapeutic target.

Dr. Parikh's research focuses on the translation and validation of novel biomarkers for the diagnosis and prognosis of acute kidney injury. Progress in kidney diseases has been hamstrung by significant heterogeneity within the current disease definitions, which are largely based on serum creatinine. Dr. Parikh's research has addressed this critical challenge by developing biomarkers of renal tubular injury, repair, and inflammation to dissect this heterogeneity. He has assembled multicenter longitudinal prospective cohorts for translational research studies across several clinical settings of acute kidney injury and chronic kidney disease for the efficient translation of novel biomarkers.

His research is dedicated to the process of applying discoveries generated in the laboratory and in preclinical experiments, the development of clinical studies, and the design of clinical trials. Dr. Parikh's studies have refined the clinical definition in perioperative acute kidney injury and hepatorenal syndrome, developed strategies to reduce kidney discard in deceased donor transplantation, and advanced regulatory approvals of kidney injury biomarkers. He has also developed biomarkers to identify rapid progressors of early diabetic kidney disease before derangements in serum creatinine. Dr. Parikh's research goal is to translate our understanding of pathophysiological mechanisms into clinical practice and improve the outcomes in patients with kidney disease.

Dr. Parikh has also been the recipient of numerous honors, including the 2017 Young Investigator Award from the American Society of Nephrology.

Work in the Philip Smith Lab explores several key topics within the field of sleep medicine. We investigate the role of obesity and neural control in sleep-disordered breathing as well as the impact of metabolic function on sleep apnea. We also research the ways in which HIV and its treatments impact a patient’s sleep. Our studies have included the effects of HIV and highly active antiretroviral therapy (HAART) on both sleep and daytime function as well as the relationship between systemic inflammation and sleep apnea in men with HIV.

The Lane laboratory is focused on understanding molecular mechanisms underlying chronic rhinosinusitis, particularly the pathogenesis of nasal polyps, as well as inflammation on the olfactory epithelium. Diverse techniques in molecular biology, immunology, and physiology are utilized to study epithelial cell innate immunity, olfactory loss, and response to viral infection. Ongoing work explores how epithelial cells of the sinuses and olfactory mucosa participate in the immune response and contribute to chronic inflammation. The lab creates and employs transgenic mouse models of chronic nasal/sinus inflammation to support research in this area. Collaborations are in place with the School of Public Health to explore mechanisms of anti-viral immunity in influenza and COVID-19.

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.