The Li Gao Lab researches functional genomics, molecular genetics and epigenetics of complex cardiopulmonary and allergic diseases, with a focus on translational research applying fundamental genetic insight into the clinical setting. Current research includes implementation of high-throughput technologies in the fields of genome-wide association studies (GWAS), massively parallel sequencing, gene expression analysis, epigenetic mapping and integrative genomics in ongoing research of complex lung diseases and allergic diseases including asthma, atopic dermatitis (AD), pulmonary arterial hypertension, COPD, sepsis and acute lung injury/ARDS; and epigenetic contributions to pulmonary arterial hypertension associated with systemic sclerosis.

The Frederick Wigley Lab is interested in the signs, symptoms and causes of scleroderma. We are testing new treatments for RaynaudÕs phenomenon and scleroderma. Understanding the treatment approach to Raynaud's phenomenon and associated ischemia and how to prevent digital ulcers is important for clinicians caring for these patients. Work in our lab has provided guidance in the management of Raynaud's phenomenon and digital ischemic ulcers, including options for the practical pharmacologic and nonpharmacologic interventions.

Our work is focused on the translational human in vivo and ex vivo assessments of right ventricular (RV) function in the setting of pulmonary hypertension. Among patients with group I pulmonary arterial hypertension PAH, those with systemic-sclerosis-associated PAH (SSc-PAH) have a particularly poor prognosis and less optimal response to PAH-guided therapy. Using in vivo pressure-volume catheterization of the right ventricle, we have uncovered key deficiencies in resting and reserve RV function in the SSc-PAH group when compared to idiopathic PAH (IPAH) patients. These studies have uncovered key discoveries with regards to right ventricular-pulmonary arterial (RV-PA) coupling in PAH. In the lab, by studying myofilament function from RV endomyocardial biopsies from these same patients, we have uncovered corresponding deficiencies in myofilament contractility and calcium sensitivity as well. Ongoing work is directed towards determining the underlying mechanism of these findings, which will hopefully lead to therapeutic applications for RV failure in SSc-PAH. Further endeavors are directed towards studying RV failure in other populations, including exercise-induced PH, PH secondary to left-heart disease, and the left ventricular assist device population.