Research in the Eliseo Guallar Lab focuses on the epidemiology and prevention of cardiovascular diseases. We have a special interest in the roles played by mercury, arsenic, lead and cadmium in cardiovascular disease development. Our methodological interests include determining threshold effects in epidemiological studies and applying statistical methods to epidemiological problem-solving.

Research in the Jochen Steppan Lab primarily focused on vascular stiffness related to aging. We are currently researching LOXL2 (lysine-oxidase-like-2), which might be intimately involved in the development or progression of vascular stiffness. We aim to better understand LOXL2's role in the vasculature and hope that this work leads to the characterization of a novel therapeutic target. This is important in the treatment of cardiovascular diseases in the aging population.

Researchers in the Adrian Dobs Lab study topics that include gonadal dysfunction, hyperlipidemia, diabetes mellitus, and the relationship between sex hormones and heart disease. We currently are investigating male gonadal function—with particular interest in new forms of male hormone replacement therapy—and hormonal changes related to aging.

Researchers in the Ami Shah Lab study scleroderma and Raynaud’s phenomenon. We examine the relationship between cancer and scleroderma, with a focus on how and if cancer causes scleroderma to develop in some patients. We are currently conducting clinical research to study ways to detect cardiopulmonary complications in patients with scleroderma, biological and imaging markers of Raynaud’s phenomenon, and drugs that improve aspects of scleroderma.

The Daniel Nyhan Lab studies vascular changes that accompany aging to determine the underlying causes and find ways to reverse the process. One goal of our research is to identify the factors that cause vascular stiffness. Our hope is that our work in vascular biology will lead to new ways to improve vascular compliance and thereby improve cardiovascular function and perioperative risk.

The Elizabeth Selvin Lab examines the intersection of epidemiology, clinical policy and public health policy. One of our key goals is to use the findings of epidemiologic research to inform the screening, diagnosis and treatment of diabetes, cardiovascular disease and kidney disease. Much of our work looks at biomarkers and diagnostics related to diabetes and diabetes complications. Our findings — linking hemoglobin A1c (HbA1c) to diabetic complications and identifying the role of A1c in diabetes diagnosis — have influenced clinical practice guidelines.

Work in the Wei Dong Gao Lab primarily focuses on heart failure and defining molecular and cellular mechanisms of contractile dysfunction. We use molecular biology and proteomic techniques to investigate the changes that myofilament proteins undergo during heart failure and under drug therapy. We're working to determine the molecular nature of nitroxyl (HNO) modification of tropomyosin.

Investigators in the Lakshmi Santhanam Lab examine the fundamental mechanisms behind cardiovascular disease. They are particularly interested in better understanding how nitric oxide-mediated S-nitrosylation (a post-translational protein modification) impacts protein function and trafficking in the vasculature as well as how this relationship influences matrix remodeling and vascular stiffening.

Research in the Lisa Yanek Lab focuses on cardiovascular disease in families and risk factor modification. Recently, we conducted a study to determine the association of lean versus fat mass with fitness in healthy, overweight and obese African Americans from families with early-onset coronary disease.

Work in the Lewis Romer Lab focuses on the responses of vascular systems to disease and injury. Using cultured human endothelial cells and fibroblasts from mice that lack expression of the FAK- or Src-family kinases, we’re exploring several topics. These include the effect of inflammatory cytokine on cell adhesion to the extracellular matrix; the role of FAK signaling in inhibiting apoptosis; and the function of FAK- and Src-family kinases in cell-matrix interactions during adhesion and motility.