The Greider lab uses biochemistry to study telomerase and cellular and organismal consequences of telomere dysfunction. Telomeres protect chromosome ends from being recognized as DNA damage and chromosomal rearrangements. Conventional replication leads to telomere shortening, but telomere length is maintained by the enzyme telomerase. Telomerase is required for cells that undergo many rounds of divisions, especially tumor cells and some stem cells. The lab has generated telomerase null mice that are viable and show progressive telomere shortening for up to six generations. In the later generations, when telomeres are short, cells die via apoptosis or senescence. Crosses of these telomerase null mice to other tumor prone mice show that tumor formation can be greatly reduced by short telomeres. The lab also is using the telomerase null mice to explore the essential role of telomerase stem cell viability. Telomerase mutations cause autosomal dominant dyskeratosis congenita. People with this disease die of bone marrow failure, likely due to stem cell loss. The lab has developed a mouse model to study this disease. Future work in the lab will focus on identifying genes that induce DNA damage in response to short telomeres, identifying how telomeres are processed and how telomere elongation is regulated.

Research in the Diane Griffin Lab focuses on the viral, cellular and immunologic determinants of diseases caused by alphaviruses and the measles virus. Our current studies aim to understand the immune-system mechanisms behind viral clearance and disease enhancement. Our team is also working to understand the pathogenesis of the measles virus, with a focus on developing new vaccines and learning how the virus induces immunosuppression.

The David Graham Lab studies the consequences of HIV interactions with the immune system, the resulting pathogenesis and how to sabotage these interactions. We apply advanced technologies like mass spectrometry to dissect processes at the molecular level. We are also actively involved in cardiovascular research and studies the ways proteins are organized into functional units in different cell types of the heart. Major projects in our lab are organized into three major areas: (1) H/SIV pathogenesis and neuropathogenesis, (2) Cardiovascular disease, and (3) High technology development

We study human B cells and neutralizing antibody responses against hepatitis C virus (HCV), hepatitis B virus (HBV), SARS-CoV-2, and respiratory syncytial virus (RSV). Our overarching hypothesis is that understanding the B cell response in individuals who naturally control infections, and those who have been vaccinated, can help us to understand the basic biology behind successful immune responses, leading to design of more effective vaccines. A particular technical strength of our laboratory is high dimensional flow cytometric analysis of antigen-specific B cells, which allows us to phenotype these rare cells, and also to sequence B cell receptor (BCR) repertoires and isolate virus-neutralizing monoclonal antibodies (mAbs).

Researchers in the Kathleen Sutcliffe Lab study organizational adaptability, reliability and resilience. Our work examines how factors such as management teams, group dynamics, information search processes, communication and learning processes affect organizational performance. Our team also studies how an organization’s design and culture affect members’ abilities to sense, manage and respond to dynamic demands. Additionally, our work seeks to better understand the factors that promote individual and organizational resilience.

The Saleh Alqahtani Lab has conducted clinical research on the management of fatty liver disease and viral hepatitis, including novel therapies. We’ve also been involved in various clinical trials related to liver cirrhosis, liver cancer and outcomes of liver transplant patients.

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.

Work in the Robert H. Brown Lab explores several topics within pulmonary physiology, with a long-term goal of understanding the structural changes in the lungs that lead to the pathophysiology of lung disease. Our core studies examine the structure-function relationship of pulmonary airways and vessels as well as their role in chronic obstructive pulmonary disease (COPD) and reactive airway disease. Recent research has involved studying the mechanisms and treatment of COPD progression, new methods for treating asthma, and lung inflation and airway hyperresponsiveness. We are also exploring the impact of HIV infection on the etiology of lung disease and the pathophysiologic consequences of lung distention.

Our lab evaluates new medications and/or techniques for the treatment of drug use disorder by conducting human laboratory studies to sensitively assess drug effects, and randomized controlled trial evaluations of medications for clinical treatment outcomes. We also focus on the development of outcome measures that are sensitive and clinically relevant.

The Franco D’Alessio Lab investigates key topics within the fields of critical care, internal and pulmonary medicine. We primarily explore immunological determinants of acute lung inflammation and repair. Our lab also investigates age-dependent lung immune response in patients with acute lung injury and acute respiratory distress syndrome (ARDS), regulatory T-cells in lung injury and repair, and modulation of alveolar macrophage innate immune response in ARDS.