Research in the Gregory Kirk Lab examines the natural history of viral infections — particularly HIV and hepatitis viruses — in the U.S. and globally. As part of the ALIVE (AIDS Linked to the Intravenous Experience) study, our research looks at a range of pathogenetic, clinical behavioral issues, with a special focus on non-AIDS-related outcomes of HIV, including cancer and liver and lung diseases. We use imaging and clinical, genetic, epigenetic and proteomic methods to identify and learn more about people at greatest risk for clinically relevant outcomes from HIV, hepatitis B and hepatitis C infections. Our long-term goal is to translate our findings into targeted interventions that help reduce the disease burden of these infections.

The Goley Lab is broadly interested in understanding cellular organization and dynamic reorganization, with particular focus on the roles of the cytoskeleton in these phenomena. We use cell biological, biochemical, genetic and structural approaches to dissect cytoskeletal processes with the aim of understanding how they work in molecular detail. Currently, we are focused on investigating the mechanisms underlying cytokinesis in bacteria. A deep understanding of cytoskeletal function in bacteria will aid in the identification of targets for novel antibiotic therapies and in efforts in synthetic biology.

Our lab is focused on determining the role of hypoxia in breast cancer metastasis. We are particularly interested in the changes in the extracellular matrix that occur under hypoxic conditions and promote cancer cell migration.

The Gail Berkenblit Lab focuses on HIV testing. We are particularly interested in the training of residents as it relates to HIV outpatient care, and the development and assessment of online curriculum.

The Gregory Diette Laboratory studies the epidemiology of lung diseases. Our focus is on asthma, chronic obstructive pulmonary disease (COPD) and environmental causes of lung disease, including allergens and particulate matter.

Our research is focused on understanding the basic mechanisms of programmed cell death in disease pathogenesis. Billions of cells die per day in the human body. Like cell division and differentiation, cell death is also critical for normal development and maintenance of healthy tissues. Apoptosis and other forms of cell death are required for trimming excess, expired and damaged cells. Therefore, many genetically programmed cell suicide pathways have evolved to promote long-term survival of species from yeast to humans. Defective cell death programs cause disease states. Insufficient cell death underlies human cancer and autoimmune disease, while excessive cell death underlies human neurological disorders and aging. Of particular interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death, particularly in the nervous system, in cancer and in virus infections. Interestingly, cell death regulators also regulate many other cellular processes prior to a death stimulus, including neuronal activity, mitochondrial dynamics and energetics. We study these unknown mechanisms. We have reported that many insults can trigger cells to activate a cellular death pathway (Nature, 361:739-742, 1993), that several viruses encode proteins to block attempted cell suicide (Proc. Natl. Acad. Sci. 94: 690-694, 1997), that cellular anti-death genes can alter the pathogenesis of virus infections (Nature Med. 5:832-835, 1999) and of genetic diseases (PNAS. 97:13312-7, 2000) reflective of many human disorders. We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). In addition, Bcl-2 family proteins have normal physiological roles in regulating mitochondrial fission/fusion and mitochondrial energetics to facilitate neuronal activity in healthy brains.

The Pomerantz Laboratory studies the molecular machinery used by cells to interpret extracellular signals and transduce them to the nucleus to affect changes in gene expression. The accurate response to extracellular signals results in a cell's decision to proliferate, differentiate or die, and it's critical for normal development and physiology. The dysregulation of this machinery underlies the unwarranted expansion or destruction of cell numbers that occurs in human diseases like cancer, autoimmunity, hyperinflammatory states and neurodegenerative disease. Current studies in the lab focus on signaling pathways that are important in innate immunity, adaptive immunity and cancer, with particular focus on pathways that regulate the activity of the pleiotropic transcription factor NF-kB.

Research in the Joseph Carrese Lab focuses on clinical ethics and professionalism, with a particular interest in medical education and examining ethical issues in the context of cultural diversity. We collaborate with colleagues to design, implement and evaluate educational curricula addressing ethics and professionalism issues in clinical practice.

Research in the Joseph Margolick Lab focuses on the many effects of HIV/AIDS on human health. We are particularly interested in the mechanisms of T-cell loss and preservation among people infected with HIV and the evaluation of human immune functions.

Dr. Hua's research has centered on the development of novel MRI technologies for in vivo functional and physiological imaging in the brain, and the application of such methods for studies in healthy and diseased brains. These include the development of human and animal MRI methods to measure functional brain activities, cerebral perfusion and oxygen metabolism at high (3 Tesla) and ultra-high (7 Tesla and above) magnetic fields. He is particularly interested in novel MRI approaches to image small blood and lymphatic vessels in the brain. Collaborating with clinical investigators, these techniques have been applied 1) to detect functional, vascular and metabolic abnormalities in the brain in neurodegenerative diseases such as Huntingdon's disease (HD), Parkinson's disease (PD), Alzheimer's disease (AD) and mental disorders such as schizophrenia; and 2) to map brain functions and cerebrovascular reactivity for presurgical planning in patients with vascular malformations, brain tumors and epilepsy.