Peter L. Strick, PhD
Dr. Strick is the Chair of Neurobiology, Director of the Systems Neuroscience Institute, and Co-Director of the CNUP and CNBC. He is a world's expert in mapping neurons in the CNS using herpes virus and recently elected member of the National Academy of Sciences. Strick's research focuses on four major issues: motor learning and the control of voluntary movement by the motor areas of the cerebral cortex; the motor and cognitive functions of the basal ganglia and cerebellum; the neural basis for the mind-body connection; and unraveling the complex neural networks that comprise the central nervous system.
Joanne Flynn, PhD
Dr. Flynn's lab studies the pathogenesis of Mycobacterium tuberculosis, the causative agent of tuberculosis. Tuberculosis kills about 2 million people every year worldwide. After a century of study of this organism, we still do not understand many basic mechanisms by which it causes disease, and how to protect against it. Their lab focuses on the host-pathogen interactions and immunology of M. tuberculosis, with the majority of studies in non-human primate models. They have pioneered the use of the cynomolgus macaque for basic biology, immunology, and pathogenesis, drug and vaccine studies, and have incorporated state-of-the-art immunologic techniques and serial imaging (PET/CT) into our studies. They also use a small new world monkey, the common marmoset, for studies of transmission of infection. They benchmark our studies against the human data obtained from collaborators. The non-human primate models of tuberculosis we have developed and used are extremely similar to tuberculosis in humans. We work closely with pathologists, veterinarians, microbiologists, immunologists and drug and vaccine experts in developing the models as well as using these models in translational studies. At the University of Pittsburgh, they have outstanding and unparalleled BSL3 facilities for studying TB in monkeys, including PET/CT imaging in the BSL3.
Simon Barratt-Boyes, BVSc, PhD, Dip ACVIM
Defining dendritic cells and macrophages in HIV/AIDS pathogenesis using the simian immunodeficiency virus (SIV) model Mononuclear phagocytes are important innate immune cells that include monocytes, macrophages, and dendritic cells (DCs), which in the human and nonhuman primate consist of two major subsets, myeloid and plasmacytoid. Given their function in antiviral immunity, dendritic cells are thought to play a protective role in HIV and SIV infection, and loss of both subsets is associated with disease progression. However, recently emphasis has been placed on the potential role of the innate immune response in chronic, generalized immune activation that is a hallmark of AIDS. In this scenario, over-active mononuclear phagocytes produce pro-inflammatory cytokines that drive chronic interferon production and inflammation in lymphoid and gut tissues. Hence there is a basic unanswered question in HIV pathogenesis: are DCs, monocytes and macrophages beneficial or detrimental to the infected host? We use the model of SIV infection of rhesus macaques, which replicates the pathogenesis of HIV-1 infection in humans and leads to simian AIDS, to address this question.
J. Timothy Greenamyre, MD, PhD
The lab is interested in mechanisms of neurological disease and neurodegeneration in general, and focuses primarily on Parkinson's disease and epilepsy. We are particularly interested in mitochondrial impairment, oxidative mechanisms and inflammation in the brain. In addition to defining pathogenic mechanisms, the lab is working to develop new therapeutic approaches including gene therapies. We use a wide variety of in vitro and in vivo models, and techniques range from molecular biology to behavior.
Bennett Van Houten, PhD
Dr. Van Houten's lab studies the formation and repair of DNA damage in nuclear and mitochondrial genomes with particular interest in the structure and function of proteins that mediate nucleotide excision repair and the role of oxidative stress in human disease; Understanding the structure and function of nucleotide excision Repair (NER) proteins, both in bacteria and in humans; Solving protein and protein-DNA structures by X-ray crystallography; Visualizing NER on DNA using single-molecule techniques, including atomic force microscopy and fluorescence microscopy using quantum dot labeling; Investigating tumor cell bioenergetics and potential strategies for therapeutic intervention.
Michael T. Lotze, MD
The DAMP Laboratories of the University of Pittsburgh were formed in 2006 to focus on the role of Damage Associated Molecular Pattern Molecules [DAMPs], released or secreted by damaged or injured cells or the inflammatory cells responding to the "danger". Initiated as a coalition of the laboratories headed up by Drs. Liang, Lotze, Tang and Zeh, they focus on the critical role of DAMPs in the initiation of chronic inflammation and the disease that often eventuates as a consequence, cancer. Many local and international collaborators are working with this group to evaluate the role of DAMPs in cancer. They are located in the G.27 Hillman Cancer Center and span fundamental studies related to the role of DAMPs and their receptors [DAMP-R] in cancer pathogenesis and persistence in transgenic and transplantable murine tumor models, closely linked with the clinical efforts to limit necrotic cell death and promote normal, and programmed [apoptotic] cell death.
The Chang-Moore lab in the Cancer Virology Program focuses on carcinogenic human herpesviruses and polyomaviruses. Our laboratory discovered the two most recent human tumor viruses, KSHV and MCV, causing Kaposi's sarcoma and Merkel cell carcinoma, respectively. Current projects involve basic investigations into how these viruses induce cell transformation. For MCV, we are focused on examining the role of large T antigen in inducing the cellular oncoprotein survivin and on examining the role of small T antigen in regulating cap-dependent protein translation. We are generating a conditionally-expressed small T antigen mouse as a potential model for Merkel cell carcinogenesis. For KSHV, we have lately been concentrating on understanding non-canonical translation proteins expressed from the LANA1 locus, and identifying unique cellular interactors with non-canonical LANA1 proteins.
Carolyn B. Coyne, PhD
Dr. Coyne's research employs aspects of cell biology, immunology, and microbiology to study multiple aspects of host-pathogen interactions. Their studies primarily focus on: (1) the identification of novel host cell innate immune molecules and pathways that regulate antiviral signaling, (2) the viral factors that attenuate host antiviral signals, and (3) the mechanisms employed by human placental trophoblasts to combat microbial access to the fetal compartment. Through these studies, they found that primate-specific microRNAs (miRNAs) that are produced almost exclusively by placental trophoblasts are secreted via exosomes and mediate protection from viral infections. They are currently dissecting the molecular basis for this protection and developing systems to study the role of these miRNAs in viral protection in vivo.
Karen A. Norris, PhD and Mark T. Gladwin, MD
Phone Dr. Norris: 412-648-8848
Email Dr. Norris: email@example.com
Dr. Norris is a Professor of Immunology and the Director of Basic Sciences in the HIV Lung Research Center. Dr. Norris conducts research in immunology and infectious diseases with emphasis on cardiopulmonary complications of HIV infection, chronic obstructive pulmonary disease and pulmonary hypertension. Dr. Norris' research efforts are focused on non-human primate (NHP) models of HIV infection and pulmonary disease. She works with a team of investigators and collaborators who provide expertise in all aspects of these studies including veterinary, pulmonary, cardiology, pathology, immunology, radiology, virology, morphometric analyses and immunology. This team has been successful in establishing the first primate model of Pneumocystis infection and she has established that SIV-associated COPD is dependent upon Pneumocystis colonization. Recent research efforts involve the development and evaluation primate models of pulmonary arterial hypertension, immune-mediated lung pathology and Pneumocystis vaccine development. Dr. Norris is highly committed to integrated studies of complex biomedical problems utilizing non-human primate models and establishing multidisciplinary, collaborative research teams to accomplish these goals.
Timothy R. Billiar, MD
Researchers in the general surgery and vascular labs are asking (and answering) some fundamental questions about how the immune system responds to cell damage. Why do some people get multiple organ failure after trauma, while others recover without complication? Why do vascular grafts fail? How does inflammation in cells and tissues of major organs affect immune responses? Can we predict how well individual patients will recover from surgery and trauma? Cell damage occurs in many situations, such as following surgery or surgical procedures, after trauma (including bone fractures) or during infection. Limiting harmful inflammation may help patients to recover from injury more quickly, and with fewer complications. Extensive mouse colonies with floxed alleles of HMGB1, TLRs, caspase 1, and others are important to the work of the group.
Peter J. Rubin, MD and Kacey Marra, PhD
Phone Dr. Marra: 412-383-8924 (office) or 412-383-8939 (lab)
Email Dr. Marra: firstname.lastname@example.org
Dr. Rubin and Dr. Marra have developed a biodegradable nerve guide that has the potential to regenerate nerves over long gaps. After demonstrating its efficacy in a rat sciatic nerve defect model, they are now examining the guide in a non-human primate median nerve defect model. If successful, they will begin clinical trials in 2014.
Michael Tsang, PhD
The lab utilizes zebrafish as a model to study early embryonic development and the utility of this model in drug discovery. The main focus is on embryonic heart development and in the adults, cardiac regeneration following injury. We are particularly interested in the role of a family of growth factors known as Fibroblast Growth Factors in these processes. We employ a variety of techniques from gene knockdown studies to the generation of transgenic zebrafish to chemical biology to address these questions. In another aspect of our lab, we have developed automated high-throughput chemical screening methodologies to identify new drugs that modulate the FGF pathway. The goal is to employ these novel agents as potential regenerative therapy.