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Displaying 11 to 20 of 49 results for pathogenesis

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  • Fuchs Laboratory

    The Fuchs Laboratory uses cellular electrophysiology, immunolabeling and electron microscopy to study synaptic connections between sensory hair cells and neurons in the cochlea. One effort focuses on an unusual cholinergic receptor that mediates efferent inhibition of hair cells, driving discovery of the molecular mechanisms, and offering a target for protection against acoustic trauma. A second topic concerns the small number of unmyelinated "type II" afferent neurons whose synaptic connectivity and response properties argue for a role as the pathway for noxious (too loud) sound. Our studies are motivated by curiosity about fundamental mechanisms, and to provide a foundation for understanding cochlear pathogenesis.

    Research Areas: synaptic connections, immunolabeling, neurons, elecrophysiology, audiology, cellular electrophysiology, hearing loss, electron microscopy, cochlea, cochlear pathogensesis

  • Gary S. Hayward Laboratory

    Research in the Gary S. Hayward Laboratory is related to human herpesvirus. Specifically, researchers are seeking to understand how the different classes of herpes viruses take control of transcription, DNA replication, cell cycle and other nuclear processes of their host cells and how they also block or evade apoptotic and immune responses in both the lytic and latent state.

    Research Areas: immunology, herpesvirus, pathogenesis, transcriptional regulation

    Lab Website

    Principal Investigator

    Gary Hayward, Ph.D.

    Department

    Oncology

  • Gregg Semenza Lab

    The Gregg Semenza Lab studies the molecular mechanisms of oxygen homeostasis. We have cloned and characterized hypoxia-inducible factor 1 (HIF-1), a basic helix-loop-helix transcription factor.

    Current research investigates the role of HIF-1 in the pathophysiology of cancer, cerebral and myocardial ischemia, and chronic lung disease, which are the most common causes of mortality in the U.S.

    Research Areas: cancer, oxygen, lung disease, genomics, HIF-1, pathogenesis, myocardial ischemia

    Principal Investigator

    Gregg Semenza, M.D., Ph.D.

    Department

    Pediatrics

  • Hamid Rabb Lab

    The Hamid Rabb Lab is involved in translational research aimed at understanding the molecular pathogenesis of kidney ischemia/reperfusion injury. We’re interested in the development of novel treatments for kidney IRI.

    Research Areas: kidney diseases, kidney ischemia/reperfusion injuries, nephrology

    Principal Investigator

    Hamid Rabb, M.D.

    Department

    Medicine

  • IBD and Autoimmune Liver Diseases Laboratory

    Investigators in the IBD and Autoimmune Liver Diseases Laboratory conduct basic and translational research in inflammatory bowel disease (IBD) and autoimmune liver diseases. One area of focus is discovering and developing biomarkers for diagnosing and prognosticating IBD and other autoimmune liver diseases (AILDs). We also are exploring the molecular pathogenesis of—and developing novel therapies for—IBD. In addition, we are working to understand the molecular reason why many IBD patients fail to respond to mainstay drug therapies—and to develop diagnostic assays that can predict non-responders before starting them on those therapies. These biomarker studies have led to our application for four U.S. and international patents.

    Research Areas: inflammatory bowel disease, Crohn’s disease, gastrointestinal system, colitis, autoimmune diseases, pathogenesis, celiac disease, liver diseases

    Lab Website

    Principal Investigator

    Xu Li, Ph.D.

    Department

    Medicine

  • J. Marie Hardwick Laboratory

    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 cel...lular 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.
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    Research Areas: cell death

  • James Hamilton Lab

    The main research interests of the James Hamilton Lab are the molecular pathogenesis of hepatocellular carcinoma and the development of molecular markers to help diagnose and manage cancer of the liver. In addition, we are investigating biomarkers for early diagnosis, prognosis and response to various treatment modalities. Results of this study will provide a molecular classification of HCC and allow us to identify targets for chemoprevention and treatment. Specifically, we extract genomic DNA and total RNA from liver tissues and use this genetic material for methylation-specific PCR (MSP), cDNA microarray, microRNA microarray and genomic DNA methylation array experiments.

    Research Areas: cancer, molecular genetics, genomics, pathogenesis, liver diseases, hepatocellular carcinoma

    Principal Investigator

    James Hamilton, M.D.

    Department

    Medicine

  • Jean Kim Lab

    The Jean Kim Laboratory performs translational research in the
    area of chronic rhinosinusitis, with a niche interest in the pathogenesis of hyperplastic nasal
    polyposis. Studies encompass clinical research to basic wet laboratory research in
    studying the underlying immune and autoimmune mediated mechanism of polyp growth and
    perpetuation of disease. Human cell and tissue culture models are used. Techniques in the
    laboratory include cell and tissue culture, real time PCR, immunoblot, ELISA, flow cytometry,
    immunohistochemistry, electron microscopy, gene array analysis, and other molecular
    approaches including genetic knockdowns. Approaches used in Dr. Kim’s clinical study
    designs include prospective and retrospective analysis of patient outcomes and clinical
    biomarkers, as wells controlled clinical trials.

    Research Areas: nasal polyps, chronic rhinosinusitis, hyperplastic nasal polyposis

  • Jerry Spivak Lab

    Research in the Jerry Spivak Lab focuses on chronic myeloproliferative disorders, particularly their molecular mechanisms and methods for distinguishing them diagnostically and interventionally. By analyzing gene expression in polycythemia vera stem cells, we have learned that patients with polycythemia vera can be differentiated from those with erythrocytosis and can be diagnosed as having either aggressive or slow-growing disease. We are also studying the roles played by specific molecular markers in the pathogenesis and diagnosis of polycythemia vera.

    Research Areas: stem cells, pathogenesis, polycythemia vera, myeloproliferative disorders

    Principal Investigator

    Jerry Spivak, M.D.

    Department

    Medicine

  • Joel Blankson Lab

    Work in the Joel Blankson Lab explores the mechanism of control of HIV-1 replication in a cohort of patients known as elite controllers or elite suppressors. These patients are HIV-1 seropositive but maintain levels of viremia that are below the limit of detection of standard clinical assays. We feel that elite suppressors represent a potential model for a therapeutic HIV vaccine. Our central hypothesis is that many of these patients are infected with fully replication-competent HIV-1 isolates that are held in check by the immune system. To test this hypothesis, we are studying many different host and viral factors in these patients.

    Research Areas: vaccines, infectious disease, HIV, pathogenesis, elite suppressors

    Principal Investigator

    Joel Blankson, M.D., Ph.D.

    Department

    Medicine

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