The Advanced Optics Lab uses innovative optical tools, including laser-based nanotechnologies, to understand cell motility and the regulation of cell shape. We pioneered laser-based nanotechnologies, including optical tweezers, nanotracking, and laser-tracking microrheology. Applications range from physics, pharmaceutical delivery by phagocytosis (cell and tissue engineering), bacterial pathogens important in human disease and cell division. Other projects in the lab are related to microscopy, specifically combining fluorescence and electron microscopy to view images of the subcellular structure around proteins.

The Kristina Nielsen Laboratory investigates neural circuits in the visual cortex that are responsible for encoding objects to understand how the visual system performs object recognition. We aim to reveal the fine-scale organization of neural circuits, with an emphasis on higher-level visual areas. We use two-photon microscopy to perform high-resolution functional imaging of visual areas in the non-human primate. We also investigate how the function of higher visual areas changes over the course of brain development in ferrets, by measuring the activity of single neurons in these areas, as well as determining the animal's visual capabilities at various developmental stages. In both types of investigations, we also rely on detailed anatomical techniques to precisely observe how the function of neuronal circuits is related to their structure.

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 interests in the Marcia Canto Lab include pancreatic neoplasms, Barrett’s esophagus and endomicroscopy. We are also interested in the use of endoscopic ultrasound to identify early-stage pancreatic cancer and its precursors.

Research in the Shigeki Watanabe Lab focuses on the cellular and molecular characterizations of rapid changes that occur during synaptic plasticity. Our team is working to determine the composition and distribution of proteins and lipids in the synapse as well as understand how the activity alters their distribution. Ultimately, we seek to discover how the misregulation of protein and lipid compositions lead to synaptic dysfunction. Our studies make use of cutting-edge electron microscopy techniques in combination with biochemical and molecular approaches.

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.

The Pathak lab is within the Division of Cancer Imaging Research in the Department of Radiology and Radiological Science. We develop novel imaging methods, computational models and visualization tools to ‘make visible’ critical aspects of cancer, stroke and neurobiology. Our research broadly encompasses the following areas: Functional and Molecular Imaging; Clinical Biomarker Development; Image-based Systems Biology and Visualization and Computational Tools. We are dedicated to mentoring the next generation of imagers, biomedical engineers and visualizers. Additional information can be found at www.pathaklab.org or by emailing Dr. Pathak.

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.

In the Lee Martin Laboratory, we are testing the hypothesis that selective vulnerability--the phenomenon in which only certain groups of neurons degenerate in adult onset neurological disorders like amyotrophic lateral sclerosis and Alzheimer's disease--is dictated by brain regional connectivity, mitochondrial function and oxidative stress. We believe it is mediated by excitotoxic cell death resulting from abnormalities in excitatory glutamatergic signal transduction pathways, including glutamate transporters and glutamate receptors as well as their downstream intracellular signaling molecules. We are also investigating the contribution of neuronal/glial apoptosis and necrosis as cell death pathways in animal (including transgenic mice) models of acute and progressive neurodegeneration. We use a variety of anatomical and molecular neurobiological approaches, including neuronal tract-tracing techniques, immunocytochemistry, immunoblotting, antipeptide antibody production, transmission electron microscopy and DNA analysis to determine the precise regional and cellular vulnerabilities and the synaptic and molecular mechanisms that result in selective neuronal degeneration.