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Andrew Lane Lab
The Lane laboratory is focused on understanding molecular mechanisms underlying chronic rhinosinusitis and particularly the pathogenesis of nasal polyps. Diverse techniques in molecular biology, immunology, physiology, and engineering are utilized to study epithelial cell innate immunity, olfactory loss, the sinus microbiome, and drug delivery to the nose and sinus cavities. Ongoing work explores how epithelial cells participate in the immune response and contribute to chronic sinonasal inflammation. The lab creates and employs transgenic mouse models of chronic sinusitis to support research in this area. Collaborations are in place with the School of Public Health to explore mechanisms of anti-viral immunity in influenza and rhinovirus, and with the University of Maryland to characterize the bacterial microbiome of the nose and sinuses in health and disease.
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, transmissi...on 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.