The Lane laboratory is focused on understanding molecular mechanisms underlying chronic rhinosinusitis, particularly the pathogenesis of nasal polyps, as well as inflammation on the olfactory epithelium. Diverse techniques in molecular biology, immunology, and physiology are utilized to study epithelial cell innate immunity, olfactory loss, and response to viral infection. Ongoing work explores how epithelial cells of the sinuses and olfactory mucosa participate in the immune response and contribute to chronic inflammation. The lab creates and employs transgenic mouse models of chronic nasal/sinus inflammation 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 COVID-19.

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.