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------------------------------------------------------------------------------------------------- Curriculum Vitae B.A.,
Pomona College, Claremont, CA ------------------------------------------------------------------------------------------------- Research Interests My laboratory focuses on the molecular, cellular, and neurophysiologic basis of glaucoma in experimental and human models. By correlating anatomic structure with the function of the glaucomatous retina, the cellular pathophysiology of glaucoma in experimental models of glaucoma is being elucidated. Molecular analysis of the glaucomatous retina using gene array analysis is providing insight into the molecular pathways associated with retinal ganglion cell death and loss of vision. In a genome wide scan of expressed genes in the glaucomatous versus the non-glaucomatous retina, my lab has identified new markers for retinal ganglion cells. We are in the midst of identifying which retinal ganglion cell-specific genes are functionally associated with glaucoma-induced cell death. These genes represent molecular targets for the development of neuroprotective therapies against glaucoma. Although most forms of glaucoma have no identifiable etiology, pseudoexfoliation (PXF) glaucoma is the most common form of glaucoma with an identifiable cause. Pseudoexfoliation glaucoma is characterized by PXF material which is deposited within the tissues of the human body and especially in the eye, which is the only known site of pathology. PXF material has eluded identification since it was first observed in the eye over a hundred years ago. Pseuodoexfoliation material has been collected from patients undergoing surgery. We are in the process of determining the nature of the pseudoexfoliation material using proteomic approaches. My lab has already identified proteins which are associated with the pathogenesis of the disease (i.e. vascular leak). By identifying and cloning the PXF material itself, genetic screening will be possible for this often occult form of glaucoma when the disease is in the early stages. Early diagnosis has implications not only for preventing optic nerve damage but also for reducing the higher surgical complication risks associated with cataract surgery in PXF patients. The molecular characterization of PXF material will also allow for the development of molecularly directed anti-glaucoma therapy based upon the molecular nature of the PXF material. As my laboratory elucidates pathways for neuroprotection in glaucoma in experimental models, we will develop and use neuroprotective agents to prevent progression of glaucomatous optic neuropathy in humans. Idiopathic intracranial hypertension (IIH) can cause severe, permanent visual field constriction due to optic nerve edema. As proof of therapeutic principle, patients with IIH may be treated with neuroprotectants in the acute phase until intracranial or retrobulbar transmural pressure is lowered either medically or surgically, including optic nerve sheath fenestration, to protect retinal cells during this period of ocular distress. We (along with Drs. Porciatti, Tse, and Lam) are prospectively studying the pathophysiology of optic nerve damage and visual field loss in patients with IIH using electrophysiology, optic nerve head imaging, and visual field analysis to understand how neuroprotective agents in addition to medical and surgical treatment can prevent vision loss. Lastly, my lab is studying the histopathologic changes involved in eyes with prior glaucoma drainage implants. Using immunohistochemical techniques to assay the expression of known wound healing molecules, we (along with Drs. Dubovy and Fantes) are developing an understanding of how the eye responds to implanted material and how this wound healing response affects the efficacy of glaucoma drainage implants in regulating intraocular pressure and minimizing optic nerve damage due to glaucoma.
Selected Publications Lee, R.K. and Gedde, S. J. 2005. Indications for Surgical Treatment in Patients with Coexisting Cataract and Glaucoma. Contemporary Ophthalmology, 4(2): 1-4. Nduaguba, C. and Lee, R.K. 2005. Glaucoma Screening: Current Trends, Economic Issues, Technology, and Challenges. Current Opinion in Ophthalmology, accepted. Lee, R.K. and Gedde, S. J. 2005. Surgical Treatment of Coexisting Cataract and Glaucoma. Contemporary Ophthalmology, 4(3):1-6. Lee, R.K. and Gedde, S. J. 2004. Surgical Management of Coexisting Cataract and Glaucoma. International Ophthalmology Clinics. 44(2): 151-166. Scott, F.D.; Monkemuller, K.E.; Lee, R.K.; and Karnam, U. 2003. Gardner's syndrome in an HIV-infected patient. Gastrointestinal Endoscopy. 57(3):429-31. Lee, R.K. and Fantes, F. 2003. Surgical Management of Glaucoma and Corneal Transplant Patients. Current Opinion in Ophthalmology, 14 (2): 95-99. Lee, R.K.; Cai, J.-P.; Deyev, V.V.; Gill, P.S.; Cabral, L.; Wood, C.; Boise, L. H.; Podack, E.R.; and Harrington Jr., W.J. 1999. AZT and Interferon-alpha Induce Apoptosis in Herpesvirus-associated Lymphomas. Cancer Research, 59: 5514-5520. Spielman, J.; Lee, R.K.; and Podack, E.R. 1998. Perforin/Fas-Ligand Double Deficiency is Associated with Macrophage Expansion and Severe Pancreatitis. J. Immunology. 161: 7063-7070. Lee, R.K.; Jasmin, B.J.; and Rotundo, R.L. 1998. Development of the Neuromuscular Junction. In: Principles of Medical Biology. Bittar, E.E. and Bittar, N., Eds. Jai Press Inc., Connecticut. Vol. 11, pgs. 187-207. Ivanov, V.N.; Lee, R. K., Podack, E.R.; and Malek, T.R. 1997. Regulation of Fas-Dependent Activation-Induced T Cell Apoptosis by cAMP Signaling: a Potential Role for Transcription Factor NF-kB. Oncogene. 14:2455-2464. Nakamura, T.; Lee, R.K.; Nam, S.Y.; Al-Ramadi, B.K.; Koni, P.A.; Bottomly, K.; Podack, E.R.; and Flavell, R.A. 1997. Reciprocal Regulation of CD30 Expression on CD4+ T cells by IL-4 and IFN-g. J. Immunology. 158: 2090-2098. Nakamura, T.; Lee, R.K.; Nam, S.Y.; Podack, E.R.; Bottomly, K.; and Flavell, R.A. 1997. Roles of IL-4 and IFN-g in Stabilizing the T Helper type 1 and 2 Phenotype. J. Immunology. 158: 2648-2653. Nishio, M.; Spielman, J.; Lee, R.K.; Nelson, D.; and Podack, E.R. 1996. CD80 (B7.1) and CD54 (intracellular adhesion molecule-1) induce target cell susceptibility to promiscuous cytotoxic T cell lysis. J. Immunology. 157: 4347-4353. Lee, R.K.; Spielman, J.; Zhao, D.Y.; Olsen, K. J.; and Podack, E.R. 1996. Perforin, Fas Ligand, and Tumor Necrosis Factor Are The Major Cytotoxic Molecules Used by Lymphokine Activated Killer Cells in Cell-Mediated Cytotoxicity. J. Immunology. 157:1919-1925. Lee, R.K.; Spielman, J.; and Podack, E.R. 1996. Bcl-2 Protects Against Fas-Based But Not Perforin-Based T-Cell Mediated Cytotoxicity. International Immunology. 8(7): 991-1000. Bowen, M.A.; Lee, R.K.; Miragliotta, G.; Nam, S.Y.; and Podack, E.R. 1996. Structure and Expression of Murine CD30 and its Role in Cytokine Production. J. Immunology. 156: 442-449. Peters, J.; Kondo, K.L.; Lee, R.K.; Lin, C.K.; Young, L.S.; and Inderlied, C.B. 1995. In Vitro Activity of Oxazolidinones Against the Mycobacterium avium Complex. J. Antimicrobial Chemotherapy. 35(5): 675-679. Jasmin, B.J.; Lee, R.K.; and Rotundo, R.L. 1993. Compartmentalization of Acetylcholinesterase mRNA and Enzyme at the Vertebrate Neuromuscular Junction. Neuron. 11: 467-477. Rotundo, R.L.; Jasmin, B.J.; Lee, R.K.; and Rossi, S.G. 1992. Compartmentalization of Acetylcholinesterase mRNA and Protein Expression in Skeletal Muscle In vitro and In vivo: Implications for Regulation at the Neuromuscular Junction. In: Multidisciplinary Approaches to Cholinesterase Functions. Schafferman, A. and Velan, B., Eds. Plenum Press, New York. pgs. 217-222. Eggerding, F.A.; Peters, J.; Lee, R.K.; and Inderlied, C.B. 1991. Detection of Rubella Virus Gene Sequences by Enzymatic Amplification and Direct Sequencing of Amplified DNA. J. Clinical Microbiology. 29(5): 945-952.
View published research articles by Dr. Lee in the National Library of Medicine ------------------------------------------------------------------------------------------------- |
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