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I am a Professor of Virology in the Department of Microbiology (http://www.md.rcm.upr.edu/micro/faculty/melendez.php), School of Medicine and direct the RCMI Translational Proteomcis Center at the University of Puerto Rico Medical Sciences Campus (UPR-MSC) http://rcmi.rcm.upr.edu/research/proteomics.html that provides clinical and basic researchers with proteomics instrumentation and services necessary to determine biomarkers for diseases that involve health disparities. I have a Ph.D. in Experimental Pathology & Immunology from Emory University School of Medicine in 1990, where I also completed two-years of post-doctoral training in Hematology and Pediatric Infectious Diseases in collaboration with the Centers for Disease Control. I also have a M.S. degree in Microbiology from University of Georgia, Athens in 1981, and a Medical Technology degree from University of Puerto Rico Medical Sciences Campus in 1979. I have been Professor of Virology since 1992 and was the Director of the Biosafety Committee at the UPR-MSC for 6 years. I am currently a Principal Investigator of and NIH funded study to understand the mechanisms of macrophage-induced HIV Neuropathogenesis using proteomics approaches.
Currently working in the project entitled: Targeting macrophage cathepsin B in HIV Neuropathogenesis. We have found important dysregulation of the cystatins B/C: cathepsin B interaction in HIV-1 infected Monocyte- derived macrophages with increased secretion of bioactive cathepsin B that may contribute to neuropathogenesis. This bioactive cathepsin B is not secreted in HIV-1 infected microglia. These studies demonstrated important differences between two macrophage populations and suggest targets for prevention of HIV associated neurological disorders (HAND). To address the roles of cystatin B/C, cathepsin B, and the proteins affected by their interactions in the progression to CI in the presence of combined anti-retroviral therapy, I have collaborated with scientists in University of Nebraska to study the proteome of blood-derived monocytes obtained from Hispanic women with the most severe form of HIV-associated neurocognitive disorder—HIV-associated dementia (HAD). Findings from these studies suggest that deficits in monocyte antioxidant proteins may lead to neuronal damage through the loss of hydrogen peroxide scavenging capabilities, thus exposing neurons to apoptosis-inducing factors. Altered monocyte functions therefore may contribute to the development and/or progression of HAD (Kraft-Terry et al, 2010). We are now conducting studies to understand the mechanisms of cathepsin B-induced neurotoxicity to target potential therapies. We are also conducting work on the proteome of macrophage from patients with mild dementia and validation of proteins from monocytes of patients with mild dementia in search of more biomarkers and targets for therapy.
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