Bienvenidos a CienciaPR, una red de recursos para todos los interesados en las ciencias y en Puerto Rico.
• B.S., Biology, Magna Cum Laude. Inter American University of Puerto Rico. Majors: Biomedical Science, Microbiology and Medical Pre-Technology.
• Biotechnology Certified. 2006. University of Puerto Rico, Arecibo Campus.
• PhD., University of Puerto Rico, Río Piedras Campus, San Juan Puerto Rico. In progress.
• Laboratory Technician II, University of Puerto Rico, Rio Piedras, Biology Department.
• Biological Science Lab Technician, NASA, (National Aeronautic Space Administration) - Cape Canaveral, Advance Life Support.
• Research Assistant, North Carolina State University, El Tallonal Natural Reserve, Arecibo, Puerto Rico.
• Biological Science Lab Technician, USDA-ARS-NAA-ERRC-PSTRU, United States Department of Agriculture- Agricultural Research Service-North Atlantic Area- Eastern Regional Research Center-Plant Science & Technology Research Unit, Wyndmoor, Pennsylvania.
• Undergraduate Research Student, Inter American University of Puerto Rico, Arecibo, Puerto Rico; Center for Environmental Education, Conservation, and Research (CECIA).
• Research Assistant on NSF projects, Inter American University of Puerto Rico, Arecibo, Puerto Rico, Science and Technology Department.
• Biological Operator I, Protein Purification, Abbott Biotechnology Limited (ABL), Barceloneta, Puerto Rico.
• QC Microbial Environmental Control (MEC) Laboratory Technician II, Microbiology, Abbott Biotechnology Limited (ABL), Barceloneta, Puerto Rico.
• Online Editor and Publisher of Biology Courses, Inter American University of Puerto Rico, Arecibo, Puerto Rico, Science and Technology Department, Biology Electronic Classroom (D-4).
• External Evaluator Assistant, University of Puerto Rico, Arecibo, Puerto Rico.
Other: 1. Fellowship from Alliance for Minority Participation (AMP). 2. RISE Fellowship
Proyect 1: Studies of congenital myasthenic syndrome (CMS) revealed mutations in acetylcholine receptor (AChR) subunit genes. These alterations either reduce expression or alter the receptor kinetic profile to decrease or increase the response to acetylcholine (ACh). Mutations that increase response to ACh and prolong activation are known to cause slow channel CMS (SCCMS). Those mutations that underlie SCCMS have been identified in different acetylcholine receptor (AChR) subunits, and in different domains of the subunits, provoking AChR channelopaties, at neuromuscular junction level. Furthermore, neuromuscular transmission is compromised because of cationic overloading after ACh binding. SCCMS is characterized by weakness and fatigability of the voluntary muscles as a result of this impaired neuromuscular transmission. Using wildtype models, several reports have demonstrated that alcohol interacts with nicotinic AChR (nAChR) (Murrell et al., 1991; Sterz et al., 1981), and produce alterations at neuromuscular junction in rats (Wali and Hayter, 1988), and frog preparations (Bradley et al., 1980). Moreover, in vitro studies demonstrated that chronic exposure to ethanol affects mRNA levels of nicotinic nAChR subunits expressed in M10 and SH-SY5Y cell lines in a receptor-dependent composition manner (Gorbounova et al., 1998). Also, recombinant human neuronal nicotinic receptors expressed in oocytes suggest that the ethanol effect depends on the receptor subunit composition (Cardoso et al., 1999). Although ethanol modulation of the nicotinic receptor at the neuromuscular junction is well documented, the very limited reports concerning the direct action of ethanol on CMS still unknown. Anecdotic evidence suggests that there is increased alcohol consumption in CMS patients. The presence of slow channels mutations related to CMS in these patients led us to question the possible effect of the mutations on the receptor in response to alcohol. Using transgenic mice models of SCCMS, electrophysiological, molecular and confocal microscopy approaches, we are investigating the role of alcohol in aV249F, a mutation that cause SCCMS. The long term goal of this project is to determine the effects of alcohol in a dissimilar panel of SCCMS, both in vivo and in vitro. The overall results from this study will provide a new insight in understanding the role of alcohol in CMS pathogenesis progression and the tools to develop prevention strategies.
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