Emily Talago is graduating with a Bachelor of Science degree in Biotechnology with a minor in Chemistry, and is finishing the Master of Science degree in Biotechnology this summer. Following graduation, she plans to first and foremost take a relaxing vacation before pursuing an occupation in industry, with future plans of obtaining a fellowship and completing a doctorate degree. Emily is the former president of the Marywood Student Affiliate Chapter of the American Chemical Society and was awarded the 2009 Medal for Excellence in Biotechnology. She chose to participate in the Honors Program in order to study biotechnology in contexts other than her immediate science field, and to explore implications of life science technologies across varied disciplines. Emily would like to thank her faculty mentors, Dr. Lisa Antoniacci of Marywood, and Dr. Edward Schmidt of Montana State for their invaluable guidance and support throughout this project. She extends gratitude to her reader, Dr. Philip Jenkins, for awakening her passion for biomedical ethics. She also thanks Dr. Michael Kiel, Dr. Jay Clymer, and Christina Elvidge for their assistance in Honors Enrichment courses, everyone from the REU/CBS program at Montana State University- especially Anneke Metz, her sister Liz for cleaning up after her and giving her a place to live, her parents for their unyielding encouragement even in the face of explosions, concoctions, and unidentifiable experiments, her brother Aaron for his sanity-retaining comic relief, and all of her family, friends, classmates and coworkers for their constant love, support, and extreme patience over the years.
Director: Dr. Lisa Antonacci
Reader: Dr. Philip Jenkins
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A transgenic mice line lacking 111 amino acids of the 135 aa N terminus of the TATA binding protein: tbpΔN/ΔN undergoes two crisis points exhibiting substantial lethality. The first during gestation has been attributed to the activity of maternal lymphocytes (Hobbs et al., 2002). The second occurs between birth and weaning. Analysis showed that during this time mutant ΔN/ΔN mice are only ~50% body mass and exhibit severe steatosis in hepatocytes compared to their wild type littermates. After weaning, mutants regain normal size, recover from the fat accumulation and appear to thrive as overtly normal adults. The second crisis corresponds to the nursing period in which mice are switched from a carbohydrate rich diet to a lipid rich diet. In order to determine whether there is a cause and effect relationship in mutants between the lipidrich breastfeed period and the recorded variances in liver histology and gene expression, adults of both genotypes were placed on high fat diets. Livers harvested exhibited results that mimicked data obtained from juvenile mutants and external appearance suggesting histology would also show lipid accumulation in hepatocytes. Also addressed is the question of potential for molecular genetic research of liver diseases to increase accuracy of disease diagnosis in a culture of social stigmas against alcohol-related liver disease.
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