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Articles 1 - 10 of 10
Full-Text Articles in Medical Genetics
The Ethical Dilemmas Epigenetic Editing In Utero Presents To Christians, Victoria Hendrix
The Ethical Dilemmas Epigenetic Editing In Utero Presents To Christians, Victoria Hendrix
Senior Honors Theses
The development of CRISPR epigenetic editing technology was initially impactful due to its potential for disease treatment. However, despite the potential benefits of epigenetic technology, there exist ethical dilemmas surrounding its use in utero. The review of the ethical dilemmas of epigenetic editing in utero from a Christian perspective showed that research in epigenetic editing is promising, yet fraught with peril. The basic ethical issues of epigenetic editing in utero stem from its inaccuracy, lack of research concerning its effects on offspring, an incomplete understanding of gene interactions, and its connection to eugenics. The ethical concerns particularly relevant to Christians …
The Revolutionary Genome Editor: Crispr-Cas9 Systems, Grace Spade
The Revolutionary Genome Editor: Crispr-Cas9 Systems, Grace Spade
Senior Honors Theses
Genetic engineering is the modification of an organism's genetic material to alter its traits through adding, deleting, or changing specific genes. CRISPR-Cas9 systems are groundbreaking tools for genetic engineering, in short utilizing a molecule called RNA to guide a protein called Cas9 to a specific location in DNA to add, delete, or replace genes. The history of how the CRISPR-Cas9 systems came into existence, how it was adapted from a natural defense system in bacteria, and its mechanism of action in both are explained. Its applications, both present and future, competing genetic modifiers, advantages and disadvantages, and the ethical dilemmas …
Epigenetic Pathogenesis Of Neurological Disorders In Utero And Considerations For Genetic Counseling, Lauren Juga
Epigenetic Pathogenesis Of Neurological Disorders In Utero And Considerations For Genetic Counseling, Lauren Juga
Senior Honors Theses
Epigenetic modifications are a major focus of study in the pathogenesis of many disorders regarding metabolism, aging, neurodevelopment, and neurodegeneration. Epigenetic mechanisms are present throughout life but are especially vital to guiding fetal development. The precise timing of gene activation and deactivation guides stem cell differentiation through each embryonic stage. After exposure to environmental stimuli, gene expression can be altered by transcription factors, resulting in observable phenotypes and even pathology. Here, the epigenetic mechanisms responsible for the pathogenesis of neurodevelopmental and neuropsychiatric disorders are explored in response to environmental perturbations in utero. The present goal is to identify correlations between …
Causes Of Color Blindness: Function And Failure Of The Genes That Detect Color, Dylan Taylor
Causes Of Color Blindness: Function And Failure Of The Genes That Detect Color, Dylan Taylor
Senior Honors Theses
Color blindness affects nearly 10% of the entire population, with multiple types of color blindness from various genetic mutations. In the following sections, the nature of light and how the human eye perceives light will be discussed. Afterward, the major forms of color blindness and their genetic causes will be considered. Once these genetic causes have been established, the current method for diagnosing color blindness will be investigated, followed by a discussion of the current treatments available to those with color blindness. Finally, a brief discussion will address possible future work for color blindness with the hope of finding better …
Genetic Relationships And Therapeutic Options For Relapsed Acute Lymphoblastic Leukemia, Hailie Shertzer
Genetic Relationships And Therapeutic Options For Relapsed Acute Lymphoblastic Leukemia, Hailie Shertzer
Senior Honors Theses
Acute lymphoblastic leukemia (ALL) is the most common form of cancer among children and can be lethal to the adult population. Though 80% of patients with ALL reach complete remission after treatment, about 20% of those diagnosed fail to remain cancer-free. Genetic rearrangements are the hallmark of relapsed ALL, but the mechanism by which these rearrangements occur is still unclear. Recent research suggests these mutations may be detectable during initial diagnosis. If researchers are able to accurately assess the probability of relapse during diagnosis by analyzing the genome of the leukemic cells, the likelihood of administering effective therapy would increase. …
Hutchinson-Gilford Progeria Syndrome Vascular Pathology: A Focused Review, Danielle M. Eschedor
Hutchinson-Gilford Progeria Syndrome Vascular Pathology: A Focused Review, Danielle M. Eschedor
Senior Honors Theses
Hutchinson-Gilford Progeria is an accelerated aging disorder caused by a de novo point mutation in the LMNA gene which codes for an intermediate filament of the nuclear lamina called lamin A. The point mutation at c.1824C>T causes a 50-amino-acid deletion that removes the binding site for Zmpste24, a metalloprotease responsible for defarnesylating prelamin A and producing mature lamin A. Without the ability to be defarnesylated, the mutated protein, called progerin, is more lipophilic and has a myriad of cytotoxic effects. As cardiovascular disease is the most common cause of death in HGPS patients, it is important for both healthcare …
Gene Expression Profiling In An Alzheimer's Disease Mouse Model, Matthew R. Dalton
Gene Expression Profiling In An Alzheimer's Disease Mouse Model, Matthew R. Dalton
Senior Honors Theses
Explaining precisely how Alzheimer’s disease (AD)—the world’s most common form of dementia—materializes in the human brain has proven to be one of the most elusive ends in modern medicine. Progressive memory loss, neurodegeneration, and the presence of abnormal protein aggregates of amyloid-beta (Aβ) and neurofibrillary tangles (NFT) characterize this disease. Genome sequencing provides researchers with the ability to better identify disease-related changes in gene expression, some of which may play a role in the initiation and progression toward the AD-like state. Intimate interactions between tissues have been observed in many diseases, particularly between the brain and blood. This analysis seeks …
Intimin Likely Used To Cause Disease During Competition With Commensal Escherichia Coli, Dominique J. Richburg
Intimin Likely Used To Cause Disease During Competition With Commensal Escherichia Coli, Dominique J. Richburg
Senior Honors Theses
The intimin gene in the Locus of Enterocyte Effacement (LEE) island of pathogenicity is the primary attachment mechanism in Citrobacter rodentium. Intimin is a bacterial adhesin (protein) that attaches to obtain a niche/nutrient and thrive within the intestine. Intimin was deleted within C. rodentium to study colonization and pathogenesis in the murine intestine. Additionally, C. rodentium is an attaching/effacing pathogen, and a useful murine model in understanding Enterohemorrhagic Escherichia coli (EHEC) infection in humans. E. coli and C. rodentium cause gastroenteritis in humans and mice, respectively. C. rodentium is a murine pathogen commonly used to model gastrointestinal disease because …
Gene Expression And Alzheimer's Disease: Evaluation Of Gene Expression Patterns In Brain And Blood For An Alzheimer's Disease Mouse Model, Amanda Hazy
Senior Honors Theses
Previous studies have established a causative role for altered gene expression in development of Alzheimer’s disease (AD). These changes can be affected by methylation and miRNA regulation. In this study, expression of miRNA known to change methylation status in AD was assessed by qPCR. Genome-wide expression changes were determined by RNA-sequencing of mRNA from hippocampus and blood of control and AD mice. The qPCR data showed significantly increased expression of Mir 17 in AD, and sequencing data revealed 230 genes in hippocampus, 58 genes in blood, and 8 overlapping genes showing significant differential expression (p value ≤ 0.05). Expression data …
Childhood Obesity And Familial Hypercholesterolemia: Genetic Diseases That Contribute To Cardiovascular Disease, Alyssa Caudle
Childhood Obesity And Familial Hypercholesterolemia: Genetic Diseases That Contribute To Cardiovascular Disease, Alyssa Caudle
Senior Honors Theses
Childhood obesity occurs as the result of an imbalance between caloric intake and energy expenditure. Genetic risk factors for obesity have become an area of research due to its permanency. Mutated genes such as Fat Mass and Obesity Associated (FTO), Leptin (LEP), Leptin Receptor (LEPR), Melanocortin 4 Receptor (MC4R), Adiponectin C1Q and Collagen Domain Containing (ADIPOQ), Proprotein Convertase Subtilisin/Kexin Type 1 (PCSK1), and Peroxisome Proliferator-Activated Receptor Gamma (PPARG) all contribute to the development of childhood obesity. In the presence of high cholesterol caused by obesity, the genetic condition known as familial hypercholesterolemia is exacerbated. Familial hypercholesterolemia is caused by a …