Master of Science, The Ohio State University, 2023, Dentistry

Purpose: The aim of this pre-post design study was to determine the usability and feasibility of a virtual simulation-based learning experience to educate pediatric dental providers regarding human papilloma virus (HPV) and the HPV vaccine. Methods: Sixteen residents at one pediatric dental residency program were recruited. All residents completed a pre-simulation survey to assess their baseline knowledge, skills, and attitudes toward discussing HPV with patients. Participants then completed a telehealth standardized patient encounter where they were tasked with discussing HPV and the HPV vaccine with a teenage patient and their parent. All participants then completed an online learning experience. Following this exercise, participants repeated the same standardized patient encounter and then completed a post-simulation survey to assess changes from baseline. Results: There was a significant difference between pre and post survey responses for eight of eleven questions (p<0.05) and pre and post standardized patient encounter performance for two of twelve vaccine discussion elements (p<0.05). Participants reported increased knowledge regarding discussing HPV and its connection to overall and oral health, as well as increased confidence in discussing common side effects and safety of the vaccine. Participants showed improved performance in communicating the safety and efficacy of the vaccine as well as sharing age-based dosing recommendations. Most participants reported the simulation equipped them with new knowledge and that they plan on applying at least one new thing they learned into their future clinical practice. Conclusions: Standardized patient encounters and virtual learning experiences are an accessible and effective way to increase knowledge regarding HPV and the HPV vaccine that exists among dental trainees and help dental providers feel confident aligning their recommendation for the HPV vaccine with the guidelines set by dental professional organizations (open full item for complete abstract)

Committee: Homa Amini DDS, MPH, MS (Advisor); Janice Townsend DDS, MS (Committee Member); Erin Gross DDS, PhD, MS (Committee Member) Subjects: Dentistry; Education; Health Education

PHD, Kent State University, 2007, College of Biomedical Sciences

Invasive uterine cervical cancer represents a major disease burden in women worldwide. Persistent Human Papillomavirus (HPV) infection is the primary risk factor for the development of cervical carcinoma. My research project involves exploring the mechanisms by which natural lignans may suppress viral oncogene function, as a novel approach to inhibit HPV induced precancerous and cancerous lesions. HPV is a small double-stranded DNA virus that contains two viral oncogenes, E6 and E7, that block the actions of the tumor suppressor proteins p53 and Rb, respectively. Our laboratory discovered that the mammalian lignans enterolactone and enterodiol increase the stability of the p53 protein and restore its functions, leading to the expression of downstream targets of p53. These mammalian lignans are derived from the parent plant lignans, secoisolariciresinol and matairesinol, via intestinal modifications of the compounds. My work has demonstrated that treatment with enterolactone represses E6 mRNA levels and E6 and E7 protein levels, with unchanging mRNA levels of p53 in HPV positive HeLa and CaSki cells. These results suggest that the ability of this lignan to induce stability of p53 occurs at a post-translational level. In addition, the functionality of p53 was examined. Induction of downstream targets of p53, such as p21 and Bax protein indicates that the p53 pathway is intact. Detection of apoptosis in cervical cancer cells was measured with a clonogenic survival assay, by activation of caspase 3, by DNA fragmentation using the TUNEL assay, as well as by repression of the anti-apoptotic protein Bcl-2. To test for the genotoxic potential of enterolactone, the comet assay was performed. The results failed to show formation of comet tails, indicating that no DNA damage was induced by the lignan. Taken together, these data unfold the mechanism by which enterolactone overcomes HPV mediated cell cycle dysregulation. More importantly, my data strongly suggests that a natural (open full item for complete abstract)

Committee: Angelo DeLucia (Advisor) Subjects: