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Item Native Hawaiian Values and Identity: An Interpretive Phenomenological Analysis of Kānaka ʻŌiwi Educators and Educator Leaders(Creighton University, 2025)The topic of this dissertation in practice is centered around Native Hawaiian identity and the intersection between Native Hawaiian identity and how Native Hawaiian values shape that identity. The purpose was to explore the role that Native Hawaiian values play in shaping the identity of Kānaka ʻŌiwi (Native Hawaiians) educators and educator leaders with an aim of advancing the existing scholarship about Native Hawaiian values and identity. A qualitative study using interpretive phenomenological analysis was conducted with 15 Kānaka ʻŌiwi educators and educator leaders from the Hawaiian Islands and the Continental United States, using semi-structured interviews. Major findings were Native Hawaiian values serving as foundational for identity and educational practice, certain values being more influential in shaping identity, and those values evolving to shape participants’ identities over their lifetimes. This dissertation in practice document is organized into three sections. Section 1 is a proposal with a detailed literature review and method for the proposed study. Section 2 is a submission-ready manuscript in alignment with Hūlili, a multidisciplinary research journal on Hawaiian Well-Being. Finally, Section 3 is a practitioner recommendation plan that outlines a new program called Kānaka ʻŌiwi Talk Story and shares my reflections as a practitioner-scholar and my leadership philosophy. Keywords: Native Hawaiian values, Native Hawaiian identity, Kānaka ʻŌiwi, educators, educator leaders - Loading...
Item Nebraska Criminal Justice Review: December 2025(Holy Family Ministries, Omaha, Neb., 2025-12)Content: Strengthening Democracy: Jason Witmer, by Civic Nebraska Short history of a long protest, by Fran Kaye Safe water at NCCW should not be a struggle, by Carla Walker South Omaha immigration raid and incarceration, by Joanna Lindberg Swift reaction to Pillen’s WEC-to-ICE decision, by Joanna Lindberg Residence Restrictions in Nebraska: They aren’t for everyone, by Jeanie Mezger Mental health among the forgotten population, by Teela A. Mickles Crossroads Connection supports those incarcerated at CCC-O, by Teresa Bray Unspoken Procedure, by Carla Walker Women’s Justice Commission Report: Stronger families, safer communities, by Joanna Lindberg Letters - Loading...
Item Investigation of Sensory Cell-Specific Changes in Gene Expression in Microrna-183 Family Knockout Mouse Inner Ear From Bulk RNA Sequencing Analysis(Creighton University, 2025)Hearing loss impacts a significant portion of the human population. According to a 2018 report by the World Health Organization, about 466 million people worldwide, including 34 million children, experience disabling hearing loss. Recent advances in molecular biology have emphasized the pivotal role of microRNAs in regulating gene expression during the development and maintenance of the inner ear. These small non-coding RNAs influence key biological processes such as cell differentiation, apoptosis, and oxidative stress, which are essential for maintaining cochlear function and protecting auditory sensory cells. Changes in microRNA expression have been linked to different types of hearing loss, including age-related, noise-induced, and genetic or congenital. Our lab focuses on the miRNA-183 family, which includes three microRNAs: miR-183, miR-96, and miR-182. These microRNAs are expressed in sensory neurons and sensory epithelial hair cells. The miRNA-183 family has been linked to hereditary deafness in both humans and mice.To investigate the potential roles of the miR-183 family in the inner ear, our research team conducted bulk RNA sequencing to compare newborn mouse inner ear tissues from wild-type versus miR-183 family knockout (KO) mice. Bulk RNA sequencing revealed numerous gene expression changes in the cochlear sensory epithelium and spiral ganglion due to miR-183 family loss-of-function. However, these changes in gene expression represent an average across the entire tissue and do not provide insight into cell-specific gene expression. To address this, I combined existing bulk RNA sequencing data with publicly available single-cell RNA sequencing data from the gene Expression Analysis Resource (gEAR) database to obtain cellular resolution. First, we compiled a list of differentially expressed predicted miRNA target genes, either upregulated or downregulated, that changed in expression by at least 20% due to miR-183 family KO. From this list, we selected the top 25 highly expressed genes and the top 25 most changed genes, whether upregulated or downregulated. Subsequently, we generated heatmaps in gEAR to visualize and explore cell-specific gene expression patterns of these genes across different cochlear cell types and spiral ganglion neurons. Results revealed 31 Genes of Interest (GOIs) based on hair cell specificity in the sensory epithelia at P1 and 37 GOIs based on developmental expression in the spiral ganglion from E14 to P1, representing a total of 60 individual genes. Concurrently, the human gene database GeneCards was used to gather information on the names, functions, and associated diseases, including hearing loss, of these 60 genes. Furthermore, DAVID (Database for Annotation, Visualization, and Integrated Discovery) was also utilized to perform Gene Ontology (GO) analysis, which enhanced the classification of these genes and helped identify patterns related to their potential functions in the mouse inner ear. After this thorough analysis, a total of 19 GOIs were identified: Egr1, Nnat, Plod2, Rims3, Cntn1, Idh2, Cfl1, Anp32b, Palld, Hspa2, Kif5a, Map1b, Zbtb20, Plag1, Prkce, Amotl2, Slc44a2, Dcx, and Sncb. These 19 genes stood out due to their expression patterns after KO, their cell-specific expression in single-cell analysis data, their potential involvement in hearing loss-related diseases, and their specific cellular processes (i.e., GO terms). Out of these 19 GOIs, four genes including Egr1, Nnat, Plod2, and Rims3 were selected as easily validatable targets to investigate cell-specific changes in expression resulting from miR-183 family KO by immunostaining. Collectively, these findings could advance hearing research by illustrating the impact of miR-183 family KO on specific genes involved in the development and maintenance of the inner ear and their potential effects on hearing loss. - No Thumbnail Available
Item Healthy Choices for Every Body: A Quality Improvement Project(Creighton University, 2025-12-12)In the United States, the adult obesity epidemic is a rising health concern. In the next five years it is predicted that over 85% of adults will be obese or pre-obese (Golden, 2020). Obesity is a growing problem in society, but there is limited guidance for providers on what to do after obesity has been diagnosed. Once obesity is diagnosed, there is a lack of clear, evidence-based recommendations and proven interventions, leaving providers without standardized approaches for effective management. One program showing success is the Healthy Choices for Every Body (HCEB), created jointly by the United States Department of Agriculture (USDA) and the University of Kentucky. A quality improvement project was conducted using the free HCEB program at a privately owned adult clinic in Omaha, Nebraska, to improve modifiable behavioral habits. The project population included seven obese or overweight adults with an average age of 44. Participants attended five, hour long zoom sessions on nutrition, exercise, and food safety practices. The project had five objectives with specific goals. Participants completed the Expanded Food and Nutrition Education Program-Food and Physical Activity Questionnaire (EFNEP-FPAQ) pre- and post-program, along with a satisfaction survey at the end of the study. Of the five project goals, 3 were accomplished. One result showing significance was the total score on the EFNEP-FPAQ out of a total of 182. The results pre-program (M=97.71, SD=10.981) and post-program (M=109.71, SD=7.432). Paired t-test results showed a significant increase, t(6)=-3.384, p=.015, with a mean improvement of 12 (SD diff= 3.549) and a large effect size (g=10.8). These results demonstrate the promise of a structured program, teaching lifestyle changes to help health care providers manage the growing obesity epidemic. - Loading...
Item LncRNA Nostrill Facilitates Neuronal Antiviral Responses by Promoting NFkB-Mediated Irf7 Transcription(Creighton University, 2025)Differences in antiviral and inflammatory gene expression influence viral clearance in the central nervous system. Persistent antiviral and inflammatory gene expression are associated with neurodegeneration and the development of neurodiseases. Long non-coding RNAs (LncRNAs) are key cell-specific regulators of gene transcription and are differentially expressed in antiviral responses and neurodegenerative diseases. The purpose of this study was to explore the role of the novel lncRNA Nostrill in neuronal antiviral responses using in vivo and in vitro model systems. The mouse model Theiler’s Murine Encephalomyelitis Virus-Induced Demyelinating Disease (TMEV-IDD) is a preclinical model of Multiple Sclerosis (MS) and is used to assess mouse strains resistant and susceptible to the chronic IDD phase of the infection. Few studies have investigated the mechanisms of antiviral gene expression in TMEV-IDD resistant and susceptible mice during the acute phase of infection. Differences in lncRNA expression during the acute phase, when hippocampal neurons are the primary targets of TMEV infection, may account for the unique viral pathogenesis of TMEV-IDD resistant and susceptible mice. When neuronal viral infection is at its height during the acute phase of TMEV-IDD, expression of the novel lncRNA Nostrill was evaluated in TMEV-IDD resistant and susceptible mice. In vivo, TMEV-IDD resistant and TMEV-IDD susceptible mice upregulated Nostrill in the hippocampus while only TMEV-IDD susceptible mice significantly upregulated Nostrill in the cortex. Nostrill expression was localized to NeuN positive neurons in the hippocampus and cortex. NFkB p65-mediated antiviral gene transcription was upregulated by TMEV infection and was correlated with Nostrill expression. In vitro, knockdown studies in neuronal cell lines showed that Nostrill regulated NFkB p65-mediated gene transcription and knockdown of Nostrill increased TMEV viral burden. Mechanistic studies demonstrated that Nostrill translocates to the cytoplasm with TMEV infection and that NFkB p65 is required for Nostrill transcription. Nostrill physically interacts with NFkB p65 to promote occupancy of NFkB p65 and RNA polymerase II at the Irf7 promoter. Nostrill may play a regulatory role in neuronal NFkB p65-mediated antiviral gene transcription and may be a preventative target for neurodegenerative diseases.