Glioblastoma (GB) is one of the deadliest cancers and the most common form of adult primary brain tumors. SGEF (ARHGEF26) has been previously shown to be overexpressed in GB tumors, play a role in cell invasion/migration, and increase temozolomide (TMZ) resistance.[3] It was hypothesized parental LN229 cell lines with SGEF knockdown (LN229-SGEFi) will show decreased metabolism in the MTS assay and decreased colony formation in a colony formation assay compared to parental LN229 cells after challenging the two cell lines with TMZ. For WB and co-immunoprecipitation (co-IP), parental LN229 cells with endogenous SGEF and BRCA were expected to interact and stain in the BRCA1:IP WB. LN229-SGEFi cells were expected to show very little SGEF precipitated due to shRNA targeted knockdown of SGEF. In conditions with mutations in the BRCA1 binding site (LN229-SGEFi + AdBRCAm/AdDM), SGEF expression was expected to decrease compared to parental LN229 or LN229-SGEFi cells reconstituted with WT SGEF (LN229-SGEFi + AdWT). LN229 infected with AdSGEF with a mutated nuclear localization signal (LN229-SGEFi + AdNLS12m) were expected to show BRCA and SGEF interaction since whole cell lysates were used for the co-IP. MTS data showed no significant differences in metabolism between the two cell lines at all three time points (3, 5, and 7 days). Western blot analysis was successful at imaging both SGEF and BRCA1 protein bands from whole cell lysate. The CFA showed no significant difference between cell lines after being challenged with 500uM TMZ. The co-IP immunoblot showed staining for BRCA1 and SGEF for all lysate samples, including unexpected lysates such as LN229-SGEFi, LN229-SGEFi + AdBRCAm, and LN229-SGEFi + AdDM. These results suggested either an indirect protein interaction between BRCA1 and SGEF, an additional BRCA binding site not included in the consensus, or possible detection of the translocated SGEF in knockdown cells lines since shRNA cannot enter the nucleus. Further optimization of CO-IP protocol, MTS assay, and CFA will be needed to characterize the SGEF/BRCA1 interaction and its role in cell survival.

Americans today face an age of information overload. With the evolution of Media 3.0, the internet, and the rise of Media 3.5—i.e., social media—relatively new communication technologies present pressing challenges for the First Amendment in American society. Twentieth century law defined freedom of expression, but in an information-limited world. By contrast, the twenty-first century is seeing the emergence of a world that is overloaded with information, largely shaped by an “unintentional press”—social media. Americans today rely on just a small concentration of private technology powerhouses exercising both economic and social influence over American society. This raises questions about censorship, access, and misinformation. While the First Amendment protects speech from government censorship only, First Amendment ideology is largely ingrained across American culture, including on social media. Technological advances arguably have made entry into the marketplace of ideas—a fundamental First Amendment doctrine—more accessible, but also more problematic for the average American, increasing his/her potential exposure to misinformation. <br/><br/>This thesis uses political and judicial frameworks to evaluate modern misinformation trends, social media platforms and current misinformation efforts, against the background of two misinformation accelerants in 2020, the COVID-19 pandemic and U.S. presidential election. Throughout history, times of hardship and intense fear have contributed to the shaping of First Amendment jurisprudence. Thus, this thesis looks at how fear can intensify the spread of misinformation and influence free speech values. Extensive research was conducted to provide the historical context behind relevant modern literature. This thesis then concludes with three solutions to misinformation that are supported by critical American free speech theory.

The goal of this project was to design and create a genetic construct that would allow for <br/>tumor growth to be induced in the center of the wing imaginal disc of Drosophila larvae, the <br/>R85E08 domain, using a heat shock. The resulting transgene would be combined with other <br/>transgenes in a single fly that would allow for simultaneous expression of the oncogene and, in <br/>the surrounding cells, other genes of interest. This system would help establish Drosophila as a <br/>more versatile and reliable model organism for cancer research. Furthermore, pilot studies were <br/>performed, using elements of the final proposed system, to determine if tumor growth is possible <br/>in the center of the disc, which oncogene produces the best results, and if oncogene expression <br/>induced later in development causes tumor growth. Three different candidate genes were <br/>investigated: RasV12, PvrACT, and Avli.

Empathy includes multiple components, including empathic concern, perspective-taking, and motivation to empathize. Various perspective-taking interventions have been found to be useful in increasing empathy. Games can be utilized as such interventions, especially when they involve perspective-taking components. The similarities between tabletop roleplaying games and various empathy-building interventions suggests that tabletop roleplaying games may be an intervention option that is already played for enjoyment. This study examines the influence of tabletop roleplaying games on motivation to empathize. Participants played a short tabletop roleplaying game and then were asked to choose between describing and empathizing with refugee targets over a series of trials. There is a potential main effect of tabletop roleplaying games on motivation to empathize, but this main effect is absent when controlling for self-other-overlap. It appears that self-other-overlap influences motivation to empathize. However, this study was underpowered, and the main effect of roleplay may have been detected if more participants were involved. Thus, there is potential that tabletop roleplaying games may influence motivation to empathize, and future research should examine this while considering the limitations of this study.

Fetal androgen exposure and childhood experiences are believed to contribute to the development and organization of the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes, which are responsible for the regulation and release of stress and sex hormones, respectively. Evidence suggests the HPA and HPG axes can couple in response to childhood adversity, and that hormonal dysregulation contributes to psychopathological disorders such as anxiety and depression. Recent research also suggests self-compassion interventions could reduce PTSD symptoms, and that the experience of childhood trauma is related to increased empathy. Still, little is known regarding the impact of fetal androgen exposure on PTSD susceptibility and the relationships between self-compassion, compassion for others, and empathy. The current study aims to determine whether fetal androgen exposure mitigates PTSD susceptibility, and to clarify the relationships between empathy, compassion for others, self-compassion, and PTSD symptoms. A sample of 208 adults completed an online survey designed to measure fetal androgen exposure, childhood maltreatment, self-compassion, compassion for others, empathy, and PTSD symptoms. Findings show a significant difference in PTSD symptoms between individuals in high and low fetal androgen exposure groups, and significant correlations were discovered between empathy and compassion for others, empathy and self-compassion, but not compassion for others and self-compassion. Future studies could explore the extent to which fetal androgen exposure influences PTSD symptom susceptibility and the clinical implications therein.