In an effort to address the lack of literature in on-campus active travel, this study aims to investigate the following primary questions:<br/>• What are the modes that students use to travel on campus?<br/>• What are the motivations that underlie the mode choice of students on campus?<br/>My first stage of research involved a series of qualitative investigations. I held one-on-one virtual interviews with students in which I asked them questions about the mode they use and why they feel that their chosen mode works best for them. These interviews served two functions. First, they provided me with insight into the various motivations underlying student mode choice. Second, they provided me with an indication of what explanatory variables should be included in a model of mode choice on campus.<br/>The first half of the research project informed a quantitative survey that was released via the Honors Digest to attract student respondents. Data was gathered on travel behavior as well as relevant explanatory variables.<br/>My analysis involved developing a logit model to predict student mode choice on campus and presenting the model estimation in conjunction with a discussion of student travel motivations based on the qualitative interviews. I use this information to make a recommendation on how campus infrastructure could be modified to better support the needs of the student population.
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.