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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.
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.
The synergistic effects between Vorinostat and Tamoxifen observed through a phase II study on breast cancer patients resistant to hormone therapy may involve more than the modulation of ER-alpha to reverse Tamoxifen resistance in ERBC cells. RT-qPCR of genes expressed in Tamoxifen resistant cells, trefoil factor 1(TFF1) and v-myc avian myelocytomatosis viral oncogene homolog (MYC), were evaluated along with ESR1 and Diablo as a control. MYC was observed to have increased expression in the treated cells, whereas the other genes had a decrease in their expression levels after the cells were treated for 3 days with Vorinostat IC30 of 1 µM. As for targeting the AR, MCF7 Tamoxifen sensitive and resistant cells were not affected by the AR antagonists to determine an IC50. The cell viability for all MCF7 sub-clones only decreased for high concentrations of 5.56 µM - 50 µM in Bicalutamide and 16.67 µM – 50 µM of MDV1300. Furthermore, hormone depletion of MCF7 G11 Tamoxifen resistant sub-clones did not show a great response to DHT stimulation or the AR antagonists. In the RT-qPCR, the MCF7 G11 cells showed an increase in mRNA expression for ER, AR, and PR after 4 hours of treatment with estradiol. As for the DHT treatment, ER, AR, PR, and PSA had a minimal increase in the fold change, but the fold change in AR was less than in the estradiol treatment. The Mayo Clinic will investigate the possible usage of AR as a biomarker through immunohistochemistry.