The literature indicates that poor body image is linked to worse academic performance and more depressive symptomatology. There is also a negative impact of depressive symptoms on academic performance found in prior studies. However, no prior study has examined the relationships between body esteem, depression, and academic achievement by gender. Studies have found that girls are at higher risk for developing depressed moods and that girls have greater depression symptoms compared to boys (Petersen et al., 1991; Patil et al., 2018). In addition, girls in general have higher levels of academic achievement and obtain higher grades than boys in high school (Fortin et al., 2013; Marsh et al., 1985). Given the gender differences in these important outcomes, it is crucial to address the potential gender differences in the relationship between body esteem, depression, and academic achievement. To address this lack of knowledge, this study aims to investigate the whether gender differences exist in 1) the relationship between body esteem and academic performance, 2) the relationship between depressive symptoms and academic performance, and 3) the relationship between body esteem and depressive symptoms.
Characterization of the Novel Fluoride Resistant Gene flr-3 in C. elegans
Creator:
Honey, Kendra
Date of publication:
August 25, 2022
Abstract Tesim:
The nematode Caenorhabditis elegans is a simple model organism used to better understand the mechanistic basis of human health and disease, as most cellular, molecular, and genetic pathways are conserved to humans. We have identified DRL-1 as a Mitogen Activated Protein (MAP) kinase responsible for proper growth and lipid homeostasis in C. elegans. The flr- 3 mutation, which was identified in a forward genetic screen, has been previously shown to confer fluoride resistance, however the molecular identity of flr-3 remains unknown. To investigate the function of flr-3, we examined its role in development and lipid reallocation, as well as compared flr-3 mutant phenotypes to the drl-1 mutant. Our results indicated that flr-3 genocopies drl-1, displaying defects in growth and lipid reallocation, indicating that it may function within the same pathway. Additionally, a complementation cross revealed that flp-2, a known mutation in the flr-3 mutant strain, does not the cause the flr-3 mutant phenotypes, leaving the genetic identity of flr-3 unknown.
The Effect of PFAS on Breast Cancer Cell Invasiveness
Creator:
Miranda Buzetta, Abel Andre
Date of publication:
August 15, 2022
Abstract Tesim:
Perfluorooctanoic acid (PFOA) is a known persistent organic pollutant and carcinogen. The stability of carbon-fluorine bonds lend to its application as a robust coating in various consumer goods and military-grade firefighting foam. This same quality allows for significant buildup in exposed soil and groundwater, leading to bioaccumulation in the bodies of living organisms. In the U.S., detectable levels of PFOA are ubiquitously present in population blood serum samples. Epidemiological studies have linked PFAS toxicity to tumorigenesis involved in liver cancer, pancreatic cancer, testicular cancer and breast cancer. The purpose of the present study is to analyze how short-term exposure to different concentrations of PFOA interact with ERɑ-positive and triple-negative breast cancer cell lines. Specifically, the study focused on the effects in epithelial to mesenchymal transition (EMT), which cancer cells undergo during the first stage of metastasis.
Role of SKN-1 in mediating CEH-60 transcriptional activity in oxidative stress response in C. elegans
Creator:
Kwon, Jinny
Date of publication:
August 12, 2022
Abstract Tesim:
Oxidative stress is a state of imbalance between the activities of reactive oxygen species (ROS) and the activities of the antioxidants (AOX) that detoxify the reactive intermediates or repair the resulting damage. Impaired ROS management contributes to aging and disease through oxidative degradation of lipids in cell membranes disrupting the DNA, proteins, and cellular functions. In C. elegans animals undergoing oxidative stress, SKN-1 accumulates in the intestinal nuclei to induce downstream stress response genes to restore the redox balance. CEH-60/PBX is an intestinal transcription factor that opposes this pathway by repressing genes that promote longevity and stress responses. To uncover the activity of CEH-60 in oxidative stress response and the role of SKN-1 in mediating this activity, I measured the survival of ceh-60 mutants as well as animals with both CEH-60 and intestinal SKN-1 knocked out under oxidative stress conditions. I found that ceh-60 mutant animals with intestinal SKN-1 additionally knocked out displayed extended lifespan compared to ceh-60 single mutants, suggesting that loss of ceh-60 may not require SKN-1 to upregulate stress response genes. Thus, in wildtype animals, CEH-60 may have different mechanistic ways to repress stress response and longevity other than via SKN-1. Another possible explanation to my findings is that SKN-1 carries out most of its stress response activity in the non-intestinal tissues.