In vitro studies are critical for elucidating the mechanisms contributing to disease development, such as how diet-induced obesity leads to increased risk and incidence of breast cancer. However, they are often limited to short-term trials which fail to mimic the prolonged exposure to energy excess that contributes to obesity development. This project investigates how acute and chronic exposure to the saturated fatty acid, palmitic acid, affects the oxidative stress response in MCF-7 breast cancer cells. In excess, palmitic acid increases cellular lipid load and can lead to the production of reactive oxygen species (ROS), ultimately resulting in inflammation and cellular damage. However, chronic exposure to low doses of oxidative stressors have been shown to be protective against acute stress events via a biologic process termed hormesis. The study compares short-term and long-term treatments to determine whether continuous exposure amplifies oxidative stress or activates cellular defense mechanisms. To do this, I have already been culturing MCF-7 cells in a low dose of palmitic acid, and will continue to do so for 3 months. Once cells have been chronically exposed to a low dose (50 µM) of palmitic acid, they will be acutely treated with a high dose (250 µM) of palmitic acid for 24-48 hr. Basal ROS production (before high dose treatment) will be compared ROS production after the high dose treatment in cells that have been chronically exposed to palmitic acid. Cells that have not been chronically exposed will serve as our controls. These studies will help us understand how chronic exposure to saturated fats, as occurs with diet-induced obesity, alters oxidative balance in breast cancer cells and contribute to a better understanding of how diet influences cancer progression and cellular stress responses.

Background: Chronic stress among older adults increases risk for depression, anxiety, cardiovascular disease, and cognitive decline. Nature-based interventions may improve psychosocial and physiological stress outcomes, though longitudinal evidence in aging populations remains limited.

Methods: A convenience sample of community-dwelling older adults (N = 21; M age = 74.14 ± 4.59 years; range 65–85) participated in a six-week Nature Rx intervention study conducted in partnership with the Fort Worth Botanic Garden and Texas Christian University. The program included three two-week modules meeting twice weekly: garden yoga, forest bathing, and vegetable gardening. Repeated measures for the Well-Being/Personal Health Index (WPHI), positive and negative affect, nature-relatedness, outdoor activity minutes were assessed at baseline and at three subsequent time points across the program. Measures for handgrip strength (HGS), and salivary cortisol were assessed at the beginning of the first and sixth weeks, respectively. Friedman tests with Bonferroni-adjusted post hoc comparisons evaluated changes in psychosocial outcomes. Paired t-tests and repeated-measures ANOVA assessed physiological outcomes. Analyses were conducted using available cases due to incomplete measurements across time points.

Results: WPHI scores did not significantly change over time, χ²(3, n = 18) = 1.886, p = .596. Positive affect significantly increased, χ²(3, N = 18) = 13.437, p = .004, with higher final scores compared with baseline (padj = .012) and Post 2 (padj = .018). Negative affect also showed a significant overall time effect, χ²(3, N = 18) = 11.131, p = .011, though pairwise differences were not significant after adjustment. Nature-relatedness and outdoor minutes did not change (all p > .05). HGS remained stable, t(18) = −1.08, p = .294, and strength classification did not significantly change (Wilcoxon W = 3.00, p = .157). Salivary cortisol significantly decreased from pre- to post-intervention, t(21) = 7.653, p < .001 (d = 1.63); ANOVA confirmed a significant condition effect, F(1, 12) = 33.09, p < .001, ηp² = .734.

Conclusion: The intervention was associated with increased positive affect and statistically significant reductions in physiological stress, despite minimal changes in global well-being or muscular strength. These findings suggest short-term nature-based programs reduce stress burden in older adults. Larger controlled studies are needed to confirm these preliminary results.

The transcription factor, Nuclear factor erythroid 2-related factor 2 (NRF2), functions by activating genes that help protect the body against oxidative stress, inflammation, and various toxins. Thus, identification of small molecules that can increase NRF2 activity could be helpful to increase the body’s natural defense system against chronic disease. The goal of this interdisciplinary project is to use cell lines generated by the Montgomery lab (Nutrition) that express a fluorescent NRF2 reporter to test a small library of novel compounds generated by the Green lab (Chemistry) for their NRF2 activation capacity. First, our reporter system will be validated with known NRF2 activators. We will then use a luciferase reporter assay to screen 15 novel compounds for their capacity to activate NRF2 compared to the known standards. These data can then be used to inform both labs about their antioxidant capacity and help optimize their furthered development and utility.

Prebiotic sodas are marketed as healthy alternatives to traditional soda, but these claims have not yet been substantiated by research. This study evaluated the effects of fasted consumption of the prebiotic sodas Olipop and Poppi, compared with Diet Coke and Coca-Cola Original, on blood glucose, insulin, glucagon-like-peptide-1 (GLP-1), satiety, gastrointestinal symptoms, and beverage preference. A single-blind, repeated-measures design was employed with 10 participants. Participants completed four randomly assigned trials with a one-week washout period between each. During each visit, blood samples and satiety questionnaires were collected at baseline and throughout a two-hour trial. Beverage preference was assessed post-consumption, and gastrointestinal symptoms were evaluated using a follow-up questionnaire 24h post-intervention. The results from this study are expected to be completed by mid-April (by SRS).

The overall goal of our study is to understand how excess adiposity in women with and without
confounding cardiometabolic risk factors influences breast cancer cell growth and oxidative stress
signaling. I have already collected preliminary data indicating that activity of the antioxidant response
gene, NRF2, and expression of NRF2 targets are decreased in serum from obese subject, regardless of
phenotype. We investigated the functional consequences of these responses
by measuring and quantifying differences in reactive oxygen species (ROS) production. We also
investigated if these changes could lead to changes in breast cancer cell growth. To
investigate this, MCF7 breast cancer cells was grown in 6 distinct treatment groups reflecting varied
human metabolic health: CON (healthy control), NWO (normal weight obese), MUO (metabolically
unhealthy obese), and MHO (metabolically healthy obese), alongside the standard fetal bovine serum-
containing media a negative control. Reactive oxygen species production was assessed using a reagent
that fluoresces when it becomes oxidized by ROS. We expect cells grown in serum from obese subjects
will have higher levels of ROS production and increased invasive capacity. However, the results have yet
to be processed as of Mar 6. This research could demonstrate how total systemic metabolic health
influences oxidative stress responses and invasive potential, linking gene expression to real functional
outcomes. These insights could heavily inform medical assessments.