GEOL2026BENFORD38105 GEOL
Type: Graduate
Author(s):
Joshua Benford
Geological Sciences
Advisor(s):
Esayas Gebremichael
Geological Sciences
Coastal wetlands are critical ecosystems located at the dynamic interface between terrestrial and marine environments, shaped by the intricate interactions among sediment transport and deposition processes, geomorphology, hydrodynamics, and biogeochemical processes. They offer essential services, acting as a primary defense against storm surge flooding and reducing cyclone wind wave energy. However, the sustainability of coastal freshwater wetlands is increasingly threatened by natural and anthropogenic stressors, including sea level rise and land subsidence. The latter process alters coastal morphology and, in combination with saltwater intrusion, which is primarily driven by unsustainable groundwater pumping rates, contributes to the salinization of the soil, leading to a severe decline in freshwater wetlands' spatial extent and significantly reducing the ecosystem services they provide. Wetlands are particularly important in areas such as the Texas Gulf Coast, including regions extending from the Galveston to Beaumont County coasts, where there is a recurrence of cyclone events causing severe devastation, sprawling urbanization extending toward the coasts, and extreme use of groundwater resources to meet the demands of the growing population. This study utilizes an approach that incorporates remote sensing datasets and analysis techniques, including deep learning methods facilitated by GeoAI, and field-based geophysical methods to explore the following key objectives: (1) quantify spatial and temporal changes in coastal wetland extent and type from 2000 to 2024 in response to major stressors; (2) investigate the hydrogeological conditions of the critical zone in areas experiencing declining freshwater wetland coverage, assessing the impacts of environmental stressors on the wetland critical zone using key indicators such as subsurface erosion and other morphological indicators (3) evaluate how shifts in wetland dynamics influence their ability to mitigate cyclone-related hazards and examine corresponding spatiotemporal variations in methane emissions.
INTR2026CISNEROS16653 INTR
Type: Undergraduate
Author(s):
Adrian Cisneros
Interdisciplinary
Advisor(s):
Keith Whitworth
Interdisciplinary
NTDT2026HARNEN24287 NTDT
Type: Graduate
Author(s):
Katie Harnen
Nutritional Sciences
Advisor(s):
Elisa Marroquin
Nutritional Sciences
Elisa Marroquin
Nutritional Sciences
Ryan Porter
Interdisciplinary
View PresentationBackground: Glucagon-like peptide 1 (GLP-1) is a key gut hormone regulating glucose homeostasis and satiety. This triple-blind, crossover, placebo-controlled randomized study investigated the effect of an L-Arginine-based supplement on active GLP-1 secretion, appetite, and food intake.
Methods: Sixteen participants (N=16) completed three conditions: a placebo and two doses of the supplement (Low-Dose, 5g; High-Dose, 10g). Supplements were consumed at time 0, and an ad libitum meal was consumed at 60 minutes. Serum samples were collected at eight time points over 120 minutes to assess circulating active GLP-1 levels.
Results: Supplementation with L-Arginine significantly augmented circulating GLP-1 levels compared to the control condition. Both doses triggered an immediate, transient rise in GLP-1, followed by a robust and significantly enhanced post-meal response relative to placebo. Analysis of the Area Under the Curve (AUC) confirmed this finding: total GLP-1 exposure was 607% greater in the High-Dose group (~ 340n pg/ml/min, p < 0.0001) and 544% greater in the Low-Dose group (~130 pg/ml/min, p = 0.0076) compared to placebo (~ 50 pg/ml/min). No significant differences in GLP-1 concentrations were observed between the two supplement doses. Secondary analyses found no differences in subsequent food intake or subjective hunger ratings between conditions, a result likely limited by the study’s power for these secondary variables (eta ~ 0.023).
Conclusions: L-Arginine is a potent secretagogue for GLP-1. These findings demonstrate that supplementation significantly increases the body's overall exposure to this crucial gut hormone, suggesting a potential role for L-Arginine in supporting metabolic health.
PHYS2026AGBOOLA46197 PHYS
Type: Undergraduate
Author(s):
Ayo Agboola
Physics & Astronomy
Advisor(s):
Hana Dobrovolny
Physics & Astronomy
PHYS2026CRAWFORD34680 PHYS
Type: Undergraduate
Author(s):
Judah Crawford
Physics & Astronomy
Mason McClure
Physics & Astronomy
Advisor(s):
Anton Naumov
Physics & Astronomy
Graphene quantum dots GQDs possess broad potential in bioimaging and optoelectronics due to their unique optical properties, tunable structure, aqueous solubility, and minimal in vivo and in vitro toxicity. However, despite their solubility, GQD fluorescence may be quenched through interactions with water molecules and aggregation via non radiative decay pathways that reduce emission efficiency. Inspired by the ability of surfactants to prevent quenching interactions for single walled carbon nanotubes, we investigate their utility in preserving GQD fluorescence. Five structurally distinct surfactants, sodium dodecyl sulfate SDS, sodium dodecylbenzene sulfonate SDBS, sodium deoxycholate SDC, sodium cholate SC, and Pluronic F127, are tested across a range of concentrations for preserving fluorescence of top down and bottom up synthesized GQDs to determine optimal conditions. This work reveals that surfactant structure and concentration can non-linearly affect GQD emission in the visible and near-infrared, with SC and SDC providing maximum concentration dependent fluorescence increase. Zeta potential and dynamic light scattering measurements are conducted for each surfactant and GQD system to quantify interfacial charge, colloidal stability, and aggregate size distributions. The present study provides mechanistic understanding of how surfactants influence GQD photophysics, offering strategies to optimize GQD based probes for biomedical imaging and photonic applications establishing a structure-to-function framework that links solution phase organization to fluorescence emission.
PHYS2026MADUPUR48006 PHYS
Type: Undergraduate
Author(s):
Ayur Madupur
Physics & Astronomy
Advisor(s):
Hana Dobrovonly
Physics & Astronomy
PHYS2026PASAM20074 PHYS
Type: Undergraduate
Author(s):
Anvitha Pasam
Physics & Astronomy
Advisor(s):
Hana Dobrovonly
Physics & Astronomy
PHYS2026PAUL9096 PHYS
Type: Graduate
Author(s):
Himish Paul
Physics & Astronomy
Ugur Topkiran
Physics & Astronomy
Diya Vashani
Physics & Astronomy
Advisor(s):
Anton Naumov
Physics & Astronomy
PHYS2026SINGARAVELAN43081 PHYS
Type: Undergraduate
Author(s):
Sanjith Singaravelan
Physics & Astronomy
Advisor(s):
Hana Dobrovonly
Physics & Astronomy
PHYS2026VASHANI17113 PHYS
Type: Graduate
Author(s):
Diya Vashani
Physics & Astronomy
Himish Paul
Physics & Astronomy
Ugur Topkiran
Physics & Astronomy
Advisor(s):
Anton Naumov
Physics & Astronomy
PHYS2026VENGADESWARAN17472 PHYS
Type: Undergraduate
Author(s):
Lakshitha Vengadeswaran
Physics & Astronomy
Advisor(s):
Hana Dobrovolny
Physics & Astronomy
BIOL2025ALLEN28009 BIOL
Type: Graduate
Author(s):
Dalton Allen
Biology
Justin Hunt
Biology
Marlo Jeffries
Biology
Laurel Skrnich
Biology
Advisor(s):
Marlo Jeffries
Biology
Location: Basement, Table 9, Position 1, 1:45-3:45
(Presentation is private)Mysid shrimp (Americamysis bahia) have been utilized in routine marine toxicity assessments for decades. While mysids are a well-established model, there a key gaps in understanding how chemical exposure impacts their endocrine systems. Crustacean growth occurs through molting (i.e., shedding old exoskeleton), a process regulated by hormones, primarily ecdysteroids. Ecdysteroids are a class of steroid hormones that share similar chemical structures to vertebrate hormones (i.e., 17β-estradiol and testosterone), which have been suggested to disrupt molting in some invertebrates. Through powerful tools, like transcriptomics, potential genetic biomarkers may be identified following chemical exposure. These biomarkers could provide the basis for future research aimed at screening endocrine disrupting compounds using invertebrate models. The objectives of this work were to 1) assess whether known vertebrate endocrine disruptors (e.g., 17β-estradiol and trenbolone) would induce alterations in molting and growth and, 2) compare gene expression profiles between vertebrate endocrine disruptors and a model ecdysteroid (i.e., ponasterone A) using transcriptomic analysis. Ponasterone A induced predictable alterations in mass, molting, and ecdysteroid-related gene expression, reinforcing both the use of this compound as a positive control and these endpoints for assessing invertebrate endocrine disruptors. Vertebrate endocrine disruptors induced varied responses in the endpoints assessed, but neither acted in a manner comparable to ponasterone A. Future work may investigate the potential for differentially expressed genes identified in the transcriptomic analysis for screening of invertebrate endocrine disruptors.
BIOL2025BERTRAND46552 BIOL
Type: Graduate
Author(s):
Morgan Bertrand
Biology
Gary Boehm
Psychology
Logun Gunderson
Psychology
Advisor(s):
Michael Chumley
Biology
Location: SecondFloor, Table 6, Position 2, 11:30-1:30
View PresentationMetabolic syndrome (MetS) is a cluster of concurrent cardiometabolic risk factors, including increased waist circumference, hypertension, elevated triglyceride level, reduced high-density lipoprotein (HDL) cholesterol level, and hyperglycemia. The key pathophysiology of MetS is insulin resistance, resulting in a disruption of glucose and lipid metabolism in the liver and adipose tissue, which increases the risk of type II diabetes, cardiovascular disease, and stroke. The development of insulin resistance and related conditions is multifaceted, but risk can be mitigated with lifestyle modifications, including improved nutrition. In the US, a typical American diet (TAD) is full of highly processed foods high in saturated fats and refined sugars and is associated with increased insulin resistance and obesity risk. In contrast, adherence to a plant-based Mediterranean diet (MD) rich in unsaturated fats, fiber, and non-refined carbohydrates has been found to reduce disease risk. Despite the contrasting nutritional compositions, the average macronutrient distributions of these two human diet styles are similar (approximately 50% kcal carbohydrates, 15% kcal protein, and 35% kcal fat). Due to the comparable macronutrient ratios but contrasting nutritional composition, direct comparative analysis could uncover metabolic and cellular differences relating to their associated health outcomes.
There are few rodent studies in the literature that directly compare a TAD and MD. Further, studies often utilize a high-fat diet, consisting of 40-60% kcal fat, or individual nutrient supplements, such as olive oil, rather than comprehensive diet models. To address these limitations, our lab developed comprehensive, macronutrient-matched TAD and MD models that more closely mimic human diets in the U.S. and Mediterranean, respectively. A previous study in our lab found that six months of TAD consumption resulted in elevated body weight, increased inflammation, and excess hepatic lipid deposition, in comparison to the MD. Our current study looked to further characterize MetS under this diet model, specifically investigating obesity, insulin resistance, and dyslipidemia markers. Male and female C57BL/6J mice consumed either the TAD or MD from the age of 4 to 7 months. We found that after three months on diet, there were elevations in hepatic steatosis and serum cholesterol levels in both males and females on the TAD. However, other findings suggested early signs of insulin resistance in TAD males, but not females. Future studies will investigate MetS after 6 months on diet to better elucidate insulin resistance development and potential sex differences.
BIOL2025BOEHLY47210 BIOL
Type: Undergraduate
Author(s):
Nicholas Boehly
Biology
Bridey Brown
Biology
Emersyn Jorski
Biology
Advisor(s):
Dr Matthew Hale
Biology
Location: SecondFloor, Table 9, Position 1, 1:45-3:45
View PresentationNick Boehly, Bridey Brown, Emersyn Jorski, Matthew Hale
Texas Christian University, Department of Biology
Previous studies have shown that nutrition plays a key role in influencing epigenetic markers. Additionally, changes in gene expression have been linked to the development of Alzheimer’s disease (AD). However, it is unclear how, and to what effect, nutrition influences changes in the epigenome. To that end, we divided mice into groups and exposed them to two different diets 1) a typical American diet (TAD) and 2) a Mediterranean diet (MD). Although it is known that diet can induce epigenetic modification, it is unknown if these changes are heritable. There has been little research that has focused on the offspring of the mice fed with these diets. Therefore, this experiment will focus on how the diets of parental mice affect their offspring’s methylation patterns of previously identified candidate genes linked to the development of AD. Prefrontal cortex samples from F1 mice, whose parents were exposed to MD or TAD, were removed, and the RNA was extracted and reverse transcribed into cDNA. This cDNA will display levels of expression by 10 distinct genes that have been linked to AD in previous studies. Our goal is to identify correlations between nutrition and the development of AD through modifications of gene expression. Moreover, this data will help illustrate how inheritance of epigenetic modifications can influence gene expression in subsequent generations.
BIOL2025CARLTON20951 BIOL
Type: Undergraduate
Author(s):
Drew Carlton
Biology
Dalton Allen
Biology
Marlo Jeffries
Biology
Katie Solomons
Biology
Reagan Spickard
Biology
Advisor(s):
Marlo Jeffries
Biology
Location: Basement, Table 15, Position 2, 1:45-3:45
View PresentationThe Trinity River is an important body of water to the state of Texas as it is a source of drinking water for the Dallas-Fort Worth and Houston Metropolitan areas, a popular location for recreational activities, and an ecologically significant habitat for a variety of organisms. Due to its urban location, the Trinity River is subject to potential heavy metal pollution from wastewater treatment plant discharge, road runoff, and industrial activities. Heavy metal exposure has been shown to cause significant adverse impacts on aquatic organisms; thus, this project aimed to evaluate the presence and biological impact of heavy metals in sediment and surface water samples collected from the Trinity River. Water samples collected from the Trinity River were tested for the presence of heavy metals using ICP-OES. Larval fathead minnows were also exposed to sediment and surface water samples collected from the Trinity River and gene expression levels of five biomarkers were measured. Metallothionein was used as a biomarker of exposure to heavy metals, catalase and superoxide dismutase were used as biomarkers of oxidative stress, and heat shock proteins 70 and 90 were used as biomarkers of generalized stress. The results of this study provide insight into the extent of heavy metal contamination in the Trinity River, as well as its potential impact on aquatic life.
BIOL2025CHADWICK36742 BIOL
Type: Undergraduate
Author(s):
Braden Chadwick
Biology
Alex Caron
Biology
Sheridan O'Coyne
Biology
Katherine Richey
Biology
Mikaela Stewart
Biology
Advisor(s):
Shauna McGillivray
Biology
Location: Basement, Table 15, Position 1, 11:30-1:30
View PresentationAs increasing antimicrobial resistance continues to limit treatment options for bacterial infections, several new approaches have sought to avoid the challenges faced by traditional antibiotics. One such approach is targeting virulence factors, which are necessary for pathogens to evade host defenses and establish infection but not for survival outside the host. This strategy could provide an effective form of treatment while reducing selective pressures for bacteria to evolve resistance mechanisms. Studies have shown that the ClpXP proteolytic complex is essential for virulence in Bacillus anthracis and that deletion of the ClpX subunit increases sensitivity to the cell-envelope-targeting antibiotics penicillin and daptomycin as well as the human antimicrobial peptide LL-37. Previously, we used computational modeling to identify commercially available inhibitors of the ClpXP complex and demonstrated that one, ritanserin, mimics the phenotype of a B. anthracis ΔclpX knockout mutant in antimicrobial susceptibility assays. In this study, we evaluated ritanserin in comparison to four other inhibitors identified during the same screen—siramesine, xaliproden, fluspirilene, and R59022—by determining the fractional inhibitory concentration (FIC) index of each when used in combination with penicillin. Notably, all inhibitors used except R59022 have undergone at least phase II clinical trials for other purposes. We found that two out of the three inhibitors with the highest predicted binding affinity, ritanserin and siramesine, exhibited synergistic interaction with penicillin, while the remainder of the interactions were indifferent. Our results further demonstrate the potential of structural biology techniques to identify and repurpose existing drugs for use as novel antibiotics.
BIOL2025CHAMBERS17534 BIOL
Type: Undergraduate
Author(s):
Nia Chambers
Biology
Advisor(s):
Giri Akkaraju
Biology
Location: SecondFloor, Table 8, Position 1, 11:30-1:30
View PresentationChronic inflammation is a major contributor to neurological damage in diseases such as Alzheimer’s, which currently affects nearly 7 million Americans. The NF-kB signaling pathway plays a critical role in mediating inflammatory responses, as it regulates the expression of several pro-inflammatory cytokines, such as TNF-alpha, that exacerbate neuroinflammation. This study investigates the effectiveness of novel compounds in regulating TNF-alpha induced NFkB activation, using a luciferase reporter assay.
BIOL2025CRONK60206 BIOL
Type: Undergraduate
Author(s):
Sophie Cronk
Biology
Cassidy Hunter
Biology
Katherine Lesslie Lesslie
Biology
Aeron Pennington
Biology
Advisor(s):
Shauna McGillivray
Biology
Location: Third Floor, Table 5, Position 1, 11:30-1:30
View PresentationExpanding the Potential for Bacteriophage Therapy: Isolation of Phages against ESKAPE Pathogens
Sophie Cronk, Katherine Lesslie, Cassidy Hunter, Aeron Pennington, Shauna M McGillivray
Bacteriophages are viruses that selectively infect bacteria and propagate to overtake the host species.
They are also being developed as a treatment for otherwise drug-resistant infections. Though
bacteriophage therapy has not been FDA approved; it has been used in cases of compassionate care.
Because of the success in these cases, bacteriophage is offering a promising alternative to antibiotics
in the fight against antibiotic resistance. One issue in mainstream bacteriophage use is them
selectivity. Phages infect a specific bacterial species or a particular strain within the species.
Therefore, multiple phages may be required in a ‘phage cocktail’ to ensure there is a phage infects a
target bacterial strain. The goal of our bacteriophage study was to gather data about
where phages are heavily populated and to refine protocols to ensure optimal bacteriophage
collection. Bacteriophage that attacks different bacterial hosts tends to be found in locations
that commonly accumulates that specific host bacteria. A secondary goal is to isolate as many phages as
possible against bacterial species known as the ESKAPE pathogens. The ESKAPE pathogens are Staphylococcus aureus, Enterobacter
aerogenes, Pseudomonas aeruginosa and Klebsiella pneumoniae. These are clinically relevant
because their antibiotic resistance poses a threat to public health due to their ability to cause severe
infections. We have successfully isolated bacteriophage for Pseudomonas aeruginosa, Klebsiella,
and Enterobacter and we are actively exploring different environments for phage that will infect
S. aureus.
BIOL2025DOLT7187 BIOL
Type: Undergraduate
Author(s):
Audrey Dolt
Biology
Chrissy Baker
Biology
Precious Castillo
Biology
Hayes Martin
Biology
Jamison Speed
Biology
Mikaela Stewart
Biology
Advisor(s):
Mikaela Stewart
Biology
Location: Basement, Table 11, Position 1, 11:30-1:30
View PresentationBRCA1 and PALB2 proteins suppress tumor formation by promoting homologous recombination when DNA damage has occurred. Mutations in BRCA1 and PALB2 are associated with a higher prevalence of breast and ovarian cancers. It is established that phosphorylation of BRCA1 and PALB2 occurs in or near the coiled-coil region of both proteins. This domain is utilized by both proteins to heterodimerize, so we hypothesize that phosphorylation events could affect BRCA1/PALB2 interaction affinity. We are using Isothermal Titration Calorimetry and Circular Dichroism to determine if phosphorylation affects the structure or function of minimized binding domains from BRCA1 and PALB2. We will present our findings from the PALB2 phosphorylation sites which, contrary to our hypothesis, do not affect binding to BRCA1, as well as forthcoming data on the BRCA1 phosphorylation sites. In addition, we are using the minimized constructs and similar techniques to study questions regarding the effect of variants of unknown significance on the structure and function of these regions. While we have many variants remaining to test, thus far we find that the coiled-coil structure is destabilized by the introduction of proline variants in particular; therefore these variants disrupt the binding between PALB2 and BRCA1 and are more likely to be detrimental. We will present a summary of the variants tested to date and our working hypothesis regarding structure and function disruptions in the coiled-coil domains of BRCA1 and PALB2.
BIOL2025DURMAZ1537 BIOL
Type: Undergraduate
Author(s):
Lal Durmaz
Biology
Advisor(s):
Giridhar Akkaraju
Biology
Location: Third Floor, Table 3, Position 3, 1:45-3:45
View PresentationInflammation is a natural and beneficial response to injury and pathogen invasion. However, chronic inflammation is linked to the progression of various neurodegenerative diseases. Although the exact etiology is unknown, Alzheimer’s disease is associated with the overactivation of the NF-kB inflammatory pathway. NF-kB is a transcription factor that, in an unstimulated cell, is sequestered in the cytoplasm as a complex with its inhibitor, IκBα. When the pathway is activated by an external signal, IκBα is phosphorylated and subsequently degraded in the proteasome. Liberated NF-κB translocates to the nucleus, where it acts as a transcription factor for pro-inflammatory genes, highlighting its potential as a therapeutic target. Our research investigates the exact point of interference of novel anti-inflammatory drugs (provided by P2D Biosciences) with the NF-kB pathway through Western blotting and immunofluorescence.
BIOL2025FINDLATER29190 BIOL
Type: Undergraduate
Author(s):
Nicholas Findlater
Biology
Madelynn Farhat
Biology
Advisor(s):
Thushara Galbadage
Interdisciplinary
Giridhar Akkaraju
Biology
Location: SecondFloor, Table 9, Position 1, 11:30-1:30
View PresentationNeurodegenerative diseases such as Parkinson’s and Alzheimer’s disease are characterized by progressive neuronal loss, often driven by oxidative stress. The accumulation of reactive oxygen species (ROS) contributes to cellular damage, making oxidative stress a key factor in disease pathology. Caenorhabditis elegans, a genetically tractable model with conserved stress response pathways and neuronal structures, provides an effective system for studying oxidative stress and neurodegeneration. This study aims to establish an optimized oxidative stress assay in C. elegans to evaluate protective effects against ROS-induced damage. Wild-type (N2) C. elegans were synchronized via a bleaching protocol to generate a uniform population of young adults. Lifespan and survival assays were performed using tert-butyl hydroperoxide (tBHP) to induce oxidative stress, testing concentrations of 10, 1, 0.1, and 0.01 mM. Higher concentrations (10 and 1 mM) resulted in rapid mortality of C. elegans within 3 and 9 hours, respectively, whereas lower concentrations (0.1 and 0.01 mM) allowed survival beyond 12 hours. Based on these findings, an optimal tBHP concentration will be used to further refine this oxidative stress model. This study provides foundational data for investigating the efficacy of potential antioxidant molecules in reducing ROS-related damage. By using the C. elegans model, future research will focus on identifying molecular mechanisms of oxidative stress response and evaluating therapeutic candidates for neurodegenerative diseases.
BIOL2025GILL20345 BIOL
Type: Undergraduate
Author(s):
Namandeep Gill
Biology
Dean Williams
Biology
Advisor(s):
Dean Williams
Biology
Location: Basement, Table 2, Position 3, 11:30-1:30
View PresentationAlligator weed (Alternanthera philoxeroides) is a highly invasive species that threatens waterways, agriculture, and ecosystems worldwide. While herbicide treatments have successfully managed populations in Mississippi, they have been less effective in Australia and New Zealand. This research investigated whether genetic differences among populations contribute to these inconsistencies in control effectiveness. To test this, we genotyped alligator weed samples from Mississippi, Australia, and New Zealand using chloroplast DNA markers to identify haplotypes. Results revealed significant genetic variation among regions. Mississippi populations exhibited greater haplotype diversity, with Ap1 and Ap3 being dominant, whereas Australia and New Zealand were primarily composed of Ap2, Ap3, and Ap5. The genetic lineages used in Mississippi herbicide trials did not directly match those found in Australia and New Zealand, suggesting that differences in herbicide response may be linked to genetic variation. These findings indicate that current herbicide trials may not accurately predict effectiveness in non-U.S. regions. Future testing on genetically relevant populations will improve control strategies, ensuring more effective management of alligator weed globally.
BIOL2025GONZALES58202 BIOL
Type: Undergraduate
Author(s):
Lilli Gonzales
Biology
Daisy Carrillo
Environmental Sciences
Hermela Leul
Nutritional Sciences
Zoie Munoz
Dean's office
Kelley Wyatt
Biology
Advisor(s):
Christina Ayala
Biology
Location: SecondFloor, Table 1, Position 1, 1:45-3:45
View PresentationEmpowerHer STEM Club is an after-school program dedicated to encouraging young girls to explore careers in science, technology, engineering, and mathematics (STEM). In collaboration with E.M. Daggett Elementary School, the program seeks to address the gender gap in STEM fields, where women currently hold only 28% of STEM occupations. Research suggests that early mentorship plays a crucial role in shaping young women's academic and career aspirations.
EmpowerHer STEM Club provides mentorship and hands-on learning experiences to inspire and support young girls in their STEM interests. The program introduces students to diverse STEM fields through interactive experiments that complement their classroom curriculum. Additionally, participants learn about various STEM careers and the achievements of influential women in these fields. Through this engaging approach, EmpowerHer STEM Club fosters curiosity, confidence, and a passion for STEM while building connections with the next generation of leaders.
BIOL2025HERGET63787 BIOL
Type: Undergraduate
Author(s):
Ana Herget
Biology
Giridhar Akkaraju
Biology
Advisor(s):
Giridhar Akkaraju
Biology
Location: Basement, Table 7, Position 3, 1:45-3:45
View PresentationAlzheimer’s Disease (AD), the most common form of dementia, currently impacts almost seven million people in the United States over the age of 65. It is predicted that by 2060 over 13 million people in the United States will be affected by AD, which is why there is a growing demand for treatments. Amyloid ꞵ plaques and phosphorylated tau proteins are both associated with the progression of the AD pathology since they play a role in the disruption of neuronal integrity. These aggregated proteins along with other molecules, such as lipopolysaccharide (LPS), lead to increased inflammation by activating the NFκB pathway. The NFκB pathway controls the production of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNFɑ); however, if it is overactive, it can lead to harmful inflammation.The company P2D Biosciences provides novel compounds designed to reduce inflammation, but the exact mode of action of these compounds is unknown. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) can be utilized to measure cytokine mRNA from BV2 cells that have been pretreated with the drugs and then with LPS. In this project we screened multiple compounds provided by P2D Biosciences to evaluate their use as anti-inflammatory agents to treat AD.
BIOL2025HERRINGTON1009 BIOL
Type: Undergraduate
Author(s):
Lauren Herrington
Biology
Advisor(s):
Mikaela Stewart
Biology
Location: Third Floor, Table 8, Position 1, 1:45-3:45
View PresentationBRCA1 is a tumor suppressor protein that normally acts with its partner, BARD1, to facilitate DNA repair, regulation of the cell cycle, and regulation of gene expression. The Caenorhabditis elegans homologs of BRCA1 and BARD1, BRC-1 and BRD-1, respectively, retain these key functions and thus make C. elegans a suitable model organism for studying the functions of BRCA1. While the functions of BRCA1 and BRC-1 are well characterized, the molecular mechanisms by which these functions are carried out is still unclear. For example, BRCA1 and BRC-1 possess E3 ubiquitin ligase activity towards histone H2A in nucleosomes, but it is unknown how this contributes to tumor suppression. While inherited mutations that disrupt tumor suppression lack E3 ligase activity, they also interfere with other critical molecular functions, such as BARD1 binding. To pinpoint the role of E3 ligase activity, we aim to characterize a mutant construct of BRC-1 in C. elegans that lacks E3 ubiquitin ligase activity towards histone H2A but retains the ability to bind BRD-1. In vitro ubiquitination assays demonstrate that our candidate for this mutant of BRC-1, Trip A, is ligase-dead towards histone H2A in nucleosomes. Co-purification of BRC-1 and BRD-1 in which only BRC-1 contained the histidine tag revealed that BRC-1:BRD-1 binding is retained in the Trip A mutant. While these results demonstrate that Trip A meets in vitro requirements for a ligase-dead mutant, further in vivo experiments are needed to confirm its suitability. If confirmed as a suitable ligase-dead mutant through in vivo experiments, Trip A can be expressed in C. elegans to identify which functions of BRC-1 depend on E3 ubiquitin ligase activity towards histone H2A in nucleosomes.