Dyslexia is a prevalent developmental disorder characterized by unexpected reading difficulty in children and adults with otherwise normal IQ and intelligence. Dyslexia is a heterogeneous disorder and a variety of deficits are observed in the population, with auditory perception and rapid stimulus processing occurring most frequently. Genetic variants are likely related to this heterogeneity. One such gene that has been reliably linked to dyslexia is the neural migration gene DCDC2. Suppression of this gene in a rat model dramatically impairs speech-sound discrimination ability from a stream of rapidly-presented auditory stimuli (Centanni et al., 2016), suggesting a potential role for this gene in rapid stimulus processing deficits in humans and supporting a prior study linking this gene to reading speed (Neef et al., 2017). One potential casualty of processing speed impairments is the ability to process unpredictable stimuli. In the current study, we designed a rapid speech sound discrimination and prediction task to evaluate whether the rapid speech sound impairment previously linked with Dcdc2 also causes deficits on a prediction task. If increased presentation rate impairs the ability to process unpredictable stimuli, then the addition of a stable predictor sound should improve performance. To test this hypothesis, homozygous Dcdc2-knockout, heterozygous, and wild type rats were trained to respond to a target sound /dad/ in a stream of rapidly presented distractors in the presence or absence of a predictor sound /bad/, which occurred reliably prior to the target in 40% of trials. In wild type rats, the results indicate the presence of a predictor enhances response to the target /dad/ at low speeds, but as the stimulus presentation rate increased the rats began responding to the predictor /bad/ rather than the target. I will present these findings as well as pilot data from rats with Dcdc2 knockout to investigate the role of this gene on the response to a stable predictor.

A recent study (Petursdottir & Oliveira, accepted pending revision) found that when comparing equivalence-based instruction (EBI) to a complete instruction (CI) control condition using concurrent training and equal mastery criteria, EBI did not inherently produce faster or better learning than CI. However, this study included only a single EBI training structure. The purpose of the present experiment was to (a) evaluate the efficiency of linear series (LS) and one-to-many (OTM) EBI protocols relative to CI, and (b) to assess transfer of function following the three arrangements. Sixty undergraduate students were assigned to one of three groups (CI, EBI-OTM and EBI-LS), all of which received training to establish three 4-member stimulus classes. In the class establishment phase (ABCD training), the CI and EI groups were presented with 36 and 9 types of trials, respectively. After achieving mastery criterion, the ABCD test included all possible trial types, with no feedback. After achieving criterion on the ABCD test, all participants proceeded to transfer of function phase, in which they were taught to execute different motor responses to one stimulus in each class, and then tested with the remaining stimuli in each class. Results suggest the OTM protocol, but not the LS protocol, was more efficient than CI. The three groups performed equally well on the transfer-of-function test.

Language learning in adulthood is often important for personal or vocational reasons, but learning a second language after the sensitive period ends is time-consuming and retention is difficult. Research has suggested that cervical vagus nerve stimulation (cVNS) can help to improve cognitive function (Sjogren et, al. 2002) and working memory in patients (Sun et al., 2017). Transcutaneous auricular vagus nerve stimulation (taVNS), a less invasive method, activates similar brain structures as cVNS (Yakunina, Kim, & Nam, 2016). Recently, our lab demonstrated that taVNS paired with training improved letter-sound learning in typically-developing young adults (Thakkar et al., under review). The current study was designed to evaluate this approach in language learning. During a training session, they were exposed to 30 words in Palau, their English translations, and a picture that corresponded to the word while receiving either active or sham stimulation to the outer left ear. Each stimulus was repeated 10 times. At the end of training, a free-recall test was given where participants saw a trained word and provided the English translation. After one week, participants completed the same free-recall test of English translations to evaluate retention of the 30 trained words. While data collection is still in progress, we are seeing trends in the hypothesized direction such that those receiving active stimulation recall more words after training and at retention than those receiving sham stimulation.

Adopted children often have trauma–related emotional and behavioral problems, such as depression, anger, and anxiety, and these problems can continue to exist after adoption. Post-adoption, the adoptive family’s impact on these problems is not well understood. The current study examines the relationship between adopted children’s trauma symptoms and family communication – a construct that is associated with child social-emotional adjustment in traditional, biological families. Data was collected from adoptive families who were recruited to participate in a therapeutic family intervention. The results revealed a significant negative correlation between family communication and trauma-related emotional and behavioral problems in adopted children; specifically, the healthier the family communicated, the less problems the adopted child exhibited. Further, we wanted to determine if a similar relationship was found between biological children’s emotional problems in adoptive families and family communication. The results revealed a similar relationship: the healthier the family communicated, the less emotional problems the biological children experienced. The results of this study indicate that family communication may be a significant factor when considering the severity of adopted children’s trauma-related emotional and behavioral problems post-adoption.

As the threat of antimicrobial-resistant infections continues to rise, the need for novel antibiotics grows. Targeting virulence factors in bacterial pathogens is one potential strategy for antibiotic development because inhibiting virulence would decrease the ability of the pathogen to evade the host immune response. This strategy may decrease the development of resistance since the treatment is not directly bactericidal and there is less selective pressure put on the bacteria population. Our goal is to discover new virulence genes in Bacillus anthracis that could potentially be a therapeutic target. Specifically, we are interested in finding genes that allow B. anthracis to acquire iron from the host. For bacterial pathogens, iron is critical for growth and often a limiting nutrient in the host. It has been linked with proper functioning of electron transfer proteins and superoxide dismutase enzymes. In B. anthracis infection, iron is acquired from host hemoglobin through a hemolytic pathway, but the complete mechanism of this is unknown. Approximately 1000 transposon mutants of B. anthracis were screened for the inability to acquire iron from hemoglobin, and five were deficient in acquiring iron from hemoglobin in in vitro assays. Of those five mutant strains, only one (9F12) also exhibited an in vivo phenotype using the wax worm model of infection. The gene disrupted in the 9F12 transposon mutant is the dUTPase/aminopeptidase gene. Our aim in this study is to confirm that the disruption of the dUTPase gene leads to the inability to acquire iron from hemoglobin in B. anthracis. Using targeted mutagenesis, we created an insertional mutant strain to disrupt the dUTPase gene and we are currently testing it, along with WT and 9F12, for the ability to grow in iron-limited conditions with or without hemoglobin. Confirmation of this phenotype will demonstrate that the dUTPASE/aminopeptidase gene is important for iron acquisition from hemoglobin and will support further studies to understand the role of this gene in the virulence of B. anthracis.

Aquatic parameters such as increased temperatures and dissolved oxygen levels is critical in determining the survival and ability to thrive of trout species, including the Bonneville cutthroat trout. Bonneville cutthroat trout (Oncorhynchus clarkia Utah), a subspecies of Yellowstone cutthroat trout, originated in the Bonneville Basin and is native to many river basins in Utah, Wyoming, Idaho, and Nevada(Duff 1996). East Canyon Creek is a headwater tributary in the Weber River Basin of northern Utah, and a stream where Bonneville cutthroat trout are native. However, due to the introduction of nonnative trout and multiple causes of habitat quality decline, they no longer occur in the stream. Over the summer of 2018, I participated in data collection which assessed the habitat qualities of East Canyon Creek. This data includes temperature, aquatic, and riparian qualities. Data on the corresponding summer for dissolved oxygen is available as well. When compared to Colorado’s Coldwater Criteria, it appears that the temperatures of East Canyon Creek exceeded the acute (22.1°C) and chronic (17.0°C) upper thermal thresholds for cutthroat trout(Todd et al 2008). When compared to the acute (5.0 mg/L) and chronic (6.0 mg/L) dissolved oxygen minimum concentrations(Null et al 2017), East Canyon Creek’s concentrations appear to have dropped below the identified concentrations. The objective of this paper is to statistically analyze the temperature and dissolved oxygen data on East Canyon Creek from 2018, and determine if a restoration project of Bonneville cutthroat trout in East Canyon Creek would be successful. Through the data analysis, we have found that water temperatures during the summer months have significantly exceeded both acute and chronic upper survival limits, and that dissolved oxygen concentrations are significantly lower than the minimum chronic survival level, indicating that East Canyon Creek is not yet suitable for a successful reintroduction of Bonneville cutthroat trout.

The BRCA1 gene encodes an 1863 amino acid protein that is relevant in many essential biological pathways, most notably DNA damage response and tumor suppression. In many instances, BRCA1's functions depend on interaction with other cellular components. One such binding partner is P53, another important tumor-suppressing protein that cooperates with BRCA1 to inhibit cancer cell growth. However, the nature of this interaction is not yet fully understood. Here we developed a biochemical assay to investigate the exact binding site for P53 in the central domain of BRCA1. The discovery of such binding sites allows future studies to identify the precise amino acid residues involved in binding and better predict the effect of mutations in the binding site on BRCA1's ability to inhibit carcinogenesis.

Breast cancer (BC) is the second most commonly diagnosed cancer among American women after skin cancer. Traditional treatments of BC include surgery, radiation, and chemotherapy therapy; however, these treatments are non-specific and potentially kill peripheral, healthy cells. There emerges a need for more specific treatments, most notably to develop chemotherapy agents that target a unique feature of the cancer cells. Interestingly, 70% of BC cells upregulate estradiol-dependent pathway, a characteristic essential for rapid cell growth. Current BC drugs, such as Herceptin and Tamoxifen, have targeted this pathway to preferentially kill BC cells. However, most women relapse within 15 years due to drug-resistance. Thus, there is a need for new chemotherapeutic drugs. Our research group studies a novel estrogen-receptor targeting drug: Est-3-Melex. This compound has the estradiol molecule linked to a DNA alkylating agent, Melex. We hypothesize that Est-3-Melex enters the cancer cells via an interaction between the estradiol moiety and the estrogen receptor alpha (ER-alpha). ER-alpha then enters the nucleus and binds to Estrogen Response Elements on the DNA. This movement positions the Melex moiety on the DNA and allows the transfer of a methyl group to the N3 adenine on the DNA. In this project, we test the hypothesized mechanism of action of our compound. Since Est-3-Melex has a DNA methylation component (Melex) conjugated to estrogen, our hypothesis is that after the drug binds to the estrogen receptor in the cytosol, it translocates to the nucleus, specifically methylates the N3-region of adenine bases, eventually triggering cell death.

Alzheimer’s Disease (AD) is the 6th leading cause of death in the US. More than 44 million people worldwide, including 5.7 million Americans, are living with this neurodegenerative disease, and those numbers continue to climb. One of the features associated with AD is a disrupted sleep/wake cycle. Sleep is essential for many psychological and biological functions. A reported 35.3% of adults get less than the minimum 7 hours of sleep per night recommended by the National Sleep Foundation. Evidence suggests a bidirectional relationship between sleep loss and AD. Previous research indicates that disruptions in sleep often precede symptoms of AD such as cognitive impairments and memory loss. Chronic sleep loss has been associated with increased amyloid-beta and proinflammatory cytokines in the brain. Extended release of these proinflammatory cytokines can lead to increases in amyloid beta in the brain, which aggregates to form plaques that disrupt neuronal communication, a hallmark of AD. The aim of the present study was to elucidate the interaction between chronic sleep restriction, inflammation, and AD pathology in C57BL6/J mice. Our lab has previously demonstrated that mice administered seven consecutive days of LPS, a bacterial mimetic, exhibit increases in amyloid beta and proinflammatory cytokines in the brain, as well as cognitive deficits. Furthermore, research from our lab has shown that stress can exacerbate the effects of LPS. Healthy C57BL6/J adult mice were subjected to the multiple platform method of sleep disruption for 10 hours per day for 6 weeks. After receiving 7 consecutive days of either LPS or saline injections, animals were subjected to contextual fear conditioning to assess cognitive functioning, and hippocampal amyloid beta levels were quantified. While 7 days of LPS administration did not increase amyloid beta or cognitive deficits in contextual fear conditioning, chronic sleep restriction was associated with deficits in contextual fear acquisition and increased levels of hippocampal amyloid beta compared to control groups. Therefore, chronic sleep loss may have detrimental effects to cognitive function through increasing amyloid beta levels in the hippocampus. Given the large percentage of adults reporting getting less than the minimum recommended 7 hours of sleep per night, combined with the alarming climb in rates of AD and a growing body of work suggesting a link between these trends, investigating the detrimental effects of not getting enough sleep is an essential area of study.

Stress has been linked to altering acute and long-term inflammatory responses. Stress has been shown to activate inflammatory responses, specifically microglial activation in the brain. While acute inflammation is one of the first responses to fighting disease and infection, prolonged inflammation has been associated with neurogenerative disease such as Alzheimer’s disease. Stress at critical periods of development, known as early life stress (ELS) has been linked to chronic dysregulation of the hypothalamic-pituitary adrenal (HPA) axis, depression and alterations to microglial cells. The goal of this study is to investigate the effect of stress in mice during early development through maternal stress during pregnancy and the impact on neuroinflammation in adult offspring. In utero, offspring are vulnerable to the harmful effects of pro-inflammatory cytokines due to stress experienced by adult mice, following an ELS timeline. Three conditions were utilized: (1) mice undergoing stress during the entire pre-natal period and with the early post-natal period, (2) mice undergoing stress during the early postnatal period, and (3) mice undergoing no additional stress at any point. For mice in the combination-stress condition, there was an immunosuppressive effect through downregulation of pro-inflammatory cytokines. These data support existing publications that indicate an immunosuppressive role of prenatal stress, leaving the host less protected against chronic disease.

Males and females differ with regard to their immune response to a pathogen. Previous studies have observed males having reduced pathogen resistance. This suggests that they may be responding to pathogens differently. However, few studies have compared male and female immune responses following pathogen exposure. The purpose of this study was to examine sex-based differences in pathogen resistance and immune responses following exposure to a pathogen in adult fathead minnows (Pimephales promelas). To accomplish this, fish were bacterially infected with Yersinia ruckeri and the immune system’s ability to respond was monitored. Additionally, genes that are known to turn on during the immune response initiation were measured quantitatively providing insight into the molecular effect in minnows. At the whole organism level, male fish were less able to survive pathogen infection relative to female fish. At the tissue level, both male and female pathogen injected fish had decreased hematocrit percentages compared to the fish injected with a saline solution but did not differ from each other. At the molecular level, increased gene expression of interleukin 1β was seen in pathogen-injected males compared to pathogen-injected females and both sham-injected sexes indicating that pathogen-injected males mounted a larger inflammatory response at the molecular level. Taken together, this evidence suggests that the increased mortality observed among males earlier in the exposure to the pathogen may be due to the upregulated inflammatory response rather than the effects of the pathogen itself.

Alzheimer’s disease (AD) is a very prevalent neurodegenerative disorder and is the 6th leading cause of death in the United States. Alzheimer’s disease (AD) is characterized by widely distributed amyloid plaques and neurofibrillary tangles, and is clinically associated with a progressive decline in memory and other cognitive functions. The major protein component of neuritic plaques is amyloid beta peptide. Several pieces of evidence have indicated that amyloid beta accumulates to form oligomeric states in the AD brain and cause the cognitive dysfunction commonly seen in patients. While a decrease in cognitive function is considered a hallmark of the disease, AD patients also exhibit decreased motor abilities and difficulties learning new motor tasks. Our lab’s previous investigations found voluntary running to decreased amyloid beta burden in C57/BL6 mice. The present experiment seeks to further explore the mechanism through which exercise induced amyloid beta clearance occurs. Previous studies have pointed to the function of the glymphatic system in the clearance of amyloid beta. The level and distribution of aquaporin 4 (AQP4) in the vascular endfeet of astrocytes is crucial to the normal function of the glymphatic system. Our experiment sought to determine a more detailed analysis of the role of AQP4 in the glymphatic clearance of amyloid beta. Using TGN-020, a selective AQP4 antagonist, we hope to further determine the importance of glymphatic clearance of amyloid beta in C57/BL6 mice through exercise. We hypothesize that mice receiving intraperitoneal TGN injections, thus blocking the function of AQP4, will experience decreased glymphatic clearance of amyloid beta. Understanding the process of amyoid beta clearance can aid in treatments for both the pathological and clinical affects associated with AD.

Bacillus anthracis is a Gram-positive bacterium that causes anthrax in humans. It is a significant microorganism in that many proteins important to virulence or pathogenesis are highly conserved in many other pathogenic bacteria. Our lab has previously identified the protein ClpX in Bacillus anthracis as metabolically significant in antibiotic resistance. Specifically, B. anthracis lacking the ClpX gene (ΔClpX) are significantly more susceptible to antibiotics that target the bacterial cell wall such as penicillin than the wild type. ClpX has multiple functions; primarily it interacts with ClpP to form a proteolytic complex that degrades dysfunctional or obsolete proteins. ClpX also has an independent chaperone function, moving proteins around the cell. This project has focused on determining if the pathway of decreased antibiotic resistance in mutant B. anthracis is dependent on ClpX interactions with ClpP, or if ClpX can function independently. To test this, a point mutation (I265E) was made in the ClpX gene at the site that has been previously identified as the site of interaction between ClpX and ClpP in Staphylococcus aureus. The ClpX genes in B. anthracis and S. aureus exhibit a high degree of conservation particularly in this region, and it is expected that this site will also be critical for ClpX and ClpP interaction in B. anthracis. The mutated ClpX gene (I265E) has been confirmed with sequencing and has been transformed as an inducible expression plasmit into the ΔClpX B. anthracis strain. The next step is to perfom growth assays in antibiotics such as penicillin to ascertain if the mutated expression vector can restore antibiotic resistance to ΔClpX.

The proper function of the Breast Cancer susceptibility gene 1 (BRCA1) and its subsequent protein in the human body is vital to healthy individuals. The malfunction of BRCA1 due to a mutation is associated with an increased risk of breast or ovarian cancer of up to 80%. The key to understanding whether a mutation in BRCA1 will lead to higher risk of cancer is its location. Many of its interactions with other proteins take place in the central region of BRCA1. Currently, little is known about how mutations located in this region affect BRCA1 structure and function. The central region is where BRCA1 interacts with another tumor suppressor called PALB2 to perform DNA repair. The central region site studied in this project can be activated as a response to DNA damage, influencing BRCA1 and PALB2 interaction to generate a damage repair response. We show how activation of BRCA1 affects its structure and function on the molecular level. The accomplish this we created three mutations in the central region that mimic activation of BRCA1 to identify possible significant changes in protein-protein interactions using biochemistry and structural biology techniques like Isothermal titration calorimetry and circular dichroism.

   Alzheimer’s disease (AD) is a neurodegenerative disease resulting in dementia and memory impairment in patients. Research is immensely important as there are currently no treatments available to slow, prevent, or cure the damage inflicted upon individuals. The brain dysfunction in AD is marked by an increase in amyloid beta (Aβ), the protein responsible for plaque deposition in the brain. The severity of the cognitive deficits positively correlates with the load of Aβ. Prior research in animal models has pointed to Aβ causing synaptic disruption. A synapse is associated with information transfer inside the brain. Neuroscientists are trying to determine if the synapse disruption caused by Aβ leads to the cognitive dysfunction seen in AD. However, it is difficult it is to visualize individual neurons inside the hippocampus. In the present study, our aim was to understand the effect that Aβ has on synapses using an immunolabeling and tissue clearing technique in an AD transgenic mouse model. The 5xFAD mouse model utilized in this study rapidly develops Aβ pathology. This model mimics the pathophysiology of AD in humans. The mouse model used was also knock-in transgenic for Green Fluorescent Protein (GFP) on mature neurons. Using immunolabeling, GFP was tagged with antibodies, thus making neurons visible under the microscope. Antibodies were also used for Aβ in order to visualize the amount of Aβ protein and its location. Images of neurons were obtained in both FAD+/GFP+ and FAD-/GFP+ mice using a conventional staining method and a tissue clearing technique. We expected the tissue clearing technique, which clears lipids from the brain, to result in enhanced visualization of neurons but this was not the case. To quantify synapses, dendritic spines were counted on individual neurons in both groups of mice. Our results showed that Aβ accumulation in FAD+ mice correlates with a decreased number of dendritic spines signifying a decrease in synaptic density.

Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder that is currently ranked as the sixth leading cause of death in the United States. Those affected by the disease experience symptoms including but not limited to mental decline, memory loss, confusion, difficulty with language, and behavioral and mood changes.  One of the hallmarks of AD is inflammation that occurs both centrally in the brain and in the periphery. While inflammation is the natural response to activation of our immune system and is critical for our survival, neuroinflammation is heavily associated with AD pathology. Two main cellular mediators involved with the inflammatory response are members of the glial cell family, microglial cells and astrocytes. When chronic inflammation is uncontrolled, it can lead to harmful cell and tissue damage. The continuous presence of damaged neurons results in the constant activation of microglia and astrocytes. This generates a neuroinflammatory environment which is thought to promote neurodegeneration. Another process commonly up regulated in the brains of aging individuals is that of oxidative stress, which plays a major role in age-related neurodegeneration and cognitive decline. The process can occur due to dysfunction of the antioxidant system, causing the accumulation of reactive oxygen species (ROS) in the brain. One of the primary biological markers of AD is the aggregation of Amyloid beta (Abeta). Abeta itself has been shown to act as a pro-inflammatory agent, promoting the activation of many inflammatory components. The accumulation of Abeta aggregates is thought to be exacerbated by essential biometal ions such as zinc and copper. Dr. Kayla Green’s lab in the TCU Chemistry Department has successfully created compounds that can simultaneously chelate metal ions and act as a powerful antioxidant. They have developed a family of compounds all consisting of N-heterocyclic amines that in turn, have the capacity to perform radical scavenging and metal ion capture. For the experimental design, BV2 neuronal cells were treated with either H202 or LPS for 16 hours. Following treatment, MTT assays were performed to measure cell viability. Once a treatment concentration was discovered that significantly decreased cell viability, varying concentrations of the N-heterocyclic amine were added to test for a recovery in overall cell viability.

Exploring the Effects of Early Life Stage Nitrate Exposure on Sexual Development and Adult Reproduction

Nitrate is a ubiquitous environmental contaminant that enters aquatic ecosystems as runoff from agricultural fertilizers, human and animal waste, and industrial processes. Previous animal studies indicate that at sublethal concentrations, nitrate acts as an anti-androgen in adult male vertebrates. However, a recent study using developing fathead minnows (Pimephales promelas) found that exposure to nitrate was correlated with increased androgen concentrations. This study sought to reconcile these conflicting results by exploring the impacts of environmentally realistic, early life stage nitrate exposure on male sexual development and adult reproduction. The main objective of this study was to identify the potential endocrine disrupting effects of nitrate across multiple levels of biological organization in male fathead minnows. Larvae less than 1 day post hatch were divided into three groups: 1) control, 2) low nitrate (50 mg/L NO3), 3) high nitrate (100 mg/L NO3) and exposed for 35 days. Gonadal gene expression of sex-steroid related genes was assessed in a subset of fish immediately following exposure. The remaining fish in each exposure group were raised in clean water until sexual maturity (115 dph) and then subjected to a 21-day breeding study, after which morphological measurements and male secondary sex characteristics were assessed. Gene expression analysis revealed that male fish in the high nitrate group had significantly decreased expression of a key enzyme in the sex steroid synthesis pathway than that of the control males. Breeding pairs in the high nitrate group also had a significant reduction in average clutch size. However, when these results are taken in conjunction with the analyses of the other target genes, breeding study endpoints, and morphological measurements, the exact effects of nitrate on the processes of sexual development and adult reproduction remain unclear.

Introduction: The purpose of this research was to determine differences in the effects of the sex hormone estrogen between the two genders on the endothelial function in vivo. Method: There was a total of forty-six college students from a liberal college in the South recruited. The forty-six students were twenty males and twenty-six females, who were divided into three groups: 20 males, 8 females (not taking any form of birth control) and 13 females (taking oral contraceptives). The participants were invited to complete a TCU approved IRB consent form and medical history questionnaire. Upon completion, the participants provided passive drool saliva for biomarker and sex hormone measurement and FMD for brachial artery flow and shear stress measurements. Results: Findings reveals that the mean age for males was 27.81 years and the mean age for females was 24.81 years. This data was found to be not significant (p = 0.0586). The BMI for males was 26.3 ± 3.59 kg/m2 and the BMI for females was 22.8 ± 2.36 kg/m2, found to be significant (p = 0.0003). 17-beta estradiol level was measured during follicular phase. There was no significant difference between men, women, and women on birth control. However, there was significant difference between male and female regarding nitrate production during the follicular phase (p = 0.0461). When comparing the post flow shear rate between women on birth control and women not on birth control, there was an increase in the shear velocity. Even though there was no significant change in sheer rate and FMD in the women on birth control, a trend toward an increase of both measures was noticed. Conclusion: There was found to be no significant difference in the effects of estrogen between men and women. Further research should be conducted to further specify the differences between women on contraceptives and men.

In partnership with UT Southwestern Moncrief Cancer Institute (MCI), the FWAYA Oncology Coalition, and TCU Pre-Health, our dedicated group of senior students at Texas Christian University aim to organize an awareness week for Adolescents and Young Adults (AYA) with cancer during the national AYA Cancer awareness week (3/31-4/6) of spring 2019 to reach students on campus. The Moncrief Cancer Institute has a leading AYA cancer program, offering individualized treatment, support, and therapy at no cost for patients who have been diagnosed with cancer. AYA oncology refers to the care and research focused on adolescents and young adults diagnosed with cancer, specifically those between the age of 15 to 39 years old. Every year 80,000 AYA’s are diagnosed with cancer in the U.S, and 600 of these patients are living in and around Tarrant County. The goal of our project is two-fold. First, we seek to raise awareness for programs and resources available to AYA patients with cancer through a campus campaign. As many members of the Texas Christian University identify between the ages of 15 and 39, we believe this cause is pertinent to TCU’s population. Second, we seek to connect the TCU community with events hosted in DFW by UT Southwestern Moncrief Cancer Institute and the FWAYA Oncology Coalition. TCU AYA Cancer Week 2019 is an Experiential
Projects that Impact the Community (EPIC) Grant project.

Hepatitis C is a disease of the liver that is caused by the Hepatitis C virus. The Hepatitis C virus (HCV) chronically infects between 130-170 million people in the world making it a significant health burden. HCV is 9.6 kb single-stranded RNA virus and a member of the Flaviviridae family of viruses which includes viruses such as Zika and Dengue. It is a smaller virus with a mature virion size between 50-80 nm. With a specific tropism for liver cells, the diseases of Hepatitis C are accordingly associated with the liver. The two predominant diseases related to HCV infection are cirrhosis and hepatocellular carcinoma. These are both caused as a result of chronic infection which occurs in about 80% of cases as opposed to acute infection which composes only 20% of cases. In order to establish a chronic infection the virus has evolved the ability to inhibit the innate immune response leading to a greater likelihood of reproduction and survival. Our specific interest was the mechanism by which HCV evades the host immune response. In previous studies we have shown that NS5A 10A, a mutant protein of NS5A, inhibits the activation of the IFN-β promoter which serves a key role in the innate immune response. In this paper we investigate the specific mechanism of the ability of NS5A 10A to interfere with the activation of the IFN-β promoter.

We are in the process of conducting a study on the effects of microgravity on Red Wiggler Earthworm decomposers. This experiment has been chosen for flight to the International Space Station to be conducted in the next several months. If we are to explore other planets in the future, we are hopeful that decomposers can grow and live successfully to bring the benefits that come with their existence. Ecosystems rely on decomposers as a building block to break down nutrients for plants. Decomposers are a critical part of an ecosystem. Earthworms play a role in in an ecosystem to constantly recycle broken down organic matter. With our experiment, we will gain more information about the growth of an Earthworm in microgravity. This experiment can help further space exploration to understand the effects of the microgravity on the growth of Earthworms.

Earthworms are crucial to the colonization of a planet due to being decomposers. They improve nutrients of the soil and they remove the dead roots, grass, and biotic factors by breaking them down. Breaking down organic matter to improve the fertility of the soil and create air pockets is such an important step in the process of decomposition. These air pockets are another benefit to the soil because it allows air flow through the soil. If we study the growth of the earthworm in microgravity, this could possibly help gain information in the process of growing produce and colonization on other celestial bodies in the future. This experiment will allow us to learn how a living organism reacts when it is growing and changing in microgravity. One part of this experiment is that we are going to compare the size of the earthworms grown in microgravity to the earthworm grown in Earth’s gravity. The growth size is a determining factor to whether earthworms are able to further space exploration and assist with the colonization of planet.

This experiment requires special handling during transportation to the International Space Station. We will be using a mini lab system provided called a Fluid Mixture Enclosure (FME) provided by the organization for the Student Spaceflights Experiment Program. This tube will be refrigerated from Burleson, TX. to NASA with a temperature of at least 40℉ or below. It will also need to be refrigerated on its return to Burleson, TX from NASA. We will follow the same experimental process with the control test on Earth.

We will be attempting to answer the question: What is the effect of microgravity vs gravity on the growth of a lentil bean? We chose this test subject to determine if lentil beans are a solution to help bone density issues and bone degeneration while astronauts are onboard the International Space Station.
While astronauts are in space, their bones degenerate and they lose muscle tone. Lentil beans can help bones and muscles develop as they contain calcium, magnesium, potassium, and protein. In our experiment, we hope to learn the effects of microgravity on plant growth ans to see if lentils grow the same in both environments. We can also use the information gathered from the lentils to conclude whether or not microgravity conditions are an adequate environment for farming and developing crops, which in turn will help determine if lentils are an appropriate crop to cultivate while on board the ISS.

Lentil beans are part of the legume family, which are usually inexpensive, nutritionally dense and a great source of protein. They are also a good source of calcium, magnesium, and potassium. Besides human consumption, lentil beans can be used for livestock feed too. In the agricultural context, the lentil beans can be utilized as a rotational crop with wheat. Lentil beans are a highly nutritious food, rich in minerals, protein, and fiber. Lentil beans are an economical source of protein, meaning it is affordable at a low-cost to prepare the beans. Lentil beans can be used as a supplement to a grain diet due to the high-protein and high-carbohydrate nutritional content.

Our hypothesis is that lentil beans will grow faster in space since there is a lesser amount of gravity in the ISS. Our experiment will help us understand how to better provide a sustainable food source for astronauts. Lentil beans, along with exercising, will allow their bones and muscles to stay strong and healthy in a microgravity environment. With our collected data after the experiment, the science community will understand how the effects of microgravity have on the growth of the lentil bean. If we explore and further understand the growth effects in microgravity of a lentil bean, this will allow us to seek deeper into understanding how other useful plants will grow in microgravity. This study will add to the research that has already been conducted. This experimental test is crucial to analyze the adjustments or changes that might need to occur to continue the legacy of the lentil bean in microgravity.

Large numbers of bats are killed at wind energy facilities world-wide and there is a pressing need to improve our understanding of why this is happening and develop effective strategies to minimize impacts. Although Texas has more installed wind energy than any other state in the U.S., there are very few publicly available data about bat mortality at Texas wind farms. This is especially true of areas that are only recently seeing wind energy development, such as far south Texas in the Rio Grande River Valley. A couple of reports suggest that northern yellow bats (Lasiurus intermedius) and southern yellow bats (Lasiurus ega) may frequently be killed at these wind energy facilities, but we know very little about population sex ratios or population structure in these two species. In collaboration with a researcher at Texas State University, San Marcos, we have extracted DNA from tissue samples taken from 88 northern yellow bats and 64 southern yellow bats killed at wind farms in Starr and Hidalgo Counties. First, we used a genetic method, in which we amplified regions of the X and Y chromosomes using PCR, to determine the sex of the bat carcasses. Next, we used a DNA barcoding approach to assess the accuracy of species identification in the field. These efforts represent the first steps in a study to evaluate genetic diversity and population structure in two species of yellow bats that will likely be negatively impacted by wind energy development.

Methylmercury (MeHg) is an environmental contaminate that has harmful effects on
wildlife. Anthropogenic sources like coal mining emit inorganic mercury (Hg) into the
atmosphere. From the atmosphere, Hg is deposited into aquatic ecosystems. Once in aquatic
ecosystems, inorganic Hg is converted to MeHg by bacteria and enters the food web. Emergent
aquatic insects (e.g. dragonflies), insects with aquatic larval stages and terrestrial adult stages,
will transport MeHg from the aquatic ecosystem to terrestrial predators like songbirds.
This project focuses on MeHg contamination of nestling Red-winged blackbirds
(Agelaius phoeniceus) from nests at the Eagle Mountain Hatchery Pond Facility. It is believed
that nestling Red-winged blackbirds (RWBL) consume aquatic-based prey, primarily odonates
(damselflies and dragonflies) but can consume terrestrial prey as well. Odonates are known to
have high levels of MeHg contamination. Although studies have attempted to observe what
RWBL parents feed nestlings, there are no studies of the actual prey composition in the
nestlings’ digestive tracts. Insects consumed by birds can be analyzed because external coverings
of insect body parts (head capsules, mandibles, legs) are composed of undigestible chiton. This study looks at nestling RWBL diets to quantify odonates in their diets. We will sort through varying fecal samples from the Pond Facility in order to determine the diet composition of the RWBL, and if the composition correlates with MeHg levels in nestlings.

In many patients with breast cancer, a mutation in their BRCA1 gene disrupts BRCA1 protein’s function as a tumor suppressor. One mechanism through which BRCA1 prevents cancer is by acting as an enzyme to attach a signaling protein called ubiquitin to a H2A, a DNA packaging protein. This attachment inhibits gene expression of DNA damaging proteins. Here, we determine whether enzymatic activity of BRCA1 towards H2A is a conserved feature in C. elegans, a microscopic worm used as a model organism.

To measure conservation, we used mutagenesis to introduce mutations into C. elegans’ BRCA1 at a region homologous to the known human H2A binding site. Similar to mutations at this site in human BRCA1, our results showed a decrease in enzymatic activity when mutations were present. This indicates that C. elegans BRCA1 and human BRCA1 use similar mechanisms of attachment to H2A. To develop tools to study this reaction in C. elegans, we need to understand the position on H2A to which ubiquitin is attached. To accomplish this, we generated C. elegans H2A using cloning to eventually determine the specific location of ubiquitin attachment.