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.
Hypoplastic Left Heart Syndrome
Alexis Damm, PA-S2
A.T. Still University: Arizona School of Health Sciences
Background: Hypoplastic left heart syndrome is a congenital heart disease that involves malformation of the left side of the heart. This etiology requires intervention after birth, and it effects 1 in 4,344 babies born in the United States (CDC, n.d.).
Clinical Case: A 4 year old male diagnosed with hypoplastic left heart syndrome prior to birth. This case study will focus on the history, diagnosis and treatment of a complication of hypoplastic left heart syndrome. The unique factors that influence this patient’s course of treatment will be highlighted in order for the disease to be better understood.
Conclusion: This clinical scenario showcases the importance of understanding birth defects, associated complications, and highlights the positive outcomes of proper pediatric care.
Reference: Center for Disease Control and Prevention. (n.d.). Congenital Heart Defects - Facts about Hypoplastic Left Heart Syndrome | CDC. Retrieved from https://www.cdc.gov/ncbddd/heartdefects/hlhs.html
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.
Author(s): Charles Edgar Biology Gary Boehm Psychology Paige Braden Psychology Kelly Brice Psychology Christopher Hagen Biology Amanda Key Biology Chumley Michael Biology Julia Peterman Psychology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology
Location: Session: 2; 2nd Floor; Table Number: 1
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.
Author(s): John Figg Biology Kelly Brice Psychology Chris Hagen Biology Claire Munster Biology Caitlyn Vilas Biology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology
Location: Session: 1; Basement; Table Number: 10
(Poster is private)
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.
(Poster is private)
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.
Author(s): Sarah Nagel Biology Kelly Brice Psychology Gabrielle Frediani Biology Christopher Hagen Biology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology
Location: Session: 1; 3rd Floor; Table Number: 8
Alzheimer’s disease (AD) is a neurodegenerative disease that leads to cognitive deficits. The brain dysfunction in AD is marked by an increase in amyloid-beta, 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 soluble Aβ causing synaptic disruption. In the present study, our aim was to understand the effect that Aβ has on synapses. We used immunolabeling 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 CNS neurons. Using immunohistochemistry, 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. Post synaptic density protein 95 (PSD-95) acted as post-synaptic marker and was also stained using immunohistochemistry. Images of synapses were obtained in both FAD+/GFP+ and FAD-/GFP+ mice. Comparing these images, we were able to determine that Aβ accumulation affects the observed number of synapses in the hippocampus.
(Poster is private)
Recently, terrestrial shoreline spiders have been proposed as biosentinels of bioaccumulative aquatic contaminants such as mercury (Hg). Terrestrial shoreline spiders become contaminated with Hg when they feed on Hg-contaminated emergent aquatic insects. Although the effect of body size on contaminant bioaccumulation in other biosentinels, such as fish, has been thoroughly examined, there has been much less research on the effect of body size on concentrations of Hg in shoreline spiders. In this study, we determined the effect of body size on Hg concentrations in six taxa of shoreline spiders belonging to four families (orb-weavers, [Araneidae], long-jawed orb-weavers, [Tetragnathidae: Tetragnatha spp.], jumping spiders [Salticidae] and wolf spiders [Lycosidae: Pardosa spp., Rabidosa spp. and Schizocosa spp.]. We collected 683 spiders during the day using sweep nets or by hand at night on May 14, June 5, 11, 20 and July 6, 2018 from 14 human-made ponds at the Lyndon B. Johnson National Grasslands, Texas, USA. Average total Hg (THg) concentrations (mean ± SE) ranged from 63 ± 4.0 ng/g to 246 ± 20.1 in Araneidae and Schizocosa spp., respectively, and were significantly different between spider taxa. We measured tibia + patella length on the first leg as a proxy for body size and found that spider THg concentration increased significantly with spider body size for Araneidae, Tetragnatha spp., Salticidae and Pardosa spp. The percent of variation in THg concentration explained by spider body size ranged from 16% to 40% for Pardosa spp. and Salticidae, respectively. This study indicates that Hg accumulation in shoreline spiders differ between spider taxa and within taxa by spider size. We recommend that future studies of Hg in shoreline spiders include assessment of spider size.
(Poster is private)
Thyroid disrupting compounds (TDCs) are known to interfere with normal thyroid hormone (TH) signaling. During embryonic and juvenile development, thyroid hormones modulate a variety of biological processes such as neurogenesis and the growth of the skeletal and muscular systems. Therefore, the majority of research on early life-stage (ELS) thyroid disruption has focused on its effects on growth and development. However, recent research has shown that ELS TDC exposure can also have adverse effects on reproduction later in life. Specifically, fathead minnows exposed to propylthiouracil (PTU), an anti-thyroid drug known to inhibit the synthesis of thyroxine (T4), during early development (from hatch through 42 days post hatch) experienced a 50% reduction in fecundity relative to controls. Interestingly, this statistically significant reduction in fecundity occurred when males, but not females, were subjected to ELS PTU exposures. After ruling out the possibility that ELS thyroid disruption altered testicular function, it was hypothesized that the observed reductions in fecundity resulted from changes in male reproductive behavior. To investigate the potential for and mechanism underlying PTU-induced alterations in male behavior, brains of PTU-exposed and control males were collected immediately after exposure for transcriptomic analysis. Of the genes that were found to be differentially expressed between the brains of PTU-exposed and control males, several were associated with axon guidance, behavior, and sex steroid signaling. Specifically, PTU-exposed males experienced significant reductions in the expression of serotonin receptor, fibronectin, estrogen receptor alpha, and aromatase. Given the known role of these genes in development and sexual differentiation of the male brain, these results provide evidence supporting the hypothesis that ELS chemically-induced hypothyroidism leads to altered neurogenesis and subsequent alterations in behavior. Overall, the results of this study may help link transcriptomic alterations in the brain to alterations in reproductive behavior, which has important population-level consequences.
Author(s): Rachel Jordan Biology Chris Hagen Biology Sofia Lopez Biology Julia Peterman Psychology Jordan White Psychology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology
Location: Session: 1; 1st Floor; Table Number: 7
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.
(Poster is private)
Alterations in neurological development and/or vision have been noted after exposures to a variety of environmental contaminants, including heavy metals, pesticides, pharmaceuticals, and estrogens. Despite the growing interest in assessing the neurotoxicity of toxicants, routine toxicity testing methods do not currently include the assessment of endpoints capable of predicting adverse impacts on neurological development. A toxicity test featuring embryonic fathead minnows - the fish embryo toxicity (FET) test - was recently developed; however, it does not include neurological-related endpoints. Development of such endpoints would expand the utility of the FET test and allow for the assessment of neurological teratogens. Previous studies have identified embryonic eye size as a potential FET test endpoint, and though there is limited evidence suggesting that these alterations are indicative of altered neurological development, studies validating the link between eye size and organism fitness are needed. The overarching goal of this project is to investigate whether reduced embryonic eye size at the conclusion of the FET test is predicative of altered vision or neurological function in larval fathead minnows. But first, assays for assessing vision and neurological function in larval fathead minnows must be developed and/or validated. Therefore, the objective of the present study was to validate methods to assess vision/neurological function in larval fathead minnows. Three assays were developed: the optomotor response assay, a feeding assay, and the c-start assay. The ability of these assays to identify alterations in the neurological function of larval fathead minnows was assessed by exposing larvae to three doses of the known neurotoxicant chlorpyrifos for 5 or 12 d. These results will be utilized in future studies investigating whether reductions in embryonic eye size are predictive of sublethal adverse effects and can also be utilized by other researchers interested in assessing vision/neurological function in larval fathead minnows.
Author(s): Sofia Lopez Biology Micah Eimerbrink Psychology Amy Hardy Biology Peterman Julia Psychology Kelsey Paulhus Biology Morgan Thompson Biology Jordon White Psychology Austin Williams Biology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology
Location: Session: 1; 2nd Floor; Table Number: 2
The pathology behind Alzheimer’s Disease (AD) consists of amyloid beta (Aβ) plaques and tau neurofibrillary tangles. Our laboratory has previously demonstrated that lipopolysaccharide (LPS) induced inflammation increases the concentration of Aβ in the hippocampus of male C57BL6/J mice. In order to elucidate the specifics behind this relationship, a group of C57BL6/J male adult mice received LPS or sterile saline injections for seven days, followed by two weeks of rest prior to receiving a second, seven-day round of LPS or sterile saline injections. Hippocampal tissue was collected and assayed following the last injection in order to quantify total Aβ levels. The results obtained showed higher levels of Aβ in the animals that underwent a single round of LPS exposure compared to their saline control, while animals exposed to two rounds of LPS showed intermediate levels of Aβ. These results suggest a decreased inflammatory response following a secondary exposure to LPS. More specifically, animals exposed to LPS for a second time showed significantly less central and peripheral inflammation four hours after LPS administration than animals with no prior exposure. The findings were then extended to adult female mice by repeating the experiment. The next goal for this research is to untangle the mechanism behind this effect.
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.
Texas horned lizards Phrynosoma cornutum are a threatened species in the state of Texas, due to population declines and extinctions, especially in the eastern part of their range. Texas horned lizards are still found in small towns in south Texas and can reach densities that are much higher (~50 lizards/ha) than in natural areas (~4-10 lizards/ha). We used models of Texas horned lizards to test whether predation levels might be lower in two south Texas towns than on a ranch that was located in south Texas. We constructed Texas horned lizard models from urethane foam, a material that is ideal for preserving marks (bites and pecks) left behind by predators. Models (n = 126) were left in the field for a period of 9 days in each location and marks left behind by predators were categorized accordingly. We conducted this experiment in June and again in August 2018. We found significantly less attempted predation events in the towns (n = 1 predation attempt) compared to the ranch (n = 60) and no differences between months. Anecdotal observations over the past 6 years also support a lack of many horned lizard predators in the towns. Our results suggest that Texas horned lizards may be under heavy predation pressure in natural environments and that lizards living in urban areas may be escaping some of this pressure leading to higher than normal lizard densities in some small Texas towns.
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.
Author(s): Gabrielle Frediani Biology Kelly Brice Psychology Christopher Hagen Biology Briar Hill Psychology Sarah Nagel Biology Filza Qureshi Psychology Gabrielle Salinas Psychology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology
Location: Session: 2; Basement; Table Number: 4
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.
(Poster is private)
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.
(Poster is private)
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.
Author(s): Brian Niebuhr Biology Sophia Cosmich Biology Phat Do Biology Sarah Nagel Biology Caroline Wade Biology
Advisor(s): Matt Chumchal Biology
Location: Session: 1; Basement; Table Number: 2
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.
Author(s): Dustin Rhoads Biology Dean Williams Biology
Advisor(s): Dean Williams Biology Sarah Hill Psychology John Horner Biology Laura Luque Biology
Location: Session: 2; 3rd Floor; Table Number: 8
Most of the literature on the basic ecology of Texas Horned Lizards cites "cryptic color pattern" as the first line of defense against predation in this taxon, and yet the degree to which horned lizards actually color-match their backgrounds has never been quantified. Texas zoos and state wildlife agencies are releasing captive-bred hatchlings and translocated adults to parts of their former range; however, the new populations are not self-sustaining, with the majority of releases lost to predation. Background color-matching has not been quantified for these reintroduction efforts but may be important to take into account when moving lizards into a new habitat where predation may be higher if they are not closely color-matched to the local soils. I quantify background color-matching in this taxon across its known range in the United States and in Mexico from in situ photos taken, as found, in the wild. I also present background color-matching variation and trends both within and between phenotypically and genetically diverse populations and ask whether lizards more closely match their local soil colors than soils from other areas. Finally, I suggest a method for zoos and wildlife agencies to score coloration in their captive populations of lizards, thus possibly enabling these institutions to objectively take into account color-matching a priori as an applied conservation strategy to potentially increase the survival of reintroduced Texas Horned Lizards.
Author(s): Alyssa Sanchez Biology Sara Gutierrez Cortazar Biology Carolyne Harvey Biology Heston Irons Biology Sohan Islam Biology Ashlyn Johns Biology
Advisor(s): Magnus Rittby Biology
Location: Session: 2; 2nd Floor; Table Number: 3
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.