Social connection, and the protection it provides, was a determining factor for our ancient ancestors’ ability to achieve their evolutionary goals of survival and reproduction. In turn, social exclusion, the loss of this connection, posed a serious threat to these goals, spurring the development of several cognitive and behavioral recovery strategies to combat its harmful effects. One potential strategy for women following experiences of social exclusion is increased motivation to engage in short-term sexual relationships that may quickly alleviate the safety and affiliative concerns associated with social exclusion. However, the relationship between social exclusion and women’s short-term mating (STM) motives remains relatively unexamined. The present research investigated the influence of social exclusion on women’s STM motives, and how individual differences in chronic concerns about exclusion influence this relationship. I predicted that being socially excluded, compared to included, would lead women to have increased STM motives. Furthermore, I predicted that individuals’ differences in chronic concerns about exclusion would moderate this relationship. To test these hypotheses, I primed feelings of social exclusion and inclusion using the future alone paradigm, and then measured several dimensions of unpartnered women’s self-reported STM motives (including sexual unrestrictedness, openness to sexual intercourse, and desired mate investment). Results did not support the hypothesized relationship. Instead, they indicated that excluded women exhibited lower STM motives, specifically less sexual unrestrictedness, than included women. However, this relationship was moderated by chronic exclusion concerns, such that, for socially excluded women, the more chronically concerned with social exclusion they were, the greater their expressed sexual unrestrictedness. For social included women, their trait exclusion concerns were unrelated to their expressed sexual unrestrictedness. Thus, for women that have chronically high exclusion concerns, increased sexual unrestrictedness following social exclusion may be a compensatory mechanism to mitigate the negative effects of being excluded. The implications of these findings for women’s interpersonal and intimate relationships will be discussed.

Alzheimer’s Disease (AD) is the most common form of dementia that mainly impacts the brain, specifically inducing neuronal cell death in the central nervous system. AD is characterized by the secretion of the protein Tau, and the formation of plaques made up of Beta-amyloid protein. Tau and Beta-amyloid plaques activate the secretion of inflammatory cytokines by microglial cell. The resulting inflammation triggers neuronal cell death, which leads to damage and cognitive decline over time. The cytokines secreted by microglial cells activate the Nf-kB signaling pathway. Activation of Nf-kB results in gene expression and secretion of TNF-a, a cytokine known to be associated with inflammation. This leads to a feedback mechanism that results in greater inflammation.
Our lab has demonstrated that a variety of anti-inflammatory compounds derived from IDT (iso-indolin dithione), targets the Nf-kB pathway by reducing the levels of TNF-a at the protein/translational level. BV-2 cells, a mouse microglial cell line were used in this study. Inflammation was stimulated by exposing these cells to LPS to trigger the activation of the Nf-kB signaling pathway. We hypothesize that the drugs tested reduce levels of TNF-a secreted by BV-2 mouse microglial cells, and therefore, block the development of disease-associated CNS inflammation seen in Alzheimer’s disease

Bacillus anthracis is a gram-positive bacterial pathogen that causes the deadly infectious disease anthrax. Bacillus anthracis contains two plasmids, pX01, and pX02. These plasmids were found to be necessary for the virulence of B. anthracis. However, Bacillus anthracis contains over 5,000 chromosomal genes and we believe that there are additional virulence genes that have yet to be discovered. Our lab constructed a transposon mutant library with random disruptions in the B. anthracis Sterne genome to screen for novel virulence factors. This library has been successfully used to identify the chromosomal genes clpX and yceGH and show their importance for B. anthracis virulence. To find additional novel virulence genes, we used the same transposon library and screened around 1,000 mutants using hydrogen peroxide, a reactive oxygen species (ROS). ROS are involved in the immune defense and the mutants that are attenuated in its presence may have a disrupted gene that contributes to the pathogenicity of B. anthracis. We obtained two mutants that were repeatedly susceptible to hydrogen peroxide in vitro. To determine the virulence of these mutants in an animal model, we will be performing an in vivo assay using the waxworm, Galleria Mellonella. Mutants that have reduced virulence in G. mellonella will be further tested to determine the location of the transposon in the genome to find out which genes are disrupted. The findings of this research could be used as potential therapeutic drug targets and could offer insight into the mechanisms that B. anthracis uses for its pathogenesis.

Mercury (Hg) is released by coal-burning power plants and artisanal gold mines into the atmosphere. Mercury deposited from the atmosphere into aquatic ecosystems can be converted into a neurotoxic form, methyl mercury (MeHg). In aquatic ecosystems, Hg biomagnifies which can affect organisms feeding at higher trophic positions. However, monitoring Hg in the environment to assess the risk to biota is not straightforward. For example, measuring Hg in sediment may not reflect the amount of Hg bioaccumulating in organisms. This difference in the Hg in the sediment and the amount bioaccumulating is partly determined by the bioavailability of Hg. Measuring bioavailability is very complex so sentinels can be used to detect Hg in food chains. Sentinels are defined as organisms that accumulate Hg within their tissues without significant adverse effects. Riparian spiders have been proposed as sentinels. Riparian spiders eat emerging aquatic insects which transport Hg from aquatic ecosystems and because of this, riparian spiders are sentinels of aquatic Hg contamination. The objective of this study was to measure Hg levels in wolf spiders (family: Lycosidae). From May 2021- June 2021, spiders were collected at four sites, two on the Clear Fork and two on the West Fork of the Trinity River, and the spiders were preserved in 95% ethanol. The spiders were sorted based on sex and their body size was measured. Hg will be analyzed using direct mercury analysis. This study attempts to determine the effect of sex and body size on the amount of Hg in wolf spiders, factors that have not been assessed previously. It also attempts to detect differences in the concentration of Hg between the Clear Fork and the West Fork of the Trinity River.

In the pathogenesis of neurodegenerative inflammatory diseases, such as Alzheimer’s disease, there is an abnormal buildup of redox metal ions that associate with β-amyloid plaques and convert oxygen into oxygen radicals. These radicals are highly reactive with cellular components and lead to oxidative stress that induces damage and death of neuronal cells which is associated with the cognitive decline of Alzheimer’s disease. Bifunctional macrocyclic compounds with antioxidant properties are a promising potential therapeutic to reduce levels of reactive oxygen species (ROS) and increase neuronal cell survival via the ability to chelate dysregulated metal ions and radical scavenging. In this project, novel macrocyclic compounds were tested for their efficacy in reducing intracellular levels of H2O2-induced ROS and H2O2-induced cytotoxicity. Intracellular ROS levels and cell survival were quantified in FRDA and BV-2 cells using the DCFH-DA and MTT cytotoxicity assays.

Alzheimer’s disease (AD) is often associated with chronic inflammation and cognitive dysfunction. In studying how AD-like pathologies change and affect learning and memory, our lab aims to optimize an object location memory (OLM) testing paradigm in mice. Briefly, a mouse is placed into an arena with two identical objects for a training session. Four hours later, one of the objects is moved to a novel location, and the mouse is placed back into the arena for the testing session. Because mice exhibit a preference for novelty, memory is assessed as the amount of time the mouse spends exploring the moved object divided by the total time spent exploring both objects. Our goal is to identify testing parameters that make this task both accurate and efficient for our lab’s use, as we will add this learning paradigm to a battery of behavioral tests to be used in future experiments. In the current study, the OLM protocol will be performed twice according to two different experimental timelines that test the effects of adding an additional training session to the original protocol.

BRCA1 is a gene found in humans that, when mutated, has been linked to breast and ovarian cancer. A homolog version of this gene, known as brc-1, exists in an organism called the Caenorhabditis elegans. This is a species of nematode worm that has the potential to be used as a model organism to study this homolog gene that is associated with human breast cancer. Previous studies with C. elegans have shown links between the brc-1 gene and DNA damage responses, cytochrome p450, or cyp, transcription levels, and ratios of male phenotype worms. This project focused on studying whether these brc-1 functions are dictated by the enzymatic activity of the protein made by this gene. To measure these phenotypes, we used a strain of C. elegans with a brc-1 mutation engineered to lack enzymatic activity of the BRCA1 protein toward nucleosomes. In order to determine how this lack of enzymatic activity affects brc-1 functions, we measured levels of reactive oxygen species (serving as a proxy for DNA damage), numbers of male offspring, and cyp levels in the mutant and wild-type C. elegans. Our initial results indicate the effects of enzymatic activity towards nucleosomes on the aforementioned phenotypes.

Our project focused on the conservation of activity of the protein BRD1 in C. elegans. C. elegans is a strong model organism for our study because BRD-1 is the worm ortholog to BARD1 in humans. Specifically, our focus is on its function as an enzyme to attach ubiquitin to the H2A tail of nucleosomes. We studied a structural mutation of BRD-1 that we predicted would interfere with its ability to bind its substrate, the nucleosome. We hypothesized that BRD-1 is bound to the nucleosome at this mutation site based on prior research in the human protein. Therefore, we integrated mutations found in humans into the DNA that codes for C. elegans BRD-1. A typical mutagenesis protocol was used to implement the mutations and then we expressed the proteins in E. coli cells. After that, nucleosomes were reconstituted by dialysis, and enzyme activity was assessed using a ubiquitination assay. These assays showed that BRD-1 in C. elegans does bind the nucleosome demonstrating conservation of the BARD1 function. Determining that function is conserved allowed us to determine that C. elegans is an appropriate organism to test mutations found in humans. This research has future clinical potential due to the ability to test mutations encountered in humans using a model organism and can aid with clinical treatment plans to help avoid the development of cancer.

Many anti-inflammatory drugs are currently in use to treat neuroinflammation in the brain which can result from Alzheimer's disease, Parkinson's disease, traumatic brain injury, and more. In collaboration with a company, P2Dbiosciences, we are testing drugs that can modulate the function of inflammatory cytokines such as TNF-alpha, with the goal of reducing neuroinflammation and thus benefiting people suffering from the neurodegeneration and cognitive decline associated with neuroinflammation. We hypothesize these drugs work by inhibiting the signaling associated with inflammatory cytokines.
Two different assays were developed to identify the mechanism of action of these cytokine modulating anti-inflammatory drugs. BV2 cells in culture were used for these assays to model how the drug affects mouse microglial cells (immune cells resident in the brain). The first assay uses a luciferase reporter gene to determine if NF-kB promoter activity is disrupted when cells are treated with drug. The second assay uses quantitative RT-PCR (qPCR) to measure changes in TNF-alpha mRNA levels when cells are treated with drug. Levels of TNF-alpha mRNA were also quantified over a period of time following drug treatment to determine whether the degradation time of the TNF-alpha mRNA was affected by treatment.

Invasive species, such as the Red Imported Fire Ant (Solenopsis invicta, hereafter, RIFA), can negatively impact native species via predation and modifying prey behavior. RIFA exist in two colony types, monogyne (single queen) and polygyne (multiple queens), and polygyne colonies are known to contain higher densities of fire ants than monogyne colonies. Texas horned lizard (Phrynosoma cornutum) eggs and hatchlings are suspected prey of RIFA’s foraging and aggressive behaviors. In this study, we collected fire ants from Karnes City and Kenedy to determine if Texas horned lizard density is lower around polygyne colonies. We collected and sequenced 30 ants, of which 20 were RIFA. Counter to our expectations, there seemed to be no correlation between RIFA colony type and Texas horned lizard density. Furthermore, we found evidence that monogyne and polgyne colonies were coexisting. In future studies, we think larger sampling sizes and determining ratios of polygyne to monogyne colonies within the same area would be useful for further testing the hypothesis that colony type may affect horned lizard density.