Although wind energy facilities are a growing source of renewable, clean energy, they have been shown to contribute to increasing bat mortalities which could threaten the persistence of bat populations. This study aims to expand what we know about the biology and behavior of bat species impacted by wind energy development. Recent research has indicated that yellow bats (Lasiurus spp) are killed at wind energy facilities in the Rio Grande Valley of south Texas. We have limited understanding of the population biology or movement patterns in these species, so the extent to which wind turbine mortality may impact these bats is currently unknown. As part of ongoing research in our labs, I extracted DNA from 18 tissue samples collected from northern yellow bats (Lasiurus intermedius) at a wind energy facility in Willacy county, Texas in 2015. I amplified a region of the mtDNA, the COI locus, and will compare genetic diversity of these samples to a larger data set from wind energy facilities in nearby Starr and Hidalgo Counties that were studied in 2016 and 2017. Together, these datasets will improve our understanding of Lasiurus intermedius genetic diversity and population structure, and have the potential to provide much needed insights into the potential impacts of wind energy development on bats in southern North America.

The student hasn't submitted any abstract yet.

Mutations in BReast CAncer 1 protein (BRCA1) play a crucial role in DNA damage control such as double-strand DNA break repair mechanisms. Mutations in BRCA1 increase the chance of disrupted genetic integrity by its contributions to the development of breast cancer. BRCA1 must bind to its partner protein PABL2 (Partner and Localizer to BRCA2) in order to properly carry out its function in the repair mechanism pathway, but its conformation once bound to PALB2 is not clear. In its inactive state, PALB2 is known to remain in an alpha-helical coiled-coil homodimer conformation. Through this observation, we hypothesized that the intrinsically disordered region of BRCA1 on its binding surface will undergo a conformational change into an alpha-helical form. In order to test this hypothesis, we first created a truncated BRCA1, making it 50 amino acids long, then conducted nuclear magnetic resonance (NMR) experiments. Through the NMR experiments, we found that the binding interface of BRCA1 does change its conformation into a helical state, forming a coiled-coil heterodimer upon binding with PALB2.

The proper functioning of the protein PALB2 is vital to preventing tumor formation within breast tissues in individuals. Upon the detection of DNA damage, PALB2 and BRCA1 bind to each other along with BRCA2 to form a DNA repair complex. This complex then repairs DNA double-strand breaks in order to prevent the accumulation of DNA damage that leads to breast cancer. While both BRCA1 and BRCA2 have been extensively studied, a lot of information about the structure and function of PALB2 remains unknown. It is thought that BRCA1 and PALB2 bind via PALB2’s coiled-coil domain; however, how variants of unknown significance (VUS) affect this binding interaction is largely unknown. Further, while some of these VUS have been studied in vivo, cheaper and easier in vitro methods to measure their effect on binding affinity have yet to be formulated. Thus, we hypothesized that isothermal titration calorimetry (ITC) could be used as an in vitro testing method for assessing the effects of VUS within the coiled-coil domain of PALB2 on the binding event between PALB2 and BRCA1. Further, we hypothesized that a decrease in binding between the two proteins as measured by ITC would correlate with a decrease in DNA repair as measured in vivo. We tested the efficacy of this method by creating seven mutations within the coiled-coil domain of PALB2 and measuring the binding event of PALB2 to BRCA1 via ITC. Our results strongly suggest that the binding event is enthalpic in nature and can be adequately measured via ITC as evidenced by the correlation between our in vitro data and previous in vivo data.

Evaluating sex-specific differences in cellular immune function in a small fish model, the fathead minnow

Andrew Mielcuszny
Department of Biology

Advisor: Dr. Marlo Jeffries

Previous studies in the Jeffries lab have shown that male and female fathead minnows differ in their ability to fight and survive bacterial infections. Specifically, males have significantly higher rates of mortality upon infection than females. Despite this, few studies have sought to identify the sex-specific differences in specific immune processes that underlie the observed differences in survival following pathogen infection. The purpose of this study was to examine the sex-specific differences in phagocytic cell activity, a key innate immune response in which immune cells engulf and destroy pathogens. To evaluate phagocytic cell activity, kidney cells were isolated from male and female adult fathead minnows and their ability to phagocytose fluorescently-labeled E. coli was measured. The relative phagocytic cell activity of male and female fathead minnows will be presented in an effort to explain whether differences in phagocytosis contribute to differences in pathogen resistance.

Mercury (Hg) is found in the environment in excess of historic baselines throughout the globe because of widespread atmospheric emissions of inorganic mercury (IHg) from anthropogenic sources such as coal-fired power plants and artisanal gold mines. In aquatic ecosystems, Ihg deposited from the atmosphere is converted by bacteria to methylmercury (MeHg), a bioavailable neurotoxin that adversely affects the health of vertebrates including humans and wildlife. Because IHg deposition varies across the landscape, it is necessary to monitor MeHg levels in aquatic food webs of individual waterbodies. This is a challenge because there are millions of river miles and lakes in the U.S. Shoreline spiders that feed on MeHg-contaminated emergent aquatic insects have been proposed as sentinel species to monitor MeHg contamination. Sentinel species are species which serve to map the bioavailable fraction of pollution in an ecosystem by retaining the pollutants in their tissue. The objective of this study was to test the hypothesis that shoreline spiders can be used as sentinels to evaluate MeHg contamination of river food webs. Our study focused on the Clear and West forks of the Trinity River. A pilot study in 2016 indicated the two forks have different levels of MeHg contamination. From June to August 2019, we collected over 1000 long-jawed orb weaver spiders (Tetragnathidae) along the shorelines of the two forks of the river. Spiders were preserved in 95% ethanol and sorted by leg length into different size categories. Mercury was analyzed using direct Hg analysis. Concentrations of Hg in spiders increased with spider size and was higher in the Clear Fork than the West Fork. A follow up study confirmed that fish in the Clear Fork had higher concentrations of MeHg than in the West Fork. This is one of the first studies to demonstrate that shoreline spiders can be used as sentinels of MeHg contamination in river ecosystems.

For this project, I mapped potential river otter habitat in the Dallas/Fort Worth metroplex based on literature data on known river otter habitat preferences in Texas. I will use this data along with GIS data on land use/cover/vegetation and distance from suitable water bodies, to determine where in the DFW river otters may prefer to live. This project is interesting and informative because in recent years more urban run-ins with river otters have been documented in the DFW. So knowing where they might like to be is good information for citizens to have, as river otters continue to make a comeback in numbers in the state of Texas.

Carnivorous plants inhabit nutrient-poor environments and supplement nutrient acquisition by capturing and digesting insect prey. Carnivorous adaptations have been hypothesized to be beneficial only in environments with high water and light availability. We hypothesized that plant morphology would change in response to resource availability, exhibiting traits that increase carnivory when light is abundant and exhibiting traits that increase photosynthesis when light is limited. In a field manipulation in Leon County, Texas, we examined the effects of feeding, shading, and their interaction on the morphology of the pitcher plant, Sarracenia alata. We employed a two-factor, cross-classified design, with shading (two levels, shaded and unshaded) and prey capture (two levels, fed and unfed) as factors. Eighty plants were haphazardly assigned to one of four treatments: (1) unshaded and fed (control); (2) shaded and fed; (3) unshaded and unfed; and (4) shaded and unfed. When light availability was reduced, plants produced pitchers that had smaller diameters, which is reflective of a photosynthetic morphology. Unfed plants exhibited reduced growth (produced fewer pitchers and had lower sum of pitcher heights). There was a significant interaction effect on estimated seasonal aboveground biomass: shading had no effect on the mass of unfed plants, but shading reduced the mass of fed plants. As the season progressed, competing vegetation reduced light availability to all pitchers. Plants in all treatments began to produce pitchers that were blade-like with a small, non-functional opening and a widened keel. This morphology would maximize light capture at the expense of prey capture. This experiment provides support for a theoretical model that suggests that carnivorous traits are only beneficial under conditions of high light availability. It also emphasizes the importance of periodic burns of carnivorous plant bogs to remove vegetation, thereby reducing light competition.

Bacillus anthracis is a bacterium that causes the deadly disease anthrax and has been used in bioterrorism. We are looking to investigate what genes within the chromosomal DNA contribute to the virulence of Bacillus anthracis. In this study, we screened a transposon library of B. anthracis ‘knock-out’ mutants for susceptibility to reactive oxygen species used by the immune system. A broad in vitro hydrogen peroxide screen was performed on 1,953 transposon mutants, and after several rounds of in vitro screening, 40 mutants were identified as consistently attenuated in the presence of hydrogen peroxide. Four of these mutants were then tested in the invertebrate model, Galleria mellonella, to assess virulence in an animal model. Mutants with phenotypes that repeated in both assays were prioritized for characterization. The location of the transposon insertion in one of the mutants was successfully identified. Identifying these novel genes contributing to the bacterium’s virulence will provide a better understanding of B. anthracis pathogenesis and may provide potential targets for combatting anthrax.

The bacterium Bacillus anthracis, the causative agent for the disease anthrax, possesses two plasmids that contribute significantly to virulence. Besides plasmids, certain chromosomal genes also contribute. In previous studies, our lab discovered that the chromosomally encoded ClpX gene is essential for virulence in B. anthracis. ClpX is an ATPase that is part of the ClpXP proteasome found in many bacteria. Loss of ClpX in B. anthracis Sterne results in increased susceptibility to cell wall targeting antibiotics like penicillin and daptomycin. However, the mechanism behind ClpX’s role in antibiotic resistance is not understood as it is likely that multiple pathways are affected by the loss of this global protease. We recently conducted a microarray to find which genes are up or down regulated in ClpX compared to wild-type (WT) B. anthracis. 119 genes had disrupted regulation and several of these had been connected to cell-wall active antibiotics like penicillin. In this study, we focused on three of these genes: MsrA, GlpF, and SigM. We confirmed the microarray results and showed that MsrA, GlpF, and SigM gene expression in our ClpX strains significantly differs from the wild-type B. anthracis Sterne via QPCR. Insertional knockout mutants were made for GlpF and SigM to test whether these genes were necessary for antibiotic resistance. We are currently testing these mutants in penicillin and daptomycin to assess their phenotypes. We found that loss of SigM results in increased susceptibility to penicillin and are currently studying the effect of daptomycin on SigM and GlpF. We will test the virulence of both mutants in our invertebrate animal model G. mellonella. This will hopefully provide better understanding on the mechanism behind ClpX’s antibiotic resistance.

Studies have shown that males and females differ with regard to their ability to survive pathogen infections. The fathead minnow is a newly developed model for immunotoxicity; 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 be expressed 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.

Pollen transfer among flowers contributes to genetic diversity and the maintenance of plant populations through the production of seeds. Decreased pollen receipt can result in fewer offspring. This is known as pollen limitation. We conducted field and laboratory experiments in a population of Sarracenia alata in Leon County, Texas in 2019 to examine 1) the effect of floral herbivory by the pitcher plant moth, Exyra semicrocea, on pollen availability and 2) the impact of pollen receipt on seed quantity and 3) seed quality. We found that floral herbivory significantly decreased the number and mass of anthers in flowers, and that a high pollen load significantly increased the number of seeds produced compared to low-pollen and control flowers. We found no differences in offspring quality among different pollen treatments based on germination traits. Pollen limitation occurs in S. alata and may pose a conservation risk when paired with other ecological disturbances.

Bacillus anthracis is a gram-positive, spore-forming bacterium and the causative agent of the deadly disease anthrax. The B. anthracis genome consists of chromosomal genes and the pXO1 and pXO2 plasmids that strongly contribute to the bacteria’s deadly nature. While the virulence factors associated with the plasmids have been extensively studied, we believe there are still undiscovered chromosomal genes that may also have important virulence factors. To identify novel chromosomal genes associated with B. anthracis virulence, we screened a transposon mutant library of B. anthracis Sterne strain for increased sensitivity to reactive oxygen species. Reactive oxygen species, such as hydrogen peroxide, have many functions in mammalian immune defenses and wild type B. anthracis is able to subvert this host defense. Sensitivity to reactive oxygen species was tested through in vitro hydrogen peroxide assays and after several rounds of screening, eight mutants were confirmed as susceptible. We next tested whether any of these mutants were attenuated in vivo using our invertebrate animal model, Galleria mellonella and found several mutants with decreased virulence. We are currently working on determining the location of the transposon insertion to find which chromosomal gene is disrupted. This could lead to the discovery of novel B. anthracis virulence genes and eventually possible treatment targets for future anthrax outbreaks and attacks.

The swim performance assay is a behavioral assessment used to measure cardiovascular function in fish. Previously, the laminar flow assay (LFA) has been the standard method of assessing swim performance in adult fish to measure their cardiac output. The spinning task assay (STA) is a novel, accessible method of assessing swim performance; however, previous studies have not compared the two methods. Additionally, there is little documentation of swim performance in larval fish, a more sensitive study subject for toxicological research. Therefore, the aim of this research is to compare the swim performance of fish in the LFA to those in the STA to determine which method is better for assessing swim performance in larval fathead minnows (Pimephales promelas). In this study, the percent of fish that fail to swim in the LFA is inversely proportional to the age of the fish, but in the STA, there is no correlation between percent failure and fish age. Results show that as fish increase in size, swim performance in the LFA improves, making it a more representative, predictable assay. Results from the STA indicate that swim performance in fish does not improve with size and performance in the STA is not correlated with performance in the LFA. Ucrit values from the LFA have less variation than those from the STA. The results of this study show that the LFA is a more suitable modality for assessing swim performance in larval fathead minnows.

Predator-prey dynamics play an integral role in shaping and regulating wildlife communities; however, recent studies have shown a decoupling of these relationships in urbanized areas. Trickle-down effects from the disruption of this trophic interaction have the potential to produce impacts that are far-reaching, altering other critical dynamics within the ecosystem. The purpose of my study was to characterize raptor activity and levels of predation in a large urban forest, the Great Trinity Forest in Dallas, TX. To quantify the extent of urbanization, I used ArcGIS Pro’s (version 2.2.0) image classification wizard with supervised, object-based classification on 50-cm pixel resolution, multi-band remote sensing imagery to estimate the percent of impervious surface. Then, from May to August 2019, I conducted weekly raptor surveys and deployed urethane foam prey mimics (snakes and mice) at 18 survey locations along an urban-to-rural gradient within this forest. In total, I detected 161 raptors representing 8 species throughout the season and found no relationship between raptor activity or diversity and degree of urbanization. Of the 732 prey models deployed, 61 showed signs of being depredated whereas 23 were missing and therefore had an unknown fate. Similar to the raptor results, overall predation on mice and snake models showed no relationship with degree of urbanization. Based on markings on the depredated models and photographs from field cameras, raptors appeared to target the snake mimics with no evidence of predation attempts on mice. And finally, I found no significant relationship between raptor activity and predation on snake models. Collectively, these results suggest either increasing levels of urbanization have no effect on raptor-prey dynamics within the Great Trinity Forest or there is low predatory response from raptors in regard to prey mimics.

Ectoparasites are a vital but often overlooked part of ecosystem dynamics, which have been shown to be negatively correlated with growth and decreased body condition in various vertebrate species. Texas horned lizards living in natural environments are known to harbor red mites (Acarina sp.), but the impact and density of these mites on lizards living in urban environments is not well known. Using weekly surveys during the summer of 2018, we examined the ectoparasite loads on Texas horned lizards (n = 87) from 11 different sites in Kenedy and Karnes City, Texas. We counted mites and recorded where they were found on the lizard’s body. We also determined the sex, age (juvenile versus adult), and body condition (body weight/SVL) of each captured lizard. We found significant differences in the number of mites between males and females, with males exhibiting heavier parasite loads, and also between different sites within the same town. We found no correlation between body condition and number of mites present. We present the first known research of ectoparasite loads of Texas horned lizards from an urban environment. Although the sample size is small, our data suggest that ectoparasite loads of Texas horned lizards from natural environments have lower mite loads than lizards found in an urban environment. These findings deserve further exploration to see if urban environments play a role in increased parasitism.

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.

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.

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.