Benthic foraminifera are single-celled organisms that are a useful proxy of environmental conditions. They can provide insights into water quality, sediment composition, and ecological changes. In the past, urban bays of Puget Sound developed chemical toxicity in sediments surpassing acceptable state limits. Recent mitigation efforts have brought most chemicals within limits. However, foraminifera health parameters continue to show signs of poor environmental conditions including increased test dissolution and decreased species richness and density. Studies on individual embayments are necessary to understand local variations and utilize foraminifera in an effective monitoring program. In this study, we investigated how the percentage of dissolved foraminifera varies based on distance from shore in Elliot Bay, Seattle. We obtained grab samples through the Washington Department of Ecology collected in 2021 from multiple sites in Elliot Bay. We processed the samples and picked up to 300 foraminifera from each sample then calculated the percentage of dissolved Elphedilla hannai, the most common calcareous species in Elliot Bay. Additionally, we reviewed foraminiferal densities, species richness, and diversity for distance from shore. We found that the percentage of dissolved Elphedilla hannai increased closer to shore and with decreased depth. These results suggest a spatial influence on the health of foraminifera.  As Elliot Bay is a major maritime hub, its shorelines are heavily industrialized, and areas both shallower and closer to shore may be experiencing higher levels of anthropogenic activities. This study highlights potential water quality gradients in urbanized embayments such as Elliot Bay, contributing to our overarching aim of understanding interactions between foraminiferal health and environmental factors in urbanized embayments.

TAR DNA binding protein 43 (TDP-43) is an RNA/DNA binding protein that forms pathological aggregates in most amyotrophic lateral sclerosis (ALS) and half of frontotemporal lobar degeneration (FTLD) cases. Knockout of TDP-43 in animal models leads to neurodegeneration and motor deficits, but overexpression of wildtype TDP43 leads to the same events; therefore, TDP43 protein homeostasis is critical to prevent ALS/FTLD. To achieve this homeostasis, TDP-43 autoregulates its own mRNA splicing, resulting in multiple TDP-43 isoforms, some of which go through non-sense mediated decay to regulate overall TDP43 levels. However, other isoforms encode unique proteins with differing C-termini, leading to variable cellular localization. It is unknown if these alternative, protein-coding isoforms are predominantly associated with ALS/FTLD or if aging changes the frequency of these isoforms. To determine how TDP43 overexpression yields these different isoforms and interacts with aging and ALS-like symptoms, we created a novel approach to overexpress human TDP43 via Adeno-Associated Virus (AAV) delivered through retro-orbital injection, leading to ALS-like motor deficits. Surprisingly, when tested in older and younger mice, we found the older mice were paradoxically protected from severe motor deficits and mortality. To determine if tardbp alternative splicing is linked to ALS-like symptoms and aging, I designed and validated primers and protocols to measure the nine tardbp mRNA isoforms in mice via quantitative real-time polymerase chain reaction (qRT-PCR). I have started to determine if hTDP43 overexpression leads to differential splicing compared to mice injected with a sham AAV in these old and young mice. Once this is done, we will clone the most interesting differentially spliced isoform in an AAV and inject that AAV and a full-length TDP43 AAV into mice to see if the spliceform causes increased toxicity, manifesting in worsening motor deficits and mortality.

Cortisol is a stress hormone that plays a role in several vital processes throughout our body, including immune and metabolic regulation and stress responses. Typically, cortisol follows a diurnal pattern, peaking in the morning and gradually declining as the day goes on. More blunted cortisol diurnal slopes have been associated with chronic stress and poor sleep. In Autumn Quarter 2023, we investigated the relationship between diurnal cortisol patterns and hours of sleep among 20 University of Washington (UW) students as part of a class project. Over three days, participants self-collected saliva samples immediately after waking and at 8 PM and answered daily survey questions about sleep, stress, and behavior. Saliva samples were analyzed by students for cortisol concentrations using an in-house enzyme immunoassay protocol. We calculated the diurnal slope by finding the quotient of the difference between the AM and PM cortisol concentrations and the difference between collection times. For this study, we calculated the average slope across the three sampling days for each individual, and the average hours of sleep across the three days. We found that sleeping less than 7 hours per night was associated with a blunted cortisol response. We are investigating if this pattern replicates across UW students using prior class data sets from 2020-2023. Understanding the relationship between these variables, including how sleep interacts with hormones like cortisol, is crucial for gaining insight into how stress influences students' academic performance and can inspire further research.

Indigenous populations in Latin America are socially disadvantaged groups that often experience insufficient access to everyday necessities. With climate change raising global temperatures, heat-related illnesses are rising in vulnerable groups, especially among communities in heat-prone environments. The Qom is a population indigenous to the Gran Chaco, a tropical dry ecozone with average summer temperatures well over 90°F ( <33°C). Most of the Qom today are located in the rural Argentinian province of Formosa, and the majority live below the poverty line, further limiting their accessibility to health services. Access to interventions that mitigate extreme heat, such as air conditioning, is also not feasible for most Qom families. The Chaco Area Reproductive Ecology (CARE) program has worked with Qom communities in Formosa for over 20 years, most often in the community of Namqom (~ pop. 5000). A current aim of the CARE program is to gain insight into the therapeutic itineraries that Namqom residents rely on the most, particularly for heat-related illnesses such as heat stroke, heat exhaustion, and heat cramps. If not addressed these illnesses can be fatal, and can exacerbate health conditions for vulnerable individuals. This study aims to identify what factors exaggerate or prevent heat-related illnesses to explore further what type of interventions can be created and implemented within the Namqom community to mitigate this issue becoming more widespread. This poster presents findings from a scoping review to inform our study design. This review will identify and synthesize findings to date on the following topics: (1) human biological and behavioral adaptations to living in the Gran Chaco and similar ecozones and; (2) the specific health risks among vulnerable groups (infants, children, pregnant women, elderly, individuals with underlying health conditions) that are exacerbated by heat stress.

Budding yeast cultures grown in limited sulfate conditions are overtaken by cells with an inverted triplication of the gene SUL1, which encodes for a sulfate transporter. The extra copies of the sulfate transporter provide a selective advantage because these cells outcompete other yeast cells for the limiting resource. To explain the mechanism behind this type of amplification the Brewer and Dunham Labs proposed a model (Origin Dependent Inverted Repeat Amplification or ODIRA), which requires both a DNA replication origin and inverted repeats flanking SUL1. ODIRA starts with a DNA replication error involving replication fork regression that leads to an extrachromosomal DNA intermediate. This intermediate then replicates and recombines into the genome, producing the observed amplification. Because similar triplications are observed in the human genome, including in human disorders, the mechanism of ODIRA offers insights into human genome evolution and disease. While the yeast research is consistent with ODIRA, we still do not know which proteins are responsible for the process. I am testing whether the genes RAD5 and RAD54 — involved in fork regression and strand switching, respectively — are involved in ODIRA. To do so, I am measuring the ODIRA frequency in strains with each gene deleted compared to a wild-type control. If either gene deletion leads to a statistically significant change in ODIRA frequency compared to the wild-type strain, I can conclude this gene is involved in ODIRA. To measure ODIRA frequency, I grow the deletion strains under selection for DNA recombination events and use whole chromosome gel electrophoresis and Southern blotting to detect ODIRA events. Preliminary data analysis suggests that there is a reduction in ODIRA events when either RAD5 or RAD54 is deleted, indicating that these genes are likely needed for ODIRA. These results may provide insight into how inverted triplications may arise.