Zooplankton are important primary consumers in the marine food web and lead an important role in carbon cycling in the open ocean. Understanding what influences zooplankton community composition can help us understand the impacts of climate change on this delicate relationship. Current research shows that zooplankton communities change based on currents and chemical cues, but there is a lack of data about the community structure of zooplankton in the Western Equatorial Pacific, specifically between 5°S and 5°N along 167°W. Data was collected from 28 December 2023, through 10 January 2024, on the R/V Thomas G. Thompson near American Samoa. A closing zooplankton net with 200μm mesh was used for net tows from 200m to surface at stations between 5°S and 5°N along the 167°W longitudinal line. Net tows were processed by counting and identifying zooplankton groups from subsamples and data was converted to abundance utilizing standard equations in RStudio. Zooplankton abundance increased from 5°S to the equator and decreased after the equator to 5°N. Species diversity (Shannon-Weiner) was lowest at the equator and highest at 5°N and 1°S. Calanoid copepods had the highest abundance over all sites, and north of the equator, calanoid copepods and gelatinous zooplankton (larvaceans) dominated most of the species composition. There were no significant relationships between species community composition and temperature, salinity, nutrients, or currents. With many processes occurring with zooplankton in the open ocean, it may be that multiple variables are impacting the resulting diversity and abundance relationships. Additionally, data was collected during the 2023 – 2024 Strong El Niño, which could have impacted the abundances and species presence due to higher water temperature and stronger currents. Monitoring zooplankton composition over time is vital for monitoring the health of our oceans as it has implications for global fisheries and carbon cycling.

The synthesis of key organic molecules often requires toxic, expensive, non-reusable reduction agents and extreme conditions. In recent years, electrochemistry has emerged as a sustainable alternative to standard methods, but this approach is often hindered by high energy barriers for electron transfer to the substrate. Electrocatalysts address this challenge by shuttling charge between the electrode and dissolved substrates, accessing lower transfer barriers, and reducing the overall energy needed. Current electrocatalysts, however, cannot stabilize reactive intermediates, which often leads to harmful side reactions and degradation of the electrode. We hypothesize that redox-active supramolecular cages can address this limitation by both shuttling charge and providing unique microenvironments capable of stabilizing intermediates. Previously, we synthesized two tetrahedral supramolecular cages that incorporate redox-active perylene diimide (PDI) and pyromellitic diimide (PMDI) motifs. Using cyclic voltammetry, we then showed that both cages can lower the voltages required for the electroreduction of vicinal dihalides to alkenes, indicating electrocatalysis. To better understand these results, I used density-functional theory (DFT) calculations to obtain computer models of the PDI and PMDI cages. These DFT-optimized structures revealed significant differences in charge density between redox centers due to electron-donating functional groups, which may explain why the PMDI cage lowered the substrate reduction voltages more than the PDI cage. With these models, I have also studied the shape and volume of the cages’ internal cavities, thereby providing information about substrate compatibility. I am conducting additional DFT analysis to understand how modifications to the ligand motifs may alter the electrocatalytic behavior. By continuing to investigate supramolecular cages for reductive electrocatalysis, I aim to contribute to the development of low-waste synthetic strategies for the production of alkenes and other commercially significant organic compounds.

Asthma exacerbations often begin and increase in severity at night. Though animal models have shown molecular circadian rhythm involvement in immune and inflammatory responses, little is known about how circadian rhythms impact responses in humans or diseases such as asthma. BMAL1/ARNTL, CRY1, NR1D1, and PER2 are the genes that form the “cellular clock” by which cells tell time. Our hypothesis is that core circadian gene expression is maintained in an expected, rhythmic manner in epithelial cells from donors with asthma. We use an ex vivo model with human airway epithelial cells cultured at an air-liquid interface in a temperature cycled incubator to mimic the epithelia of the human airway. After temperature cycling to synchronize cellular circadian cycles, RNA collection occurs every four hours over a 48-hour period. After RNA isolation, I perform reverse-transcriptase quantitative polymerase chain (RT-qPCR) on a planned eight donor lines (4 healthy/4 asthmatic) to measure the gene expression of the four clock forming genes. In three asthmatic donor lines, I have found that core circadian rhythmicity is maintained in asthmatic epithelial cells and resembles the circadian rhythm expression in eight healthy donor lines previously analyzed. Shown through a preliminary study conducted by the lab, genes linked to asthma in the IL-17 signaling pathway have altered circadian rhythms of gene expression. In the future, I will use qPCR to study immune and inflammatory genes to confirm the altered rhythmicity across a wider scope of donor lines. In addition, I will analyze gene expression in different subsets of asthma to investigate whether altered circadian regulation contributes to asthma subtypes, such as T2-low which has been linked to IL-17 signaling pathway dysregulation. Investigating the differences in asthma-related circadian gene expression is essential to the development of chronotherapeutics – therapies that take into account time of day.

The immune system and inflammatory responses to viral infections are regulated by molecular circadian rhythms in mouse models. Mice infected with influenza just prior to their active phase have a mortality rate four times higher than mice infected just prior to their rest phase. As a result, circadian rhythms are hypothesized to regulate viral replication and early immune responses in airway epithelia during viral infections. Prior work has shown circadian cycles regulate gene expression in human epithelial cells. However, the influence of time of infection on viral replication in human airway epithelia has not yet been explored. We hypothesized that circadian-synchronized human airway epithelial cells would demonstrate differential viral replication and immune responses when infected at two different times of day. To address this gap, we differentiated primary epithelial cells from healthy children at an air-liquid interface to create an ex vivo cellular model of the human airway. Airway epithelial cells underwent circadian synchronization using temperature cycled incubators and were exposed on the apical surface to human rhinovirus-16 at time 0 and 12 hours during a circadian cycle. The RNA from seven total cell lines was sequenced and viral genome copy number was quantified at hour 96 following infection using GeneSig qPCR. Infection at hour 12 led to two-fold higher viral genome copy number 96 hours after infection as compared to hour 0. Infection late in the circadian phase (time 12) leads to increased viral replication at the airway epithelium and may explain the difference in mortality in mouse models of viral infection. Ongoing work is investigating immune responses based on time of infection. In the future, we will investigate changes in circadian regulation of viral infection in airway epithelia from healthy children and children with airway diseases such as asthma.

The cerebellum, which accounts for 10% of human brain volume, contains approximately 80% of all brain neurons and has long been understudied relative to the cerebral cortex. During development, the cerebellar ventricular zone (VZ) is a transient progenitor zone which generates all cerebellar GABAergic (inhibitory) neurons. This includes Purkinje cells (PCs) and PAX2+ interneuronal progenitors (PIPs). While the mouse cerebellar VZ has been relatively well characterized, there is limited knowledge about its human counterpart. In this study, we investigated organization of progenitors and birth of neurons derived from the human cerebellar VZ, uncovering several notable features. Specifically, I conducted image analysis in conjunction with immunohistology (IHC) assays to (1) identify different cell types and marker gene expression across developmental stages and (2) quantify proliferative cells at different stages of development. We found that a substantial number of PCs are generated during embryonic development, particularly within the first 50 post-conception days, within a compact two-week timeframe. This occurs well before the onset of cerebral neurogenesis, with interneuronal differentiation commencing during early fetal development. Neuronal differentiation predominantly occurs from the inner and outer subventricular zones (SVZ), zones which are completely absent in the mouse developing cerebellum, with the initial wave of differentiation occurring from the outer SVZ. Significantly, relative to mice, we observed variations in migratory patterns and the quantity of PC plates, including a subset of PCs that retain the expression of cell cycle genes several weeks after these cells leave progenitor zones. This work extends our knowledge of human-specific birth and organization of progenitors and neurons originating from the ventricular zone and cellular and molecular differences in ventricular zone progenitors, Purkinje cells, and PIPs across different developmental ages.
 

The COVID-19 pandemic has reshaped our social dynamics, leading to a decline in in-person interactions across American society. This shift has raised concerns about increased loneliness and diminished social connections, with significant ramifications for mental health. College students, in particular, are likely to feel the impact of reduced social interaction, given its centrality to academic and campus life.The aim of our study is to determine the relationship between the amount of time University of Washington undergraduates spend interacting with others while feeling socially connected and their perceived levels of anxiety. Our cross-sectional study used an anonymous online survey to measure hours spent socializing per week, and self-perceived anxiety levels amongst 18–24-year-old undergraduate students. We will collect data through convenience sampling in February 2024 distributing our survey via social media and direct outreach. We will conduct our analysis including prevalence ratios, descriptive statistics and qualitative content analysis. We hypothesize that UW undergraduate students spend 35 hours a week interacting with others and that low social interaction would be correlated with high self-perceived anxiety levels, adjusting for >4 roommates and >40 hours spent working per week.Our findings could hold potential significance for public health initiatives aimed at addressing population-level mental well-being, reducing anxiety, and enhancing access to effective mental health care interventions.

Undergraduate students experience high levels of stress, with approximately 75 to 80% of college students reporting moderate stress and 10 to 12% reporting severe stress. Cross-sectional research has shown that students drink more heavily and frequently on days they experience a greater number of life stressors. In our cross-sectional study, we investigated the association between the amount of self-perceived stress undergraduate students (aged 18-24) at the UW-Seattle Campus have and the amount of alcohol they consumed during a week in the Winter 2024 Academic Quarter. Study participants reported perceived stress (how often they felt overwhelmed by situations in their lives), by responding to 10 prompts from the Perceived Stress Scale (PSS), using a 0 (Never) to 4 (Very often) scale. Study participants also reported the number of servings of alcohol (as defined by the National Institute of Health) they consumed during that week. From these responses, we calculated prevalence ratios and compared alcohol usage between participants who had high perceived stress versus low perceived stress. We hypothesized that UW undergraduate students with high perceived stress would consume 25% more alcohol than their peers with low perceived stress, during a one week period. Our study showed that the prevalence of high alcohol consumption was 1.3 (CI: 0.5, 3.5) times as high among those with high perceived stress compared to those without. These results indicate no significant association between our exposure and outcome, in part due to our small sample size (N=78). We believe that further research is needed, with a larger sample size, to better understand the true association between perceived stress and alcohol consumption on our campus.