Acute Pancreatitis (AP) is a sudden inflammatory condition of the pancreas that can lead to significant mortality. Despite its rising prevalence and associated healthcare burden, treatment options remain limited to supportive care, with mortality rates in severe cases reaching 30%. Activin A is a key contributor to AP, interacting with the ACVR2A receptor to regulate various pathophysiological processes, including inflammation through immune cell recruitment. This study hypothesizes that activin A binds to ACVR2A to activate the ERK pathway, leading to increased NF-κB expression and elevated production of pro-inflammatory cytokines, including TNF-α and IL-1β. Experiments were designed using the 266-6 immortalized pancreatic acinar cell line and RAW 264.7 macrophages. These cells will be cultured for western blot analysis, ELISA assays, and transwell migration assays following activin A stimulation. Lower ERK phosphorylation and reduced NF-κB expression are expected when cells are treated with ACVR2A inhibitors in combination with activin A, compared to activin A treatment alone. ELISA assays are anticipated to confirm increased TNF-α and IL-1β production in 266-6 cells following activin A treatment. Macrophage migratory capacity is expected to increase when exposed to conditioned media from activin A-treated 266-6 cells. These findings will provide insights into the role of activin A in AP pathophysiology, potentially identifying new therapeutic targets for mitigating pancreatic inflammation and immune cell recruitment.

Pancreatic Ductal Adenocarcinoma (PDAC) is a deadly disease without prognostic tools for early detection or effective therapeutic strategies. Activin A is a cytokine that is upregulated in tumor and stromal cells that surround the tumor in PDAC and acts as a promoter of metastasis. Activin A has also been shown to stimulate the AKT pathway which is proto-oncogenic. Here, we set out to test the hypothesis that activin A drives PDAC development through the AKT pathway. Western blots for proteins of the AKT pathway (phospho-PRAS40 and phospho-β-catenin) and transwell migration assays will be performed on PanC1 pancreatic cancer cells stimulated with activin A. Additionally, inhibitors of the activin A receptor subtype 2A (ACVR2A) and the AKT pathway will be included to delineate receptor-specific effects. Given activin's known role for simulating the AKT pathway, it is expected that activin A stimulation will phosphorylate and trigger increased migratory capacity of PanC1 pancreatic cancer cells. Inhibitor experiments will confirm that these effects are ACVR2A specific. This data will identify if activin A is a novel therapeutic target in late stage PDAC, a disease with limited targeted pharmacological treatments. 

While taking multiple general science courses and dance courses as a double-degree student, I have devised creative ways to balance my studying and dance training. One involved creating dance choreography to memorize organic chemistry reactions, which inspired me to choreograph a dance piece named after the motor cortex “Homunculus” for Aura Dance Company’s (RSO) annual spring show in 2023. This sparked my interest in organizing a project to teach this learning structure that may be useful to others. With help from Professor Hannah Wiley and MFA candidate Beth Twigs, I designed dance workshops for my peers to learn more about neuroscience and dance. NeuroDance is a multidimensional project to educate students about neuroscience through dance-making tools. The project involved organizing workshops where participants learned movements inspired by molecular neuroscience, neuroanatomy, and skeletal anatomy. Participants modeled ions, neurons, and planes of movement through facilitated movement phrases and seeds. To assess learning outcomes, quizzes were given before and after the workshops. Volunteers were recruited from on-campus social, dance, and neuroscience groups, and outreach will occur via social media and posters. The data from the learning aspect of these workshops house the scientific results, but the movement observed served as the foundation for a larger choreographic work presented in the Department of Dance’s Dance Majors Concert (2025). The physicality and repetition inherent in dance offer a unique and enriching platform for learning. I aim further to explore the potential of dance education in STEM with this pilot study.

 Marine debris, classified as solid, man-made litter and material that has been lost or discarded in the ocean, is a persistent pollution issue in coastal regions around the world, and Puget Sound is not an exception. This research investigates the distribution and abundance of marine debris across various regions of Puget Sound and how they are changing over time. Since 1987, the Washington Department of Fish and Wildlife (WDFW) has conducted annual trawls to assess bottom fish populations in Puget Sound. The contents of these trawls provide valuable representation of the soft-bottom habitat, including the organisms and debris inhabiting the seafloor. The WDFW’s extensive records of these surveys include the location, depth, type, and abundance of debris collected in each trawl. With this dataset, I explore spatial patterns in different types of debris, examine trends in abundance over the last two decades, and identify hotspots for debris accumulation in Puget Sound. The results of this study contribute to a deeper understanding of the dispersal of aluminum, plastic, glass, fishing gear, and other debris that lie at the bottom of Puget Sound. Insights on these patterns are vital to informing effective clean up and guiding prevention efforts to create cleaner and safer waters for both humans and marine life. 

A subset of voltage-gated potassium channels, Kv2s, are responsible for the majority of the perisomatic delayed rectifier current in pyramidal neurons of the neocortex. Mutations in these ion channels and their associated proteins cause developmental epilepsy, but the cellular mechanisms underlying this remain less clear. Previously, we have shown that the two members of the Kv2 family of voltage-gated potassium channel α-subunits, Kv2.1 and Kv2.2, are expressed differently depending upon the type of neuron in rodent primary sensory and motor neocortex. There are two major subclasses of layer 5 (L5) pyramidal neurons in the neocortex, extratelencephalic (ET) and intratelencephalic (IT) neurons, that are distinguished by their projection targets and laminar distribution. ET neurons, enriched in L5b of the neocortex, send projections to subcortical structures, whereas IT neurons, primarily located in L5a, project within the telencephalon. In rodents, ET neurons are enriched in Kv2.1, but not Kv2.2. Here, we tested whether these features extend to the association cortices of primates, particularly the prefrontal cortex and temporal cortex, which are essential for various higher-order cognitive functions, including recognition, attention, and planning. Using immunohistochemistry against Kv2.1 and Kv2.2, we showed that these subunits have distinct laminar distributions in the dorsolateral prefrontal cortex (dlPFC) and temporal cortex (TCx). Kv2.1 was predominantly expressed in L5b, whereas Kv2.2 was more concentrated in layer 2 (L2) and L5a. Using a tarantula toxin, Guanxitoxin (GxTx), to block the Kv2-mediated current, we found that, similar to what we observed previously in rodents, the role of Kv2 channels differs depending on the L5 neuron type. GxTx makes L5 ET neurons fire repetitive bursts, whereas GxTx makes L5 IT neurons less excitable. Together, these results support distinct roles for Kv2.1 and Kv2.2 in regulating excitability across ET and IT neurons in the association cortex of the macaque.