The project aims to explore and experiment, through critical and creative geovisualization practice and pedagogy, innovative ways to embody, imagine, and represent the more nuanced social and spatial understanding of the Capitol Hill Organized Protest (CHOP). Specifically, we plan to implement qualitative forms of representation and analysis into the CHOP digital geographical archive as new data and layers. It involves analyzing individual graffiti, the messages, and patterns of speech, memories shared in the interactive map, as well as data collected from the field visit and interviews/conversations with the participants of the CHOP through the transformation of various modes of data and analysis that value representation in different ways. It draws on disruptive approaches from black digital geographies and critical and socially-relevant GIS to challenge how meaning is made from digital data. Yet, the project’s objective is not just to map these data and representation in/of the CHOP, but the opposite—remaking and even re-imagining through a process of humanistic sense of place-making. We engaged in multiple conversations with both direct and indirect stakeholders, fostering a comprehensive understanding of the diverse perspectives surrounding the CHOP. Direct stakeholders included individuals who had lived and experienced similar conflicts in Seattle’s history with the WTO protests, which provided invaluable insights that allowed for direct comparisons to the circumstances within the CHOP. Indirect stakeholders include individuals who contributed greatly by offering their perspectives on approaching potential challenges of the project. We put forward critical and creative geovisual processes that can draw connections between local community-based participatory and policy work, and how these diverse evolutions of critical GIS and geovisualization tell a more complex and nuanced story about the CHOP by relating to social, political, and cultural practices and as a way of engaged knowledge production.

Though Seattle’s reputation is for economic and technological prosperity, some Seattle high schools do not nurture students with the academic and professional rigor needed to partake in their local economy. This project examines the relationship between poverty and income in the City of Seattle and secondary education outcomes in Seattle Public Schools (SPS). The project puts forward the concept and practice of community mapping and GIS (Geographic Information Systems) for representation and visualization. Conducting a mixed-methods research using both qualitative and secondary research analyses, we uncover education narratives and outcomes in SPS while considering socioeconomic and political influences. SPS and state government online databases provided relevant information such as school graduation rate, college-readiness index, census tract poverty percentage, average annual income, and income inequality. We also conducted an online survey on SPS counselors, inquiring about their perception and input behind local socioeconomic contributions to the SPS curriculum and school life. In visualizing our research data, we utilized ArcGIS Pro, sectioning Seattle by SPS school zones and census tract, organizing our data by poverty percentage and income level through bivariate analysis, and juxtaposing them with education outcomes in SPS. Altogether, employing a social community investigation in conjunction with our mapping process allows for a deeper geospatial analysis that can be used as a tool to highlight socio-economic issues. In light of the socio-economic problems in Seattle, SPS counselors infer that other variables such as rich community sentiment, domestic and scholastic support, extracurricular involvement, and an overall meaningful life balance can contribute to successful education. Though our work establishes the relationship between high poverty percentage, low income, and poor education outcomes, we found that specific education metrics such as graduation rates do not necessarily entail success beyond secondary education. We proposed to use other metrics, such as the college readiness index, to infer education outcomes more accurately.

Traditionally known for its toxicity, hydrogen sulfide (H₂S) also possesses physiological roles as an endogenous gaseous signaling molecule in multiple biological processes. Previous research has demonstrated changes in levels of H₂S-producing enzymes during oxidative stress, hypoxia, and inflammation in various tissues including the liver and heart. H₂S protects cells from cytotoxicity in part by promoting the synthesis of glutathione, neutralizing reactive oxygen species, and inhibiting apoptosis signaling pathways. Thiol methyltransferases TMT1A and TMT1B can methylate endogenous H₂S to methanethiol. TMT1B has been shown to have a potential role in mediating the toxic effects of methanethiol. Gene silencing of TMT1B was found to significantly alleviate the observed cytotoxicity induced by methanethiol in human bronchial epithelial cells (16HBE). Methanethiol may induce harm to human respiratory tract cells, and understanding the mechanisms involved, including the role of TMT1B, could potentially lead to insights for mitigating these harmful effects. Doxorubicin (Dox) is a widely used chemotherapy drug for the treatment of various cancers but can induce oxidative stress in cells. In my preliminary experiments, I assessed the cell viability of HepG2 liver cells that were supplemented with various concentrations of NaSH (H₂S donor) and sodium methanethiolate (NaSMe, MeSH donor), followed by Dox treatment. Supplementing the cells with H₂S significantly increased cell viability in the presence of doxorubicin, while the methanethiol had no effect. The goal of my project is to identify H₂S-dependent protective pathways during cellular stress in HepG2 versus cardiomyocytes. My preliminary data indicates that both H₂S and its metabolite, methanethiol, may alter cellular responses following treatment of exogenous compounds that induce cellular stress such as CoCl₂, hydrogen peroxide and Dox. My goal is to pinpoint genes altered during the stress response. This understanding of H₂S-dependent pathways may pave the way for designing novel therapeutics that maintain or enhance H₂S levels.

Acute pancreatitis is an abrupt and painful inflammation of the pancreas that is often associated with serious complications and high mortality rates. Current diagnostic and therapeutic options remain limited, underscoring the need for novel strategies based on the underlying mechanisms of the disease. Our previous research suggests a key role for activin A, a member of the Transforming Growth Factor β (TGF-β) superfamily, in modulating inflammatory responses. Notably, activin A appears to trigger the c-Jun N-terminal kinase (JNK) pathway, a crucial member in macrophage activation during inflammatory diseases. This study aims to explore the role of activin A and the pJNK signaling pathway in macrophages during the pathogenesis of acute pancreatitis. Our investigation involves cell culture experiments using the RAW264.7 macrophage cell line, qPCR and Western blot analysis to identify protein alterations in activin-stimulated macrophages, and transwell migration assays to examine macrophage’s migratory ability toward chemoattractant after activin stimulation. We predict that activin A-stimulated macrophages would have increased JNK activation, increasing macrophage infiltration in inflamed tissues and polarization toward the pro-inflammatory subtype, potentially exacerbating the severe inflammatory response of acute pancreatitis. Our study is expected to reveal novel pathogenic mechanisms of acute pancreatitis and pave the way for the development of more effective diagnostic and therapeutic strategies for this disease.