This project investigates the effects of Chile’s 2020-2021 pension withdrawals on household consumption across food, housing, transportation, healthcare, and education. I use existing socio-economic household survey data for my analysis. Chile’s Covid response allowed civilians to withdraw up to 30% of their pensions, impacting 11 million workers and reducing pension assets by an estimated 22% of GDP. This policy mirrors actions in 30 other countries globally, now facing similar challenges. This research aims to address the literature gap in consumption research, and provide a framework for policymakers in affected nations to understand how the pension funds were used in terms of consumption. My role encompasses everything, from design to analysis. First, I make sure the two groups being compared (Chilean households who withdrew funds and who did not) were on similar spending paths before the withdrawals happened, known as pre-trend analysis. I use statistical tools, such as t-tests, to check if those trends were similar—basically confirming that the two groups were spending similarly before the policy change. Second, I use a statistical model, called Difference-in-Differences (DiD), to isolate the specific effect of the withdrawals from other things that might have affected spending. Third, I look at how the pension withdrawals affected retirees and non-retirees as well as different income demographics, to see if the impact was the same or different for everyone, known as heterogeneity analysis. As this project is in-progress, I assume I would find a statistically significant, varied impact on household consumption. I anticipate increased spending on essential purchases since the Covid crisis led to many financial difficulties that affected households' spending. These findings can help inform younger generations around the world about their decisions regarding their own retirement planning decisions, as this global issue disrupted their retirement savings.

In Adoptive Cell Therapy (ACT), a novel modality of cancer therapy, immune cells can be engineered with T cell receptors (TCRs) to aid in targeting specific antigens presented on the surface of cancer cells. However, TCR-T cells often have limited persistence after transfer into patients, which has hampered the effectiveness of this therapy for solid tumors. Last year, our lab identified LSD1 as a target for drug inhibition, which is an enzyme that alters the epigenome of cells via histone modifications. My project aims to understand the mechanism of LSD1 inhibitor drugs, as well as the effect of these drugs on two types of T cells: cytotoxic CD8+ cells and helper CD4+ cells. In addition to understanding how LSD1 drugs work, I also ask exactly how CD4+ cells enhance the function of CD8+ cells in tumor killing. Which receptors on CD8+ cells are activated by helper T cells, what is the signal phosphorylation pathway transducing the "helping" signal from receptors, and what downstream epigenetic regulators play a role in translating the "helping" signal into better function in CD8+ T cells? To assess these interactions, I will generate a diverse population of CD8+ T cells with targeted receptor knockouts, known as a receptor library. Similar libraries will be generated for epigenetic regulators as well as kinases/phosphatases. The performance of T cells will be assessed via coculture assays, where T cells can kill tumor cells but not fully eliminate the tumor because of periodic addition of new tumor cells. At the end of the coculture period, we will assess gRNAs enriched in dysfunctional populations, which will identify genes critical to CD8+ T cell function. This project aims to provide enhanced function of T cells that are better suited for applications in clinic.

All organisms develop from a single, symmetrical cell. That symmetry must be broken at several points during embryogenesis to develop into a complex, intricate form of life. The earliest symmetry breaking event in vertebrates is the formation of the dorsal organizer, a signaling center that establishes dorsal-ventral and anterior-posterior axes. β-catenin signaling is highly conserved in the dorsal organizer and utilized during cancer proliferation. However, the mechanisms employed in selective β-catenin stabilization are still not fully understood, due in part to limited vertebrate embryological models. Established model organisms for development, like fish and frogs, pre-pattern their dorsal organizer through maternal determinants, which is lacking in mammalian model organisms who break symmetry with self-organization. Remarkably, the African Turquoise Killifish, Nothobranchius furzeri, lack a pre-pattern. This presents a strong model organism, N. furzeri, to investigate mechanisms of self-organization. In this work, I explore the metabolic shifts and mechanical forces as two potential drivers of selective β-catenin stabilization. To investigate whether fluctuations in intracellular pH (pHi) stabilize β-catenin, I created a Tol-2 mediated transgenic pHi reporter line. Using light sheet microscopy, I observed that pHi fluctuations occur after β-catenin is stabilized in the incipient dorsal organizer. This ruled out pHi as the initializing factor of β-catenin stabilization. Next, I will explore whether mechanical forces drive embryonic symmetry breaking. This model posits that local microtubules-generated forces are transduced by focal adhesions into biochemical signals, enabling selective β-catenin stabilization. To evaluate this model, I will develop a transgenic toolkit to visualize microtubules polymerization and focal adhesion signaling with pharmacological and dominant negative approaches. These experiments will elucidate the mechanism responsible for symmetry breaking in N. furzeri and potentially conserved regulators of Β-catenin signaling, foundational to our understanding of development and cancer research.

Approximately 320 million years ago, teleost fish experienced a whole-genome duplication event, which is theorized to have contributed to developmental and morphological innovations that enhanced the reproductive success of their modern descendants. However, the role of duplicated genes in the genesis of novel cell types remains unknown. Here we show that the African Turquoise Killifish (Nothobranchius furzeri) possesses a novel immune lineage specified prior to gastrulation—a far earlier stage than observed in other teleosts. Surprisingly, through single-cell RNA sequencing, we found that this lineage unexpectedly expresses nanos1b, a duplicated paralog of nanos1, a gene well known for its role in germline development across vertebrates. To verify this novel expression of nanos1b in immune cells before gastrulation, I performed RNA in situ hybridization to visualize the expression of nanos1b, eomes (a mesodermal marker), and lcp1 (a marker of mature immune cells). The results revealed co-expression of nanos1b with both eomes and lcp1, supporting the hypothesis that nanos1b expression links the myeloid lineage to the developing mesoderm. These investigations will help elucidate the pathway through which the killifish embryo fast-tracks the production of immune cells during early development.