Macrophages play a critical role in cardiovascular disease through metabolic adaptations, yet the underlying genetic architecture governing these stress responses remains largely unknown. To investigate the metabolic response of macrophages, we analyzed bulk transcriptomic microarray data of macrophage samples representing 92 inbred strains of the Hybrid Mouse Diversity Panel (HMDP). Using Compass, a flux balance analysis algorithm based on transcriptome data, we predicted continuous biochemical reaction activities under control and oxidized phospholipid (OxPL)-treated conditions. Comparing these predicted fluxes uncovered significant changes in response to OxPL and across the genetic variation of the HMDP. Significantly increased reactions with OxPL treatment included amino acid transport pathways necessary for glutathione synthesis and iron (Fe2+) efflux mechanisms that function to prevent cellular ferroptosis. Ongoing work aims to leverage the genetic variation in the HMDP to identify the genetic drivers of these changes and prioritize candidate genes for further study.

Tuberculosis (TB), caused by Mycobacterium tuberculosis, is an infectious disease that significantly impacts global health. Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) is a receptor expressed on myeloid cells that promotes the formation of lipid droplet-rich (‘foamy’) macrophages when activated, creating an anti-inflammatory environment that allows for bacterial survival. The mycobacterial cell wall contains external lipid components known as mycolic acids and phthiocerol dimycocerosates (PDIM), which are known virulence factors that serve as TREM2 ligands and activate its downstream signaling cascade. This study investigates the role of TREM2 in foamy cell formation in response to mycolic acids and PDIM, in which I hypothesize that TREM2 induces macrophage lipid droplet accumulation in response to these lipids. Here, I utilize Oil Red staining to visualize lipid droplet accumulation and show that mycolic acids and PDIM induce lipid droplet accumulation in monocyte-derived macrophages (MDMs) of 5 donors, resulting in approximately a 1.5-fold and 2-fold increase, respectively, relative to untreated samples. My findings demonstrate that mycolic acids and PDIM alter macrophage lipid metabolism by promoting lipid droplet accumulation and foamy macrophage formation, contributing to disease persistence. Overall, this can advance the understanding of immune response and macrophage lipid metabolism during mycobacterial infection and may inform future therapeutic strategies for TB.

Piezoelectricity is a specialized property of specific solid materials that generates an electrical voltage through mechanical stress or vice versa. The charge generated by this interaction is suitable to generate stimuli compatible with bioelectricity. This demonstrates potential for enhanced regenerative therapies and self-sufficient, multiuse micro drug-delivery devices. Piezoelectric technologies are gaining more space in medical diagnostics as well, and their market worth is expected to reach 46 billion USD in 2030 (MarketsandMarkets, 2025). However, the toxicity of some efficient piezoelectric materials such as lead zirconate titanite (PZT) raises concerns regarding their biological applications (Wang et al, 2025). This work is an exploratory research which reviews current literature on the topic and examines pathways for piezoelectricity in Biomedical applications, as well as their feasibility. It aims to find an answer for how and when piezoelectricity-reliant therapies are superior compared to other methods in both efficiency and scalability, contributing to future research with more concrete data in promising piezoelectric applications.

Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness worldwide, with age and genetic background representing major risk factors. The trabecular meshwork (TM) plays a critical role in maintaining intraocular pressure homeostasis, and its dysfunction is strongly implicated in POAG pathogenesis. Given the limited regenerative capacity of TM cells and the eye’s continual exposure to environmental stressors, we hypothesize that somatic mutations acquired over an individual’s lifetime may give rise to glaucoma-causing variants, increasing disease risk even in the absence of predisposing germline variants. To explore this, we conducted a proof-of-concept analysis to assess whether somatic variants can be detected in TM cells using publicly available scRNA-seq data. Variant calling was performed with scAllele, followed by genotyping using a Bayesian framework incorporating priors based on population allele frequencies. Our analysis identified somatic variants in TM cells, supporting the feasibility of this approach. However, this study is limited by the use of short-read sequencing, which is biased toward transcript ends and may fail to capture variants outside these regions. Despite these constraints, our findings establish a foundation for detecting somatic mutations in TM cells. Future work can extend this framework to examine associations between somatic mutation burden and glaucoma risk, potentially improving understanding of disease mechanisms.

This abstract has been withheld from publication.