Pulmonary hypertension (PH) is a progressive pulmonary vascular disease characterized by increased pulmonary arterial pressure leading to right ventricular (RV) failure and death. While inflammation is established in the lungs and RV, emerging evidence suggests the presence of a multi-organ inflammatory response in PH. We hypothesize that PH is characterized by coordinated inflammatory signaling across multiple organs such as the lungs, RV, spinal cord, liver, and kidneys. Monocrotaline (MCT) and Sugen-hypoxia (SuHx), are established models of PH and RV failure, predominantly established in rats. PH was induced in rat models, tissues were collected, RNA sequencing was performed, transcriptomic datasets were analyzed, and common candidate genes were identified in certain organs. Bioinformatic results revealed consistent upregulation of inflammatory pathways across multiple organs including TNF alpha signaling via NFKB, IL-6/JAK-STAT3 signaling, IL-2/JAK-STAT5 signaling, IFN alpha response, IFN gamma response, and inflammatory response pathways. These findings were cross-referenced with available human transcriptomic datasets for select organs, confirming the presence of key inflammatory signatures in PH patients. This study characterizes PH as a multi-organ inflammatory disease, enabling future work to reveal targeted gene therapies based on identified inflammatory genes. Future work will also explore sex–differences in inflammatory response and its relation to multi-organ inflammation.

Persistent infection with high-risk human papillomavirus (hrHPV) remains a critical concern for young women living with perinatal HIV, who exhibit higher rates of abnormal cytology despite vaccination. Vaginal microbiome dysbiosis has been associated with hrHPV persistence through potential mechanisms including induced inflammation and carcinogenic metabolites released due to epithelial disruption; however, the complex interactions among the microbiome, host immune response, and local metabolic activity remain understudied. Utilizing longitudinal samples and clinical data from the PHACS III cohort, we integrated three distinct datasets: microbiome composition (16S rRNA sequencing), host immune responses (Luminex multiplex cytokine assays), and metabolome composition (mass spectrometry profiling). Data integration was performed using multivariate association modeling and dimensionality reduction techniques to identify co-associated multi-omics clusters. Our analysis revealed a highly interconnected landscape, characterized by extensive, significant correlations between microbial taxa, local metabolites, and host cytokines. We identified specific interaction networks where microbial-metabolic signatures correlate with altered cytokine expression. These findings characterize the functional architecture of the vaginal environment and identify candidate biomarkers of HPV persistence. This integrated framework provides a foundation for developing precision interventions and refining cervical cancer screening guidelines.

Previous work has identified heterogeneous, plastically interchangeable cellular states in glioma tumors that mirror normal neurodevelopmental programs using single-cell RNA sequencing and other multiomic data. However, the transitions among these states remained poorly understood, despite their potential relevance for therapies targeting specific cellular subpopulations and state transitions. This study consolidated these glioma cellular states and characterized their hierarchical relationships. The inferred states were consistent with previously reported reference states, as supported by overlapping state-defining transcriptomic signatures and concordant tumor cell state assignments. Pseudotime analysis further identified putative developmental trajectories of glioma cells by projecting them into a principal component space derived from normal differentiating neural stem cells. These findings were validated using cell entropy measurements and gene set enrichment analyses based on normal neural developmental stages. The inferred trajectories were also evaluated for their association with glioblastoma progression through survival analysis and comparisons across WHO glioma grades. These analyses defined developmental relationships among glioma cellular states and provided a framework for understanding state transitions that may ultimately inform glioma diagnosis and therapy.

Somatostatin (SST) neurons in the tuberal nucleus (TN) of the hypothalamus regulate feeding behavior in mice. Gonadal hormone state has been found to modulate the effects of this neuronal population on feeding. We investigated how gonadal signals regulate food intake via TN-SST neurons. We hypothesize that TN-SST neurons integrate metabolic and reproductive hormones to regulate food intake. To discern whether ovarian and testicular hormones modulate feeding via TN-SST neurons, we performed gonadectomies (GDX) and TN-SST ablation on male and female mice. We observed that caspase ablation in sham GDX females did not recapitulate the previously reported decreases in feeding. In males, loss of testicular hormones reduced food intake, and surprisingly, TN-SST ablation blocked this effect. To understand how androgen signaling modulates TN-SST-controlled feeding behavior, we first stained for the co-expression of androgen receptor and SST in the TN. Afterwards, to determine if testosterone was the androgen modulating this interaction, we studied feeding behavior of GDX male mice with and without ablated TN-SST neurons relative to non-GDX controls. Finally, we are studying if an androgen receptor knockout in the TN will yield similar results to GDX. Establishing bidirectional effects between metabolic and reproductive states advances understanding of sex differences, expands the scientific community’s understanding of metabolic and hormonal disorders and presents opportunities for possible therapies.

Brugada syndrome is a cardiac arrhythmia disorder often caused by abnormal sodium channel gating that disrupts normal electrical conduction in the heart. My project investigates how the Brugada-associated G24S mutation in the SNTA1 scaffolding protein alters the function of the cardiac voltage-gated sodium channel Nav1.5. Using site-directed mutagenesis, in vitro mRNA synthesis, Xenopus laevis oocyte microinjection, and two-electrode voltage clamp electrophysiology, I compared Nav1.5 expressed alone, with SNTA1 wild type, and with the G24S mutant. Wild-type SNTA1 shifted Nav1.5 activation toward more hyperpolarized potentials and increased current amplitude, suggesting enhanced channel opening. In contrast, the G24S mutation caused a rightward shift in both activation and steady-state inactivation, indicating impaired channel opening and reduced normal gating control. These findings support a loss-of-function effect of the G24S mutation that may reduce sodium current availability and contribute to the electrophysiological defects underlying Brugada syndrome. This work improves our understanding of how SNTA1-associated mutations alter Nav1.5 behavior and may help guide future precision therapies for inherited cardiac arrhythmias such as Brugada syndrome.