Talia
Marx
Sponsor: Laura Van Winkle, Ph.D. VM: Anat Physio & Cell Biology Chronic exposure to air pollution has been strongly associated with increased risks for neurologic and respiratory diseases, such as Alzheimer's disease (AD) and pulmonary fibrosis. Traffic- Related air pollution (TRAP), which is a major contributing factor to outdoor air pollution, consists of particulate matter (PM) and gases produced from vehicle exhausts. Here, we hypothesize that chronic TRAP exposure promotes AD pathogenesis by promoting neuroinflammation secondary to pulmonary inflammation. To test this hypothesis, we exposed transgenic rats expressing AD- susceptible genes to PM and/or gas from light- and heavy- duty vehicles (LDV+HDV) or LDV-only, beginning at 1 month of age; controls were exposed to filtered air. Results from immunohistochemical analysis of fixed lung sections showed significant changes in alveolar macrophage populations after 11- months of exposure in males but not in females. The effects of TRAP exposure on macrophages were source-dependent. Males exposed to PM matter and gas from LDV+HDV experienced a significant increase in pro-fibrotic macrophages, while males only exposed to PM and gas from LDV-only exhaust had the opposite effect and had a reduced number of pro-fibrotic macrophages. No significant differences in pro-inflammatory macrophages were observed across all TRAP exposures in both males and females. PPARγ Lipid Nanoparticles for the Treatment of Obesity
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Authors:
Talia Marx
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Over 650 million adults are obese worldwide, and that number continues to rise. Obesity is a chronic low grade inflammatory disease, where white adipose tissue expansion recruits macrophages which polarize to a pro-inflammatory state called M1. Both the pro-inflammatory macrophages and the anti- inflammatory, M2, macrophages release cytokines such as interleukin-6 (IL-6) and interleukin-10 (IL-10) respectively. PPAR? is a transcription factor that can be found in the nucleus of the M2 macrophage and promotes M2 polarization. Our goal is to use lipid nanoparticles to deliver a PPAR?-based therapeutic directly into adipose tissue in order to promote macrophage polarization toward the M2 state, which will be quantified by cytokine response. Both in vitro and in vivo experiments were performed using fluorescent microscopy, ELISA, qPCR, and histology. The results of the trials found that PPAR?-LNPs lowered levels of pro- inflammatory cytokines such as IL-6, and increased expression of fat browning and thermogenesis-associated genes such as Ucp1. Histology found a significant decrease in lipid droplet accumulation in treated mice. Overall, PPAR?-LNP demonstrates a highly effective and safe nanoparticle-based strategy against chronic inflammation. Language and Cultural Sensitivity: Enhancing Patient Care at Nadezhda Clinic Michael Maslianka
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UC Davis / Biomedical Engineering / 2026
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Talia Marx