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Open Access Publications from the University of California

Scholarly Works (3 results)

  • Thesis
  • Peer Reviewed
UC Riverside Electronic Theses and Dissertations (2014)

Light-duty passenger cars and large ocean-going vessels represent two particle emission sources that have the ability to affect human health, climate change and air quality in local communities and worldwide. Driving speed and engine technology are two factors that can affect vehicle emissions. In California, drivers can drive upwards of 70% at speeds above the posted limits. This can cause high uncertainty when modeling vehicle emissions. The first part of this thesis examines both high-speed driving and direct-injection effects on particle concentration and composition while the second part examines the effectiveness of a scrubber technology to remove particulate matter (PM) from large ocean-going vessel emissions. The results show that high-speed driving can affect both total particle count and composition significantly as well as direct-injection technology. Ocean-going vessels equipped with a scrubber are effective at removing gaseous SO2, however, they are not as effective at removing PM or black carbon (BC).

    Cover page: Particle Emissions From Vehicles (SI-PFI and SI-DI) at High Speed and From Large Ocean-Going Vessels
    • Article
    • Peer Reviewed
    2016 Publications (2016)
      Cover page: Understanding particles emitted from spray and wall-guided gasoline direct injection and flex fuel vehicles operating on ethanol and iso-butanol gasoline blends
      • Article
      • Peer Reviewed
      UC Irvine Previously Published Works (2021)

      Purpose

      Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease characterized by an extensive fibroinflammatory stroma, which includes abundant cancer-associated fibroblast (CAF) populations. PDAC CAFs are heterogeneous, but the nature of this heterogeneity is incompletely understood. The Hedgehog pathway functions in PDAC in a paracrine manner, with ligands secreted by cancer cells signaling to stromal cells in the microenvironment. Previous reports investigating the role of Hedgehog signaling in PDAC have been contradictory, with Hedgehog signaling alternately proposed to promote or restrict tumor growth. In light of the newly discovered CAF heterogeneity, we investigated how Hedgehog pathway inhibition reprograms the PDAC microenvironment.

      Experimental design

      We used a combination of pharmacologic inhibition, gain- and loss-of-function genetic experiments, cytometry by time-of-flight, and single-cell RNA sequencing to study the roles of Hedgehog signaling in PDAC.

      Results

      We found that Hedgehog signaling is uniquely activated in fibroblasts and differentially elevated in myofibroblastic CAFs (myCAF) compared with inflammatory CAFs (iCAF). Sonic Hedgehog overexpression promotes tumor growth, while Hedgehog pathway inhibition with the smoothened antagonist, LDE225, impairs tumor growth. Furthermore, Hedgehog pathway inhibition reduces myCAF numbers and increases iCAF numbers, which correlates with a decrease in cytotoxic T cells and an expansion in regulatory T cells, consistent with increased immunosuppression.

      Conclusions

      Hedgehog pathway inhibition alters fibroblast composition and immune infiltration in the pancreatic cancer microenvironment.
        Cover page: Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic CancerHedgehog Signaling in Pancreatic Cancer
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