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Open Access Publications from the University of California

Scholarly Works (6 results)

  • Thesis
  • Peer Reviewed
UC Berkeley Electronic Theses and Dissertations (2022)

Emerging semiconductors have begun to rival conventional silicon with breakthroughs in improved performance and novel and affordable processing techniques. As the applications for emerging semiconductors are explored, there is a clear need to understand the hierarchical nature of these materials to fully optimize their functionality. Consistently reproducingthe assembly and electronic functionality of organic semiconductors, for example, remains difficult given their propensity for variable molecular packing and morphology due to weak bonding interactions. As another case, metal halide perovskite semiconductors demonstrate intriguing photophysics that may change when confined in nanostructure forms. One technique alone cannot comprehensively interrogate the repercussions of changes in the molecular structure to the microstructure, morphology, and ensuing electronic functionality of a semiconductor. Only a multimodal characterization approach enables an extensive multiscale insight into the structure-function dynamics of semiconducting materials and devices.

Chapter 1 first introduces organic semiconductor properties and device applications. Common thin film processing methods and modification strategies are discussed along with the formation of crystalline microstructures in thin films. Next, a suite of characterization techniques that span multiple length and time scales are shared to inform on how one maystrategically combine individual techniques to characterize structure, morphology, and dynamics.

Chapter 2 describes a multimodal imaging study of organic semiconductor, rubrene, thin films. Scanning transmission X-ray microscopy reveals and quantifies the disappearance of orientational discontinuities in a hybrid crystalline microstructure, which is corroborated at higher spatial resolution with 4D-scanning transmission electron microscopy. In situ polarized optical microscopy during thermal annealing uncovers Arrhenius behavior for rubrene crystallization and that the finite substrate thermalization rate leads to the formation of the observed hybrid crystalline microstructure. This study emphasizes the role of temperature in organic semiconductor crystallization, and highlights the challenges and opportunities for thin film design protocols.

Chapter 3 focuses on characterizing the anisotropic behavior of inorganic lead halide perovskite (CsPbBr3) nanowires and nanowire bundles. Stroboscopic scattering interferometric microscopy shows exciton diffusion and trapping in the nanowire bundles. We use transient absorption microscopy to probe the polarization-resolved excited-state dynamics of thenanowire bundles. Coupled with polarization-resolved fluorescence, we determine that the splitting of the band-edge exciton states is driven by the shape anisotropy and a long-range exchange interaction. This study demonstrates the power of optical pump-probe microscopies to resolve charge transport and excited-state dynamics in individual structures.

This dissertation highlights the complexities of characterizing soft semiconductor thin films and nanostructures across multiple length and time scales. Despite the challenges in implementing a multimodal approach, the knowledge acquired about the semiconductors, such as defects in packing, grain boundaries, and charge carrier dynamics, is invaluable for guiding future design principles that incorporate semiconducting materials into novel technology.

    Cover page: Mapping multiscale relationships in soft semiconductor structure and function with multimodal characterization
    • Article
    • Peer Reviewed
    UC Berkeley Previously Published Works (2020)
    Inorganic lead halide perovskite nanostructures show promise as the active layers in photovoltaics, light emitting diodes, and other optoelectronic devices. They are robust in the presence of oxygen and water, and the electronic structure and dynamics of these nanostructures can be tuned through quantum confinement. Here we create aligned bundles of CsPbBr3 nanowires with widths resulting in quantum confinement of the electronic wave functions and subject them to ultrafast microscopy. We directly image rapid one-dimensional exciton diffusion along the nanowires, and we measure an exciton trap density of roughly one per nanowire. Using transient absorption microscopy, we observe a polarization-dependent splitting of the band edge exciton line, and from the polarized fluorescence of nanowires in solution, we determine that the exciton transition dipole moments are anisotropic in strength. Our observations are consistent with a model in which splitting is driven by shape anisotropy in conjunction with long-range exchange.
      Cover page: Effect of Anisotropic Confinement on Electronic Structure and Dynamics of Band Edge Excitons in Inorganic Perovskite Nanowires
      • Article
      • Peer Reviewed
      UCLA Previously Published Works (2023)
      With age, skeletal muscle stem cells (MuSCs) activate out of quiescence more slowly and with increased death, leading to defective muscle repair. To explore the molecular underpinnings of these defects, we combined multiomics, single-cell measurements, and functional testing of MuSCs from young and old mice. The multiomics approach allowed us to assess which changes are causal, which are compensatory, and which are simply correlative. We identified glutathione (GSH) metabolism as perturbed in old MuSCs, with both causal and compensatory components. Contrary to young MuSCs, old MuSCs exhibit a population dichotomy composed of GSHhigh cells (comparable with young MuSCs) and GSHlow cells with impaired functionality. Mechanistically, we show that antagonism between NRF2 and NF-κB maintains this bimodality. Experimental manipulation of GSH levels altered the functional dichotomy of aged MuSCs. These findings identify a novel mechanism of stem cell aging and highlight glutathione metabolism as an accessible target for reversing MuSC aging.
        Cover page: Multiomics reveals glutathione metabolism as a driver of bimodality during stem cell aging.
        • Article
        • Peer Reviewed
        UC Berkeley Previously Published Works (2019)
        Chronic or excess glucocorticoid exposure causes lipid disorders such as hypertriglyceridemia and hepatic steatosis. Angptl4 (angiopoietin-like 4), a primary target gene of the glucocorticoid receptor in hepatocytes and adipocytes, is required for hypertriglyceridemia and hepatic steatosis induced by the synthetic glucocorticoid dexamethasone. Angptl4 has also been shown to be required for dexamethasone-induced hepatic ceramide production. Here, we further examined the role of ceramide-mediated signaling in hepatic dyslipidemia caused by chronic glucocorticoid exposure. Using a stable isotope-labeling technique, we found that dexamethasone treatment induced the rate of hepatic de novo lipogenesis and triglyceride synthesis. These dexamethasone responses were compromised in Angptl4-null mice (Angptl4-/-). Treating mice with myriocin, an inhibitor of the rate-controlling enzyme of de novo ceramide synthesis, serine palmitoyltransferase long-chain base subunit 1 (SPTLC1)/SPTLC2, decreased dexamethasone-induced plasma and liver triglyceride levels in WT but not Angptl4-/- mice. We noted similar results in mice infected with adeno-associated virus-expressing small hairpin RNAs targeting Sptlc2. Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Cζ (PKCζ) are two known downstream effectors of ceramides. We found here that mice treated with an inhibitor of PKCζ, 2-acetyl-1,3-cyclopentanedione (ACPD), had lower levels of dexamethasone-induced triglyceride accumulation in plasma and liver. However, small hairpin RNA-mediated targeting of the catalytic PP2A subunit (Ppp2ca) had no effect on dexamethasone responses on plasma and liver triglyceride levels. Overall, our results indicate that chronic dexamethasone treatment induces an ANGPTL4-ceramide-PKCζ axis that activates hepatic de novo lipogenesis and triglyceride synthesis, resulting in lipid disorders.
          Cover page: An ANGPTL4-ceramide-protein kinase Cζ axis mediates chronic glucocorticoid exposure-induced hepatic steatosis and hypertriglyceridemia in mice.
          • Article
          • Peer Reviewed
          UCLA Previously Published Works (2022)
          Short-term fasting is beneficial for the regeneration of multiple tissue types. However, the effects of fasting on muscle regeneration are largely unknown. Here, we report that fasting slows muscle repair both immediately after the conclusion of fasting as well as after multiple days of refeeding. We show that ketosis, either endogenously produced during fasting or a ketogenic diet or exogenously administered, promotes a deep quiescent state in muscle stem cells (MuSCs). Although deep quiescent MuSCs are less poised to activate, slowing muscle regeneration, they have markedly improved survival when facing sources of cellular stress. Furthermore, we show that ketone bodies, specifically β-hydroxybutyrate, directly promote MuSC deep quiescence via a nonmetabolic mechanism. We show that β-hydroxybutyrate functions as an HDAC inhibitor within MuSCs, leading to acetylation and activation of an HDAC1 target protein p53. Finally, we demonstrate that p53 activation contributes to the deep quiescence and enhanced resilience observed during fasting.
            Cover page: Fasting induces a highly resilient deep quiescent state in muscle stem cells via ketone body signaling
            • Article
            • Peer Reviewed
            UC Berkeley Previously Published Works (2019)
            Chronic or excess glucocorticoid exposure causes lipid disorders such as hypertriglyceridemia and hepatic steatosis. Angptl4 (angiopoietin-like 4), a primary target gene of the glucocorticoid receptor in hepatocytes and adipocytes, is required for hypertriglyceridemia and hepatic steatosis induced by the synthetic glucocorticoid dexamethasone. Angptl4 has also been shown to be required for dexamethasone-induced hepatic ceramide production. Here, we further examined the role of ceramide-mediated signaling in hepatic dyslipidemia caused by chronic glucocorticoid exposure. Using a stable isotope-labeling technique, we found that dexamethasone treatment induced the rate of hepatic de novo lipogenesis and triglyceride synthesis. These dexamethasone responses were compromised in Angptl4-null mice (Angptl4-/-). Treating mice with myriocin, an inhibitor of the rate-controlling enzyme of de novo ceramide synthesis, serine palmitoyltransferase long-chain base subunit 1 (SPTLC1)/SPTLC2, decreased dexamethasone-induced plasma and liver triglyceride levels in WT but not Angptl4-/- mice. We noted similar results in mice infected with adeno-associated virus-expressing small hairpin RNAs targeting Sptlc2. Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Cζ (PKCζ) are two known downstream effectors of ceramides. We found here that mice treated with an inhibitor of PKCζ, 2-acetyl-1,3-cyclopentanedione (ACPD), had lower levels of dexamethasone-induced triglyceride accumulation in plasma and liver. However, small hairpin RNA-mediated targeting of the catalytic PP2A subunit (Ppp2ca) had no effect on dexamethasone responses on plasma and liver triglyceride levels. Overall, our results indicate that chronic dexamethasone treatment induces an ANGPTL4-ceramide-PKCζ axis that activates hepatic de novo lipogenesis and triglyceride synthesis, resulting in lipid disorders.
              Cover page: An ANGPTL4–ceramide–protein kinase Cζ axis mediates chronic glucocorticoid exposure–induced hepatic steatosis and hypertriglyceridemia in mice
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