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Open Access Publications from the University of California

Scholarly Works (11 results)

  • Thesis
  • Peer Reviewed
UC Irvine Electronic Theses and Dissertations (2016)

BACKGROUND: Cardiovascular disease is the leading cause of death in the United States. Short-term exposures to air pollution have been associated with acute increases in cardiovascular hospitalization and mortality. However, the causative chemical components and underlying pathophysiological mechanisms remain to be clarified.

METHODS: We conducted a cohort panel study involving 97 elderly subjects living in the Los Angeles metropolitan area. Weekly, we measured microvascular function, represented by reactive hyperemia index (RHI), and airway and circulating biomarkers of oxidative stress and inflammation, including exhaled breath condensate malondialdehyde (EBC MDA), fractional exhaled nitric oxide, oxidized low-density lipoprotein, and plasma interleukin-6 (IL-6) over 12 weeks. Exposures included 7-day personal nitrogen oxides (NOX), daily ambient pollutants, including particulate matter size <0.25 µm in aerodynamic diameter (PM2.5), ozone, carbon monoxide (CO), black carbon (BC), and NOx, five-day average PM measured in three size-fractions and characterized by chemical components including transition metals, PM oxidative potential, and electrophilic potential. CAlifornia LINE Source Dispersion Model, version 4 (CALINE4) was used to estimate individual exposure to local traffic-generated NOx. Associations between clinical outcomes and pollutants were assessed using linear mixed effects regression models. Potential effect modification by demographic characteristics and CALINE4-modeled NOx was assessed by adding interaction terms to these models.

RESULTS: RHI was inversely associated with daily ambient traffic-related air pollutants (BC, NOX, and CO), other mobile-source components/tracers (polycyclic aromatic hydrocarbons, elemental carbon, and hopanes), PM oxidative potential, and transition metals, and was positively associated electrophilic potential. We found significant positive associations of airway oxidative stress (EBC MDA), and inflammation (IL-6) with traffic-related air pollutants, ultrafine particles, and transition metals. The observed associations were generally stronger among subjects at higher local traffic-generated NOx (estimated by CALINE4). Associations between systemic oxidative stress and inflammation biomarkers and air pollutants were mostly non-significant, expect for positive associations that observed for IL-6 and traffic-related air pollutants at 1-day averages.

CONCLUSIONS: Short-term exposure to pollutants with high oxidative potential (traffic-related pollutants, ultrafine particles, and transition metals) was associated with impaired microvascular function and increased airway oxidative stress and inflammation in elderly adults. Chronic exposure to residential NOx may further strengthen the observed associations.

    Cover page: Cardiovascular, Oxidative Stress, and Inflammatory Consequences of Short-term Exposure to Chemically-characterized Air Pollution in an Elderly Cohor
    • Article
    • Peer Reviewed
    LBL Publications (2024)
    China’s cement industry emits over 1 Gt of carbon dioxide (CO2) annually, or 3% of global CO2 emissions. Urgent decarbonization efforts of the Chinese cement industry are needed to meet China and global community’s climate commitments. Prior studies on this topic primarily relied on supply-side technologies and end-of-pipe solutions, presenting one singular pathway to net zero without exploring multiple trajectories. This study adds value to the existing research by constructing and evaluating two different pathways toward net-zero emissions in China’s cement industry: the Energy Technology Pathway (ETP) and the Circular Economy Pathway (CEP). Both pathways aim for net-zero emissions but diverge in their prioritization and emphasis. The Energy Technology Pathway focused on supply-side technologies such as green hydrogen and CCS, while the Circular Economy Pathway focused on demand-side strategies, centered on materials and resources. The study showed both pathways can achieve a comparable level of emission reduction, reducing 94-95% of CO2 emissions by 2060 from the 2020 level. Notably, the role of CCS is limited in the CEP, contributing only 5% and 22% of total emission reductions by 2030 and 2060, respectively. The majority of the emission reductions in CEP are achieved through a combination of material-focused innovations and circular economy strategies, such as increasing the use of supplemental cementitious materials (SCMs), advancing alternative cements, integrating material efficiency practices in product lifecycle phases, and adopting alternative fuels (e.g., industrial wastes and agricultural byproducts). Policy support on materials and the circular economy will be critical. We recommend updating codes and standards to allow performance-based cement products, providing R&D support on alternative cements, developing implementation guides to disseminate material efficiency practices, and improving material/waste collection, sorting, and recycling systems.
      Cover page: Evaluating Net-Zero Emission Pathways for China’s Cement Industry
      • Article
      • Peer Reviewed
      UC San Diego Previously Published Works (2022)

      Background and aims

      Patient-reported outcome measures (PROMs) provide a wholesome view of patient well-being. We conducted a retrospective cohort study to evaluate whether PROMs inform risk of unplanned healthcare utilization in patients with IBD.

      Methods

      We identified adult patients with IBD who completed at least two surveys in a large Internet-based cohort within 1 year. We evaluated the association between baseline patient characteristics, disease activity indices, medication use, and PROMs, assessed using NIH Patient-Reported Outcome Measurement Information System (PROMIS) and subsequent risk of incident hospitalization (at time of first follow-up) within 1 year, and readmission within 1 year (in patients with hospitalization at first follow-up), using multivariable logistic regression.

      Results

      Of 7902 patients with IBD (45.5 year, 72% females, 63% Crohn's disease), 1377 (17.4%) were hospitalized within 1 year. Among PROMs, pain interference (adjusted OR per 5-point increase in PROMIS, 1.09; 95% CI 1.05-1.14), but not depression, anxiety, fatigue or sleep disturbance, was predictive of higher risk of hospitalization. Prior surgery or hospitalization, symptomatic disease, biologic, and corticosteroid use were also associated with higher risk of hospitalization. Of 521 patients hospitalized with IBD, 133 (25.5%) were readmitted within 1 year. Anxiety and pain interference were predictive of higher risk of readmission, whereas depression was associated with lower risk of readmission.

      Conclusions

      In a large Internet-based cohort study, PROMs may have a modest effect on modifying risk of unplanned healthcare utilization in patients with IBD, with pain interference being most consistently associated with increased risk of hospitalization and readmission.
        Cover page: Patient-Reported Outcomes and Risk of Hospitalization and Readmission in Patients with Inflammatory Bowel Diseases
        • Article
        • Peer Reviewed
        LBL Publications (2023)
        Decarbonized power systems are critical to mitigate climate change, yet methods to achieve a reliable and resilient near-zero power system are still under exploration. This study develops an hourly power system simulation model considering high-resolution geological constraints for carbon-capture-utilization-and-storage to explore the optimal solution for a reliable and resilient near-zero power system. This is applied to 31 provinces in China by simulating 10,450 scenarios combining different electricity storage durations and interprovincial transmission capacities, with various shares of abated fossil power with carbon-capture-utilization-and-storage. Here, we show that allowing up to 20% abated fossil fuel power generation in the power system could reduce the national total power shortage rate by up to 9.0 percentages in 2050 compared with a zero fossil fuel system. A lowest-cost scenario with 16% abated fossil fuel power generation in the system even causes 2.5% lower investment costs in the network (or $16.8 billion), and also increases system resilience by reducing power shortage during extreme climatic events.
          Cover page: A net-zero emissions strategy for China’s power sector using carbon-capture utilization and storage
          • Article
          • Peer Reviewed
          UC Irvine Previously Published Works (2016)

          Background

          Short-term exposure to ambient air pollution has been associated with acute increases in cardiovascular hospitalization and mortality. However, causative chemical components and underlying pathophysiological mechanisms remain to be clarified. We hypothesized that endothelial dysfunction would be associated with mobile-source (traffic) air pollution and that pollutant components with higher oxidative potential to generate reactive oxygen species (ROS) would have stronger associations.

          Methods

          We carried out a cohort panel study in 93 elderly non-smoking adults living in the Los Angeles metropolitan area, during July 2012-February 2014. Microvascular function, represented by reactive hyperemia index (RHI), was measured weekly for up to 12 weeks (N = 845). Air pollutant data included daily data from regional air-monitoring stations, five-day average PM chemical components and oxidative potential in three PM size-fractions, and weekly personal nitrogen oxides (NOx). Linear mixed-effect models estimated adjusted changes in microvascular function with exposure.

          Results

          RHI was inversely associated with traffic-related pollutants such as ambient PM2.5 black carbon (BC), NOx, and carbon monoxide (CO). An interquartile range change increase (1.06 μg/m(3)) in 5-day average BC was associated with decreased RHI, -0.093 (95 % CI: -0.151, -0.035). RHI was inversely associated with other mobile-source components/tracers (polycyclic aromatic hydrocarbons, elemental carbon, and hopanes), and PM oxidative potential as quantified in two independent assays (dithiothreitol and in vitro macrophage ROS) in accumulation and ultrafine PM, and transition metals.

          Conclusions

          Our findings suggest that short-term exposures to traffic-related air pollutants with high oxidative potential are major components contributing to microvascular dysfunction.
            Cover page: Associations between microvascular function and short-term exposure to traffic-related air pollution and particulate matter oxidative potential.
            • Article
            • Peer Reviewed
            UC Irvine Previously Published Works (2016)

            Background

            Exposure to air pollution has been associated with cardiorespiratory morbidity and mortality. However, the chemical constituents and pollution sources underlying these associations remain unclear.

            Method

            We conducted a cohort panel study involving 97 elderly subjects living in the Los Angeles metropolitan area. Airway and circulating biomarkers of oxidative stress and inflammation were measured weekly over 12 weeks and included, exhaled breath condensate malondialdehyde (EBC MDA), fractional exhaled nitric oxide (FeNO), plasma oxidized low-density lipoprotein (oxLDL), and plasma interleukin-6 (IL-6). Exposures included 7-day personal nitrogen oxides (NOx), daily criteria-pollutant data, five-day average particulate matter (PM) measured in three size-fractions and characterized by chemical components including transition metals, and in vitro PM oxidative potential (dithiothreitol and macrophage reactive oxygen species). Associations between biomarkers and pollutants were assessed using linear mixed effects regression models.

            Results

            We found significant positive associations of airway oxidative stress and inflammation with traffic-related air pollutants, ultrafine particles and transition metals. Positive but nonsignificant associations were observed with PM oxidative potential. The strongest associations were observed among PM variables in the ultrafine range (PM <0.18µm). It was estimated that an interquartile increase in 5-day average ultrafine polycyclic aromatic hydrocarbons was associated with a 6.3% (95% CI: 1.1%, 11.6%) increase in EBC MDA and 6.7% (95% CI: 3.4%, 10.2%) increase in FeNO. In addition, positive but nonsignificant associations were observed between oxLDL and traffic-related pollutants, ultrafine particles and transition metals while plasma IL-6 was positively associated with 1-day average traffic-related pollutants.

            Conclusion

            Our results suggest that exposure to pollutants with high oxidative potential (traffic-related pollutants, ultrafine particles, and transition metals) may lead to increased airway oxidative stress and inflammation in elderly adults. This observation was less clear with circulating biomarkers.
              Cover page: Associations of oxidative stress and inflammatory biomarkers with chemically-characterized air pollutant exposures in an elderly cohort.
              • Article
              • Peer Reviewed
              UCLA Previously Published Works (2021)
              The family of coronavirus are named for their crown shape. Encoded by the genetic material inherited from the coronavirus itself, this intrinsic well-known "viral corona" is considered an "inherited corona". After contact with mucosa or the entrance into the host, bare coronaviruses can become covered by a group of dissolved biomolecules to form one or multiple layers of biomolecules. The layers acquired from the surrounding environment are named the "acquired corona". We highlight here the possible role of the acquired corona in the pathogenesis of coronaviruses, which will generate fresh insight into the nature of various coronavirus-host interactions.
                Cover page: Inherited and acquired corona of coronavirus in the host: Inspiration from the biomolecular corona of nanoparticles
                • Article
                • Peer Reviewed
                UC Berkeley Previously Published Works (2024)
                Fatigue failure is invariably the most crucial failure mode for metallic structural components. Most microstructural strategies for enhancing fatigue resistance are effective in suppressing either crack initiation or propagation, but often do not work for both synergistically. Here, we demonstrate that this challenge can be overcome by architecting a gradient structure featuring a surface layer of nacre-like nanolaminates followed by multi-variant twinned structure in pure titanium. The polarized accommodation of highly regulated grain boundaries in the nanolaminated layer to cyclic loading enhances the structural stability against lamellar thickening and microstructure softening, thereby delaying surface roughening and thus crack nucleation. The decohesion of the nanolaminated grains along horizonal high-angle grain boundaries gives rise to an extraordinarily high frequency (≈1.7 × 103 times per mm) of fatigue crack deflection, effectively reducing fatigue crack propagation rate (by 2 orders of magnitude lower than the homogeneous coarse-grained counterpart). These intriguing features of the surface nanolaminates, along with the various toughening mechanisms activated in the subsurface twinned structure, result in a fatigue resistance that significantly exceeds those of the homogeneous and gradient structures with equiaxed grains. Our work on architecting the surface nanolaminates in gradient structure provides a scalable and sustainable strategy for designing more fatigue-resistant alloys.
                  Cover page: Nacre-like surface nanolaminates enhance fatigue resistance of pure titanium.
                  • Article
                  • Peer Reviewed
                  UC Berkeley Previously Published Works (2015)
                  Impaired insulin-mediated suppression of hepatic glucose production (HGP) plays a major role in the pathogenesis of type 2 diabetes (T2D), yet the molecular mechanism by which this occurs remains unknown. Using a novel in vivo metabolomics approach, we show that the major mechanism by which insulin suppresses HGP is through reductions in hepatic acetyl CoA by suppression of lipolysis in white adipose tissue (WAT) leading to reductions in pyruvate carboxylase flux. This mechanism was confirmed in mice and rats with genetic ablation of insulin signaling and mice lacking adipose triglyceride lipase. Insulins ability to suppress hepatic acetyl CoA, PC activity, and lipolysis was lost in high-fat-fed rats, a phenomenon reversible by IL-6 neutralization and inducible by IL-6 infusion. Taken together, these data identify WAT-derived hepatic acetyl CoA as the main regulator of HGP by insulin and link it to inflammation-induced hepatic insulin resistance associated with obesity and T2D.
                    Cover page: Hepatic acetyl CoA links adipose tissue inflammation to hepatic insulin resistance and type 2 diabetes.
                    • Article
                    • Peer Reviewed
                    UC San Francisco Previously Published Works (2023)
                    Cell senescence deters the activation of various oncogenes. Induction of senescence is, therefore, a potentially effective strategy to interfere with vital processes in tumor cells. Sphingosine-1-phosphate receptor 1 (S1PR1) has been implicated in various cancer types, including ovarian cancer. The mechanism by which S1PR1 regulates ovarian cancer cell senescence is currently elusive. In this study, we demonstrate that S1PR1 was highly expressed in human ovarian cancer tissues and cell lines. S1PR1 deletion inhibited the proliferation and migration of ovarian cancer cells. S1PR1 deletion promoted ovarian cancer cell senescence and sensitized ovarian cancer cells to cisplatin chemotherapy. Exposure of ovarian cancer cells to sphingosine-1-phosphate (S1P) increased the expression of 3-phosphatidylinositol-dependent protein kinase 1 (PDK1), decreased the expression of large tumor suppressor 1/2 (LATS1/2), and induced phosphorylation of Yes-associated protein (p-YAP). Opposite results were obtained in S1PR1 knockout cells following pharmacological inhibition. After silencing LATS1/2 in S1PR1-deficient ovarian cancer cells, senescence was suppressed and S1PR1 expression was increased concomitantly with YAP expression. Transcriptional regulation of S1PR1 by YAP was confirmed by chromatin immunoprecipitation. Accordingly, the S1PR1-PDK1-LATS1/2-YAP pathway regulates ovarian cancer cell senescence and does so through a YAP-mediated feedback loop. S1PR1 constitutes a druggable target for the induction of senescence in ovarian cancer cells. Pharmacological intervention in the S1PR1-PDK1-LATS1/2-YAP signaling axis may augment the efficacy of standard chemotherapy.
                      Cover page: S1PR1 regulates ovarian cancer cell senescence through the PDK1-LATS1/2-YAP pathway.
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