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Open Access Publications from the University of California

Scholarly Works (61 results)

  • Thesis
  • Peer Reviewed
UC Irvine Electronic Theses and Dissertations (2020)

The depletion of fossil fuels and the urgency of reducing greenhouse gas emissions demonstrate a pressing need for alternative energy sources. Currently, natural gas consumption is a major contributor to global warming, not only due to the carbon dioxide emissions in the combustion products but also due to natural gas leakage in the mining, transmission and storage facilities. Therefore, replacing the pipeline natural gas with renewable gas can decrease greenhouse gas emissions as well as reduce dependence on fossil fuels. This dissertation investigated the feasibility of blending renewable gases (i.e., biogas, hydrogen), into existing natural gas transmission and distribution pipelines from the perspective of fuel properties and combustion performance of residential appliances.

The fuel interchangeability technical barriers and challenges were first investigated, including fuel properties, flowrate control, flame performance, etc.. Moreover, the source of reddish hydrogen flame color was also investigated experimentally. The results indicated that hydrogen cracking and embrittlement could be a concern influencing flame appearance. A multi-fuel blending system was fabricated under this dissertation to generate fuel mixtures of various percentages. Burner configurations of existing residential burners were investigated, and representative self-aspirating burners were selected to conduct fuel interchangeability testing on different fuel classes. Monitored combustion performance included ignition behaviors, blowoff/flashback limits, emissions (CO, UHCs, NO, NO2, N2O, NH3, etc.), efficiency, burner temperature, combustion noise, etc.. It was found that CO and UHCs emissions and the risk of flame blow-off increase significantly when the CO2 percentage in the fuel exceeds 5 vol%. Self-aspirating burners were found to have distinct H2 tolerance levels with a limiting factor of the flashback, which is more inclined to occur at ignition conditions. This limited the H2 injection limits below 20 vol%. At a low level of H2 addition to natural gas, most of the combustion performance of the tested self-aspirating devices didn’t differ much and some of them were improved, which shows a positive sign for natural gas replacement with renewable hydrogen for self-aspirating flames

    Cover page: Impact of Increased Renewable Gases in Natural Gas on Combustion Performance of Self-aspirating Flames
    • Thesis
    • Peer Reviewed
    UC San Diego Electronic Theses and Dissertations (2020)

    Regulated neural circuit activity is essential for cognitive ability and behavioral activities whereas aberrant circuit function is a hallmark of disorders, including Autism Spectrum Disorders and epilepsy. However, the specific mechanisms of regulating neural circuit remain obscure. This study uses a unique C. elegans model of circuit hyperactivity, a gain-of-function mutation in a nicotinic acetylcholine receptor subunit, acr-2(gf). The acr-2(gf) gene product functions in acetylcholine motor neurons and results in a disrupted neural circuit by hyperactivating the acetylcholine excitatory motor neurons and causing impaired locomotion with stochastic muscle convulsions. From previous genetic screening, a functional linkage has been found between neuronal activity and one missense mutation within conserved translation initiation factor eif-3.g, allowing suppression on acr-2(gf) convulsion. The aim of my master thesis is to identify genes affecting motor neural circuit function through eif-3.g and acr-2(gf). Specifically, I am involved in analyzing mutations isolated from a genetic suppressor screen for genes that restored convulsion rate in eif-3.g(ju807); acr-2(gf) animals. I identified one eif-3.g suppressor as protein translation repressor lin-66, which encodes for heterochronic gene downregulating development. We speculate that gene lin-66 gene is one of the targets of or participate in eif-3.g function in motor neurons. Our studies provide fundamental mechanism for future implication on understanding the regulation between motor neurons and translational initiation factors.

      Cover page: Investigating roles of the protein translation initiation factor EIF-3.G in regulating neuronal circuit activity in Caenorhabditis elegans.
      • Article
      • Peer Reviewed
      UCLA Previously Published Works (2009)
      Zebrafish teeth develop on pharyngeal jaws in the 5th branchial arch, but early tooth development is remarkably similar to mammals (Borday-Birraux et al., Evol Dev 8:130, 2006). Recently, eve1 has been shown to be associated with the primary tooth (4V1) and early ameloblast development, the enamel organ precursor (Laurenti et al., Dev Dyn 230:727, 2004). dax1 is initially expressed in the 5th branchial arch in zebrafish at approximately 26 h postfertilization (hpf) and colocalizes with eve1 expression at ~48 hpf. Embryos injected with dax1 morpholino show downregulation of eve1 expression. Based on the zebrafish observations, we demonstrated novel DAX1 expression in normal human dental, benign ameloblastoma, and malignant ameloblastoma tissues. The association of NR0B1 and its protein product DAX1 with primary tooth development and ameloblastoma tumorigenesis is an association not previously described.
        Cover page: The expression of nr0b1, the earliest gene in zebrafish tooth development, is a marker for human tooth and ameloblastoma formation
        • Article
        • Peer Reviewed
        UC San Diego Previously Published Works (2024)
        Protein translation initiation is a conserved process involving many proteins acting in concert. The 13 subunit eukaryotic initiation factor 3 (eIF3) complex is essential for assembly of the pre-initiation complex that scans mRNA and positions ribosome at the initiation codon. We previously reported that a gain-of-function (gf) mutation affecting the G subunit of the Caenorhabditis elegans eIF3 complex, eif-3.g(gf), selectively modulates protein translation in the ventral cord cholinergic motor neurons. Here, through unbiased genetic suppressor screening, we identified that the gene lin-66 mediates eif-3.g(gf)-dependent protein translation in motor neurons. LIN-66 is composed largely of low-complexity amino acid sequences with unknown functional domains. We combined bioinformatics analysis with in vivo functional dissection and identified a cold-shock domain in LIN-66 critical for its function. In cholinergic motor neurons, LIN-66 shows a close association with EIF-3.G in the cytoplasm. The low-complexity amino acid sequences of LIN-66 modulate its subcellular pattern. As cold-shock domains function broadly in RNA regulation, we propose that LIN-66 mediates stimulus-dependent protein translation by facilitating the interaction of mRNAs with EIF-3.G.
          Cover page: C. elegans LIN-66 mediates EIF-3/eIF3-dependent protein translation via a cold-shock domain.
          • Article
          • Peer Reviewed
          UC San Francisco Previously Published Works (2016)
          CYP2W1 is a recently discovered human cytochrome P450 enzyme with a distinctive tumor-specific expression pattern. We show here that CYP2W1 exhibits tight binding affinities for retinoids, which have low nanomolar binding constants, and much poorer binding constants in the micromolar range for four other ligands. CYP2W1 converts all-transretinoic acid (atRA) to 4-hydroxyatRA and all-transretinol to 4-OH all-transretinol, and it also oxidizes retinal. The enzyme much less efficiently oxidizes 17β-estradiol to 2-hydroxy-(17β)-estradiol and farnesol to a monohydroxylated product; arachidonic acid is, at best, a negligible substrate. These findings indicate that CYP2W1 probably plays an important role in localized retinoid metabolism that may be intimately linked to its involvement in tumor development.
            Cover page: Catalytic Activities of Tumor-Specific Human Cytochrome P450 CYP2W1 Toward Endogenous Substrates
            • Article
            • Peer Reviewed
            UCLA Previously Published Works (2016)

            Background

            Cardiac maturation during perinatal transition of heart is critical for functional adaptation to hemodynamic load and nutrient environment. Perturbation in this process has major implications in congenital heart defects. Transcriptome programming during perinatal stages is an important information but incomplete in current literature, particularly, the expression profiles of the long noncoding RNAs (lncRNAs) are not fully elucidated.

            Methods and results

            From comprehensive analysis of transcriptomes derived from neonatal mouse heart left and right ventricles, a total of 45 167 unique transcripts were identified, including 21 916 known and 2033 novel lncRNAs. Among these lncRNAs, 196 exhibited significant dynamic regulation along maturation process. By implementing parallel weighted gene co-expression network analysis of mRNA and lncRNA data sets, several lncRNA modules coordinately expressed in a developmental manner similar to protein coding genes, while few lncRNAs revealed chamber-specific patterns. Out of 2262 lncRNAs located within 50 kb of protein coding genes, 5% significantly correlate with the expression of their neighboring genes. The impact of Ppp1r1b-lncRNA on the corresponding partner gene Tcap was validated in cultured myoblasts. This concordant regulation was also conserved in human infantile hearts. Furthermore, the Ppp1r1b-lncRNA/Tcap expression ratio was identified as a molecular signature that differentiated congenital heart defect phenotypes.

            Conclusions

            The study provides the first high-resolution landscape on neonatal cardiac lncRNAs and reveals their potential interaction with mRNA transcriptome during cardiac maturation. Ppp1r1b-lncRNA was identified as a regulator of Tcap expression, with dynamic interaction in postnatal cardiac development and congenital heart defects.
              Cover page: Decoding the Long Noncoding RNA During Cardiac Maturation
              • Article
              • Peer Reviewed
              UCLA Previously Published Works (2023)
              Endothelial-mesenchymal transition (EndMT) drives the endothelium to contribute to vascular calcification in diabetes mellitus. In our previous study, we showed that glycogen synthase kinase-3β (GSK3β) inhibition induces β-catenin and reduces mothers against DPP homolog 1 (SMAD1) to direct osteoblast-like cells toward endothelial lineage, thereby reducing vascular calcification in Matrix Gla Protein (Mgp) deficiency. Here, we report that GSK3β inhibition reduces vascular calcification in diabetic Ins2Akita/wt mice. Cell lineage tracing reveals that GSK3β inhibition redirects endothelial cell (EC)-derived osteoblast-like cells back to endothelial lineage in the diabetic endothelium of Ins2Akita/wt mice. We also find that the alterations in β-catenin and SMAD1 by GSK3β inhibition in the aortic endothelium of diabetic Ins2Akita/wt mice are similar to Mgp-/- mice. Together, our results suggest that GSK3β inhibition reduces vascular calcification in diabetic arteries through a similar mechanism to that in Mgp-/- mice.
                Cover page: GSK3β Inhibition Reduced Vascular Calcification in <i>Ins2<sup>Akita/+</sup></i> Mice.
                • Article
                • Peer Reviewed
                UCLA Previously Published Works (2019)
                In this manuscript, phosphine-dependent [3 + 3] and [4 + 3] annulation reactions of allenoate with aziridines were disclosed. The alkyldiphenylphosphine-promoted [4 + 3] annulation of allenoate with aziridines has been achieved under mild conditions, providing biologically interesting functionalized tetrahydroazepines in moderate to excellent yield with moderate to excellent regioselectivity and diastereoselectivity.
                  Cover page: Phosphine-promoted [4 + 3] annulation of allenoate with aziridines for synthesis of tetrahydroazepines: phosphine-dependent [3 + 3] and [4 + 3] pathways
                  • Article
                  • Peer Reviewed
                  UCLA Previously Published Works (2024)
                  Vascular calcification is a severe complication of cardiovascular diseases. Previous studies demonstrated that endothelial lineage cells transitioned into osteoblast-like cells and contributed to vascular calcification. Here, we found that inhibition of cyclin-dependent kinase (CDK) prevented endothelial lineage cells from transitioning to osteoblast-like cells and reduced vascular calcification. We identified a robust induction of CDK1 in endothelial cells (ECs) in calcified arteries and showed that EC-specific gene deletion of CDK1 decreased the calcification. We found that limiting CDK1 induced E-twenty-six specific sequence variant 2 (ETV2), which was responsible for blocking endothelial lineage cells from undergoing osteoblast differentiation. We also found that inhibition of CDK1 reduced vascular calcification in a diabetic mouse model. Together, the results highlight the importance of CDK1 suppression and suggest CDK1 inhibition as a potential option for treating vascular calcification.
                    Cover page: CDK1 inhibition reduces osteogenesis in endothelial cells in vascular calcification.
                    • Article
                    • Peer Reviewed
                    UC San Francisco Previously Published Works (2016)
                    Cholest-4-en-3-one, whether added exogenously or generated intracellularly from cholesterol, inhibits the growth ofMycobacterium tuberculosiswhen CYP125A1 and CYP142A1, the cytochrome P450 enzymes that initiate degradation of the sterol side chain, are disabled. Here we demonstrate that a 16-hydroxy derivative of cholesterol, which was previously reported to inhibit growth ofM. tuberculosis, acts by preventing the oxidation of the sterol side chain even in the presence of the relevant cytochrome P450 enzymes. The finding that (25R)-cholest-5-en-3β,16β,26-triol (1) (and its 3-keto metabolite) inhibit growth suggests that cholesterol analogs with non-degradable side chains represent a novel class of anti-mycobacterial agents. In accord with this, two cholesterol analogs with truncated, fluorinated side chains have been synthesized and shown to similarly block the growth in culture ofM. tuberculosis.
                      Cover page: Cholesterol Analogs with Degradation-resistant Alkyl Side Chains Are Effective Mycobacterium tuberculosis Growth Inhibitors*
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