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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 (2013)

Since Barack Obama's presidential campaign of 2008, media outlets have changed how race is covered and framed during political campaigns. In the so-called "post-racial" era of American politics when race is supposed to matter less, we are still very much attuned to stories that are framed by racial conflict. When the media wraps a "racial mode of interpretation" around a conflict between two candidates, there are potential electoral penalties involved for either a white or black candidate who becomes entangled in such a controversy.

This project describes this process and provides empirical evidence that individuals' political judgments of candidates can be changed when exposed to such framing. Through a series of three survey experiments that simulate the effect of race-salient media coverage on voters, I find that there are statistically significant electoral penalties--in some cases, more than 10 percentage points--when respondents learn new information about a candidate that either assigns blame for a "race play" or connects him and his opponent to racial controversy. There is also evidence that the media plays a significant role in assigning blame for playing the race card. More respondents were willing to assign blame to a particular candidate when they read news stories in which a media analyst blamed that candidate.

While past literature has focused on racial priming processes that activate white resentment through implicit or explicit cues in campaign ads, this research demonstrates that there may be an important learning process that has been overlooked. Media coverage with an explicit racial mode of interpretation may activate a broader backlash effect among respondents regardless of their racial resentment scores.

    Cover page: The Influence of Explicit Racial Cues on Candidate Evaluation
    • Article
    • Peer Reviewed
    UC Santa Barbara Previously Published Works (2022)
    Biosensors and bioassays, both of which employ proteins and nucleic acids to detect specific molecular targets, have seen significant applications in both biomedical research and clinical practice. This success is largely due to the extraordinary versatility, affinity, and specificity of biomolecular recognition. Nevertheless, these receptors suffer from an inherent limitation: single, saturable binding sites exhibit a hyperbolic relationship (the "Langmuir isotherm") between target concentration and receptor occupancy, which in turn limits the sensitivity of these technologies to small variations in target concentration. To overcome this and generate more responsive biosensors and bioassays, here we have used the sequestration mechanism to improve the steepness of the input/output curves of several bioanalytical methods. As our test bed for this we employed sensors and assays against neutrophil gelatinase-associated lipocalin (NGAL), a kidney biomarker for which enhanced sensitivity will improve the monitoring of kidney injury. Specifically, by introducing sequestration we have improved the responsiveness of an electrochemical aptamer based (EAB) biosensor, and two bioassays, a paper-based "dipstick" assay and an enzyme-linked immunosorbent assay (ELISA). Doing so we have narrowed the dynamic range of these sensors and assays several-fold, thus enhancing their ability to measure small changes in target concentration. Given that introducing sequestration requires only the addition of the appropriate concentration of a high-affinity "depletant," the mechanism appears simple and easily adaptable to tuning the binding properties of the receptors employed in a wide range of biosensors and bioassays.
      Cover page: The sequestration mechanism as a generalizable approach to improve the sensitivity of biosensors and bioassays
      • Article
      • Peer Reviewed
      UC Santa Barbara Previously Published Works (2021)
      Electrochemical aptamer-based (EAB) sensors, composed of an electrode-bound DNA aptamer with a redox reporter on the distal end, offer the promise of high-frequency, real-time molecular measurements in complex sample matrices and even in vivo. Here we assess the extent to which switching the aptamer terminus that is electrode-bound and the one that is redox-reporter-modified affects the performance of these sensors. Using sensors against doxorubicin, cocaine, and vancomycin as our test beds, we find that both signal gain (the relative signal change seen in the presence of a saturating target) and the frequency dependence of gain depend strongly on the attachment orientation, suggesting that this easily investigated variable is a worthwhile parameter to optimize in the design of new EAB sensors.
        Cover page: Switching the aptamer attachment geometry can dramatically alter the signalling and performance of electrochemical aptamer-based sensors
        • Article
        Proceedings of the Annual Meeting of the Cognitive Science Society, Volume 40 (2018)
        Previous research has demonstrated that speakers changephonetic forms in response to variability in their immediatelinguistic milieu, such that they converge with an interlocutor.While much is known about the impact of social dynamics onthis process, the impact of individual variability in cognitionand perception is less well-explored. The present study seeksto examine the impact of these individual differences onphonetic convergence during a naturalistic conversation,comparing convergence in autism spectrum disorder (ASD)and typical development. Results showed a small effect oftemporal convergence within typically developing dyads,compared with evidence of divergence within ASD dyads.While preliminary, this pattern of results suggests that socialmotivation may play a more important role in phoneticconvergence than sensory accounts (such as self-monitoring).
          Cover page: Reduced Phonetic Convergence in Autism Spectrum Disorder
          • Article
          • Peer Reviewed
          UC San Diego Previously Published Works (2020)

          Background

          Protein disulfide isomerase (PDI) proteins are part of the thioredoxin protein superfamily. PDIs are involved in the formation and rearrangement of disulfide bonds between cysteine residues during protein folding in the endoplasmic reticulum and are implicated in stress response pathways.

          Methods

          Eight children from four consanguineous families residing in distinct geographies within the Middle East and Central Asia were recruited for study. All probands showed structurally similar microcephaly with lissencephaly (microlissencephaly) brain malformations. DNA samples from each family underwent whole exome sequencing, assessment for repeat expansions and confirmatory segregation analysis.

          Results

          An identical homozygous variant in TMX2 (c.500G>A), encoding thioredoxin-related transmembrane protein 2, segregated with disease in all four families. This variant changed the last coding base of exon 6, and impacted mRNA stability. All patients presented with microlissencephaly, global developmental delay, intellectual disability and epilepsy. While TMX2 is an activator of cellular C9ORF72 repeat expansion toxicity, patients showed no evidence of C9ORF72 repeat expansions.

          Conclusion

          The TMX2 c.500G>A allele associates with recessive microlissencephaly, and patients show no evidence of C9ORF72 expansions. TMX2 is the first PDI implicated in a recessive disease, suggesting a protein isomerisation defect in microlissencephaly.
            Cover page: Recurrent homozygous damaging mutation in TMX2, encoding a protein disulfide isomerase, in four families with microlissencephaly
            • Article
            • Peer Reviewed
            UC Davis Previously Published Works (2020)

            Objectives

            To approximate the rate of familial myasthenia gravis and the coexistence of other autoimmune disorders in the patients and their families.

            Design

            Retrospective cohort study.

            Setting

            Clinics across North America.

            Participants

            The study included 1032 patients diagnosed with acetylcholine receptor antibody (AChR)-positive myasthenia gravis.

            Methods

            Phenotype information of 1032 patients diagnosed with AChR-positive myasthenia gravis was obtained from clinics at 14 centres across North America between January 2010 and January 2011. A critical review of the epidemiological literature on the familial rate of myasthenia gravis was also performed.

            Results

            Among 1032 patients, 58 (5.6%) reported a family history of myasthenia gravis. A history of autoimmune diseases was present in 26.6% of patients and in 28.4% of their family members.

            Discussion

            The familial rate of myasthenia gravis was higher than would be expected for a sporadic disease. Furthermore, a high proportion of patients had a personal or family history of autoimmune disease. Taken together, these findings suggest a genetic contribution to the pathogenesis of myasthenia gravis.
              Cover page: Epidemiological evidence for a hereditary contribution to myasthenia gravis: a retrospective cohort study of patients from North America
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