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Open Access Publications from the University of California

Scholarly Works (8 results)

  • Article
  • Peer Reviewed
Berkeley Undergraduate Journal, Volume 25, Issue 3 (2012)

The Castro district in San Francisco, California presents itself as the “Gay Mecca,” a safe haven for LGBT-identified individuals. However, demographics of and observations in the Castro illuminate quite a different story. On weekend nights, several low-income queer men and women of color consistently congregate on the corner of Market and Castro St., quite literally at the margins of Castro social life. Essentially, the marginal positioning of these low-income queer people of color on this corner results from a double exclusion, from their home neighborhoods and from the Castro. In their home neighborhoods, these individuals are marginalized due to their sexuality, and in the Castro they are marginalized due to their race and socioeconomic class. The corner of Market and Castro, then, is significant to these low-income queer people of color for a variety of reasons, including emotional and socioeconomic support, but namely in regard to identity formation. While marginalized, these low-income queer people of color manage to carve out a small space, however policed or challenged, that provides them with the platform to play with and embody their multiple, intersecting identities that they are unable to fully express in other spaces.

    Cover page: Community and Exclusion in the Gay Mecca
    • Thesis
    • Peer Reviewed
    UC Santa Cruz Electronic Theses and Dissertations (2020)

    This dissertation attempts to understand the emergence and development of the Open Insulin Project, a community laboratory-based project to create an open-source protocol for affordable bioengineered insulin. It seeks to situate this effort within broader trends in the capitalization of the biosciences and biomedicine and to explore its potential and struggles as a resistance effort working against these prevailing trends. It draws on roughly three years of ethnographic study, including participant-observation within the Project and interviews with key members and associates. It argues that the Open Insulin Project is the product of a contradiction within biocapital and that it represents a new phenomenon: antibiocapital. It further explores the ways in which appropriating bioengineering constrains a would-be antibiocapitalist Project and compels such an effort to conform to the sociopolitical order of biocapital. Situating the Project within a broader trend of amateur bio, it argues that the emergence of amateur bio social movements creates the potential for reimagining rights and governance in the contemporary biosciences, though this potential may be limited by the presence and influence of powerful interests. Finally, it argues that this Project and efforts like it provide unique opportunities for collaboration between the social, natural, and engineering sciences that could overcome some of the limitations of past efforts, including those under the banner of Ethical, Legal, and Social Implications/Aspects (ELSI/A) research and “post-ELSI” efforts in synthetic biology. Such collaborations challenge the approaches of both social scientists and projects like Open Insulin.

      Cover page: Biologics of Resistance: The Open Insulin Project and the Promise of AntibiocapitalCreative Commons 'BY-NC-SA' version 4.0 license
      • Article
      • Peer Reviewed
      UC Irvine Previously Published Works (2019)
      Institutions should value teaching and service, and not just research, when considering faculty for promotion and tenure.
        Cover page: When it comes to teaching and tenure it is time to walk the walk
        • Article
        • Peer Reviewed
        UC Davis Previously Published Works (2014)
        The length of the mitotic spindle varies among different cell types. A simple model for spindle length regulation requires balancing two forces: pulling, due to micro-tubules that attach to the chromosomes at their kinetochores, and pushing, due to interactions between microtubules that emanate from opposite spindle poles. In the budding yeast Saccharomyces cerevisiae, we show that spindle length scales with kinetochore number, increasing when kinetochores are inactivated and shortening on addition of synthetic or natural kinetochores, showing that kinetochore-microtubule interactions generate an inward force to balance forces that elongate the spindle. Electron microscopy shows that manipulating kinetochore number alters the number of spindle microtubules: adding extra kinetochores increases the number of spindle microtubules, suggesting kinetochore-based regulation of microtubule number.
          Cover page: Chromosomal attachments set length and microtubule number in the S. cerevisiae mitotic spindle
          • Article
          • Peer Reviewed
          Matriptase is an epithelia-specific membrane-anchored serine protease that has received considerable attention in recent years because of its consistent dysregulation in human epithelial tumours, including breast cancer. Mice with reduced levels of matriptase display a significant delay in oncogene-induced mammary tumour formation and blunted tumour growth. The abated tumour growth is associated with a decrease in cancer cell proliferation. Here we demonstrate by genetic deletion and silencing that the proliferation impairment in matriptase-deficient breast cancer cells is caused by their inability to initiate activation of the c-Met signalling pathway in response to fibroblast-secreted pro-HGF. Similarly, inhibition of matriptase catalytic activity using a selective small-molecule inhibitor abrogates the activation of c-Met, Gab1 and AKT, in response to pro-HGF, which functionally leads to attenuated proliferation in breast carcinoma cells. We conclude that matriptase is critically involved in breast cancer progression and represents a potential therapeutic target in breast cancer.
            Cover page: Targeting matriptase in breast cancer abrogates tumour progression via impairment of stromal-epithelial growth factor signalling
            • Article
            • Peer Reviewed
            UC Davis Previously Published Works (2018)
            Poison frogs acquire chemical defenses from the environment for protection against potential predators. These defensive chemicals are lipophilic alkaloids that are sequestered by poison frogs from dietary arthropods and stored in skin glands. Despite decades of research focusing on identifying poison frog alkaloids, we know relatively little about how environmental variation and subsequent arthropod availability impacts alkaloid loads in poison frogs. We investigated how seasonal environmental variation influences poison frog chemical profiles through changes in the diet of the Climbing Mantella (Mantella laevigata). We collected M. laevigata females on the Nosy Mangabe island reserve in Madagascar during the wet and dry seasons and tested the hypothesis that seasonal differences in rainfall is associated with changes in diet composition and skin alkaloid profiles of M. laevigata. The arthropod diet of each frog was characterized into five groups (i.e. ants, termites, mites, insect larvae, or other) using visual identification and cytochrome oxidase 1 DNA barcoding. We found that frog diet differed between the wet and dry seasons, where frogs had a more diverse diet in the wet season and consumed a higher percentage of ants in the dry season. To determine if seasonality was associated with variation in frog defensive chemical composition, we used gas chromatography / mass spectrometry to quantify alkaloids from individual skin samples. Although the assortment of identified alkaloids was similar across seasons, we detected significant differences in the abundance of certain alkaloids, which we hypothesize reflects seasonal variation in the diet of M. laevigata. We suggest that these variations could originate from seasonal changes in either arthropod leaf litter composition or changes in frog behavioral patterns. Although additional studies are needed to understand the consequences of long-term environmental shifts, this work suggests that alkaloid profiles are relatively robust against short-term environmental perturbations.
              Cover page: Seasonal changes in diet and chemical defense in the Climbing Mantella frog (Mantella laevigata).
              • Article
              • Peer Reviewed
              UC Davis Previously Published Works (2023)
              Impairment of vascular pathways of cerebral β-amyloid (Aβ) elimination contributes to Alzheimer disease (AD). Vascular damage is commonly associated with diabetes. Here we show in human tissues and AD-model rats that bloodborne islet amyloid polypeptide (amylin) secreted from the pancreas perturbs cerebral Aβ clearance. Blood amylin concentrations are higher in AD than in cognitively unaffected persons. Amyloid-forming amylin accumulates in circulating monocytes and co-deposits with Aβ within the brain microvasculature, possibly involving inflammation. In rats, pancreatic expression of amyloid-forming human amylin indeed induces cerebrovascular inflammation and amylin-Aβ co-deposits. LRP1-mediated Aβ transport across the blood-brain barrier and Aβ clearance through interstitial fluid drainage along vascular walls are impaired, as indicated by Aβ deposition in perivascular spaces. At the molecular level, cerebrovascular amylin deposits alter immune and hypoxia-related brain gene expression. These converging data from humans and laboratory animals suggest that altering bloodborne amylin could potentially reduce cerebrovascular amylin deposits and Aβ pathology.
                Cover page: Aβ efflux impairment and inflammation linked to cerebrovascular accumulation of amyloid-forming amylin secreted from pancreas
                • Article
                • Peer Reviewed
                UC San Diego Previously Published Works (2024)
                Hypoxia-inducible factor pathway genes are linked to adaptation in both human and nonhuman highland species. EPAS1, a notable target of hypoxia adaptation, is associated with relatively lower hemoglobin concentration in Tibetans. We provide evidence for an association between an adaptive EPAS1 variant (rs570553380) and the same phenotype of relatively low hematocrit in Andean highlanders. This Andean-specific missense variant is present at a modest frequency in Andeans and absent in other human populations and vertebrate species except the coelacanth. CRISPR-base-edited human cells with this variant exhibit shifts in hypoxia-regulated gene expression, while metabolomic analyses reveal both genotype and phenotype associations and validation in a lowland population. Although this genocopy of relatively lower hematocrit in Andean highlanders parallels well-replicated findings in Tibetans, it likely involves distinct pathway responses based on a protein-coding versus noncoding variants, respectively. These findings illuminate how unique variants at EPAS1 contribute to the same phenotype in Tibetans and a subset of Andean highlanders despite distinct evolutionary trajectories.
                  Cover page: Functional EPAS1/HIF2A missense variant is associated with hematocrit in Andean highlanders
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