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Open Access Publications from the University of California

Scholarly Works (8 results)

  • Article
Contemporary Music Score Collection (2020)
    Cover page: Voyagers
    • Article
    Contemporary Music Score Collection (2020)
    This music score was submitted for the Kaleidoscope 2020 Call for Scores, an open access collaboration with the UCLA Music Library.
      Cover page: Grneta Variations
      • Article
      Contemporary Music Score Collection (2020)
        Cover page: Playing for our lives
        • Article
        • Peer Reviewed
        Proceedings of the Annual Meeting of the Berkeley Linguistics Society, Volume 1 (1975)
          Cover page: On the Origin of Several Medio-passive Personal Endings in Indo-European
          • Article
          • Peer Reviewed
          Proceedings of the Annual Meeting of the Berkeley Linguistics Society, Volume 2 (1976)
            Cover page: Etymology of Greek agalma, agallō, agallomai
            • Article
            • Peer Reviewed
            UCLA Previously Published Works (2002)
            Apoptosis depends critically on regulated cytoskeletal reorganization events in a cell. We demonstrate that death effector domain containing DNA binding protein (DEDD), a highly conserved and ubiquitous death effector domain containing protein, exists predominantly as mono- or diubiquitinated, and that diubiquitinated DEDD interacts with both the K8/18 intermediate filament network and pro-caspase-3. Early in apoptosis, both cytosolic DEDD and its close homologue DEDD2 formed filaments that colocalized with and depended on K8/18 and active caspase-3. Subsequently, these filamentous structures collapsed into intracellular inclusions that migrated into cytoplasmic blebs and contained DEDD, DEDD2, active caspase-3, and caspase-3-cleaved K18 late in apoptosis. Biochemical studies further confirmed that DEDD coimmunoprecipitated with both K18 and pro-caspase-3, and kinetic analyses placed apoptotic DEDD staining prior to caspase-3 activation and K18 cleavage. In addition, both caspase-3 activation and K18 cleavage was inhibited by expression of DEDDDeltaNLS1-3, a cytosolic form of DEDD that cannot be ubiquitinated. Finally, siRNA mediated DEDD knockdown cells exhibited inhibition of staurosporine-induced DNA degradation. Our data suggest that DEDD represents a novel scaffold protein that directs the effector caspase-3 to certain substrates facilitating their ordered degradation during apoptosis.
              Cover page: DEDD regulates degradation of intermediate filaments during apoptosis
              • Article
              • Peer Reviewed
              Western Journal of Emergency Medicine: Integrating Emergency Care with Population Health, Volume 17, Issue 2 (2016)

              Introduction: Clinicians are urged to decrease radiation exposure from unnecessary medical procedures. Many emergency department (ED) patients placed in an observation unit (EDOU) do not require chest pain evaluation with a nuclear stress test (NucST). We sought to implement a simple ST algorithm that favors non-nuclear stress test (Non-NucST) options to evaluate the effect of the algorithm on the proportion of patients exposed to radiation by comparing use of NucST versus Non-NucST pre- and post-algorithm.

              Methods: An ST algorithm was introduced favoring Non-NucST and limiting NucST to a subset of EDOU patients in October 2008. We analyzed aggregate data before (Jan-Sept 2008, period 1) and after (Jan-Sept 2009 and Jan-Sept 2010, periods 2 and 3 respectively) algorithm introduction. A random sample of 240 EDOU patients from each period was used to compare 30-day major adverse cardiac events (MACE). We calculated confidence intervals for proportions or the difference between two proportions.

              Results: A total of 5,047 STs were performed from Jan-Sept 2008-2010. NucST in the EDOU decreased after algorithm introduction from period 1 to 2 (40.7%, 95% CI [38.3-43.1] vs. 22.1%, 95% CI [20.1-24.1]), and remained at 22.1%, 95% CI [20.3-24.0] in period 3. There was no difference in 30-day MACE rates before and after algorithm use (0.1% for period 1 and 3, 0% for period 2).

              Conclusion: Use of a simple ST algorithm that favors non-NucST options decreases the proportion of EDOU chest pain patients exposed to radiation exposure from ST almost 50% by limiting NucST to a subset of patients, without a change in 30-day MACE.

                Cover page: Reduction in Radiation Exposure through a Stress Test Algorithm in an Emergency Department Observation UnitCreative Commons 'BY' version 4.0 license
                • Article
                • Peer Reviewed
                UC San Diego Previously Published Works (2018)
                Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.
                  Cover page: Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
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