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Open Access Publications from the University of California

Scholarly Works (133 results)

  • Article
Research Summaries (2003)

Through the National Sea Grant’s Oyster Disease Research Program, scientists from around the country are being funded to find approaches to restoring the ecological and commercial viability of oyster beds.This one-page publication highlights the efforts of Dr. Jane Burns of the Theodore Gildred Cancer Center at UC San Diego’s School of Medicine to create a genetically engineered,disease-resistant version of the commercially important oyster, Crassostrea virginica. Conceptually, this could be achieved by inserting appropriate genes from a horseshoe crab—the crab produces antimicrobial proteins that make it immune to disease—into an oyster genome. Though simple in theory, in practice it requires the development of many intermediary techniques and tools.

    Cover page: Creation of a Molluscan Cell Line
    • Article
    • Peer Reviewed
    UC San Diego Previously Published Works (2018)
      Cover page: Finding Kawasaki Disease
      • Article
      • Peer Reviewed
      UC San Diego Previously Published Works (2023)
      Although elegant work has detailed the clinical presentation, immune response and disease outcome of multisystem inflammatory syndrome in children, many questions remain. Studies in 2022 have explored the nature of the vascular injury, the role of the SARS-CoV-2 spike protein and the association with the current variants of the virus.
        Cover page: MIS-C: myths have been debunked, but mysteries remain
        • Article
        • Peer Reviewed
        UC San Diego Previously Published Works (2017)
        [first paragraph of article]The mainstay of therapy for acute Kawasaki disease (KD) is intravenous immunoglobulin (IVIG), which was first described in a case series from Japan and later proven through a nationwide clinical trial in the U.S. published in 1986. Since completion of the initial clinical trials, many questions have arisen regarding the nuances of KD treatment. In the absence of an evidence base, what follows is an attempt to devise rational responses to these questions that draw upon common sense and the personal experience of this author. 
          Cover page: Frequently asked questions regarding treatment of Kawasaki disease
          • Article
          • Peer Reviewed
          UC San Diego Previously Published Works (2018)
          Dr. Kawasaki saw his first case of the disease that would come to bear his name in 1961. His meticulous description of the clinical syndrome persists as the case definition to the present day. This review chronicles the emergence and recognition of Kawasaki disease in Asia and Western countries and articulates the old disease/new disease controversy.
            Cover page: History of the worldwide emergence of Kawasaki disease
            • Article
            • Peer Reviewed
            UC San Diego Previously Published Works (2015)
            The introduction of intravenous immunoglobulin (IVIG) for modulation of inflammation in acute Kawasaki disease was a great therapeutic triumph. However, three decades later, the mechanisms underlying immune regulation by IVIG are only beginning to be revealed. Stimulation of an immature myeloid population of dendritic cells that secretes IL-10 and the elucidation of Fc-specific natural regulatory T cells provide insights into the mechanisms of IVIG. Other potential mechanisms include provision of agent-specific neutralizing antibody, anti-idiotype and anti-cytokine antibodies, blockade of activating Fcγ receptors and stimulation of the inhibitory FcγRIIb receptor. New initiatives must seek to understand the mechanisms of IVIG in order to replace it one day with more affordable and more targeted therapies.
              Cover page: The immunomodulatory effects of intravenous immunoglobulin therapy in Kawasaki disease
              • Article
              • Peer Reviewed
              UC San Diego Previously Published Works (2018)

              Purpose of review

              Kawasaki disease presents many challenges to the diverse group of physicians who care for these patients including infectious disease specialists, rheumatologists, and cardiologists. Here we review some of the progress being made toward improved understanding of disease pathogenesis, treatment, and long-term outcomes.

              Recent findings

              Epidemiologic studies in different populations documented increasing numbers of cases in countries with high physician awareness of the disease. These data suggest true increases in patient numbers rather than increases because of increased case ascertainment. Adequately powered clinical trials for adjunctive therapies continue to be an unmet need. Long-term consequences of damage to the arterial wall and myocardium are beginning to emerge and systematic, longitudinal observational studies are needed to better define outcomes.

              Summary

              The unknown cause, lack of a specific diagnostic test, and uncertain future for patients who develop permanent cardiovascular damage all require further study.
                Cover page: New insights into cardiovascular disease in patients with Kawasaki disease
                • Thesis
                • Peer Reviewed
                UC San Diego Electronic Theses and Dissertations (2016)

                Background

                Genetic variation in calcium signaling pathways is associated with Kawasaki disease (KD) susceptibility and coronary artery aneurysms (CAA). Expression quantitative trait locus analysis for KD-associated variants in calcium/sodium channel gene solute carrier family 8 member 1 (SLC8A1) revealed an effect on expression of urotensin 2 (UTS2). We investigated the role of UTS2 in KD pathogenesis by measuring levels of UTS2 and its receptor in blood and tissues.

                Results

                UTS2 transcript levels determined by reverse transcription polymerase chain reaction were higher in whole blood of KD subjects homozygous for three risk alleles in SLC8A1 (p=0.002-0.006). Increased levels of plasma UTS2 varied as a function of SLC8A1 genotype (p=0.008-0.04). UTS2 transcript levels in a microarray dataset for 131 subjects remained higher in the convalescent phase of KD in subjects with aneurysms. Immunohistochemical staining identified UTS2 and UTS2R expression in mononuclear inflammatory cells and spindle-shaped cells in the coronary arterial wall of a KD patient with CAA and in a femoral endarterectomy specimen from an adult patient with peripheral aneurysms following KD in childhood.

                Discussion

                Host genetics influences UTS2 levels, which may contribute to inflammation and cardiovascular damage in KD

                  Cover page: Urotensin 2 in Kawasaki disease pathogenesis
                  • Article
                  Research Final Reports (2003)

                  The focus is on research conducted and the progress made toward the achievement of all specific aims outlined in the original proposal. Three abstracts describing aspects of our work in oysters were presented at national and international meetings. Specific Aim: Test methods of introducing pantropic vectors into C. virginica embryos to create transgenic oysters

                    Cover page: Toward the genetic engineering of disease resistance in oysters
                    • Article
                    • Peer Reviewed
                    UC San Diego Previously Published Works (2017)
                    Background: A growing population of young adults is presenting to cardiologists with late manifestations of Kawasaki disease (KD) that include cardiomyopathy, ischemia, and infarction. The management of these conditions differs in important ways from atherosclerotic heart disease, and yet there is little awareness in the adult cardiology community regarding the special challenges posed by the cardiovascular sequelae of KD. Methods: Observations were made on a population of 140 adult KD patients enrolled in the San Diego Adult KD Collaborative Study. Results: Coronary artery aneurysms resulting from KD in childhood are associated with a high risk of thrombosis and stenosis at the inlet or outlet of the aneurysm. These aneurysms are often highly calcified and may contain a large thrombus burden that may obscure the true size of the aneurysm. Pitfalls in the management of these patients stem largely from failure to recognize the nature of the lesions, which leads to attempts to dilate highly calcified stenotic segments and undersizing of stents. Intravascular ultrasound is helpful in appreciating the true dimensions of the aneurysm, which may be filled with thrombus. Thrombolysis and use of anti-platelet agents followed by systemic anti-coagulation are appropriate management strategies for patients presenting with acute infarction. Bypass grafting with the internal thoracic arteries can be a successful strategy, but care must be taken to avoid competitive flow through the native vessel leading to graft failure. In contrast to the individuals who developed coronary artery aneurysms, young adults who had documented normal echocardiograms associated with their acute KD in childhood and who have no evidence of calcium deposition in the arterial wall as assessed by computed tomography (CT) calcium score appear to have no increased cardiovascular risk in the medium term. Long-term outcomes for adults post-KD in childhood are still being defined. Conclusions: KD poses special management challenges for the adult cardiologist who must recognize the unique features of the cardiovascular lesions in this growing population of patients.
                      Cover page: Management of sequelae of Kawasaki disease in adults
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