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      <src>https://socictopen.socict.org/files/original/1f298a1106fa82cd314a1d85d0bb48a9.pdf</src>
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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Coronavirus</text>
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            <name>Description</name>
            <description>An account of the resource</description>
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                <text>Dominio científico: Coronavirus</text>
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    <name>Text</name>
    <description>A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.</description>
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        <element elementId="50">
          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation</text>
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          <name>Creator</name>
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              <text>Jaideep Chakladar, Wei  Tse Li, Weg  M. Ongkeko, Abby  C. Lee, Chengyu Chen, Eric  Y. Chang, Jessica Wang-Rodriguez</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>The COVID-19 pandemic caused by the SARS-CoV-2 virus, overlaps with the ongoing epidemics of cigarette smoking and electronic cigarette (e-cig) vaping. However, there is scarce data relating COVID-19 risks and outcome with cigarette or e-cig use. In this study, we mined three independent RNA expression datasets from smokers and vapers to understand the potential relationship between vaping/smoking and the dysregulation of key genes and pathways related to COVID-19. We found that smoking, but not vaping, upregulates ACE2, the cellular receptor that SARS-CoV-2 requires for infection. Both smoking and use of nicotine and flavor-containing e-cigs led to upregulation of pro-inflammatory cytokines and inflammasome-related genes. Specifically, chemokines including CCL20 and CXCL8 are upregulated in smokers, and CCL5 and CCR1 are upregulated in flavor/nicotine-containing e-cig users. We also found genes implicated in inflammasomes, such as CXCL1, CXCL2, NOD2, and ASC, to be upregulated in smokers and these e-cig users. Vaping flavor and nicotine-less e-cigs, however, did not lead to significant cytokine dysregulation and inflammasome activation. Release of inflammasome products, such as IL-1B, and cytokine storms are hallmarks of COVID-19 infection, especially in severe cases. Therefore, our findings demonstrated that smoking or vaping may critically exacerbate COVID-19-related inflammation or increase susceptibility to COVID-19.</text>
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          <name>Date</name>
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              <text>2020</text>
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          <name>Subject</name>
          <description>The topic of the resource</description>
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              <text>covid-19, SARS-CoV-2, ACE2, tobacco, electronic cigarettes, Vaping</text>
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          <name>Identifier</name>
          <description>An unambiguous reference to the resource within a given context</description>
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              <text>10.3390/ijms21155513</text>
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          <name>Source</name>
          <description>A related resource from which the described resource is derived</description>
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              <text>Epidemiology and Health</text>
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          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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              <text>Korean Society of Epidemiology</text>
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          </elementTextContainer>
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        <element elementId="38">
          <name>Coverage</name>
          <description>The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant</description>
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              <text>Biology (General), Chemistry</text>
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