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1.
Front Psychol ; 13: 847522, 2022.
Article in English | MEDLINE | ID: covidwho-1952611

ABSTRACT

Purpose: COVID-19 pandemic is a significant threat toward the public health. However, the discussion of the mechanism of media literacy's effect in fighting against pandemic is limited. Thus, this study aims to explore the mechanism with a sociocognitive perspective. Methods: A survey was administrated to 420 college students in China. PROCESS macro of SPSS was applied to analyze the data and test the moderated mediation effect. Results: The moderated mediation model of media literacy, proxy efficacy, self-efficacy, and official media use was tested and supported. Official media use was a negative moderator on the association between media literacy and proxy efficacy. Conclusion: The study explored the media literacy's role as a determinant of proxy efficacy and self-efficacy, which contributed to the sociocognitive theory.

2.
Frontiers in psychology ; 13, 2022.
Article in English | EuropePMC | ID: covidwho-1871273

ABSTRACT

Purpose COVID-19 pandemic is a significant threat toward the public health. However, the discussion of the mechanism of media literacy’s effect in fighting against pandemic is limited. Thus, this study aims to explore the mechanism with a sociocognitive perspective. Methods A survey was administrated to 420 college students in China. PROCESS macro of SPSS was applied to analyze the data and test the moderated mediation effect. Results The moderated mediation model of media literacy, proxy efficacy, self-efficacy, and official media use was tested and supported. Official media use was a negative moderator on the association between media literacy and proxy efficacy. Conclusion The study explored the media literacy’s role as a determinant of proxy efficacy and self-efficacy, which contributed to the sociocognitive theory.

3.
Nat Cell Biol ; 23(12): 1314-1328, 2021 12.
Article in English | MEDLINE | ID: covidwho-1559292

ABSTRACT

The lung is the primary organ targeted by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), making respiratory failure a leading coronavirus disease 2019 (COVID-19)-related mortality. However, our cellular and molecular understanding of how SARS-CoV-2 infection drives lung pathology is limited. Here we constructed multi-omics and single-nucleus transcriptomic atlases of the lungs of patients with COVID-19, which integrate histological, transcriptomic and proteomic analyses. Our work reveals the molecular basis of pathological hallmarks associated with SARS-CoV-2 infection in different lung and infiltrating immune cell populations. We report molecular fingerprints of hyperinflammation, alveolar epithelial cell exhaustion, vascular changes and fibrosis, and identify parenchymal lung senescence as a molecular state of COVID-19 pathology. Moreover, our data suggest that FOXO3A suppression is a potential mechanism underlying the fibroblast-to-myofibroblast transition associated with COVID-19 pulmonary fibrosis. Our work depicts a comprehensive cellular and molecular atlas of the lungs of patients with COVID-19 and provides insights into SARS-CoV-2-related pulmonary injury, facilitating the identification of biomarkers and development of symptomatic treatments.


Subject(s)
COVID-19/genetics , Lung/metabolism , Transcriptome/genetics , Alveolar Epithelial Cells/metabolism , Alveolar Epithelial Cells/pathology , Alveolar Epithelial Cells/virology , COVID-19/metabolism , Fibrosis/metabolism , Fibrosis/pathology , Fibrosis/virology , Humans , Lung/pathology , Lung/virology , Proteomics/methods , SARS-CoV-2/pathogenicity
4.
Natl Sci Rev ; 7(12): 1868-1878, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-1087785

ABSTRACT

Systematic autopsy and comprehensive pathological analyses of COVID-19 decedents should provide insights into the disease characteristics and facilitate the development of novel therapeutics. In this study, we report the autopsy findings from the lungs and lymphatic organs of 12 COVID-19 decedents-findings that evaluated histopathological changes, immune cell signature and inflammatory factor expression in the lungs, spleen and lymph nodes. Here we show that the major pulmonary alterations included diffuse alveolar damage, interstitial fibrosis and exudative inflammation featured with extensive serous and fibrin exudates, macrophage infiltration and abundant production of inflammatory factors (IL-6, IP-10, TNFα and IL-1ß). The spleen and hilar lymph nodes contained lesions with tissue structure disruption and immune cell dysregulation, including lymphopenia and macrophage accumulation. These findings provide pathological evidence that links injuries of the lungs and lymphatic organs with the fatal systematic respiratory and immune malfunction in critically ill COVID-19 patients.

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