ABSTRACT
In order to better understand the impact of COVID-19 on the free-floating bike-sharing (FFBS) system and the potential role of FFBS played in the pandemic period, this study explores the impact mechanism of travel frequency of FFBS users before and after the pandemic. Using the online questionnaire collected in Nanjing, China, we first analyze the changes of travel frequency, travel distance, and travel duration in these two periods. Then, two ordered logit models are applied to explore the contributing factors of the weekly trip frequency of FFBS users before and after COVID-19. The results show that: (1) While the overall travel duration and travel distance of FFBS users decreased after the pandemic, the trip frequency of FFBS users increased as the travel duration increased. (2) Since COVID-19, attitude perception variables of the comfort level and the low travel price have had significantly positive impacts on the weekly trip frequency of FFBS users. (3) Respondents who use FFBS as a substitution for public transport are more likely to travel frequently in a week after the outbreak of COVID-19. (4) The travel time in off-peak hours of working days, weekends, and holidays has a significantly positive correlation with the trip frequency of FFBS users. Finally, several relevant policy recommendations and management strategies are proposed for the operation and development of FFBS during the similar disruptive public health crisis.
ABSTRACT
OBJECTIVES: Coronavirus disease 2019 (COVID-19) is an acute respiratory infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 can damage the myocardium directly, or activate the immune system, trigger a cytokine storm, and cause inflammatory cells to infiltrate the myocardial tissue and damage the myocardium. This study is based on the sequencing data to analyze the changes in gene expression of cardiomyocytes and macrophages after SARS-CoV-2 infection, and explore the potential effects of SARS-CoV-2 on the heart and immune system. METHODS: The public data set GSE151879 was retrieved. The online software Network Analyst was used to preprocess the data, and the differentially expressed genes (DEGs) [log2(fold change)>2, adjusted P-value<0.05] screening between the infection group and the control group in cardiomyocytes, human embryonic stem cell-derived cardiomyocytes, and macrophages were screened. Consistent common differentially expressed genes (CCDEGs) with the same expression pattern in cardiomyocytes and macrophages were obtained, and the online analysis software String was used to conduct enrichment analysis of their biological functions and signal pathways. Protein-protein interaction network, transcription factor-gene interaction network, miRNA-gene interaction network and environmental chemical-gene interaction network were established, and Cytoscape 3.72 was used to perform visualization. RESULTS: After data standardization, the data quality was excellent and it can ensure reliable results. Myocardial cell infection with SARS-CoV-2 and gene expression spectrum were changed significantly, including a total of 484 DEGs in adult cardiomyoblasts, a total of 667 DEGs in macrophages, and a total of 1 483 DEGs in human embryo source of cardiomyopathy. The Stum, mechanosensory transduction mediator homolog (STUM), dehydrogenase/reductase 9 (DHRS9), calcium/calmodulin dependent protein kinase II beta (CAMK2B), claudin 1(CLDN1), C-C motif chemokine ligand 2 (CCL2), TNFAIP3 interacting protein 3 (TNIP3), G protein-coupled receptor 84 (GPR84), and C-X-C motif chemokine ligand 1 (CXCL1) were identical in expression patterns in 3 types of cells. The protein-protein interaction suggested that CAMK2B proteins may play a key role in the antiviral process in 3 types of cells; and silicon dioxide (SiO2), benzodiazepine (BaP), nickel (Ni), and estradiol (E2) affect anti-SARS-CoV-2 processes of the 3 types of cells. CONCLUSIONS: CAMK2B, CLDN1, CCL2, and DHRS9 genes play important roles in the immune response of cardiomyocytes against SARS-CoV-2. SiO2, BaP, Ni, E2 may affect the cell's antiviral process by increasing the toxicity of cardiomyocytes, thereby aggravating SARS-CoV-2 harm to the heart.