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INTRODUCTION: The outbreak of COVID-19 has significantly impacted travel behavior. However, few studies have analyzed the impact of COVID-19 on adolescent travel behavior. This article analyzed the impact of COVID-19 on adolescent travel behavior using questionnaire survey data. METHODS: This paper first used confirmatory factor analysis (CFA) to explore the psychological factors related to the adolescents' perceptions about the severity of COVID-19. The study then established a logit model to study the effects of COVID-19 in different phases (before, during, and after the epidemic peak), demographic characteristics, and the role of psychological factors on their travel behavior. RESULTS: The results show that the phase of COVID-19 did not significantly impact the adolescents' choice of short-distance travel. The frequency of outings per week, the number of exercise sessions per week, and willingness to travel by public transportation decreased significantly in the outbreak phase. Meanwhile, the perception of the severity of COVID-19 significantly impacted adolescent travel behavior. CONCLUSION: This research demonstrates that COVID-19 has led adolescents to reduce their frequency of outings, and they try not to use public transportation. Adolescents appear to be traveling more cautiously in the outbreak phase and the post-epidemic phase.
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The Ankyrin repeat domain 49 (ANKRD49) is an evolutionarily conserved protein, which is related to mediate protein-protein interaction. However, the function of ANKRD49 in human glioma remains elusive. Mining through The Cancer Genome Atlas (TCGA) database, we found that the expression of ANKRD49 was increased in glioma tissues and that high expression of ANKRD49 was strongly associated with high disease grade and poor overall survival. To investigate the role of ANKRD49 in malignant glioma, lentivirus expressing shRNA targetting ANKRD49 was constructed in U251 and U87 malignant glioma cells. We demonstrated that ANKRD49 knockdown reduced the proliferation rate of U251 and U87 cells. Further mechanism analysis indicated that depletion of ANKRD49 led to the cell-cycle arrest and induced apoptosis in U251 and U87 cells. ANKRD49 knockdown also changed the expression of key effectors that are involved in stress response, cell cycle, and apoptosis, including p-HSP27 (heat shock protein 27), p-Smad2 (SMAD family member 2), p-p53, p-p38, p-MAPK (mitogen-activated protein kinase), p-SAPK/JNK (stress-activated protein kinase/c-jun n-terminal kinase), cleveagated Caspase-7, p-Chk1 (checkpoint kinase 1), and p-eIF2a (eukaryotic translation initiation factor 2a). Taken together, our findings implicate that ANKRD49 promotes the proliferation of human malignant glioma cells. ANKRD49 maybe an attractive target for malignant glioma therapy.