How fear of COVID-19 promotes posttraumatic growth during COVID-19 epidemic: A moderated mediation model.

OBJECTIVE: Recent studies have shown that the COVID-19 lockdown contributes to the psychological and physical stress of college students, who are forced to adjust to this tough time. The objective of this study was to explore how positive coping behaviors and fear of COVID-19 predicted posttraumatic growth (PTG) among Chinese college students in Wuhan during the latest lockdown. METHOD: Chinese college students in Wuhan (N = 982) aged 18-30 were recruited and completed an online survey, which assessed the fear of COVID-19, positive coping, reflective rumination, and PTG. RESULTS: Chinese college students reported high levels of PTG at the total scale (79.4%) and subdomains (83.7%). Fear of COVID-19 can not only directly influence PTG, but can also indirectly affect PTG through the mediating role of positive coping. Additionally, reflective rumination moderates the association between fear of COVID-19 and positive coping, whereby fear of COVID-19 promotes positive coping in college students with a higher level of reflective rumination. CONCLUSION: PTG in college students is the result of both positive behavior and reflective cognition during the COVID-19 pandemic in China. Therefore, in order to promote students' positive psychological changes, students should be encouraged to interpret situations positively and take proactive responses. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Apatinib regulates the growth of gastric cancer cells by modulating apoptosis and autophagy.

Apatinib is a novel, highly selective small-molecule inhibitor of the tyrosine kinase VEGFR-2. Although its safety and efficacy in the treatment of advanced gastric cancer (GC) and other solid tumors have been confirmed, the precise molecular mechanism underlying its efficacy remains unclear. The purpose of this study was to investigate the mechanism by which apatinib regulates the biological functions of GC cells in vitro. The CCK-8 assay was used to detect the inhibitory effect of apatinib at different concentrations on the proliferation of SGC7901 and MKN45 human GC cells. The effects of apatinib on apoptosis, autophagy, and cell cycle-related genes in SGC7901 and MKN45 cells were detected by Western blotting and real-time quantitative PCR (RT-qPCR). JC-1 staining, flow cytometry, Hoechst 33342 staining, dansylcadaverine (MDC) staining, and Transwell assays were used to detect the effects of apatinib on apoptosis, the cell cycle, autophagy, and invasion and migration capacities, respectively, in SGC7901 and MKN45 cells. The inhibitory effect of apatinib on the proliferation of GC cells was dependent on concentration. Apatinib significantly promoted apoptosis and autophagy. It also altered the cell cycle distribution and inhibited the invasion and migration of GC cells. In general, apatinib inhibited the proliferation of GC cells by promoting apoptosis and autophagy, regulating the cell cycle and inhibiting the invasion and migration capacities of GC cells.

Role, function and regulation of the thymocyte selection-associated high mobility group box protein in CD8+ T cell exhaustion.

Thymocyte selection-associated high mobility group box protein (TOX), a member of the high-motility group box (HMG) protein superfamily, is an evolutionarily conserved DNA-binding protein. It functions as a transcription factor that modulates transcriptional programs by binding to DNA in a structure-dependent manner. It has been well established that TOX is required for the development of CD4+ T cells, natural killer (NK) cells and innate lymphoid cells (ILCs), as well as the autoimmunity mediated by CD8+ T cells. Recently, emerging evidence supports an essential role for TOX in the induction of T cell exhaustion in the setting of tumor or chronic viral infection by mediating transcriptional and epigenetic changes, which are cardinal hallmarks of exhausted T cells. Moreover, TOX plays a key role in the persistence of antigen-specific T cells and in the mitigation of tissue damage caused by immunopathology over the course of tumorigenesis and chronic infection. Additionally, TOX contributes to the high level of programmed cell death protein 1 (PD-1) on the cell surface by participating in the process of endocytic recycling of PD-1. In this review, we summarize the most recent information about the role of TOX in the process of T cell exhaustion, which enriches our understanding of the molecular mechanisms of CD8+ T cell exhaustion upon chronic antigen stimulation and reveals promising therapeutic targets for persisting infection and cancer.