Background The mental health of students is affected by COVID-19. We aim to evaluate the anxiety and depression symptoms among college students during COVID-19 pandemic, analyze the influence factors that contribute to college students’ anxiety and depression symptoms, and provide some suggestions for improving the mental health of college students. Methods With 179 college students participating, an online questionnaire consisting of a general questionnaire, Generalized Anxiety Disorder (GAD-7), and Patient Health Questionnaire (PHQ-9) was conducted in universities in Shanghai. The anxiety and depression symptoms among college students were evaluated using GAD-7 and PHQ-9 scales, and influence factors were analyzed using an unordered multi-class Logistic regression model. Results The reliability and validity of the GAD-7 and PHQ-9 scales were good (reliability ≥ 0.9, validity = 100%). The incidence of anxiety was 32.4%, of which were 23.5%, 8.4%, and 0.6% in mild, moderate, and severe, respectively; and the incidence of depression was 46.40%, of which in mild, moderate, moderate to severe, and severe were 28.5%, 10.1%, 7.3%, and 0.6%, respectively. Multivariate analysis revealed that male students with strong psychological quality, who were not easily affected by the COVID-19 pandemic, who received less negative or false information, and who had a strong grasp of psychology and related knowledge were less likely to suffer from mild or moderate anxiety symptoms [OR (95% CI) 0.18 (0.04, 0.81), 0.12 (0.05, 0.33), 0.23 (0.06, 0.89) and 0.07 (0.01, 0.74)]. Furthermore, college students who were not affected by the COVID-19 pandemic were less likely to suffer from mild, moderate, and moderate to severe depression symptoms [OR (95% CI) 0.23 (0.08, 0.65), 0.22 (0.05, 0.93), 0.10 (0.02, 0.54)]. Conclusion The GAD-7 and PHQ-9 scales are suitable for evaluating anxiety and depression symptoms in college students. The COVID-19 pandemic was associated with a high incidence of anxiety and depression symptoms among college students, although gender and mental state fluctuations during the pandemic, negative and false information, and exposure to psychology and related courses were the main influencing factors.
Objectives Chemokines have been suggested to play significant roles in the progression of malignant cancers. This study aimed to identify the chemokines related to malignant progression in thyroid carcinoma. Methods The mRNA expression levels of 52 chemokines were compared between differentiated thyroid cancer (DTC) samples and normal thyroid tissues from The Cancer Genome Atlas database; survival analysis was then performed on the basis of differentially expressed chemokines. A retrospective study was conducted on the level of differentially expressed chemokines in 76 DTC patients. Functional pathway analysis was performed to explore chemokine-related regulatory mechanisms. Results We identified 20 chemokines with differentially expressed mRNA levels through publicly available data. High levels of CCL22 and CCL26 were found to be related with metastasis in clinical DTC samples. High levels of CCL22 were found to be significantly related to poor prognosis in DTC patients. Pathway analyses revealed that cytokines might affect cancer progression through cytokine-cytokine receptor and cytokine-interleukin interactions. Conclusions CCL22 and CCL26 could serve as prognostic biomarkers in thyroid carcinoma.
PLA2R1 is a novel gene that is aberrantly expressed in a variety of malignancies. However, the role and mechanism of PLA2R1 in thyroid cancer has not been elucidated. We aimed to uncover the underlying mechanism of PLA2R1 in thyroid cancer. We collected 115 clinical specimens, including 54 tumor tissues and 61 para-cancerous tissues, who underwent surgical treatment at Shanghai Tenth Hospital. Immunohistochemical staining was used to evaluate PLA2R1 expression in differentiated thyroid cancer (DTC) tissues. The thyroid cancer cell lines 8505c and FTC133 transfected with PLA2R1 overexpression or knockdown plasmids were used for CCK8 assays and a wound healing assay. Next, we conducted coimmunoprecipitation (Co-IP) experiments and western blotting to explore the underlying mechanism of PLA2R1 in regulating the growth of thyroid cancer. We discovered that the expression of PLA2R1 was lower in the tumor tissues than in para-cancerous tissues (χ2 = 37.0, p < 0.01). The overexpression of PLA2R1 significantly suppressed thyroid cancer cell proliferation and migration, and both of these effects were partially attenuated by the knockdown of PLA2R1. Furthermore, the in vivo growth of DTC could be alleviated by the knockdown of PLA2R1. The mechanistic study revealed that PLA2R1 competed with FN1 for binding to ITGB1, inhibiting the FAK axis and epithelial-mesenchymal transition (EMT). We speculate that PLA2R1 might be a promising marker and a novel therapeutic target for thyroid cancer.
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