Background The COVID-19 pandemic has made unprecedented impact on the psychological health of university students, a population vulnerable to distress and mental health disorders. This study investigated psychiatric symptoms (anxiety, depression, and traumatic stress) during state-enforced quarantine among university students in China (N = 1912) through a cross-sectional survey during March and April 2020. Results Psychiatric symptoms were alarmingly prevalent: 67.05% reported traumatic stress, 46.55% had depressive symptoms, and 34.73% reported anxiety symptoms. Further, 19.56% endorsed suicidal ideation. We explored risk and protective factors of psychological health, including demographic variables, two known protective factors for mental health (mindfulness, perceived social support), four COVID-specific factors (COVID-19 related efficacy, perceived COVID-19 threat, perceived COVID-19 societal stigma, COVID-19 prosocial behavior) and screen media usage. Across symptom domains, mindfulness was associated with lower symptom severity, while COVID-19 related financial stress, perceived COVID-19 societal stigma, and perceived COVID-19 threat were associated with higher symptom severity. COVID-19 threat and COVID-19 stigma showed main and interactive effects in predicting all mental health outcomes, with their combination associated with highest symptom severity. Screen media device usage was positively associated with depression. Female gender and COVID-19 prosocial behavior were associated with higher anxiety, while COVID-19 self-efficacy associated with lower anxiety symptoms. Conclusions Findings suggest high need for psychological health promotion among university students during the COVID-19 pandemic and inform an ecological perspective on the detrimental role of stigma during an emerging infectious disease outbreak. Interventions targeting multi-level factors, such as promoting mindfulness and social support at individual and interpersonal levels while reducing public stigma about COVID-19, may be particularly promising. Attending to the needs of disadvantaged groups including those financially impacted by COVID-19 is needed.

Aim: Recent studies have underlined causative links between microRNA (miRNA) deregulation and cancer development. However, the relevance of abnormally expressed miRNA to tumor biology has not been well understood in hepatocellular carcinoma (HCC).Methods: A bead-based miRNA expression profiling method was performed on 20 pairs of surgically removed HCC and adjacent non-tumorous tissue (NT). Special miR-338 downregulations and miR-338 associated with clinical characteristics was validated in an extended samples set of 36 paired HCC and adjacent non-tumorous liver tissues by real-time reverse transcription polymerase chain reaction (RT-PCR) analysis.Results: Out of our bead-based microarray data, 12 upregulated and 19 downregulated miRNA were found to be associated with HCC. Further characterization of miRNA-338, in which 20 pairs of the samples were clustered clearly into two groups according to expression of miR-338, revealed that the level of miR-338 expression can be associated with clinical aggressiveness, such as, tumor size, tumor-node-metastasis stage, vascular invasion and intrahepatic metastasis. These results were validated by real-time RT-PCR analysis. Conclusion:Our study suggests that miRNA expression could have relevance to the clinical behavior of HCC and that the bead-based miRNA expression profiling method might be a suitable system to assay miRNA expression in large-scale diagnostic trails.

MicroRNAs are involved in human carcinogenesis and cancer progression. Our previous study has shown that loss of miR-338-3p expression is associated with clinical aggressiveness of hepatocellular carcinoma (HCC). However, the exact roles and mechanisms of miR-338-3p remain unknown in HCC. To determine whether and how miR-338-3p influences liver cancer cell invasion, we studied miR-338-3p in the liver cancer cell lines, and we found that miR-338-3p is down-regulated in treated cells. Forced expression of miR-338-3p in SK-HEP-1 cells suppressed cell migration and invasion, whereas inhibition of miR-338-3p in SMMC-7721 cells induced cell migration and invasion. Furthermore, smoothened (SMO) was identified as a direct target of miR-338-3p. Forced expression of miR-338-3p down-regulated SMO and matrix metalloproteinase (MMP)-9 expression, but inhibition of miR-338-3p up-regulated SMO and MMP9 expression. However, small interfering RNA targeted SMO reversed the effects induced by blockade of miR-338-3p. SMO and MMP9 were overexpressed and associated with invasion and metastasis in HCC tissues. These data indicate that miR-338-3p suppresses cell invasion by targeting the smoothened gene in liver cancer in vitro and miR-338-3p might be a novel potential strategy for liver cancer treatment.

This randomized controlled trial evaluated the effect of a mindfulness-based mobile health (mHealth) intervention, tailored to the pandemic context, among young adult students (N = 114) with elevated anxiety and/or depressive symptoms during quarantine in China, compared to a time-and attention-matched social support-based mHealth control. At baseline, postintervention (1 month), and 2-month follow-up, participants completed self-reports of primary outcomes (anxiety and depression), secondary outcomes (mindfulness and social support), and emotional suppression as a culturally relevant mechanism of change. Feasibility and acceptability were also evaluated. Using intent-to-treat (ITT) analysis, linear mixed effects models showed that compared to social support mHealth, mindfulness mHealth had a superior effect on anxiety ( p = .024, between-group d = 0.72). Both conditions improved on depression (baseline-to-FU ds > 1.10, between-group difference not significant, d = 0.36 favoring mindfulness). There was an interaction of Emotional suppression reduction × Condition in the improvement of anxiety and depression.

Background: Circular RNAs (circRNAs) represent a class of non-coding RNAs (ncRNAs) which are widely expressed in mammals and tissue-specific, of which some could act as critical regulators in the atherogenesis of cerebrovascular disease. However, the underlying mechanisms by which circRNA regulates the ectopic phenotype of endothelial cells (ECs) in atherosclerosis remain largely elusive. Methods: CCK-8, transwell, wound healing and Matrigel assays were used to assess cell viability, migration and tube formation. QRT-qPCR and Immunoblotting were used to examine targeted gene expression in different groups. The binding sites of miR-370-3p (miR-370) with TGFβR2 or hsa_circ_0003204 (circ_0003204) were predicted using a series of bioinformatic tools, and validated using dual luciferase assay and RNA immunoprecipitation (RIP) assay. The localization of circ_0003204 and miR-370 in ECs were investigated by fluorescence in situ hybridization (FISH). Gene function and pathways were enriched through Metascape and gene set enrichment analysis (GSEA). The association of circ_0003204 and miR-370 in extracellular vesicles (EVs) with clinical characteristics of patients were investigated using multiple statistical analysis. Results: Circ_0003204, mainly located in the cytoplasm of human aorta endothelial cells (HAECs), was upregulated in the ox-LDL-induced HAECs. Functionally, the ectopic expression of circ_0003204 inhibited proliferation, migration and tube formation of HAECs exposed to ox-LDL. Mechanically, circ_0003204 could promote protein expression of TGFβR2 and its downstream phosph-SMAD3 through sponging miR-370, and miR-370 targeted the 3′ untranslated region (UTR) of TGFβR2. Furthermore, the expression of circ_0003204 in plasma EVs was upregulated in the patients with cerebral atherosclerosis, and represented a potential biomarker for diangnosis and prognosis of cerebrovascular atherogenesis. Conclusions: Circ_0003204 could act as a novel stimulator for ectopic endothelial inactivation in atherosclerosis and a potential biomarker for cerebral atherosclerosis.

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Background: N6-methyladenosine (m6A) methylation, a well-known modification with new epigenetic functions, has been reported to participate in gastric cancer (GC) tumourigenesis, providing novel insights into the molecular pathogenesis of GC.However, the involvement of Wilms' tumour 1-associated protein (WTAP), a key component of m6A methylation, in GC progression is controversial. Here, we investigated the biological role and underlying mechanism of WTAP in GC. Methods: We determined WTAP expression using tissue microarrays and The CancerGenome Atlas (TCGA) data set, which was used to construct co-expression networks by weighted gene co-expression network analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Database for Annotation, Visualization and Integrated Discovery (DAVID). CIBERSORT was used to determine WTAP expression in 22 immune cell types. Results:Wilms' tumour 1-associated protein was highly expressed in GC, which indicated a poor prognosis, and WTAP expression served as an independent predictor of GC survival. By WGCNA, GO, KEGG and core gene survival analyses, we found that high WTAP expression correlated with RNA methylation and that low expression correlated with a high T cell-related immune response. CIBERSORT was used to correlate low WTAP expression with T lymphocyte infiltration. Conclusion: RNA methylation and lymphocyte infiltration are the main causes of high WTAP expression and poor prognosis, respectively. K E Y W O R D S differentially expressed genes, DNA methylation, gastric cancer, N6-methyladenosine (m6A) methylation, WTAP | 4453 LI et aL.