The Healthy Context Paradox Between Bullying and Emotional Adaptation: A Moderated Mediating Effect.

Introduction: Bullying is a significant concern for young people, with studies consistently showing a link between bullying and negative emotional consequences. However, the mechanisms that underlie this association remain unclear, particularly in terms of the classroom environment. This study aimed to explore the paradoxical phenomenon between bullying victimization and emotional adaptation among junior high school students in China, using the hypothesis of the healthy context paradox. Methods: The study involved 880 students (565 girls; Mage=14.69; SD=1.407 years), and data were collected using self-reported surveys. The findings of the study, utilizing multilevel structural equation modeling (MSEM) techniques, demonstrated a cross-level moderated effect of classroom-level bullying victimization on the relationship between individual bullying victimization and emotional adaptation. Results: Specifically, the results indicated that in classrooms with higher levels of victimization, the association between individual bullying victimization and increased depressive symptoms and State&Trait anxiety was more pronounced. These findings support the "Healthy context paradox" hypothesis in the Chinese context and provide insight into the mechanisms underlying this phenomenon. Discussion: The results suggest that the classroom environment plays a crucial role in shaping the emotional consequences of bullying and that addressing classroom victimization is crucial for promoting emotional health among young people. By understanding the mechanisms that underlie the association between bullying and emotional consequences, interventions can be developed to target the underlying factors that contribute to this paradoxical phenomenon. Overall, the study provides new insights into the complex relationship between bullying and emotional health among young people, highlighting the importance of considering the classroom environment in addressing this issue.

Clinical application of three-dimensional T1-weighted BrainVIEW in magnetic resonance imaging of cerebral venous thrombosis: a case report and literature review.

To date, there is no clinical scoring system or laboratory indicator that can rule out cerebral venous thrombosis (CVT) or provide diagnostic proof for evaluating post-treatment thrombosis recanalization during follow-up. We therefore explored an imaging method for quantitative assessment of CVT and assessed thrombotic changes during follow-up. A patient presented with severe posterior occipital distension extending to the top of the forehead and an elevated plasma D-dimer (DD2) level. Computed tomography and pre-contrast-enhanced magnetic resonance imaging revealed only a small amount of cerebral hemorrhage. Three-dimensional (3D) T1-weighted (T1W) BrainVIEW pre-contrast-enhanced magnetic resonance scanning showed subacute thrombosis in the venous sinus, and the post-contrast-enhanced scan combined with volume rendering reconstruction showed cerebral thrombosis of the venous sinus and allowed for measurement of the thrombus volume. On days 30 and 60 of post-treatment follow-up, post-contrast-enhanced scans showed progressive reduction of the thrombus volume as well as recanalization and fibrotic flow voids in the chronic thrombosis. 3D T1W BrainVIEW was helpful to observe the size of the thrombi and the situation of venous sinus recanalization during the follow-up after clinical treatment of CVT. This technique can reflect the imaging manifestations of CVT throughout the whole process to guide clinical treatment decisions.

Peste des petits ruminants virus hemagglutinin (H) induces lysosomal degradation of host cyclophilin A to facilitate viral replication.

Peste des petits ruminants virus (PPRV) is a highly contagious disease that affects sheep and goats. To better understand PPRV replication and virulence, cyclophilin A (CypA), a multifunctional goat host protein, was selected for further studies. CypA has been reported to inhibit or facilitate viral replication. However, the precise roles of CypA during PPRV infection remain unclear. Our data show for the first time that CypA suppressed PPRV replication by its PPIase activity, and PPRV infection decreased CypA protein levels. Detailed analysis revealed that PPRV H protein was responsible for the reduction of CypA, which was dependent on the lysosome pathway. No interaction was identified between H and CypA. Furthermore, the 35-58 region of H was essential for the reduction of CypA. In conclusion, our findings identify the antiviral role of CypA against PPRV and provide key insights into how PPRV H protein antagonizes host antiviral response.

LncRNA MALAT1 up-regulates VEGF-A and ANGPT2 to promote angiogenesis in brain microvascular endothelial cells against oxygen-glucose deprivation via targetting miR-145.

Stroke is one of the leading causes of death and long-term disability around the world. Angiogenesis is supposed to protect brain microvascular endothelial cells (BMECs) from oxidative and ischemic stress. Previous studies indicated that interaction between metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and miR-145 was involved in myocardial ischemia reperfusion, suggesting MALAT1 and miR-145 were also mediated with the progress of angiogenesis and cell migration in oxygen-glucose deprivation (OGD)-induced BMECs. The present study aimed to investigate the functional roles of MALAT1 in regulating miR-145 and its downstream pro-angiogenesis factors, vascular endothelial growth factor (VEGF)-A and Angiopoietin-2 (ANGPT2) during the progress of angiogenesis in OGD-induced BMECs. An in vitro OGD model was employed in mouse BMECs to mimic brain hypoxic and ischemic conditions; MTT was used to determine cell viability. qRT-PCR was used to determine the expression of long non-coding RNA (lncRNA)-MALAT1 and miR-145 under OGD conditions; in vitro tube formation assay was used to investigate angiogenic effect of MALAT1 and miR-145 The relationship between lncRNA-MALAT1/miR-145 and miR-145/VEGF-A/ANGPT2 was evaluated by qRT-PCR and Western blot, and direct binding was assessed using dual luciferase assay. Results showed that the levels of lncRNA-MALAT1 and miR-145 were up-regulated in OGD-induced BMECs. miR-145 functioned as an anti-angiogenic and pro-apoptotic factor in OGD treated BMECs via down-regulating VEGF-A and ANGPT2 directly. While lncRNA-MALAT1 enhanced the expressions of VEGF-A and ANGPT2 by targetting miR-145 to promote angiogenesis and proliferation of BMECs under OGD conditions. Our present study revealed the inhibitory functions of miR-145 on angiogenesis through direct targetting on VEGF-A and ANGPT2 for the first time and proved the protective role of lncRNA-MALAT1 for BMECs under OGD conditions through the direct regulation of miR-145.

The regulation of survival and differentiation of neural stem cells by miR-124 via modulating PAX3.

MicroRNAs (miRNAs) have crucial functions in the regulation of proliferation and differentiation of neural stem cells (NSCs). MiR-124 has been reported to be implicated in neurogenesis. However, the precise function and mechanism of miR-124 still need further verification. In this study, we identified paired box 3 (PAX3) as a potential target of miR-124 using bioinformatics approaches. Next, we found PAX3 had reversed expression pattern with miR-124 as well as TUBB3 and GFAP. Dual-luciferase assay showed that miR-124 could bind to the 3'-UTR of PAX3 mRNA and restrain its expression. It was demonstrated that overexpression and knocking down of miR-124 in NSCs could promote the survival and suppress the apoptosis of NSCs. Meanwhile, miR-124 enhanced the expression of TUBB3 and GFAP via impairing PAX3 expression. Mechanistic study revealed that augmented Akt-GSK3ß signaling pathway was the driving-force for the regulatory functions of miR-124 in NSCs. In summary, this study for the first time uncovered that miR-124 could suppress PAX3 expression, which in turn regulated the differentiation of NSCs.