The mediating effect of bullying on parental-peer support matching and NSSI behaviour among adolescents.

BACKGROUND: Being subjected to bullying is a significant risk factor for non-suicidal self-injury (NSSI) among adolescents. Parental support, peer support, and social connectedness play protective roles in mitigating NSSI in this population. However, the precise impact of the combined effects of parental and peer support on bullying and NSSI requires further investigation. METHODS: This study employed the Child and Adolescent Social Support Scale, Delaware Bullying Victimisation Scale, Social Connectedness Scale, and the Ottawa Self-Injury Inventory to survey 1277 Chinese adolescents. Polynomial regression analysis and response surface analysis were applied to examine the mediating role of bullying and social connectedness in the relationship between parental and peer support matching and NSSI. RESULTS: The results indicate that parental support (r = 0.287, P < 0.001), peer support (r = 0.288, P < 0.001), and social connectedness (r = 0.401, P < 0.001) were protective factors against NSSI in adolescents. Conversely, bullying (r = 0.425, P < 0.001) acts as a risk factor for NSSI in this population. Adolescents with low parental and peer support experienced more bullying than those with high parental and peer support, while those with low parental but high peer support experienced less bullying than those with high parental but low peer support (R^2 = 0.1371, P < 0.001). Social connectedness moderated the effect between bullying and NSSI in this model (ß = 0.006, P < 0.001). LIMITATIONS: Due to the under-representation of participants and lack of longitudinal data support, the explanatory power of causality between variables was limited. Future studies should include national samples and incorporate longitudinal studies to enhance the generalisability and robustness of the findings. CONCLUSION: This study reveals the influence mechanism of parental and peer support matching experienced by adolescents on bullying and NSSI and the moderating role of social connectedness. These findings enrich the developmental theory of adolescent NSSI and provide reference for the prevention and intervention of adolescent NSSI behaviour.

The Future of TCR-like Antibodies in Diagnosis and Potential Application Targets.

The human leukocyte antigen (HLA, also known as the major histocompatibility complex or MHC) system, is responsible for immune monitoring of the intracellular proteome of all nucleated cells. The presentation of antigen peptides separates malignant or infected cells from their healthy counterparts and forms aberrant cells tagged as the foundation for identification. Therefore, peptide-MHC molecules can give potential diagnostic targets for cancer or infection. TCR-like antibodies recognize specific peptides that bind to MHC molecules, allowing them to target Such inaccessible cytoplasmic or nuclear tumors or virus-associated antigens. It binds to MHC, presenting peptides found on the surface of target cells. These antibodies have shown promising clinical applications in diagnosing and imaging cancer and infected cells. This review presents the current situation of TCR-like antibodies and its prospects for application in the field of intracellular antigen diagnostics. It also lists the potential application targets of TCR, like antibodies in various disease diagnoses, providing valuable information for developing diagnostic reagents and selecting targets in the future.

The Impact of Academic Pressure and Peer Support on Adolescents' Loneliness: A Polynomial Regression and Response Surface Analysis.

Purpose: To explore the impact of the match between academic pressure and peer support on adolescents' sense of loneliness and examine whether social connectedness played a mediating role, using a polynomial regression and response surface analysis. Methods: A questionnaire survey was conducted with 1277 adolescents from two cities in Sichuan Province, China, to investigate their academic pressure, peer support, social connectedness, and sense of loneliness. Results: (1) Adolescents' sense of loneliness positively correlated with their level of academic pressure and negatively correlated with their degree of peer support. (2) Social connectedness played a mediating role in the relationship between academic pressure, peer support, and sense of loneliness. (3) Adolescents with high academic pressure and low peer support had weaker social connectedness than those with low academic pressure and high peer support. (4) Adolescents with high academic pressure and high peer support had stronger social connectedness than those with low academic pressure and low peer support. Discussion: The study revealed the mechanism through which a match (or mismatch) between academic pressure and peer support influenced adolescents' sense of loneliness and validated the mediating role of social connectedness. The study enriches the developmental theory of adolescent loneliness and provides research experience for future interventions targeting adolescent loneliness.

The Effect of Loneliness on Non-Suicidal Self-Injury Behavior in Chinese Junior High School Adolescents: A Moderated Mediation Model.

Purpose: This study explore the interaction between loneliness and non-suicidal self-injury behaviors (hereinafter "NSSI"), and to further examine the mediating role of self-control and the moderating role of social connection. Methods: A total of 414 junior high school students (age 14.05±0.84) in Sichuan province in China were investigated on their loneliness, self-control, social connection and NSSI by questionnaire. Results: (1) there was a significant positive correlation between loneliness and NSSI; (2) self-control played a mediating role in the relationship between loneliness and NSSI; and (3) after controlling for gender, family structure, and family economic level, the social connectedness played a moderating role in the relationship between loneliness and NSSI, as well as between self-control and NSSI. Conclusion: The results verify the relationship between loneliness and NSSI, expands and deepens the internal logical relationship between them, and provides a reference that can be used in the future for the prevention and intervention of NSSI in adolescents.

Interfacial Characteristics and Mechanical Properties of CuSn15/HT250 Prepared via Additive Manufacturing Combined with an Inconel 718 Interlayer.

Tremendous discrepancies in the positive enthalpy of mixing and the coefficient of thermal expansion emerge between the copper alloy and the gray cast iron, accounting for numerous pores and cracks in the interfacial region during the metallurgical bonding process. To enhance the interfacial bonding properties of these two refractory materials, laser-directed energy deposition was applied to fabricate the CuSn15 alloy on the HT250 substrate; meanwhile, Inconel 718 alloy, acting as the interlayer, was added to their bonding region. Firstly, the effect of the deposition process on deposition layer quality was investigated, and then the effects of Inconel 718 addition on the interfacial morphology, element distribution, phase composition, bonding strength, microhardness were studied. The results showed that a substrate (HT250) without cracks and a deposition layer (CuSn15) free from pores could be obtained via parameter optimization combined with preheating and slow cooling processes. Adding the Inconel 718 interlayer eliminated the interfacial pores and cracks, facilitated interfacial element (Cu, Fe, Ni) diffusion, and enhanced interfacial bonding strength. The interface between HT250 and CuSn15 mainly contained the FeSn2 phase, while the interfaces of the CuSn15-Inconel 718 and the Inconel 718-HT250 were mainly composed of the Ni3Sn4, Cr5Si3, FeSi2, Cr7C3. The microhardness and fracture morphology of the interfacial region in the samples with and without the interlayer were also studied. Finally, CuSn15 was also successfully deposited on the surface of the HT250 impeller with large size and complex structure, which was applied in the root blower.

High Expression of ABRACL Is Associated with Tumorigenesis and Affects Clinical Outcome in Gastric Cancer.

BACKGROUND: The ABRA C-terminal like (ABRACL) protein belongs to a novel family of low-molecular weight proteins that increase actin dynamics and cell motility. It is involved in various diseases including cancer; however, its role in gastric cancer is unclear. In this study, the expression of ABRACL in gastric cancer and its relationships with patients' clinicopathological features and survival are examined. METHODS: Sample expression profiles were downloaded from the Gene Expression Omnibus database and the Cancer Genome Atlas. ABRACL expression at the protein level in normal gastric and gastric cancer tissues was compared by using immunohistochemistry staining data provided by the Human Protein Atlas. Correlations between ABRACL expression and clinicopathological features are analyzed by chi-square tests. Patient survival was evaluated by Kaplan-Meier analysis. RESULTS: ABRACL expression is upregulated in gastric cancer tissues than in normal tissues. High ABRACL levels indicated a poor prognosis. ABRACL expression (low ABRACL, n = 96; high ABRACL, n = 96) in gastric cancer tissues (primary data from GSE15459) is significantly correlated with poor overall survival (χ2 = 4.078, p = 0.043; log-rank test). ABRACL protein levels (low ABRACL, n = 172, high ABRACL, n = 171) in gastric cancer tissues (primary data from www.kmplot.com ) are significantly correlated with poor overall survival (χ2 = 4.305, p = 0.038, log-rank test). CONCLUSIONS: Our results indicate that ABRACL is highly expressed in gastric cancer and is a potential prognostic marker and therapeutic target for this disease.

MicroRNA­339­5p inhibits cell proliferation of acute myeloid leukaemia by directly targeting SOX4.

In recent decades, microRNAs (miRNAs) have been considered novel gene regulators. Dysregulated miRNAs serve crucial roles in the formation and progression of acute myeloid leukaemia (AML). Therefore, the roles of differentially expressed miRNAs in AML require extensive investigation to obtain insight into the treatment of patients with AML. The present study demonstrated significant miR­339­5p downregulation in AML samples and cell lines. miR­339­5p overexpression attenuated AML cell proliferation by inducing cell cycle arrest and promoting cell apoptosis. Additionally, sex­determining region Y­related high­mobility group box 4 (SOX4) was identified as a direct target gene of miR­339­5p in AML. Furthermore, SOX4 expression was significantly upregulated in AML samples; this upregulation was inversely correlated with the expression levels of miR­339­5p. Additionally, a series of rescue experiments demonstrated that SOX4 resumption reversed the effects of miR­339­5p overexpression on cell proliferation, cycle status and apoptosis of AML. In conclusion, miR­339­5p may serve its antiproliferative role in AML by directly targeting SOX4, which suggests that miR­339­5p may be considered an effective novel therapeutic target for treating patients with such an aggressive haematological malignancy.

miR-126 Suppresses Invasion and Migration of Malignant Glioma by Targeting Mature T Cell Proliferation 1 (MTCP1).

BACKGROUND The aim of this study was to assess the utility of miR-126 in promoting malignant glioma progression and determine if miR-126 might be a target for malignant glioma treatment. MATERIAL AND METHODS The expression of miR-126 in malignant glioma tissues and cells was detected by reverse transcription polymerase chain reaction (RT-PCR). Western blot analysis was used to detect changes in protein levels. Transwell assay was applied to assess the migration and invasion in vitro. Luciferase reporter assay was used to confirm the binding of miR-126 and mature T cell proliferation 1 (MTCP1). A nude mouse tumor model was used to assess the molecular mechanism in vivo. RESULTS The expression level of miR-126 in patients with stage III~IV malignant glioma was significant lower than that in patients with stage I~II. In different malignant glioma cell lines, the expression was significantly reduced in U87MG. Compared with the control mimics group, the expression of MTCP1 was significantly decreased. The results of Transwell assay showed that the invasiveness and migration in the miR-126 mimics group was significantly lower than in the control mimics groups. miR-126 mimics did not affect luciferase activity in the Mut-miR-126/MTCP1 group, while miR-126 mimics reduced luciferase activity by 54% in the Wt-miR-126/MTCP1 group. The results of invasion showed that the invasion ability in the miR-126 inhibitor group was significantly increased compared with that in the normal control (NC) group, while the invasion and migration abilities in the MTCP1 siRNA group were significantly increased. After 6 weeks, the tumor volume in the miR-126 inhibitor group was significantly increased, while that in the MTCP1 siRNA group was significantly decreased. CONCLUSIONS miR-126 inhibits the migration of malignant glioma cells by inhibiting MTCP1.

miR-15b Inhibits the Progression of Glioblastoma Cells Through Targeting Insulin-like Growth Factor Receptor 1.

The microRNAs (miRNAs) have been suggested as a tumor suppressor in recent years. miR-15b was reported to exert an anti-oncogenic role in the proliferation, migration, and invasion of diverse tumor cells. However, the mechanisms underlying miR-15b-mediated biology of glioblastoma are still unclear. In the present study, the expression of miR-15b was down-regulated in glioblastoma tumor tissues and U87 and U251 cells, but insulin-like growth factor receptor 1 (IGF1R) expression became up-regulated in these tumor tissues and cells (all p < 0.001). Furthermore, IGF1R expression was inversely associated with miR-15b expression. Notably, patients with lower miR-15b expression have a much shorter survival period compared with high expression (log-rank test p = 0.045). In vitro data demonstrated that miR-15b mimics inhibited the proliferation, cell cycle arrest, and invasion of U87 and U251 cells. Besides, we validated IGF1R as a direct target of miR-15b using dual luciferase assays, and IGF1R plasmids partially abrogated miR-15b mimics inhibited cell proliferation. In vivo, miR-15b mimics indeed repressed cell proliferation in mouse xenograft model. In conclusion, our study demonstrated that miR-15b inhibits the progression of glioblastoma cells through targeting IGF1R, and miR-15b can be recommended as a tumor suppressor in the progression of glioblastoma.

MicroRNA-490-3p regulates cell proliferation and apoptosis by targeting HMGA2 in osteosarcoma.

MicroRNA-490-3p (miR-490-3p) has been implicated in several human malignancies; however, its potential functions and the underlying molecular mechanisms in osteosarcoma progression remain largely unclear. Here, we showed that miR-490-3p was down-regulated in osteosarcoma cell lines. Ectopic expression of miR-490-3p decreased cell proliferation, induced G1 arrest and apoptosis in vitro and inhibited tumorigenicity in a mouse xenograft model. Furthermore, miR-490-3p bound directly to HMGA2 mRNA 3'UTR and mediated a decrease in HMGA2 mRNA and protein expression. Re-expression of HMGA2 reversed the inhibitory effects of miR-490-3p. Further investigations showed an inverse correlation between low miR-490-3p and high HMGA2 expression in osteosarcoma tissues. Taken together, our results suggest that miR-490-3p functions as a potential tumor suppressor by down-regulating HMGA2 expression directly, and it may represent a potential therapeutic target for patients with osteosarcoma.

Hugl-1 inhibits glioma cell growth in intracranial model.

Drosophila lethal (2) giant larvae (lgl) has been reported as a tumor suppressor and could regulate the Drosophila hippo signaling. Human giant larvae-1(Hugl-1), one human homologue of Drosophila lgl, also has been reported to be involved in the development of some human cancers. However, whether Hugl-1 is associated with the pathogenesis of malignant gliomas remains poorly understood. In the present work, we examined the effect of Hugl-1 on glioma cell growth both in vitro and in vivo. Firstly, we found that Hugl-1 protein levels decreased in the human glioma tissues, suggesting that Hugl-1 is involved in glioma progression. Unfortunately, either stably or transiently over-expressing Hugl-1 did not affect glioma cell proliferation in vitro. In addition, Hugl-1 over-expression did not regulate hippo signaling pathway. Interestingly, over-expression of Hugl-1 not only inhibited gliomagenesis but also markedly inhibited cell proliferation and promoted the apoptosis of U251 cells in an orthotopic model of nude mice. Taken together, this study provides the evidence that Hugl-1 inhibits glioma cell growth in intracranial model of nude mice, suggesting that Hugl-1 might be a potential tumor target for glioma therapy.