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Sports events conducted in conjunction with the curriculum may serve as a supportive factor in the development of social integration among adolescents attending school. The aim of this study is to examine how adolescent participation in various sports activities, specifically football, volleyball, athletics, and tennis, affects their level of social integration and social engagement. The study involved 400 adolescents (aged 13–15) from a single school in Ukraine. Data were collected using the Social Integration Scale (SIS-A) and the Social Engagement Scale (SCE-A), which were specifically developed for this research. The study employed a pre-test/post-test design with control and intervention groups over the course of one academic year. The results indicate that sports-based interventions were associated with improvements in social integration, with a significant increase in SIS-A scores across the four sports subgroups ( p  = .000), whereas the control group showed no significant changes. However, no significant improvements in social engagement were found in any group, including those involved in sports. This suggests that while sport may support social integration, it does not necessarily contribute to broader civic participation, particularly in the absence of explicit civic education or community-oriented activities within the intervention. The highest observed effects were in the football subgroup. Volleyball participation led to moderate improvements in social integration, while individual sports (e.g., athletics, tennis) had comparatively smaller effects. These findings underscore the importance of distinguishing between different dimensions of social development and highlight the need for more targeted approaches to enhance civic engagement among adolescents. The present results indicate that participation in sports events can contribute to social integration, although such effects should be interpreted with consideration of contextual and methodological limitations.

The high incidence of heart failure secondary to myocardial infarction (MI) has been difficult to effectively address. MI causes strong aseptic inflammation, and infiltration of different immune cells and changes in the local inflammatory microenvironment play a key regulatory role in ventricular remodeling. Therefore, the possibility of improving the prognosis of MI through targeted immunity has been of interest and importance in MI. However, previously developed immune-targeted therapies have not achieved significant success in clinical trials. Here, we propose that the search for therapeutic targets from different immune cells may be more precise and lead to better clinical translation. Specifically, this review summarizes the role and potential therapeutic targets of various immune cells in ventricular remodeling after MI, especially monocytes/macrophages and neutrophils, as a way to demonstrate the importance and potential of immunomodulatory therapies for MI. In addition, we analyze the reasons for the failure of previous immunomodulatory therapies and the issues that need to be addressed, as well as the prospects and targeting strategies of using immune cells to drive novel immunomodulatory therapies, hoping to advance the development of immunomodulatory therapies by providing evidence and new ideas.

Targeted integration of transgenes can be achieved by strategies based on homologous recombination （HR）, mi- crohomology-mediated end joining （MMEJ） or non-homologous end joining （NHEJ）. The more generally used HR is inefficient for achieving gene integration in animal embryos and tissues, because it occurs only during cell division, although MMEJ and NHEJ can elevate the efficiency in some systems. Here we devise a homology-mediated end joining （HMEJ）-based strategy, using CRISPR/Cas9-mediated cleavage of both transgene donor vector that contains guide RNA target sites and -800 bp of homology arms, and the targeted genome. We found no significant improve- ment of the targeting efficiency by the HMEJ-based method in either mouse embryonic stem cells or the neuroblas- toma cell line, N2a, compared to the HR-based method. However, the HMEJ-based method yielded a higher knock- in efficiency in HEK293T cells, primary astrocytes and neurons. More importantly, this approach achieved transgene integration in mouse and monkey embryos, as well as in hepatocytes and neurons in vivo, with an efficiency much greater than HR-, NHEJ- and MMEJ-based strategies. Thus, the HMEJ-based strategy may be useful for a variety of applications, including gene editing to generate animal models and for targeted gene therapies.

In recent years, the hydroacoustic communication MAC (Medium Access Control) protocol has attracted wide attention. Hydroacoustic communication networks suffer from issues such as long propagation delays and rapid dynamic changes in network load, which prevent the maximization of network performance through the use of a single transmission mode. In this paper, we propose a Dynamic Switching Transmission MAC protocol called the DSTM-MAC protocol. Firstly, the protocol realizes the design of dynamic switching transmission mode by adapting to changes in network load, introduces a more accurate model for total system delay, and computes parameters such as the switching threshold L and the optimal fixed contention window. Secondly, it carries out parameter design for different transmission modes and realizes dynamic concurrent transmission based on these modes, ultimately achieving the goal of maximizing network performance improvement. Finally, experiments demonstrate that the DSTM-MAC protocol surpasses the traditional DCF protocol in terms of end-to-end delay and system throughput.

Proprioception and touch serve as complementary sensory modalities to coordinate hand kinematics and recognize users’ intent for precise interactions. However, current motion-tracking electronics remain bulky and insufficiently precise. Accurately decoding both is also challenging owing to the mechanical crosstalk of endogenous and exogenous deformations. Here, we report a hyperconformal dual-modal (HDM) metaskin for interactive hand motion interpretation. The metaskin integrates a strongly coupled hydrophilic interface with a two-step transfer strategy to minimize interfacial mechanical losses. The 10-μm-scale hyperconformal film is highly sensitive to intricate skin stretches while minimizing signal distortion. It accurately tracks skin stretches as well as touch locations and translates them into polar signals, which are individually salient. This approach enables a differentiable signaling topology within one single data channel without burdening structural complexity to the metaskin. When combined with temporal differential calculations and time-series machine learning network, the metaskin extracts interactive context and action cues from the low-dimensional data. This phenomenon is further exemplified through demonstrations in contextual navigation, typing and control integration, and multi-scenario object interaction. We demonstrate this fundamental approach in advanced skin-integrated electronics, highlighting its potential for instinctive interaction paradigms and paving the way for augmented somatosensation recognition. It is challenging to effectively translate and separate complementary somatosensory information. Here, the authors present a hyperconformal metaskin that decodes hand motion and touch directly from the skin in an imperceptible way, enabling intent recognition for applications in navigation and manipulation.

Skin cutaneous melanoma (SKCM) is the world's fourth deadliest cancer, and advanced SKCM leads to a poor prognosis. Novel biomarkers for SKCM diagnosis and prognosis are urgently needed. Long non-coding RNAs (lncRNAs) provide various biological functions and have been proved to play a significant role in tumor progression. Single-cell RNA sequencing (scRNA-seq) enables genome analysis at the single-cell level. This study explored prognostic lncRNAs in SKCM based on scRNA-seq and bulk RNA sequencing data. The TCGA cohort and melanoma samples in the GEO database (GSE72056, GSE19234, GSE15605, GSE7553, and GSE81383) were included in this study. Marker genes were filtered, and ensemble lncRNAs were annotated. The clinical significance of selected lncRNAs was verified through TCGA and GEO dataset analysis. SiRNA transfection, wound-healing and transwell assays were performed to evaluate the effect of PRRT3-AS1 on cellular function. Immune infiltration of the selected lncRNAs was also exhibited. A 5-marker-lncRNAs model of significant prognostic value was constructed based on GSE72056 and the TCGA cohort. PRRT3-AS1 combined with DANCR was then found to provide significant prognostic value in SKCM. PRRT3-AS1 was filtered for its higher expression in more advanced melanoma and significant prognosis value. Cellular function experiments revealed that PRRT3-AS1 may be required for cancer cell migration in SKCM. PRRT3-AS1 was found to be related to epithelial-mesenchymal transition (EMT) signaling pathways. DNA methylation of PRRT3-AS1 was negatively related to PRRT3-AS1 expression and showed significant prognosis value. In addition, PRRT3-AS1 may suppress immune infiltration and be involved in immunotherapy resistance. PRRT3-AS1 may be a diagnostic and prognostic biomarker of SKCM.

Colorectal cancer (CRC) is the third most common malignant tumor worldwide, with high recurrence and metastasis rates significantly impacting outcomes. This study explores the role of FBXO6, a ubiquitination-related protein, in regulating CRC malignancy, particularly cell migration and invasion. Our analysis reveals that higher FBXO6 expression correlates with better prognosis in CRC patients, although its expression decreases in advanced-stage tumors. Functional studies demonstrate that FBXO6 overexpression suppresses the invasive and migratory abilities of HCT116 and RKO cells and reduces single-cell colony formation. In contrast, FBXO6 knockdown promotes these malignant traits. Immunoprecipitation and mass spectrometry analyses identified ITGB1 as a key substrate of FBXO6, with potential prognostic relevance in CRC. Subsequent in vitro assays confirmed this interaction, revealing that FBXO6 binds ITGB1 at its glycoprotein recognition site, thereby reducing ITGB1 stability and attenuating downstream FAK/PI3K/AKT/ERK signaling. ITGB1 overexpression counteracts the suppressive effects of FBXO6, restoring downstream signaling activity. In vivo xenograft models further validate these findings: FBXO6 overexpression reduces tumor growth, Ki67 levels, and ITGB1-associated signaling. Additional rescue experiments show that FBXO6 counteracts the tumor-promoting effects of ITGB1 overexpression. In conclusion, FBXO6 suppresses CRC cell proliferation, migration, and invasion by targeting ITGB1 for ubiquitination and disrupting key oncogenic signaling pathways, thereby supporting its potential as a prognostic biomarker and candidate therapeutic target in CRC.

M-type phospholipase A2 receptor (PLA2R) is the major autoantigen in adult idiopathic membranous nephropathy (IMN). Although reactive epitopes in the PLA2R domains have been identified, the clinical value of these domains recognized by anti-PLA2R antibodies remains controversial. Accordingly, this study aimed to quantitatively detect changes in the concentrations of different antibodies against epitopes of PLA2R in patients with IMN before and after treatment to evaluate the clinical value of epitope spreading. Highly sensitive time-resolved fluorescence immunoassay was used to quantitatively analyze the concentrations of specific IgG and IgG4 antibodies against PLA2R and its epitopes (CysR, CTLD1, CTLD6-7-8) in a cohort of 25 patients with PLA2R-associated membranous nephropathy (13 and 12 in the remission and non-remission groups, respectively) before and after treatment, and the results were analyzed in conjunction with clinical biochemical indicators. The concentration of specific IgG (IgG4) antibodies against PLA2R and its epitopes (CysR, CTLD1 and CTLD6-7-8) in non-remission group was higher than that in remission group. The multipliers of elevation of IgG (IgG4) antibody were 5.6(6.2) fold, 3.0(24.3) fold, 1.6(9.0) fold, and 4.2(2.6) fold in the non-remission/remission group, respectively. However, the difference in antibody concentrations between the two groups at the end of follow-up was 5.6 (85.2), 1.7 (13.1), 1.0 (5.1), and 1.5 (22.3) times higher, respectively. When detecting concentrations of specific IgG antibodies against PLA2R and its different epitopes, the remission rate was 66.67% for only one epitope at M0 and 36.36% for three epitopes at M0. When detecting concentrations of specific IgG4 antibodies against PLA2R and its different epitopes, the remission rate was 100.00% for only one epitope at M0 and 50.00% for three epitopes at M0. A trivariate logistic regression model for the combined detection of eGFR, anti-CTLD678 IgG4, and urinary protein had an AUC of 100.00%. Low concentrations of anti-CysR-IgG4, anti-CTLD1-IgG4, and anti-CTLD6-7-8-IgG4 at initial diagnosis predict rapid remission after treatment. The use of specific IgG4 against PLA2R and its different epitopes combined with eGFR and urinary protein provides a better assessment of the prognostic outcome of IMN.