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Owing to the rapid advancements in artificial intelligence (AI) technologies, there has been increasing concern about how to promote the use of AI technologies in school settings to enhance students' learning performance. Teachers' intention to adopt AI tools in their classes plays a crucial role in this regard. Therefore, it is important to explore factors affecting teachers' intention to incorporate AI technologies or applications into course designs in higher education. In this study, a structural equation modeling approach was employed to investigate teachers' continuance intention to teach with AI. In the proposed model, 10 hypotheses regarding anxiety (AN), self-efficacy (SE), attitude towards AI (ATU), perceived ease of use (PEU) and perceived usefulness (PU) were tested, and this study explored how these factors worked together to influence teachers' continuance intention. A total of 311 teachers in higher education participated in the study. Based on the SEM analytical results and the research model, the five endogenous constructs of PU, PEU, SN, and ATU explained 70.4% of the changes in BI. In this model, SN and PEU were the determining factors of BI. The total effect of ATU was 0.793, followed by SE, with a total effect of 0.554. As a result, the intentions of teachers to learn to use AI-based applications in their teaching can be predicted by ATU, SE, PEU, PU and AN. Among them, teachers' SE positively influenced teachers' PEU and ATU towards adopting AI-based applications, and also influenced PU through PEU. In addition, the relationship between teachers' SE and AN was negatively correlated, which indicated that enhancing teachers' SE could reduce their AN towards using AI-based applications in their teaching. Accordingly, implications and suggestions for researchers and school teachers are provided.

This study aims to explore a data-driven cultural background fusion method to improve the accuracy of environmental art image classification. A novel Dual Kernel Squeeze and Excitation Network (DKSE-Net) model is proposed for the complex cultural background and diverse visual representation in environmental art images. This model combines the advantages of adaptive adjustment of receptive fields using the Selective Kernel Network (SKNet) and the characteristics of enhancing channel features using the Squeeze and Excitation Network (SENet). Constructing a DKSE module can comprehensively extract the global and local features of the image. The DKSE module adopts various techniques such as dilated convolution, L2 regularization, Dropout, etc. in the multi-layer convolution process. Firstly, dilated convolution is introduced into the initial layer of the model to enhance the original art image’s feature capture ability. Secondly, the pointwise convolution is constrained by L2 regularization, thus enhancing the accuracy and stability of the convolution. Finally, the Dropout technology randomly discards the feature maps before and after global average pooling to prevent overfitting and improve the model’s generalization ability. On this basis, the Rectified Linear Unit activation function and depthwise convolution are introduced after the second layer convolution, and batch normalization is performed to improve the efficiency and robustness of feature extraction. The experimental results indicate that the proposed DKSE-Net model significantly outperforms traditional Convolutional Neural Networks (CNNs) and other existing state-of-the-art models in the task of environmental art image classification. Specifically, the DKSE-Net model achieves a classification accuracy of 92.7%, 3.5 percentage points higher than the comparative models. Moreover, when processing images with complex cultural backgrounds, DKSE-Net can effectively integrate different cultural features, achieving a higher classification accuracy and stability. This enhancement in performance provides an important reference for image classification research based on the fusion of cultural backgrounds and demonstrates the broad potential of deep learning technology in the environmental art field.

Long noncoding RNAs act as crucial regulators in plenty of human cancers, yet their potential roles and molecular mechanisms in chemoresistance are poorly understood. This study showed that a novel lncRNA, long intergenic noncoding RNA 152 (Linc00152), promoted tumor progression and conferred resistance to oxaliplatin (L-OHP)-induced apoptosis in vitro and in vivo. It antagonized chemosensitivity through acting as a competing endogenous RNA to modulate the expression of miR-193a-3p, and then erb-b2 receptor tyrosine kinase 4 (ERBB4). Knockdown of ERBB4 in colon cancer cells decreased AKT phosphorylation, which resulted in decreased L-OHP resistance. Consistent with above findings, the specific AKT signaling inhibitor and activator were used, respectively, which demonstrated that Linc00152 contributed to L-OHP resistance at least partly through activating AKT pathway. Further studies indicated that Linc00152 was increased and appeared to be an independent prognostic factor for decreased survival and increased disease recurrence in stage II and III colon cancer patients undergoing L-OHP-based chemotherapy after surgery. Collectively, our findings established Linc00152 as a candidate prognostic indicator of outcome and drug responsiveness in colon cancer patients, and the involvement of competing endogenous RNAs mechanism in Linc00152/miR-193a-3p/ERBB4/AKT signaling axis may provide a novel choice in the investigation of drug resistance.

Cancer-associated fibroblasts (CAF) play a crucial role in tumor progression and immune regulation. However, the functional heterogeneity of CAFs remains unclear. Here, we identify antigen-presenting CAFs (apCAF), characterized by high MHC II expression, in gastric cancer (GC) tumors and find that apCAFs are preferentially located near tertiary lymphoid structures. Both in vivo and in vitro experiments demonstrate that apCAFs promote T cell activation and enhances its cytotoxic and proliferative capacities, thereby strengthening T cell-mediated anti-tumor immunity. Additionally, apCAFs facilitate the polarization of macrophages toward a pro-inflammatory phenotype. These polarized macrophages, in turn, promote the formation of apCAFs, creating a positive feedback loop that amplifies anti-tumor immune responses. Notably, baseline tumors in immunotherapy responders across various cancer types exhibit higher levels of apCAFs infiltration. This study advances the understanding of CAFs heterogeneity in GC and highlights apCAFs as a potential biomarker for predicting immunotherapy response in pan-cancer. The role of cancer associated fibroblasts (CAF) in immunotherapy response of gastric cancer (GC) is elusive. Here, by single cell sequencing, spatial transcriptomic and functional evaluation, the authors identify antigen-presenting CAF (apCAF) with high MHC II, which is correlated with immunotherapy responsiveness of GC patients.

Pyruvate kinase (PK) is a key enzyme that catalyzes the dephosphorylation of phosphoenolpyruvate (PEP) into pyruvate, and is responsible for the production of ATP during glycolysis. As another important isozyme of PK, pyruvate kinase M2 (PKM2) exists in cells with high levels of nucleic acid synthesis, such as normal proliferating cells (e.g., lymphocytes and intestinal epithelial cells), embryonic cells, adult stem cells, and tumor cells. With further research, PKM2, as an important regulator of cellular pathophysiological activity, has attracted increasing attention in the process of autoimmune response and inflammatory. In this re]view, we examine the contribution of PKM2 to the human immune response. Further studies on the immune mechanisms of PKM2 are expected to provide more new ideas and drug targets for immunotherapy of inflammatory and autoimmune diseases, guiding drug development and disease treatment.

Vascular repair is considered a key restorative measure to improve long-term outcomes after ischemic stroke. N 6 -methyladenosine (m 6 A), the most prevalent internal modification in eukaryotic mRNAs, functionally mediates vascular repair. However, whether circular RNA SCMH1 (circSCMH1) promotes vascular repair by m 6 A methylation after stroke remains to be elucidated. Here, we identify the role of circSCMH1 in promoting vascular repair in peri-infarct cortex of male mice and male monkeys after photothrombotic (PT) stroke, and attenuating the ischemia-induced m 6 A methylation in peri-infarct cortex of male mice after PT stroke. Mechanically, circSCMH1 increased the translocation of ubiquitination-modified fat mass and obesity-associated protein (FTO) into nucleus of endothelial cells (ECs), leading to m 6 A demethylation of phospholipid phosphatase 3 ( Plpp3 ) mRNA and subsequently the increase of Plpp3 expression in ECs. Our data demonstrate that circSCMH1 enhances vascular repair via FTO-regulated m 6 A methylation after stroke, providing insights into the mechanism of circSCMH1 in promoting stroke recovery. The mechanisms behind how vascular repair is regulated after ischemic stroke are yet to be elucidated. Here, the authors describe that a circular RNA interacts with FTO to promote vascular repair following stroke in mice and primates via mediating m6 A modification.

SexSy composite cathode materials, which offer superior theoretical capacity compared to pure selenium and improved electrochemical properties relative to pure sulfur, have aroused considerable interest in recent decades on account of their applications in electric vehicles and energy storage grids. In the current work, the feasibility of a Co@C2N monolayer as a promising host candidate for the cathode material of Li-SexSy batteries has been evaluated using first-principles calculations, and particular efforts have been devoted to underscoring the anchoring mechanism and catalytic performance of the Co@C2N monolayer. The pronounced synergistic effects of Co-S and Li-N bonds lead to increased anchoring performance for Li2SexSy/SexSy clusters on the surface of Co@C2N monolayer, which effectively inhibit the shuttle effect. The charge density difference and Mulliken charge analysis underscores a substantial charge transfer from the Li2SexSy and SexSy clusters to the Co@C2N monolayer, which indicates a noticeable chemical interaction between them. Further electronic property calculations show that the Co@C2N monolayer can improve the electrical conductivity of cathode materials for Li-SexSy batteries by maintaining semi-metallic characteristics after anchoring of Li2SexSy/SexSy clusters. Additionally, the catalytic performance of the Co@C2N monolayer is evaluated in terms of the reduction pathway of Se8 and the decomposition energy barrier of the Li2SeS cluster, which highlights the catalytic role of the Co@C2N monolayer in the formation and decomposition of the Li2SeS cluster during the cycle processes. Overall, the Co@C2N monolayer emerges as a promising host material and catalyst for Li-SexSy batteries with remarkable anchoring and catalytic performance.

Background The long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) has been reported to be overexpressed in colorectal cancer (CRC). However, its underlying mechanisms in the progression of CRC have not been well studied. Methods To investigate the clinical significance of NEAT1, we analyzed its expression levels in a publicly available dataset and in 71 CRC samples from Fudan University Shanghai Cancer Center. Functional assays, including the CCK8, EdU, colony formation, wound healing, and Transwell assays, were used to determine the oncogenic role of NEAT1 in human CRC progression. Furthermore, RNA pull-down, mass spectrometry, RNA immunoprecipitation, and Dual-Luciferase Reporter Assays were used to determine the mechanism of NEAT1 in CRC progression. Animal experiments were used to determine the role of NEAT1 in CRC tumorigenicity and metastasis in vivo. Results NEAT1 expression was significantly upregulated in CRC tissues compared with its expression in normal tissues. Altered NEAT1 expression led to marked changes in proliferation, migration, and invasion of CRC cells both in vitro and in vivo. Mechanistically, we found that NEAT1 directly bound to the DDX5 protein, regulated its stability, and sequentially activated Wnt signaling. Our study showed that NEAT1 indirectly activated the Wnt/β-catenin signaling pathway via DDX5 and fulfilled its oncogenic functions in a DDX5-mediated manner. Clinically, concomitant NEAT1 and DDX5 protein levels negatively correlated with the overall survival and disease-free survival of CRC patients. Conclusions Our findings indicated that NEAT1 activated Wnt signaling to promote colorectal cancer progression and metastasis. The NEAT1/DDX5/Wnt/β-catenin axis could be a potential therapeutic target of pharmacological strategies.

Background Patient perceived empathy plays a major role in establishing a good doctor–patient relationship. Therefore, this study explores the relationship among patient perceived empathy, quality of doctor-patient communication, and evaluation of the doctor-patient relationship while initially investigating the possible factors influencing patient perceived empathy. Methods We used the C-CARE scale, the C-SEGUE framework, and the C-PDRQ-15 scale to measure patient perceived empathy, ratings of doctor-patient communication quality, and ratings of patient-doctor relationships, respectively. A nationwide survey was conducted among 3039 patients, aged 18 to 92 years in China. Bootstrapped mediation analysis was performed. Results The age of the patient, the grade of hospital, and the consultation duration have significant differences in the scores of patient perceived empathy. There was a significantly positive correlation among patient's perceived empathy, doctor-patient communication, and doctor-patient relationship. Patient's perceived empathy can not only directly predict doctor-patient relationship , but also predict doctor-patient relationship through the mediating effect of doctor-patient communication. Conclusion Patient perceived empathy was related to age, hospital grade, and consultation duration. Patient perceived empathy can improve the doctor-patient relationship directly and can also optimize it indirectly via doctor-patient communication. The more empathy patients feel during medical interactions, the more positive their evaluation of the doctor-patient communication process and the more harmonious the doctor-patient relationship will be. Practice implications Emphasizing the importance of empathy in clinical encounters can facilitate effective doctor-patient communication and hence strengthen the doctor-patient relationship. Respecting and understanding patients is more important than providing professional medical advice when conveying empathy.

Neutrophil extracellular traps (NETs) can cause acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) by inducing macrophage pyroptosis. The purpose of this study was to find out whether pretreatment of alpha-linolenic acid (ALA) could inhibit NETs-induced macrophage pyroptosis in sepsis-induced ALI/ARDS, as well as to identify which inflammasome is involved in this process. LPS was instilled into the trachea to establish sepsis-induced ALI/ARDS in a mouse model. ​Lung injury was assessed by microscopic examination of lung tissue after hematoxylin and eosin staining, pathology score, and bronchoalveolar lavage fluid (BALF) total protein concentration. The level of NETs in lung tissue was detected by MPO-DNA ELISA. Purified NETs, extracted from peritoneal neutrophils, induced macrophage pyroptosis . Expression of pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC) and IL-1β in the lung tissue and bone marrow-derived macrophages (BMDMs) were determined by western blotting or ELISA. Specks of Pyrin/ASC were examined by confocal immunofluorescence microscopy. Mefv (Pyrin) mice were used to study the role of Pyrin in the process of sepsis-induced ALI/ARDS. ALA alleviated LPS-induced lung injury. ALA reduced the level of NETs, pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC), and IL-1β in the lung tissue of sepsis mice. , NETs increased the expression of pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC) and IL-1β significantly in BMDMs. Pyrin protein was found to be higher and form the inflammasome with ASC in NETs challenged-BMDMs. Knockout of Mefv (Pyrin) gene fully restored the increased expression of pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC) and IL-1β and . Lung injury was alleviated significantly in Mefv (Pyrin)-/- mice as well.​ ALA suppresses all the NETs-induced changes as mentioned above. Our study is the first to demonstrate Pyrin inflammasome driving NETs-induced macrophage pyroptosis, and ALA may reduce ALI/ARDS by inhibiting the activation of the Pyrin inflammasome-driven macrophage pyroptosis.