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This study explores the influence of the Internet of Things (IoT) and Artificial Intelligence (AI)-enhanced learning models on student management in educational informatization management. A game-theoretic enhanced learning model is proposed to achieve this objective, incorporating resource scheduling strategies under fog computing and a student management system that integrates IoT and AI technologies. This model’s performance and the student management system are then tested. The results indicate that the fog computing-based hierarchical Q-learning (Q) model proposed in this study achieves faster convergence than a single Q model, reaching convergence after 80 training rounds, ten rounds earlier than the comparative algorithm. The model exhibits a lower average workload delay of 0.5 ms and fog node delay below 1 ms, showcasing significant advantages in terms of overall cost-effectiveness, thus minimizing service costs. The student management system has 3000 concurrent user connections, static page request times ranging from 0 to 25 s, login response time predominantly at 60 s, and a capacity to process up to 20 parallel tasks per second with zero errors. The system functionalities are fully realized, meeting usage demands effectively and achieving the highest average functional score of 9.03 for online interaction functionality. This study demonstrates the efficacy of the game-theoretic enhanced learning model in a fog computing environment and the positive impact of IoT and AI technologies on student management. The proposed student management system better caters to individual student needs, enhancing learning outcomes and experiences. The study's innovation lies in the integration of IoT technology with AI-enhanced learning models, coupled with the introduction of game-theoretic resource scheduling strategies, enabling the student management system to intelligently identify student requirements, allocate learning resources, and dynamically optimize the educational process, ultimately improving learning outcomes. This holds significant implications for enhancing education quality and promoting personalized student development.

Tannic acid (TA), a high-molecular-weight polyphenol, is used as a hemostasis spray and unguent for trauma wound remedy in traditional medical treatment. However, the use of tannic acid on a large-area wound would lead to absorption poisoning. In this work, a TA coating was assembled on a quartz/silicon slide, or medical gauze, via chelation interaction between TA and Fe3+ ions and for further use as a hemostasis dressing. Protein adsorption on the TA coating was further investigated by fluorescence signal, ellipsometry analysis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The adsorbed bovine serum albumin (BSA), immunoglobulin G (IgG) and fibrinogen (Fgn) on the TA coating was in the manner of monolayer saturation adsorption, and fibrinogen showed the largest adsorption. Furthermore, we found the slight hemolysis of the TA coating caused by the lysed red blood cells and adsorption of protein, especially the clotting-related fibrinogen, resulted in excellent hemostasis performance of the TA coating in the blood clotting of an animal wound. Thus, this economic, environmentally friendly, flexible TA coating has potential in medical applications as a means of preparing novel hemostasis materials.

Activation of MAVS, an adaptor molecule in Rig-I-like receptor (RLR) signaling, is indispensable for antiviral immunity, yet the molecular mechanisms modulating MAVS activation are not completely understood. Ubiquitination has a central function in regulating the activity of MAVS. Here, we demonstrate that a mitochondria-localized deubiquitinase USP18 specifically interacts with MAVS, promotes K63-linked polyubiquitination and subsequent aggregation of MAVS. USP18 upregulates the expression and production of type I interferon following infection with Sendai virus (SeV) or Encephalomyocarditis virus (EMCV). Mice with a deficiency of USP18 are more susceptible to RNA virus infection. USP18 functions as a scaffold protein to facilitate the re-localization of TRIM31 and enhances the interaction between TRIM31 and MAVS in mitochondria. Our results indicate that USP18 functions as a post-translational modulator of MAVS-mediated antiviral signaling. Ubiquitination has an important function in the regulation of antiviral immunity involving the signalling molecule MAVS. Here the authors investigate deubiquitinating enzymes and show USP18 regulates MAVS mediated antiviral signalling through modulating the ubiquitination of MAVS via promotion of interaction between MAVS and TRIM31.

BRD4 is well known for its role in super-enhancer organization and transcription activation of several prominent oncogenes including c-MYC and BCL2. As such, BRD4 inhibitors are being pursued as promising therapeutics for cancer treatment. However, drug resistance also occurs for BRD4-targeted therapies. Here, we report that BRD4 unexpectedly interacts with the LSD1/NuRD complex and colocalizes with this repressive complex on super-enhancers. Integrative genomic and epigenomic analyses indicate that the BRD4/LSD1/NuRD complex restricts the hyperactivation of a cluster of genes that are functionally linked to drug resistance. Intriguingly, treatment of breast cancer cells with a small-molecule inhibitor of BRD4, JQ1, results in no immediate activation of the drug-resistant genes, but long-time treatment or destabilization of LSD1 by PELI1 decommissions the BRD4/LSD1/NuRD complex, leading to resistance to JQ1 as well as to a broad spectrum of therapeutic compounds. Consistently, PELI1 is up-regulated in breast carcinomas, its level is negatively correlated with that of LSD1, and the expression level of the BRD4/LSD1/NuRD complex–restricted genes is strongly correlated with a worse overall survival of breast cancer patients. Together, our study uncovers a functional duality of BRD4 in superenhancer organization of transcription activation and repression linking to oncogenesis and chemoresistance, respectively, supporting the pursuit of a combined targeting of BRD4 and PELI1 in effective treatment of breast cancer.

Toxic amyloid-beta (Aβ) plaque and harmful inflammation are two leading symptoms of Alzheimer’s disease (AD). However, precise AD therapy is unrealizable due to the lack of dual-targeting therapy function, poor BBB penetration, and low imaging sensitivity. Here, we design a near-infrared-II aggregation-induced emission (AIE) nanotheranostic for precise AD therapy. The anti-quenching emission at 1350 nm accurately monitors the in vivo BBB penetration and specifically binding of nanotheranostic with plaques. Triggered by reactive oxygen species (ROS), two encapsulated therapeutic-type AIE molecules are controllably released to activate a self-enhanced therapy program. One specifically inhibits the Aβ fibrils formation, degrades Aβ fibrils, and prevents the reaggregation via multi-competitive interactions that are verified by computational analysis, which further alleviates the inflammation. Another effectively scavenges ROS and inflammation to remodel the cerebral redox balance and enhances the therapy effect, together reversing the neurotoxicity and achieving effective behavioral and cognitive improvements in the female AD mice model. Toxic amyloid-beta plaque and harmful inflammation are two leading hallmarks of Alzheimer’s disease (AD), and precise AD therapy is elusive due to the lack of dual-targeting therapy function, limited blood-brain barrier penetration, and low imaging sensitivity. Here, the authors address these issues by designing a near-infrared-II aggregation-induced emission nanotheranostic for precise AD therapy.

How the carbohydrate binding protein galectin-3 might act as a diabetogenic and tumorogenic factor remains to be investigated. Here we report that intracellular galectin-3 interacts with Rag GTPases and Ragulator on lysosomes. We show that galectin-3 senses lipopolysaccharide (LPS) to facilitate the interaction of Rag GTPases and Ragulator, leading to the activation of mTORC1. We find that the lipopolysaccharide/galectin-3-Rag GTPases/Ragulator-mTORC1 axis regulates a cohort of genes including GLUT1 , and HK2 , and PKM2 that are critically involved in glucose uptake and glycolysis. Indeed, galectin-3 deficiency severely compromises LPS-promoted glycolysis. Importantly, the expression of HK2 is significantly reduced in diabetes patients. In multiple types of cancer including hepatocellular carcinoma (HCC), galectin-3 is highly expressed, and its level of expression is positively correlated with that of HK2 and PKM2 and negatively correlated with the prognosis of HCC patients. Our study unravels that galectin-3 is a sensor of LPS, an important modulator of the mTORC1 signaling, and a critical regulator of glucose metabolism. The carbohydrate binding protein galectin-3 has been linked to diabetes and cancer. Here, authors show that galectin-3 is a sensor of LPS, an important modulator of the mTORC1 signaling, and a critical regulator of glucose metabolism.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has quickly spread worldwide and has affected more than 10 million individuals. A typical feature of COVID-19 is the suppression of type I and III interferon (IFN)-mediated antiviral immunity. However, the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive. Here, we reported that the SARS-CoV-2 membrane (M) protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway mediated by RIG-I/MDA-5–MAVS signaling. In addition, the SARS-CoV-2 M protein suppresses type I and III IFN induction stimulated by SeV infection or poly (I:C) transfection. Mechanistically, the SARS-CoV-2 M protein interacts with RIG-I, MAVS, and TBK1, thus preventing the formation of the multiprotein complex containing RIG-I, MAVS, TRAF3, and TBK1 and subsequently impeding the phosphorylation, nuclear translocation, and activation of IRF3. Consequently, ectopic expression of the SARS-CoV-2 M protein facilitates the replication of vesicular stomatitis virus. Taken together, these results indicate that the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling, which subsequently attenuates antiviral immunity and enhances viral replication. This study provides insight into the interpretation of SARS-CoV-2-induced antiviral immune suppression and illuminates the pathogenic mechanism of COVID-19.

Abiotic stressors, particularly saline-alkali stress, restrict plant growth and development. , which grows in coastal areas and exhibits high saline-alkali tolerance, serves as an ideal model for analyzing rose response mechanisms to saline-alkali stress (SAS). However, its response mechanisms have not yet been elucidated. This study examined SAS using a 150 mmol·L saline-alkali solution and analyzed the physiological and molecular response mechanisms using physiological and biochemical indicators and high-throughput RNA-sequencing technology. Under SAS, reactive oxygen species accumulation increased, resulting in extensive oxidative damage to cell membranes. In response, the superoxide dismutase, peroxidase, and catalase activities, along with the contents of soluble sugars, soluble proteins, and proline increased. Furthermore, 325, 2,197, 4,266, and 6,842 differentially expressed genes (DEGs) were identified at 6, 12, 24, and 48 h of SAS, respectively. Functional annotation and pathway enrichment analyses indicated that DEGs were primarily involved in cell wall organization, enzyme activity, biosynthesis of secondary metabolites, and photosynthesis pathways. Several structural genes from the phenylpropanoid biosynthesis pathway, including , , , , , , , and , were identified by qRT-PCR, which positively responded to SAS and peaked at 12 h. Weighted gene co-expression network analysis revealed that likely functions as the hub gene in the secondary metabolic pathway responding to SAS. This study advances understanding of saline-alkali resistance mechanisms, and the identified genes and metabolic pathways can enhance future rose breeding efforts.

As a highly pathogenic human coronavirus, SARS-CoV-2 has to counteract an intricate network of antiviral host responses to establish infection and spread. The nucleic acid-induced stress response is an essential component of antiviral defense and is closely related to antiviral innate immunity. However, whether SARS-CoV-2 regulates the stress response pathway to achieve immune evasion remains elusive. In this study, SARS-CoV-2 NSP5 and N protein were found to attenuate antiviral stress granule (avSG) formation. Moreover, NSP5 and N suppressed IFN expression induced by infection of Sendai virus or transfection of a synthetic mimic of dsRNA, poly (I:C), inhibiting TBK1 and IRF3 phosphorylation, and restraining the nuclear translocalization of IRF3. Furthermore, HEK293T cells with ectopic expression of NSP5 or N protein were less resistant to vesicular stomatitis virus infection. Mechanistically, NSP5 suppressed avSG formation and disrupted RIG-I–MAVS complex to attenuate the RIG-I–mediated antiviral immunity. In contrast to the multiple targets of NSP5, the N protein specifically targeted cofactors upstream of RIG-I. The N protein interacted with G3BP1 to prevent avSG formation and to keep the cofactors G3BP1 and PACT from activating RIG-I. Additionally, the N protein also affected the recognition of dsRNA by RIG-I. This study revealed the intimate correlation between SARS-CoV-2, the stress response, and innate antiviral immunity, shedding light on the pathogenic mechanism of COVID-19.

Highlights The review highlights recent advancements in enhancing the intrinsic physical properties of metal halide perovskite scintillators, such as improving light yield and response times, to improve their X-ray detection performance. It discusses innovative engineering strategies to effectively optimize radioluminescent light management for high-resolution X-ray imaging. The problems encountered in the application of metal halides perovskites materials for X-ray detection are summarized, and the potential development direction in the future is prospected. The relentless pursuit of advanced X-ray detection technologies has been significantly bolstered by the emergence of metal halides perovskites (MHPs) and their derivatives, which possess remarkable light yield and X-ray sensitivity. This comprehensive review delves into cutting-edge approaches for optimizing MHP scintillators performances by enhancing intrinsic physical properties and employing engineering radioluminescent (RL) light strategies, underscoring their potential for developing materials with superior high-resolution X-ray detection and imaging capabilities. We initially explore into recent research focused on strategies to effectively engineer the intrinsic physical properties of MHP scintillators, including light yield and response times. Additionally, we explore innovative engineering strategies involving stacked structures, waveguide effects, chiral circularly polarized luminescence, increased transparency, and the fabrication of flexile MHP scintillators, all of which effectively manage the RL light to achieve high-resolution and high-contrast X-ray imaging. Finally, we provide a roadmap for advancing next-generation MHP scintillators, highlighting their transformative potential in high-performance X-ray detection systems.