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Advances in brain–computer interfaces (BCIs) have enabled direct and functional connections between human brains and computing systems. Recent developments in artificial intelligence have also significantly improved the ability to detect brain activity patterns. In particular, using steady-state visual evoked potentials (SSVEPs) in BCIs has enabled noticeable advances in human activity monitoring and identification. However, the lack of publicly available electroencephalogram (EEG) datasets has limited the development of SSVEP-based BCI systems (SSVEP-BCIs) for human activity monitoring and assisted living. This study aims to provide an open-access multicategory EEG dataset created under the SSVEP-BCI paradigm, with participants performing forward, backward, left, and right movements to simulate directional control commands in a virtual environment developed in Unity. The purpose of these actions is to explore how the brain responds to visual stimuli of control commands. An SSVEP-BCI system is proposed to enable hands-free control of a virtual target in the virtual environment allowing participants to maneuver the virtual target using only their brain activity. This work demonstrates the feasibility of using SSVEP-BCIs in human activity monitoring and assessment. The preliminary experiment results indicate the effectiveness of the developed system with high accuracy, successfully classifying 89.88% of brainwave activity.

Driven by government-led digital transformation initiatives and the rapid development of blockchain technology, low-carbon supply chain management is increasingly confronted with the dual imperative of investing in low-carbon technologies while effectively integrating blockchain systems to maximise corporate profits. This study examines low-carbon product supply chains by assessing the impact of government subsidy policies on manufacturers’ investment decisions in low-carbon technology, particularly in the context of blockchain adoption. Using a game-theoretic framework, four distinct supply chain models are developed to reflect scenarios with and without blockchain adoption and to compare the effects of technology-oriented and output-based subsidy policies. The findings suggest that larger subsidies encourage greater investment in low-carbon technologies, with higher total subsidy amounts having a stronger incentive effect. Notably, in the absence of blockchain technology, technology subsidy policies result in higher product pricing. However, when blockchain is introduced, manufacturers strategically increase wholesale prices to capture a greater share of the subsidy benefits, with the extent of the price adjustment depending on the subsidy amount. To effectively stimulate consumer purchases, policymakers should carefully consider the implications of implementing technology subsidies in markets lacking blockchain infrastructure. In addition, strengthening consumer trust in green products motivates manufacturers to intensify their efforts to reduce emissions, leading to higher wholesale and retail prices without dampening demand. These findings highlight the crucial roles of both subsidy mechanisms and blockchain technology in developing efficient low-carbon supply chain strategies. This study also introduces a unified analytical framework that defines the boundaries of low-carbon technology investments across various policy and technological scenarios, offering valuable insights for policymakers, industry stakeholders, and researchers.

Cancer‐associated fibroblasts (CAFs) are essential players in the tumor microenvironment (TME) due to their roles in facilitating tumor progression and metastasis. It is worth noting that the high‐metastatic hepatocellular carcinoma (HCC) cell‐derived exosomes have exhibited the ability to transform normal fibroblasts into CAFs, which further fosters the lung metastasis of low‐metastatic HCC cells. Yet, the mechanisms underlying this tumor exosome‐induced metastatic niche formation are poorly explored. In this study, the secreted protein arginyl aminopeptidase (RNPEP) was highly expressed in the plasma of patients with HCC. In addition, high‐metastatic HCC cells showed augmented RNPEP expression levels in their exosomes. These exosomes induced obvious CAF‐like properties in the human fibroblast cell line MRC‐5, as evidenced by the increased CAF marker expression, and enhanced migratory ability. More strikingly, the secretions from high‐metastatic tumor exosome‐educated MRC‐5 cells increased tumor stemness and promoted epithelial–mesenchymal transition (EMT) in MHCC‐97L cells, a low‐metastatic HCC cell line. However, the knockdown of RNPEP in exosomes from high‐metastatic HCC cells abated the changes described above. Animal studies in vivo highlighted the pro‐tumor and pro‐metastatic effects of exosomal RNPEP on MHCC‐97L cells by inducing CAF activation. Furthermore, tumor‐derived exosomal RNPEP induced the activation of NF‐κB signaling in MRC‐5 cells, a critical pathway associated with CAF activation. Collectively, these results provide novel insight into tumor‐derived exosomal RNPEP for its crosstalk with CAFs during HCC lung metastasis. This study demonstrates a novel mechanism underlying the communications between high‐metastatic HCC cells, CAFs, and low‐metastatic HCC cells. The tumor‐derived exosomal RNPEP, which induced the activation of CAFs to promote HCC lung metastatic progression, could be a potential target for further development of HCC therapeutic strategies.

Chimeric antigen receptors (CARs) can redirect T cells against antigen-expressing tumors, and each component plays an important role in the function and anti-tumor efficacy. It has been reported that using human sequences or a low affinity of CAR single-chain variable fragments (scFvs) in the CAR binding domains is a potential way to enhance the function of CAR-T cells. However, it remains largely unknown how a lower affinity of CARs using humanized scFvs affects the function of CAR-T cells until recently. We used different humanized anti-HER2 antibodies as the extracellular domain of CARs and further constructed a series of the CAR-T cells with different affinity. We have observed that moderately reducing the affinity of CARs (light chain variable domain (V )-based CAR-T) could maintain the anti-tumor efficacy, and improved the safety of CAR therapy both and compared with high-affinity CAR-T cells. Moreover, T cells expressing the V domain only antibody exhibited long-lasting tumor elimination capability after multiple challenges , longer persistence and lower cytokine levels . Our findings provide an alternative option for CAR-T optimization with the potential to widen the use of CAR T cells.

Sepsis‐induced acute kidney injury (SI‐AKI) causes renal dysfunction and has a high mortality rate. Protein arginine methyltransferase‐1 (PRMT1) is a key regulator of renal insufficiency. In the present study, we explored the potential involvement of PRMT1 in SI‐AKI. A murine model of SI‐AKI was induced by cecal ligation and perforation. The expression and localization of PRMT1 and molecules involved in the transforming growth factor (TGF)‐β1/Smad3 and interleukin (IL)‐6/signal transducer and activator of transcription 3 (STAT3) signaling pathways were detected in mouse kidney tissues by western blot analysis, immunofluorescence, and immunohistochemistry. The association of PRMT1 with downstream molecules of the TGF‐β1/Smad3 and IL‐6/STAT3 signaling pathways was further verified in vitro in mouse renal tubular epithelial cells. Cecal ligation and perforation caused epithelial–mesenchymal transition, apoptosis, and inflammation in renal tissues, and this was alleviated by inhibition of PRMT1. Inhibition of PRMT1 in SI‐AKI mice decreased the expression of TGF‐β1 and phosphorylation of Smad3 in the renal cortex, and downregulated the expression of soluble IL‐6R and phosphorylation of STAT3 in the medulla. Knockdown of PRMT1 in mouse renal tubular epithelial cells restricted the expression of Cox‐2, E‐cadherin, Pro‐caspase3, and phosphorylated Smad3 (involved in the TGF‐β1‐mediated signaling pathway), and also blocked IL‐6/soluble IL‐6R, inducing the expression of Cox‐2 and phosphorylated‐STAT3. In conclusion, our findings suggest that inhibition of PRMT1 mitigates SI‐AKI by inactivating the TGF‐β1/Smad3 pathway in the cortex and the IL‐6/STAT3 pathway in the medulla. Our findings may aid in the identification of potential therapeutic target molecules for SI‐AKI. Protein arginine methyltransferase‐1 (PRMT1) is a key regulator of renal dysfunction caused by sepsis‐induced acute kidney injury (SI‐AKI). Inhibition of PRMT1 alleviates SI‐AKI by inactivating the transforming growth factor (TGF)‐β1/Smad3 pathway in the cortex and interleukin (IL)‐6/signal transducer and activator of transcription 3 (STAT3) pathway in the medulla. PRMT1 may be a potential therapeutic target molecule for SI‐AKI.

Blastocystis sp. is an important gastrointestinal parasite with global distribution, prevalent in humans, farmed animals, and wildlife. Therefore, this study aimed to investigate the prevalence and genetic diversity of Blastocystis sp. in Asiatic brush-tailed porcupines ( Atherurus macrourus ), bamboo rats ( Rhizomys pruinosus ), and masked palm civets ( Paguma larvata ) in Hainan Province, China. A total of 900 fecal samples were collected from three farmed animal species including 257 porcupines, 360 rats, and 283 civets. Genomic DNA was extracted from each fecal sample and Blastocystis sp. was detected by PCR at the small subunit ribosomal RNA ( SSU rRNA) gene. A phylogenetic tree was constructed using the maximum likelihood method. Blastocystis sp. was detected in 47 (5.2%) fecal samples: 12 (4.7%) Asiatic brush-tailed porcupines, 8 (2.2%) bamboo rats, and 27 (9.5%) masked palm civets. Three known Blastocystis sp. subtypes, including ST1, ST4, ST5, and one unnamed subtype (unST), were found in one, 19, 26, and one animal, respectively. Subtypes ST4 and unST were detected in porcupines, ST4 in rats, and ST1 and ST5 in civets. Our results suggest that the three farmed animal species reported in this study could serve as reservoirs for potentially zoonotic Blastocystis sp. subtypes and transmit this parasite to humans, other farmed animals, and wildlife. Blastocystis sp. est un parasite gastro-intestinal important avec une distribution mondiale, répandu chez les humains, les animaux d’élevage et la faune. Par conséquent, cette étude visait à étudier la prévalence et la diversité génétique de Blastocystis sp. chez les athérures à longue queue ( Atherurus macrourus ), les rats des bambous ( Rhizomys pruinosus ) et les civettes masquées ( Paguma larvata ) dans la province de Hainan, en Chine. Au total, 900 échantillons fécaux ont été collectés sur ces trois espèces animales d’élevage dont 257 athérures, 360 rats et 283 civettes. L’ADN génomique a été extrait de chaque échantillon fécal et Blastocystis sp. a été détecté par PCR au niveau du gène de la petite sous-unité de l’ARN ribosomal. Un arbre phylogénétique a été construit en utilisant la méthode du maximum de vraisemblance. Blastocystis sp. a été détecté dans 47 (5,2 %) échantillons fécaux : 12 (4,7 %) athérures, 8 (2,2 %) rats et 27 (9,5 %) civettes. Trois sous-types de Blastocystis sp., dont ST1, ST4, ST5 et un sous-type sans nom (unST), ont été trouvés respectivement chez 1, 19, 26 et 1 animal. Les sous-types ST4 et unST ont été détectés chez les athérures, ST4 chez les rats et ST1 et ST5 chez les civettes. Nos résultats suggèrent que les trois espèces animales d’élevage concernées par cette étude pourraient servir de réservoirs à des sous-types potentiellement zoonotiques de Blastocystis sp. et transmettre ce parasite aux humains, à d’autres animaux d’élevage et à la faune.

BackgroundCurrently, an epidermal growth factor receptor variant III (EGFRvIII)-specific peptide (PEPvIII) vaccine has not achieved satisfactory outcomes in several clinical trials for glioblastoma. This is probably due to the poor immunogenicity of the PEPvIII peptide vaccine and the harshly immunosuppressive tumor microenvironment. Hence, identifying strategies to enhance tumor-specific T cell immune responses and reverse immune suppression is crucial for achieving the maximum beneficial therapeutic effect.MethodsTo enhance the immunogenicity of the PEPvIII vaccine, we have developed a novel oncolytic adenovirus-based vaccine by genetically incorporating the PEPvIII peptide into the adenovirus hexon protein, naming this construct Ad5-D24-PEPvIII. However, the upregulation of programmed cell death-ligand 1 (PD-L1) expression in the tumor microenvironment following oncolytic virus therapy may limit its therapeutic effectiveness. To address this, we first attempted to co-express soluble programmed cell death 1 (sPD-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the E4 region of Ad5-D24-PEPvIII. Subsequently, we combined the oncolytic adenovirus-based PEPvIII vaccine carrying GM-CSF with a PD-L1 inhibitor. Two immunocompetent mouse glioma models were used to evaluate their antitumor effects in vivo. The immune cell status within the tumor microenvironment was assessed using flow cytometry and immunohistochemistry. CD8+ T cell immune responses were evaluated by ELISA.ResultsLocal administration of Ad5-D24-PEPvIII, which presents high copies of tumor-specific antigen PEPvIII in the hexon protein, successfully activated PEPvIII-specific T cell responses. Co-expression of sPD-1 and GM-CSF in the E4 region of Ad5-D24-PEPvIII could increase the release of proinflammatory cytokines, activate myeloid cells and promote the maturation of dendritic cells, thereby further enhancing the activation and proliferation of CD8+ T cells targeting tumor antigens. More importantly, when the oncolytic adenovirus-based PEPvIII vaccine carrying GM-CSF was combined with a PD-L1 inhibitor, it could also broaden the tumor antigenic epitopes and significantly inhibit tumor growth in immunocompetent glioma mouse models.ConclusionOur work suggests that the efficient presentation of PEPvIII, achieved by modifying the hexon protein of the oncolytic adenovirus, combined with the adjuvant function of GM-CSF and blockade of the PD-1/PD-L1 axis, significantly enhances the therapeutic efficacy of the PEPvIII vaccine against glioblastoma. In addition, this combination strategy also provides a promising and personalized treatment for patients with cancer.

Transmissible gastroenteritis virus (TGEV) is a highly contagious gastrointestinal virus that causes diarrhea, vomiting, anorexia, dehydration, and weight loss in piglets. In clinical practice, it often occurs in mixed infections with other pathogens, and is therefore difficult to diagnose and prevent. It mainly harms piglets of about 2 weeks old, causing huge losses on farms. The clinical confirmation of TGEV usually requires a laboratory diagnosis, but traditional PCR and immunofluorescence assays have some limitations. Moreover, most farms in China are ill-equipped to accurately diagnose the disease. Therefore, a new detection method with high sensitivity and specificity and less dependence on instrumentation is required. We used recombinase polymerase amplification (RPA), combined with the nuclease characteristics of the activated Cas13a protein to establish a visual CRISPR-Cas13a-assisted detection method for TGEV by adding a reporter RNA with fluorescent and quenching moieties to the system. We selected the optimal RPA primer and best CRISPR RNA (crRNA). The reaction system was optimized and its repeatability, specificity, and sensitivity verified. The TGEV detection system did not cross-react with other common diarrhea viruses, and its detection limit was 10 copies, which is similar with the sensitivity of qPCR. We successfully established an RPA-CRISPR-Cas13a-assisted detection method, and used this detection system to analyze 123 pig blood samples. qPCR was used as the gold standard method. The sensitivity, specificity, positive coincidence rate, and negative coincidence rate of the new method were 100, 98.93, 96.66, and 100%, respectively.

Wind tunnel tests are carried out for the Commonwealth Advisory Aeronautical Research Council (CAARC) high-rise building with a scale of 1:400 in exposure categories D. The distribution law of extreme pressure coefficients under different conditions is studied. Probability distribution fitting is performed on the measured area-averaged extreme pressure coefficients. The general extreme value (GEV) distribution is preferred for probability distribution fitting of extreme pressure coefficients. From the comparison between the area-averaged coefficients and the value from GB50009-2012, it is indicated that the wind load coefficients from GB50009-2012 may be non-conservative for the CAARC building. The area reduction effect on the extreme wind pressure is smaller than that on the mean wind pressure from the code. The recommended formula of the area reduction factor for the extreme pressure coefficient is proposed in this study. It is found that the mean and the coefficient of variation (COV) for the directionality factors are 0.85 and 0.04, respectively, when the orientation of the building is given. If the uniform distribution is given for the building’s orientation, the mean value of the directionality factors is 0.88, which is close to the directionality factor of 0.90 given in the Chinese specifications.

β‐Sitosterol is a natural compound with demonstrated anti‐cancer properties against various cancers. However, its effects on hepatocellular carcinoma (HCC) and the underlying mechanisms are not well understood. This study aims to investigate the impact of β‐sitosterol on HCC. In this study, we investigated the effects of β‐sitosterol on HCC tumour growth and metastasis using a xenograft mouse model and a range of molecular analyses, including bioinformatics, real‐time PCR, western blotting, lentivirus transfection, CCK8, scratch and transwell assays. The results found that β‐sitosterol significantly inhibits HepG2 cell proliferation, migration and invasion both in vitro and in vivo. Bioinformatics analysis identifies forkhead box M1 (FOXM1) as a potential target for β‐sitosterol in HCC treatment. FOXM1 is upregulated in HCC tissues and cell lines, correlating with poor prognosis in patients. β‐Sitosterol downregulates FOXM1 expression in vitro and in vivo. FOXM1 overexpression mitigates β‐sitosterol's inhibitory effects on HepG2 cells. Additionally, β‐sitosterol suppresses epithelial–mesenchymal transition (EMT) in HepG2 cells, while FOXM1 overexpression promotes EMT. Mechanistically, β‐sitosterol inhibits Wnt/β‐catenin signalling by downregulating FOXM1, regulating target gene transcription related to HepG2 cell proliferation and metastasis. β‐Sitosterol shows promising potential as a therapeutic candidate for inhibiting HCC growth and metastasis through FOXM1 downregulation and Wnt/β‐catenin signalling inhibition.