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HighlightsThe electrochemical techniques utilizing metal-organic frameworks (MOFs)-based catalysts for converting CO2 into chemical species are discussed.The structure–activity relationship of MOF-based catalysts in electrocatalytic CO2 reduction reactions is thoroughly reviewedThe challenges and opportunities of large-scale applications of MOF-based materials in electrochemical CO2 reduction reactions are discussed, and possible directions for the future development of MOFs and their derivatives are outlined.Electrochemically reducing CO2 to more reduced chemical species is a promising way that not only enables the conversion of intermittent energy resources to stable fuels, but also helps to build a closed-loop anthropogenic carbon cycle. Among various electrocatalysts for electrochemical CO2 reduction, multifunctional metal–organic frameworks (MOFs) have been employed as highly efficient and selective heterogeneous electrocatalysts due to their ultrahigh porosity and topologically diverse structures. Up to now, great progress has been achieved in the design and synthesis of highly active and selective MOF-related catalysts for electrochemical CO2 reduction reaction (CO2RR), and their corresponding reaction mechanisms have been thoroughly studied. In this review, we summarize the recent progress of applying MOFs and their derivatives in CO2RR, with a focus on the design strategies for electrocatalysts and electrolyzers. We first discussed the reaction mechanisms for different CO2RR products and introduced the commonly applied electrolyzer configurations in the current CO2RR system. Then, an overview of several categories of products (CO, HCOOH, CH4, CH3OH, and multi-carbon chemicals) generated from MOFs or their derivatives via CO2RR was discussed. Finally, we offer some insights and perspectives for the future development of MOFs and their derivatives in electrochemical CO2 reduction. We aim to provide new insights into this field and further guide future research for large-scale applications.

Proton exchange membrane water electrolysis stands as a promising technology for sustainable hydrogen production, although its viability hinges on minimizing platinum (Pt) usage without sacrificing catalytic efficiency. Central to this challenge is enhancing the intrinsic activity of Pt while ensuring the stability of the catalyst. We herein present a Mo 2 TiC 2 MXene-supported Pt nanocluster catalyst (Mo 2 TiC 2 -Pt NC ) that requires a minimal Pt content (36 μg cm −2 ) to function, yet remains highly active and stable. Operando spectroscopy and theoretical simulation provide evidence for anomalous charge transfer from the MXene substrate to Pt NC , thus generating highly efficient electron-rich Pt sites for robust hydrogen evolution. When incorporated into a proton exchange membrane electrolyzer, the catalyst affords more than 8700 h at 200 mA cm −2 under ambient temperature with a decay rate of just 2.2 μV h −1 . All the performance metrics of the present Mo 2 TiC 2 -Pt NC catalysts are on par with or even surpass those of current hydrogen evolution electrocatalysts under identical operation conditions, thereby challenging the monopoly of high-loading Pt/C-20% in the current electrolyzer design. Reducing platinum use is vital for sustainable hydrogen production via proton exchange membrane water electrolysis. Here, the authors report a Mo₂TiC₂ MXene-supported platinum nanocluster catalyst that requires minimal platinum content and operates efficiently for over 8700 h.

Background Gastric cancer stem cells (GCSCs) are key contributors to tumorigenesis, recurrence and metastasis, complicating gastric cancer (GC) treatment. Rhaponticin (RA), a potential novel anticancer drug, has unexplored effects on GCSCs. Methods GCSCs were isolated using CD133 and CD166 markers with magnetic bead separation method and then evaluated their response to the IC50 concentrations of RA (16.90 µg/mL for BGC-823 and 22.18 µg/mL for SGC-7901), and effects on cell proliferation, migration, invasion, and stemness were measured. We analyzed the GCSC-related microarray dataset GSE111556 and explored RA’s role in restoring programmed cell death ligand 1 (PD-L1) function in CD133+/CD166 + cells post-PD-L1 knockdown. RA’s impact on tumour growth and immune microenvironment was assessed in a xenograft mouse model. Results The CD133+/CD166 + subpopulation exhibited stem-like characteristics, with the highest proportion in BGC-823 (38.85%) and SGC-7901 (43.81%) cells. These cells formed tumour spheres and had increased expression of stemness markers Sox2 and Oct-4 (compared to the parental cell line, P  < 0.001). RA treatment showed no toxicity to normal GES-1 cells but reduced the viability of CD133+/CD166 + cells in a dose-dependent manner, with IC50 values of 16.90 µg/ml for BGC-823 and 22.18 µg/ml for SGC-7901. RA also decreased the proportion of CD133+/CD166 + cells and their stem-like properties ( P  < 0.001). Analysis of the GEO database identified PD-L1 as a key target gene of RA, with high expression in GC tissues. Knocking down PD-L1 in CD133+/CD166 + cells and introducing RA did not significantly change PD-L1 expression ( P >0.05), suggesting RA’s effect may be PD-L1 dependent. In a xenograft mouse model, the tumour size in the RA treatment group was approximately one-sixth that of the CD133+/CD166 + group ( P  < 0.001). Post-RA treatment, there was an elevation in the expression levels of CD4 and CD8, alongside a reduction in PD-L1 expression ( P  < 0.001). Conclusions RA suppresses GCSC stem - like phenotype by inhibiting PD - L1 and enhancing T cell tumour infiltration in the studied models. These findings suggest that RA may have potential for further exploration as a candidate for GC treatment, but extensive preclinical and clinical studies are required to determine its true therapeutic value. Highlights The CD133+/CD166 + human GC cell subpopulation has the phenotypic characteristics of tumor stem-like cells. RA suppressed the stem-like cell phenotype of CD133+/CD166 + human GC cell subpopulation. PD-L1 is a key target gene of RA. RA prevents the stemness and aggressive phenotype of human CD133+/CD166 + GC cell subsets by inhibiting PD-L1. RA regulates the tumor microenvironment in CD133+/CD166 + xenograft mice by suppressing PD-L1.

The identification of particular types of damage in wind turbine blades using acoustic emission (AE) techniques is a significant emerging field. In this work, a 45.7-m turbine blade was subjected to flap-wise fatigue loading for 21 days, during which AE was measured by internally mounted piezoelectric sensors. This paper focuses on using unsupervised pattern recognition methods to characterize different AE activities corresponding to different fracture mechanisms. A sequential feature selection method based on a k-means clustering algorithm is used to achieve a fine classification accuracy. The visualization of clusters in peak frequency−frequency centroid features is used to correlate the clustering results with failure modes. The positions of these clusters in time domain features, average frequency−MARSE, and average frequency−peak amplitude are also presented in this paper (where MARSE represents the Measured Area under Rectified Signal Envelope). The results show that these parameters are representative for the classification of the failure modes.

Various physical information can be leaked while the encryption algorithm is running in the device. Side-channel analysis exploits these leakages to recover keys. Due to the sensitivity of deep learning to the data features, the efficiency and accuracy of side channel analysis are effectively improved with the application of deep learning algorithms. However, a considerable part of existing reserches are based on traditional neural networks. The effectiveness of key recovery is improved by increasing the size of the network. However, the computational complexity of the algorithm increases accordingly. Problems such as overfitting, low training efficiency, and low feature extraction ability also occur. In this paper, we construct an improved lightweight convolutional neural network based on the feature fusion network. The new network and the traditional neural networks are respectively applied to the side-channel analysis for comparative experiments. The results show that the new network has faster convergence, better robustness and higher accuracy. No overfitting has occurred. A heatmap visualization method was introduced for analysis. The new network has higher heat value and more concentration in the key interval. Side-channel analysis based on feature fusion network has better performance, compared with the ones based on traditional neural networks.

Glioblastoma (GBM) is the most common and deadly malignant tumor of the nervous system. RIMS1, a member of the RAS gene superfamily, plays a critical role in signaling pathways regulating cell growth and differentiation. However, the prognostic value of RIMS1, particularly its relationship with immune cell infiltration in gliomas, has not been fully explored. RIMS1 expression in glioblastoma cells and tissues was assessed using bioinformatics platforms. The association between RIMS1 expression levels and overall survival was analyzed using Kaplan-Meier analysis and Cox regression model. To evaluate the proliferative and migratory capacity of GBM cells, we conducted CCK-8, colony formation, transwell, and scratch assays. With data from The Cancer Genome Atlas (TCGA), we investigated the correlation between RIMS1 expression and immune cell infiltration levels and assessed the prognostic impact of RIMS1 on GBM patient survival, focusing on its potential involvement in immune pathways. Lower RIMS1 expression was associated with poorer overall survival and was linked to patient age, gender, and tumor grade. Importantly, RIMS1 expression showed a significant correlation with immune cell infiltration levels, suggesting that RIMS1 influences glioblastoma survival, at least in part, through immune-related mechanisms. In glioblastoma patients, elevated RIMS1 expression may serve as an independent prognostic biomarker, potentially through its impact on immune cell infiltration.

For the routine target detection algorithm in the underwater complex environment to obtain the image of the existence of blurred images, complex background and other phenomena, leading to difficulties in model feature extraction, target miss detection and other problems. Meanwhile, an improved YOLOv7 model is proposed in order to improve the accuracy and real-time performance of the underwater target detection model. The improved model is based on the single-stage target detection model YOLOv7, incorporating the CBAM attention mechanism in the model, so that the feature information of the detection target is weighted and enhanced in the spatial dimension and the channel dimension, capturing the local relevance of feature information, making the model more focused on target feature information, improved detection accuracy, and using the SPPFCSPC module, reducing the computational effort of the model while keeping the model perceptual field unchanged, improved inference speed of the model. After a large number of comparison experiments and ablation experiments, it is proved that our proposed ACFP-YOLO algorithm model has higher detection accuracy compared with Efficientdet, Faster-RCNN, SSD, YOLOv3, YOLOv4, YOLOv5 models and the latest YOLOv7 model, and is more accurate for target detection tasks in complex underwater environments advantages.

Non-homologous end joining (cNHEJ) is a major pathway to repair double-strand breaks (DSBs) in DNA. Several core cNHEJ are involved in the progress of the repair such as KU70 and 80, DNA-dependent protein kinase catalytic subunit (DNA-PKcs), Artemis, X-ray repair cross-complementing protein 4 (XRCC4), DNA ligase IV, and XRCC4-like factor (XLF). Recent studies have added a number of new proteins during cNHEJ. One of the newly identified proteins is Paralogue of XRCC4 and XLF (PAXX), which acts as a scaffold that is required to stabilize the KU70/80 heterodimer at DSBs sites and promotes the assembly and/or stability of the cNHEJ machinery. PAXX plays an essential role in lymphocyte development in XLF-deficient background, while XLF/PAXX double-deficient mouse embryo died before birth. Emerging evidence also shows a connection between the expression levels of PAXX and cancer development in human patients, indicating a prognosis role of the protein. This review will summarize and discuss the function of PAXX in DSBs repair and its potential role in cancer development.

Parental histones, the carriers of posttranslational modifications, are deposited evenly onto the replicating DNA of sister chromatids in a process dependent on the Mcm2 subunit of DNA helicase and the Pole3 subunit of leading-strand DNA polymerase. The biological significance of parental histone propagation remains unclear. Here we show that Mcm2-mutated or Pole3-deleted mouse embryonic stem cells (ESCs) display aberrant histone landscapes and impaired neural differentiation. Mutation of the Mcm2 histone-binding domain causes defects in pre-implantation development and embryonic lethality. ESCs with biased parental histone transfer exhibit increased epigenetic heterogeneity, showing altered histone variant H3.3 and H3K27me3 patterning at genomic sites regulating differentiation genes. Our results indicate that the lagging strand pattern of H3.3 leads to the redistribution of H3K27me3 in Mcm2-2A ESCs. We demonstrate that symmetric parental histone deposition to sister chromatids contributes to cellular differentiation and development. Mcm2 mutation or Pole3 deletion in mouse embryonic stem cells leads to asymmetric parental histone distribution and impaired neural differentiation. Mutation of the Mcm2 histone-binding domain causes defects in pre-implantation development and embryonic lethality.

BackgroundOH2 is a genetically engineered oncolytic herpes simplex virus type 2 designed to selectively amplify in tumor cells and express granulocyte-macrophage colony-stimulating factor to enhance antitumor immune responses. We investigated the safety, tolerability and antitumor activity of OH2 as single agent or in combination with HX008, an anti-programmed cell death protein 1 antibody, in patients with advanced solid tumors.MethodsIn this multicenter, phase I/II trial, we enrolled patients with standard treatment-refractory advanced solid tumors who have injectable lesions. In phase I, patients received intratumoral injection of OH2 at escalating doses (106, 107 and 108CCID50/mL) as single agent or with fixed-dose HX008. The recommended doses were then expanded in phase II. Primary endpoints were safety and tolerability defined by the maximum-tolerated dose and dose-limiting toxicities (DLTs) in phase I, and antitumor activity assessed per Response Evaluation Criteria in Solid Tumors (RECIST version 1.1) and immune-RECIST in phase II.ResultsBetween April 17, 2019 and September 22, 2020, 54 patients with metastatic cancers were enrolled. Forty patients were treated with single agent OH2, and 14 with OH2 plus HX008. No DLTs were reported with single agent OH2 in phase I. Four patients, having metastatic mismatch repair-proficient rectal cancer or metastatic esophageal cancer, achieved immune-partial response, with two from the single agent cohort and two from the combination cohort. The duration of response were 11.25+ and 14.03+ months for the two responders treated with single agent OH2, and 1.38+ and 2.56+ months for the two responders in the combination cohort. The most common treatment-related adverse event (TRAE) with single agent OH2 was fever (n=18, 45.0%). All TRAEs were of grade 1–2, except one case of grade 3 fever in the 108CCID50/mL group. No treatment-related serious AEs occurred. Single agent OH2 induced alterations in the tumor microenvironment, with clear increases in CD3+ and CD8+ cell density and programmed death-ligand 1 expression in the patients’ post-treatment biopsies relative to baseline.ConclusionsIntratumoral injection of OH2 was well-tolerated, and demonstrated durable antitumor activity in patients with metastatic esophageal and rectal cancer. Further clinical development of OH2 as single agent or with immune checkpoint inhibitors in selected tumor types is warranted.