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In this study, a low-cost and easily recyclable porous green adsorbent (magnetic porous loofah biochar, MPLB) was synthesized by modifying the almost zero-cost loofah biochar material with Fe 3 O 4 . The successful synthesis of the material was demonstrated by XRD, FTIR, SEM, VSM, and BET. In addition, the material exhibits outstanding magnetic separation performance (40.01 umg/g) allowing for rapid recovery within just 90 s. The adsorption process of phenol on MPLB was found to be spontaneous and endothermic. The experimental data fit exceptionally well with the pseudo-second-order kinetic model and Langmuir model ( R 2  > 0.99), indicating that the dominant adsorption mechanisms involved monolayer adsorption and chemisorption. These interactions were attributed to host–guest interaction, π–π conjugation, hydrogen bonding, and pore filling. The maximum adsorption capacity calculated using the Langmuir model at 298 K is 39.4 mg/g. Importantly, even after undergoing seven cycles of recycling, MPLB retained 78% of its initial adsorption capacity. In simulated experiments employing MPLB for phenol removal in actual wastewater, an impressive removal rate of 96.4% was achieved. In conclusion, MPLB exhibits significant potential as an effective adsorbent for phenol removal in wastewater. Graphical abstract

The continuous imbalance of the diabetic wound microenvironment is an important cause of chronic nonhealing, which manifests as a vicious cycle between excessive accumulation of reactive oxygen species (ROS) and abnormal healing. Regulating the microenvironment by suppressing wound inflammation, oxidative stress, and bacterial infection is a key challenge in treating diabetic wounds. In this study, ROS‐responsive hydrogels are developed composed of silk fibroin methacrylated (SFMA), modified collagen type III (rCol3MA), and lipid nanoparticles (LNPs). The newly designed hydrogel system demonstrated stable physicochemical properties and excellent biocompatibility. Moreover, the release of antimicrobial peptide (AMP) and puerarin (PUE) demonstrated remarkable efficacy in eradicating bacteria, regulating inflammatory responses, and modulating vascular functions. This multifunctional hydrogel is a simple and efficient approach for the treatment of chronic diabetic infected wounds and holds tremendous potential for future clinical applications. The prevalence of diabetes‐related chronic non‐healing wounds presents a daunting challenge to healthcare professionals worldwide. In the study, a hydrogel system is designed that responds dynamically to the unique microenvironment of diabetic wounds. By integrating silk fibroin methacrylated (SFMA), modified collagen type III (rCol3MA), lipid nanoparticles (LNPs), antimicrobial peptide (AMP), and puerarin (PUE), the hydrogel embodies the convergence of cutting‐edge biomaterials science and compassionate patient care.

For a SLAM system operating in a dynamic indoor environment, its position estimation accuracy and visual odometer stability could be reduced because the system can be easily affected by moving obstacles. In this paper, a visual SLAM algorithm based on the Yolov4-Tiny network is proposed. Meanwhile, a dynamic feature point elimination strategy based on the traditional ORBSLAM is proposed. Besides this, to obtain semantic information, object detection is carried out when the feature points of the image are extracted. In addition, the epipolar geometry algorithm and the LK optical flow method are employed to detect dynamic objects. The dynamic feature points are removed in the tracking thread, and only the static feature points are used to estimate the position of the camera. The proposed method is evaluated on the TUM dataset. The experimental results show that, compared with ORB-SLAM2, our algorithm improves the camera position estimation accuracy by 93.35% in a highly dynamic environment. Additionally, the average time needed by our algorithm to process an image frame in the tracking thread is 21.49 ms, achieving real-time performance.

Haze seriously affects the visual quality of road inspection images and contaminates the discrimination of key road objects, which thus hinders the execution of road inspection work. The basic assumptions of the classical dark-channel prior are not suitable for road images containing light-colored lane lines and vehicles, while typical deep dehazing networks lack physical model interpretability, and they focus on global dehazing effects, neglecting the preservation of object features. For this reason, this paper proposes a Dark-Channel Soft-Constrained and Object-Perception-Enhanced Deep Dehazing Network (DCSC-OPE-Net) for the information recovery of road inspection images. The network is divided into two modules: a dark-channel soft-constrained dehazing module and a near-view object-perception-enhanced module. Unlike the traditional dark-channel algorithms that impose strong constraints on dark pixels, a dark-channel soft-constrained loss function is constructed to ensure that the features of light-colored vehicles and lane lines are effectively maintained. To avoid resolution loss due to patch-based dark-channel processing for image dehazing, a resolution enhancement module is used to strengthen the contrast of the dehazed image. To autonomously perceive and enhance key road features to support road inspection, edge enhancement loss combined with a transmission map is embedded into the network to autonomously discover near-view objects and enhance their key features. The experiments utilize public datasets and real road inspection datasets to validate the performance of the proposed DCSC-OPE-Net compared with typical networks using dehazing evaluation metrics and road object recognition metrics. The experimental results demonstrate that the proposed DCSC-OPE-Net can obtain the best dehazing performance, with an NIQE score of 4.5 and a BRISQUE score of 18.67, and obtain the best road object recognition results (i.e., 83.67%) among the comparison methods.

Naked cuticle homolog 1 (NKD1), which is expressed at low levels in many tumors, is considered an inhibitor of the Wnt/β‐catenin pathway, but it is highly expressed in colon cancer and can promote colon cancer cell proliferation. miRNAs are involved in the occurrence and progression of many tumors. However, miRNAs that can regulate NKD1 and the mechanisms by which NKD1 regulates tumor progression remain ambiguous. This research aims to reveal the potential regulatory network of NKD1 in colon cancer. miRNA data downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were analyzed by bioinformatics to screen for potential miRNAs targeting NKD1. Let‐7b‐5p was found to inhibit proliferation, migration, and invasion of colon cancer cells targeting NKD1. Further studies suggested that let‐7b‐5p can modulate Wnt signaling activity, and the nuclear accumulation of β‐catenin was significantly restrained by let‐7b‐5p through targeting NKD1. Moreover, NKD1 could prohibit the expression of the APC protein. Further studies manifested that NKD1 bound to APC and promoted the ubiquitination degradation of APC through restraining the expression of the deubiquitinating enzyme USP15 and blocking the combination between USP15 and APC. Functionally, NKD1 enhanced the proliferation and migration of colon cancer cells by inhibiting APC expression. This research revealed a novel mechanism by which the let‐7b‐5p‐NKD1‐APC‐β‐catenin signaling pathway inhibited colon cancer cell progression. Targeting NKD1, let‐7b‐5p inhibits ubiquitination degradation of APC and activation of Wnt signaling pathway, thus inhibiting proliferation, migration and invasion of colon cancer cells. In addition, NKD1 can promote the ubiquitination degradation of APC by inhibiting the binding of APC to the deubiquitinating enzyme USP15.

Diabetic wound healing remains a significant clinical challenge because of hyperglycaemia-induced cellular senescence, impaired angiogenesis, and chronic inflammation. To address these issues, we developed a multifunctional hydrogel (GelMA/PNS/Alg@IGF-1) that integrates gelatine methacryloyl (GelMA), Panax notoginseng saponins (PNS), and sodium alginate microspheres encapsulating insulin-like growth factor-1 (IGF-1). This hydrogel was engineered to achieve gradient and sustained release of bioactive agents to target senescence and promote vascular repair. In vitro studies demonstrated that the hydrogel significantly reduced oxidative stress, suppressed senescence markers and senescence-associated secretory phenotypes, and restored endothelial cell function under high-glucose conditions by inhibiting NF-κB pathway activation. Transcriptomic analysis revealed the modulation of pathways linked to inflammation, apoptosis, and angiogenesis. This hydrogel accelerated diabetic wound closure in a rat model in vivo and enhanced collagen deposition, granulation tissue formation, and neovascularization. Furthermore, the hydrogel mitigated oxidative stress and cellular senescence and promoted tissue remodelling. The synergistic effects of PNS and IGF-1 within the hydrogel established a pro-regenerative microenvironment to address both pathological ageing and vascular dysfunction. These findings highlight GelMA/PNS/Alg@IGF-1 as a promising therapeutic platform for diabetic wound management, as this material offers dual anti-senescence and proangiogenic efficacy to overcome the complexities of chronic wound healing. Graphical abstract

Transport infrastructure plays a crucial role in facilitating the high-quality development of new urbanization. Based on the provincial panel data of 31 provinces in China from 2013 to 2020, this study empirically analyzed the impact and mechanism of transportation infrastructure on the high-quality development of new urbanization from multiple perspectives. The results showed that transportation infrastructure can significantly promote the development of new urbanization, and the promoting effect was significantly positive in the eastern and western regions, while it was positive but not significant in the central region. Transportation infrastructure can promote the development of new urbanization by promoting industrial agglomeration. When the population density is lower than the corresponding threshold value, the transport infrastructure can significantly promote the development of new urbanization; when the population density is higher than the corresponding threshold value, the transport infrastructure will significantly hinder the development of new urbanization. Transport infrastructure has a significant positive spatial spillover effect on the development of new urbanization, and the positive spatial spillover effect has been significant in the eastern, central and western regions.

Background DNA methylation plays a crucial role in species development and environmental adaptation. In mammals, there are significant dietary changes from infancy to adulthood. Notably, the red panda transitions from milk consumption as juveniles to a bamboo-based diet as adults, with significant alterations in food characteristics and nutritional content. However, the regulatory role of DNA methylation in this process remains unclear. In this study, we investigate the regulatory role of DNA methylation on the expression of digestive and metabolic genes in the liver and pancreas during the red panda’s dietary transition from suckling stage to adulthood. Results Our findings reveal significant differences in DNA methylation patterns before and after dietary transition, highlighting the specific alterations in the methylation profiles of genes involved in lipid, carbohydrate, and amino acid metabolism. We found that perilipin-4 ( PLIN4 ) is hypomethylated and highly expressed in the liver of adult red pandas, facilitating lipid droplet formation and storage, crucial for adapting to the low-fat content in bamboo. In contrast, genes like lipoprotein lipase ( LPL ), crucial for lipid breakdown, exhibited hypermethylated with low-expression patterns, reflecting a reduced lipid metabolism capacity in adults. Carbohydrate metabolism-related genes like ADH4 and FAM3C are hypomethylated and highly expressed in adults, enhancing glycogen production and glucose utilization. Genes involved in protein metabolism like CTSZ and GLDC , exhibit hypomethylated with high-expression and hypermethylated with low-expression patterns in the pancreas of adults, respectively, contributing to protein metabolism balance post-weaning. Conclusion This study reveals the regulatory role of DNA methylation in the dietary transition of red pandas from milk to bamboo and provides methylation evidence for the molecular regulation of adaptive expression of digestive and metabolic genes in red pandas with specialized diets.

DNA–RNA hybrids triggered by double-strand breaks (DSBs) are crucial intermediates during DSB repair, and their timely resolution requires numbers of RNA helicases, including DEAD box 1 (DDX1). However, how these helicases are recruited to DSB-induced hybrids in time remains largely unclear. Here, we revealed that squamous cell carcinoma antigen recognized by T cells 3 (SART3) promotes DDX1 binding to DNA–RNA hybrids at DSBs for optimal homologous recombination (HR) repair. SART3 itself associates with DNA–RNA hybrids and PAR chains and accumulates at DSBs in both PARylation- and DNA–RNA hybrids-dependent fashion. SART3 also associates with DDX1 and is necessary for DDX1 enrichment at DSBs. The defective SART3-DDX1 association observed in cells expressing the cancer-associated variant SART3-R836W impairs not only the accumulation of DDX1, but also hybrid removal and HR efficiency. Moreover, SART3 promotes DNA end resection through enhancing USP15-BARD1 association and BRCA1-BARD1 retention. Together, our study reveals an role of SART3 in DSB repair, rendering SART3 a promising target for cancer therapy. Transient R-loops form around DSBs must be timely removed for HR repair. Here, the authors show that SART3 promotes DDX1 helicase binding to DSBs for optimal DNA-RNA hybrid removal, and enhances USP15-BARD1 association for efficient DNA end resection.

RAD18, an important ubiquitin E3 ligase, plays a dual role in translesion DNA synthesis (TLS) and homologous recombination (HR) repair. However, whether and how the regulatory mechanism of O-linked N-acetylglucosamine (O-GlcNAc) modification governing RAD18 and its function during these processes remains unknown. Here, we report that human RAD18, can undergo O-GlcNAcylation at Ser130/Ser164/Thr468, which is important for optimal RAD18 accumulation at DNA damage sites. Mechanistically, abrogation of RAD18 O-GlcNAcylation limits CDC7-dependent RAD18 Ser434 phosphorylation, which in turn significantly reduces damage-induced PCNA monoubiquitination, impairs Polη focus formation and enhances UV sensitivity. Moreover, the ubiquitin and RAD51C binding ability of RAD18 at DNA double-strand breaks (DSBs) is O-GlcNAcylation-dependent. O-GlcNAcylated RAD18 promotes the binding of RAD51 to damaged DNA during HR and decreases CPT hypersensitivity. Our findings demonstrate a novel role of RAD18 O-GlcNAcylation in TLS and HR regulation, establishing a new rationale to improve chemotherapeutic treatment.