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By integrating statistical modeling and data analysis techniques, we systematically assess the carbon emission performance of the ceramic industry and propose targeted emission reduction pathways. Firstly, the entropy weight TOPSIS model is employed to quantitatively evaluate the carbon emission performance of the three major Chinese ceramic production areas: Foshan, Jingdezhen, and Zibo. Through data-driven quantitative analysis, it is disclosed that the carbon emission intensity in Foshan is significantly higher than that in the other two regions (with a relative closeness degree of 0.5185). The key issues identified include high energy consumption in the production process, a high reliance on raw coal, and insufficient investment in environmental protection. Furthermore, through the XGBoost-SHAP combined modeling, the key drivers of carbon emissions are precisely identified from multi-dimensional data. It is found that the elasticity coefficient of raw coal in the carbon emission proportion is as high as 25.84%, while the potential for substitution with natural gas is remarkable. Based on statistical prediction techniques, a carbon emission trend model under the scenario of energy structure optimization is constructed, predicting that after reaching a peak in 2017, Foshan’s carbon emissions will continue to decline, with the proportion of raw coal dropping to 48% and that of natural gas rising to 10%, thereby verifying the feasibility of the green transformation. Additionally, a multi-agent carbon trading simulation model is constructed to explore the emission reduction behaviors of enterprises under different carbon price scenarios. This study not only achieves precise quantitative analysis of carbon emissions through statistical method innovation but also verifies the feasible paths of low-carbon transformation through data modeling.

The coherent integration of multiple pulses can improve the detection performance of weak targets. However, in the process of coherent integration, serious echo envelope migration exists when the target moves fast. A method named keystone transform has been proposed to solve this problem. Nevertheless, for wideband radars, the problem of energy dispersal increases the difficulties of Doppler ambiguity searching. Thus, in this paper, a Doppler ambiguity searching method based on energy accumulation is proposed. The effectiveness of the algorithm is verified by the simulations. (4 pages)

High quality CaF2: Yb, Er @ mesoporous SiO2 core-shell nanoparticles were prepared by coating silica shell onto solvothermal synthesized CaF2: Yb, Er nanoparticles through reverse microemulsion and liquid crystal template processes. The phase identification, morphology and upconversion luminescence properties of CaF2: Yb, Er @SiO2 core-shell nanoparticles were investigated in detail. The results show that CaF2: Yb, Er nanocrystals are of cubic structure and SiO2 shell is mesoporous. The core-shell structure has little effect on the upconversion properties of CaF2: Yb, Er nanoparticles. And the nanocomposites with upconversion luminescent CaF2: Yb, Er nanocrystals core and a mesoporous silica shell are potential photocontrollable drug vehicles.

Cancer cells are frequently confronted with metabolic stress in tumor microenvironments due to their rapid growth and limited nutrient supply. Metabolic stress induces cell death through ROS-induced apoptosis. However, cancer cells can adapt to it by altering the metabolic pathways. AMPK and AKT are two primary effectors in response to metabolic stress: AMPK acts as an energy-sensing factor which rewires metabolism and maintains redox balance. AKT broadly promotes energy production in the nutrient abundance milieu, but the role of AKT under metabolic stress is in dispute. Recent studies show that AMPK and AKT display antagonistic roles under metabolic stress. Metabolic stress-induced ROS signaling lies in the hub between metabolic reprogramming and redox homeostasis. Here, we highlight the cross-talk between AMPK and AKT and their regulation on ROS production and elimination, which summarizes the mechanism of cancer cell adaptability under ROS stress and suggests potential options for cancer therapeutics.

Visual Simultaneous Localization and Mapping (V-SLAM) plays a crucial role in the development of intelligent robotics and autonomous navigation systems. However, it still faces significant challenges in handling highly dynamic environments. The prevalent method currently used for dynamic object recognition in the environment is deep learning. However, models such as Yolov5 and Mask R-CNN require significant computational resources, which limits their potential in real-time applications due to hardware and time constraints. To overcome this limitation, this paper proposes ADM-SLAM, a visual SLAM system designed for dynamic environments that builds upon the ORB-SLAM2. This system integrates efficient adaptive feature point homogenization extraction, lightweight deep learning semantic segmentation based on an improved DeepLabv3, and multi-view geometric segmentation. It optimizes keyframe extraction, segments potential dynamic objects using contextual information with the semantic segmentation network, and detects the motion states of dynamic objects using multi-view geometric methods, thereby eliminating dynamic interference points. The results indicate that ADM-SLAM outperforms ORB-SLAM2 in dynamic environments, especially in high-dynamic scenes, where it achieves up to a 97% reduction in Absolute Trajectory Error (ATE). In various highly dynamic test sequences, ADM-SLAM outperforms DS-SLAM and DynaSLAM in terms of real-time performance and accuracy, proving its excellent adaptability.

A MIL series metal‒organic framework (MOF), MIL-100(Fe), was successfully synthesized at the nanoscale and fully characterized by TEM, TGA, XRD, FTIR, DLS, and BET. A toxicological assessment was performed using two different cell lines: human normal liver cells (HL-7702) and hepatocellular carcinoma (HepG2). In vitro cytotoxicity of MIL-100(Fe) was evaluated by the MTT assay, LDH releasing rate assay, DAPI staining, and annexin V/PI double staining assay. The safe dose of MIL-100(Fe) was 80 μg/mL. It exhibited good biocompatibility, low cytotoxicity, and high cell survival rate (HL-7702 cells’ viability >85.97%, HepG2 cells’ viability >91.20%). Therefore, MIL-100(Fe) has a potential application as a drug carrier.

Oridonin (ORI) is a natural active ingredient with strong anticancer activity. But its clinical use is restricted due to its poor water solubility, short half-life, and low bioavailability. The aim of this study is to utilize the metal organic framework material MOF-5 to load ORI in order to improve its release characteristics and bioavailability. Herein, MOF-5 was synthesized by the solvothermal method and direct addition method, and characterized by Scanning Electron Microscopy (SEM), X-Ray Diffraction (XRD), Fourier Transform Infrared Spectrometer (FTIR), Thermogravimetric Analysis (TG), Brunauer–Emmett–Teller (BET), and Dynamic Light Scattering (DLS), respectively. MOF-5 prepared by the optimal synthesis method was selected for drug-loading and in vitro release experiments. HepG2 cells were model cells. MTT assay, 4′,6-diamidino-2-phenylindole (DAPI) staining and Annexin V/PI assay were used to detect the biological safety of blank carriers and the anticancer activity of drug-loaded materials. The results showed that nano-MOF-5 prepared by the direct addition method had complete structure, uniform size and good biocompatibility, and was suitable as an ORI carrier. The drug loading of ORI@MOF-5 was 52.86% ± 0.59%. The sustained release effect was reliable, and the cumulative release rate was about 87% in 60 h. ORI@MOF-5 had significant cytotoxicity (IC50:22.99 μg/mL) and apoptosis effect on HepG2 cells. ORI@MOF-5 is hopeful to become a new anticancer sustained release preparation. MOF-5 has significant potential as a drug carrier material.

Cuproptosis is a recently discovered form of cell death that is mediated by copper (Cu) and is a non-apoptotic form of cell death related to oligomerization of lipoylated proteins and loss of Fe-S protein clusters. Since its discovery, cuproptosis has been extensively studied by researchers for its mechanism and potential applications in the treatment of cancer. Therefore, this article reviews the specific mechanism of cuproptosis currently studied, as well as its principles and strategies for use in anti-cancer treatment, with the aim of providing a reference for cuproptosis-based cancer therapy.

Sustained-release preparation is a hot spot in antitumor drug research, where the first task is to select suitable drug carriers. Research has revealed that carboxylic acid iron metal–organic frameworks (MOFs), constructed from iron (Fe) ions and terephthalic acid, are nontoxic and biocompatible. Due to the breathing effect, the skeleton of this mesoporous material is flexible and can reversibly adapt its pore size through drug adsorption. Therefore, we chose one kind of Fe-MOF, MIL-53(Fe), as a carrier for the anticancer drug oridonin (Ori). In this work, we report the design and synthesis of MIL-53(Fe) and explore its ability as a transport vehicle to deliver Ori. MIL-53(Fe) is characterized by scanning electron microscopy and X-ray powder diffraction. A loading capacity of 56.25 wt % was measured by high performance liquid chromatography. This carrier was safe and nontoxic (cell viability > 95.27%), depending on the results of 3-(4,5-dimethylthiazol-2-yl)--2,5-diphenyltetrazolium bromide assays, lactate dehydrogenase assays, and Annexin V-fluoresce isothiocyanate/propidium iodide double-staining assays. After loading the drug, the structure of the MIL-53(Fe) was not destroyed, and Ori was amorphous in MIL-53(Fe). Based on an analysis of the Ori release profile, results suggest that it lasts for more than seven days in vitro. The cumulative release rate of Ori at the seventh day was about 82.23% and 91.75% in phosphate buffer saline solution at 37 °C under pH 7.2 and pH 5.5, respectively. HepG2 cells were chosen to study the cytotoxicity of Ori@MIL-53(Fe), and the results show that the anticancer ratio of Ori@MIL-53(Fe) system reaches 90.62%. Thus, MIL-53 can be used as a carrier for anticancer drugs and Ori@MIL-53(Fe) is a promising sustained-release drug delivery system for the cancer therapy.

Background Trastuzumab is a first‐line targeted therapy for human epidermal growth factor receptor‐2 (HER2)‐positive gastric cancer. However, the inevitable occurrence of acquired trastuzumab resistance limits the drug benefit, and there is currently no effective reversal measure. Existing researches on the mechanism of trastuzumab resistance mainly focused on tumor cells themselves, while the understanding of the mechanisms of environment‐mediated drug resistance is relatively lacking. This study aimed to further explore the mechanisms of trastuzumab resistance to identify strategies to promote survival in these patients. Methods Trastuzumab‐sensitive and trastuzumab‐resistant HER2‐positive tumor tissues and cells were collected for transcriptome sequencing. Bioinformatics were used to analyze cell subtypes, metabolic pathways, and molecular signaling pathways. Changes in microenvironmental indicators (such as macrophage, angiogenesis, and metabolism) were verified by immunofluorescence (IF) and immunohistochemical (IHC) analyses. Finally, a multi‐scale agent‐based model (ABM) was constructed. The effects of combination treatment were further validated in nude mice to verify these effects predicted by the ABM. Results Based on transcriptome sequencing, molecular biology, and in vivo experiments, we found that the level of glutamine metabolism in trastuzumab‐resistant HER2‐positive cells was increased, and glutaminase 1 (GLS1) was significantly overexpressed. Meanwhile, tumor‐derived GLS1 microvesicles drove M2 macrophage polarization. Furthermore, angiogenesis promoted trastuzumab resistance. IHC showed high glutamine metabolism, M2 macrophage polarization, and angiogenesis in trastuzumab‐resistant HER2‐positive tumor tissues from patients and nude mice. Mechanistically, the cell division cycle 42 (CDC42) promoted GLS1 expression in tumor cells by activating nuclear factor kappa‐B (NF‐κB) p65 and drove GLS1 microvesicle secretion through IQ motif‐containing GTPase‐activating protein 1 (IQGAP1). Based on the ABM and in vivo experiments, we confirmed that the combination of anti‐glutamine metabolism, anti‐angiogenesis, and pro‐M1 polarization therapy had the best effect in reversing trastuzumab resistance in HER2‐positive gastric cancer. Conclusions This study revealed that tumor cells secrete GLS1 microvesicles via CDC42 to promote glutamine metabolism, M2 macrophage polarization, and pro‐angiogenic function of macrophages, leading to acquired trastuzumab resistance in HER2‐positive gastric cancer. A combination of anti‐glutamine metabolism, anti‐angiogenesis, and pro‐M1 polarization therapy may provide a new insight into reversing trastuzumab resistance.