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Pancreatic cancer is characterized by high malignancy, low early diagnosis rates, and poor prognosis. Approximately 15%-20% of patients at initial diagnosis have resectable pancreatic cancer, 20%-30% have borderline resectable pancreatic cancer, and over 50% are present with unresectable. Surgical resection remains the only potentially curative treatment option available, but the unique anatomical position of the pancreatic head necessitates complex gastrointestinal reconstruction after resection, which may lead to severe complications such as grade B/C pancreatic fistulas and bleeding. Comprehensive preoperative preparation and individualized postoperative management are crucial to reducing perioperative complications, enhancing patient quality of life, and expediting the initiation of adjuvant therapy. This article reviews perioperative integrated management strategies for patients with pancreatic cancer, drawing on literature and our center's experience, including nutritional therapy, psychological support, preoperative jaundice reduction, neoadjuvant treatment, the prevention and management of pancreatic fistulas and postoperative bleeding, with the aim of improving clinical outcomes and overall survival rates.

Metabolic reprogramming provides tumors with an energy source and biofuel to support their survival in the malignant microenvironment. Extensive research into the intrinsic oncogenic mechanisms of the tumor microenvironment (TME) has established that cancer-associated fibroblast (CAFs) and metabolic reprogramming regulates tumor progression through numerous biological activities, including tumor immunosuppression, chronic inflammation, and ecological niche remodeling. Specifically, immunosuppressive TME formation is promoted and mediators released via CAFs and multiple immune cells that collectively support chronic inflammation, thereby inducing pre-metastatic ecological niche formation, and ultimately driving a vicious cycle of tumor proliferation and metastasis. This review comprehensively explores the process of CAFs and metabolic regulation of the dynamic evolution of tumor-adapted TME, with particular focus on the mechanisms by which CAFs promote the formation of an immunosuppressive microenvironment and support metastasis. Existing findings confirm that multiple components of the TME act cooperatively to accelerate the progression of tumor events. The potential applications and challenges of targeted therapies based on CAFs in the clinical setting are further discussed in the context of advancing research related to CAFs. [ABSTRACT FROM AUTHOR]

Various amounts of TiSi2 (30, 40, and 50 wt.%) were added to 3 mol% yttria stabilized tetragonal zirconia polycrystals (3Y‐TZP) to fabricate 3Y‐TZP/TiSi2 composites by vacuum sintering. The effects of the TiSi2 added amount, as well as the sintering temperature on the microstructure, mechanical, and electrical characteristics of the 3Y‐TZP/TiSi2 composites were examined. The sintered samples consisted of three phases: tetragonal (t‐ZrO2), TiSi2, and reaction product Ti5Si3. The maximum bending strength and relative density of the composites, reaching 501.20 MPa and 98.59% respectively, were achieved at a TiSi2 content of 30 wt.% and sintering temperature of 1500°C. The resistivity of 3Y‐TZP/TiSi2 composites showed a nonlinear decrease with increasing TiSi2 content. These results indicated that 3Y‐TZP/TiSi2 composites had a typical percolation threshold phenomenon due to the different TiSi2 content and a conductivity model of 3Y‐TZP/TiSi2 composites at room temperature was founded on the generalized effective medium equation. The resistivity of the composites could optionally adjust between 102 and 10−4Ω·cm with 30–50 wt.% TiSi2 under room temperature. Overall, the 3Y‐TZP/TiSi2 composites show great potential for applications in the heat‐not‐burn tobacco field. [ABSTRACT FROM AUTHOR]

Femtosecond laser processing technology has been used to achieve controlled processing of microtips array on the surface of polycrystalline LaB6 blocks. Under the condition of ensuring the integrity of the geometric morphology of the tips array, the tips with a height of 10 μm and a radius of curvature of 1 μm can be processed. The distribution of tips in the array is uniform, the morphology is complete, the crystal structure and physical phase of LaB6 have not changed after processing, which breaks through the technical problems of difficult processing and poor geometry consistency about polycrystalline rare-earth hexaboride tips emitter, and the processing area is no longer limited by the small size of single crystals. The field emission performance test indicated that the turn-on electric field is 2.8 V/μm, and the current density is 467.9 mA/cm2 when the applied electric field reached 9.4 V/μm. [ABSTRACT FROM AUTHOR]

Retinal vessel segmentation plays a vital role in the medical field, facilitating the identification of numerous chronic conditions based on retinal vessel images. These conditions include diabetic retinopathy, hypertensive retinopathy, glaucoma, and others. Although the U-Net model has shown promising results in retinal vessel segmentation, it tends to struggle with fine branching and dense vessel segmentation. To further enhance the precision of retinal vessel segmentation, we propose a novel approach called transformer dilated convolution attention U-Net (TDCAU-Net), which builds upon the U-Net architecture with improved Transformer-based dilated convolution attention mechanisms. The proposed model retains the three-layer architecture of the U-Net network. The Transformer component enables the learning of contextual information for each pixel in the image, while the dilated convolution attention prevents information loss. The algorithm efficiently addresses several challenges to optimize blood vessel detection. The process starts with five-step preprocessing of the images, followed by chunking them into segments. Subsequently, the retinal images are fed into the modified U-Net network introduced in this paper for segmentation. The study employs eye fundus images from the DRIVE and CHASEDB1 databases for both training and testing purposes. Evaluation metrics are utilized to compare the algorithm's results with state-of-the-art methods. The experimental analysis on both databases demonstrates that the algorithm achieves high values of sensitivity, specificity, accuracy, and AUC. Specifically, for the first database, the achieved values are 0.8187, 0.9756, 0.9556, and 0.9795, respectively. For the second database, the corresponding values are 0.8243, 0.9836, 0.9738, and 0.9878, respectively. These results demonstrate that the proposed approach outperforms state-of-the-art methods, achieving higher performance on both datasets. The TDCAU-Net model presented in this study exhibits substantial capabilities in accurately segmenting fine branching and dense vessels. The segmentation performance of the network surpasses that of the U-Net algorithm and several mainstream methods. [ABSTRACT FROM AUTHOR]

1,4-Naphthoquinone scaffold-derived compounds has shown considerable pharmacological properties against cancer, including acute myeloid leukemia (AML) However, its impact and mechanisms in AML are uncertain. In this study, the mechanisms of 1,4-naphthoquinone scaffold-derived compounds against AML were investigated via network pharmacology, molecular docking and molecular dynamics simulation. ASINEX database was used to collect the 1,4-naphthoquinone scaffold-derived compounds, and compounds were extracted from the software to evaluate their drug similarity and toxicity. The potential targets of compounds were retrieved from the SwissTargetPrediction Database and the Similarity Ensemble Approach Database, while the potential targets of AML were obtained from the GeneCards databases and Gene Expression Omnibus. The STRING database was used to construct a protein–protein interaction (PPI) network, topologically and Cyto Hubb plugin of Cytoscape screen the central targets. After selecting the potential key targets, the gene ontology (GO) function annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed for the intersection targets, and a network map of "compounds-potential targets-pathway-disease" were constructed. Molecular docking of the compounds with the core target was performed, and core target with the strongest binding force and 1,4-naphthoquinone scaffold-derived compounds was selected for further molecular dynamics simulation and further molecular mechanics/Poisson–Boltzmann surface area (MM/PBSA) approach verification. In addition, the Bloodspot database was applied to perform the overall survival of core targets. A total of 19 1,4-naphthoquinone scaffold-derived compounds were chosen out, and then 836 targets of compounds, 96 intersection targets of AML were screened. Core targets include STAT3, TLR4, HSP90AA1, JUN, MMP9, PTPRC, JAK2, PTGS2, KIT and CSF1R. GO functional enrichment analysis revealed that 90 biological processes, 10 cell components and 12 molecular functions were enriched while KEGG pathway enrichment analysis revealed 34 enriched signaling pathways. Analysis of KEGG enrichment hinted that these 10 core genes were located in the pathways in cancer, suggesting that 1,4-naphthoquinone scaffold-derived compounds had potential activity against AML. Molecular docking analysis revealed that the binding energies between 1,4-naphthoquinone scaffold-derived compounds and the core proteins were all higher than − 6 kcal/mol, indicating that the 10 core targets all had strong binding ability with compounds. Moreover, a good binding capacity was inferred from molecular dynamics simulations between compound 7 and MMP9. The total binding free energy calculated using the MM/GBSA approach revealed values of − 6356.865 kcal/mol for the MMP9-7 complex. In addition, Bloodspot database results exhibited that HSP90AA1, MMP9 and PTPRC were associated with overall survival. The findings provide foundations for future studies into the interaction underlying the anti-AML potential of compounds with 1,4-naphthoquinone-based scaffold structures. Compounds with 1,4-naphthoquinone-based scaffold structures exhibits considerable potential in mitigating and treating AML through multiple targets and pathways. [ABSTRACT FROM AUTHOR]

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Background: Breast cancer is the second leading cause of cancer-related death in women, and drug resistance during treatment is a major challenge. However, the mechanisms underlying drug resistance are not fully understood. Here we applied whole-exome sequencing (WES) to clarify resistant rules to Herceptin and tyrosine kinase inhibitors (TKIs). Methods: There are 12 HER2+ breast cancer patients who were done WES. Samples from tumor and surrounding tissues underwent DNA sequencing and analysis. Various experimental and bioinformatics techniques were employed, including genomic capture, mutation analysis (Genome Analysis Toolkit (GATK), etc.), bioinformatics assessments, and drug-gene interaction investigations. Ultimately, the study explored the association of APOB gene expression with breast cancer recurrence rates, immune cell infiltration, and drug response. Results: The C > T mutation frequency was highest in the Herceptin-insensitive (HI) and verification groups, codenamed YI, contrasting with the Herceptin-sensitive (HE) group. No microsatellite instability (MSI)-H patients were in the HE group, but both HI and YI groups had 1 each. Significant differences in transition-transversion (TiTv) were observed in the HI and YI groups rather than the HE group. In the TKI- insensitive (TI) group, C > T mutations were highest, differing from the TKI-sensitive (TE) group. TE group included 2 MSI-H patients. Significant differences in TiTv were found in the TI group rather than the TE group. Mutated APOB may resist Herceptin and TKI, increasing immune infiltration. We identified potential drugs targeting it. Conclusions: Our study suggested that a higher percentage of C > T mutations, significant differences in TiTv, and MSI-H status may indicate Herceptin resistance, while a higher percentage of C > T mutations, significant differences in TiTv, and the absence of MSI-H may indicate TKI resistance in breast cancer patients. For patients resistant to both Herceptin and TKI, mutated APOB may play a crucial role in resistance. [ABSTRACT FROM AUTHOR]