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Pancreatic surgery is characterized by great trauma, difficult operation, high risk and high complication rate. Minimally invasive, refined and standardized pancreatic surgery is the future trend. With its advantages of high precision, high safety, and more realistic and clear operating field, robotic pancreatic surgery has gradually become the preferred method of pancreatic surgery worldwide. In the past 10 years, more than a dozen large pancreas centers in China have matured to carry out robotic pancreatic surgery, including pancreaticoduodenectomy, pancreaticocaudectomy, pancreatic tumor enucleation, middle pancreatectomy, total pancreatectomy, pancreaticodectomy with duodenum preserved and other pancreatic surgery methods. However, there are still some problems in robotic pancreatic surgery, such as complex system construction, lack of force feedback, inadequate imaging fusion, and immature remote operation. Pancreatic surgeons should continue to carry out high-quality clinical studies on robotic pancreatic surgery to verify its safety and effectiveness, and standardize robotic pancreatic surgery with the accumulation of experience.

The development of high-performance and cost-effective electrocatalysts toward the oxygen evolution reaction (OER) is remarkably desirable but challenging. Herein, we design and fabricate a sea urchin-like S-doped Ni(OH)2 electrocatalyst on nickel foam using a simple hydrothermal method, followed by treatment with Na2S solution. The introduction of S not only modulates the electronic structure of Ni(OH)2, but also improves the electronic conductivity, thus enhancing the OER performance of Ni(OH)2. Owing to the free-standing feature, modified electronic structure, and sea urchin-like structure, the optimized S-Ni(OH)2–30 min delivers excellent OER performance with overpotentials of 306 and 392 mV at 10 and 100 mA cm−2, respectively, Tafel slope of 89.2 mV dec−1, and stability for 30 h at 50 mA cm−2. This work demonstrates the importance of incorporating S in Ni(OH)2 to optimize the electronic structure for improving OER activity and provides a promising pathway to synthesize Ni(OH)2-based electrocatalysts. [ABSTRACT FROM AUTHOR]

Background: Pancreatic cancer is a highly aggressive neoplasm characterized by poor diagnosis. Amino acids play a prominent role in the occurrence and progression of pancreatic cancer as essential building blocks for protein synthesis and key regulators of cellular metabolism. Understanding the interplay between pancreatic cancer and amino acid metabolism offers potential avenues for improving patient clinical outcomes. Methods: A comprehensive analysis integrating 10 machine learning algorithms was executed to pinpoint amino acid metabolic signature. The signature was validated across both internal and external cohorts. Subsequent GSEA was employed to unveil the enriched gene sets and signaling pathways within high- and low-risk subgroups. TMB and drug sensitivity analyses were carried out via Maftools and oncoPredict R packages. CIBERSORT and ssGSEA were harnessed to delve into the immune landscape disparities. Single-cell transcriptomics, qPCR, and Immunohistochemistry were performed to corroborate the expression levels and prognostic significance of this signature. Results: A four gene based amino acid metabolic signature with superior prognostic capabilities was identified by the combination of 10 machine learning methods. It showed that the novel prognostic model could effectively distinguish patients into high- and low-risk groups in both internal and external cohorts. Notably, the risk score from this novel signature showed significant correlations with TMB, drug resistance, as well as a heightened likelihood of immune evasion and suboptimal responses to immunotherapeutic interventions. Conclusion: Our findings suggested that amino acid metabolism-related signature was closely related to the development, prognosis and immune microenvironment of pancreatic cancer. [ABSTRACT FROM AUTHOR]

In this study, CO2 reacted with a curing agent through nucleophilic addition to form ammonium salts, enabling the stable capture and internal release of CO2, which achieved gas-phase nucleation and foaming. Additionally, the introduction of wave-absorbing agents improved the absorption mechanism and promoted uniform foaming. This nucleation-free foaming process relies on the induced growth of gas nuclei and the synergistic effect of the wave-absorbing agents, effectively preventing the uneven foaming issues caused by traditional nucleating agents. Ultimately, a lightweight epoxy foam absorbing material (LFAM) was developed. BET tests showed that 2.0 wt% carbon-based wave-absorbing agents (LFAMs–A2) expanded the material's volume to 4.6 times its original size, forming a uniform porous structure. VNA tests revealed that LFAMs–A2 achieved a minimum reflection loss of −13.25 dB and an absorption bandwidth of 3.7 GHz in the 12–18 GHz range. The material with 2.0 wt% ferrite-based wave-absorbing agents (LFAMs–C2) achieved a minimum reflection loss of −26.83 dB at 16.6 GHz and an absorption bandwidth of 5.3 GHz, nearly covering the Ku band. DSC tests indicated that the material maintained good thermal stability at 150 °C. This study provides a new approach for lightweight coatings and structural optimization, with broad application potential in 5G communications, microwave anechoic chambers, and aerospace fields. [ABSTRACT FROM AUTHOR]

Pancreatic cancer remains one of the most lethal malignant diseases. Gemcitabine‐based chemotherapy is still one of the first‐line systemic treatments, but chemoresistance occurs in the majority of patients. Recently, accumulated evidence has demonstrated the role of the tumour microenvironment in promoting chemoresistance. In the tumour microenvironment, pancreatic stellate cells (PSCs) are among the main cellular components, and extracellular vesicles (EVs) are common mediators of cell‒cell communication. In this study, we showed that SP1‐transcribed miR‐31‐5p not only targeted LATS2 in pancreatic cancer cells but also regulated the Hippo pathway in PSCs through EV transfer. Consequently, PSCs synthesized and secreted protein acidic and rich in cysteins (SPARC), which was preferentially expressed in stromal cells, stimulating Extracellular Signal regulated kinase (ERK) signalling in pancreatic cancer cells. Therefore, pancreatic cancer cell survival and chemoresistance were improved due to both the intrinsic Hippo pathway regulated by miR‐31‐5p and external SPARC‐induced ERK signalling. In mouse models, miR‐31‐5p overexpression in pancreatic cancer cells promoted the chemoresistance of coinjected xenografts. In a tissue microarray, pancreatic cancer patients with higher miR‐31‐5p expression had shorter overall survival. Therefore, miR‐31‐5p regulates the Hippo pathway in multiple cell types within the tumour microenvironment via EVs, ultimately contributing to the chemoresistance of pancreatic cancer cells. [ABSTRACT FROM AUTHOR]