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To identify key genes and shared pathogenic pathways associated with acute pancreatitis-associated acute lung injury (AP-ALI), through bioinformatics analysis, and to provide potential molecular targets for the diagnosis and treatment of AP-ALI. The cerulein-induced severe acute pancreatitis (SAP) mouse lung tissue dataset (GSE244335), lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse lung tissue dataset (GSE216943), and human AP patient peripheral blood dataset (GSE194331) were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened. Subsequently, we conducted a series of bioinformatic analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and protein-protein interaction (PPI) network construction. The PPI network was constructed and hub genes were screened. Cross-species consistency of key pathways was verified using the human dataset. A total of 469 and 153 DEGs were screened from GSE244335 and GSE216943, respectively, with 94 overlapping common DEGs. GO/KEGG enrichment analyses showed that these common DEGs were mainly enriched in immune-inflammatory responses, chemokine receptor binding, and NF-κB signaling pathways. PPI network analysis identified the top 10 hub genes in mice (IL-1β, CCL3, CXCL2, CXCL10, CCL2, CXCL9, CXCL1, CXCR2, TLR2, TNF). Ten hub genes (S100A9, ARG1, RETN, etc.) were screened from the human AP dataset (GSE194331). Cross-species comparison of mouse lung tissue and human peripheral blood revealed 6 common GO-BP terms related to systemic inflammatory responses, suggesting shared mechanisms between local lung injury and systemic inflammation in AP. The identified hub genes (e.g., IL-1β, CXCL2) and the IL-17/NF-κB signaling pathway represent candidate molecular signatures implicated in AP-ALI. These computational findings generate testable hypotheses regarding inflammatory mechanisms, potentially highlighting shared systemic inflammatory processes between mouse lung injury and human peripheral blood. Direct validation in human pulmonary tissue or bronchoalveolar lavage fluid is warranted to confirm their local pathogenic relevance.

Quantum efficiency (QE) is a critical metric for assessing the performance of industrial digital cameras. The current EMVA1288 standard relies on monochromatic light for QE measurements. Comprehensive QE tests across the visible spectrum often involve elaborate setups and extensive data acquisition. Additionally, such tests may not fully capture camera performance under broadband illumination, which is frequently encountered in industrial applications. This study introduces the concept of average quantum efficiency (AQE) using white light sources and proposes a novel testing method. Systematic experiments and data analyses were performed on two industrial digital cameras under white light sources with different spectral distributions. The results suggest that AQE testing offers a practical and efficient means to evaluate camera performance under broadband illumination, complementing existing monochromatic QE measurement methods.

High-Resolution Range Profile (HRRP) radar recognition suffers from data scarcity challenges in real-world applications. We present HRRPGraphNet++, a framework combining dynamic graph neural networks with meta-learning for few-shot HRRP recognition. Our approach generates graph representations dynamically through multi-head self attention (MSA) mechanisms that adapt to target-specific scattering characteristics, integrated with a specialized meta-learning framework employing layer-wise learning rates. Experiments demonstrate state-of-the-art performance in 1-shot (82.3%), 5-shot (91.8%), and 20-shot (94.7%) settings, with enhanced noise robustness (68.7% accuracy at 0 dB SNR). Our hybrid graph mechanism combines physical priors with learned relationships, significantly outperforming conventional methods in challenging scenarios.

Background Anterior cervical discectomy and fusion (ACDF) is a common surgical procedure for treating cervical spine diseases, but its anterior approach can lead to complications such as dysphagia and carotid artery injury due to the large incision. However, performing ACDF under a percutaneous endoscopic approach can effectively mitigate these issues. Considering the need for smaller-sized cages in endoscopic procedures, this study explores the feasibility of using small-sized cages for percutaneous endoscopic ACDF surgery. Methods The finite element method is used in this paper to construct cervical spine surgical models with three different sizes of cages implanted, studying the impact of size on cervical biomechanical performance. The dimensions of the cages remain constant in length and height, with a length of 14 mm and a height of 6 mm, and widths of 7 mm, 10 mm, and 14 mm, respectively. Results In a complete fusion state, the range of motion of the surgery level decreased, while adjacent segments showed a compensatory increase in range of motion. Intervertebral disc pressure increased in adjacent discs during flexion and extension. Facet joint pressure in the operated segments generally decreased across all conditions compared to the intact model, but in non-surgical segments exhibited varied compensatory increases under different conditions. Smaller cages led to increased von Mises stress on the cage and endplates, with stress distribution varying by motion condition. Conclusion The results show that, using a 10 mm wide polyetheretherketone cage in complete fusion does not significantly affect postoperative vertebral stability or adjacent segment degeneration risk. Additionally, the risk of subsidence is relatively low, making it a suitable cage option for percutaneous endoscopic ACDF surgery.

Background Acute lung injury (ALI) is a critical inflammatory response syndrome that rapidly develops into acute respiratory distress syndrome (ARDS). Currently, no effective therapeutic modalities are available for patients with ALI/ARDS. According to recent studies, inhibiting both the release of pro-inflammatory cytokines and the formation of reactive oxygen species (ROS) as early as possible may be a promising therapy for ALI. Results In this study, a ROS-responsive nano-delivery system based on oxidation-sensitive chitosan (Ox-CS) was fabricated for the simultaneous delivery of Ce NPs and RT. The in vitro experiments have shown that the Ox-CS/Ceria-Resatorvid nanoparticles (Ox-CS/CeRT NPs) were rapidly and efficiently internalised by inflammatory endothelial cells. Biological evaluations validated the significant attenuation of ROS-induced oxidative stress and cell apoptosis by Ox-CS/CeRT NPs, while maintaining mitochondrial function. Additionally, Ox-CS/CeRT NPs effectively inhibited the release of pro-inflammatory factors. After intraperitoneal ( i.p. ) administration, Ox-CS/CeRT NPs passively targeted the lungs of LPS-induced inflamed mice and released the drug activated by the high ROS levels in inflammatory tissues. Finally, Ox-CS/CeRT NPs significantly alleviated LPS-induced lung injury through inhibiting both oxidative stress and pro-inflammatory cytokine expression. Conclusions The created Ox-CS/CeRT NPs could act as a prospective nano-delivery system for a combination of anti-inflammatory and anti-oxidant therapy of ALI. Graphical Abstract

Fibroblast growth factors (FGFs) and their receptors (FGFRs) play critical roles in many biological processes and developmental functions. Chromosomal translocation of FGFRs result in the formation of chimeric FGFR fusion proteins, which often cause aberrant signaling leading to the development and progression of human cancer. Due to the high recurrence rate and carcinogenicity, oncogenic FGFR gene fusions have been identified as promising therapeutic targets. Erdafitinib and pemigatinib, two FGFR selective inhibitors targeting FGFR fusions, have been approved by the U.S. Food and Drug Administration (FDA) to treat patients with urothelial cancer and cholangiocarcinoma, respectively. Futibatinib, a third-generation FGFR inhibitor, is under phase III clinical trials in patients with FGFR gene rearrangements. Herein, we review the current understanding of the FGF/FGFRs system and the oncogenic effect of FGFR fusions, summarize promising inhibitors under clinical development for patients with FGFR fusions, and highlight the challenges in this field.

Pancreatic adenocarcinoma is by far the deadliest type of cancer. Inflammation is one of the important risk factors in tumor development. However, it is not yet clear whether deterioration in pancreatic cancer patients is related to inflammation, as well as the underlying mechanism. In addition, JNK is abnormally activated in pancreatic cancer cells and the JNK inhibitor C66 reduces the inflammatory microenvironment in the tumor. Therefore, the aim of this study was to evaluate the role of C66 in the proliferation and migration of pancreatic cancer. Our results showed that various inflammatory cytokines, such as IL-1β, IL-6, IL-8, and IL-15, were more expressed in pancreatic cancer than in the matching normal tissue. Furthermore, C66, a curcumin analogue with good anti-inflammatory activity, inhibited the proliferation and migration of pancreatic cancer cells in a dose-dependent manner, and effectively inhibited the expression of the above inflammatory factors. Our previous research demonstrated that C66 prevents the inflammatory response by targeting JNK. Therefore, in this study, JNK activity in pancreatic cancer cells was investigated, revealing that JNK was highly activated, and the treatment with C66 inhibited the phosphorylation of JNK. Next, shJNK was used to knockdown JNK expression in pancreatic cancer cells to further confirm the role of JNK in the proliferation and migration of this tumor, as well as in the inflammatory tumor microenvironment (TME). The results demonstrated that JNK knockdown could significantly inhibit the proliferation and migration of pancreatic cancer. Moreover, the low JNK expression in pancreatic cancer cells significantly inhibited the expression of various inflammatory factors. These results indicated that C66 inhibited the progression of pancreatic cancer through the inhibition of JNK-mediated inflammation.

Diabetes manifests as chronic inflammation and leads to the development diabetic cardiomyopathy (DCM). Targeting key proteins in inflammatory signaling may provide new therapy for DCM. In this study, the authors explore the pharmacological effects and mechanisms of Schisandrin B (Sch B), a natural compound with anti‐inflammatory activity against DCM. It is shown that Sch B prevents high‐level glucose (HG)‐induced hypertrophic and fibrotic responses in cultured cardiomyocytes. RNA sequencing and inflammatory qPCR microarray show that Sch B mainly affects myeloid differentiation primary response 88 (MyD88)‐dependent inflammatory gene expression in HG‐challenged cardiomyocytes. Further studies indicate that Sch B directly binds to and inhibits MyD88 activation, but does not alter MyD88‐independent Toll‐like receptor signaling in vivo and in vitro. Inhibiting or silencing MyD88 is associated with reduced levels of HG‐induced inflammatory cytokines and myocardial injuries in vitro. Treatment of type 1 and type 2 diabetic mice with Sch B protects heart function, reduces myocardial injuries, and decreases secretion of inflammatory cytokines. Cardiomyocyte‐specific MyD88 knockout also protects mice against cardiac inflammation and injury in type 1 diabetic mice. In conclusion, these studies show that cardiomyocyte MyD88 plays an apathogenetic role in DCM and Sch B specifically targets MyD88 to reduce inflammatory DCM. Hyperglycemia/high‐concentration glucose (HG) activates Toll‐like receptors (TLRs)‐MyD88 in cardiomyocytes and heart tissues. MyD88‐mediated activation of TAK1‐MAPKs/NF‐κB signaling causes increased production of inflammatory factors, leading to cardiomyocyte hypertrophy and fibrosis. Schisandrin B is able to bind to the TIR domain of MyD88, potentially through Thr‐272 and Arg‐288 sites. Such binding suppresses TAK1‐MAPKs/NF‐κB activation and attenuates inflammatory diabetic cardiomyopathy.

The relationship between the expression of the SATB2 and CDX2 proteins and common molecular changes and clinical prognosis in colorectal cancer (CRC) still needs further clarification. We collected 1180 cases of CRC and explored the association between the expression of SATB2 and CDX2 and clinicopathological characteristics, molecular alterations, and overall survival of CRC using whole-slide immunohistochemistry. Our results showed that negative expression of SATB2 and CDX2 was more common in MMR-protein-deficient CRC than in MMR-protein-proficient CRC (15.8% vs. 6.0%, P  = 0.001; 14.5% vs. 4.0%, P  = 0.000, respectively). Negative expression of SATB2 and CDX2 was more common in BRAF -mutant CRC than in BRAF wild-type CRC (17.2% vs. 6.1%, P  = 0.003; 13.8% vs. 4. 2%; P  = 0.004, respectively). There was no relationship between SATB2 and/or CDX2 negative expression and KRAS , NRAS , and PIK3CA mutations. The lack of expression of SATB2 and CDX2 was associated with poor histopathological features of CRC. In multivariate analysis, negative expression of SATB2 (P = 0.030), negative expression of CDX2 (P = 0.043) and late clinical stage (P = 0.000) were associated with decreased overall survival of CRC. In conclusion, the lack of SATB2 and CDX2 expression in CRC was associated with MMR protein deficiency and BRAF mutation, but not with KRAS , NRAS and PIK3CA mutation. SATB2 and CDX2 are prognostic biomarkers in patients with CRC.

Purpose This study examines how digital transformation affects the operational performance of Chinese manufacturing firms, with a focus on multidimensional impact mechanisms. Design/methodology/approach Using the “Technology-Organization-External Network” framework, we analyze a dataset from 2,346 listed Chinese manufacturing firms (2011–2021) to empirically test the impact of digital transformation on operational performance. Findings Digital transformation significantly improves manufacturing enterprises’ performance by enhancing innovation effectiveness, boosting labor productivity, increasing organizational management efficiency, reducing supply chain dependence and strengthening capital market recognition. The transformation’s effect evolves from negative to positive over time, emphasizing the need for sustained investment. Originality/value This study innovatively proposes the “Technology-Organization-External Network” framework to reveal the multidimensional mechanisms. It further validates the long-term benefits of digital transformation and highlights the importance of external conditions such as digital infrastructure, financial development and industry competition intensity.