The Northern Sea Route (NSR) makes travel between Europe and Asia shorter and quicker than a southern transit via the Strait of Malacca and Suez Canal. It provides greater access to Arctic resources such as oil and gas. As global warming accelerates, melting Arctic ice caps are likely to increase traffic in the NSR and enhance its commercial viability. Due to the harsh Arctic environment imposing threats to the safety of ship navigation, it is necessary to assess Arctic navigation risk to maintain shipping safety. Currently, most studies are focused on the conventional assessment of the risk, which lacks the validation based on actual data. In this study, actual data about Arctic navigation environment and related expert judgments were used to generate a structured data set. Based on the structured data set, extreme gradient boosting (XGBoost) and alternative methods were used to establish models for the assessment of Arctic navigation risk, which were validated using cross-validation. The results show that compared with alternative models, XGBoost models have the best performance in terms of mean absolute errors and root mean squared errors. The XGBoost models can learn and reproduce expert judgments and knowledge for the assessment of Arctic navigation risk. Feature importance (FI) and shapley additive explanations (SHAP) are used to further interpret the relationship between input data and predictions. The application of XGBoost, FI, and SHAP is aimed to improve the safety of Arctic shipping using advanced artificial intelligence techniques. The validated assessment enhances the quality and robustness of assessment.
In advanced diabetic kidney disease (DKD), tubulointerstitial fibrosis (TIF) is a key histopathological lesion accompanying progressive renal functional decline. However, the tubular mechanisms that drive tubulointerstitial fibrogenesis remain incompletely understood. N-acetyltransferase 10 (NAT10) mediates mRNA N4-acetylcytidine (ac4C) modification, but its role and therapeutic potential in DKD are unknown. We investigated NAT10 regulation and function using cultured tubular cells, diabetic mouse models, patient kidney specimens, and tubule-specific Nat10 knockout mice, together with pharmacological treatment using guanosine diphosphate disodium salt. High glucose or diabetes increased tubular NAT10 abundance in cultured cells, mouse kidneys, and human DKD tissues through activation of NF-κB signaling. Mechanistically, NAT10 in tubular cells stabilized Brd4 and Pfkm mRNAs through ac4C modification, activating the STAT3/TGF-β and lactate/H3K18 lactylation pathways. These pathways synergistically promoted fibroblast activation through NOTCH/SMAD3 signaling and formed a positive feedback loop with NF-κB. Tubule-specific Nat10 deletion reduced Brd4 and Pfkm expression, suppressed the associated signaling cascades, and mitigated kidney fibrosis in the DKD model. Consistently, guanosine diphosphate disodium salt alleviated renal injury and fibrosis in db/db mice. Thus, NAT10 drives tubular fibrosis through ac4C-dependent profibrotic signaling, supporting NAT10 inhibition as a potential therapeutic strategy for DKD.