Estimating the water quality index based on interpretable machine learning models.

The water quality index (WQI) is an important tool for evaluating the water quality status of lakes. In this study, we used the WQI to evaluate the spatial water quality characteristics of Dianchi Lake. However, the WQI calculation is time-consuming, and machine learning models exhibit significant advantages in terms of timeliness and nonlinear data fitting. We used a machine learning model with optimized parameters to predict the WQI, and the light gradient boosting machine achieved good predictive performance. The machine learning model trained based on the entire Dianchi Lake water quality data achieved coefficient of determination (R2), mean square error, and mean absolute error values of 0.989, 0.228, and 0.298, respectively. In addition, we used the Shapley additive explanations (SHAP) method to interpret and analyse the machine learning model and identified the main water quality parameter that affects the WQI of Dianchi Lake as NH4+-N. Within the entire range of Dianchi Lake, the SHAP values of NH4+-N varied from -9 to 3. Thus, in future water environmental governance, it is necessary to focus on NH4+-N changes. These results can provide a reference for the treatment of lake water environments.

Fructose Metabolism in Tumor Endothelial Cells Promotes Angiogenesis by Activating AMPK Signaling and Mitochondrial Respiration.

Angiogenesis is vital for tumor growth and metastasis. Emerging evidence suggests that metabolic reprogramming in endothelial cells (EC) may affect angiogenesis. Here, we showed that multiple regulators in the fructose metabolism pathway, especially fructose transporter SLC2A5 and fructose-metabolizing enzyme ketohexokinase (KHK), were upregulated in tumor endothelial cells from hepatocellular carcinoma (HCC). In mouse models with hepatoma xenografts or with Myc/sgp53-induced liver cancer, dietary fructose enhanced tumor angiogenesis, tumor growth, and metastasis, which could be attenuated by treatment with an inhibitor of SLC2A5. Furthermore, vessel growth was substantially increased in fructose-containing Matrigel compared with PBS-Matrigel. Inhibiting fructose metabolism in EC cells in vivo using EC-targeted nanoparticles loaded with siRNA against KHK significantly abolished fructose-induced tumor angiogenesis. Fructose treatment promoted the proliferation, migration, and tube formation of ECs and stimulated mitochondrial respiration and ATP production. Elevated fructose metabolism activated AMPK to fuel mitochondrial respiration, resulting in enhanced EC migration. Fructose metabolism was increased under hypoxic conditions as a result of HIF1α-mediated upregulation of multiple genes in the fructose metabolism pathway. These findings highlight the significance of fructose metabolism in ECs for promoting tumor angiogenesis. Restricting fructose intake or targeting fructose metabolism is a potential strategy to reduce angiogenesis and suppress tumor growth. SIGNIFICANCE: Fructose metabolism in endothelial cells fuels mitochondrial respiration to stimulate tumor angiogenesis, revealing fructose metabolism as a therapeutic target and fructose restriction as a dietary intervention for treating cancer.