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Superconducting materials have extremely high application value in our life. At present, the discovery of new superconducting materials relies on the experience of experts through a large number of "trial and error" experiments. Obtaining the properties of superconductors also requires a large number of experiments. In this paper, we propose to use the XGBoost model to identify superconductors, reaching 0.986 in accuracy. We apply the deep forest algorithm to predict the critical temperature of superconductors and the coefficient of determination reaches 0.944. We propose to apply the same algorithm to predict the forbidden band width of materials and the coefficient of determination reaches 0.917. A new sub-network structure is constructed to predict the Fermi level of materials and the coefficient of determination reaches 0.984. All of these algorithms have state-of-the-art performance. Finally, the model is tested with a publicly available dataset to identify 50 candidate superconducting materials with a critical temperature greater than 90K.

Background and aim: Small ubiquitin–like modifier (SUMO)-specific protease (SENP)3 is a protease molecule that responds to reactive oxygen species (ROS) with high sensitivity. However, the role of ROS and SENP3 in the formation of nasal polyps (NPs) remains unclear. This study aimed to explore how SENP3 influenced the outcome of chronic rhinosinusitis (CRS) by altering macrophage function, that is, the formation of NPs. Methods: The alternative activation of macrophage (M2) was detected with CD68+CD206+ in humans and CD206+ in mice. The nasal mucosa of patients with CRS was tested using flow cytometry (CD68, CD80, and CD206) and triple-color immunofluorescence staining (CD68, CD206, and SENP3). The bone marrow–derived macrophages from SENP3 knockout and control mice were stimulated with interleukin (IL)-4 and IL-13 to analyze alternative macrophage polarization in vitro. An animal model of eosinophil infiltration rhinitis was constructed using SENP3 knockout mice. CD206 was detected by immunofluorescence staining. The thickening of eosinophil-infiltrated mucosa was detected by Luna staining. Results: The number of CD68+ CD206+ M2 increased in the nasal mucosa of patients with CRS with NP (CRSwNP) compared with patients with CRS without NP (CRSsNP), but with no significant difference between the groups. SENP3 knockout increased the polarization of F4/80+CD206+M2. Meanwhile, the number of CD206+M2 significantly increased in the osinophil infiltration rhinitis model constructed using SENP3 knockout mice and controls, with a more obvious proliferation of the nasal mucosa. Conclusion: The downregulation of the expression of macrophage SENP3 in the nasal mucosa in osinophil infiltration rhinitis promoted the formation of NPs. Trial registration: This study was retrospective and did not involve any health interventions for human participants.