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Inflammatory bowel diseases (IBD) are chronic inflammatory disorders affecting the digestive tract, including ulcerative colitis and Crohn's disease. Ruscogenin, a prominent steroidal sapogenin present in radix ophiopogon japonicus, has shown a protective effect on attenuating the inflammatory response associated with inflammatory diseases, but the efficacy of ruscogenin in IBD remains unclear. The aim of this study is to explore the effect of ruscogenin on intestinal barrier dysfunction and inflammatory responses as well as the underlying mechanism in ulcerative colitis. A dextran sulfate sodium salt (DSS)-induced C57BL/6 mouse colitis model was employed for the in vivo studies, while in vitro experiments were performed in THP-1 cells and human intestinal epithelial cells involved in inducing inflammatory responses and pyroptosis using LPS/nigericin. The results indicated that ruscogenin treatment attenuated the symptoms of ulcerative colitis, reduced the release of inflammatory cytokines and the expression of pyroptosis-associated proteins, and restored the integrity of the intestinal epithelial barrier in colon tissue in mice. Moreover, ruscogenin inhibited LPS/nigericin-induced pyroptosis in THP-1 cells. Mechanically, ruscogenin inhibited NLRP3 inflammasome activation and canonical pyroptosis, at least in part, through the suppression of the TLR4/NF-κB signaling pathway. These findings might provide new insights and a solid foundation for further exploration into the therapeutic potential of ruscogenin in the treatment of IBD. [ABSTRACT FROM AUTHOR]

Ulcerative colitis is a chronic inflammatory bowel disorder that is hard to cure once diagnosed. Bisdemethoxycurcumin has shown positive effects on inflammatory diseases. However, the underlying bioactive interaction between bisdemethoxycurcumin and ulcerative colitis is unclear. The objective of this study was to determine the core target and potential mechanism of action of bisdemethoxycurcumin as a therapy for ulcerative colitis. The public databases were used to identify potential targets for bisdemethoxycurcumin and ulcerative colitis. To investigate the potential mechanisms, the protein-protein interaction network, gene ontology analysis, and Kyoto encyclopedia of genes and genomes analysis have been carried out. Subsequently, experimental verification was conducted to confirm the findings. A total of 132 intersecting genes of bisdemethoxycurcumin, as well as ulcerative coli-tis-related targets, were obtained. SRC, EGFR, AKT1, and PIK3R1 were the targets of highest potential, and the PI3K/Akt and MAPK pathways may be essential for the treatment of ulcerative colitis by bisdemethoxycurcumin. Molecular docking demonstrated that bisdemethoxycurcumin combined well with SRC, EGFR, PIK3R1, and AKT1. Moreover, the in vitro experiments suggested that bisdemethoxycurcumin might reduce LPS-induced pro-inflammatory cytokines levels in RAW264.7 cells by suppressing PI3K/Akt and MAPK pathways. Our study provided a comprehensive overview of the potential targets and molecular mechanism of bisdemethoxycurcumin against ulcerative colitis. Furthermore, it also provided a theoretical basis for the clinical treatment of ulcerative colitis, as well as compelling evidence for further study on the mechanism of bisdemethoxycurcumin in the treatment of ulcerative colitis. [ABSTRACT FROM AUTHOR]

As asymmetric interior permanent magnet synchronous motor (AIPMSM) has excellent performance but complicated topological structure, a novel high-resolution encoding and edge smoothing method is proposed for topology optimization of the asymmetric rotor of interior permanent magnet synchronous motor (IPMSM) in this study. This method aims to solve complex electromagnetic design problems with time-dependent performance through a multi-objective genetic algorithm (MOGA) integrated with a high-resolution encoding and edge smoothing method. The complex structure is represented by a high-resolution image-like matrix and then vectorized by the edge smoothing method. Therefore, the commonly used discrete binary encoded variables related to the finite element (FE) model are replaced with a vectorized topological structure and other control variables. In this sense, high-resolution matrix and edge smoothing methods are used for the first time to represent the rotor topology of AIPMSMs. Compared with the traditional topology optimization method, the proposed method has the advantage of expressing more complex and vectorized topological structures; meanwhile, the obtained performance is accurate and trustworthy using conventional FE simulation. Numerical results show that a stable convergence is achieved with the avoidance of checkerboards and material overlapping. It is shown that the proposed method can find solutions with better performances, in comparison with the reference model. [ABSTRACT FROM AUTHOR]

The demand for fast magnetic field approximation for the optimal design of electromagnetic devices is urgent nowadays. However, due to the lack of a publicly available dataset and the unclear definition of each parameter in the magnetic field dataset, the expansion of data-driven magnetic field approximation is severely limited. This study presents a physics-informed generative adversarial network (PIGAN), as well as a permanent magnet linear synchronous motor (PMLSM)-based magnetic field dataset, for fast magnetic field approximation. It includes the current density, material distribution, electromagnetic material properties, and other parameters of the electric machine. Physics-informed loss functions are utilized in the training process, making the output governed by Maxwell's equation. Different slot-pole combinations of the PMLSM are involved in the dataset to extend the generalization of PIGAN. Some indicators for the further evaluation of magnetic approximation performance, including image-based metrics and calculation methods for the performance of electric motors, are presented in this study. Some challenges of magnetic field approximation using PIGAN are also discussed. The effectiveness of the physics-informed method is verified by comparing the magnetic field approximation results and the performance analysis results of the PMLSM with FEM, and the speed of PIGAN is approximately 40 times faster than that of FEM, while the accuracy is similar. [ABSTRACT FROM AUTHOR]

Ulcerative colitis is a chronic inflammatory bowel disorder that is hard to cure once diagnosed. Bisdemethoxycurcumin has shown positive effects on inflammatory diseases. However, the underlying bioactive interaction between bisdemethoxycurcumin and ulcerative colitis is unclear. The objective of this study was to determine the core target and potential mechanism of action of bisdemethoxycurcumin as a therapy for ulcerative colitis. The public databases were used to identify potential targets for bisdemethoxycurcumin and ulcerative colitis. To investigate the potential mechanisms, the protein-protein interaction network, gene ontology analysis, and Kyoto encyclopedia of genes and genomes analysis have been carried out. Subsequently, experimental verification was conducted to confirm the findings. A total of 132 intersecting genes of bisdemethoxycurcumin, as well as ulcerative coli-tis-related targets, were obtained. SRC, EGFR, AKT1, and PIK3R1 were the targets of highest potential, and the PI3K/Akt and MAPK pathways may be essential for the treatment of ulcerative colitis by bisdemethoxycurcumin. Molecular docking demonstrated that bisdemethoxycurcumin combined well with SRC, EGFR, PIK3R1, and AKT1. Moreover, the in vitro experiments suggested that bisdemethoxycurcumin might reduce LPS-induced pro-inflammatory cytokines levels in RAW264.7 cells by suppressing PI3K/Akt and MAPK pathways. Our study provided a comprehensive overview of the potential targets and molecular mechanism of bisdemethoxycurcumin against ulcerative colitis. Furthermore, it also provided a theoretical basis for the clinical treatment of ulcerative colitis, as well as compelling evidence for further study on the mechanism of bisdemethoxycurcumin in the treatment of ulcerative colitis.