DC Traction Power Supply System Based on Modular Multilevel Converter Suitable for Energy Feeding and De-icing

A novel DC traction power supply system suitable for energy feeding and de-icing is proposed in this paper for an urban rail transit catenary on the basis of the full bridge submodule (FBSM) modular multilevel converter (MMC). The FBSM-MMC is a novel type of voltage source converter (VSC) and can directly control the output DC voltage and conduct bipolar currents, thus flexibly controlling the power flow of the urban rail transit catenary. The proposed topology can overcome the inherent disadvantages of the output voltage drop in the diode rectifier units, increase the power supply distance and reduce the number of traction substations. The flexible DC technology can coordinate multiple FBSM-MMCs in a wide area and jointly complete the bidirectional control of catenary power flow during the operation of the electric locomotive, so as to realize the local consumption and optimal utilization of the recovered braking energy of the train. In addition, the FBSM-MMCs can also adjust the output current when the locomotive is out of service to prevent the catenary from icing in winter. The working modes of the proposed topology are illustrated in detail and the control strategy is specially designed for normal locomotive operations and catenary de-icing. Simulation cases conducted by PSCAD/EMTDC validate the proposed topology and its control strategy.

Both IDO1 and TDO contribute to the malignancy of gliomas via the Kyn–AhR–AQP4 signaling pathway

Indoleamine 2,3-dioxygenase 1(IDO1),indoleamine 2,3-dioxygenase 2(IDO2),and tryptophan 2,3-dioxygenase(TDO)initiate the first step of the kynurenine pathway(KP),leading to the transformation of L-tryptophan(Trp)into L-kynurenine(Kyn)and other downstream metabolites.Kyn is known as an endogenous ligand of the aryl hydrocarbon receptor(AhR).Activation of AhR through TDO-derived Kyn is a novel mechanism to support tumor growth in gliomas.However,the role of IDO1 and IDO2 in this mechanism is still unknown.Herein,by using clinical samples,we found that the expression and activity of IDO1 and/or TDO(IDO1/TDO)rather than IDO2 were positively correlated with the pathologic grades of gliomas.The expression of IDO1/TDO rather than IDO2 was positively correlated with the Ki67 index and overall survival.The expression of IDO1/TDO was positively correlated with the expression of aquaporin 4(AQP4),implying the potential involvement of IDO1/TDO in glioma cell motility.Mechanistically,we found that IDO1/TDO accounted for the release of Kyn,which activated AhR to promote cell motility via the Kyn–AhR–AQP4 signaling pathway in U87MG glioma cells.RY103,an IDO1/TDO dual inhibitor,could block the IDO1/TDO–Kyn–AhR–AQP4 signaling pathway and exert anti-glioma effects in GL261 orthotopic glioma mice.Together,our results showed that the IDO1/TDO–Kyn–AhR–AQP4 signaling pathway is a new mechanism underlying the malignancy of gliomas,and suggest that both IDO1 and TDO might be valuable therapeutic targets for gliomas.

Correction:Both IDO1 and TDO contribute to the malignancy of gliomas via the Kyn-AhR-AQP4 signaling pathway

In the process of collating the raw data,the authors noticed the inadvertent mistakes in Fig.4h&6g that need to be corrected.The correct data are provided as follows.The key findings of the article are not affected by the corrections.We apologize for the inadvertent mistakes.The authors mistakenly placed the wrong representative image showing the invasion ability of U87MG cells in the IFN-γ+1-MT group.The correct version of Fig.4h is shown above.