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The dynamics of current controller is usually neglected for simplification when assessing microgrid transient stability. Utilizing the Takagi–Sugeno method, this letter thoroughly examines the effects of current controller on transient stability estimations and reveals that completely ignoring the dynamics of current controller can cause overestimation on transient stability. The findings highlight a significant overestimation on lower boundary of angle about 29.2% even if current controller performs fast dynamics with bandwidth more than 28 times the fundamental frequency. Recognizing the impracticality of including current controller dynamics in microgrids with multiple converters, this letter proposes a stability-enhanced method through phase compensation in the current controller, which can improve the accuracy of transient stability assessments while still omitting current controller dynamics. In addition, a guideline for parameter design of phase compensation is provided. Theoretical findings are verified by hardware-in-loop experimental results based on OPAL-RT platform.

ABSTRACTCurrently, abnormally elevated rail potential exists in the DC traction power system, which greatly threatens the safe operation of the line. In order to realize the reflux safety, timetable optimization of multitrain based on improved Seeker Optimization Algorithm (SOA) is proposed to suppress the rail potential of the system. Firstly, the simulation model of the system is built and the calculation process of rail potential is proposed. Secondly, an optimization model based on maximum rail potential is formulated, where the dwell time is the decision variable and is adjusted to change the regenerative power distribution of the system. Finally, the improved SOA is used to handle the optimization model. Compared with the maximum rail potential before optimization, the simulation results demonstrate that the maximum rail potential is reduced by 55.5% with the proposed method, which greatly improves the reflux safety of the multi-train subway system.

Nanozymes have been developed to overcome the inherent limitations of natural enzymes, such as their low stability and high cost. However, their efficacy has been hindered by their relatively low specificity and activity. Here, we demonstrate the self-assembly of individual copper nanoclusters (CuNCs) via a simple yet fast (10 min) DNA nanosheet (DNS)-templated method, enhancing the peroxidase-like activity and specificity of CuNCs. Furthermore, we demonstrate the successful assembly of CuNCs on different DNA nanostructures by atomic force microscopy (AFM), transmission electron microscopy (TEM), and X-ray photoelectron spectroscopy (XPS). The resulting micron-scale ultrathin DNA nanosheet-templated CuNCs (DNS@CuNCs) exhibit exceptional catalytic activity, with a specific activity reaching 1.79 × 103U mg–1. Investigation into the catalytic process reveals that the enhanced activity and specificity arise from disparities in active intermediate content before and after CuNCs assembly. Significantly, the DNS@CuNCs-based biosensor demonstrates remarkable anti-interference capabilities, enabling the detection of H2O2in undiluted human serum for the first time with a detection limit of 0.99 μM.

Hypoxia, and hypoxia inducible factor-1 (HIF-1), can induce tumor resistance to radiation therapy. To overcome hypoxia-induced radiation resistance, recent studies have described nanosystems to improve tumor oxygenation for immobilizing DNA damage and simultaneously initiate oxygen-dependent HIF-1α degradation. However, HIF-1α degradation is incomplete during tumor oxygenation treatment alone. Therefore, tumor oxygenation combined with residual HIF-1 functional inhibition is crucial to optimizing therapeutic outcomes of radiotherapy. Here, a reactive oxygen species (ROS) responsive nanoplatform is reported to successfully add up tumor oxygenation and HIF-1 functional inhibition. This ROS responsive nanoplatform, based on manganese dioxide (MnO2) nanoparticles, delivers the HIF-1 inhibitor acriflavine and other hydrophilic cationic drugs to tumor tissues. After reacting with overexpressed hydrogen peroxide (H2O2) within tumor tissues, Mn2+and oxygen molecules are released for magnetic resonance imaging and tumor oxygenation, respectively. Cooperating with the HIF-1 functional inhibition, the expression of tumor invasion-related signaling molecules (VEGF, MMP-9) is obviously decreased to reduce the risk of metastasis. Furthermore, the nanoplatform could relieve T-cell exhaustion viadownregulation of PD-L1, whose effects are similar to the checkpoint inhibitor PD-L1 antibody, and subsequently activates tumor-specific immune responses against abscopal tumors. These therapeutic benefits including increased X-ray-induced damage, downregulated resistance, and T-cell exhaustion related proteins expression achieved synergistically the optimal inhibition of tumor growth. Overall, this designed ROS responsive nanoplatform is of great potential in the sensitization of radiation for combating primary and metastatic tumors.

Abraxane® (Abx), an FDA approved albumin-bound paclitaxel nano-formulation, is one of the most common chemical drugs for the treatment of metastatic triple-negative breast cancer (mTNBC). However, acquired resistance and metastasis are critical factors that limit the treatment of mTNBC by Abx. In particular, both the tumor hypoxic microenvironment and the increase in hydrogen peroxide (H2O2) levels viapaclitaxel stimulation primarily mediate the resistance to chemotherapy, where multiple drug resistance proteins such as P-gp and tumor invasion-related cytokines such as VEGF are continuously activated to pump out chemical drugs and aggravate tumor metastasis, respectively. Therefore, it is of great importance to combine tumor oxygenation with commercial chemical drugs for overcoming the acquired resistance and metastasis. In this study, a facile method was developed to deposit manganese dioxide (MnO2) onto the surface of Abraxane® (Abx) to form MnO2-modified Abx (M-Abx). The modification process did not change the critical characteristics of the parent Abx, which might have great potential for application in clinics for the treatment of mTNBC. Tumor oxygenation mediated by M-Abx specifically occurs within the H2O2-overexpressed tumor microenvironment, and significantly downregulates the content of tumor progression-related proteins, such as HIF-1α, P-gp, and VEGF. Ultimately, M-Abx treatment results in about a 2-fold increase in inhibition efficiency of tumor growth in both primary and metastatic tumors compared with traditional Abx therapy. Therefore, oxygen-rich chemotherapy was realized to efficiently sensitize paclitaxel, relieve acquired resistance and inhibit tumor metastasis.