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The independent DC bus structure multiport power electronic transformer (IDBS-MPET) is a novel power electronic transformer designed to integrate multiple DC sources and DC loads. Due to the configuration of DC ports, which are directly constructed by the parallel connection of dual active bridge (DAB) converters, the distribution of DC sources and DC loads among the three phases becomes unbalanced. In cases where the load power at certain ports is too high, this imbalance may lead to the over-modulation of the front-end H-bridge (HB). Since the output power at a certain port in the IDBS-MPET is constrained by the loads at other ports, this paper proposes a multiport steady-state power flow allocation method. This method establishes the load sensitivity correlation factor to enable all the ports to adjust power cooperatively based on it. By applying the proposed steady-state power flow allocation method, iterative calculations continuously update the priority of all the ports and their load sensitivity correlation factors. This process ensures that the power flow converges to a steady-state solution. Simulation results for two different IDBS-MPETs demonstrate that the power flow at all the ports effectively meets load requirements, while the front-end HB avoids over-modulation, ensuring the safe and stable operation of the IDBS-MPET. The results validate the effectiveness of the proposed steady-state power flow allocation method. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is characterized by pronounced immune escape and resistance to chemotherapy-induced apoptosis. Preliminary investigations revealed a marked overexpression of gasdermin E (GSDME) in GBM. Notably, cisplatin (CDDP) demonstrated a capacity of inducing pyroptosis by activating caspase-3 to cleave GSDME, coupled with the release of proinflammatory factors, indicating the potential as a viable approach of inducing anti-tumor immune activation. For the effective delivery of CDDP, the CDDP-polyphenol nanocomplexes were prepared, and catalase and copper ions were incorporated to fortify structural integrity, enhance glutathione (GSH) responsiveness, and ameliorate tumor hypoxia. Additionally, BV2 microglial cells were engineered to overexpress programmed death-1 (PD-1), and the membrane is employed for nanocomplex coating, effectively blocking the CDDP-induced upregulation of programmed death ligand 1 (PD-L1). Furthermore, the angiopep-2 peptide was modified to efficiently cross the blood brain barrier and specifically target GBM cells. In vitro analyses confirmed potent cytotoxicity and characteristic induction of pyroptosis. In vivo assays corroborated the enhancement of tumor targeting, culminating in an obvious suppression of tumor proliferation. A notable activation of immune cells was observed within tumors and lymph nodes, indicative of a synergistic effect of chemotherapy and immunotherapy, underscoring its potential as a safe and efficacious therapeutic strategy against GBM. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction, characterized by high morbidity and mortality, has now become a serious health hazard for human beings. Conventional surgical interventions to restore blood flow can rapidly relieve acute myocardial ischemia, but the ensuing myocardial ischemia-reperfusion injury (MI/RI) and subsequent heart failure have become medical challenges that researchers have been trying to overcome. The pathogenesis of MI/RI involves several mechanisms, including overproduction of reactive oxygen species, abnormal mitochondrial function, calcium overload, and other factors that induce cell death and inflammatory responses. These mechanisms have led to the exploration of antioxidant and inflammation-modulating therapies, as well as the development of myocardial protective factors and stem cell therapies. However, the short half-life, low bioavailability, and lack of targeting of these drugs that modulate these pathological mechanisms, combined with liver and spleen sequestration and continuous washout of blood flow from myocardial sites, severely compromise the expected efficacy of clinical drugs. To address these issues, employing conventional nanocarriers and integrating them with contemporary biomimetic nanocarriers, which rely on passive targeting and active targeting through precise modifications, can effectively prolong the duration of therapeutic agents within the body, enhance their bioavailability, and augment their retention at the injured myocardium. Consequently, these approaches significantly enhance therapeutic effectiveness while minimizing toxic side effects. This article reviews current drug delivery systems used for MI/RI, aiming to offer a fresh perspective on treating this disease. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to construct an ischemic cardiomyocyte-targeted and ROS-responsive drug release system to reduce myocardial ischemia-reperfusion injury (MI/RI). Methods: We constructed thioketal (TK) and cardiac homing peptide (CHP) dual-modified liposomes loaded with puerarin (PUE@TK/CHP-L), which were expected to deliver drugs precisely into ischemic cardiomyocytes and release drugs in response to the presence of high intracellular ROS levels. The advantages of PUE@TK/CHP-L were assessed by cellular pharmacodynamics, in vivo fluorescence imaging and animal pharmacodynamics. Results: PUE@TK/CHP-L significantly inhibited apoptosis and ferroptosis in H/R-injured cardiomyocytes and also actively targeted ischemic myocardium. Based on these advantages, PUE@TK/CHP-L could significantly enhance the drug's ability to attenuate MI/RI. Conclusion: PUE@TK/CHP-L had potential clinical value in the precise treatment of MI/RI. Article highlights Myocardial ischemia-reperfusion injury (MI/RI) is a series of pathological changes caused by revascularisation after myocardial infarction, for which there is no effective treatment. Excessive production of reactive oxygen species (ROS) is an important predisposing factor for MI/RI. Apoptosis and ferroptosis of cardiomyocytes are important pathological mechanisms of myocardial ischemia-reperfusion injury and both are closely related to excessive intracellular ROS. We have successfully synthesized ROS-responsive and cardiac-targeted liposomes loaded with puerarin (PUE@TK/CHP-L). It was found that PUE@TK/CHP-L could target ischemic myocardium. In vivo and ex vivo results showed that PUE@TK/CHP-L can effectively reduce the level of myocardial oxidative stress and decrease cardiomyocyte apoptosis and ferroptosis. These results suggested that PUE@TK/CHP-L could hopefully be a promising drug carrier for mitigating MI/RI. [ABSTRACT FROM AUTHOR]

Acute inflammation has the potential for the recruitment of immune cells, inhibiting tumor angiogenesis, metastasis, and drug resistance thereby overcoming the tumor immunosuppressive microenvironment caused by chronic inflammation. Here, an acute inflammation inducer using bacteria outer membrane vesicles (OMVs) loaded in thermal‐sensitive hydrogel (named OMVs‐gel) for localized and controlled release of OMVs in tumor sites is proposed. OMVs trigger neutrophil recruitment and amplify acute inflammation inside tumor tissues. The hydrogel ensures drastic inflammation is confined within the tumor, addressing biosafety concerns that the direct administration of free OMVs may cause fatal effects. This strategy eradicated solid tumors safely and rapidly. The study further elucidates one of the possible immune mechanisms of OMVs‐gel therapy, which involves the assembly of antitumor neutrophils and elastase release for selective tumor killing. Additionally, tumor vascular destruction induced by OMVs‐gel results in tumor darkening, allowing for combinational photothermal therapy. The findings suggest that the use of OMVs‐gel can safely induce acute inflammation and enhance antitumor immunity, representing a promising strategy to promote acute inflammation application in tumor immunotherapy. [ABSTRACT FROM AUTHOR]

Combining actual conditions, power demand forecasting is affected by various uncertain factors such as meteorological factors, economic factors, and diversity of forecasting models, which increase the complexity of forecasting. In response to this problem, taking into account that different time step states will have different effects on the output, the attention mechanism is introduced into the method proposed in this paper, which improves the deep learning model. Improved models of convolutional neural networks (CNN) and long short-term memory (LSTM) that combine the attention mechanism are proposed respectively. Finally, according to the verification results of actual examples, it is proved that the proposed method can obtain a smaller error and the prediction performance are better compared with other models.

Owing to the diverse connection configurations of dual active bridge converters, a multiplicity of low-voltage DC port structures are anticipated to emerge in the independent DC bus structure multiport power electronic transformer (IDBS-MPET). An inadequate low-voltage DC port structure exacerbates the power imbalance in IDBS-MPET, presenting a risk of overmodulation even when transmitting relatively low levels of power. To overcome this limitation, a design scheme of IDBS-MPET topology based on the maximum power transmission capability of the low-voltage DC ports is proposed in this paper. Three topology design rules are derived from the maximum power transmission capability results of more than 80 typical IDBS-MPET topologies. The symmetrical triple cross-phase connection structure, the symmetrical double cross-phase connection structure and the single-phase connection structure are sequentially identified as the three most optimal structures of low-voltage DC ports. By employing the proposed design methodology, each low-voltage DC port achieves its maximum power transfer capability relative to other configurations. The effectiveness of the proposed design scheme is validated by an optimal designed IDBS-MPET topology with six low-voltage DC ports. [ABSTRACT FROM AUTHOR]