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This paper proposes a model predictive current control (MPCC) method for a three-leg two-phase voltage source inverter to reduce the ripple of the output current. The proposed MPCC method is based on discrete space vector modulation, which is implemented by eliminating nonlinear modulation regions and generating virtual voltage vectors based on the stationary reference voltage vector axis. In addition, based on a voltage angle estimated using load parameters, the candidate voltage vectors in a specific region are generated, which reduces the calculation burden. Subsequently, the cost function is calculated using these candidate voltage vectors, and the optimal voltage vector selected using the proposed MPCC method is more accurate than the vector selected using the conventional MPCC method. Therefore, by applying the proposed method to increase the number of virtual voltage vectors, it is possible to obtain a delicate reference voltage. Consequently, the total harmonic distortion of the output current is reduced, resulting in an increase in power quality. The effectiveness and feasibility of the proposed method are verified through simulations and experiments. [ABSTRACT FROM AUTHOR]

Aggregation and misfolding of α-Synuclein (α-Syn), a causative agent for Parkinson's disease (PD), and oxidative stress are tightly implicated in the pathogenesis of PD. Although more than 20 genes including HtrA2 have been identified as causative genes for PD, the molecular mechanisms underlying the pathophysiological functions between HtrA2 and α-Syn in the pathogenesis of PD remain unclear. This study shows that HtrA2 serine protease selectively recognizes and interacts with the NAC region of α-Syn. Interestingly, we found that HtrA2 causes proteolysis of α-Syn to prevent mitochondrial accumulation of α-Syn, thereby inhibiting the production of reactive oxygen species (ROS) in the mitochondria. We have further demonstrated that HtrA2 knockdown promotes α-Syn-mediated mitochondrial ROS production, thereby activating microglial cells. This study is the first to demonstrate that the HtrA2/α-Syn cellular partner may play a crucial role in the pathogenesis of PD and provide new insights into the pathological processes and effective therapeutic strategies for PD. [Display omitted] • HtrA2 selectively interacts with the hydrophobic NAC site of α-Syn. • HtrA2 prevents mitochondrial accumulation of α-Syn by proteolysis of α-Syn. • α-Syn–induced ROS in mitochondria was reduced by HtrA2. • Inactivation of HtrA2 caused α-Syn accumulation in microglia. • Inactivation of HtrA2 leads to an increase in mitochondrial ROS in the microglia. [ABSTRACT FROM AUTHOR]

Background: Immune checkpoint inhibitors unleash inhibitory signals on T cells conferred by tumors and surrounding stromal cells. Despite the clinical efficacy of checkpoint inhibitors, the lack of target expression and persistence of immunosuppressive cells limit the pervasive effectiveness of the therapy. These limitations may be overcome by alternative approaches that co-stimulate T cells and the immune microenvironment. Methods: We analyzed single-cell RNA sequencing data from multiple human cancers and a mouse tumor transplant model to discover the pleiotropic expression of the Interleukin 7 (IL-7) receptor on T cells, macrophages, and dendritic cells. Results: Our experiment on the mouse model demonstrated that recombinant IL-7 therapy induces tumor regression, expansion of effector CD8 T cells, and pro-inflammatory activation of macrophages. Moreover, spatial transcriptomic data support immunostimulatory interactions between macrophages and T cells. Conclusion: These results indicate that IL-7 therapy induces anti-tumor immunity by activating T cells and pro-inflammatory myeloid cells, which may have diverse therapeutic applicability. [ABSTRACT FROM AUTHOR]