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Abstract The harmonic compensation of SAPF (shunt active power filter) may trigger harmonic oscillation due to the interaction with grid impedance and non‐linear loads, which distorts the power quality. In previous research, the relevant mechanism has been studied. However, the SAPF generally employs complex harmonic detection algorithm, which significantly increases the computational demands. The SAPF in full compensation mode can effectively solve this problem. But the modification of harmonic detection link may change the oscillation mechanism and previous stabilization methods need to be re‐evaluated. Therefore, this paper establishes the small signal model of the SAPF system in full compensation mode and investigates its oscillation mechanism. It is revealed that harmonic compensation and passive resonance collectively induce the harmonic oscillation. Based on the model, the working mechanism and application performance of the main stabilization methods proposed in the past (harmonic virtual admittance and harmonic compensation canceling) are analyzed and compared. However, neither of them can achieve effective stabilization without sacrificing the performance of compensation. Consequently, the harmonic phase compensation method is proposed to achieve the stabilization of the SAPF system in full compensation mode without affecting normal compensation. Finally, simulations and experiments are performed to verify the mechanism analysis and proposed methods.

Abstract Shunt active power filter (SAPF) has emerged as a promising solution for mitigating harmonic distortions. Due to the interaction between the current inner‐loop of SAPF, source impedance and non‐linear loads, harmonic oscillation issue arises and adversely affects the stability of the system, thus in turn exacerbating the harmonic distortion. However, previous studies paid less attention to the value of phase adjustment in improving the dynamic behaviour of the loop and thus stabilizing harmonic oscillation. Taking the dynamic characteristics between source impedance and non‐linear load into consideration, this paper models and analyzes the SAPF system with source current direct control to reveal the law of full harmonic compensation oscillation. Based on the analysis, an enhanced phase adjustment strategy using load current feedforward is proposed and designed to stabilize harmonic oscillation, while maintaining a favourable trade‐off between stability and harmonic compensation performance. The small‐signal model validated for stability analysis and the effectiveness of proposed stabilization strategy are verified by simulation and experiment.

With the rapid development and application of renewable energy, the advantages of DC distribution system are becoming more and more obvious. In the DC distribution system, the DC transformer is a component that connects different voltage DC bus and realizes the connection between DC bus and the renewable energy. Its efficiency and dynamic performance are of great significance. Among them, DAB has been widely studied. In DAB, the current stress is related to the conduction loss of switches. Therefore, this paper first studies the basic principle and basic electrical characteristics under DPS control, and uses the KKT condition to solve the optimization problem with the goal of optimizing the current stress. In order to improve the dynamic performance, this paper proposes power compensation control considering the difference between the theoretical calculation and the actual transmission power. Finally, the simulation is built in PLECS. By comparing SPS control and the optimized control in this paper, it is proved that the optimized control in this paper can reduce the current stress and reduce the loss under the same transmission power. Compared with the traditional PI control, the power compensation control can improve the start-up time and reduce the output voltage variation and recovery time when the load suddenly changes.

Abstract Osteoblasts play an important role in the regulation of bone homeostasis throughout life. Thus, the damage of osteoblasts can lead to serious skeletal diseases, highlighting the urgent need for novel pharmacological targets. This study introduces chemical genetics strategy by using small molecule forskolin (FSK) as a probe to explore the druggable targets for osteoporosis. Here, this work reveals that transglutaminase 2 (TGM2) served as a major cellular target of FSK to obviously induce osteoblast differentiation. Then, this work identifies a previously undisclosed allosteric site in the catalytic core of TGM2. In particular, FSK formed multiple hydrogen bonds in a saddle‐like domain to induce an “open” conformation of the β‐sandwich domain in TGM2, thereby promoting the substrate protein crosslinks by incorporating polyamine. Furthermore, this work finds that TGM2 interacted with several mitochondrial homeostasis‐associated proteins to improve mitochondrial dynamics and ATP production for osteoblast differentiation. Finally, this work observes that FSK effectively ameliorated osteoporosis in the ovariectomy mice model. Taken together, these findings show a previously undescribed pharmacological allosteric site on TGM2 for osteoporosis treatment, and also provide an available chemical tool for interrogating TGM2 biology and developing bone anabolic agent.

Summary: Background: The E2F family of transcription factors play a crucial role in the development of various cancers. However, E2F members lack targetable binding pockets and are typically considered “undruggable”. Unlike canonical small-molecule therapeutics, molecular glues mediate new E3 ligase–protein interactions to induce selective proteasomal degradation, which represents an attractive option to overcome these limitations. Methods: Human proteome microarray was utilized to identify a natural product-derived molecular glue for targeting E2F2 degradation. Co-IP analysis with stable isotope labeling of amino acids in cell culture (SILAC)-based quantitative proteomics was carried out to further explore the E3 ligase for E2F2 degradation. Findings: In this study, we identified a molecular glue bufalin, which significantly promoted E2F2 degradation. Unexpectedly, E2F2 underwent ubiquitination and proteasomal degradation via a previously undisclosed atypical E3 ligase, zinc finger protein 91 (ZFP91). In particular, we observed that bufalin markedly promoted E2F2-ZFP91 complex formation, thereby leading to E2F2 polyubiquitination via K48-linked ubiquitin chains for degradation. E2F2 degradation subsequently caused transcriptional suppression of multiple oncogenes including c-Myc, CCNE1, CCNE2, MCM5 and CDK1, and inhibited hepatocellular carcinoma growth in vitro and in vivo. Interpretation: Collectively, our findings open up a new direction for transcription factors degradation by targeting atypical E3 ligase ZFP91. Meanwhile, the chemical knockdown strategy with molecular glue may promote innovative transcription factor degrader development in cancer therapy. Funding: This work was financially supported by the National Key Research and Development Project of China (2022YFC3501601), National Natural Sciences Foundation of China (81973505, 82174008, 82030114), and China Postdoctoral Science Foundation (2019M650396), the Fundamental Research Funds for the Central Universities.

Sleep loss impacts a broad range of brain and cognitive functions. However, how sleep deprivation affects risky decision‐making remains inconclusive. This study used functional MRI to examine the impact of one night of total sleep deprivation (TSD) on risky decision‐making behavior and the underlying brain responses in healthy adults. In this study, we analyzed data from N = 56 participants in a strictly controlled 5‐day and 4‐night in‐laboratory study using a modified Balloon Analogue Risk Task. Participants completed two scan sessions in counter‐balanced order, including one scan during rested wakefulness (RW) and another scan after one night of TSD. Results showed no differences in participants' risk‐taking propensity and risk‐induced activation between RW and TSD. However, participants showed significantly reduced neural activity in the anterior cingulate cortex and bilateral insula for loss outcomes, and in bilateral putamen for win outcomes during TSD compared with RW. Moreover, risk‐induced activation in the insula negatively correlated with participants' risk‐taking propensity during RW, while no such correlations were observed after TSD. These findings suggest that sleep loss may impact risky decision‐making by attenuating neural responses to decision outcomes and impairing brain‐behavior associations. Previous studies have suggested that sleep loss affects various neurobehavioral functions including decision‐making. However, the impact of sleep deprivation on risky decision‐making remains controversial. This study examined the impact of total sleep deprivation on risky decision‐making in the brain through a modified Balloon Analogue Risk Task. Results demonstrate that sleep loss may impact risky decision‐making by attenuating the brain's responses to the decision outcomes and impairing the relationship between brain and behavior. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that advanced neuroimaging modalities such as arterial spin labelling (ASL) might have prognostic utility for pediatric concussion. This study aimed to: 1) examine group differences in global and regional brain perfusion in youth with concussion or orthopedic injury (OI) at 72 h and 4 weeks post-injury; 2) examine patterns of abnormal brain perfusion within both groups and their recovery; 3) investigate the association between perfusion and symptom burden within concussed and OI youths at both time-points; and 4) explore perfusion between symptomatic and asymptomatic concussed and OI youths. Youths ages 10.00-17.99 years presenting to the emergency department with an acute concussion or OI were enrolled. ASL-magnetic resonance imaging scans were conducted at 72 h and 4 weeks post-injury to measure brain perfusion, along with completion of the Health Behavior Inventory (HBI) to measure symptoms. Abnormal perfusion clusters were identified using voxel-based z-score analysis at each visit. First, mixed analyses of covariance (ANCOVAs) investigated the Group*Time interaction on global and regional perfusion. Post hoc region of interest (ROI) analyses were performed on significant regions. Second, within-group generalized estimating equations investigated the recovery of abnormal perfusion at an individual level. Third, multiple regressions at each time-point examined the association between HBI and regional perfusion, and between HBI and abnormal perfusion volumes within the concussion group. Fourth, whole–brain one-way ANCOVAs explored differences in regional and abnormal perfusion based on symptomatic status (symptomatic vs. asymptomatic) and OIs at each time-point. A total of 70 youths with a concussion [median age (interquartile range; IQR) = 12.70 (11.67-14.35), 47.1% female] and 29 with an OI [median age (IQR) = 12.05 (11.18-13.89), 41.4% female] were included. Although no Group effect was found in global perfusion, the concussion group showed greater adjusted perfusion within the anterior cingulate cortex/middle frontal gyrus (MFG) and right MFG compared with the OI group across time-points (ps ≤ 0.004). The concussion group showed lower perfusion within the right superior temporal gyrus at both time-points and bilateral occipital gyrus at 4 weeks, (ps ≤ 0.006). The number of hypoperfused clusters was increased at 72 h compared with 4 weeks in the concussion youths (p < 0.001), but not in the OIs. Moreover, Group moderated the HBI-perfusion association within the left precuneus and superior frontal gyrus at both time-points, (ps ≤ 0.001). No association was found between HBI and abnormal perfusion volume within the concussion group at any visits. At 4 weeks, the symptomatic sub-group (n = 10) showed lower adjusted perfusion within the right cerebellum and lingual gyrus, while the asymptomatic sub-group (n = 59) showed lower adjusted perfusion within the left calcarine, but greater perfusion within the left medial orbitofrontal cortex, right middle frontal gyrus, and bilateral caudate compared with OIs. Yet, no group differences were observed in the number of abnormal perfusion clusters or volumes at any visit. The present study suggests that symptoms may be associated with changes in regional perfusion, but not abnormal perfusion levels. [ABSTRACT FROM AUTHOR]