Holographic Three-Dimensional Virtual Reality and Augmented Reality Display Based on 4K-Spatial Light Modulators

In this paper, we propose a holographic three-dimensional (3D) head-mounted display based on 4K-spatial light modulators (SLMs). This work is to overcome the limitation of stereoscopic 3D virtual reality and augmented reality head-mounted display. We build and compare two systems using 2K and 4K SLMs with pixel pitches 8.1 μm and 3.74 μm, respectively. One is a monocular system for each eye, and the other is a binocular system using two tiled SLMs for two eyes. The viewing angle of the holographic head-mounted 3D display is enlarged from 3.8 ∘ to 16.4 ∘ by SLM tiling, which demonstrates potential applications of true 3D displays in virtual reality and augmented reality

Inhibition of SAT1 alleviates chondrocyte inflammation and ferroptosis by repressing ALOX15 expression and activating the Nrf2 pathway

Aims: Osteoarthritis (OA) is the most common chronic pathema of human joints. The pathogenesis is complex, involving physiological and mechanical factors. In previous studies, we found that ferroptosis is intimately related to OA, while the role of Sat1 in chondrocyte ferroptosis and OA, as well as the underlying mechanism, remains unclear. Methods: In this study, interleukin-1β (IL-1β) was used to simulate inflammation and Erastin was used to simulate ferroptosis in vitro. We used small interfering RNA (siRNA) to knock down the spermidine/spermine N1-acetyltransferase 1 (Sat1) and arachidonate 15-lipoxygenase (Alox15), and examined damage-associated events including inflammation, ferroptosis, and oxidative stress of chondrocytes. In addition, a destabilization of the medial meniscus (DMM) mouse model of OA induced by surgery was established to investigate the role of Sat1 inhibition in OA progression. Results: The results showed that inhibition of Sat1 expression can reduce inflammation, ferroptosis changes, reactive oxygen species (ROS) level, and lipid-ROS accumulation induced by IL-1β and Erastin. Knockdown of Sat1 promotes nuclear factor-E2-related factor 2 (Nrf2) signalling. Additionally, knockdown Alox15 can alleviate the inflammation-related protein expression induced by IL-1β and ferroptosis-related protein expression induced by Erastin. Furthermore, knockdown Nrf2 can reverse these protein expression alterations. Finally, intra-articular injection of diminazene aceturate (DA), an inhibitor of Sat1, enhanced type II collagen (collagen II) and increased Sat1 and Alox15 expression. Conclusion: Our results demonstrate that inhibition of Sat1 could alleviate chondrocyte ferroptosis and inflammation by downregulating Alox15 activating the Nrf2 system, and delaying the progression of OA. These findings suggest that Sat1 provides a new approach for studying and treating OA. Cite this article: Bone Joint Res 2024;13(3):110–123

Mitoquinone alleviates osteoarthritis progress by activating the NRF2-Parkin axis

Summary: Osteoarthritis (OA) is a prevalent degenerative disease of the elderly. The NRF2 antioxidant system plays a critical role in maintaining redox balance. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant. This research aimed to determine whether MitoQ alleviated OA and the role of the NRF2/Parkin axis in MitoQ-mediated protective effects. In interleukin (IL)-1β-induced OA chondrocytes, MitoQ activated the NRF2 pathway, reducing extracellular matrix (ECM) degradation and inflammation. MitoQ also increased glutathione peroxidase 4 (GPX4) expression, leading to decreased levels of reactive oxygen species (ROS) and lipid ROS. Silencing NRF2 weakened MitoQ’s protective effects, while knockdown of Parkin upregulated the NRF2 pathway, inhibiting OA progression. Intra-articular injection of MitoQ mitigated cartilage destruction in destabilized medial meniscus (DMM)-induced OA mice. Our study demonstrates that MitoQ maintains cartilage homeostasis in vivo and in vitro through the NRF2/Parkin axis. We supplemented the negative feedback regulation mechanism between NRF2 and Parkin. These findings highlight the therapeutic potential of MitoQ for OA treatment

Bone age assessment based on three-dimensional ultrasound and artificial intelligence compared with paediatrician-read radiographic bone age: protocol for a prospective, diagnostic accuracy study

Introduction Radiographic bone age (BA) assessment is widely used to evaluate children’s growth disorders and predict their future height. Moreover, children are more sensitive and vulnerable to X-ray radiation exposure than adults. The purpose of this study is to develop a new, safer, radiation-free BA assessment method for children by using three-dimensional ultrasound (3D-US) and artificial intelligence (AI), and to test the diagnostic accuracy and reliability of this method.Methods and analysis This is a prospective, observational study. All participants will be recruited through Paediatric Growth and Development Clinic. All participants will receive left hand 3D-US and X-ray examination at the Shanghai Sixth People’s Hospital on the same day, all images will be recorded. These image related data will be collected and randomly divided into training set (80% of all) and test set (20% of all). The training set will be used to establish a cascade network of 3D-US skeletal image segmentation and BA prediction model to achieve end-to-end prediction of image to BA. The test set will be used to evaluate the accuracy of AI BA model of 3D-US. We have developed a new ultrasonic scanning device, which can be proposed to automatic 3D-US scanning of hands. AI algorithms, such as convolutional neural network, will be used to identify and segment the skeletal structures in the hand 3D-US images. We will achieve automatic segmentation of hand skeletal 3D-US images, establish BA prediction model of 3D-US, and test the accuracy of the prediction model.Ethics and dissemination The Ethics Committee of Shanghai Sixth People’s Hospital approved this study. The approval number is 2022-019. A written informed consent will be obtained from their parent or guardian of each participant. Final results will be published in peer-reviewed journals and presented at national and international conferences.Trial registration number ChiCTR2200057236

IRF1 regulation of ZBP1 links mitochondrial DNA and chondrocyte damage in osteoarthritis

Abstract Background Z-DNA binding protein 1 (ZBP1) is a nucleic acid sensor that is involved in multiple inflammatory diseases, but whether and how it contributes to osteoarthritis (OA) are unclear. Methods Cartilage tissues were harvested from patients with OA and a murine model of OA to evaluate ZBP1 expression. Subsequently, the functional role and mechanism of ZBP1 were examined in primary chondrocytes, and the role of ZBP1 in OA was explored in mouse models. Results We showed the upregulation of ZBP1 in articular cartilage originating from OA patients and mice with OA after destabilization of the medial meniscus (DMM) surgery. Specifically, knockdown of ZBP1 alleviated chondrocyte damage and protected mice from DMM-induced OA. Mechanistically, tumor necrosis factor alpha induced ZBP1 overexpression in an interferon regulatory factor 1 (IRF1)-dependent manner and elicited the activation of ZBP1 via mitochondrial DNA (mtDNA) release and ZBP1 binding. The upregulated and activated ZBP1 could interact with receptor-interacting protein kinase 1 and activate the transforming growth factor-beta-activated kinase 1-NF-κB signaling pathway, which led to chondrocyte inflammation and extracellular matrix degradation. Moreover, inhibition of the mtDNA-IRF1-ZBP1 axis with Cyclosporine A, a blocker of mtDNA release, could delay the progression of DMM-induced OA. Conclusions Our data revealed the pathological role of the mtDNA-IRF1-ZBP1 axis in OA chondrocytes, suggesting that inhibition of this axis could be a viable therapeutic approach for OA

High-performance liquid metal electromagnetic actuator fabricated by femtosecond laser

Small-scale electromagnetic soft actuators are characterized by a fast response and simple control, holding prospects in the field of soft and miniaturized robotics. The use of liquid metal (LM) to replace a rigid conductor inside soft actuators can reduce the rigidity and enhance the actuation performance and robustness. Despite research efforts, challenges persist in the flexible fabrication of LM soft actuators and in the improvement of actuation performance. To address these challenges, we developed a fast and robust electromagnetic soft microplate actuator based on a laser-induced selective adhesion transfer method. Equipped with unprecedentedly thin LM circuit and customized low Young’s modulus silicone rubber (1.03 kPa), our actuator exhibits an excellent deformation angle (265.25°) and actuation bending angular velocity (284.66 rad·s ^−1 ). Furthermore, multiple actuators have been combined to build an artificial gripper with a wide range of functionalities. Our actuator presents new possibilities for designing small-scale artificial machines and supports advancements in ultrafast soft and miniaturized robotics

Tuning the Solvent Alkyl Chain to Tailor Electrolyte Solvation for Stable Li-Metal Batteries

1,2-Dimethoxyethane (DME) has been considered as the most promising electrolyte solvent for Li-metal batteries (LMBs). However, challenges arise from insufficient Li Coulombic efficiency (CE) and poor anodic stability associated with DME-based electrolytes. Here, we proposed a rational molecular design methodology to tailor electrolyte solvation for stable LMBs, where shortening the middle alkyl chain of the solvent could reduce the chelation ability, while increasing the terminal alkyl chain of the solvent could increase the steric hindrance, affording a diethoxymethane (DEM) solvent with ultra-weak solvation ability. When serving as a single solvent for electrolyte, a peculiar solvation structure dominated by contact ion pairs (CIPs) and aggregates (AGGs) was achieved even at a regular salt concentration of 1 m, which gives rise to anion-derived interfacial chemistry. This illustrates an unprecedentedly high Li||Cu CE of 99.1% for a single-salt single-solvent (non-fluorinated) electrolyte at ∼1 m. Moreover, this 1 m DEM-based electrolyte also remarkably suppresses the anodic dissolution of Al current collectors and significantly improves the cycling performance of high-voltage cathodes. This work opens up new frontiers in engineering electrolytes toward stable LMBs with high energy densities

Molecular Design of Asymmetric Cyclophosphamide as Electrolyte Additive for High-Voltage Lithium-Ion Batteries

Elevating the charging voltage could greatly promote the energy density of lithium-ion batteries (LIBs) with LiNixMnyCozO2 cathodes, although challenges arise from severe parasitic reactions and rapid capacity decay at high voltage, especially for nickel-rich cathodes. Herein, by incorporating various useful functionalities into one single molecule, we rationally design and synthesize a new class of five-membered asymmetric cyclophosphamides as electrolyte additives to enable stable cycling of high-voltage LIBs. It is demonstrated that the strong Lewis-base feature of the P–N bond can effectively scavenge the detrimental HF and H2O in the electrolyte. Meanwhile, the five-membered ring with an asymmetric amine moiety undergoes ring-opening polymerization to generate a highly robust and thin polymeric cathode–electrolyte interphase. Benefiting from the above merits, the asymmetric cyclophosphamide additive significantly suppresses decomposition of the electrolyte, dissolution of the transitional metals, and structural damage to the cathode, thus markedly improving the cycling stability and Coulombic efficiency of both high-voltage coin and pouch LIBs (up to 4.6 V)