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Liquid-liquid phase separation promotes the formation of membraneless condensates that mediate diverse cellular functions, including autophagy of misfolded proteins. However, how phase separation participates in autophagy of dysfunctional mitochondria (mitophagy) remains obscure. We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. Here, we show that the ubiquitinated mitochondrial Nur77 forms membraneless condensates capable of sequestrating damaged mitochondria by interacting with the UBA domain of p62/SQSTM1. However, tethering clustered mitochondria to the autophagy machinery requires an additional interaction mediated by the N-terminal intrinsically disordered region (IDR) of Nur77 and the N-terminal PB1 domain of p62/SQSTM1, which confers Nur77-p62/SQSTM1 condensates with the magnitude and liquidity. Our results demonstrate how composite multivalent interaction between Nur77 and p62/SQSTM1 coordinates to sequester damaged mitochondria and to connect targeted cargo mitochondria for autophagy, providing mechanistic insight into mitophagy. How phase separation participates in mitophagy remains unclear. Here the authors show that Nur77 and p62/SQSTM1 through “head-to-head” and “tail-to-tail” interactions form membraneless condensates capable of sequestering dysfunctional mitochondria and tethering them to autolysosome for degradation.

Valve switching is one of the most important power losses in digital hydraulics. In this paper, a dynamic Zero-Flowrate-Switching (ZFS) control method is developed for hydraulic/pneumatic systems. The proposed control strategy is to actively reduce the flowrate passing through the valve to zero before switching off the valve. To realize it, an accessory line, in which a RLC oscillator is applied to generate a sinusoidal flowrate, is allocated parallel to the main control line for flowrate regulation. The pressure, with high frequency and small amplitude wave outputs from a regular piston pump, is used to drive the RLC oscillator. To evaluate the performance of this strategy, mathematical models for switching power loss and pressure pulses are developed and characteristic analysis is conducted. The results show that the energy loss of the system when applying the dynamic ZFS controller is reduced to 16% compared to that of a normal hydraulic system without a dynamic ZFS controller; moreover, pressure pulses in a dynamic ZFS system are much more minor than those in a Hard-Switching system.

Monocular depth estimation (MDE) is a cornerstone task in 2D/3D scene reconstruction and recognition with widespread applications in autonomous driving, robotics, and augmented reality. However, existing state-of-the-art methods face a fundamental trade-off between computational efficiency and estimation accuracy, limiting their deployment in resource-constrained real-world scenarios. It is of high interest to design lightweight but effective models to enable potential deployment on resource-constrained mobile devices. To address this problem, we present RepACNet, a novel lightweight network that addresses this challenge through reparameterized asymmetric convolution designs and CNN-based architecture that integrates MLP-Mixer components. First, we propose Reparameterized Token Mixer with Asymmetric Convolution (RepTMAC), an efficient block that captures long-range dependencies while maintaining linear computational complexity. Unlike Transformer-based methods, our approach achieves global feature interaction with tiny overhead. Second, we introduce Squeeze-and-Excitation Consecutive Dilated Convolutions (SECDCs), which integrates adaptive channel attention with dilated convolutions to capture depth-specific features across multiple scales. We validate the effectiveness of our approach through extensive experiments on two widely recognized benchmarks, NYU Depth v2 and KITTI Eigen. The experimental results demonstrate that our model achieves competitive performance while maintaining significantly fewer parameters compared to state-of-the-art models.

Effective transfection of genetic molecules such as DNA usually relies on vectors that can reversibly uptake and release these molecules, and protect them from digestion by nuclease. Non-viral vectors meeting these requirements are rare due to the lack of specific interactions with DNA. Here, we design a series of four isoreticular metal-organic frameworks (Ni-IRMOF-74-II to -V) with progressively tuned pore size from 2.2 to 4.2 nm to precisely include single-stranded DNA (ssDNA, 11–53 nt), and to achieve reversible interaction between MOFs and ssDNA. The entire nucleic acid chain is completely confined inside the pores providing excellent protection, and the geometric distribution of the confined ssDNA is visualized by X-ray diffraction. Two MOFs in this series exhibit excellent transfection efficiency in mammalian immune cells, 92% in the primary mouse immune cells (CD4+ T cell) and 30% in human immune cells (THP-1 cell), unrivaled by the commercialized agents (Lipo and Neofect). Non-viral vectors are important for transfection but can be limited in the uptake, protection and release of ssDNA. Here, the authors report on the design of metal-organic-framework vectors with precisely controlled pore geometry and demonstrate the vector in the transfection of immune cells.

Highly efficient multi-dimensional data storage and extraction are two primary ends for the design and fabrication of emerging optical materials. Although metasurfaces show great potential in information storage due to their modulation for different degrees of freedom of light, a compact and efficient detector for relevant multi-dimensional data retrieval is still a challenge, especially in complex environments. Here, we demonstrate a multi-dimensional image storage and retrieval process by using a dual-color metasurface and a double-layer integrated perovskite single-pixel detector (DIP-SPD). Benefitting from the photoelectric response characteristics of the FAPbBr 2.4 I 0.6 and FAPbI 3 films and their stacked structure, our filter-free DIP-SPD can accurately reconstruct different colorful images stored in a metasurface within a single-round measurement, even in complex environments with scattering media or strong background noise. Our work not only provides a compact, filter-free, and noise-robust detector for colorful image extraction in a metasurface, but also paves the way for color imaging application of perovskite-like bandgap tunable materials. A compact, filter-free, double-layer perovskite single-pixel detector enables simultaneous recognition of overlapping dual-color metasurface images in complex environments.

The rapid evolution of eavesdropping technologies has encouraged regular updates and improvement of encryption systems. Developing a detector-dependent optical encryption scheme to tightly connect the decryption and imaging processes offers great potential to prevent eavesdropping. By designing an optically programmable dual-band photodetector, a color image encryption scheme where the photodetector functions as both a detector and a critical decryption key is demonstrated here. The distinctive optically programmable property of the photodetector enables the manipulation of its long-wavelength sensitivity via short-wavelength photonic stimulation, leading to different imaging outputs between single-pixel imaging and point-scan imaging, which therefore demonstrates a capability to decrypt information hidden in color images. This detector-dependent decryption method can effectively prevent potential information leaks when other detectors are used as eavesdropping devices. Our encryption paradigm opens new avenues for color image encryption using photodetectors, enhancing encryption security by introducing a device-based dimension. Owing to different outputs between single-pixel imaging and point-scan imaging, an optically programmable dual-band perovskite photodetector enables a high-security detector-dependent color image encryption scheme by integrating imaging and decryption processes.

Road networks play a fundamental role in our daily life. It is of importance to extract the road structure in a timely and precise manner with the rapid evolution of urban road structure. Recently, road network extraction using deep learning has become an effective and popular method. The main shortcoming of the road extraction using deep learning methods lies in the fact that there is a need for a large amount of training datasets. Additionally, the datasets need to be elaborately annotated, which is usually labor-intensive and time-consuming; thus, lots of weak annotations (such as the centerline from OpenStreetMap) have accumulated over the past a few decades. To make full use of the weak annotations, we propose a novel semi-weakly supervised method based on adversarial learning to extract road networks from remote sensing imagery. Our method uses a small set of pixel-wise annotated data and a large amount of weakly annotated data for training. The experimental results show that the proposed approach can achieve a maintained performance compared with the methods that use a large number of full pixel-wise annotations while using less fully annotated data.

Radiation-induced lung injury (RILI) is one of the most common and fatal complications of thoracic radiotherapy, whereas no effective interventions are available. Andrographolide, an active component extracted from Andrographis paniculate , is prescribed as a treatment for upper respiratory tract infection. Here we report the potential radioprotective effect and mechanism of Andrographolide on RILI. C57BL/6 mice were exposed to 18 Gy of whole thorax irradiation, followed by intraperitoneal injection of Andrographolide every other day for 4 weeks. Andrographolide significantly ameliorated radiation-induced lung tissue damage, inflammatory cell infiltration, and pro-inflammatory cytokine release in the early phase and progressive fibrosis in the late phase. Moreover, Andrographolide markedly hampered radiation-induced activation of the AIM2 inflammasome and pyroptosis in vivo. Furthermore, bone marrow-derived macrophages (BMDMs) were exposed to 8 Gy of X-ray radiation in vitro and Andrographolide significantly inhibited AIM2 inflammasome mediated-pyroptosis in BMDMs. Mechanistically, Andrographolide effectively prevented AIM2 from translocating into the nucleus to sense DNA damage induced by radiation or chemotherapeutic agents in BMDMs. Taken together, Andrographolide ameliorates RILI by suppressing AIM2 inflammasome mediated-pyroptosis in macrophage, identifying Andrographolide as a novel potential protective agent for RILI.

Dexmedetomidine (DEX) is an anesthetic that is widely used in the clinic, and it has been reported to exhibit paradoxical effects in the progression of multiple solid tumors. In this study, we sought to explore the mechanism by which DEX regulates hepatocellular carcinoma (HCC) progression underlying liver fibrosis. We determined the effects of DEX on tumor progression in an orthotopic HCC mouse model of fibrotic liver. A coculture system and a subcutaneous xenograft model involving coimplantation of mouse hepatoma cells (H22) and primary activated hepatic stellate cells (aHSCs) were used to study the effects of DEX on HCC progression. We found that in the preclinical mouse model of liver fibrosis, DEX treatment significantly shortened median survival time and promoted tumor growth, intrahepatic metastasis and pulmonary metastasis. The DEX receptor (ADRA2A) was mainly expressed in aHSCs but was barely detected in HCC cells. DEX dramatically reinforced HCC malignant behaviors in the presence of aHSCs in both the coculture system and the coimplantation mouse model, but DEX alone exerted no significant effects on the malignancy of HCC. Mechanistically, DEX induced IL-6 secretion from aHSCs and promoted HCC progression via STAT3 activation. Our findings provide evidence that the clinical application of DEX may cause undesirable side effects in HCC patients with liver fibrosis.Liver cancer: Common anesthetic can accelerate tumor progressionResearchers warn against using the anesthetic dexmedetomidine (DEX) in liver cancer patients after indications that it promotes tumor growth. Concerns have been raised that certain anesthetics, including DEX, can accelerate the progression of cancerous tumors, but the precise effects of DEX on liver cancer tumors are unclear. Most liver cancers develop in patients who already have fibrosis, a build-up of scarred tissue in the liver. This tissue accumulation stems from the activation of hepatic stellate cells (HSCs) during liver damage. Using human cancer cell lines and mouse models, Aimin Li and Xue Ning at the Southern Medical University, Guangzhou, China and co-workers demonstrated that DEX interacts with HSCs via a receptor protein on their cell surface, further enhancing activation levels. Activated HSCs in turn secrete factors that accelerate tumor growth and invasion.

Aberrant activation of NLRP3 inflammasome has an important function in the pathogenesis of various inflammatory diseases. Although many components and mediators of inflammasome activation have been identified, how NLRP3 inflammasome is regulated to prevent excessive inflammation is unclear. Here we show NLRP3 inflammasome stimulators trigger Src homology-2 domain containing protein tyrosine phosphatase-2 (SHP2) translocation to the mitochondria, to interact with and dephosphorylate adenine nucleotide translocase 1 (ANT1), a central molecule controlling mitochondrial permeability transition. This mechanism prevents collapse of mitochondrial membrane potential and the subsequent release of mitochondrial DNA and reactive oxygen species, thus preventing hyperactivation of NLRP3 inflammasome. Ablation or inhibition of SHP2 in macrophages causes intensified NLRP3 activation, overproduction of proinflammatory cytokines IL-1β and IL-18, and increased sensitivity to peritonitis. Collectively, our data highlight that, by inhibiting ANT1 and mitochondrial dysfunction, SHP2 orchestrates an intrinsic regulatory loop to limit excessive NLRP3 inflammasome activation. The NLRP3 inflammasome is central to a variety of inflammatory diseases, but how it is regulated to prevent excessive inflammation is not clear. Here the authors show that NLRP3 activation causes SHP2 translocation to the mitochondria to interact with and dephosphorylate ANT1, thus stabilizing the mitochondria and preventing release of proinflammatory mitochondrial DNA and ROS.