ABSTRACTUnderwater smart adhesives with switchable adhesion have attracted significant attention for applications in marine engineering and biomedical fields. However, achieving both robust adhesion and rapid on‐demand detachment in aquatic environments remains a critical challenge. Inspired by the diving bell spider, we propose a design strategy based on heterogeneous wettability surfaces to achieve switchable adhesion between two surfaces. The heterogeneous wettability surface design confines the oil phase within air cavities formed in superhydrophobic (lipophilic) regions, thereby creating annular oil rings, which establish stable oil/water interfaces that spatially isolate the internal water bridge from the external aquatic environment. The Laplace pressure difference generated at the oil/water interfaces induces robust adhesion between surfaces. In addition, the adhesion strength can be linearly enhanced by constructing multiple, uniformly arranged oil/water interfaces. Rapid on‐demand separation can also be achieved through controlled electrolysis of the internal water bridge by applying voltage between the surfaces. Finally, we demonstrate the practical applicability of this adhesive by integrating it into an unmanned underwater vehicle (UUV) for efficient underwater anchoring and ship‐hull hitchhiking, highlighting its broad application potential in underwater engineering scenarios.

ABSTRACTLead‐based semiconductors play a critical role in emerging high‐performance optoelectronics. For scalable, cost‐effective fabrication, recycling lead waste from spent lead‐acid batteries has proven a promising strategy. Nevertheless, achieving device‐grade semiconductor quality from recycled sources remains a critical unresolved challenge. Here, we present the first additive‐assisted lead recycling strategy, in which trace amounts of KCl are introduced during the recycling process to enable the formation of high‐purity PbI2. The incorporated KCl enhances crystallization and removes impurities, while residual KCl further improves the colloidal stability and photophysical properties of PbS quantum dots (QDs), addressing key challenges in their direct synthesis. The resulting PbS QD solar cells with KCl additive achieved a power conversion efficiency of 13.3%, surpassing those fabricated with commercial PbI2 (12.1%) and recycled PbI2 without the additive (11.0%). Moreover, CsPbI3 QDs synthesized from KCl‐assisted PbI2 exhibited enhanced surface integrity, stronger photoluminescence, and longer carrier lifetimes, and the resulting solar cells delivered a superior efficiency of 16.6%, outperforming devices fabricated from commercial PbI2 (15.4%), demonstrating the universality of this approach across different lead‐based QD systems. This work establishes a sustainable, additive‐assisted metallurgy‐semiconductor coupling strategy, providing an energy‐efficient pathway to convert lead waste into high‐purity semiconductor precursors for advanced optoelectronic devices.

ABSTRACTCar sickness, an enormous vehicular travel challenge, affects a significant proportion of the population. Pharmacological interventions are limited by adverse side effects, and effective nonpharmacological alternatives remain to be identified. Here, we introduce a novel attention‐shifting method based on a closed‐loop, artificial intelligence (AI)‐driven, wearable mindfulness brain–computer interface (BCI) to alleviate car sickness. As the user performs an attentional task, i.e., focusing on breathing as in mindfulness, with a wearable headband, the BCI collects and analyzes electroencephalography (EEG) data via a convolutional neural network to assess the user's mindfulness state and provide real‐time audiovisual feedback. This approach might sustainedly shift the user's attention from physiological discomfort toward the BCI‐based mindfulness practices, thereby mitigating car sickness symptoms. The efficacy of the proposed method was rigorously evaluated in two real‐world experiments, namely, short and long car rides, with a large cohort of more than 100 participants susceptible to car sickness. Remarkably, over 83% of the participants rated the BCI‐based attention shifting as effective, with significant reductions in car sickness severity, particularly in individuals with severe symptoms. Furthermore, EEG data analysis revealed a neurobiological signature of car sickness, which provided mechanistic insights into the efficacy of the BCI‐based attention shifting for alleviating car sickness. This study proposes a wearable, nonpharmacological intervention for car sickness, validated in a relatively large‐scale study involving over 100 participants in real‐world car riding. These findings, derived from a between‐cohort comparison, support the potential of this approach to improve the travel experience for car sickness sufferers and represent a novel practical application of BCI technology.

ABSTRACTMacrophages show great potential for application in cellular immunotherapy, but are limited by immune checkpoints (ICBs). Immune checkpoint inhibitors (ICIs) can effectively block immune escape pathways and alleviate immune suppression in the tumor microenvironment (TME). Here, we constructed hypoxia response bacteria (HRB) that specifically expressed CD47 antibody (aCD47) under hypoxic conditions in the TME, enabling the in situ synthesis of ICIs at the tumor site. In addition, this study further prepared responsive liposomes for encapsulating the STING agonist cGAMP and modified them by covalent attachment to the HRB surface to form the composite material HRB@LC. This composite system can synergistically block CD47‐SIRPα‐mediated immune escape and activate the STING signal pathway, thereby enhancing systemic antitumor immune responses and significantly improving the efficacy of immunotherapy.

ABSTRACTGenetic mutations cause approximately 80% of rare human diseases, highlighting the urgent need for precise genome editing. Since clustered regularly interspaced short palindromic repeat (CRISPR)‐CRISPR‐associated 9 (Cas9) nucleases were first used for genome editing in 2012, genome editing technologies have rapidly advanced. Base editors, derived from the CRISPR‐Cas system, were developed to introduce specific point mutations without requiring DNA double‐strand breaks, and subsequently, prime editing (PE) technology was created to enable insertions, deletions, and all types of point mutations. The precision and versatility of PE make it a promising tool for clinical applications. However, PE has potential limitations, including low editing efficiency and limited capacity for large‐scale manipulation. To overcome these limitations, research has been continuously conducted to improve PE efficiency and expand its capabilities. Therefore, this review aims to highlight current efforts and future directions for developing and improving PE‐related tools.

ABSTRACTBronchopulmonary dysplasia (BPD) disrupts the process of alveolar development, characterized by damage to alveolar epithelial type II cells (AEC II). The present study aims to evaluate the impact of the tryptophan‐derived metabolite indole‐3‐propionic acid (IPA) on postnatal pulmonary development in BPD. Metabolomics indicated that tryptophan metabolic dysfunction is associated with BPD, with IPA emerging as a key metabolite that co‐varies at neonatal levels in both clinical and experimental BPD. Supplementation with IPA protected against hyperoxia‐induced alveolar simplification, which was characterized by increased pro‐proliferative, anti‐apoptotic, and pro‐transdifferentiation activities. Mechanistically, we evaluated circular dichroism (CD), molecular docking, surface plasmon resonance (SPR), and immunoprecipitation techniques, and speculated that IPA exerted its inhibitory effect on phosphorylation of vesicle associated membrane protein 8 (VAMP8) through direct molecular binding. This interaction influenced the assembly of the soluble N‐ethylmaleimide‐sensitive factor attachment protein receptor (SNARE) complex and subsequently promotes autophagosome‐lysosome fusion. In summary, IPA alleviates hyperoxia‐induced alveolar arrest by promoting autophagosome‐lysosome fusion via inhibition of VAMP8 phosphorylation, which is suggestive of a promising therapeutic target of BPD.