Background and Aims: Metabolic syndrome (MS) is a progressive metabolic disease characterized by obesity and multiple metabolic disorders. Tryptophan (Trp) is an essential amino acid, and its metabolism is linked to numerous physiological functions and diseases. However, the mechanisms by which Trp affects MS are not fully understood.

Methods and Results: In this study, experiments involving a high-fat diet (HFD) and fecal microbiota transplantation (FMT) were conducted to investigate the role of Trp in regulating metabolic disorders. In a mouse model, Trp supplementation inhibited intestinal farnesoid X receptor (FXR) signaling and promoted hepatic bile acid (BA) synthesis and excretion, accompanied by elevated levels of conjugated BAs and the ratio of non-12-OH to 12-OH BAs in hepatic and fecal BA profiles. As Trp alters the gut microbiota and the abundance of bile salt hydrolase (BSH)-enriched microbes, we collected fresh feces from Trp-supplemented mice and performed FMT and sterile fecal filtrate (SFF) inoculations in HFD-treated mice. FMT and SFF not only displayed lipid-lowering properties but also inhibited intestinal FXR signaling and increased hepatic BA synthesis. This suggests that the gut microbiota play a beneficial role in improving BA metabolism through Trp. Furthermore, fexaramine (a gut-specific FXR agonist) reversed the therapeutic effects of Trp, suggesting that Trp acts through the FXR signaling pathway. Finally, validation in a finishing pig model revealed that Trp improved lipid metabolism, enlarged the hepatic BA pool, and altered numerous glycerophospholipid molecules in the hepatic lipid profile.

Conclusion: Our studies suggest that Trp inhibits intestinal FXR signaling mediated by the gut microbiota–BA crosstalk, which in turn promotes hepatic BA synthesis, thereby ameliorating MS.

Concrete is the most widely used and highest-volume basic material in the word today. Enhancing its toughness, including tensile strength and deformation resistance, can boost the structural load-bearing capacity, minimize cracking, and decrease the amount of concrete and steel required in engineering projects. These advancements are crucial for the safety, durability, energy efficiency, and emission reduction of structural engineering. This paper systematically summarized the brittle characteristics of concrete and the various structural factors influencing its performance at multiple scales, including molecular, nano-micro, and meso-macro levels. It outlines the principles and impacts of concrete toughening and crack prevention from both internal and external perspectives, and discusses recent advancements and engineering applications of toughened concrete. In situ polymerization and fiber reinforcement are currently practical and highly efficient methods for enhancing concrete toughness. These techniques can boost the matrix's flexural strength by 30% and double its fracture energy, achieving an ultimate tensile strength of up to 20 MPa and a tensile strain exceeding 0.6%. In the future, achieving breakthroughs in concrete toughening will probably rely heavily on the seamless integration and effective synergy of multi-scale toughening methods.

The vast potential of medical big data to enhance healthcare outcomes remains underutilized due to privacy concerns, which restrict cross-center data sharing and the construction of diverse, large-scale datasets. To address this challenge, we developed a deep generative model aimed at synthesizing medical data to overcome data sharing barriers, with a focus on breast ultrasound (US) image synthesis. Specifically, we introduce CoLDiT, a conditional latent diffusion model with a transformer backbone, to generate US images of breast lesions across various Breast Imaging Reporting and Data System (BI-RADS) categories. Using a training dataset of 9,705 US images from 5,243 patients across 202 hospitals with diverse US systems, CoLDiT generated breast US images without duplicating private information, as confirmed through nearest-neighbor analysis. Blinded reader studies further validated the realism of these images, with area under the receiver operating characteristic curve (AUC) scores ranging from 0.53 to 0.77. Additionally, synthetic breast US images effectively augmented the training dataset for BI-RADS classification, achieving performance comparable to that using an equal-sized training set comprising solely real images (P = 0.81 for AUC). Our findings suggest that synthetic data, such as CoLDiT-generated images, offer a viable, privacy-preserving solution to facilitate secure medical data sharing and advance the utilization of medical big data.

Comorbid anxiety in chronic pain is clinically common, with a comorbidity rate of over 50%. The main treatments are based on pharmacological, interventional, and implantable approaches, which have limited efficacy and carry a risk of side effects. Here, we report a terahertz (THz, 10¹² Hz) wave stimulation (THS) technique, which exerts nonthermal, long-term modulatory effects on neuronal activity by reducing the binding between nano-sized glutamate molecules and GluA2, leading to the relief of pain and comorbid anxiety-like behaviors in mice. In mice with co-occurring anxiety and chronic pain induced by complete Freund's adjuvant (CFA) injection, hyperactivity was observed in glutamatergic neurons in the anterior cingulate cortex (ACC^Glu). Using whole-cell recording in ACC slices, we demonstrated that THS (34 THz) effectively inhibited the excitability of ACC^Glu. Moreover, molecular dynamics simulations showed that THS reduced the number of hydrogen bonds bound between glutamate molecules and GluA2. Furthermore, THS target to the ACC in CFA-treatment mice suppressed ACC^Glu hyperactivity and, as a result, alleviated pain and anxiety-like behaviors. Consistently, inhibition of ACC^Glu hyperactivity by chemogenetics mimics THS-induced antinociceptive and antianxiety behavior. Together, our study provides evidence for THS as an intervention technique for modulating neuronal activity and a viable clinical treatment strategy for pain and comorbid anxiety.

Exposure to airborne fine particulate matter (PM_2.5) is strongly associated with poor fertility and ovarian damage. However, the mechanism underlying this remains largely unclear. Here, we found that PM_2.5 markedly impaired murine ovarian reserve, decreased hormone levels, and aggravated ovarian inflammation. Circulating interleukin-6 (IL-6) was elevated in PM_2.5-exposed mice and was further confirmed to mediate this damage by IL-6 recombinant protein intervention. PM_2.5 exposure led to increased alveolar macrophage infiltration in the lungs. However, alveolar macrophage clearance with clodronate liposomes could not fully reverse the elevated IL-6 levels and ovarian injury, suggesting that alveolar macrophages were probably not the only source of circulating IL-6. Further experiments indicated that IL-6 mainly targeted ovarian theca–interstitial cells and impaired testosterone synthesis via suppressing the peroxisome proliferator-activated receptor γ (PPARγ) pathway. In addition, apoptosis of granulosa cells and restriction of follicular growth were observed in co-cultures with IL-6-treated theca–interstitial cells, which could be further reversed by the PPARγ agonist. Moreover, IL-6-neutralizing antibodies ameliorated PM_2.5-induced ovarian damage. Notably, increased levels of circulating IL-6 were observed in premature ovarian aging patients and were inversely associated with their ovarian function. In summary, our findings offer a mechanistic explanation for PM_2.5-induced ovarian dysfunction and verify IL-6 as a biomarker and potential therapeutic target.

Osteoporosis presents a marked global public health challenge, characterized by deficient osteogenesis and a deteriorating immune microenvironment. Conventional clinical interventions primarily target osteoclast-mediated bone damage, yet lack a comprehensive therapeutic approach that balances bone formation and resorption. Herein, we introduce a bone-targeted nanocomposite, A-Z@Pd(H), designed to address these challenges by integrating diverse functional components. The nanocomposite incorporates internal hydrogen-carrying nanozymes, which effectively scavenge multiple reactive oxygen species (ROS) and synergistically engage the autophagy–lysosome pathway to accelerate endogenous ROS degradation in macrophages. This mechanism disrupts the vicious cycle of autophagic dysfunction–ROS accumulation–macrophage inflammation. In addition, external metal–organic frameworks release zinc ions (Zn²⁺) in response to the acidic osteoporotic environment, thereby promoting osteogenesis. In a murine model of osteoporosis, intravenous administration of A-Z@Pd(H) leads to preferential accumulation in the femur, thereby remodeling the osteoporotic microenvironment through immune regulation, osteogenesis promotion, and osteoclast inhibition. These findings suggest that this system composed of hydrogen therapy and ion therapy may be a promising candidate for bone-targeted comprehensive therapy in osteoporosis.

The current biopsychosocial medical models have substantial limitations and require to form an improved scientific medical model. This new model should consider human health holistically, emphasizing the integrity of life and focusing on the impact of physiological spaces, natural factors, and the interaction between individuals and their environment. We propose a “life–society–nature medical model” that provides novel perspectives for innovation in basic medical theory, the integration of Traditional Chinese and Western medicine, disease diagnosis, therapy and prevention, as well as the development of new therapeutic agents, scientific instruments, and approaches to medical education.

MXenes, a class of 2-dimensional transition metal carbides and nitrides, have garnered important attention due to their remarkable electrical and thermal conductivity, high photothermal conversion efficiency, and multifunctionality. This review explores the potential of MXene materials in various thermal applications, including thermal energy storage, heat dissipation in electronic devices, and the mitigation of electromagnetic interference in wearable technologies. Recent advancements in MXene composites, such as MXene/bacterial cellulose aerogel films and MXene/polymer composites, have demonstrated enhanced performance in phase change thermal storage and electromagnetic interference shielding, underscoring their versatility and effectiveness. Although notable progress has been made, challenges remain, including the need for a deeper understanding of photothermal conversion mechanisms, improvements in mechanical properties, exploration of diverse MXene types, and the development of sustainable synthesis methods. This paper discusses these aspects and outlines future research directions, emphasizing the growing importance of MXenes in addressing energy efficiency, health, and safety concerns in modern applications.

The contact time of the droplet impacting on solid surfaces can be markedly reduced by 40% to 50% by breaking the symmetric behaviors with the help of the surface structures and motion, which is crucial to diverse applications involving anti-icing, anti-erosion, self-cleaning, etc. Herein, it is interesting to note that the contact time can be further decreased up to 60% on a moving ridge surface because of corresponding synergy, inspired by flying insects or wind-dispersal seeds. In the present work, the synergistic mechanisms of the reduction in contact time have been revealed by analyzing the 3 basic features, called Leaf-type, Ear-type, and Butterfly-type, according to their morphological and dynamical behaviors. Therefore, a universal theoretical model has arrived by introducing normal and tangential Weber numbers, beyond previous descriptions. Importantly, our study discovers a generalized scaling law of −0.52 between the contact time and new composite Weber number (We_com), which is feasible to stationary and moving surfaces, suggesting that the limit reduction rate on a moving ridge surface tends to 78%. The present work provides an insight to optimize the corresponding application efficiency by coupling the surface structure and motion.

Spermatogenesis is a sophisticated biological process by which spermatogonial stem cells (SSCs) undergo self-renewal and differentiation into spermatozoa. Molecular mechanisms underlying fate determinations of human SSCs by key genes and signaling pathways remain elusive. Here, we report for the first time that Yes1-associated transcriptional regulator (YAP1) is required for fate determinations of SSCs and male fertility by interacting with RAD21 and targeting NEDD4 in humans and mice. YAP1 was mainly located at cell nuclei of human SSCs. YAP1 silencing resulted in the decreases in proliferation and DNA synthesis as well as an enhancement in apoptosis of human SSCs both in vivo and in vitro. RNA sequencing and real-time polymerase chain reaction assays identified NEDD4 as a target of YAP1, and NEDD4 knockdown inhibited the proliferation of human SSCs and increased their apoptosis. Furthermore, YAP1 interacted with RAD21 to regulate NEDD4 transcription in human SSCs. Importantly, YAP1 abnormalities were found to be associated with non-obstructive azoospermia (NOA) as manifested as lower expression level of YAP1 in testicular tissues of NOA patients and YAP1 single-nucleotide variants (SNVs) in 777 NOA patients. Finally, Yap1 germline conditional knockout (cKO) mice assumed mitotic arrest, low sperm count, and motility. Collectively, these results highlight a critical role of YAP1 in determining the fate determinations of human SSCs and male infertility through the YAP1/RAD21/NEDD4 pathway. This study provides new insights into the genetic regulatory mechanisms underlying human spermatogenesis and the pathogenesis of NOA, and it offers new targets for gene therapy of male infertility.

The wide-bandgap semiconductor material Ga₂O₃ exhibits great potential in solar-blind deep-ultraviolet (DUV) photodetection applications, including none-line-of-sight secure optical communication, fire warning, high-voltage electricity monitoring, and maritime fog dispersion navigation. However, Ga₂O₃ photodetectors have traditionally faced challenges in achieving both high responsivity and fast response time, limiting their practical application. Herein, the Ga₂O₃ solar-blind DUV photodetectors with a suspended structure have been constructed for the first time. The photodetector exhibits a high responsivity of 1.51 × 10¹⁰ A/W, a sensitive detectivity of 6.01 × 10¹⁷ Jones, a large external quantum efficiency of 7.53 × 10¹² %, and a fast rise time of 180 ms under 250-nm illumination. Notably, the photodetector achieves both high responsivity and fast response time simultaneously under ultra-weak power intensity excitation of 0.01 μW/cm². This important improvement is attributed to the reduction of interface defects, improved carrier transport, efficient carrier separation, and enhanced light absorption enabled by the suspended structure. This work provides valuable insights for designing and optimizing high-performance Ga₂O₃ solar-blind photodetectors.

Atrazine (AT), a widely utilized chemical herbicide, causes widespread contamination of agricultural water bodies. Recently, exposure to AT has been linked to the development of age-related neurodegenerative diseases (NDs), suggesting its neurotoxicity potential. As an endocrine disruptor, AT targets the hypothalamus, a crucial part of the neuroendocrine system. However, the toxicological mechanism of AT exposure to the hypothalamus and its correlation with ND development remain unexplored. Our results indicated that AT exposure caused significant morphological and structural damage to the hypothalamus, leading to the loss of mature and intact neurons and microglial activation. Furthermore, hypothalamic neural stem cells (HtNSCs) were recruited to areas of neuronal damage caused by AT. Through in vivo and in vitro experiments, we clarified the outcomes of AT-induced HtNSC recruitment alongside the loss of mature/intact neurons. Mechanistically, AT induces senescence in these recruited HtNSCs by activating integrated stress response signaling. This consequently hinders the repair of damaged neurons by inhibiting HtNSC proliferation and differentiation. Overall, our findings underscore the pivotal role of the integrated stress response pathway in AT-induced HtNSC senescence and hypothalamic damage. Additionally, the present study offers novel perspectives to understand the mechanisms of AT-induced neurotoxicity and provides preliminary evidence linking AT contamination to the development of NDs.

Disease-associated microglia (DAM) are observed in neurodegenerative diseases, demyelinating disorders, and aging. However, the spatiotemporal dynamics and evolutionary trajectory of DAM during the progression of amyotrophic lateral sclerosis (ALS) remain unclear. Using a mouse model of ALS that expresses a human SOD1 gene mutation, we found that the microglia subtype DAM begins to appear following motor neuron degeneration, primarily in the brain stem and spinal cord. Using reverse transcription quantitative polymerase chain reaction, RNAscope in situ hybridization, and flow cytometry, we found that DAM increased in number as the disease progressed, reaching their peak in the late disease stage. DAM responded to disease progression in both SOD1^G93A mice and sporadic ALS and C9orf72-mutated patients. Motor neuron loss in SOD1^G93A mice exhibited 2 accelerated phases: P90 to P110 (early stage) and P130 to P150 (late stage). Some markers were synchronized with the accelerated phase of motor neuron loss, suggesting that these proteins may be particularly responsive to disease progression. Through pseudotime trajectory analysis, we tracked the dynamic transition of homeostatic microglia into DAM and cluster 6 microglia. Interestingly, we used the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to deplete microglia in SOD1^G93A mice and observed that DAM survival is independent of CSF1R. An in vitro phagocytosis assay directly confirmed that DAM could phagocytose more beads than other microglia subtypes. These findings reveal that the induction of the DAM phenotype is a shared cross-species and cross-subtype characteristic in ALS. Inducing the DAM phenotype and enhancing its function during the early phase of disease progression, or the time window between P130 and P150 where motor neuron loss slows, could serve as a neuroprotective strategy for ALS.

Chirality has garnered significant attention in the scientific community since its discovery by Louis Pasteur over a century ago. It has been showing a profound impact on chemical, biomedical, and materials sciences. Significant progress has been made in controlling molecular chirality, as evidenced by the several Nobel Prizes in chemistry awarded in this area, particularly for advancements in the asymmetric catalytic synthesis of molecules with central and axial chirality. However, the exploration of new types of chirality has been largely stagnant for more than half a century, likely due to the complexity and challenges inherent in this field. In this work, we present the discovery of a novel type of chirality—staircase chirality as inspired by the design and synthesis of unnatural amino acid derivatives. The architecture of staircase chirality is characterized by 2 symmetrical phenyl rings anchored by a naphthyl pier, with the rings asymmetrically displaced due to the influence of chiral auxiliaries at their para positions. This unique staircase chiral framework has been thoroughly characterized using spectroscopic techniques, with its absolute configuration definitively confirmed by x-ray diffraction analysis. Remarkably, one of the staircase molecules exhibits 4 distinct types of chirality: central, orientational, turbo, and staircase chirality, a combination that has not been previously documented in the literature. Computational studies using density functional theory (DFT) calculations were conducted to analyze the relative energies of individual staircase isomers, and the results are in agreement with our experimental findings. We believe that this discovery will open up a new research frontier in asymmetric synthesis and catalysis, with the potential to make a substantial impact on the fields of chemistry, medicine, and materials science.

The NLRP3 inflammasome plays a critical role in various inflammatory conditions. However, despite extensive research in targeted drug development for NLRP3, including MCC950, clinical success remains elusive. Here, we discovered that the activated NLRP3 inflammasome complex (disc-NLRP3) and the activating mutation L351P exhibited resistance to MCC950. Through investigations using the small-molecule compound polydatin, HSP90α was found to stabilize both the resting (cage-NLRP3) and activated state (disc-NLRP3) of NLRP3 complexes, sustaining its activation. Our mechanistic studies revealed that polydatin specifically targets HSP90α, binding to it directly and subsequently interfering with the HSP90α-NLRP3 interaction. This disruption leads to the dissipation of cage-NLRP3, disc-NLRP3 complexes and NLRP3 L351P. Importantly, genetic and pharmacological inactivation of HSP90α effectively reduced NLRP3 inflammasome activation and alleviated cerulein-induced acute pancreatitis. These therapeutic effects highlight the clinical potential of HSP90α inhibition. Our findings demonstrate that HSP90α is crucial for the stability of both the resting and activated states of the NLRP3 inflammasome during its sustained activation, and targeting HSP90α represents a promising therapeutic strategy for diseases driven by the NLRP3 inflammasome.

Breast cancer (BC) often spreads to bones, leading to bone metastasis (BM). Current targeted therapies have limited effectiveness in the treatment of this condition. Osteoclasts, which contribute to bone destruction, are crucial in supporting tumor cell growth in the bones. Breast cancer bone metastasis (BCBM) treatments have limited efficacy and can cause adverse effects. Ononin exhibits anticancer properties against various cancers. The study examined the impact of ononin on the BCBM and the signaling pathways involved. Our study utilized a variety of experimental techniques, including cell viability assays, colony formation assays, wound-healing assays, Transwell migration assays, Western blot analysis, and tartrate-resistant acid phosphatase (TRAP) staining. We examined the effects of ononin on osteoclastogenesis induced in MDA-MB-231 conditioned medium- and RANKL-treated RAW 264.7 cells. In a mouse model of BCBM, ononin reduced tumor-induced bone destruction. Ononin treatment effectively inhibited proliferation and colony formation and reduced the metastatic capabilities of MDA-MB-231 cells by suppressing cell adhesion, invasiveness, and motility and reversing epithelial–mesenchymal transition (EMT) markers. Ononin markedly suppressed osteoclast formation and osteolysis-associated factors in MDA-MB-231 cells, as well as blocked the activation of the mitogen-activated protein kinase (MAPK) pathway in RAW 264.7 cells. Ononin treatment down-regulated the phosphorylation of MAPK signaling pathways, as confirmed using MAPK agonists or inhibitors. Ononin treatment had no adverse effects on the organ function. Our findings suggest that ononin has therapeutic potential as a BCBM treatment by targeting the MAPK pathway.

To explore whether the metabolic state reprogramming approach may be used to explore previously unknown metabolic pathways that contribute to antibiotic resistance, especially those that have been neglected in previous studies, pyruvate reprogramming was performed to reverse the resistance of multidrug-resistant Edwardsiella tarda. Surprisingly, we identified a pyruvate-regulated glutathione system that occurs by boosting glycine, serine, and threonine metabolism. Moreover, cysteine and methionine metabolism played a key role in this reversal. This process involved pyruvate-depressed glutathione and pyruvate-promoted glutathione oxidation, which was attributed to the elevated glutathione peroxidase and depressed glutathione reductase that was inhibited by glycine. This regulation inhibited reactive oxygen species (ROS) degradation and thereby elevated ROS to eliminate E. tarda. Loss of metB, gpx, and gor of the metabolic pathways increased and decreased resistance, respectively, both in vitro and in vivo, thereby supporting the hypothesis of a pyruvate–cysteine–glutathione system/glycine–ROS metabolic pathway. The role of this metabolic pathway in drug resistance and reprogramming reversal was demonstrated in laboratory-evolved gentamicin-resistant E. tarda and other clinically isolated multidrug- and carbapenem-resistant pathogens. Thus, we reveal a less studied antibiotic resistance metabolic pathway along with the mechanisms involved in its reversal.

The effective and translational strategy to regenerate knee meniscal fibrocartilage remained challenging. Herein, we first identified vascular smooth muscle cells (VSMCs) transdifferentiated into fibrochondrocytes and participated in spontaneous meniscal regeneration using smooth muscle cell lineage tracing transgenic mice meniscal defect model. Then, we identified low-intensity pulsed ultrasound (LIPUS) acoustic stimulus enhanced fibrochondrogenic transdifferentiation of VSMCs in vitro and in vivo. Mechanistically, LIPUS stimulus could up-regulate mechanosensitive ion channel Piezo1 expression and then activate the transforming growth factor β1 (TGFβ1) signal, following repression of the Notch signal, consequently enhancing fibrochondrogenic transdifferentiation of VSMCs. Finally, we demonstrated that the regular LIPUS stimulus enhanced anisotropic native-like meniscal fibrocartilage tissue regeneration in a beagle canine subtotal meniscectomy model at 6 months postoperatively. The single-cell RNA sequencing analysis confirmed the role of VSMC fibrochondrogenic transdifferentiation in meniscal regeneration.

Photoelectrochemistry provides an important application in the production of high-value-added chemicals. However, photoelectrochemical organic transformation with high product selectivity remains a challenge. Until now, various technologies have been developed to promote the selectivity of photoelectrochemical high-value-added chemical production. Herein, a novel ion-shielding heterogeneous photoelectrocatalysis strategy for the production of trifluoromethyl group (CF₃)-containing compounds with high selectivity is described.

Neutrophils are essential in combating invading pathogens such as Plasmodium parasites, but the participation of their subpopulations and mechanisms in resistance to parasite infection are not fully understood. Our study identified a marked increase in Ly6G⁺ neutrophils in response to P. berghei ANKA infection. Depletion of these cells rendered mice more susceptible to infection. Elevated interleukin-17 (IL-17) levels, which increased the Ly6G⁺ neutrophil population, were also found to contribute to this protective effect. IL-17 depletion led to reduced neutrophil numbers and increased susceptibility. Furthermore, dihydroartemisinin (DHA) treatment enhanced neutrophil-mediated immune responses through up-regulation of CD18 and CXCR4 factors. These findings revealed key mechanisms of neutrophil and IL-17 interactions in malaria protection and highlighted DHA's potential to promote neutrophil function in combating malaria.

Metamaterials hold great potential to enhance the imaging performance of magnetic resonance imaging (MRI) as auxiliary devices, due to their unique ability to confine and enhance electromagnetic fields. Despite their promise, the current implementation of metamaterials faces obstacles for practical clinical adoption due to several notable limitations, including their bulky and rigid structures, deviations from optimal resonance frequency, and inevitable interference with the radiofrequency (RF) transmission field in MRI. Herein, we address these restrictions by introducing a flexible and smart metamaterial that enhances sensitivity by conforming to patient anatomies while ensuring comfort during MRI procedures. The proposed metamaterial selectively amplifies the magnetic field during the RF reception phase by passively sensing the excitation signal strength, remaining “off” during the RF transmission phase. Additionally, the metamaterial can be readily tuned to achieve a precise frequency match with the MRI system through a controlling circuit. The metamaterial presented here paves the way for the widespread utilization of metamaterials in clinical MRI, thereby translating this promising technology to the MRI bedside.

Radiative cooling has witnessed substantial progress while its performance is constrained by the thermal reciprocal Kirchhoff's law. Violating Kirchhoff's law to pursue nonreciprocal radiative cooling seems promising; however, the energy conservation requirement and radiant flux integrated over the entire hemisphere make the nonreciprocal benefit insignificant. This commentary discusses the practical limits of nonreciprocal radiative cooling and points toward the future direction of directional radiative cooling.

Living microorganisms can perform directed migration for foraging in response to a chemoattractant gradient. We report a biomimetic strategy that rotary F_oF₁-ATPase (adenosine triphosphatase)-propelled flasklike colloidal motors exhibit positive chemotaxis resembling the chemotactic behavior of bacteria. The streamlined flasklike colloidal particles are fabricated through polymerization, expansion, surface rupture, and re-polymerizing nanoemulsions composed of triblock copolymers and ribose. The as-synthesized particles enable the incorporation of thylakoid vesicles into the cavity, ensuring a geometric asymmetric nanoarchitecture. The chemical gradient in the neck channel across flasklike colloidal motors facilitates autonomous movement at a speed of 1.19 μm/s in a ΔpH value of 4. Computer simulations reveal the self-actuated flasklike colloidal motors driven by self-diffusiophoretic force. These flasklike colloidal motors display positive directional motion along an adenosine diphosphate (ADP) concentration gradient during adenosine triphosphate (ATP) synthesis. The positive chemotaxis is ascribed that the phosphorylation reaction occurring inside colloidal motors generates 2 distinct phoretic torques at the bottom and the opening owing to the diffusion of ADP, thereby a continuous reorientation motion. Such a biophysical strategy that nanosized rotary protein molecular motors propel the directional movement of a flasklike colloidal motor holds promise for designing new types of biomedical swimming nanobots.

Cryogenic crystal bolometer plays a crucial role in searching for neutrinoless double-beta (0νββ) decay, which is a rare process that could determine the Majorana nature of neutrinos. The flagship bolometer experiment—CUORE (Cryogenic Underground Observatory for Rare Events)—operating at the Gran Sasso underground laboratory [Laboratori Nazionali del Gran Sasso (LNGS)] as the world's first ton-scale bolometric detector has achieved great success and well demonstrated advantages of the bolometric technology for the 0νββ study. The proposed upgrade of CUORE—the CUPID project—aims to achieve higher sensitivity with orders of magnitude background reduction by utilizing scintillating crystals and dual readout technology to exclude most of the background events dominated by alpha particles. Although CUPID has outstanding advantages over CUORE, further increasing the detection capability to fully explore the effective neutrino mass region for the inverted neutrino mass hierarchy and possibly to discover Majorana neutrinos remains a technical challenge ahead. In this prospective, we discuss strategies toward future technology development to further enhance the experimental sensitivity.

Personalized healthcare monitoring is a transformative tool for preventing potential risks and enhancing health status, particularly through molecular-level insights. Advances in nanotechnology, smart devices, and artificial intelligence (AI) have revolutionized personalized healthcare, especially in point-of-care testing (POCT), enabling early detection and timely intervention. Recently, surface-enhanced Raman spectroscopy (SERS) technology, particularly with flexible chips, has shown immense promise in this field due to its in situ, rapid, specific, and efficient detection capabilities. In this review, we highlight recent advancements in flexible SERS chips for personalized healthcare monitoring, demonstrating their effectiveness in target sampling and detection. Importantly, we provide a comprehensive overview of potential applications of flexible SERS chips in personalized healthcare, address current challenges, and propose future development directions. We also explore the future development of miniaturized Raman devices to broaden their applications in personalized healthcare monitoring. Additionally, we underscore the important role of AI in enhancing data processing and analysis. Our aim is to offer a thorough guide on integrating SERS into personalized healthcare monitoring, promising a new era of health management.