Room-temperature (RT) terahertz (THz) detection finds widespread applications in security inspection, communication, biomedical imaging, and scientific research. However, the state-of-the-art detection strategies are still limited by issues such as low sensitivity, narrow response range, slow response speed, complex fabrication techniques, and difficulties in scaling up to large arrays. Here, we present a high-sensitivity, broadband-response, and high-speed RT THz detection strategy by utilizing a deep subwavelength metal–semiconductor–metal (MSM) structure. The spontaneously formed 2-dimensional electron gas (2DEG) at the CdTe/PbTe interface provides a superior transport channel characterized by high carrier concentration, low scattering, and high mobility. The synergy of the electromagnetic induced well effect formed in the MSM structure, and the efficient and rapid transport capabilities of the 2DEG channel give rise to an impressive performance improvement. The proposed 2DEG photodetector exhibits a broad frequency range from 22 to 519 GHz, an ultralow noise equivalent power of 3.0 × 10⁻¹⁴ W Hz^−1/2 at 166 GHz, and a short response time of 6.7 μs. This work provides an effective route for the development of high-performance RT THz detection strategies, paving the way for enhanced THz technology applications.

Slow wound healing in the elderly has attracted much attention recently due to the associated infection risks and decreased longevity. The “brain–skin axis” theory suggests that abnormalities in the brain and nervous system can lead to skin degeneration because abnormal mental states, like chronic stress, can have negative physiological and functional effects on the skin through a variety of processes, resulting in delayed wound healing and accelerated skin aging. However, it remains unclear whether maintaining a youthful brain has beneficial effects on aged skin healing. In light of this, we identified youthful brain-derived extracellular vesicles (YBEVs) and created a composite GelMA hydrogel material that encourages scarless wound healing in aged skin. We found that YBEVs reduce the expression of senescence, senescence-associated secretory phenotypes, and inflammation-associated proteins, and even restore dysfunction in senescent cells. Furthermore, by encouraging collagen deposition, angiogenesis, epidermal and dermal regeneration, and folliculogenesis, we demonstrated that YBEV-containing composite hydrogels accelerated scarless wound healing in skin wounds of aged rats. The pro-repairing speed and effect of this composite hydrogel even matched that of young rats. Subsequent proteomic analysis revealed the presence of numerous proteins within YBEVs, some of which may play a role in the regulation of skin energy intake, particularly through oxidative phosphorylation and mitochondrial function. In conclusion, the findings suggest that maintaining a youthful brain could potentially alleviate skin aging, and the proposed YBEVs-GelMA hydrogel emerges as a promising strategy for addressing age-related impairments in skin healing.

Disruption of acylcarnitine homeostasis results in life-threatening outcomes in humans. Carnitine–acylcarnitine translocase deficiency (CACTD) is a scarce autosomal recessive genetic disease and may result in patients' death due to heart arrest or respiratory insufficiency. However, the reasons and mechanism of CACTD inducing respiratory insufficiency have never been elucidated. Herein, we employed lipidomic techniques to create comprehensive lipidomic maps of entire lungs throughout both prenatal and postnatal developmental stages in mice. We found that the acylcarnitines manifested notable variations and coordinated the expression levels of carnitine–acylcarnitine translocase (Cact) across these lung developmental stages. Cact-null mice were all dead with a symptom of respiratory distress and exhibited failed lung development. Loss of Cact resulted in an accumulation of palmitoyl-carnitine (C16-acylcarnitine) in the lungs and promoted the proliferation of mesenchymal progenitor cells. Mesenchymal cells with elevated C16-acylcarnitine levels displayed minimal changes in energy metabolism but, upon investigation, revealed an interaction with sterile alpha motif domain and histidine-aspartate domain-containing protein 1 (Samhd1), leading to decreased protein abundance and enhanced cell proliferation. Thus, our findings present a mechanism addressing respiratory distress in CACTD, offering a valuable reference point for both the elucidation of pathogenesis and the exploration of treatment strategies for neonatal respiratory distress.

The emergence and prevalence of methicillin-resistant Staphylococcus aureus (MRSA) severely compromises conventional β-lactam antibiotics efficacy and poses an extensive global health challenge. Given the close relationship between docosahexaenoic acid (DHA) and metabolic alterations, this study aimed to reveal the novel function of DHA to potentiate β-lactam antibiotics activity through a lipid peroxidation mechanism. Additionally, DHA exhibited significant inhibitory effects on the catalytic function of β-lactamase through interactions with active residues. Herein, the dual-faceted mechanisms of perturbation of lipid metabolism and β-lactamase catalytic inhibition achieved the potentiated antibacterial efficacy of β-lactam antibiotics in combination with DHA against MRSA. Furthermore, to enhance the pharmacodynamic performance and stability of DHA, amoxicillin and DHA co-loaded nanoemulsions (Amo/DHA-NEs) were prepared via high-energy emulsification. Intriguingly, we found that Amo/DHA-NEs effectively rescued MRSA-induced infections in the murine infection models, as evidenced by the superior bacterial clearance and mitigated inflammation. Collectively, this work reveals a potentially exploitable link between DHA-driven metabolic reprogramming and β-lactams resistance, and we propose combination therapies of DHA and β-lactams targeting the emerging threat of MRSA infections.

Prussian blue and Prussian blue analogs are widely used in sodium-ion batteries (SIBs). In this study, we upcycle the degraded Prussian blue directly into layered materials for SIBs through thermal treatment. Prussian blue thermally decomposes to form metal oxides, which then recrystallize into layered metal oxides with metal–nitrogen bond on their surface under suitable temperature conditions. This transformation method is similar to solid-state synthesis, allowing for the pre-addition of necessary components before material conversion to optimize the composition and integrity of the target materials. Based on in situ x-ray diffraction observations of the crystal structure changes of Prussian blue at different temperatures, we demonstrate 1,000 °C as the optimal temperature for converting to layered materials. These materials exhibit an initial discharge capacity of 122.3 mAh g⁻¹ and good rate and cycling stability. We hope that this research will promote the sustainable development of the SIB industry.

Gain-of-function mutations of Notch2 cause the rare autosomal dominant disorder known as Hajdu–Cheney syndrome (HCS). Most patients with HCS develop congenital heart disease; however, the precise mechanisms remain elusive. Here, a murine model expressing the human Notch2 intracellular domain (hN2ICD) in cardiomyocytes (hN2ICD-Tg^CM) was generated and the mice spontaneously developed ventricular diastolic dysfunction with preserved ejection fraction and cardiac hypertrophy. Ectopic hN2ICD expression promoted cardiomyocyte hypertrophy by suppressing adenylosuccinate lyase (ADSL)-mediated adenosine 5′-monophosphate (AMP) generation, which further enhanced the activation of the mammalian target of rapamycin complex 1 pathway by reducing AMP-activated kinase activity. Hairy and enhancer of split 1 silencing abrogated hN2ICD-induced cardiomyocyte hypertrophy by increasing Adsl transcription. Importantly, pharmacological activation of AMP-activated kinase ameliorated cardiac hypertrophy and dysfunction in hN2ICD-Tg^CM mice. The frameshift mutation in Notch2 exon 34 (c.6426dupT), which causes early-onset HCS, induces AC16 human cardiomyocyte hypertrophy through suppressing ADSL-mediated AMP generation. Thus, targeting Notch2-mediated purine nucleotide metabolism may be an attractive therapeutic approach to heart failure treatment.

The intricate relationship between cancer, circadian rhythms, and aging is increasingly recognized as a critical factor in understanding the mechanisms underlying tumorigenesis and cancer progression. Aging is a well-established primary risk factor for cancer, while disruptions in circadian rhythms are intricately associated with the tumorigenesis and progression of various tumors. Moreover, aging itself disrupts circadian rhythms, leading to physiological changes that may accelerate cancer development. Despite these connections, the specific interplay between these processes and their collective impact on cancer remains inadequately explored in the literature. In this review, we systematically explore the physiological mechanisms of circadian rhythms and their influence on cancer development. We discuss how core circadian genes impact tumor risk and prognosis, highlighting the shared hallmarks of cancer and aging such as genomic instability, cellular senescence, and chronic inflammation. Furthermore, we examine the interplay between circadian rhythms and aging, focusing on how this crosstalk contributes to tumorigenesis, tumor proliferation, and apoptosis, as well as the impact on cellular metabolism and genomic stability. By elucidating the common pathways linking aging, circadian rhythms, and cancer, this review provides new insights into the pathophysiology of cancer and identifies potential therapeutic strategies. We propose that targeting the circadian regulation of cancer hallmarks could pave the way for novel treatments, including chronotherapy and antiaging interventions, which may offer important benefits in the clinical management of cancer.

Spermatogonial stem cells (SSCs) are essential for initiating and maintaining normal spermatogenesis, and notably, they have important applications in both reproduction and regenerative medicine. Nevertheless, the molecular mechanisms controlling the fate determinations of human SSCs remain elusive. In this study, we identified a selective expression of APBB1 in dormant human SSCs. We demonstrated for the first time that APBB1 interacted with KAT5, which led to the suppression of GDF15 expression and consequent inhibition of human SSC proliferation. Intriguingly, Apbb1^−/− mice assumed the disrupted spermatogenesis and markedly reduced fertility. SSC transplantation assays revealed that Apbb1 silencing enhanced SSC colonization and impeded their differentiation, which resulted in the impaired spermatogenesis. Notably, 4 deleterious APBB1 mutation sites were identified in 2,047 patients with non-obstructive azoospermia (NOA), and patients with the c.1940C>G mutation had a similar testicular phenotype with Apbb1^−/− mice. Additionally, we observed lower expression levels of APBB1 in NOA patients with spermatogenic arrest than in obstructive azoospermia patients with normal spermatogenesis. Collectively, our findings highlight an essential role of APBB1/KAT5/GDF15 in governing human SSC fate decisions and maintaining normal spermatogenesis and underscore them as therapeutic targets for treating male infertility.

Acute respiratory distress syndrome (ARDS) survivors often suffer from long-term psychiatric disorders such as depression, but the underlying mechanisms remain unclear. Here, we found marked alterations in the composition of gut microbiota in both ARDS patients and mouse models. We investigated the role of one of the dramatically changed bacteria—Akkermansia muciniphila (AKK), whose abundance was negatively correlated with depression phenotypes in both ARDS patients and ARDS mouse models. Specifically, while fecal transplantation from ARDS patients into naive mice led to depressive-like behaviors, microglial activation, and intestinal barrier destruction, colonization of AKK or oral administration of its metabolite—propionic acid—alleviated these deficits in ARDS mice. Mechanistically, AKK and propionic acid decreased microglial activation and neuronal inflammation through inhibiting the Toll-like receptor 4/nuclear factor κB signaling pathway. Together, these results reveal a microbiota-dependent mechanism for ARDS-related depression and provide insight for developing a novel preventative strategy for ARDS-related psychiatric symptoms.