ABSTRACT Dynamic and real‐time sensing of taste is increasingly important for food safety and pharmaceutical quality control, yet the development of advanced sensors for each taste, especially those for bitterness, remains limited. The challenge has been lying on developing suitable receptors for bitter compounds that are capable of reversible operation. Here, we present a graphene‐based taste sensor that integrates a quinine‐specific aptamer, enabling selective molecular recognition with high sensitivity and operational stability. Especially, unlike previous sensors, which were irreversible or required regeneration steps, our design achieves fully reversible quinine‐specific capture and release. Combined with previously developed taste sensors by the authors, graphene‐based electronic tongue was demonstrated to differentiate four different taste compounds and even complex beverages. This work highlights the strong potential of the graphene‐based sensors with aptamer receptors as reliable and tunable platforms for advanced taste sensing and real‐time analysis.
ABSTRACT Chimeric antigen receptor (CAR)‐T cell therapy has emerged as a groundbreaking treatment for cancer. After decades of research, it is now being actively explored for a broader range of immune‐mediated diseases, particularly cancer and autoimmune disorders. Significant progress has been made in both understanding technological advancements and addressing the intrinsic limitations of this engineered cellular therapy. However, the clinical efficacy and safety of CAR‐T cells remain influenced by several factors, including the immunosuppressive tumour microenvironment (TME), the continuous mutational evolution of tumour cells, the prohibitive cost of production limiting accessibility, and the immune‐related toxicities associated with biologic treatments. Given these substantial challenges, a paradigm shift is urgently needed – from conceptualizing CAR‐T cells solely as “engineered immune cells” to recognizing them as “programmable intelligent systems.” This review proposes a dynamic immune engineering framework, advocating that the next generation of CAR‐T cells be conceived as programmable immune systems capable of sensing, responding to, and self‐regulating immune responses. This evolving approach positions dynamic immune regulation as the core principle underlying immune system function. Ultimately, this review aims to provide a conceptual and theoretical foundation for the development of next‐generation CAR‐T therapies that are not only highly effective but also cost‐efficient and globally accessible.
ABSTRACT Deciphering the structure‐activity relationship on Cu‐based electrocatalysts is critical to rationally optimize their performances in CO 2 to multicarbon (C 2+ ) conversion, which nonetheless remains highly challenging due to their ill‐defined and electrochemically unstable structures. Herein, this study explores Cu‐based molecular hybrids with defined structures to establish structure‐activity relationships in CO 2 ‐C 2+ electrocatalysis, where a Ni(II) phthalocyanine anchored on Cu 2 O nanocubes via 2‐(3‐thienyl)ethoxy groups outperforms its Co(II) analog and unmodified prototype in C 2+ synthesis (78.3% selectivity, 330 mA . cm −2 ), rivaling top catalysts. Structural analysis revealed the functional 2‐(3‐thienyl)ethoxy anchors pose superior Cu 2 O affinity to retain the Cu(I) structure and the grafted metal phthalocyanines during catalysis. Such stabilized and well‐defined catalyst structures enable the structure‐activity relationship unveiled by in situ spectroscopies and theoretical calculations. The results show that the synergy between the molecular metal centers and surface Cu atoms fine‐tunes the energy barriers for both CO transfer and *OCCO hydrogenation, which are minimized by the optimal Cu‐S‐Ni coordination endowing abundant Cu(I)Cu(0)‐paired active sites with an electron‐rich Ni center. This work demonstrates the essential role of metal‐ligand cooperativity in C‐C coupling and successfully bridges mechanistic insights with catalyst design for efficient CO 2 ‐C 2+ conversion.
ABSTRACT Chronic stress potentially accelerates aging and increases age‐related disease risk. However, the underlying mechanisms and organ specificity remain unclear. Utilizing a 12‐month unpredictable chronic mild stress (UCMS) mouse model, we revealed chronic stress significantly exacerbates systemic inflammation, causing widespread tissue damage and lifespan shortening. Integrated single‐cell RNA sequencing analysis of multiple tissues suggests a common feature of lymphocyte reduction and myeloid cell expansion. The lungs and kidneys exhibited pronounced stress responses, including epigenetic dysregulation and mitochondrial dysfunction. Both β‐nicotinamide mononucleotide (NMN) and compound medicine Bazi Bushen (BZBS) effectively alleviate the UCMS‐induced aging phenotypes. BZBS restores immune system homeostasis and reduces stress/inflammation levels in various tissues. Bioactive compounds from BZBS constituents —Schisandra chinensis (Turcz.) Baill. and Cnidium monnieri (L.) Cusson— improved mitochondrial function via AMPK‐SIRT‐PGC‐1α signaling activation. The present study underscores the importance of early intervention in chronic stress to prevent or delay age‐related diseases, with significant implications for public health strategies aimed at healthy aging.
