Discrete-modulated coherent-state continuous-variable quantum key distribution (DMCS-CVQKD) is of great value for its simple implementation. However, the traditional DMCS-CVQKD scheme cannot tolerate the high channel excess noise and channel loss, compared to the Gaussian-modulated scheme, and its error correction is still difficult. In this paper, we propose a discrete-modulated coherent-state basis-encoding quantum key distribution (DMCS-BE-QKD) protocol, where the secret keys are encoded in the random choice of 2 measurement bases, i.e., the conjugate quadratures X and P of discrete-modulated coherent states, and it only needs simple binary sequence error correction. We analyze the secret key rate of DMCS-BE-QKD protocol under individual and collective attacks in the linear Gaussian channel. The results show that DMCS-BE-QKD can greatly enhance the ability to tolerate the channel loss and excess noise compared to the original DMCS-CVQKD protocol, which can tolerate approximately 40 dB more channel loss compared to the original DMCS-CVQKD for the realistic value of noise. Finally, a proof-of-principle experiment is conducted under a 50.5-km optical fiber to verify the feasibility of DMCS-BE-QKD. It is based on the consistent physical procedures of the traditional DMCS-CVQKD, which makes it perfectly compatible to deployed terminals and can serve as a multiplier for the practical secure quantum cryptography communication in harsh environments.

This commentary highlights the importance and implications of the study “Quadruple-band synglisis enables high thermoelectric efficiency in earth-abundant tin sulfide crystals”, led by C. Chang and L. Zhao, published in Science. They improved the thermoelectric efficiency by activating quadruple-band synglisis and facilitating carrier transport in tin sulfide crystals, and successfully developed an optical pump–terahertz probe technique in reflection mode to diagnose the carrier dynamics for high-conductivity bulk thermoelectric materials. This study inspires mutual promotion and complementary development between the fields of thermoelectrics and terahertz technology.

Oxalate-induced crystalline kidney injury is a common form of crystal nephropathy. The accumulation of calcium oxalate (CaOx) crystal could lead to renal epithelium injury and inflammation. The underlying cellular events in kidney after CaOx crystal formation are largely unknown. This study was aimed to gain a better understanding of mouse kidney function in the development of renal CaOx formation. The study utilized a mouse CaOx model to analyze the cellular response at 5 time points using single-cell RNA sequencing and investigate the interaction of different cells during renal CaOx crystal formation. Additionally, the study investigated the communication between these cells and macrophages, as well as the role of chemokines in recruiting infiltrating macrophages. RNA velocity analysis uncovered an alternative differentiation pathway for injured and S1 proximal tubule cells, which mainly communicate with macrophages through the SPP1–CD44 pair, along with the expression of proinflammatory factors and stone matrix genes during renal CaOx crystal formation. Furthermore, resident Fn1 macrophages were found to express chemokines, such as CCL2, which recruited infiltrating macrophages. The CCL2 secretion was mediated by the CD44–AKT pathway. Blocking CCL2 decreased the expression of injury markers in the kidney, including CLU, LCN2, and KIM-1, and inhibited CaOx crystal deposition. The study identified potential cell types and target genes involved in renal tubule injury in oxalate-related crystal nephropathy. The findings shed light on the cellular processes that contribute to the formation and damage caused by CaOx crystals within the kidney, which could lead to the development of potential cell types and target genes for treating this condition.

Vascular inflammatory aging is strongly associated with multimorbidity, including immunosenescence. Here, bioinformatic analysis indicated elevated expression of the lysozyme (LYZ) gene in age-dependent vascular diseases. Lyz1 deficiency led to vascular inflammatory aging, including damage to indicators related to oxidative stress, vascular function, and inflammation in the serum and vascular tissues of wild-type (WT) and Lyz1^−/− mice. The 16S ribosomal RNA sequencing of intestinal contents revealed increased Bifidobacterium and its metabolism of acetate, butyrate, omega-muricholic acid, propionate, and valeric acid in Lyz1^−/− mice compared with that in WT mice. Additionally, RNA sequencing of vascular tissues identified differentially expressed genes in Lyz1^−/− mice compared with those in WT mice, as well as enrichment of the common phosphatidylinositol 3-kinase (PI3K)–Akt signaling pathway. Vascular inflammatory aging phenotypes were detected in the blood vessels of antibiotic-treated and germ-free mice, and the PI3K–Akt signaling pathway was inhibited. Importantly, intravenous LYZ administration worsened the pathological conditions, whereas oral LYZ administration successfully restored the gut microbial balance and reversed the vascular inflammatory aging phenotypes. Collectively, this study establishes LYZ as a novel biomarker for age-related vascular diseases and the gut microbiota–PI3K–Akt axis as a promising therapeutic target.

To improve the treatment outcomes for large bone defects and osteoporosis, researchers have been committed to reducing bone loss and accelerating bone regeneration through cell transplantation, biomaterial intervention, and biophysical stimulation over the past few decades. Magnetism, as a noninvasive biophysical stimulus, has been employed in the repair of the musculoskeletal system, achieving a series of promising results. In this review, we provide a retrospective analysis and perspective of research on magnetic-driven bone regeneration and functional reconstruction. This review aims to delineate safe and efficient magnetic application modalities and to summarize the potential mechanisms by which magnetism regulates the behavior of skeletal lineage cells, thereby providing insights for the expansion and translational application of magnetic-driven regenerative medicine.

Nitrite reductases (NiRs) are natural enzymes that facilitate the reduction of nitrite. They are essential for the microbial nitrogen cycle and play a vital role in regulating numerous physiological and pathological processes associated with nitric oxide (NO) in living organisms. By the merits of protein engineering, a variety of artificial NiR mimics have been developed. These include traditional artificial proteins, metal-azacycle complexes, and nanozymes such as metal, metal oxide/sulfide nanoparticles, metal-organic frameworks, bioinorganic nanohybrids, and advanced single-atom nanozymes. This development marks an important milestone in broadening the application of enzyme-like catalytic nitrite reduction across various fields, such as biomedicine, biosensing, food science, and environmental science. In this review, we first outline the different types of NiRs, along with their active center structures and catalytic mechanisms, drawing from recent research and discoveries. We then classify the reported NiR mimic materials, discussing their active center structures and enzyme-like catalytic mechanisms. Additionally, we explore the potential future applications and challenges facing NiR mimics in the field of biomedicine.

It has been demonstrated that glutamine is a key player in boosting endothelial cell (EC) proliferation. However, despite its importance, the role of endothelial glutaminolysis in diabetes remains largely unexplored. Our research aimed to investigate the function of glutaminolysis in ECs within the context of diabetes and to evaluate the potential therapeutic effects of salvianolic acid B (SalB) and α-ketoglutarate (α-KG) on diabetic vascular complications. Histological analysis of skin wounds in diabetic patients revealed delayed restoration of vascularization and collagen synthesis during wound healing, accompanied by decreased glutaminase 1 (GLS1) expression and reduced colocalization with the EC marker platelet-endothelial cell adhesion molecule-1 (CD31). Additionally, a significant decline in GLS1 activity and expression was observed in ECs isolated from diabetic hearts. In vitro studies using cultured ECs demonstrated that exposure to high glucose and high fat (HGHF) reduced GLS1 expression and suppressed glutaminolysis, impairing EC proliferation and tube formation. These adverse effects were mitigated by treatment with SalB or supplementation with α-KG plus nonessential amino acids (NEAAs). Among diabetic mice subjected to myocardial ischemia/reperfusion (MI/R), SalB administration or α-KG supplementation promoted myocardial revascularization and improved cardiac dysfunction. Notably, endothelial-specific GLS1 deletion in mice blocked the beneficial effects afforded by SalB but not those afforded by α-KG. Furthermore, SalB administration accelerated angiogenesis and cutaneous wound healing in diabetic mice, and these influences were removed by pharmacological inhibition of GLS1 using bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl) ethyl sulfide (BPTES) or genetic deletion of endothelial GLS1. These findings indicate that defective endothelial glutaminolysis contributes to impaired angiogenesis and poor ischemic tissue repair in diabetes. Improving endothelial glutaminolysis by treatment with SalB or metabolic supplementation with α-KG promotes angiogenesis and ischemic tissue repair in diabetic mice, emphasizing the possibility of GLS1 as a treatment target.

Background: Ischemic heart disease is a leading cause of mortality and disability worldwide among cardiovascular conditions. Myocardial ischemia–reperfusion injury (MIRI) occurs following percutaneous coronary intervention, during which neutrophils generate neutrophil extracellular traps (NETs) in response to injury. This study aims to elucidate the mechanisms underlying NET activation and its impact on MIRI. Methods: Sham and MIRI rat models were established. Various techniques, including enzyme-linked immunosorbent assay, hematoxylin and eosin staining, Masson staining, and transmission electron microscopy, were used to assess endothelial cell injury and myocardial tissue inflammation. Immunofluorescence was employed to evaluate NET activation in tissues, peripheral blood neutrophils, and protein colocalization. MitoTracker and ER-Tracker staining were conducted to assess the formation of mitochondria-associated membranes (MAMs). Extracted NETs were applied to conduct microvascular endothelial cell tube formation assay and flow cytometry. RNA-sequencing and immunoprecipitation–mass spectrometry were applied to determine the key regulators. Flow cytometry and Western blot were used to assess Ca²⁺ and mitophagy levels in neutrophils. Deoxyribonuclease I, NET inhibitor, was injected into MIRI rats to evaluate the in vivo effects of NET modulation on MIRI severity. Results: MIRI was often accompanied by cardiac microvascular endothelial cell (CMEC) injury and inflammation. Lactate mediated H3K18 lactylation at the MICU3 promoter in neutrophils, enhancing its transcription and leading to elevated MICU3 levels. Besides, lactate also promoted the interaction between MICU3 and AASR1, stabilizing MICU3 through lactylation. Up-regulated MICU3 interacted with VDAC1, facilitating MAM formation, excessive Ca²⁺ uptake, mitochondrial dysfunction, mitophagy activation, and NET activation. Elevated NET level exacerbated CMEC dysfunction, further aggravating MIRI. Conclusion: Lactate-driven MICU3 transcriptional activation and stabilization facilitates NET formation, contributing to MIRI development.

Isovaleryl-CoA (coenzyme A) dehydrogenase (IVD) plays a pivotal role in the catabolism of leucine, converting isovaleryl-CoA to 3-methylcrotonyl-CoA. Dysfunction of IVD is linked to isovaleric acidemia (IVA), a rare metabolic disorder characterized by the accumulation of toxic metabolites. In this study, we present the cryo-electron microscopy structures of human IVD, resolved both in its apo form and in complex with its substrates, isovaleryl-CoA and butyryl-CoA. Our findings reveal a tetrameric architecture with distinct substrate-binding pockets that facilitate the enzyme's preference for short branched-chain acyl-CoAs. Key residues involved in FAD binding and substrate interaction were identified, elucidating the catalytic mechanism of IVD. Additionally, we investigated the impact of various disease-associated hotspot mutations derived from different regions, demonstrating their effects on enzyme stability and activity. Notably, mutations such as A314V, S281G/F382V, and E411K resulted in substantial loss of function, while others exhibited milder effects, which is consistent with our structural analyses. These insights enhance our understanding of IVD's enzymatic properties and provide a foundation for developing targeted therapies for IVA.

Hydrogel microparticles that can effectively deliver mesenchymal stem cells (MSCs) are expected to accelerate wound repair progress. Attempts in the area are focusing on improving the functions of the microparticles and MSCs to promote the therapeutic effect. Here, inspired by the topological morphology of ice branches, we propose novel freeze-derived anisotropic porous microparticles for hepatocyte growth factor (HGF)-overexpressing MSCs (MSCs^HGF) loading and wound healing. The microparticles were fabricated by introducing microfluidic methacrylated gelatin pre-gel droplets into low-temperature silicone oil, followed by photo-cross-linking and freeze-drying processes. Drawing an advantage from the biocompatible chemical composition and the structured pore arrangement of the microparticles, MSCs^HGF can be efficiently encapsulated and released, maintaining continuous HGF secretion to enhance cell migration and support vascular regeneration. Leveraging these characteristics, we have shown that MSCs^HGF-loaded porous microparticles could substantially promote angiogenesis, polarize macrophages toward the M2 phenotype, and reduce inflammation during the wound repair process, consequently enhancing skin wound repair efficiency. Thus, we believe that our MSCs^HGF-integrated freeze-derived anisotropic porous microparticles hold promising prospects for clinical wound-healing applications.