大连医科大学

The chemical composition of Mg-based welding wires plays a decisive role in determining the microstructure and mechanical properties of wire arc additive-manufactured (WAAM) components. Herein, an innovative CO2 -induced wire fabrication strategy was proposed to achieve the in-situ synthesis of T2-Al2 MgC2 phase within the AZ91D Mg-based alloy. The fine T2-Al2 MgC2 phase was synthesized through the insitu reaction between CO2 and AZ91D Mg-based alloy, after which Mg-based welding wires were prepared through hot extrusion and used for WAAM of thin-walled structures. Microstructural evolution, mechanical properties, and the refinement mechanism of the T2-Al2 MgC2 phase during the WAAM process were investigated. The as-built WAAM components were characterized by a predominantly equiaxed microstructure and an average grain size of approximately 14.7 & micro;m. Grain refinement was attributed to the orientation relationship (0 0 01) T2 -Al2 Mg C2 //(0 0 01)alpha- Mg , which enabled T2-Al2 MgC2 to act as effective heterogeneous nuclei for alpha-Mg. MgO nanoparticles were synchronously formed to impede grain-boundary migration and suppress the coarsening of the B-Mg17 Al12 . The horizontal direction of the components exhibited an ultimate tensile strength of 320.6 MPa and an elongation of 9.2 %, while the vertical direction showed corresponding values of 269.2 MPa and 6.8 %, respectively. Furthermore, the components exhibited pronounced quasi-cleavage fracture characteristics. This work provides a new pathway for developing high-performance Mg-based welding wires suitable for the WAAM process. (c) 2026 Published by Elsevier Ltd on behalf of The editorial office of Journal of Materials Science & Technology.

Cognitive impairment (CI), spanning mild memory issues to severe dementia, impacts over 55 million people worldwide and have a significant effect that strains health, economy, and caregiving. Surprisingly, it occurs at any age. The glial cell ecosystem, particularly astrocyte-microglia crosstalk, is pivotal for brain homeostasis and cognitive function across the lifespan. Intriguingly, in recent discoveries, dysregulation of ecosystem contributes to neurodevelopmental disorders (NDDs), adult cognitive decline, and neurodegenerative diseases like Alzheimer’s disease (AD), and astrocyte-derived interleukin-3 (IL-3), acting via the IL-3/CD123-related signals, may act as a key regulatory mediator of microglial function. Over the past few decades, extensive researches have been devoted to investigating aging-related regulatory factors with the aim of deciphering the “code” underlying cognitive developmental abnormalities, premature cognitive decline, and neurodegeneration. Astrocyte-microglia crosstalk governs age-dependent glial turnover via senescence-sensitive IL-3. Under pathological conditions, perturbed turnover’s association with age-stratified CI and its regulators is poorly understood. This review integrates current evidence on glial crosstalk, cellular senescence, and repopulation to elucidate age-specific CI driven by dysregulated glial turnover, while identifying key biomarkers that can predict aging processes. Looking ahead, therapeutic strategies targeting the IL-3/CD123-related signals regulating glial crosstalk hold promise for advancing interventions in immune-mediated CI across the lifespan.

Regulatory T cells (Tregs) play a pivotal role in promoting immune tolerance during organ transplantations, prompting a critical shift from conventional immunosuppression to active immune regulation in therapeutic paradigms. This review synthesizes recent advances in Treg-based therapies for liver, kidney, and heart transplantations, highlighting their capacity to modulate immune responses and prevent allograft rejection, with preclinical studies and early-phase clinical trials demonstrating the safety and feasibility of autologous polyclonal Treg therapy for enhancing graft survival. Despite these promising results, widespread clinical application faces challenges including complex manufacturing, cellular stability in inflammatory environments, and lack of standardized potency assays. Therefore, this review critically assesses emerging strategies, such as antigen-specific chimeric antigen receptor (CAR)-Tregs for precise immune targeting and gene-edited, “off-the-shelf” allogeneic Tregs, aimed at improving scalability and accessibility. By providing a comprehensive overview of current progress and remaining obstacles, this review guides future research and supports the clinical translation of Treg-based therapies to ultimately improve long-term outcomes for transplant recipients.

Diabetic foot ulcers are serious skin wounds that affect many people with diabetes, often leading to severe infections or even the loss of a limb. This paper explores how artificial intelligence —computer programs that can learn from data—is changing the way doctors find and treat these wounds. By reviewing 68 recent studies, we looked at how these smart technologies analyze different types of medical images to help patients. Our findings show that AI can help doctors identify health risks much earlier than traditional methods. These computer tools are also excellent at measuring how a wound is healing and predicting which treatments will work best for each individual. Because AI can spot tiny patterns in images that the human eye might miss, it makes medical care more precise and consistent. In conclusion, using AI to manage diabetic foot wounds offers a powerful way to improve patient health. By helping doctors make better, data-driven decisions, this technology can lead to faster healing and reduce the risk of serious complications for people living with diabetes.

Atherosclerosis is a chronic inflammatory disease influenced by host–microbiota interactions beyond traditional risk factors. Microbial communities in the oral cavity, gut, and blood contribute to vascular dysfunction through metabolic and immune mechanisms, yet an integrated perspective across these compartments remains lacking. This narrative review synthesizes current evidence on the distinct and interconnected roles of oral, gut, and blood microbiotas in atherosclerosis pathogenesis. We critically evaluate key microbial metabolites, trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acids, and their mechanisms of host metabolic and immune modulation. We also examine cross-compartment interactions, emerging multi-omics approaches, and the translational potential of microbiota-targeted interventions. Oral pathogens promote systemic inflammation and endothelial activation. Gut-derived metabolites such as TMAO exacerbate foam cell formation and impair reverse cholesterol transport, whereas SCFAs exert protective effects via immune modulation and gut barrier maintenance. Emerging evidence suggests that blood microbial components contribute to vascular inflammation, though methodological challenges remain. Multi-omics integration (metagenomics, metabolomics, host genomics) reveals interconnected metabolic networks linking microbial activity to atherosclerosis. Microbiota-targeted strategies, including dietary modulation, TMA lyase inhibitors, and probiotics, show promise for risk stratification and therapeutic intervention. The human microbiota regulates atherosclerosis through immunometabolic metabolites, offering promising biomarkers and therapeutic targets. However, clinical translation requires addressing interindividual variability, establishing causality, and standardizing methodologies. This review provides an integrated framework for leveraging microbiota–host interactions in precision cardiovascular medicine. Oral, gut, and blood microbiotas form an interconnected ecosystem that collectively contributes to atherosclerosis pathogenesis through niche-specific microbial communities and bidirectional cross-compartment signaling. Microbial metabolites, including TMAO, SCFAs, and secondary bile acids, serve as critical mediators linking microbial activity to host lipid metabolism, immune regulation, and endothelial dysfunction. Multi-omics integration (metagenomics, metabolomics, and host genomics) enables mechanistic insights into microbiota–host interactions and facilitates the discovery of composite biomarkers for improved cardiovascular risk stratification. Microbiota-targeted interventions, such as dietary modulation, TMA lyase inhibitors, probiotics, and prebiotics, offer promising therapeutic strategies for restoring metabolic homeostasis and mitigating atherosclerosis progression. Translating microbiota research into clinical practice requires addressing key challenges, including establishing causality, standardizing methodologies across studies, and accounting for interindividual variability to enable personalized cardiovascular care.