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Infection, as a common postoperative complication of orthopedic surgery, is the main reason leading to implant failure. Silver nanoparticles (AgNPs) are considered as a promising antibacterial agent and always used to modify orthopedic implants to prevent infection. To optimize the implants in a reasonable manner, it is critical for us to know the specific antibacterial mechanism, which is still unclear. In this review, we analyzed the potential antibacterial mechanisms of AgNPs, and the influences of AgNPs on osteogenic-related cells, including cellular adhesion, proliferation, and differentiation, were also discussed. In addition, methods to enhance biocompatibility of AgNPs as well as advanced implants modifications technologies were also summarized.

Prosthesis-associated infections are one of the main causes of implant failure; thus it is important to enhance the long-term antibacterial ability of orthopedic implants. Titanium dioxide nanotubes (TNTs) are biomaterials with good physicochemical properties and biocompatibility. Owing to their inherent antibacterial and drug-loading ability, the antibacterial application of TNTs has received increasing attention. In this review, the process of TNT anodizing fabrication is summarized. Also, the mechanism and the influencing factors of the antibacterial property of bare TNTs are explored. Furthermore, different antibacterial strategies for carrying drugs, as well as modifications to prolong the antibacterial effect and reduce drug-related toxicity are discussed. In addition, antibacterial systems based on TNTs that can automatically respond to infection are introduced. Finally, the currently faced problems are reviewed and potential solutions are proposed. This review provides new insight on TNT fabrication and summarizes the most advanced antibacterial strategies involving TNTs for the enhancement of long-term antibacterial ability and reduction of toxicity. Keywords: antibacterial property, drug delivery, titanium dioxide nanotube, orthopedic implant, surface modification

The development of unstable carotid atherosclerotic plaques is associated with the induction of neutrophil extracellular traps (NETs) via the activation of diverse inflammatory mediators in the circulating bloodstream. However, the underlying mechanisms through which NETs influence the microenvironment of atherosclerotic plaques and contribute to the development of unstable carotid plaques remain largely elusive. The objective of this study was to elucidate the role of myeloid differentiation protein 1 (MD-1, LY86 )-induced NETs underlying the crosstalk between unstable plaque formation and the plaque microenvironment. We employed bioinformatics analysis to identify key genes associated with carotid-unstable plaque, followed by comprehensive validation using various experimental approaches on tissue specimens and plasma samples classified based on pathological characteristics. Patients with carotid-unstable plaques exhibited elevated plasma concentrations of MD-1 ( LY86 ), while patients with stable plaques demonstrated comparatively lower levels. Furthermore, soluble MD-1 was found to induce the formation of NETs through activation of Toll-like receptor signaling pathway. The proliferative and immature vascularization effects of NETs on endothelial cells, as well as their inhibitory impact on cell migration, are directly correlated with the concentration of NETs. Additionally, NETs were found to activate the NF-κB signaling pathway, thereby upregulating ICAM1, VCAM1, MMP14, VEGFA, and IL6 expression in both Human umbilical vein endothelial cells (HUVECs) and HAECs. Subsequently, a significant increase in intraplaque neovascularization by NETs results in poor carotid plaque stability, and NETs in turn stimulate macrophages to produce more MD-1, generating a harmful positive feedback loop. Our findings suggest that soluble MD-1 in the bloodstream triggers the production of NETs through activation of the Toll-like receptor signaling pathway and further indicate NETs mediate a crosstalk between the microenvironment of the carotid plaque and the neovascularization of the intraplaque region. Inhibiting NETs formation or MD-1 secretion may represent a promising strategy to effectively suppress the development of unstable carotid plaques. NETs influence carotid plaque microenvironment and neovascularization Atherosclerosis, a disease where arteries get blocked with fat, is a main cause of heart disease and stroke. Predicting which atherosclerotic plaques will cause heart attacks is hard. Researchers analyzed gene data from unstable and stable carotid plaques, focusing on neutrophils and a protein called MD-1. The study involved 30 patients and 10 healthy volunteers to understand how MD-1 and neutrophils contribute to plaque instability. The main finding is that MD-1 could be a biomarker for unstable plaques, offering a new target for therapies to prevent major heart events. This progress in understanding the molecular mechanisms behind plaque instability could lead to better prevention strategies for heart disease. Future research may focus on developing treatments that target MD-1 and neutrophils to stabilize plaques and reduce the risk of heart attacks. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

The exogenous excitation requirement and electron-hole recombination are the key elements limiting the application of catalytic therapies. Here a tumor microenvironment (TME)-specific self-triggered thermoelectric nanoheterojunction (Bi 0.5 Sb 1.5 Te 3 /CaO 2 nanosheets, BST/CaO 2 NSs) with self-built-in electric field facilitated charge separation is fabricated. Upon exposure to TME, the CaO 2 coating undergoes rapid hydrolysis, releasing Ca 2+ , H 2 O 2 , and heat. The resulting temperature difference on the BST NSs initiates a thermoelectric effect, driving reactive oxygen species production. H 2 O 2 not only serves as a substrate supplement for ROS generation but also dysregulates Ca 2+ channels, preventing Ca 2+ efflux. This further exacerbates calcium overload-mediated therapy. Additionally, Ca 2+ promotes DC maturation and tumor antigen presentation, facilitating immunotherapy. It is worth noting that the CaO 2 NP coating hydrolyzes very slowly in normal cells, releasing Ca 2+ and O 2 without causing any adverse effects. Tumor-specific self-triggered thermoelectric nanoheterojunction combined catalytic therapy, ion interference therapy, and immunotherapy exhibit excellent antitumor performance in female mice. The exogenous excitation requirement and electron-hole pair recombination are the key factors limiting the application of catalytic therapies. Here, the authors address these limitations by designing a tumor microenvironment-specific self-triggered thermoelectric nanoheterojunction with a self-built-in electric field that facilitates charge separation for cancer treatment.

Bone regeneration remains a great clinical challenge. Two-dimensional materials, especially graphene and its derivative graphene oxide, have been widely used for bone regeneration. Since its discovery in 2014, black phosphorus (BP) nanomaterials including BP nanosheets and BP quantum dots have attracted considerable scientific attention and are considered as prospective graphene substitutes. BP nanomaterials exhibit numerous advantages such as excellent optical and mechanical properties, electrical conductivity, excellent biocompatibility, and good biodegradation, all of which make them particularly attractive in biomedicine. In this review, we comprehensively summarize recent advances of BP-based nanomaterials in bone regeneration. The advantages are reviewed, the different synthesis methods of BP are summarized, and the applications to promote bone regeneration are highlighted. Finally, the existing challenges and perspectives of BP in bone regeneration are briefly discussed.

Thermoelectric therapy has been emerging as a promising and versatile strategy for targeting malignant tumors treatment. However, the lack of effective time-space controlled triggering of thermoelectric effect in vivo limits the application of thermoelectric therapy. Here a magnetically triggered thermoelectric heterojunction (CuFe 2 O 4 /SrTiO 3 , CFO/STO) for synergistic thermoelectric/chemodynamic/immuno-therapy is developed. The efficient magnetothermal nanoagent (CFO) is synthesized using the hydrothermal method, and thermoelectric nanomaterials (STO) are grown on its surface to create the heterojunction. To enhance oral delivery efficiency, a fusion membrane (M) of Staphylococcus aureus and macrophage cell membranes are coated the CFO/STO heterojunction, enabling effective targeting of orthotopic colorectal cancer. Once the CFO/STO@M reaches the tumor region, in vitro alternating magnetic field (AMF) stimulation activates the catalytic treatment through a magnetic-thermo-electric energy cascade conversion effect. Additionally, the immunogenic death of tumor cells, down-regulating vascular endothelial growth factor and heat shock protein HSP70, increasing expression of endothelial cell adhesion molecule (ICAM-1/VCAM-1), and M1 polarization of macrophages contribute to tumor immunotherapy. Overall, the magnetically triggered thermoelectric heterojunction based on CFO/STO@M shows remarkable antitumor capability in female mice, offering a promising approach to broaden both the scope of application and the effectiveness of catalytic therapy. Thermoelectric therapy is promising for cancer treatment, but is limited by the lack of effective spatiotemporal control of thermoelectric effect in vivo. Here, the authors report a spatiotemporally controllable nanodevice that allows a precise and efficient magnetic-thermo-electric cascade energy conversion in vivo to mediate the thermoelectric/chemodynamic/immunotherapy of colorectal cancer.

The traditional Chinese medicine has been reported to be valid for cardiovascular and cerebrovascular diseases. However, its active components for the protection of ischemic stroke are not clear. We aimed to explore the active components of against ischemic stroke as well as its potential mechanisms. We investigated the brain protective effects of extracts from , total glycosides (TGs), polysaccharides (PSs), and oligosaccharides (OSs) in a rat model of middle cerebral artery occlusion-reperfusion (MCAO/R). 2, 3, 5-Triphenyltetrazolium chloride (TTC) staining was used to assess the cerebral infarction volume, and Evans blue assay was adopted to assess the blood-brain barrier (BBB) permeability. Then, the expressions CD31, α-SMA, PDGFRβ, SYN, PSD95, MAP-2, ZO-1, claudin-5, occludin, Keap-1, and Nrf-2 were analyzed using western blotting or immunofluorescence, and the activities MDA, SOD, CAT, and GSH-Px were analyzed using kits. TGs treatment remarkably decreased neurological deficit scores and infarction volumes, promoted angiogenesis and neural remodeling, and effectively maintained blood-brain-barrier integrity compared with the model group. Furthermore, TGs significantly decreased MDA levels and increased antioxidant activities (SOD, CAT, and GSH-Px) in brains. Meanwhile, TGs remarkably downregulated Keap-1 expression and facilitated Nrf-2 nuclear translocation. On the contrary, no protective effects were observed for PSs and OSs groups. TGs are the main active components of against MCAO/R-induced cerebral injury, and protection is mainly the Nrf-2/Keap-1 pathway.

Prosthesis-associated infections and aseptic loosening are major causes of implant failure. There is an urgent need to improve the antibacterial ability and osseointegration of orthopedic implants. Zinc oxide nanoparticles (ZnO-NPs) are a common type of zinc-containing metal oxide nanoparticles that have been widely studied in many fields, such as food packaging, pollution treatment, and biomedicine. The ZnO-NPs have low toxicity and good biological functions, as well as antibacterial, anticancer, and osteogenic capabilities. Furthermore, ZnO-NPs can be easily obtained through various methods. Among them, green preparation methods can improve the bioactivity of ZnO-NPs and strengthen their potential application in the biological field. This review discusses the antibacterial abilities of ZnO-NPs, including mechanisms and influencing factors. The toxicity and shortcomings of anticancer applications are summarized. Furthermore, osteogenic mechanisms and synergy with other materials are introduced. Green preparation methods are also briefly reviewed.

The precise targeted delivery of therapeutic agents to deep regions of the brain is crucial for the effective treatment of various neurological diseases. However, achieving this goal is challenging due to the presence of the blood‒brain barrier (BBB) and the complex anatomy of the brain. Here, a biomimetic self‐propelled nanomotor with cascade targeting capacity is developed for the treatment of neurological inflammatory diseases. The self‐propelled nanomotors are designed with biomimetic asymmetric structures with a mesoporous SiO2 head and multiple MnO2 tentacles. Macrophage membrane biomimetic modification endows nanomotors with inflammatory targeting and BBB penetration abilities The MnO2 agents catalyze the degradation of H2O2 into O2, not only by reducing brain inflammation but also by providing the driving force for deep brain penetration. Additionally, the mesoporous SiO2 head is loaded with curcumin, which actively regulates macrophage polarization from the M1 to the M2 phenotype. All in vitro cell, organoid model, and in vivo animal experiments confirmed the effectiveness of the biomimetic self‐propelled nanomotors in precise targeting, deep brain penetration, anti‐inflammatory, and nervous system function maintenance. Therefore, this study introduces a platform of biomimetic self‐propelled nanomotors with inflammation targeting ability and active deep penetration for the treatment of neurological inflammation diseases. A biomimetic drug‐loaded self‐propelled MnO2‐Au‐mSiO2@Cur nanomotor is developed with an asymmetric octopus‐type antenna structure that can target brain inflammation across the blood–brain barrier, realize deep penetration during inflammation, enhance the anti‐inflammatory effect and promote the polarization of microglia from the M1 to the M2 phenotype.

Glioblastoma multiform (GBM) is the most common malignant primary brain tumor in adults. Radiotherapy plus concomitant and adjuvant TMZ chemotherapy is the current standard of care for patients with GBM. Matrix metalloproteinases (MMPs), a family of zinc-dependent endopeptidases, are key modulators of tumor invasion and metastasis due to their ECM degradation capacity. The aim of the present study was to identify the most informative MMP member in terms of prognostic and predictive ability for patients with primary GBM. The mRNA expression profiles of all MMP genes were obtained from the Chinese Glioma Genome Atlas (CGGA), the Repository for Molecular Brain Neoplasia Data (REMBRANDT) and the GSE16011 dataset. MGMT methylation status was also examined by pyrosequencing. The correlation of MMP9 expression with tumor progression was explored in glioma specimens of all grades. Kaplan-Meier analysis and Cox proportional hazards regression models were used to investigate the association of MMP9 expression with survival and response to temozolomide. MMP9 was the only significant prognostic factor in three datasets for primary glioblastoma patients. Our results indicated that MMP9 expression is correlated with glioma grade (p<0.0001). Additionally, low expression of MMP9 was correlated with better survival outcome (OS: p = 0.0012 and PFS: p = 0.0066), and MMP9 was an independent prognostic factor in primary GBM (OS: p = 0.027 and PFS: p = 0.032). Additionally, the GBM patients with low MMP9 expression benefited from temozolomide (TMZ) chemotherapy regardless of the MGMT methylation status. Patients with primary GBMs with low MMP9 expression may have longer survival and may benefit from temozolomide chemotherapy.