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Clear elucidation of the connection between chemical structure and biological action mechanisms is the key issue preventing the successful development of nanomedicines. Herein, employing essential trace element selenium (Se) as an example, we fabricate organic-inorganic covalent Se hybrid by anchoring Se atom to polyethylene glycol chain during carbonization to form organic Se-C and inorganic Se-Se bonds in one system to integrate the advantages of both species. The weak covalent Se-Se bond breaks down in response to redox stimuli, thus releases organic Se with stronger electron transfer ability to scavenge free radicals, and forms highly active inorganic Se, which further releases free Se atom to trigger selenoprotein synthesis and activation, ultimately reverses reperfusion injury in male-mice ischemic stroke, and improves neurological restoration. This work provides a unique Se atom reprogramming strategy to design highly bioactive hybrid Se species with clear chemical nature and action mechanisms. Developing potent and biocompatible antioxidative nanomedicines is beneficial for reversing ischemic reperfusion injury, but hindered by a lack of understanding of biological action mechanisms. Here, the authors report bioactive organic-inorganic covalent selenium hybrid nanoparticles, and elucidate their mechanisms of action in suppressing reperfusion-induced injury of ischemic stroke.

Selenium (Se) is a crucial element in selenoproteins, key biomolecules for physiological function in vivo. As a selenium‐rich organ, the central nervous system can express all 25 kinds of selenoproteins, which protect neurons by reducing oxidative stress and inflammatory response. However, decreased Se levels are prevalent in a variety of neurological disorders, which is not conducive to the treatment and prognosis of patients. Thus, the biological study of Se has emerged as a focal point in investigating the pivotal role of trace elements in neuroprotection. This paper presents a comprehensive review of the pathogenic mechanism of neurological diseases, the protective mechanism of Se, and the neurological protective function of selenoproteins. Additionally, the application of Se as a neuroprotective agent in neurological disorder therapy, including ischemic stroke, Alzheimer's, Parkinson's, and other neurological diseases, is summarized. The present review aims to offer novel insights and methodologies for the prevention and treatment of neurological disorders with trace Se, providing a scientific basis for the development of innovative Se‐based neuroprotectants to promote their clinical application against neurological diseases. Selenium (Se) is a crucial element in selenoproteins, key biomolecules for physiological function in vivo. Central nervous system can express all 25 kinds of selenoproteins, which protect neurons by reducing oxidative stress and inflammatory response. Neuroprotection is being investigated through the biological study of Se. In this review, novel insights are presented for the prevention and treatment of neurological disorders with trace Se, providing scientific evidence for the development of innovative Se‐based neuroprotectants.

Exploring efficient and low‐toxicity radiosensitizers to break through the bottleneck of radiation tolerance, immunosuppression and poor prognosis remains one of the critical developmental challenges in radiotherapy. Nanoheterojunctions, due to their unique physicochemical properties, have demonstrated excellent radiosensitization effects in radiation energy deposition and in lifting tumor radiotherapy inhibition. Herein, they doped selenium (Se) into prussian blue (PB) to construct a nano‐heterojunction (Se@PB), which could promote the increase of Fe2+/Fe3+ ratio and conversion of Se to a high valence state with Se introduction. The Fe2+‐Se‐Fe3+ electron transfer chain accelerates the rate of electron transfer on the surface of the nanoparticles, which in turn endows it with efficient X‐ray energy transfer and electron transport capability, and enhances radiotherapy physical sensitivity. Furthermore, Se@PB induces glutathione (GSH) depletion and Fe2+ accumulation through pro‐Fenton reaction, thereby disturbs the redox balance in tumor cells and enhances biochemical sensitivity of radiotherapy. As an excellent radiosensitizer, Se@PB effectively enhances X‐ray induced mitochondrial dysfunction and DNA damage, thereby promotes cell apoptosis and synergistic cervical cancer radiotherapy. This study elucidates the radiosensitization mechanism of Se‐doped nanoheterojunction from the perspective of the electron transfer chain and biochemistry reaction, which provides an efficient and low‐toxic strategy in radiotherapy. For the development of highly effective and low‐toxic radiosensitizers, herein, the study develops a nano‐heterojunction (Se@PB) containing Fe2+‐Se‐Fe3+ electron transfer chains, which is inspired by the high safety of the trace elements selenium (Se) and Prussian blue (PB), and the unique activities of Se in strong electron contribution and its redox properties. The Se@PB nano‐heterojunction containing Fe2+‐Se‐Fe3+ chain exerts physical and biochemical radiosensitization by accelerating electron transfer and redox dyshomeostasis.

Surface defect detection on steel components is crucial for quality control in polysilicon production. However, this task remains challenging due to tiny defect sizes, irregular geometries, complex backgrounds, and low contrast. To address these issues, we propose MSEOD-DDFusionNet (Multi-Scale and Effective Object-Detection Diffusion Fusion Network), a novel multi-scale diffusion-enhanced attention network. The network integrates four specialized modules: MTECAAttention (Multi-Scale Texture Enhancement Channel-Aware Attention) for lossless multi-scale feature fusion, ODConv (Omni-Dimensional Dynamic Convolution) for dynamic adaptation to irregular geometries, LMDP (Local Multi-Scale Discriminative Perception) for selective noise suppression and micro-defect amplification, and DDFusion (Diffusion-Driven Feature Fusion) for scene-aware noise modeling. Pruning further reduces computational complexity while improving accuracy. Extensive experiments on the specialized DDTE dataset and public benchmarks demonstrate state-of-the-art performance. Our model achieves 82.6% and 61.6% on DDTE, while maintaining a high inference speed of 193.5 FPS with only 8.46M parameters. It also shows excellent generalization across NEU-DET, GC10-DET, and cross-domain tasks, providing an efficient and accurate solution for industrial defect inspection.

The systemic inflammatory response index (SIRI), a novel inflammation maker, has proven to be associated with prognostic outcomes in various diseases. However, few studies have been conducted assessing how SIRI may influence outcomes of patients on peritoneal dialysis (PD). Herein, we assessed the predictive value of SIRI on mortality all-cause mortality, including cardiovascular disease (CVD) in PD patients. A total of 646 PD patients were enrolled in this study. PD patients received regular PD treatments at the Zhujiang Hospital from 1 January 2011 to 31 December 2018. SIRI values could be computed as follows: neutrophil count × monocyte count/lymphocyte count. Patients were divided into two groups according to the median level of SIRI. Cox regression analysis and Kaplan-Meier methods were applied to analyze the relationship between SIRI and mortality outcomes in PD patients. During the median 31-month follow-up period, 97 (15.0%) PD patients died from all-causes, and 47 (49.0%) died of CVD. Kaplan-Meier analyses revealed that a high SIRI corresponded to the high mortality of all-cause deaths, including CVD (both p < 0.001) in patients on PD. After adjusting for potential confounders, the higher SIRI level was significantly associated with an increased all-cause mortality (HR: 2.007, 95% CI: 1.304-3.088, p = 0.002) and cardiovascular mortality (HR: 2.847, 95% CI: 1.445-5.608, p = 0.002). SIRI was a promising predictor of mortality in PD patients, with a higher SIRI corresponding to increased risk of mortality.

Low persistence, metabolic dysfunction in microenvironment, and tumor‐derived immunosuppression of Natural killer (NK) cells in patients are greatly limited the successful clinical application of NK cell‐based cancer immunotherapy. Interestingly, herein that human serum albumin‐encapsulated black phosphorus quantum dots (BPQDs@HSA) can effectively augment antitumor efficacy of clinical patients‐derived NK cell immunotherapy is found. As the donor of phosphate group, BPQDs@HSA binds with the protein of phosphatidylinositol 4‐phosphate 5‐kinase type‐1 gamma (PIP5K1A) and activates the downstream PI3K‐Akt and mTOR signaling pathways to reprogram cell metabolism of glycolysis and further promote the oxidative phosphorylation, sequentially maintains the cell viability and immunity of NK cells. And multiomics analysis is therefore conducted to reveal the underlying immunoregulation mechanisms, and that BPQDs@HSA can interact with the Toll‐like receptor (TLR) on the NK cell surface and increase the expression level of mTOR, and thus activate downstream NF‐κB signalling pathways to regulate cytokine secretion and enhance immune tumoricidal is found. BPQDs@HSA can also enhance immune surveillance, relieve immune suppression, and inhibit tumor immune escape. Collectively, this study not only demonstrates a successful strategy for nanomedicine‐potentiated immune‐cancer therapy, but also sheds light on the understanding of interface between nanomedicine and immune cells activation. Herein a successful strategy for cancer treatment by nanomedicine‐potentiated NK cell immunotherapy is presented. BPQDs@HSA activates PI3K‐Akt‐mTOR signaling pathways to reprogram cell metabolism of glycolysis and further promote the oxidative phosphorylation, sequentially maintains the cell viability and immunity of NK cells. BPQDs@HSA can also enhance immune tumoricidal and immune surveillance, relieve immune suppression, and inhibit tumor immune escape.

Nanomaterials-based drug delivery systems display potent applications in cancer therapy, owing to the enhanced permeability and retention effect and diversified chemical modification. In this study, we have tailored and synthesized different sized mesoporous silica nanoparticles (MSNs) through reactant control to investigate the relevancy of nanoparticle size toward anticancer efficacy and suppressing cancer multidrug resistance. The different sized MSNs loaded with anticancer ruthenium complex (RuPOP) and conjugated with folate acid (FA) to enhance the selectivity between cancer and normal cells. The nanosystem (Ru@MSNs) can specifically recognize HepG2 hepatocellular carcinoma cells, thus enhance accumulation and selective cellular uptake. The smaller sized (20 nm) Ru@MSNs exhibit higher anticancer activity against HepG2 cells, while the larger sized (80 nm) Ru@MSNs exhibit higher inhibitory effect against DOX-resistant hepatocellular carcinoma cells (R-HepG2). Moreover, Ru@MSNs induced ROS overproduction in cancer cells, leading to DNA damage and p53 phosphorylation, consequently promoting cancer cells apoptosis. Ru@MSNs (80 nm) also inhibited ABCB1 and ABCG2 expression in R-HepG2 cells to prevent drug efflux, thus overcome multidrug resistance. Ru@MSNs also inhibited tumor growth in vivo without obvious toxicity in major organs of tumor-bearing nude mice. Taken together, these results verify the size effects of MSNs nanosystem for precise cancer therapy.

Background Cancer cell membrane-camouflaged nanotechnology for metal complex can enhance its biocompatibility and extend the effective circulation time in body. The ruthenium polypyridyl complex (RuPOP) has extensive antitumor activity, but it still has disadvantages such as poor biocompatibility, lack of targeting, and being easily metabolized by the organism. Cancer cell membranes retain a large number of surface antigens and tumor adhesion molecules CD47, which can be used to camouflage the metal complex and give it tumor homing ability and high biocompatibility. Results Therefore, this study provides an electrostatic adsorption method, which uses the electrostatic interaction of positive and negative charges between RuPOP and cell membranes to construct a cancer cell membrane-camouflaged nano-platform (RuPOP@CM). Interestingly, RuPOP@CM maintains the expression of surface antigens and tumor adhesion molecules, which can inhibit the phagocytosis of macrophage, reduce the clearance rate of RuPOP, and increase effective circulation time, thus enhancing the accumulation in tumor sites. Besides, RuPOP@CM can enhance the activity of cellular immune response and promote the production of inflammatory cytokines including TNF-α, IL-12 and IL-6, which is of great significance in treatment of tumor. On the other hand, RuPOP@MCM can produce intracellular ROS overproduction, thereby accelerating the apoptosis and cell cycle arrest of tumor cells to play an excellent antitumor effect in vitro and in vivo. Conclusion In brief, engineering cancer cell membrane-camouflaged metal complex is a potential strategy to improve its biocompatibility, biological safety and antitumor effects.

Oilseed rape is sensitive to soil phosphorus deficiencies. In contrast, white lupin is widely used as a model plant because it has efficient phosphorus utilization. Therefore, soil fertility and microbial composition in the rhizospheres of oilseed rapes and root exudate metabolites were compared under monocropping and intercropping systems. The main purpose was to explore whether the phosphorus absorption of rapeseed can be promoted by intercropping with white lupine. In comparison with oilseed rape monoculture (RR), the results showed that the contents of soil-available phosphorus, microbial biomass and phosphorus in the rhizospheres of oilseed rapes in the intercropping system (RL) were all higher than those of RR. Meanwhile, in comparison with RR, not only phosphorus-solubilizing bacteria, such as Streptomyces, Actinomadura and Bacillus, but also phosphorus-solubilizing fungi, such as Chaetomium, Aspergillus, Penicillium, were enriched in the rhizospheres of the oilseed rape under the RL system. Moreover, more abundant soil bacterial functions, organic acids and metabolites were also detected in root exudates of the oilseed rapes under the RL system. All of the above results suggest that soil phosphorus availability in the rhizospheres of oilseed rape could be improved by intercropping with white lupin. Additionally, soil phosphorus-solubilizing microorganisms, that are enriched in the rhizospheres of oilseed rapes under RL systems, have an important function in the improvement of phosphorus absorption of rapeseed by intercropping with white lupin.

Selenium nanoparticle (SeNP)-based nanotherapeutics have become an emerging cancer therapy, while effective drug delivery remains a technical hurdle. A theranostic approach, through which imaging companions are integrated with SeNPs, will allow image-guided drug delivery and, therefore, is highly desirable. Traditional methods require the chemical conjugation of imaging agents to the surface of nanoparticles, which may impede the later clinical translation. In this study, we developed a label-free strategy in which lentinan-functionalized SeNPs (LNT-SeNPs) are detected using MRI by the hydroxyl protons carried on LNT molecules. The in vitro phantom study showed that LNT and LNT-SeNPs have a strong CEST signal at 1.0 ppm apart from the water resonance, suggesting an in vivo detectability in the µM concentration range. Demonstrated on CT26 colon tumor cells, LNT-SeNPs exert a strong anticancer effect (IC50 = 4.8 μM), prominently attributed to the ability to generate intracellular reactive oxygen species. However, when testing in a mouse model of CT26 tumors, administration of LNT-SeNPs alone was found unable to deliver sufficient drugs to the tumor, leading to poor treatment responses. To improve the drug delivery, we co-injected LNT-SeNPs and TNF-α, a previously reported drug that could effectively damage the endothelial cells in the tumor vasculature, thereby increasing drug delivery to the tumor. Our results revealed a 75% increase in the intratumoral CEST MRI signal, indicating a markedly increased delivery efficiency of LNT-SeNPs when combined with TNF-α. The combination therapy also resulted in a significantly enhanced treatment outcome, as revealed by the tumor growth study. Taken together, our study demonstrates the first label-free, SeNP-based theranostic system, in which LNT was used for both functional surface coating and CEST MRI signal generating. Such a theranostic LNT-SeNP system is advantageous because it requires chemical labeling and, therefore, has high biocompatibility and low translatable barriers.