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The objective of this study was to investigate the specific role of nitric oxide (NO) in the early response of hulless barley roots to copper (Cu) stress. We used the fluorescent probe diaminofluorescein-FM diacetate to establish NO localization, and hydrogen peroxide (H 2 O 2 )-special labeling and histochemical procedures for the detection of reactive oxygen species (ROS) in the root apex. An early production of NO was observed in Cu-treated root tips of hulless barley, but the detection of NO levels was decreased by supplementation with a NO scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO). Application of sodium nitroprusside (a NO donor) relieved Cu-induced root inhibition, ROS accumulation and oxidative damage, while c-PTIO treatment had a synergistic effect with Cu and further enhanced ROS levels and oxidative stress. In addition, the Cu-dependent increase in activities of superoxide dismutase, peroxidase and ascorbate peroxidase were further enhanced by exogenous NO, but application of c-PTIO decreased the activities of catalase and ascorbate peroxidase in Cu-treated roots. Subsequently, cell death was observed in root tips and was identified as a type of programed cell death (PCD) by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The addition of NO prevented the increase of cell death in root tips, whereas inhibiting NO accumulation further increased the number of cells undergoing PCD. These results revealed that NO production is an early response of hulless barley roots to Cu stress and that NO contributes to Cu tolerance in hulless barley possibly by modulating antioxidant defense, subsequently reducing oxidative stress and PCD in root tips.

Digestive tract-related cancers account for four of the top ten high-risk cancers worldwide. In recent years, cancer immunotherapy, which exploits the innate immune system to attack tumors, has led to a paradigm shifts in cancer treatment. Gut microbiota modification has been widely used to regulate cancer immunotherapy. Dietary compounds and traditional Chinese medicine (TCM) can alter the gut microbiota and its influence on toxic metabolite production, such as the effect of iprindole on lipopolysaccharide (LPS), and involvement in various metabolic pathways that are closely associated with immune reactions. Therefore, it is an effective strategy to explore new immunotherapies for gastrointestinal cancer to clarify the immunoregulatory effects of different dietary compounds/TCMs on intestinal microbiota. In this review, we have summarized recent progress regarding the effects of dietary compounds/TCMs on gut microbiota and their metabolites, as well as the relationship between digestive cancer immunotherapy and gut microbiota. We hope that this review will act as reference, providing a theoretical basis for the clinical immunotherapy of digestive cancer via gut microbiota modulation.

Falls are a critical safety risk in aging societies, causing severe injuries and fatalities, particularly in urban public buildings where elderly visitors frequently gather. Cultural and heritage spaces such as museums and galleries present additional challenges for monitoring due to complex lighting, reflective display cases, and fluctuating visitor densities, underscoring the need for reliable fall detection systems that can be seamlessly deployed without intrusive infrastructure. This study proposes an interpretable, lightweight fall detection and alert system based on the YOLOv11-SEFA architecture. The model integrates P2 feature enhancement and SimAM attention into the YOLOv11n backbone, achieving consistent detection reliability while maintaining low computational cost. A four-layer sensing-to-cloud pipeline is combined with random forest classification of six-dimensional structural features to predict multi-level fall risk, with feature importance analysis verifying aspect ratio, distance to camera, and crowd presence as key predictors aligned with safety logic. The system demonstrates stable performance across confusion matrices, PR curves, and ROC-AUC learning curves, indicating operational feasibility and edge suitability. Practical tests show sub-270 ms latency, low power and bandwidth requirements, and smooth integration into weak-current infrastructures. Pilot validation at Rochfort Gallery, a restored 1920s heritage building in North Sydney, demonstrates feasibility under real-world conditions, supporting future deployment in smart city health and safety applications.

Paclitaxel (PTX) has been suggested to be a promising front-line drug for gastric cancer (GC), while P-glycoprotein (P-gp) could lead to drug resistance by pumping PTX out of GC cells. Consequently, it might be a hopeful way to combat drug resistance by inhibiting the out-pumping function of P-gp. In this study, we developed a drug delivery system incorporating PTX onto polyethylene glycol (PEG)-modified and oxidized sodium alginate (OSA)-functionalized graphene oxide (GO) nanosheets (NSs), called PTX@GO-PEG-OSA. Owing to pH/thermal-sensitive drug release properties, PTX@GO-PEG-OSA could induced more obvious antitumor effects on GC, compared to free PTX. With near infrared (NIR)-irradiation, PTX@GO-PEG-OSA could generate excessive reactive oxygen species (ROS), attack mitochondrial respiratory chain complex enzyme, reduce adenosine-triphosphate (ATP) supplement for P-gp, and effectively inhibit P-gp's efflux pump function. Since that, PTX@GO-PEG-OSA achieved better therapeutic effect on PTX-resistant GC without evident toxicity. In conclusion, PTX@GO-PEG-OSA could serve as a desirable strategy to reverse PTX's resistance, combined with chemo/photothermal/photodynamic therapy.

Plant parasitic nematodes respond to root exudates to locate their host roots. In our studies second stage juveniles of Heterodera glycines , the soybean cyst nematode (SCN), quickly migrated to soybean roots in Pluronic F-127 gel. Roots of soybean and non-host Arabidopsis treated with the ethylene (ET)-synthesis inhibitor aminoethoxyvinylglycine (AVG) were more attractive to SCN than untreated roots, and significantly more nematodes penetrated into roots. Moreover, Arabidopsis ET insensitive mutants ( ein2, ein2-1, ein2-5, ein3-1, ein5-1 , and ein6 ) were more attractive than wild-type plants. Conversely, the constitutive triple-response mutant ctr1-1 , was less attractive to SCN. While ET receptor gain-of-function mutant ein4-1 attracted more SCN than the wild-type, there were no significant differences in attractiveness between another gain-of-function ET receptor mutant, etr1-3 , or the loss-of-function mutants etr1-7 and ers1-3 and the wild type. Expression of the reporter construct EBS: β-glucuronidase ( GUS ) was detected in Arabidopsis root tips as early as 6 h post infection, indicating that ET signaling was activated in Arabidopsis early by SCN infection. These results suggest that an active ET signaling pathway reduces root attractiveness to SCN in a way similar to that reported for root-knot nematodes, but opposite to that suggested for the sugar beet cyst nematode Heterodera schachtii .

The tumor immune microenvironment (TIME) is associated with tumor prognosis and immunotherapy response. Here we develop and validate a CT-based radiomics score (RS) using 2272 gastric cancer (GC) patients to investigate the relationship between the radiomics imaging biomarker and the neutrophil-to-lymphocyte ratio (NLR) in the TIME, including its correlation with prognosis and immunotherapy response in advanced GC. The RS achieves an AUC of 0.795–0.861 in predicting the NLR in the TIME. Notably, the radiomics imaging biomarker is indistinguishable from the IHC-derived NLR status in predicting DFS and OS in each cohort (HR range: 1.694–3.394, P  < 0.001). We find the objective responses of a cohort of anti-PD-1 immunotherapy patients is significantly higher in the low-RS group (60.9% and 42.9%) than in the high-RS group (8.1% and 14.3%). The radiomics imaging biomarker is a noninvasive method to evaluate TIME, and may correlate with prognosis and anti PD-1 immunotherapy response in GC patients. Tumour microenvironment has been linked with immunotherapy response in gastric cancer. Here, the authors use CT-based radiomics to predict neutrophils-to-lymphocyte ratio and response to immunotherapy.

Gastric cancer (GC) is a serious disease with high morbidity and mortality rates worldwide. Chemotherapy plays a key role in GC treatment, while inevitable drug resistance and systematic side effects hinder its clinical application. Fenton chemistry-based chemodynamic therapy (CDT) has been used as a strategy for cancer ferroptosis, and the CDT efficiency could be enhanced by photothermal therapy (PTT). With the trend of treatment and diagnosis integration, the combination of magnetic resonance imaging (MRI) and CDT/PTT exhibits enormous progress. Herein, we constructed a platform based on PEGylated manganese-containing polydopamine (PDA) nanoparticles, named as PEG-PDA@Mn (PP@Mn) NPs. The PP@Mn NPs were stable and globular. Furthermore, they demonstrated near-infrared (NIR)-triggered PTT and Fenton-like reaction-based CDT effects and T1-weighted MRI capabilities. According to in vitro studies, the PP@Mn NPs trigger ferroptosis in cancer cells by producing abundant reactive oxygen species (ROS) via a Fenton-like reaction combined with PTT. Furthermore, in vivo studies showed that, under MRI guidance, the PP@Mn NPs combined with the PTT at the tumor region, have CDT anti-tumor effect. In conclusion, the PP@Mn NPs could provide an effective strategy for CDT/PTT synergistic ferroptosis therapy for GC.

Molecular biomarkers that predict disease progression might promote drug development and therapeutic strategies in aggressive cancers, such as gastric cancer (GC). High-throughput mRNA sequencing (RNA-seq) revealed that collagen type X alpha 1 (COL10A1) is a disease progression-associated gene. Analysis of 103 GC patients showed that high COL10A1 mRNA expression was associated with GC metastasis and reduced survival. We analyzed the COL10A1 promoter using the UCSC genome website and JASPAR database, and we found potential SOX9 binding site. Here, we demonstrated that SOX9 and COL10A1 were both up-regulated in GC. We observed a positive correlation between the expression patterns of SOX9 and COL10A1 in GC cells and tissues. The results of electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP) assay and promoter reporter indicated that SOX9 could directly bind to the COL10A1 gene promoter and activate its transcription. Biological function experiments showed that COL10A1 regulated the migration and invasion of GC cells. Knockdown COL10A1 inhibited lung and abdominal cavity metastasis in a nude mouse model. Moreover, transforming growth factor-β1 (TGF-β1) treatment up-regulated the phosphorylation of Smad2 and increased SOX9 and COL10A1 expression. COL10A1 was confirmed to be a potential inducer of epithelial-to-mesenchymal transition (EMT). SOX9 was essential for COL10A1-mediated EMT, and cell migration, invasion and metastasis. Co-expression of SOX9 and COL10A1 was associated with tumor progression and was strongly predictive of overall survival in GC patients. In summary, this study elucidated the mechanistic link between COL10A1 and the TGF-β1-SOX9 axis. These findings indicated that COL10A1 might play a crucial role in GC progression and serve as a potential biomarker and therapeutic target in GC patients.

Peritoneal metastasis predicts poor prognosis of gastric cancer (GC) patients, and the underlying mechanisms are poorly understood. The 2-DIGE, MALDI-TOF/TOF MS and single-cell transcriptome were used to detect differentially expressed proteins among normal gastric mucosa, primary GC and peritoneal metastatic tissues. Lentiviruses carrying shRNA and transcription activator-like effector nuclease technology were used to knock down myosin heavy chain 9 (MYH9) expression in GC cell lines. Immunofluorescence, immune transmission electron microscopy, chromatin fractionation, co-immunoprecipitation, and assays for chromatin immunoprecipitation, dual luciferase reporter, agarose-oligonucleotide pull-down, flow cytometry and cell anoikis were performed to uncover nuclear MYH9-induced β-catenin ( ) transcription . Nude mice and conditional transgenic mice were used to investigate the findings . We observed that MYH9 was upregulated in metastatic GC tissues and was associated with a poor prognosis of GC patients. Mechanistically, we confirmed that MYH9 was mainly localized in the GC cell nuclei by four potential nuclear localization signals. Nuclear MYH9 bound to the promoter through its DNA-binding domain, and interacted with myosin light chain 9, β-actin and RNA polymerase II to promote transcription, which conferred resistance to anoikis in GC cells and . Staurosporine reduced nuclear MYH9 S1943 phosphorylation to inhibit transcription, Wnt/β-catenin signaling activation and GC progression in both orthotropic xenograft GC nude mouse and transgenic GC mouse models. This study identified that nuclear MYH9-induced CTNNB1 expression promotes GC metastasis, which could be inhibited by staurosporine, indicating a novel therapy for GC peritoneal metastasis.

Background The molecular mechanisms underlying lymph node metastasis (LNM) in gastric cancer (GC) remain poorly understood. This study investigated HOXA9’s role in driving LNM via metabolic reprogramming. Methods Integrated analysis of gastric cancer RNA sequencing data and clinical specimens was performed. Functional validation involved HOXA9 overexpression and knockdown in AGS and HGC-27 cell lines, c-MYC silencing by siRNA, and glycolytic inhibition using 2-deoxyglucose (2-DG, 2.5 mM). In vitro assays evaluated proliferation (CCK-8), apoptosis (Annexin V/PI), migration/invasion (Transwell), lymphangiogenesis (HLEC tubulogenesis), and metabolism (Seahorse analyser). In vivo, effects were evaluated using a popliteal LNM mouse model ( n  = 6/group) and administered exogenous lactate (20 mM) to restore levels. Results HOXA9 was significantly upregulated in LNM-positive GC tissues (1.3-fold, p  = 0.0006) and predicted poor survival (HR = 1.57, p  = 1.7 × 10⁻⁵). HOXA9 overexpression enhanced GC cell proliferation (2.5-fold, p  < 0.0001), invasion (1.6-fold, p  = 0.0002), and migration (2.0-fold, p  < 0.0001), while suppressing apoptosis. Mechanistically, HOXA9 directly bound the c-MYC promoter, thereby upregulating glycolytic enzymes (HIF-1α, HK2, GLUT1, PDK1, LDHA) and increasing lactate secretion (1.7-fold, p  = 0.005). The resultant lactate-rich microenvironment stimulated lymphangiogenesis (1.4-fold, p  < 0.01) and endothelial cell migration (1.8-fold, p  < 0.001). These effects were significantly reversed by c-MYC knockdown or 2-DG treatment, with 2-DG reducing lymphangiogenesis by 37.56% ( p  < 0.0001). In vivo, HOXA9 knockdown reduced LNM burden (66% reduction in node volume, 83% lower metastasis rate), and this effect was markedly rescued by lactate supplementation. Conclusions HOXA9 promotes GC LNM by activating the c-MYC-glycolysis-lactate axis, which remodels the lymphatic niche. This axis represents a targetable pathway for GC therapy.