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ABSTRACT Background Phosphorus (P) is an essential mineral element required in large quantities by plants. Globally, the availability of P in many soils is poor. Breeding crops that can acquire and utilise this limited resource with high efficiency is an important goal for agricultural sustainability in the future. The mapping and cloning of quantitative trait loci (QTLs) provides an effective tool in analyzing the genetic mechanisms underlying P efficiency and breeding P-efficient varieties. Scope This paper describes the QTL mapping of traits related to P efficiency which impact on shoot biomass or yield of crops in the past 20 years. It summarises the progress of studies on crop P-efficiency related QTLs and discusses the challenges for the cloning of QTLs. It proposes a scheme to develop crop genotypes with improved P efficiency. It also describes emerging methods, such as QTL-seq, genome-wide association analysis, and RNA-seq, that aid the rapid identification of P-efficiency related genes in crops. Conclusion Traits conferring P efficiency are heritable. Thus, it is feasible to incorporate phenotyping and selection for P efficiency in crop breeding programs. Identification of QTLs for target traits is a key step to enhancing the P efficiency of crops. Numerous QTLs have been identified that affect P efficiency in key crops, but few causal genes have been identified and breeding P-efficient crop varieties using marker-assisted selection (MAS) has not progressed far. The challenge now is to identify the specific genes controlling P-efficiency related traits. The availability of complete genome sequences for more crops, and the combination of conventional linkage mapping, association mapping, QTL-seq, transcriptomics and gene editing technologies can accelerate the cloning and confirmation of genes underlying QTL affecting P-efficiency related traits. Knowledge of these genes will be helpful in revealing the molecular mechanisms underlying P efficiency in crops, as well as providing the opportunity to improve crop P efficiency through MAS or gene manipulation.

With the aging of the population, the incidence of osteoporosis (OP) is on the rise, but the ecology of immune cell subpopulations in OP is poorly understood. Therefore, identifying cell subpopulations involved in promoting the development of OP may facilitate the development of new treatments. Based on bioinformatics analysis, we constructed a single-cell landscape of the OP microenvironment and identified immune cell subpopulations in OP to further explore the role of different subpopulations in the abnormal bone microenvironment. Among macrophages (Mac), the Mac_OLR1 subpopulation has an M1-like phenotype and significantly activates cytokine and osteoclast differentiation pathways, interacting with osteoclasts via the HBEGF-CD9 axis. In neutrophils (Neut), the Neut_RSAD2 subpopulation significantly activated cytokine and osteoclast differentiation pathways and had a high neutrophil extracellular trap (NET) score, and H1FX was identified as its potential regulator. In effector memory T (Tem) cells, the Tem_CCL4 subpopulation significantly activated osteoclast differentiation and immune inflammation-related pathways and highly expressed proinflammatory molecules such as CCL4, CCL4L2, CCL5 and IFNG. In B cells, the abundance of the B_ACSM3 subpopulation was significantly increased in the OP group and the osteoclast differentiation pathway was significantly activated, and MYB was identified as its potential regulator. In summary, we identified several immune cell subpopulations that may be involved in promoting the formation of OP, further identified the transcription factors that regulate these subpopulations, and speculated that the development of OP may be accompanied by immune inflammatory responses mediated by these subpopulations. These findings provide candidate molecules and cells for future OP research and may help facilitate the development of new therapies.

Combining information from multispectral images into a fused image is informative and beneficial for human or machine perception. Currently, multiple photodetectors with different response bands are used, which require complicated algorithms and systems to solve the pixel and position mismatch problem. An ideal solution would be pixel-level multispectral image fusion, which involves multispectral image using the same photodetector and circumventing the mismatch problem. Here we presented the potential of pixel-level multispectral image fusion utilizing colloidal quantum dots photodiode array, with a broadband response range from X-ray to near infrared and excellent tolerance for bending and X-ray irradiation. The colloidal quantum dots photodiode array showed a specific detectivity exceeding 10 12 Jones in visible and near infrared range and a favorable volume sensitivity of approximately 2 × 10 5  μC Gy −1 cm −3 for X-ray irradiation. To showcase the advantages of pixel-level multispectral image fusion, we imaged a capsule enfolding an iron wire and soft plastic, successfully revealing internal information through an X-ray to near infrared fused image. Multispectral images suffer of pixel and position mismatch, due to the multiple sensor approach. Here, Li et al., demonstrate a flexible PbS colloidal quantum dots (CQDs) photodiode array with a broadband response range from X-ray to near infrared, enabling multi-spectral images by one single sensor.

Gastrodiae Rhizoma (tianma, TM), a traditional medicine that has food and medicine homology, faces controversy over retaining its epidermis (tianma pi, TP) during processing due to unclear phytochemical value. This study presents the first integrated approach combining GC–IMS, UHPLC–MS, and Caenorhabditis elegans (C. elegans) aging models to compare TP with the tuber core (tianma xin, TX). The results include the following: (1) A total of forty-seven volatile compounds were identified by GC–IMS, including 12 key aroma substances via relative odor activity value (ROAV ≥ 1), of which seven ((Z)-4-heptenal, β-citronellol, hexanal, 1-pentanol, 1-octen-3-one, 2-methylpropanol, and 2-butanone) were enriched in TP. (2) Non-targeted metabolomics revealed 1025 metabolites via UHPLC–MS, highlighting phenylpropanoid biosynthesis as the primary differential pathway (p < 0.05). Phenylpropanoids and polyketides exhibited predominant enrichment in TP (|log2FC| > 2, VIP > 1, p < 0.01). (3) In C. elegans models, TP outperformed TX in pharyngeal pumping (4.16%, p < 0.05), while both extended stress-resistant lifespan (p < 0.01). In conclusion, TP plays an essential role in establishing the characteristic odor profile of TM and retaining bioactive components, particularly phenylpropanoids. Preserving TP during processing optimally maintains the distinctive aroma profile and pharmacological value of TM, which provides valuable guidance for industrial utilization.

With the continuous expansion of power grids and the advancement of ultra-high voltage (UHV) projects, transmission lines are increasingly traversing areas characterized by micro-terrain. These localized topographic features can intensify meteorological effects, thereby increasing the risks of hazards such as conductor icing and galloping, directly threatening operational stability. Enhancing the disaster resilience of transmission lines in such environments requires accurate and efficient terrain identification. However, conventional recognition methods often neglect the spatial alignment of the transmission lines, limiting their effectiveness. This paper proposes a deep learning-based recognition framework that incorporates a dual-branch network architecture and a cross-branch spatial attention mechanism to address this limitation. The model explicitly captures the spatial correlation between transmission lines and surrounding terrain by utilizing line alignment information to guide attention along the line corridor. A semi-synthetic dataset, comprising 6495 simulated samples and 130 real-world samples, was constructed to facilitate model training and evaluation. Experimental results show that the proposed model achieves classification accuracies of 94.6% on the validation set and 92.8% on real-world test cases, significantly outperforming conventional baseline methods. These findings demonstrate that explicitly modeling the spatial relationship between transmission lines and terrain features substantially improves recognition accuracy, offering important support for hazard prevention and resilience enhancement in UHV transmission systems.

Background Lung adenocarcinoma (LUAD) is a common type of lung cancer with a high risk of metastasis, but the exact molecular mechanisms of metastasis are not yet understood. Methods This study acquired single-cell transcriptomics profiling of 11 distal normal lung tissues, 11 primary LUAD tissues, and 4 metastatic LUAD tissues from the GSE131907 dataset. The lung multicellular ecosystems were characterized at a single-cell resolution, and the potential mechanisms underlying angiogenesis and metastasis of LUAD were explored. Results We constructed a global single-cell landscape of 93,610 cells from primary and metastatic LUAD and found that IGF2BP2 was specifically expressed both in a LUAD cell subpopulation (termed as LUAD_IGF2BP2), and an endothelial cell subpopulation (termed as En_IGF2BP2). The LUAD_IGF2BP2 subpopulation progressively formed and dominated the ecology of metastatic LUAD during metastatic evolution. IGF2BP2 was preferentially secreted by exosomes in the LUAD_IGF2BP2 subpopulation, which was absorbed by the En_IGF2BP2 subpopulation in the tumor microenvironment. Subsequently, IGF2BP2 improved the RNA stability of FLT4 through m 6 A modification, thereby activating the PI3K-Akt signaling pathway, and eventually promoting angiogenesis and metastasis. Analysis of clinical data showed that IGF2BP2 was linked with poor overall survival and relapse-free survival for LUAD patients. Conclusions Overall, these findings provide a novel insight into the multicellular ecosystems of primary and metastatic LUAD, and demonstrate that a specific LUAD_IGF2BP2 subpopulation is a key orchestrator promoting angiogenesis and metastasis, with implications for the gene regulatory mechanisms of LUAD metastatic evolution, representing themselves as potential antiangiogenic targets.

Acute myocardial infarction (AMI) poses a significant global mortality burden. Utilizing bio informatics, this study explored cellular aging-related genes (CARGs) and mitochondrial-related genes (MRGs). in AMI Public AMI datasets were analyzed using differential expression and weighted gene co-expression network analysis (WGCNA) to identify 1,373 differentially expressed genes (DEGs), of which 643 were upregulated and 730 downregulated. A turquoise module related to cellular aging was identified by gene set variation analysis (WGCNA). Venn analysis revealed 37 candidate genes intersecting DEGs, key module genes, and MRGs. Machine learning, receiver operating characteristic (ROC) analysis, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) validated Isopentenyl-diphosphate delta-isomerase 1 (IDI1) and phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1) as key AMI genes. A comprehensive lncRNA-miRNA-mRNA network was constructed, and Cyclosporine showed strong binding affinities with IDI1 (-6.2 kcal/mol) and PMAIP1 (-4.8 kcal/mol), indicating therapeutic potential. This study may provide insights into AMI pathogenesis and highlight potential drug targets for further investigation.

As a severe metabolic disease, type 2 diabetes mellitus (T2DM) has become a serious threat to human health in recent years. Gastrodin, as a primary chemical constituent in Gastrodia elata Blume, has antidiabetic effects. However, the possible mechanisms are unclear. The aim of the present study was to investigate the effects and possible mechanisms of gastrodin on the treatment of T2DM. In vivo , after treatment with gastrodin for 6 weeks, fasting blood glucose levels, blood lipid metabolism, and insulin sensitivity index values were remarkably reduced compared with those of the diabetic control group. The values of aspartate aminotransferase and alanine aminotransferase also showed that gastrodin alleviates liver toxicity caused by diabetes. Moreover, gastrodin relieved pathological damage to the pancreas in T2DM rats. In vitro , gastrodin alleviated insulin resistance by increasing glucose consumption, glucose uptake, and glycogen content in dexamethasone-induced HepG2 cells. The Western blotting results showed that gastrodin upregulated the expression of insulin receptors and ubiquitin-specific protease 4 (USP4) and increased the phosphorylation of GATA binding protein 1 (GATA1) and protein kinase B (AKT) in vivo and in vitro . Furthermore, gastrodin decreased the ubiquitin level of the insulin receptor via UPS4 and increased the binding of GATA1 to the USP4 promoter. Additionally, administration of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway inhibitors MK-2206 and LY294002 abolished the beneficial effects of gastrodin. Our results indicate that gastrodin promotes the phosphorylation of GATA1 via the PI3K/AKT pathway, enhances the transcriptional activity of GATA1, and then increases the expression level of USP4, thereby reducing the ubiquitination and degradation of insulin receptors and ultimately improving insulin resistance. Our study provides scientific evidence for the beneficial actions and underlying mechanism of gastrodin in the treatment of T2DM.

Objective To elucidate the mechanism through which tumor-associated neutrophil extracellular traps (NETs) contribute to the progression of colorectal cancer (CRC), characterize cellular populations within the CRC tumor microenvironment (TME), and identify potential therapeutic targets. Methods We retrieved the single-cell RNA-seq datasets of CRC from GEO, and performed clustering analysis and subgroup analysis on the quality-controlled single-cell transcriptome data. Subsequently, we interrogated signaling pathways, biological functions, developmental trajectories, survival outcomes, gene regulatory networks, and cellular communication among distinct cell subgroups to delineate tumor heterogeneity during CRC progression. Results Our analyses reveal that the DACH1 + and NKD1 + CRC subgroups play vital roles in the initiation, progression, and metastasis of CRC. PPIF + neutrophil subgroups promote NETs formation and CRC progression by facilitating mitochondrial reactive oxygen species (mtROS) production. Meanwhile, the C1QC + Mac, RACK1 + Tem, RACK1 + B, and RACK1 + Plasma subgroups exert certain immunosuppressive effects within CRC TME, thus promoting CRC progression. Moreover, RACK1 may serve as a key ecological niche gene in CRC. Furthermore, PPIF + neutrophils modulate the TME via TNFSF14–TNFRSF14 and TNFSF14-LTBR checkpoint axes, thereby sustaining the CRC progression. Conclusion Our research findings have revealed the biological characteristics of CRC under the influence of NETs. Altogether, this study underlines the therapeutic potential value of targeting NETs-related mechanisms in the context of CRC.