Search Results (6,035)

Despite the widespread adoption of BIM, information exchange across disciplines remains hindered by heterogeneous structures at the tabular data level, particularly when integrating data across multiple discipline-specific models. Manual mapping, rigid templates, or one-off programming scripts are labor-intensive and difficult to scale, limiting automated querying, cross-model aggregation, and schedule-level analytics. This study proposes a lightweight, workflow-driven approach for semantic normalization and cross-model integration of BIM schedule data, with optional script-supported workflow configuration used only to assist the configuration of deterministic, rule-guided mapping logic, rather than serving as a core analytical method. By introducing a customizable subcategory layer, the workflow enables fine-grained semantic alignment and efficient normalization across diverse schedule datasets, implemented through lightweight Python scripting and rule-guided semantic matching used solely as a supporting mechanism for deterministic field mapping. Using structural, architectural, and HVAC models, we demonstrate a stepwise process including data cleaning, hierarchical classification, consistency checking, batch analytics, and automated computation of cross-model metrics such as opening-to-wall ratios. Sample-based validation confirms the workflow’s reliability, achieving semantic mapping agreement rates above 95% and reducing manual processing time by more than 85%. The workflow is readily extensible to other disciplines and modeling conventions, supporting high-throughput data integration for tasks such as design coordination, semantic alignment, RFI reduction, accelerated design reviews, and data-driven decision making. Overall, rather than introducing a new algorithm, the contribution of this work lies in formalizing a reusable, schedule-level workflow abstraction that enables consistent semantic alignment and automated cross-model aggregation without relying on rigid ontologies or training-intensive learning-based models. Any optional tooling used during workflow configuration is auxiliary and does not constitute a standalone learning-based method requiring model training or performance benchmarking. This provides a reusable methodological foundation for scalable, schedule-level BIM data integration and cross-model analytics. Full article

Background/Objectives: Having longer mesocotyls is beneficial for the deep-sowing tolerance of rice, which is important for seedling establishment. Methods: Here, we performed transcriptome analysis of the elongating mesocotyl of Zhengdao 209 in response to three different sowing depths to identify the pivotal genes regulating rice mesocotyl elongation. Results: Three groups with different mesocotyl lengths were compared using transcriptome analysis, and 60 common differentially expressed genes were detected. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that these genes are primarily involved in phenylpropanoid biosynthesis, cutin suberine and wax biosynthesis, the plant mitogen-activated protein kinase signaling pathway, diterpenoid biosynthesis, cyanoamino acid metabolism, carbon fixation in photosynthetic organisms, flavonoid biosynthesis, and glutathione metabolism. Furthermore, weighted gene co-expression network and hierarchical clustering analyses showed that most of the differentially expressed genes are implicated in phenylpropanoid biosynthesis, carbon metabolism, photosynthesis antenna proteins, and plant–pathogen interactions. Among the genes involved in phenylpropanoid biosynthesis processes, the expression levels of OsPHT3 and LOC_Os04g59260 increased, while OsCCR1, OsPGIP4, and LOC_Os01g45110 expression decreased with increasing sowing depth. Among the genes involved in the mitogen-activated protein kinase signaling pathway, the expression levels of LOC_Os07g03319 and LOC_Os07g03580 increased, while LOC_Os07g03409 decreased with increasing sowing depth. Among the genes involved in diterpenoid biosynthesis processes, the expression levels of OsCYP76M5 and OsCYP71Z2 decreased, while OsCYP71Z21 increased with increasing sowing depth. Furthermore, the expression levels of these genes were analyzed using quantitative real-time polymerase chain reaction, which confirmed the transcriptome analysis results. Conclusions: This study identified candidate genes governing rice mesocotyl length and provides novel insights into the molecular regulatory mechanisms underlying mesocotyl elongation in rice. Full article

Background: Ionizing radiation (IR) induces profound bone marrow (BM) injury by disrupting hematopoietic stem cell (HSC) homeostasis, leading to acute myelosuppression and long-term hematopoietic dysfunction. Although transcriptome-wide analyses have advanced our understanding of radiation responses, the key molecular networks and hub genes governing post-irradiation BM injury remain incompletely defined. Methods: This study aimed to systematically identify radiation-responsive pathways and central genes in BM after irradiation through an integrative bioinformatics approach based on RNA sequencing (RNA-seq). Public RNA-seq data from mouse BM HSCs collected 3 days after whole-body irradiation were analyzed. Differentially expressed genes (DEGs) were identified using two independent statistical frameworks to improve the robustness of the results. Functional analysis was performed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Protein–protein interaction (PPI) networks were constructed using STRING, and hub genes were identified using network topology parameters. Results: Both analysis pathways consistently demonstrated extensive transcriptome reprogramming after irradiation. DEGs were primarily enriched in processes related to cytokine signaling, hematopoietic lineage regulation, immune response, and extracellular matrix remodeling. KEGG analysis highlighted cytokine–cytokine receptor interaction, hematopoietic cell lineage, JAK-STAT signaling, and PI3K-Akt signaling as key molecular axes. GSEA further supported coordinated changes in pathways related to inflammatory response, stress response, and metabolic reprogramming. PPI network analysis identified four consensus hub genes, namely Il6, Cd34, Gypa, and Pdgfrb, which are related to inflammatory signaling, hematopoietic regulation, erythroid dynamics, and microenvironmental remodeling, respectively. Conclusion: This integrative bioinformatics study demonstrates that radiation-induced BM injury is associated with coordinated activation of inflammatory cytokine networks, alterations in the hematopoietic program, and microenvironmental restructuring. The hub genes identified in this study may represent candidate regulatory genes or molecular indicators potentially involved in the response to radiation-induced hematopoietic damage. Full article

Scholarly knowledge graphs integrate bibliographic records from heterogeneous sources and therefore require controlled, auditable deduplication. This paper presents OntoDup, an ontology-driven approach that models entity matching as a governed decision process: Matching outcomes are recorded as reified assertions enriched with governance state, evidence, provenance and operational metadata, while a separate operational view is exposed through policy-driven materialization of consumable identity links. We evaluate OntoDup on the DBLP-ACM and DBLP-Scholar benchmarks under two regimes: (i) a pre-blocked setting using the benchmark candidate lists to compare matching methods under a fixed candidate set, and (ii) an end-to-end setting that generates candidates from the graph with DeepBlocker and applies governed triage and materialization. We report operational precision/recall/$F_1$ computed directly on the graph via SPARQL aggregations, characterize governance workload through state distributions, and quantify inference cost for LLM-based matchers via token and latency metadata attached to assertions. For end-to-end evaluation, we anchor operational links against a full positive reference encoded as idealized validations derived from the benchmark labels, enabling analysis of missed positives in terms of governance status and materialization policy. The experiments show that OntoDup enables evaluation at the level of consumable identity links, review workload, and inference cost, revealing operational trade-offs that are not visible from pairwise matching metrics alone. Full article

Background: In an earlier murine model of myocardial infarction (MI), we showed that CD8 cells and myeloid dendritic cells (mDCs) infiltrate the infarcted myocardium within the first week. However, in humans, the spatial interplay between CD8⁺ T cells and dendritic cells in the spatial context of human myocardial infarction remains underexplored. Objective: In the present study, we applied spatial transcriptomics and functional assays to characterize immune–stromal dynamics in infarcted myocardium and peripheral blood. Methods & Results: Spatial transcriptomics analysis of infarcted human myocardium at days 2 and 6 post-MI, combined with peripheral blood flow cytometry and EPC colony-forming assays, was performed. Cell composition, pathway enrichment, and cell-to-cell communication analyses were conducted to map immune–stromal cells’ dynamics across time points. Spatial mapping identified dynamic shifts in immune, fibroblast, and endothelial populations, with fibroblasts and endothelial cells remaining abundant throughout. CD8⁺ T cells accumulated in ischemic regions while their circulating levels declined. Gene Ontology and pathway analyses of CD8A⁺ transcripts revealed enrichment of proinflammatory and NF-κB survival programs. ITGAX/CD33/THBD⁺ APCs progressively increased within infarct zones, activating antigen-presentation and leukocyte chemotaxis pathways. Early (day 2) APC–endothelial crosstalk showed the strongest predicted recruitment signals for CD8⁺ T cells, which diminished by day 6. Finally, EPC colony-forming capacity showed a tendency for reduction in MI patients and inversely correlated with coronary lesion burden, indicating impaired vascular repair potential. Conclusions: This integrative spatial and functional study demonstrates that APC-driven CD8⁺ recruitment and EPC dysfunction are key features of human MI. Immune–endothelial niches facilitate early cytotoxic T-cell infiltration, while progenitor depletion limits vascular regeneration. These findings provide mechanistic insight into immune–vascular imbalance during infarct healing and highlight potential therapeutic targets to modulate inflammation and restore vascular repair. Full article

The design and manufacturing of carbon-fiber-reinforced polymer (CFRP) structures in aerospace require balancing high structural performance with cost-efficient, reproducible production. Conventional design and planning methods are often fragmented across disciplines, causing data discontinuities and limited traceability. This paper introduces a graph-based design language (GBDL) information architecture that integrates CFRP design and manufacturing within a unified, model-based framework. The approach formalizes engineering knowledge through process ontologies and graph-based data models linking geometry, material, tooling, and process parameters in a consistent, machine-interpretable form. Each step, from geometry derivation and structural design to prepreg hand lay-up and automated fiber placement, is represented within a shared design graph to ensure data consistency, transparency, and automated assessment of lead time, labor, cost, waste, and energy consumption. Although current implementations address selected use cases with partially automated interfaces, the architecture establishes a scalable foundation for full interoperability. A helicopter-frame case study demonstrates the applicability and adaptability of the method. Full article

Construction sites implement various safety management activities, including toolbox meetings, risk assessments, and safety knowledge assessments, to reduce accidents. Multiple-choice question (MCQ)-based assessments are widely used to evaluate worker safety competencies. However, the effectiveness of MCQ assessments depends critically on distractor quality; incorrect options must be plausible enough to challenge uninformed respondents while remaining clearly distinguishable from knowledgeable ones. Manual distractor creation requires substantial expertise and is prone to inconsistency, whereas large language models (LLMs) often generate options that lack domain relevance. This paper proposes context-aware multipath adaptive safety scoring (CoMPASS), an algorithm that integrates construction safety domain knowledge with LLM capabilities for MCQ distractor generation. CoMPASS operates through two pathways: CoMPASS-H leverages a hierarchical hazard factor ontology for hazard identification questions, whereas CoMPASS-R uses hybrid retrieval-augmented generation (RAG) for risk control questions. An evaluation using 50 real construction accident cases with a robotic assessment test (RAT) using frontier LLMs as virtual examinees demonstrated that CoMPASS-R achieved a 90% quality pass rate, whereas all baseline methods failed to meet the composite quality criteria. The proposed framework provides a scalable approach to generating assessment content that supports effective safety management at construction sites. Full article

Pluripotent stem cell (PSC) differentiation is orchestrated by intricate autocrine and paracrine signaling networks. Among these, exosomes, key components of the cellular secretome, are implicated as crucial mediators of intercellular communication via delivery of bioactive molecules, including microRNAs (miRNAs). This study investigated the role of exosomal miRNAs in stem cell differentiation using Dgcr8-deficient mouse embryonic stem cells (mESCs), which are incapable of producing mature miRNAs. Although the differentiation capacity was markedly impaired in these cells, partial restoration was observed following treatment with exosomes derived from differentiating wild-type mESCs. Exosomal miRNA uptake was confirmed, and gene ontology analysis revealed significant enrichment of pathways associated with cell fate determination, morphogenesis, and apoptosis regulation. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that exosomal miRNAs modulated multiple osteoinductive signaling cascades, notably the MAPK and TGF-β pathways, in Dgcr8-deficient cells. Apoptotic markers were also downregulated, suggesting a protective effect conferred by the exosomal cargo. Collectively, our results suggest that exosome-mediated delivery of miRNAs may represent a fundamental mechanism by which pluripotent stem cells coordinate stress responses and differentiation trajectories, providing novel insights into the regulation of embryogenesis. Full article

The safety of titanium dioxide (TiO₂), widely used in foods and personal care products, has been of on-going concern. Adverse effects of TiO₂ have been reported, suggesting risk to human health. To evaluate its potential epigenotoxicity, the effect of exposure to a TiO₂ product, to which humans could be exposed, on microRNA (miRNA) expression (a primary epigenetic mechanism) was investigated using human cell lines (Caco-2, HCT116 (colorectal) and HepG2, SNU387 (liver)) relevant to human exposure. The effect of TiO₂ nanomaterial exposure on expression levels of miRNA was determined using the TaqMan Array Human microRNA A+B Card Set v3.0 platform. Differentially expressed miRNAs were identified (SNU387 (n = 112), HepG2 (n = 97), Caco-2 (n = 94), and HCT116 (n = 53)). Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) functional enrichment analysis of target genes provided insights into the roles of modulating pathways, which can be associated with diseases. Top 10 KEGG pathways in each cell line included MAPK signaling pathway, Axon guidance, cell cycle, Hippo signaling pathway, and Endocytosis. Findings from the study clearly demonstrate the impact of TiO₂ exposure on miRNA expression, supporting the potential involvement of this epigenetic mechanism in its biological responses. Hence, epigenetic studies are important for the complete assessment of the potential risk from exposure. Full article

This paper develops Tone as Ontology, a structural account of being grounded in the invariants of generative systems. We articulate the ontological significance of tone, distinguishing this foundational work from a companion paper that explores its methodological application and formalization. We redefine “tone” as the structural profile of constraints that allows entities to maintain coherence under transformation. The tonal ontology formalizes three invariants—Resonance, Responsibility, and Closure—as conditions of persistence that bridge operational and metaphysical ontology. Concretely, we specify Resonance (relational continuity via recursive feedback), Responsibility (traceable accountability that conserves integrity across transformations), and Closure (recursive self-consistency enabling bounded openness). In contrast to informational or substance-based views, tonal being is understood as the conservation of structure through change. The resulting framework unites physical coherence, informational integrity, and ontological continuity into a generative ontology of integrity, suggesting that to exist is to maintain one’s tone. This paper addresses fundamental questions in meta-ontology, demonstrates how tone generates classical ontological frameworks, and advances a conceptual reorientation for understanding existence as resonant persistence. It outlines testable implications across philosophy of mind, AI ethics, and social/environmental theory. Overall, tonal ontology is presented as a post-informational, structurally grounded account of being. Full article

Ochratoxin A (OTA), a prevalent food contaminant, is closely linked to the development of various cancers, including clear cell renal cell carcinoma (ccRCC). However, the potential mechanisms remain to be explored. In this study, we employed network toxicology, machine learning, and molecular docking techniques to systematically investigate the potential molecular mechanisms underlying OTA-associated ccRCC. We normalized transcriptional data from two Gene Expression Omnibus (GEO) datasets and analyzed it using differential expression analysis and weighted gene co-expression network analysis (WGCNA), identifying 3224 ccRCC-associated target genes. These were intersected with 232 predicted OTA target genes, yielding a total of 56 overlapping targets. The results of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these targets were primarily enriched in critical biological processes, including extracellular matrix remodeling, immune microenvironment regulation, signaling pathway transduction, cellular metabolism, and protein homeostasis. Machine learning analysis identified “glmBoost + RF” (a sequential combination of feature selection and classifier) as the optimal model, from which nine key genes were extracted. SHapley Additive exPlanations (SHAP) analysis revealed five core genes (IGFBP3, ITGA5, PYGL, SLC22A8, LTB4R), with IGFBP3 and ITGA5 serving as the principal driver genes of the model. Validation of the model’s diagnostic efficacy and single-cell transcriptome analysis indicated that the core genes exhibited significant differential expression patterns, cell-type-specific expression characteristics, and high independent diagnostic efficacy. Molecular docking analyses predicted stable interactions between OTA and the core target proteins. These findings suggest potential molecular links between OTA exposure and ccRCC, providing a foundation for hypothesis generation and future experimental validation. Full article

Background: Recurrent vulvovaginal candidiasis (RVVC) is a chronic inflammatory disease primarily caused by Candida albicans (C. albicans). Its pathogenesis remains incompletely understood, and clinical management is challenged by recurrence and drug resistance. Ferroptosis, an iron-dependent form of programmed cell death driven by lipid peroxidation, has been implicated in various infectious and inflammatory diseases. However, its role in RVVC remains unclear, with a particular lack of evidence from clinical samples and animal experiments. Objective: This study aimed to investigate the association between RVVC and ferroptosis. First, we analyzed high-throughput sequencing data from human RVVC samples in the Gene Expression Omnibus (GEO) database to identify the expression profile of ferroptosis-related genes. Second, using an established murine model of chronic vulvovaginal candidiasis (CVVC), we validated changes in ferroptosis-related markers in vaginal tissues in vivo. Furthermore, an in vitro model of C. albicans-infected bone marrow-derived macrophages (BMDMs) was employed to explore the underlying mechanisms. This study provides experimental evidence for elucidating the pathogenesis of RVVC and exploring novel therapeutic strategies. Methods: The RVVC-related gene expression dataset GSE278036 was obtained from the GEO database. Differentially expressed genes (DEGs) were screened using the DESeq2 algorithm and intersected with ferroptosis-related genes from the FerrDb database to identify key targets. A protein–protein interaction (PPI) network was constructed using the STRING database and Cytoscape software, and hub genes were identified via the Betweenness centrality algorithm. Functional and pathway analyses, including gene set enrichment analysis (GSEA), Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and WikiPathways, were performed. Immune infiltration analysis characterized the immune microenvironment in RVVC patients. A CVVC mouse model was established in vivo, and a C. albicans-BMDMs infection model was established in vitro. The ferroptosis inhibitor ferrostatin-1 (Fer-1) was administered to investigate the pathological function and regulatory mechanisms of ferroptosis in RVVC at the molecular, cellular, and tissue levels. Results: Differential analysis identified 3132 DEGs in RVVC, which intersected with ferroptosis-related genes to yield 194 key targets. Among them, 20 hub genes were identified, including ferroptosis regulators and inflammatory factors. Functional enrichment analysis confirmed that these shared targets regulate RVVC pathology through a “ferroptosis-inflammation-immunity” multi-pathway network. Immune infiltration analysis revealed a specific immune disorder in RVVC patients characterized by “activation of the pro-inflammatory innate immune axis and suppression of the adaptive immune axis,” which was closely associated with ferroptosis-related genes. In vivo and in vitro experiments confirmed that C. albicans infection induced ferroptosis in vaginal tissues and macrophages, as manifested by lipid ROS accumulation, Fe²⁺ overload, GSH depletion, downregulation of GPX4 and SLC7A11, upregulation of ACSL4, 4-HNE, and MDA, and mitochondrial structural damage. Macrophages were identified as key target cells for ferroptosis, and their ferroptosis led to impaired antifungal function. Fer-1 treatment significantly inhibited ferroptosis, reduced vaginal histopathological damage and inflammatory cell infiltration, decreased fungal burden, downregulated abnormally elevated inflammatory factors, and restored Th1/Th2 immune balance. Furthermore, Fer-1 preserved macrophage viability and enhanced their antifungal killing capacity. Conclusions: This study provides the first evidence linking RVVC to ferroptosis through a combination of clinical data analysis and experiments, suggesting that ferroptosis is involved in its pathological process. These findings offer a new perspective for elucidating RVVC pathogenesis and developing targeted therapeutic strategies. Full article

Wuweiganlu (WGL) is a traditional formulation widely applied in the treatment of rheumatoid arthritis (RA), yet the identity of its bioactive constituents remains inadequately defined. In this study, ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) and untargeted serum metabolomics were employed to characterize the active components of WGL. Fraxin was identified as a principal compound from WGL. To investigate its therapeutic mechanism in RA, a series of in silico and experimental approaches were conducted. Network pharmacology analysis and RNA sequencing identified heat shock protein family member 8 (HSPA8) as a potential molecular target of Fraxin, which was further validated by molecular docking studies. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that Fraxin exerts its effects primarily by modulating cell apoptosis through the PI3K signaling pathway. In vitro experiments demonstrated that Fraxin significantly reduced inflammatory responses and downregulated HSPA8 expression in lipopolysaccharide (LPS)-stimulated fibroblast-like synoviocytes (FLs) and macrophages. In vivo, Fraxin administration markedly reduced paw swelling, alleviated bone deformities, and improved bone volume fraction (BV/TV) in male IL1RA-deficient mice exhibiting spontaneous arthritis. Histological analysis confirmed that Fraxin attenuated joint inflammation by modulating the inflammatory microenvironment. Additionally, Fraxin inhibited synovial hyperplasia by regulating mitochondrial membrane potential collapse in FLs. Functional assays revealed that this regulation occurred via the inhibition of HSPA8/PI3K/AKT signaling axis, thereby suppressing aberrant FLS proliferation and contributing to the attenuation of RA progression. Full article

Recently, a shift from substance-based to process-based ontologies of living beings and biological entities has been widely advocated, largely on the grounds that traditional substance thinking, by encouraging biological reductionism, fails to adequately capture the nature of biological wholes. Process-based approaches are instead taken to provide a more appropriate metaphysical framework for the constitutive dynamicity of living systems. These arguments, however, have been criticized for relying on overly reductive characterizations of substances, which both classical and contemporary accounts describe as inherently involving change and activity. In this essay, I address the substance-versus-process debate from the perspective of contemporary cell biology. I argue that conceiving the cell as a substance is not only compatible with the centrality of processes, but that the cell continues to function as the fundamental reference point in biology precisely because it entails processuality as intrinsic to its dynamic mode of being. Within this framework, subcellular entities are identified by their functional subservience to the cellular whole. On this basis, I propose an empirically grounded criterion for distinguishing between purely processual and substance-like subcellular entities. Processual entities, such as the Golgi complex and the nucleolus, lack dedicated repair systems and tend to disassemble upon inhibition of specific metabolic activities. By contrast, substance-like entities, including cell-derived organelles such as the mitochondrion and the nucleus, depend for their persistence on specific repair systems, and their eventual dismantling under non-permissive conditions cannot be straightforwardly understood as the mere interruption of a process, but instead appears as the outcome of an active, regulated response. Full article

Infertility is a prevalent clinical issue which disrupts normal human life and exerts an impact on fertility rates within the population. The increase in environmental pollutants, including acetyl tributyl citrate (ATBC), has given rise to concerns regarding their potential toxicity in infertility-related disorders. Icariin exhibits therapeutic effects on infertility, yet its mechanism of action against plasticiser-induced reproductive disorders remains unclear. This study aims to elucidate the potential toxicological targets and molecular mechanisms of ATBC-induced infertility, as well as the therapeutic targets and mechanisms of icariin in treating ATBC-induced reproductive disorders, through network toxicology, molecular-docking techniques and molecular dynamics simulation. Utilising the component-target database SwissTargetPrediction, the Similarity Ensemble Approach, PharmMapper, the ChEMBL database, and disease databases including the Therapeutic Target Database, OMIM, GeneCards, and DrugBank, 63 targets for ATBC-induced infertility and 33 targets for icariin treatment were identified. Screening via the STRING platform and Cytoscape 3.10.1 software yielded four core targets for ATBC-induced infertility—HSP90AA1, PIK3CA, CASP3, HRAS—and four core targets for icariin treatment—IL6, TNF, STAT3, and INS. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed that ATBC-induced infertility correlates with pathways including pathways in cancer, prostate cancer, and PI3K-Akt signalling pathways. Conversely, the core targets of icariin therapy for related reproductive disorders are closely associated with tumour-associated signalling pathways and the AGE-RAGE signalling pathway. Molecular-docking and molecular dynamics simulation further confirmed the strong binding interactions between ATBC and infertility-related targets, as well as between icariin and core targets for treating reproductive disorders. This provides a theoretical foundation for understanding ATBC’s toxicological targets and the complex molecular mechanisms underpinning icariin’s treatment of infertility. It informs the development of strategies for icariin to prevent and treat infertility caused by exposure to ATBC-containing plastics or excessive ATBC contact. Full article