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ToxiVerse: chemical bioprofiling, toxicity data sharing and customizable predictive modeling.

MOTIVATION: Chemical toxicity assessment is critical for drug development and environmental safety. Computational models have emerged as a promising alternative to animal testing and now play a significant role in efficiently evaluating new chemicals. To address the urgent need for user-friendly machine learning tools in computational toxicology, we developed ToxiVerse, a public web-based platform. RESULTS: ToxiVerse provides automatic chemical bioprofiling, curated toxicity datasets, and a predictive modeling interface designed for researchers who lack programming expertise. The platform comprises three integrated modules: (i) Bioprofiler, which provides chemical descriptors by combining chemical-bioactivity data from PubChem assays with a machine learning-based data gap-filling procedure; (ii) Database, which hosts ∼50 000 curated chemicals covering diverse toxicity endpoints; and (iii) Cheminformatics, which enables dataset upload, chemical curation, and automatic generation of quantitative structure-activity relationship models for toxicity prediction. AVAILABILITY: The tool is accessible at www.toxiverse.com, and source code is available at https://github.com/zhu-research-group/toxiverse.

Quantitative Structure-Activity Relationship

Bacterial polar metabolites modulate β-amyloid toxicity and cholinergic dysfunction in models of Alzheimer's disease.

Alzheimer's disease is characterized by progressive neurodegeneration driven by β-amyloid (Aβ) toxicity, oxidative stress, and cholinergic dysfunction. In this study, we investigated whether polar metabolites derived from a cultivable bacterial isolate could modulate Aβ-associated neurodegenerative phenotypes in complementary experimental models. A bioactivity-guided approach identified an aqueous fraction with high antioxidant capacity in DPPH, FRAP, and ORAC assays. In a transgenic Drosophila melanogaster model expressing human Aβ, treatment with this fraction significantly reduced amyloid accumulation and attenuated neurodegenerative histopathological alterations. In human SH-SY5Y neuronal cultures, the metabolites improved cell viability under therapeutic, but not preventive, conditions following exposure to aggregated Aβ. The aqueous fraction also exhibited significant inhibitory activity against acetylcholinesterase and butyrylcholinesterase. Whole-genome sequencing assigned the bioactive isolate to the genus Providencia, with comparative genomic analyses suggesting its placement within a distinct taxonomic lineage. Metabolomic profiling by LC-ESI-MS/MS revealed a diverse set of polar metabolites, including metabolites putatively annotated based on spectral matching, previously associated with neuroprotective and cholinesterase-modulating activities. Collectively, these findings demonstrate that bacterial polar metabolites can modulate key pathological features of Alzheimer's disease, supporting their relevance for mechanistic studies of Aβ toxicity and cholinergic dysfunction.

Animals

Integrating structure and experimental data annotations with computational modeling framework for predicting micro-nanoplastics toxicities.

The wide use of plastic materials leads to increased emissions of micro-nanoplastics (MNPs) into the environment, raising significant concerns about their impact on human health. Traditional experimental approaches for assessing MNPs toxicity are costly, time-consuming, and there are no experimental protocols that are universally acceptable. Computational modeling using machine learning (ML) approaches provides an efficient alternative to MNP toxicity assessment. However, most modeling studies of MNPs are limited due to the lack of high-quality data and there are few previous modeling studies considering complex structures of MNPs for model training. To address this challenge, we constructed three MNP datasets with popular toxicity endpoints from various resources and used nanostructure annotation techniques to create virtual MNPs (vMNPs) for all MNP structures. The MNP structures were digitalized from annotated vMNPs, and geometrical descriptors were calculated using the Delaunay Tessellation approach. Moreover, important experimental information, such as concentrations and cell lines, were transformed into extra training variables. Partial least squares regression (PLSR) models were built using both experimental and geometrical descriptors and validated through a leave-one-out cross validation procedure. The resulting models showed reasonable performance in predicting toxicity potentials of MNPs for the three endpoints in the present datasets. Moreover, an additional library of vMNPs with their predicted properties and bioactivities was constructed, directing further research of new MNPs. This study provides three novel ML models for MNPs by integrating geometrical and experimental descriptors, which have the potential to assess new MNPs for their toxicity. The modeling strategy developed in this study can be easily expanded to model other MNP toxicity endpoints and create promising new models for MNP toxicity assessments.

Data annotation

Exploring the Translation of Organ-on-a-Chip Technology for Human-Relevant Diagnostic Biomarkers.

Microphysiological systems (MPSs) are gaining traction as a viable alternative model for toxicity studies. Further characterization is necessary to explore the full translational potential of MPSs to human physiology, along with the utility of these platforms to serve as a diagnostic tool. Multiomics analyses have emerged as a key means for identifying host biomarkers associated with chemical and drug exposure. Correlations between published human omics and MPS technology omics data will inform the potential of organ chips to accurately represent human responses and provide an alternative approach for improved biomarker discovery for toxicity assessment and exposure identification. To interrogate these potential overlaps, TissUse Chip3 multiorgan chips (MOCs) seeded with kidney organoids, liver organoids, and respiratory tract tissue were exposed to low, therapeutic, and toxic doses of acetaminophen (n = 4 for each condition) for 24 h and subjected to proteomic and metabolomic analysis. The data from our organ chips are largely consistent with biomarkers and dysregulations identified in published human omics data, in vitro and in vivo data, to include the identification of several known acetaminophen metabolites and biotransformation products. These data suggest that organ chips may be a suitable surrogate for human biomarker identification and drug or hazardous chemical exposure diagnosis.

Humans

Pentatricopeptide repeat protein targeting CUG repeat RNA ameliorates RNA toxicity in a myotonic dystrophy type 1 mouse model.

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystemic disorder caused by the expansion of a CTG-triplet repeat in the 3' untranslated region of the dystrophia myotonica protein kinase (DMPK) gene. It results in the transcription of toxic RNAs that contain expanded CUG repeats (CUGexp). Splicing factors, such as muscleblind-like 1 (MBNL1), are sequestered by CUGexp, thereby disrupting the normal splicing program that is essential for various cellular functions. Pentatricopeptide repeat (PPR) proteins, originally found in plants, regulate RNA in organelles by binding in a sequence-specific manner. Here, we designed PPR proteins that specifically bind to the hexamer of CUG repeat RNAs (CUG-PPRs) and showed that CUG-PPR1 could ameliorate RNA toxicity induced by CUGexp in cell models of DM1. A single systemic recombinant adeno-associated virus (AAV9) vector-mediated gene delivery of CUG-PPR1 demonstrated long-term therapeutic effects on myotonia and restored splicing activity in a mouse model of DM1. These results highlight the potential of PPR molecules to target pathogenic RNA sequences in DM1 and potentially other RNA-mediated disorders.

Animals

Harnessing the Power of Large Language Models for Drug Discovery: A Systematic Review of Current Applications and Future Directions.

INTRODUCTION: The demand for inventive approaches to drug discovery has increased due to the rising costs, time, and failure rates in pharmaceutical research. Large Language Models (LLMs), with their sophisticated natural language processing and generative capabilities, have become potent instruments that have the potential to revolutionize biomedical research. The function of LLMs in different phases of drug development is methodically examined in this article. METHODS: The PRISMA 2020 principles were adhered to in this systematic study. A thorough search for research published between 2018 and 2025 was done using PubMed, Scopus, Web of Science, and Google Scholar. The search terms "large language model," "transformer," "drug discovery," and important sub-domains (such as "de-novo design" and "ADMET") were merged, and two reviewers independently screened the results. Predetermined inclusion and exclusion criteria were used to filter studies for relevance. 98 studies out of the 1,285 records that were initially retrieved met the requirements for the final qualitative synthesis. RESULTS: 98 studies that demonstrated the use of LLMs in various drug discovery domains were found during the review. These covered molecular generation, genomics, protein-ligand modeling, ADME/T and toxicity profiling, drug-target interaction and DTI prediction, and biomedical text mining. 42 different LLM-based tools were mapped, including BioBERT, SciSpacy, Drug- LLM, DNA-BERT, GPT-4, and ChatGPT. Predictive accuracy, hypothesis creation, target prioritization, and multi-modal data integration all showed notable gains with these techniques. DISCUSSION: By providing scalable, precise, and effective solutions for data-driven drug discovery, LLMs are revolutionizing the pharmaceutical industry. They allow for the creation of hypotheses and individualized insights across multi-modal biological data, and they perform better than conventional approaches in a number of subdomains. Improvements in performance were task-dependent; the most consistent gains occurred for biomedical text mining, disease-genedrug relationship mapping and drug-target interaction prediction tasks. Yet most evidence for clinical applications is still derived from retrospective studies and benchmark datasets, suggesting a higher need for prospective validation. CONCLUSION: There is revolutionary potential in incorporating LLMs into drug discovery processes. Clinical translation and regulatory uptake will depend heavily on collaborative validation, ethical deployment, and standardization as models become more multimodal and interpretable. Before normal use, extensive prospective benchmarking and head-to-head comparisons with established chemoinformatics pipelines are necessary.

De novo design

From molecular responses to environmental monitoring: advances and translational gaps in omics approaches in fish environmental toxicology.

Fish occupy a central position in aquatic ecosystems and serve as important bioindicators for environmental monitoring, as well as powerful translational models for understanding toxic mechanisms conserved across higher vertebrates. In recent years, omics techniques have proven to be powerful tools to address complex environmental questions that conventional toxicology methods cannot answer. Despite this potential, a critical translational gap remains between molecular findings and their use in ecological risk assessment frameworks. This review critically synthesizes advances across omics techniques including epigenomics, transcriptomics, metabolomics and proteomics and their integration. Special emphasis is placed on methodological considerations and practical aspects of these techniques in fish environmental toxicology and environmental monitoring. Evidence from single-omics studies suggests conserved biomarker signatures across species while characterizing complex phenomena like non-monotonic dose-response relationships, mixture toxicity and transgenerational and stereoselective effects with implications for population level monitoring. Multi-omics studies, especially those involving triple omics, further enhance mechanistic resolution by reconstructing adverse outcome pathways. We further evaluate using case studies when additional molecular layers provide critical insight and when they offer limited advantage, a strategic distinction with direct implications in environmental monitoring programmes. Finally, current limitations and future directions that will ultimately bridge the translational gap and hold promise for advancing mechanistic ecotoxicology and predictive environmental monitoring are discussed.

Animals

DHX9 Inhibition Enhances Paclitaxel Sensitivity by Inducing Mitotic Failure in Ovarian and Endometrial Cancers.

Recurrent high-grade serous ovarian carcinoma (HGSOC) and endometrial cancer remain major clinical challenges with limited effective treatment options. DExH-box helicase 9 (DHX9), a DNA/RNA helicase essential for genomic stability, has not yet been explored as a therapeutic target in gynecologic cancers. In this study, we show that a selective DHX9 inhibitor (DHX9i) suppresses proliferation in a subset of HGSOC and endometrial cancer cell lines by inducing DNA damage, chromosomal instability, and mitotic failure. This effect was independent of microsatellite instability status and prior resistance to platinum or PARP inhibitors. Genomic analysis indicated that DHX9i resistance was unlikely to be driven by single-gene mutations but was instead associated with copy-number alterations in mitotic spindle and microtubule-regulating genes in both HGSOC and endometrial cancer. Transcriptomic profiling further revealed consistent alterations in microtubule- and spindle-associated pathways in DHX9i-resistant models following DHX9i treatment. Mechanistically, DHX9i induced mitotic defects in DHX9i-sensitive models, whereas resistant lines maintained mitotic integrity. Given the convergence of resistance-associated features on microtubule-related pathways, we combined DHX9i with the microtubule-stabilizing agent paclitaxel to enhance mitotic stress. This combination triggered mitotic disruption and enhanced cytotoxicity in DHX9i-resistant cells. In vivo, the combination led to sustained tumor regression and prolonged survival in both DHX9i-sensitive and DHX9i-resistant models without notable toxicity. Overall, our findings define genomic, transcriptomic, and phenotypic characteristics associated with differential responses to DHX9i and support the clinical evaluation of the DHX9i-paclitaxel combination as a therapeutic strategy in recurrent gynecologic cancers.

Female

The Hematological Variations and Effect of Cadmium Induced Toxicity on Mammary Tumors Development in Albino Mice. A Comparative Model Study on the Effect of Heavy Metals in Human Breast Cancer.

INTRODUCTION: Breast cancer develops in breast tissues, in ducts and lobules. It affects both genders, though it is uncommon in men. Hematological variations are important considerations and deficiencies in metals can negatively impact human health. Cadmium is highly toxic and plays role in breast cancer progression. This study was designed for hematological variations and cadmium induced toxicity in mice and humans causing breast cancer. METHODS: Mice, obtained from local supplier, housed at university laboratory for 11 weeks, exposed to cadmium. Following dissection, blood and organs were harvested for examination. Histological analysis of liver and mammary gland tissues was conducted. RESULTS: Affected mice had higher Hb, RBC, HCT, MCV, and MCH, while humans showed lower Hb, HCT, and MCV but similar RBC and MCH. Other blood values also show changes. Histopathology revealed changes in mammary glands (higher cadmium led to increased fat deposition, degeneration of alveolar epithelial cells, and a reduction in alveolar milk lumen size, indicating compromised glandular function) and liver damage (vacuolation, lipid accumulation, fibrosis, and collagen deposition, was noticeable with prolonged cadmium). These changes causes liver fibrosis and impaired mammary gland function. DISCUSSION: The cadmium exposure induces distinct hematological alterations and severe tissues damage, reflecting species-specific responses. The observed liver fibrosis and mammary gland dysfunction emphasize cadmium's potential to compromise critical organ functions over time. CONCLUSION: Significant effects of cadmium exposure in mice were observed. Histological damage was seen in mammary glands and liver. Further research on protective measures and dose-response relationships for cadmium exposure is needed.

Animals

Uncovering parental exposure risks of TCPP: Impaired development and metabolic homeostasis in zebrafish offspring.

As brominated flame retardants are phased out, tris (1‑chloro-2-propyl) phosphate (TCPP), a phosphorus-based flame retardant, has emerged as a prominent detectable flame retardant in the environment. However, TCPP has been found to exhibit endocrine-disrupting effects on organisms, raising significant safety concerns. In our study, we utilized the zebrafish model to explore the toxic effects of parental TCPP exposure on offspring and uncover its regulatory mechanisms through metabolomics analysis. Moreover, the impact on the nervous system and lipid metabolism was examined through behavioral analysis and specific staining. Our findings demonstrated that both embryonic and parental TCPP exposure induced developmental disorders in larvae, along with decreased locomotor activity and disordered lipid metabolism homeostasis. Parental exposure to TCPP, exhibiting stronger developmental toxicity than direct embryonic exposure, notably led to reductions in crucial energy substrates such as amino acids and carbohydrates. Meanwhile, embryonic TCPP exposure primarily affected the endogenous lipid-related metabolites including phospholipids, lipid-soluble vitamins, steroids and fatty acids, promoting lipid accumulation in larval liver and subcutaneous tissue. What's more, continuously parental and embryonic exposure showed the most pronounced effects on zebrafish development and metabolic regulation. Our study highlights the risk posed by parental exposure to TCPP on offspring zebrafish, underscoring the need for comprehensive consideration of the impact from parental exposure in pollutants regulation.

Animals

Bioactivity and developmental toxicity of Raphanus raphanistrum: integrating phytochemistry, in vitro assays, and zebrafish model.

Raphanus raphanistrum L. (wild radish), a member of the Brassicaceae family, is an edible herb widely utilized in traditional medicine for the treatment of various ailments. This study aimed to evaluate the chemical composition, antioxidant capacity, enzyme inhibitory potential, and cytotoxic activity of extracts derived from its aerial parts. Among the tested extracts, the 70% ethanol extract contained the highest total phenolic content. A total of 38 compounds, mainly phenolic acids and flavonoids, were identified by HPLC-ESI-MS/MS analysis. The aqueous extract contained the highest levels of individual phenolic compounds, particularly ferulic acid and p-coumaric acid. The 70% ethanol extract showed the strongest antioxidant activity in all assays. The ethyl acetate extract exhibited the highest acetylcholinesterase and α-amylase inhibitory activities. Cytotoxicity assays revealed that the 70% ethanol extract was active against A549 lung cancer cells with an IC50 value of 56.77 µg mL-1 and a selectivity index of 1.6. In vivo zebrafish developmental toxicity assays demonstrated dose-dependent embryotoxic effects. Early exposure (0 hpf) caused increased mortality, reduced hatching, and morphological abnormalities, such as axial curvature and pericardial edema, whereas exposure at 72 hpf showed markedly reduced sensitivity. Overall, the findings suggest that R. raphanistrum is a promising natural source of bioactive compounds that could be used in the nutraceutical, pharmaceutical and cosmeceutical industries.

Journal Article

Organoids and microphysiological systems: Promising models for accelerating AAV gene therapy studies.

The FDA has predicted that at least 10-20 gene therapy products will be approved by 2025. The surge in the development of such therapies can be attributed to the advent of safe and effective gene delivery vectors such as adeno-associated virus (AAV). The enormous potential of AAV has been demonstrated by its use in over 100 clinical trials and the FDA's approval of two AAV-based gene therapy products. Despite its demonstrated success in some clinical settings, AAV-based gene therapy is still plagued by issues related to host immunity, and recent studies have suggested that AAV vectors may actually integrate into the host cell genome, raising concerns over the potential for genotoxicity. To better understand these issues and develop means to overcome them, preclinical model systems that accurately recapitulate human physiology are needed. The objective of this review is to provide a brief overview of AAV gene therapy and its current hurdles, to discuss how 3D organoids, microphysiological systems, and body-on-a-chip platforms could serve as powerful models that could be adopted in the preclinical stage, and to provide some examples of the successful application of these models to answer critical questions regarding AAV biology and toxicity that could not have been answered using current animal models. Finally, technical considerations while adopting these models to study AAV gene therapy are also discussed.

Animals

Elucidation of the immunotoxicity of PEDOT: PSS on RAW264.7 macrophages by oxidative stress, inflammatory response, and NF-κB pathway activation.

Poly(3,4-ethylenedioxythiophene): poly(styrenesulfonate) (PEDOT: PSS) nanoparticles, widely used conductive polymers, pose environmental and health risks due to their nanoscale dispersion. However, the characteristics of PEDOT: PSS in aquatic systems and the underlying mechanisms of its toxicity in animal and cell models remain poorly understood. This study aimed to investigate the toxicological effects of PEDOT: PSS nanoparticles on macrophages, with a focus on RAW 264.7 cells. After an acute exposure to PEDOT: PSS nanoparticles at different concentrations (5, 10, 20 μg/mL), we observed significant impairments in cell viability, proliferation, migration, adhesion, and phagocytosis, as well as morphological alterations. Concurrently, there was a marked upregulation of inflammatory markers, including reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), indicating the induction of oxidative stress and inflammation. Mechanistically, PEDOT: PSS nanoparticles activated the nuclear factor kappa B (NF-κB) signaling pathway, a key regulator of inflammatory responses, suggesting that they may mediate inflammatory responses and cell damage via activation of the NF-κB signaling pathway. These findings reveal the toxic mechanism of PEDOT: PSS nanoparticles in macrophages and provide new insights into their biological safety implications.

Animals

Natural language processing-based model to predict radiation pneumonitis in patients with locally advanced non-small cell lung cancer undergoing chemoradiotherapy: a retrospective cohort study.

BACKGROUND: Radiation pneumonitis (RP) remains a significant treatment-related toxicity in patients with unresectable, locally advanced non-small cell lung cancer (NSCLC) undergoing chemoradiotherapy (CRT). Most existing predictive models rely on static baseline demographic or dosimetry variables and lack real-time clinical applicability. We developed a novel predictive framework that integrates longitudinal symptom data extracted from clinical notes using natural language processing (NLP) with clinical and dosimetry features to improve early RP prediction. METHODS: We retrospectively identified 227 patients with locally advanced NSCLC treated with definitive CRT at a high-volume cancer center in the United States. We included all patients older than 18 years who were diagnosed between Jan 1, 2006, and Dec 31, 2022 with histologically or cytologically confirmed unresectable Stage 2 or 3 NSCLC and treated with conformal radiotherapy to a minimum dose of ≥45 Gy with or without chemotherapy. Of these, 31 RP events were identified through manual adjudication using radiologic criteria and chart review. NLP was used to extract the temporal relationship of 16 pre-specified symptoms with treatment from over 100,000 clinical notes spanning pre- and during-treatment intervals. We trained and validated machine learning models on combinations of baseline clinical data, radiation dosimetry, and NLP-derived symptom features. Model performance was evaluated using a nested cross-validation framework, with an outer cross-validation loop reserved for performance assessment and an inner cross-validation loop used for model training and integration, and summarized using area under the receiver operating characteristic curve (AUC) and partial AUC (pAUC) at high specificity thresholds. Clinical utility was evaluated using decision curve analysis (DCA). FINDINGS: The best-performing model incorporated longitudinal NLP features and achieved a median AUC of 0.759 (90% confidence interval 0.753-0.766), significantly outperforming baseline models using only dosimetry (AUC 0.613) or clinical variables (AUC 0.635). NLP-based features such as cough trajectory, shortness of breath, and wheezing were among the most important predictors. Inclusion of NLP-derived symptom data improved early identification of high-risk patients, particularly in the clinically relevant high-specificity range (pAUC 0.021 vs. 0.010 for dosimetry alone). DCA showed that the calibrated MLP model provided greater net benefit than default strategies of treating all or no patients across clinically relevant threshold possibilities. INTERPRETATION: In this early work, NLP-based extraction of longitudinal symptoms from routine clinical documentation meaningfully enhances RP prediction in patients undergoing CRT for NSCLC. This approach leverages existing electronic health record infrastructure to deliver real-time, scalable, and interpretable risk estimates, offering a pathway toward potential early intervention and personalized toxicity management. The model and DCA requires external and prospective validation before clinical deployment; as such, future work should focus on this validation and integration into clinical decision support systems. FUNDING: AstraZeneca.

Chemoradiotherapy

Deletion of the Salmonella pathogenicity island 2 gene, spiC, in attenuated Salmonella Typhimurium VNP20009 optimizes its potential for bacterial schwannoma therapy.

UNLABELLED: Recent advances in systems biology and immunotherapy have spurred the investigation of bacteria as therapeutic vehicles for cancer treatment. Currently, Bacillus Calmette-Guérin remains the only FDA-approved bacterial cancer therapy; it is a live attenuated mycobacterium that is indicated for the treatment and prophylaxis of carcinoma in situ of the urinary bladder and for the prophylaxis of primary or recurrent papillary tumors following transurethral resection. Although safety concerns have been raised, attenuated Salmonella Typhimurium strains such as VNP20009 have advanced to clinical trials targeting fast-growing human tumors. Notably, this strain induces robust immunological control of slow-growing tumors such as NF2-related schwannomatosis (NF2-SWN) in preclinical murine models. Here, we genetically characterize VNP20009 with the goal of constructing genetically defined attenuated strains that retain its promising therapeutic features while improving safety. Specifically, we investigated the contribution of the Salmonella pathogenicity island I (SPI-1) and SPI-2 type III secretion systems to antitumor efficacy and biosafety. Mutation of the SPI-1 gene sipB, a key structural component required for SPI-1 type III secretion system function, partially reduced tumor control in NF2-SWN murine schwannoma models, suggesting that bacterial invasion alone does not fully account for antitumor activity. In contrast, deletion of the SPI-2 gene spiC, a key effector required for intracellular survival, preserved robust tumor regression in NF2-SWN murine schwannoma models while improving safety and reducing systemic toxicity. To create a genetically defined and tractable platform, we generated two attenuated strains-AST101 and AST101-ΔspiC-which retain key mutations present in VNP20009 but lack ill-characterized background mutations. In the syngeneic NF2-SWN mouse schwannoma model, both strains significantly suppressed tumor growth compared to PBS. Collectively, these findings support the development of rationally engineered Salmonella Typhimurium strains with enhanced safety and preserved antitumor efficacy. IMPORTANCE: Given long-standing safety concerns surrounding the therapeutic use of live bacteria, we constructed a ΔspiC mutant of VNP20009 and demonstrated that it provides a markedly improved safety profile while retaining antitumor efficacy in NF2-related schwannomatosis mouse schwannoma models. In addition, we created two genetically defined Salmonella Typhimurium strains, AST01 and AST01-ΔspiC, which incorporate the key-targeted mutations found in VNP20009 and VNP20009-ΔspiC, respectively. These engineered strains offer a well-defined genetic background, enabling precise investigation of the bacterial traits responsible for Salmonella Typhimurium-mediated tumor control and thus further improvement of attenuated strains optimized for bacteriotherapy of neoplasms.

Salmonella typhimurium

Sample Preparation of Caenorhabditis elegans for GC-MS-Based Metabolomics in Toxicity Assessment.

The nematode Caenorhabditis elegans, widely recognized as a model organism due to its ease of breeding and well-characterized genomes, boasts complete digestive, reproductive, and endocrine systems, as well as conserved signaling pathways shared with mammals. It has become an invaluable resource for metabolomics research, particularly in examining responses to chemical or environmental factors and toxicity assessments. In this article, we provide detailed, step-by-step protocols for cultivating C. elegans and conducting metabolomics analyses, specifically focusing on sample preparation for GC-MS analysis in response to toxic compound treatments. We highlight the critical choice of extraction solvent, introducing two representative systems for extracting metabolites from C. elegans.

Animals

hPSC models in cancer mechanisms and therapeutic discovery.

Despite major advances in cancer genomics and immunotherapy, the field remains limited by experimental models that fail to faithfully recapitulate human tumor initiation, genetic context, and immune-tumor interactions. Traditional animal and immortalized cell models often lack predictive power for therapeutic response and toxicity. Recent advances in human pluripotent stem cell (hPSC) technology have transformed this landscape, enabling the generation of patient-specific cancer models, multicellular organoids and assembloids, and scalable immune effector cells. These platforms now permit mechanistic dissection of tumorigenesis, reconstruction of human tumor microenvironments, and development of off-the-shelf immunotherapies. This review will synthesize these emerging findings, define key technological and biological gaps, and outline future directions for integrating hPSC-based modeling into precision oncology and translational cancer research.

cancer immunotherapy

Integrating RNA sequencing with deep learning-based metabolic toxicity prediction: A new perspective on screening prioritized liquid crystal monomers.

Nearly 99 % of liquid crystal monomers (LCMs) toxicological data remains gaps, especially to aquatic organisms. Herein, this study proposes a rapid and high-throughput screening method for identifying priority LCMs in natural water. Using six fluorinated LCMs (LCMsF) with significant enrichment characteristics in zebrafish as examples, RNA sequencing revealed that LCMsF-induced metabolic disturbances are predominant, including 28 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway abnormalities attributed to 498 differentially expressed genes. Notably, the intricate sequencing process resulted in the inability to rapid identify additional 857 LCMsF that may induce metabolic disturbances. To address this, LCMsT-MTP, a predictive deep learning model based on RNA sequencing, was developed. This model integrates a comprehensive representation of LCMsF structures and metabolic toxicity target sequences. LCMsT-MTP improves upon traditional methods that are limited to single targets and mechanisms by facilitating the simultaneous identification of 21 metabolic toxicities induced by LCMsF. In addition, the LCMsT-MTP model was further applied to non-fluorinated LCMs (LCMsNone F) that satisfy the applicability domains test. Accordingly, a metabolic toxicity priority list of LCMs was proposed, with ∼95 % of LCMs classified as high or medium risk. Priority list validation by molecular dynamics confirmed that the interactions of LCMsF/LCMsNone F and metabolic toxicity targets in representative KEGG pathways were distinct.

Animals