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Verrault, M.

Publications and source records attributed to Verrault, M..

2 recordsLinked to original sources

h5adify: neuro-symbolic metadata harmonizationenables scalable AnnData integration with locallarge language models

BackgroundThe rapid growth of public single-cell and spatial transcriptomics repositories has shifted the main bottleneck for atlas-scale integration from data generation to metadata heterogeneity. Even when datasets are released in the AnnData H5AD format, inconsistent column naming, partial annotations, and mixed gene identifier conventions frequently prevent reproducible merging, downstream benchmarking, and reuse in foundation model training. Automated approaches that resolve semantic inconsistency while preserving biological validity are therefore essential for scalable data reuse. ResultsWe present h5adify, a neuro-symbolic toolkit that combines deterministic biological inference with locally deployed large language models to transform heterogeneous AnnData objects into schema-normalized, integration-ready representations. The framework performs metadata field discovery, gene identifier harmonization, optional paper-aware extraction, and consensus resolution with explicit uncertainty logging. Benchmarking four open-weight model families deployed through Ollama (Gemma, Llama, Mistral, and Qwen) demonstrates that small local models achieve high semantic accuracy in metadata resolution with low hallucination rates and modest computational requirements. In controlled simulations introducing annotation noise into single-cell and Visium-like datasets, harmonization improves integration benchmarking and reduces spurious batch effects. Application to sex-annotated glioblastoma datasets recovers biologically coherent microenvironmental patterns and cell type-specific genomic differences not explained by differential expression alone. ConclusionsTogether, h5adify provides a reproducible framework for evaluating LLM-assisted biocuration and enables scalable, privacy-preserving metadata harmonization for modern single-cell atlases and foundation model pipelines. These results demonstrate that modular neuro-symbolic integration of deterministic biological inference and small local language models can effectively resolve semantic heterogeneity while remaining computationally accessible.

bioinformatics↗

Identification of inter- and intra-tumoral molecular phenotypes steering temozolomide resistance in patient-derived glioblastoma cells.

BackgroundRadiation therapy and chemotherapy using Temozolomide are the standard adjuvant treatments for patients with glioblastoma. Despite maximal treatment prognosis is still poor largely due to the emergence of Temozolomide resistance. This resistance is closely linked to the widely recognized inter- and intra-tumoral heterogeneity in glioblastoma, although the underlying mechanisms are not yet fully understood. This study aims to investigate the diverse molecular mechanisms involved in temozolomide resistance. MethodsTo induce temozolomide resistance, we subjected 21 patient-derived glioblastoma cell cultures to Temozolomide treatment for a period of up to 90 days. Prior to treatment, the cells molecular characteristics were analyzed using bulk RNA sequencing. Additionally, we performed single-cell sequencing on four of the cell cultures to track the evolution of temozolomide resistance. ResultsThe induced temozolomide resistance was associated with two distinct phenotypic behaviors, classified as "adaptive" (ADA) or "non-adaptive" (N-ADA) to temozolomide. The ADA phenotype displayed neurodevelopmental and metabolic gene signatures, whereas the N-ADA phenotype expressed genes related to cell cycle regulation, DNA repair, and protein synthesis. Single-cell RNA sequencing revealed that in ADA cell cultures, one or more subpopulations emerged as dominant in the resistant samples, whereas N-ADA cell cultures remained relatively stable. ConclusionsThe adaptability and heterogeneity of glioblastoma cells play pivotal roles in temozolomide treatment and contribute to the tumors ability to survive. Depending on the tumors adaptability potential, subpopulations with acquired resistance mechanisms may arise. Further research is necessary to deepen our understanding of these mechanisms and develop strategies to overcome them.

cancer biology↗