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Olga Papadodima

Publications and source records attributed to Olga Papadodima.

2 recordsLinked to original sources

Pre-Meta: priors-augmented retrieval for LLM-based metadata generation.

MOTIVATION: While high-throughput sequencing technologies have dramatically accelerated genomic data generation, the manual processes required for dataset annotation and metadata creation impede the efficient discovery and publication of these resources across disparate public repositories. Large language models (LLMs) have the potential to streamline dataset profiling and discovery. However, their current limitations in generalizing across specialized knowledge domains, particularly in fields such as biomedical genomics, prevent them from fully realizing this potential. This article presents Pre-Meta, an LLM-agnostic and domain-independent data annotation pipeline with an enriched retrieval procedure that leverages related priors-such as pre-generated metadata tags and ontologies-as auxiliary information to improve the accuracy of automated metadata generation. RESULTS: Validated using five selected metadata fields sampled across 1500 papers, the Pre-Meta assisted annotation experiment-without finetuning and prompt optimization-demonstrates a systemic improvement in the annotation task: shown through a 23%, 72%, and 75% accuracy gain from conventional RAG adoptions of GPT-4o mini, Llama 8B, and Mistral 7B respectively. AVAILABILITY AND IMPLEMENTATION: The code, data access, and scripts are available at: https://github.com/SINTEF-SE/LLMDap.

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Characterization of the BM88 promoter and identification of an 88 bp fragment sufficient to drive neurone-specific expression.

BM88 is a neurone-specific protein implicated in cell cycle exit and differentiation of neuronal precursors. It is widely expressed in terminally differentiated neurones but also in neuronal progenitors, albeit in lower levels. Thus BM88 expression shows a tight correlation with the progression of progenitor cells towards neuronal differentiation. Here we report the genomic organization and proximal promoter characterization of the human and mouse BM88 genes. Both promoters lie in a CpG island, are TATA-less and have multiple transcription start sites. Deletion analysis performed on the human BM88 gene revealed an 88 bp minimal promoter fragment that is preferentially active in neural cells. Importantly, this minimal promoter is sufficient to confer specific transcriptional activity in primary neurones, but not in glial cells. Within the promoter region there are four functional Sp1-binding sites. Simultaneous mutations to all four Sp1 sites results in complete loss of promoter activity. Transactivation experiments revealed that Sp1 directly activates the BM88 promoter while activation also occurs in the presence of neurogenin-1. Characterization of the promoter elements that control neurone-specific and developmental expression of BM88 should contribute to the elucidation of the transcriptional networks that regulate the transition from a proliferative neural progenitor to a post-mitotic neurone.

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