Nicola Zamboni

ChEBI-N performs ontology-based enrichment analysis on metabolomics data, identifying enriched chemical classes and demonstrating improved results with organism-specific backgrounds.

The paper integrates multi-omics data from pediatric sepsis patients to identify a reproducible inflammatory host-response axis associated with disease severity.

This study shows ACOD1 deficiency in microglia enhances inflammatory responses by altering arginine metabolism, specifically increasing argininosuccinate synthesis while reducing polyamine synthesis, dependent on ACLY.

This study systematically maps metal-binding sites in E. coli using Metal-LiP, identifies 424 candidate metal-binding proteins, and suggests functional roles for metal binding.

This study identifies coenzyme A depletion as a cause of antibiotic tolerance in Pseudomonas aeruginosa using proteomic, metabolomic, and machine learning analyses.

The paper shows that microbial metabolite release rates are negatively correlated with metabolite value, explaining variability better than other factors.

The paper identifies bacterial DNA remnants in blood immune cells of CRC and IBD patients, suggesting microbial translocation via intestinal barrier defects.

The paper shows that stress-induced changes in extracellular vesicles from mice can alter sperm and embryo transcriptomes, leading to metabolic issues in offspring.

This study identifies metabolic differences between proliferating and quiescent endothelial cells using proteomics and metabolomics, revealing distinct metabolic pathways in blood and lymphatic endothelium.

The paper profiles the metabolome of 180 cancer cell lines and identifies two major metabolic types linked to epithelial-mesenchymal transition (EMT).

MSNovelist generates small molecule structures de novo from mass spectra, outperforming database-based methods for novel compounds.

The paper uses multi-omics data from mice to identify gene-environment-age interactions and causal molecular networks linked to longevity.

The paper shows that paternal trauma alters blood metabolites and sperm transcriptomes, which can be transmitted to offspring via PPAR-mediated mechanisms.