Biology subjects

Niazi, U.

Publications and source records attributed to Niazi, U..

2 recordsLinked to original sources

bioRxiv2026

COSMOS: A FAIR-aligned infrastructure for clinical trial data validation, warehousing, and interactive discovery

1.SummaryThe Clinical Omics System for Metadata and Outcome Storage (COSMOS) is an open-source, FAIR- and GCP aligned clinical trial unit (CTU) infrastructure designed to streamline the transition of academic clinical and multi-omic trial datasets into curated, analysis-ready repositories within Secure Data Environments (SDEs). By integrating an automated Data Quality and Data Validation (DQ&DV) "Trust Layer" with a relational Structured Query Language (SQL) schema, COSMOS enables programmatic and interactive data access via R Shiny applications. Dynamic integration of omics and clinical data is achieved through analytical data structures (e.g. ExpressionSet objects) linked via relational database identifiers. This lowers technical barriers for researchers and promotes governed data reuse and secondary discovery. Availability and ImplementationCOSMOS is freely available under the GPL-3.0 license at https://github.com/at2e19/SCTU_COSMOS_DQDV_Shiny Supplementary information: Supplementary data are available at Bioinformatics online.

bioinformatics↗

bioRxiv2020

ILC1-derived TGFβ1 drives intestinal remodelling

Organoids can shed light on the dynamic interplay between complex tissues and rare cell types within a controlled microenvironment. Here, we developed gut organoid co-cultures with type-1 innate lymphoid cells (ILC1) to dissect the impact of their accumulation in inflamed intestines. We demonstrate for the first time that murine and human ILC1 secrete TGF{beta}1, driving expansion of CD44v6+ epithelial crypts. ILC1 additionally express MMP9 and drive gene signatures indicative of extracellular matrix remodelling. We therefore encapsulated human epithelial-mesenchymal intestinal organoids in MMP-sensitive, synthetic hydrogels designed to form efficient networks at low polymer concentrations. Harnessing this defined system, we demonstrate that ILC1 drive matrix softening and stiffening, which we suggest occurs through balanced matrix degradation and deposition. Our platform enabled us to elucidate previously undescribed interactions between ILC1 and their microenvironment, which suggest that they may exacerbate fibrosis and tumour growth when enriched in inflamed patient tissues.

immunology↗