<HashMap><database>bioimages</database><scores/><additional><omics_type>Unknown</omics_type><submitter/><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-BIAD1024</full_dataset_link><repository>bioimages</repository><figure_sub>Specimen</figure_sub><figure_sub>Image analysis</figure_sub><figure_sub>Study Component</figure_sub><figure_sub>organisation</figure_sub><figure_sub>Biosample</figure_sub><figure_sub>Image correlation</figure_sub><figure_sub>Associations</figure_sub><figure_sub>Image acquisition</figure_sub><pubmed_authors>Richard Benninger</pubmed_authors></additional><is_claimable>false</is_claimable><name>Beta-cell Intrinsic Dynamics Rather than Gap Junction Structure Dictates Subpopulations in the Islet Functional Network</name><description>Diabetes is caused by the inability of electrically coupled, functionally heterogeneous β-cells within the pancreatic islet to provide adequate insulin secretion. Functional networks have been used to represent synchronized oscillatory [Ca2+] dynamics and to study β-cell subpopulations, which play an important role in driving islet function. The mechanism by which highly synchronized β-cell subpopulations drive islet function is unclear. We used experimental and computational techniques to investigate the relationship between functional networks, structural (gap-junction) networks, and intrinsic β-cell dynamics in slow and fast oscillating islets. Highly synchronized subpopulations in the functional network were differentiated by intrinsic dynamics, including metabolic activity and KATP ch</description><dates><release>2024-01-22T00:00:00Z</release><modification>2024-02-15T23:28:06.967Z</modification><creation>2024-01-19T16:09:56.877Z</creation></dates><accession>S-BIAD1024</accession><cross_references/></HashMap>