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cs.AI, q-bio.NC updates on arXiv.org
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MedFuse: Multiplicative Embedding Fusion For Irregular Clinical Time Series
arXiv:2511.09247v1 Announce Type: new Abstract: Clinical time series derived from electronic health records (EHRs) are inherently irregular, with asynchronous sampling, missing values, and heterogeneous feature dynamics. While numerical laboratory measurements are highly informative, existing embedding strategies usually combine feature identity and value embeddings through additive operations, which constrains their ability to capture value-dependent feature interactions. We propose MedFuse, a
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(Multiomics OR Omics) AND (Pancreatic)
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Multi-omics analysis of long-term cultured human islets
bioRxiv [Preprint]. 2024 Dec 25:2024.12.25.626491. doi: 10.1101/2024.12.25.626491.ABSTRACTβ-cell dysfunction in pancreatic islets, characterized as either the loss of β-cell mass or the resistance of β-cell to glucose, is the leading cause of progression to diabetes. Islet transplantation became a promising approach to replenish functional β-cell mass. However, not much known about changes in islets used for transplantation after isolation. We have subjected human islets into long-term in vitro
Multi-omics analysis of long-term cultured human islets
bioRxiv [Preprint]. 2024 Dec 25:2024.12.25.626491. doi: 10.1101/2024.12.25.626491.
ABSTRACT
β-cell dysfunction in pancreatic islets, characterized as either the loss of β-cell mass or the resistance of β-cell to glucose, is the leading cause of progression to diabetes. Islet transplantation became a promising approach to replenish functional β-cell mass. However, not much known about changes in islets used for transplantation after isolation. We have subjected human islets into long-term in vitro culture (LTC) and characterized those survived islets. While most of the dysregulated genes were downregulated during LTC, specific groups of mRNA or miRNA were upregulated, and they are involved in specific pathways. In general, α-cells and β-cells of LTC-islets have elevated expressions of MAFB and MAFA genes, respectively. We also found that exocrine cells were eliminated faster than endocrine cells, and β-cells were lost at a higher rate than α-cells. Interestingly, one specific group of cells that have characteristics of immature α-cells or β-cells, were enriched in LTC-islets, revealing the possibility of transdifferentiation of α-cells to β-cells, or dedifferentiation of β-cells to α -cells, under in vitro culture. Our results suggest that there are intrinsic cellular and molecular mechanisms in pancreatic cells that are associated with their maturity and correlated with their survival ability under unfavorable living conditions.
PMID:39763987 | PMC:PMC11703225 | DOI:10.1101/2024.12.25.626491
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Nature - Issue - nature.com science feeds
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Author Correction: π-HuB: the proteomic navigator of the human body
Nature, Published online: 23 December 2024; doi:10.1038/s41586-024-08555-xAuthor Correction: π-HuB: the proteomic navigator of the human body
Author Correction: π-HuB: the proteomic navigator of the human body
Nature, Published online: 23 December 2024; doi:10.1038/s41586-024-08555-x
Author Correction: π-HuB: the proteomic navigator of the human body-
Nature - Issue - nature.com science feeds
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Collagenolysis-dependent DDR1 signalling dictates pancreatic cancer outcome
Nature, Published online: 05 October 2022; doi:10.1038/s41586-022-05169-zCleaved and intact type I collagen have different effects on pancreatic ductal adenocarcinoma (PDAC), and remodelling of type I collagen—mediated through DDR1 signalling—is a prognostic indicator for the survival of patients with PDAC.
Collagenolysis-dependent DDR1 signalling dictates pancreatic cancer outcome
Nature, Published online: 05 October 2022; doi:10.1038/s41586-022-05169-z
Cleaved and intact type I collagen have different effects on pancreatic ductal adenocarcinoma (PDAC), and remodelling of type I collagen—mediated through DDR1 signalling—is a prognostic indicator for the survival of patients with PDAC.