36 research outputs found

    Multi-agent architecture for waste minimisation in beef supply chain

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    Food waste is an alarming issue pertaining to the rising global hunger, huge environmental footprint, and high monetary value. In developing and developed nations, it occurs primarily due to inefficiencies upstream and downstream of the supply chain respectively. A common factor in both developed and developing nations is product flow within the supply chain from farms to retailers. This study aims to identify the root causes of waste generated across the product flow of the beef supply chain from farm to retailer. A workshop involving twenty practitioners of the beef industry was conducted and the collected information was transcribed and coded to generate a current reality tree, which assisted in identifying root causes of waste in the entire beef supply chain. A multi-agent architecture framework spanning the entire beef supply chain from farm to retailer is proposed, which is composed of autonomous agents capable of bringing all segments of the beef industry on a single platform and collaboratively assist them in mitigating root causes of waste. The proposed framework will aid the practitioners in the beef industry to reduce waste, improve their operational efficiency thereby raising food security, economic development whilst curbing their carbon footprint

    Metabolic re-wiring of isogenic breast epithelial cell lines following epithelial to mesenchymal transition.

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    To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked FilesEpithelial to mesenchymal transition (EMT) has implications in tumor progression and metastasis. Metabolic alterations have been described in cancer development but studies focused on the metabolic re-wiring that takes place during EMT are still limited. We performed metabolomics profiling of a breast epithelial cell line and its EMT derived mesenchymal phenotype to create genome-scale metabolic models descriptive of both cell lines. Glycolysis and OXPHOS were higher in the epithelial phenotype while amino acid anaplerosis and fatty acid oxidation fueled the mesenchymal phenotype. Through comparative bioinformatics analysis, PPAR-γ1, PPAR- γ2 and AP-1 were found to be the most influential transcription factors associated with metabolic re-wiring. In silico gene essentiality analysis predicts that the LAT1 neutral amino acid transporter is essential for mesenchymal cell survival. Our results define metabolic traits that distinguish an EMT derived mesenchymal cell line from its epithelial progenitor and may have implications in cancer progression and metastasis. Furthermore, the tools presented here can aid in identifying critical metabolic nodes that may serve as therapeutic targets aiming to prevent EMT and inhibit metastatic dissemination.Icelandic Research Counci

    EGFR Signal-Network Reconstruction Demonstrates Metabolic Crosstalk in EMT.

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    To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.Epithelial to mesenchymal transition (EMT) is an important event during development and cancer metastasis. There is limited understanding of the metabolic alterations that give rise to and take place during EMT. Dysregulation of signalling pathways that impact metabolism, including epidermal growth factor receptor (EGFR), are however a hallmark of EMT and metastasis. In this study, we report the investigation into EGFR signalling and metabolic crosstalk of EMT through constraint-based modelling and analysis of the breast epithelial EMT cell model D492 and its mesenchymal counterpart D492M. We built an EGFR signalling network for EMT based on stoichiometric coefficients and constrained the network with gene expression data to build epithelial (EGFR_E) and mesenchymal (EGFR_M) networks. Metabolic alterations arising from differential expression of EGFR genes was derived from a literature review of AKT regulated metabolic genes. Signaling flux differences between EGFR_E and EGFR_M models subsequently allowed metabolism in D492 and D492M cells to be assessed. Higher flux within AKT pathway in the D492 cells compared to D492M suggested higher glycolytic activity in D492 that we confirmed experimentally through measurements of glucose uptake and lactate secretion rates. The signaling genes from the AKT, RAS/MAPK and CaM pathways were predicted to revert D492M to D492 phenotype. Follow-up analysis of EGFR signaling metabolic crosstalk in three additional breast epithelial cell lines highlighted variability in in vitro cell models of EMT. This study shows that the metabolic phenotype may be predicted by in silico analyses of gene expression data of EGFR signaling genes, but this phenomenon is cell-specific and does not follow a simple trend.Icelandic Research Fund (RANNIS) 130591-051 152358-051 152369-05
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