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. 2021 May 6;11:9703. doi: 10.1038/s41598-021-88936-8

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Workflow leading to a conceptual model of the “chemokine switch”. (Panel A): A schematic of the analysis workflow. Time courses of inflammatory mediators were measured in trauma patients and causal interactions inferred by DyBN analysis. The inferred network topology formed the basis a Boolean model which was simulated in silico. Results were compared to clinical trajectories to refine the model. (Panels B-D): DyBN consensus network structure for Mild, Moderate and Severe Injury. Panel E: Boolean model structure with cross-regulation among chemokines MIG, IP-10, and MCP-1.