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10.1371/journal.pcbi.1004460 http://scihub22266oqcxt.onion/10.1371/journal.pcbi.1004460 C4669096!4669096!26633296     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Comput+Biol 2015 ; 11 (12): ä Nephropedia Template TP {{tp|p=26633296|t=2015. Computational Identification of Mechanistic Factors That Determine the Timing and Intensity of the Inflammatory Response |pdf=|usr=}}{{26633296}} gab.com Text Computational Identification of Mechanistic Factors That Determine the Timing and Intensity of the Inflammatory Response JO: PLoS Comput Biol http://www.kidney.de/pget.php?&tw=1&pmid=26633296 #FOAvip Timely resolution of inflammation is critical for the restoration of homeostasis in injured or infected tissue. Chronic inflammation is often characterized by a persistent increase in the concentrations of inflammatory cells and molecular mediators, whose distinct amount and timing characteristics offer an opportunity to identify effective therapeutic regulatory targets. Here, we used our recently developed computational model of local inflammation to identify potential targets for molecular interventions and to investigate the effects of individual and combined inhibition of such targets. This was accomplished via the development and application of computational strategies involving the simulation and analysis of thousands of inflammatory scenarios. We found that modulation of macrophage influx and efflux is an effective potential strategy to regulate the amount of inflammatory cells and molecular mediators in both normal and chronic inflammatory scenarios. We identified three molecular mediators ? tumor necrosis factor-? (TNF-?), transforming growth factor-? (TGF-?), and the chemokine CXCL8 ? as potential molecular targets whose individual or combined inhibition may robustly regulate both the amount and timing properties of the kinetic trajectories for neutrophils and macrophages in chronic inflammation. Modulation of macrophage flux, as well as of the abundance of TNF-?, TGF-?, and CXCL8, may improve the resolution of chronic inflammation. Twit Text FOAVip Computational Identification of Mechanistic Factors That Determine the Timing and Intensity of the Inflammatory Response ????PLoS Comput Biol http://www.kidney.de/pget.php?&tw=1&pmid=26633296 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26633296 #FOAvip English Wikipedia <ref>{{Cite pmid|26633296}}</ref> Computational Identification of Mechanistic Factors That Determine the Timing and Intensity of the Inflammatory Response #MMPMID26633296 Nagaraja S; Reifman J; Mitrophanov AY PLoS Comput Biol 2015[Dec]; 11 (12): ä PMID26633296show ga Timely resolution of inflammation is critical for the restoration of homeostasis in injured or infected tissue. Chronic inflammation is often characterized by a persistent increase in the concentrations of inflammatory cells and molecular mediators, whose distinct amount and timing characteristics offer an opportunity to identify effective therapeutic regulatory targets. Here, we used our recently developed computational model of local inflammation to identify potential targets for molecular interventions and to investigate the effects of individual and combined inhibition of such targets. This was accomplished via the development and application of computational strategies involving the simulation and analysis of thousands of inflammatory scenarios. We found that modulation of macrophage influx and efflux is an effective potential strategy to regulate the amount of inflammatory cells and molecular mediators in both normal and chronic inflammatory scenarios. We identified three molecular mediators ? tumor necrosis factor-? (TNF-?), transforming growth factor-? (TGF-?), and the chemokine CXCL8 ? as potential molecular targets whose individual or combined inhibition may robustly regulate both the amount and timing properties of the kinetic trajectories for neutrophils and macrophages in chronic inflammation. Modulation of macrophage flux, as well as of the abundance of TNF-?, TGF-?, and CXCL8, may improve the resolution of chronic inflammation. äComputational Identification of Mechanistic Factors That Determine the(epmc).pdf DeepDyve Pubget Overpricing