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10.1098/rsif.2020.0950 http://scihub22266oqcxt.onion/10.1098/rsif.2020.0950 33593209!8086847!33593209     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       J+R+Soc+Interface 2021 ; 18 (175): 20200950 Nephropedia Template TP {{tp|p=33593209|t=2021. Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19 |pdf=|usr=}}{{33593209}} gab.com Text Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19 JO: J R Soc Interface http://www.kidney.de/pget.php?&tw=1&pmid=33593209 #FOAvip While the pathological mechanisms in COVID-19 illness are still poorly understood, it is increasingly clear that high levels of pro-inflammatory mediators play a major role in clinical deterioration in patients with severe disease. Current evidence points to a hyperinflammatory state as the driver of respiratory compromise in severe COVID-19 disease, with a clinical trajectory resembling acute respiratory distress syndrome, but how this 'runaway train' inflammatory response emerges and is maintained is not known. Here, we present the first mathematical model of lung hyperinflammation due to SARS-CoV-2 infection. This model is based on a network of purported mechanistic and physiological pathways linking together five distinct biochemical species involved in the inflammatory response. Simulations of our model give rise to distinct qualitative classes of COVID-19 patients: (i) individuals who naturally clear the virus, (ii) asymptomatic carriers and (iii-v) individuals who develop a case of mild, moderate, or severe illness. These findings, supported by a comprehensive sensitivity analysis, point to potential therapeutic interventions to prevent the emergence of hyperinflammation. Specifically, we suggest that early intervention with a locally acting anti-inflammatory agent (such as inhaled corticosteroids) may effectively blockade the pathological hyperinflammatory reaction as it emerges. Twit Text FOAVip Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19 ????J R Soc Interface http://www.kidney.de/pget.php?&tw=1&pmid=33593209 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33593209 #FOAvip English Wikipedia <ref>{{Cite pmid|33593209}}</ref> Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19 #MMPMID33593209 Fadai NT; Sachak-Patwa R; Byrne HM; Maini PK; Bafadhel M; Nicolau DV Jr J R Soc Interface 2021[Feb]; 18 (175): 20200950 PMID33593209show ga While the pathological mechanisms in COVID-19 illness are still poorly understood, it is increasingly clear that high levels of pro-inflammatory mediators play a major role in clinical deterioration in patients with severe disease. Current evidence points to a hyperinflammatory state as the driver of respiratory compromise in severe COVID-19 disease, with a clinical trajectory resembling acute respiratory distress syndrome, but how this 'runaway train' inflammatory response emerges and is maintained is not known. Here, we present the first mathematical model of lung hyperinflammation due to SARS-CoV-2 infection. This model is based on a network of purported mechanistic and physiological pathways linking together five distinct biochemical species involved in the inflammatory response. Simulations of our model give rise to distinct qualitative classes of COVID-19 patients: (i) individuals who naturally clear the virus, (ii) asymptomatic carriers and (iii-v) individuals who develop a case of mild, moderate, or severe illness. These findings, supported by a comprehensive sensitivity analysis, point to potential therapeutic interventions to prevent the emergence of hyperinflammation. Specifically, we suggest that early intervention with a locally acting anti-inflammatory agent (such as inhaled corticosteroids) may effectively blockade the pathological hyperinflammatory reaction as it emerges. |Adrenal Cortex Hormones[MESH] |COVID-19/*immunology/*physiopathology[MESH] |Cytokines/immunology[MESH] |Epithelial Cells/*immunology/*virology[MESH] |Epithelium/immunology[MESH] |Humans[MESH] |Inflammation/*immunology[MESH] |Lung/pathology/*physiopathology[MESH] |Models, Immunological[MESH] |Respiratory Distress Syndrome/immunology/physiopathology[MESH]Infection, inflammation and intervention: mechanistic modelling of epi(epmc).pdf DeepDyve Pubget Overpricing