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10.1016/j.imlet.2021.09.005 http://scihub22266oqcxt.onion/10.1016/j.imlet.2021.09.005 34562551!8457906!34562551     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunol+Lett 2021 ; 240 (ä): 1-8 Nephropedia Template TP {{tp|p=34562551|t=2021. Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-19 patients |pdf=|usr=}}{{34562551}} gab.com Text Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-19 patients JO: Immunol Lett http://www.kidney.de/pget.php?&tw=1&pmid=34562551 #FOAvip Some COVID-19 patients suffer complications from anti-viral immune responses which can lead to both a dangerous cytokine storm and development of blood-borne factors that render severe thrombotic events more likely. The precise immune response profile is likely, therefore, to determine and predict patient outcomes and also represents a target for intervention. Anti-viral T cell exhaustion in the early stages is associated with disease progression. Dysregulation of T cell functions, which precedes cytokine storm development and neutrophil expansion in alveolar tissues heralds damaging pathology.T cell function, cytokine production and factors that attract neutrophils to the lung can be modified through targeting molecules that can modulate T cell responses. Manipulating T cell responses by targeting the PI3K/Akt/mTOR pathway could provide the means to control the immune response in COVID-19 patients. During the initial anti-viral response, T cell effector function can be enhanced by delaying anti-viral exhaustion through inhibiting PI3K and Akt. Additionally, immune dysregulation can be addressed by enhancing immune suppressor functions by targeting downstream mTOR, an important intracellular modulator of cellular metabolism. Targeting this signalling pathway also has potential to prevent formation of thrombi due to its role in platelet activation. Furthermore, this signalling pathway is essential for SARS-cov-2 virus replication in host cells and its inhibition could, therefore, reduce viral load. The ultimate goal is to identify targets that can quickly control the immune response in COVID-19 patients to improve patient outcome. Targeting different levels of the PI3K/Akt/mTOR signalling pathway could potentially achieve this during each stage of the disease. Twit Text FOAVip Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-19 patients ????Immunol Lett http://www.kidney.de/pget.php?&tw=1&pmid=34562551 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34562551 #FOAvip English Wikipedia <ref>{{Cite pmid|34562551}}</ref> Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-19 patients #MMPMID34562551 Abu-Eid R; Ward FJ Immunol Lett 2021[Dec]; 240 (ä): 1-8 PMID34562551show ga Some COVID-19 patients suffer complications from anti-viral immune responses which can lead to both a dangerous cytokine storm and development of blood-borne factors that render severe thrombotic events more likely. The precise immune response profile is likely, therefore, to determine and predict patient outcomes and also represents a target for intervention. Anti-viral T cell exhaustion in the early stages is associated with disease progression. Dysregulation of T cell functions, which precedes cytokine storm development and neutrophil expansion in alveolar tissues heralds damaging pathology.T cell function, cytokine production and factors that attract neutrophils to the lung can be modified through targeting molecules that can modulate T cell responses. Manipulating T cell responses by targeting the PI3K/Akt/mTOR pathway could provide the means to control the immune response in COVID-19 patients. During the initial anti-viral response, T cell effector function can be enhanced by delaying anti-viral exhaustion through inhibiting PI3K and Akt. Additionally, immune dysregulation can be addressed by enhancing immune suppressor functions by targeting downstream mTOR, an important intracellular modulator of cellular metabolism. Targeting this signalling pathway also has potential to prevent formation of thrombi due to its role in platelet activation. Furthermore, this signalling pathway is essential for SARS-cov-2 virus replication in host cells and its inhibition could, therefore, reduce viral load. The ultimate goal is to identify targets that can quickly control the immune response in COVID-19 patients to improve patient outcome. Targeting different levels of the PI3K/Akt/mTOR signalling pathway could potentially achieve this during each stage of the disease. |*COVID-19 Drug Treatment[MESH] |Animals[MESH] |COVID-19/enzymology/immunology/virology[MESH] |Fibrinolytic Agents/therapeutic use[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |MTOR Inhibitors/therapeutic use[MESH] |Molecular Targeted Therapy[MESH] |Phosphatidylinositol 3-Kinase/*metabolism[MESH] |Phosphoinositide-3 Kinase Inhibitors/therapeutic use[MESH] |Proto-Oncogene Proteins c-akt/*metabolism[MESH] |SARS-CoV-2/immunology/*pathogenicity[MESH] |TOR Serine-Threonine Kinases/*metabolism[MESH]Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-1(epmc).pdf DeepDyve Pubget Overpricing