Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1080/14728222.2020.1783243 http://scihub22266oqcxt.onion/10.1080/14728222.2020.1783243 32594778!ä!32594778 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       Expert+Opin+Ther+Targets 2020 ; 24 (8): 723-730 Nephropedia Template TP {{tp|p=32594778|t=2020. The cytokine storm of COVID-19: a spotlight on prevention and protection |pdf=|usr=}}{{32594778}} gab.com Text The cytokine storm of COVID-19: a spotlight on prevention and protection JO: Expert Opin Ther Targets http://www.kidney.de/pget.php?&tw=1&pmid=32594778 #FOAvip INTRODUCTION: The cytokine release syndrome (CRS) of COVID-19 is associated with the development of critical illness requiring multi-organ support. Further research is required to halt progression of multi-organ injury induced by hyper-inflammation. AREAS COVERED: PubMed/MEDLINE(TM) databases were accessed between May 9(th)-June 9(th), 2020, to review the latest perspectives on the treatment and pathogenesis of CRS. EXPERT OPINION: Over-activity of chemotaxis triggers a macrophage activation syndrome (MAS) resulting in the release of pro-inflammatory cytokines. IL-6 and TNF- alpha are at the forefront of hyper-inflammation. The inflammatory cascade induces endothelial activation and capillary leak, leading to circulatory collapse and shock. As endothelial dysfunction persists, there is activation of the clotting cascade and microvascular obstruction. Continued endothelial activation results in multi-organ failure, regardless of pulmonary tissue damage. We propose that targeting the endothelium may interrupt this cycle. Immuno-modulating therapies have been suggested, however, further data is necessary to confirm that they do not jeopardize adaptive immunity. Inhibition of IL-6 and the Janus Kinase, signal transducer and activator of transcription proteins pathway (JAK/STAT), are favorable targets. Remote ischemic conditioning (RIC) reduces the inflammation of sepsis in animal models and should be considered as a low risk intervention, in combination with cardiovascular protection. Twit Text FOAVip The cytokine storm of COVID-19: a spotlight on prevention and protection ????Expert Opin Ther Targets http://www.kidney.de/pget.php?&tw=1&pmid=32594778 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32594778 #FOAvip English Wikipedia <ref>{{Cite pmid|32594778}}</ref> The cytokine storm of COVID-19: a spotlight on prevention and protection #MMPMID32594778 Pearce L; Davidson SM; Yellon DM Expert Opin Ther Targets 2020[Aug]; 24 (8): 723-730 PMID32594778show ga INTRODUCTION: The cytokine release syndrome (CRS) of COVID-19 is associated with the development of critical illness requiring multi-organ support. Further research is required to halt progression of multi-organ injury induced by hyper-inflammation. AREAS COVERED: PubMed/MEDLINE(TM) databases were accessed between May 9(th)-June 9(th), 2020, to review the latest perspectives on the treatment and pathogenesis of CRS. EXPERT OPINION: Over-activity of chemotaxis triggers a macrophage activation syndrome (MAS) resulting in the release of pro-inflammatory cytokines. IL-6 and TNF- alpha are at the forefront of hyper-inflammation. The inflammatory cascade induces endothelial activation and capillary leak, leading to circulatory collapse and shock. As endothelial dysfunction persists, there is activation of the clotting cascade and microvascular obstruction. Continued endothelial activation results in multi-organ failure, regardless of pulmonary tissue damage. We propose that targeting the endothelium may interrupt this cycle. Immuno-modulating therapies have been suggested, however, further data is necessary to confirm that they do not jeopardize adaptive immunity. Inhibition of IL-6 and the Janus Kinase, signal transducer and activator of transcription proteins pathway (JAK/STAT), are favorable targets. Remote ischemic conditioning (RIC) reduces the inflammation of sepsis in animal models and should be considered as a low risk intervention, in combination with cardiovascular protection. |*Betacoronavirus/pathogenicity/physiology[MESH] |*Coronavirus Infections/immunology/therapy/virology[MESH] |*Cytokine Release Syndrome/etiology/immunology[MESH] |*Multiple Organ Failure/prevention & control/virology[MESH] |*Pandemics[MESH] |*Pneumonia, Viral/immunology/therapy/virology[MESH] |Animals[MESH] |COVID-19[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Mice[MESH] |Patient Care Management/*methods[MESH] |SARS-CoV-2[MESH]The cytokine storm of COVID-19: a spotlight on prevention and protecti(epmc).pdf DeepDyve Pubget Overpricing