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10.1080/08923973.2021.1925293 http://scihub22266oqcxt.onion/10.1080/08923973.2021.1925293 34015982!8146296!34015982     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunopharmacol+Immunotoxicol 2021 ; 43 (3): 247-258 Nephropedia Template TP {{tp|p=34015982|t=2021. Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19 |pdf=|usr=}}{{34015982}} gab.com Text Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19 JO: Immunopharmacol Immunotoxicol http://www.kidney.de/pget.php?&tw=1&pmid=34015982 #FOAvip SARS-CoV-2 is a type of beta-CoV that develops acute pneumonia, which is an inflammatory condition. A cytokine storm has been recognized as one of the leading causes of death in patients with COVID-19. ALI and ARDS along with multiple organ failure have also been presented as the consequences of acute inflammation and cytokine storm. It has been previously confirmed that SARS-CoV, as another member of the beta-CoV family, activates NLRP3 inflammasome and consequently develops acute inflammation in a variety of ways through having complex interactions with the host immune system using structural and nonstructural proteins. Numerous studies conducted on Tranilast have further demonstrated that the given drug can act as an effective anti-chemotactic factor on controlling inflammation, and thus, it can possibly help the improvement of the acute form of COVID-19 by inhibiting some key inflammation-associated transcription factors such as NF-kappaB and impeding NLRP3 inflammasome. Several studies have comparably revealed the direct effect of this drug on the prevention of inappropriate tissue's remodeling; inhibition of neutrophils, IL-5, and eosinophils; repression of inflammatory cell infiltration into inflammation site; restriction of factors involved in acute airway inflammation like IL-33; and suppression of cytokine IL-13, which increase mucosal secretions. Therefore, Tranilast may be considered as a potential treatment for patients with the acute form of COVID-19 along with other drugs. Twit Text FOAVip Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19 ????Immunopharmacol Immunotoxicol http://www.kidney.de/pget.php?&tw=1&pmid=34015982 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34015982 #FOAvip English Wikipedia <ref>{{Cite pmid|34015982}}</ref> Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19 #MMPMID34015982 Saeedi-Boroujeni A; Mahmoudian-Sani MR; Nashibi R; Houshmandfar S; Tahmaseby Gandomkari S; Khodadadi A Immunopharmacol Immunotoxicol 2021[Jun]; 43 (3): 247-258 PMID34015982show ga SARS-CoV-2 is a type of beta-CoV that develops acute pneumonia, which is an inflammatory condition. A cytokine storm has been recognized as one of the leading causes of death in patients with COVID-19. ALI and ARDS along with multiple organ failure have also been presented as the consequences of acute inflammation and cytokine storm. It has been previously confirmed that SARS-CoV, as another member of the beta-CoV family, activates NLRP3 inflammasome and consequently develops acute inflammation in a variety of ways through having complex interactions with the host immune system using structural and nonstructural proteins. Numerous studies conducted on Tranilast have further demonstrated that the given drug can act as an effective anti-chemotactic factor on controlling inflammation, and thus, it can possibly help the improvement of the acute form of COVID-19 by inhibiting some key inflammation-associated transcription factors such as NF-kappaB and impeding NLRP3 inflammasome. Several studies have comparably revealed the direct effect of this drug on the prevention of inappropriate tissue's remodeling; inhibition of neutrophils, IL-5, and eosinophils; repression of inflammatory cell infiltration into inflammation site; restriction of factors involved in acute airway inflammation like IL-33; and suppression of cytokine IL-13, which increase mucosal secretions. Therefore, Tranilast may be considered as a potential treatment for patients with the acute form of COVID-19 along with other drugs. |*COVID-19 Drug Treatment[MESH] |Anti-Inflammatory Agents/*therapeutic use[MESH] |COVID-19/immunology/pathology[MESH] |Humans[MESH] |Inflammasomes/*immunology[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/*immunology[MESH] |SARS-CoV-2/*immunology[MESH]Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibi(epmc).pdf DeepDyve Pubget Overpricing