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10.1016/j.heliyon.2021.e07200 http://scihub22266oqcxt.onion/10.1016/j.heliyon.2021.e07200 34095559!8165044!34095559     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Heliyon 2021 ; 7 (6): e07200 Nephropedia Template TP {{tp|p=34095559|t=2021. Ephrin-A1 and the sheddase ADAM12 are upregulated in COVID-19 |pdf=|usr=}}{{34095559}} gab.com Text Ephrin-A1 and the sheddase ADAM12 are upregulated in COVID-19 JO: Heliyon http://www.kidney.de/pget.php?&tw=1&pmid=34095559 #FOAvip More than 3.5 million people have died globally from COVID-19, yet an effective therapy is not available. It is, therefore, important to understand the signaling pathways that mediate disease progression in order to identify new molecular targets for therapeutic development. Here, we report that the blood serum levels of ephrin-A1 and the sheddase ADAM12 were significantly elevated in COVID-19 patients treated at SUNY Downstate Hospital of Brooklyn, New York. Both ephrin-A1 and ADAM12 are known to be involved in inflammation and regulate endothelial cell permeability, thus providing a gateway to lung injury. The clinical outcome correlated with the ephrin-A1 and ADAM12 serum levels during the first week of hospitalization. In contrast, the serum levels of TNFalpha were elevated in only a small subset of the patients, and these same patients also had highly elevated levels of the sheddase ADAM17. These data indicate that ephrin-A1-mediated inflammatory signaling may contribute to COVID-19 disease progression more so than TNFalpha-mediated inflammatory signaling. They also support the notion that, in COVID-19 inflammation, ADAM12 sheds ephrin-A1, while ADAM17 sheds TNFalpha. Furthermore, the results suggest that elevated serum levels and activity of cytokines, such as TNFalpha, and other secreted inflammatory molecules, such as ephrin-A1, are not simply due to overexpression, but also to upregulation of sheddases that release them into the blood circulation. Our results identify ephrin-A1, ADAM12, and other molecules in the ephrin-A1 signaling pathway as potential pharmacological targets for treating COVID-19 inflammation. Twit Text FOAVip Ephrin-A1 and the sheddase ADAM12 are upregulated in COVID-19 ????Heliyon http://www.kidney.de/pget.php?&tw=1&pmid=34095559 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34095559 #FOAvip English Wikipedia <ref>{{Cite pmid|34095559}}</ref> Ephrin-A1 and the sheddase ADAM12 are upregulated in COVID-19 #MMPMID34095559 Mendoza R; Saha N; Momeni A; Gabutan E; Alawad M; Dehghani A; Diks J; Lin B; Wang D; Alshal M; Fyke W; Wang B; Himanen JP; Premsrirut P; Nikolov DB Heliyon 2021[Jun]; 7 (6): e07200 PMID34095559show ga More than 3.5 million people have died globally from COVID-19, yet an effective therapy is not available. It is, therefore, important to understand the signaling pathways that mediate disease progression in order to identify new molecular targets for therapeutic development. Here, we report that the blood serum levels of ephrin-A1 and the sheddase ADAM12 were significantly elevated in COVID-19 patients treated at SUNY Downstate Hospital of Brooklyn, New York. Both ephrin-A1 and ADAM12 are known to be involved in inflammation and regulate endothelial cell permeability, thus providing a gateway to lung injury. The clinical outcome correlated with the ephrin-A1 and ADAM12 serum levels during the first week of hospitalization. In contrast, the serum levels of TNFalpha were elevated in only a small subset of the patients, and these same patients also had highly elevated levels of the sheddase ADAM17. These data indicate that ephrin-A1-mediated inflammatory signaling may contribute to COVID-19 disease progression more so than TNFalpha-mediated inflammatory signaling. They also support the notion that, in COVID-19 inflammation, ADAM12 sheds ephrin-A1, while ADAM17 sheds TNFalpha. Furthermore, the results suggest that elevated serum levels and activity of cytokines, such as TNFalpha, and other secreted inflammatory molecules, such as ephrin-A1, are not simply due to overexpression, but also to upregulation of sheddases that release them into the blood circulation. Our results identify ephrin-A1, ADAM12, and other molecules in the ephrin-A1 signaling pathway as potential pharmacological targets for treating COVID-19 inflammation. äEphrin-A1 and the sheddase ADAM12 are upregulated in COVID-19 (epmc).pdf DeepDyve Pubget Overpricing