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10.1101/2020.09.02.280180 http://scihub22266oqcxt.onion/10.1101/2020.09.02.280180 32908980!7480031!32908980     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32908980&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       bioRxiv 2020 ; ä (ä): ä Nephropedia Template TP {{tp|p=32908980|t=2020. Induction of a regulatory myeloid program in bacterial sepsis and severe COVID-19 |pdf=|usr=}}{{32908980}} gab.com Text Induction of a regulatory myeloid program in bacterial sepsis and severe COVID-19 JO: bioRxiv http://www.kidney.de/pget.php?&tw=1&pmid=32908980 #FOAvip A recent estimate suggests that one in five deaths globally are associated with sepsis (1) . To date, no targeted treatment is available for this syndrome, likely due to substantial patient heterogeneity (2,3) and our lack of insight into sepsis immunopathology (4) . These issues are highlighted by the current COVID-19 pandemic, wherein many clinical manifestations of severe SARS-CoV-2 infection parallel bacterial sepsis (5-8) . We previously reported an expanded CD14+ monocyte state, MS1, in patients with bacterial sepsis or non-infectious critical illness, and validated its expansion in sepsis across thousands of patients using public transcriptomic data (9) . Despite its marked expansion in the circulation of bacterial sepsis patients, its relevance to viral sepsis and association with disease outcomes have not been examined. In addition, the ontogeny and function of this monocyte state remain poorly characterized. Using public transcriptomic data, we show that the expression of the MS1 program is associated with sepsis mortality and is up-regulated in monocytes from patients with severe COVID-19. We found that blood plasma from bacterial sepsis or COVID-19 patients with severe disease induces emergency myelopoiesis and expression of the MS1 program, which are dependent on the cytokines IL-6 and IL-10. Finally, we demonstrate that MS1 cells are broadly immunosuppressive, similar to monocytic myeloid-derived suppressor cells (MDSCs), and have decreased responsiveness to stimulation. Our findings highlight the utility of regulatory myeloid cells in sepsis prognosis, and the role of systemic cytokines in inducing emergency myelopoiesis during severe bacterial and SARS-CoV-2 infections. Twit Text FOAVip Induction of a regulatory myeloid program in bacterial sepsis and severe COVID-19 ????bioRxiv http://www.kidney.de/pget.php?&tw=1&pmid=32908980 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32908980 #FOAvip English Wikipedia <ref>{{Cite pmid|32908980}}</ref> Induction of a regulatory myeloid program in bacterial sepsis and severe COVID-19 #MMPMID32908980 Reyes M; Filbin MR; Bhattacharyya RP; Sonny A; Mehta A; Billman K; Kays KR; Pinilla-Vera M; Benson ME; Cosimi LA; Hung DT; Levy BD; Villani AC; Sade-Feldman M; Baron RM; Goldberg MB; Blainey PC; Hacohen N bioRxiv 2020[Sep]; ä (ä): ä PMID32908980show ga A recent estimate suggests that one in five deaths globally are associated with sepsis (1) . To date, no targeted treatment is available for this syndrome, likely due to substantial patient heterogeneity (2,3) and our lack of insight into sepsis immunopathology (4) . These issues are highlighted by the current COVID-19 pandemic, wherein many clinical manifestations of severe SARS-CoV-2 infection parallel bacterial sepsis (5-8) . We previously reported an expanded CD14+ monocyte state, MS1, in patients with bacterial sepsis or non-infectious critical illness, and validated its expansion in sepsis across thousands of patients using public transcriptomic data (9) . Despite its marked expansion in the circulation of bacterial sepsis patients, its relevance to viral sepsis and association with disease outcomes have not been examined. In addition, the ontogeny and function of this monocyte state remain poorly characterized. Using public transcriptomic data, we show that the expression of the MS1 program is associated with sepsis mortality and is up-regulated in monocytes from patients with severe COVID-19. We found that blood plasma from bacterial sepsis or COVID-19 patients with severe disease induces emergency myelopoiesis and expression of the MS1 program, which are dependent on the cytokines IL-6 and IL-10. Finally, we demonstrate that MS1 cells are broadly immunosuppressive, similar to monocytic myeloid-derived suppressor cells (MDSCs), and have decreased responsiveness to stimulation. Our findings highlight the utility of regulatory myeloid cells in sepsis prognosis, and the role of systemic cytokines in inducing emergency myelopoiesis during severe bacterial and SARS-CoV-2 infections. äInduction of a regulatory myeloid program in bacterial sepsis and seve(epmc).pdf DeepDyve Pubget Overpricing