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10.3389/fimmu.2018.01511 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.01511 C6036179!6036179!30013565     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       Front+Immunol 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=30013565|t=2018. Chronic Critical Illness and the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome |pdf=|usr=}}{{30013565}} gab.com Text Chronic Critical Illness and the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=30013565 #FOAvip Dysregulated host immune responses to infection often occur, leading to sepsis, multiple organ failure, and death. Some patients rapidly recover from sepsis, but many develop chronic critical illness (CCI), a debilitating condition that impacts functional outcomes and long-term survival. The ?Persistent Inflammation, Immunosuppression, and Catabolism Syndrome? (PICS) has been postulated as the underlying pathophysiology of CCI. We propose that PICS is initiated by an early genomic and cytokine storm in response to microbial invasion during the early phase of sepsis. However, once source control, antimicrobial coverage, and supportive therapies have been initiated, we propose that the persistent inflammation in patients developing CCI is a result of ongoing endogenous alarmin release from damaged organs and loss of muscle mass. This ongoing alarmin and danger-associated molecular pattern signaling causes chronic inflammation and a shift in bone marrow stem cell production toward myeloid cells, contributing to chronic anemia and lymphopenia. We propose that therapeutic interventions must target the chronic organ injury and lean tissue wasting that contribute to the release of endogenous alarmins and the expansion and deposition of myeloid progenitors that are responsible for the propagation and persistence of CCI. Twit Text FOAVip Chronic Critical Illness and the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=30013565 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30013565 #FOAvip English Wikipedia <ref>{{Cite pmid|30013565}}</ref> Chronic Critical Illness and the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome #MMPMID30013565 Hawkins RB; Raymond SL; Stortz JA; Horiguchi H; Brakenridge SC; Gardner A; Efron PA; Bihorac A; Segal M; Moore FA; Moldawer LL Front Immunol 2018[]; 9 (ä): ä PMID30013565show ga Dysregulated host immune responses to infection often occur, leading to sepsis, multiple organ failure, and death. Some patients rapidly recover from sepsis, but many develop chronic critical illness (CCI), a debilitating condition that impacts functional outcomes and long-term survival. The ?Persistent Inflammation, Immunosuppression, and Catabolism Syndrome? (PICS) has been postulated as the underlying pathophysiology of CCI. We propose that PICS is initiated by an early genomic and cytokine storm in response to microbial invasion during the early phase of sepsis. However, once source control, antimicrobial coverage, and supportive therapies have been initiated, we propose that the persistent inflammation in patients developing CCI is a result of ongoing endogenous alarmin release from damaged organs and loss of muscle mass. This ongoing alarmin and danger-associated molecular pattern signaling causes chronic inflammation and a shift in bone marrow stem cell production toward myeloid cells, contributing to chronic anemia and lymphopenia. We propose that therapeutic interventions must target the chronic organ injury and lean tissue wasting that contribute to the release of endogenous alarmins and the expansion and deposition of myeloid progenitors that are responsible for the propagation and persistence of CCI. äChronic Critical Illness and the Persistent Inflammation, Immunosuppre(epmc).pdf DeepDyve Pubget Overpricing