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10.1186/s40635-016-0109-y http://scihub22266oqcxt.onion/10.1186/s40635-016-0109-y C5099302!5099302!27822777     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27822777&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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Intensive+Care+Med+Exp 2016 ; 4 (ä): ä Nephropedia Template TP {{tp|p=27822777|t=2016. Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis |pdf=|usr=}}{{27822777}} gab.com Text Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis JO: Intensive Care Med Exp http://www.kidney.de/pget.php?&tw=1&pmid=27822777 #FOAvip Background: Histamine assumes an important role as a major mediator in various pathologic disorders associated with inflammation and immune reactions. However, the involvement of histamine in the pathological conditions and symptoms of sepsis remains entirely unknown. In this study, we establish that histamine is identified as a contributory mediator to promoting the development of organ injury in sepsis. Methods: Histidine decarboxylase (HDC) gene knockout (HDC?/?) mice, histamine H1-/H2-receptor gene-double knockout (H1R?/?/H2R?/?) mice, and their littermate wild-type (WT) C57BL/6J mice underwent cecal ligation and puncture (CLP) or sham operation. Some WT mice were injected intraperitoneally with d-chlorpheniramine and famotidine 60 min before CLP to block H1- and H2-receptors, respectively. Results: In mice rendered septic by CLP, tissue histamine levels were elevated in association with increased HDC expression. Sepsis-induced abnormal cytokine production and multiple organ injury (lung, liver, and kidney) were significantly less pronounced in HDC?/? mice as compared with WT controls, and HDC deficiency had improved survival in sepsis. This benefit corresponded with a significant reduction in activation levels of the nuclear factor (NF)-?B signaling pathway. H1R?/?/H2R?/? mice apparently behaved similar to HDC knockout mice in reducing sepsis-related pathological changes. Pharmacological interventions with H1- and H2-receptor antagonists indicated that both H1- and H2-receptors were involved in septic lung and liver injury, whereas only H2-receptors contributed to septic kidney injury. Conclusions: In the setting of sepsis, histamine, through activation of H1- and H2-receptors, serves as an aggravating mediator to contribute to the development of sepsis-driven major end-organ failure. Electronic supplementary material: The online version of this article (doi:10.1186/s40635-016-0109-y) contains supplementary material, which is available to authorized users. Twit Text FOAVip Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis ????Intensive Care Med Exp http://www.kidney.de/pget.php?&tw=1&pmid=27822777 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27822777 #FOAvip English Wikipedia <ref>{{Cite pmid|27822777}}</ref> Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis #MMPMID27822777 Hattori M; Yamazaki M; Ohashi W; Tanaka S; Hattori K; Todoroki K; Fujimori T; Ohtsu H; Matsuda N; Hattori Y Intensive Care Med Exp 2016[Dec]; 4 (ä): ä PMID27822777show ga Background: Histamine assumes an important role as a major mediator in various pathologic disorders associated with inflammation and immune reactions. However, the involvement of histamine in the pathological conditions and symptoms of sepsis remains entirely unknown. In this study, we establish that histamine is identified as a contributory mediator to promoting the development of organ injury in sepsis. Methods: Histidine decarboxylase (HDC) gene knockout (HDC?/?) mice, histamine H1-/H2-receptor gene-double knockout (H1R?/?/H2R?/?) mice, and their littermate wild-type (WT) C57BL/6J mice underwent cecal ligation and puncture (CLP) or sham operation. Some WT mice were injected intraperitoneally with d-chlorpheniramine and famotidine 60 min before CLP to block H1- and H2-receptors, respectively. Results: In mice rendered septic by CLP, tissue histamine levels were elevated in association with increased HDC expression. Sepsis-induced abnormal cytokine production and multiple organ injury (lung, liver, and kidney) were significantly less pronounced in HDC?/? mice as compared with WT controls, and HDC deficiency had improved survival in sepsis. This benefit corresponded with a significant reduction in activation levels of the nuclear factor (NF)-?B signaling pathway. H1R?/?/H2R?/? mice apparently behaved similar to HDC knockout mice in reducing sepsis-related pathological changes. Pharmacological interventions with H1- and H2-receptor antagonists indicated that both H1- and H2-receptors were involved in septic lung and liver injury, whereas only H2-receptors contributed to septic kidney injury. Conclusions: In the setting of sepsis, histamine, through activation of H1- and H2-receptors, serves as an aggravating mediator to contribute to the development of sepsis-driven major end-organ failure. Electronic supplementary material: The online version of this article (doi:10.1186/s40635-016-0109-y) contains supplementary material, which is available to authorized users. äCritical role of endogenous histamine in promoting end-organ tissue in(epmc).pdf DeepDyve Pubget Overpricing