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10.1016/j.smim.2016.03.006 http://scihub22266oqcxt.onion/10.1016/j.smim.2016.03.006 C4987193!4987193 !27021500     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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27021500 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Semin+Immunol 2016 ; 28 (3 ): 285-91 Nephropedia Template TP {{tp|p=27021500 |t=2016. Complement inhibition in pre-clinical models of periodontitis and prospects for clinical application |pdf=|usr=}}{{27021500 }} gab.com Text Complement inhibition in pre-clinical models of periodontitis and prospects for clinical application JO: Semin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27021500 #FOAvip Periodontitis is a dysbiotic inflammatory disease leading to the destruction of the tooth-supporting tissues. Current therapies are not always effective and this prevalent oral disease continues to be a significant health and economic burden. Early clinical studies have associated periodontitis with elevated complement activity. Consistently, subsequent genetic and pharmacological studies in rodents have implicated the central complement component C3 and downstream signaling pathways in periodontal host-microbe interactions that promote dysbiosis and inflammatory bone loss. This review discusses these mechanistic advances and moreover focuses on the compstatin family of C3 inhibitors as a novel approach to treat periodontitis. In this regard, local application of the current lead analog Cp40 was recently shown to block both inducible and naturally occurring periodontitis in non-human primates. These promising results from non-human primate studies and the parallel development of Cp40 for clinical use highlight the feasibility for developing an adjunctive, C3-targeted therapy for human periodontitis. Twit Text FOAVip Complement inhibition in pre-clinical models of periodontitis and prospects for clinical application ????Semin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27021500 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27021500 #FOAvip English Wikipedia <ref>{{Cite pmid|27021500 }}</ref> Complement inhibition in pre-clinical models of periodontitis and prospects for clinical application #MMPMID27021500 Hajishengallis G ; Hajishengallis E ; Kajikawa T ; Wang B ; Yancopoulou D ; Ricklin D ; Lambris JD Semin Immunol 2016[Jun]; 28 (3 ): 285-91 PMID27021500 show ga Periodontitis is a dysbiotic inflammatory disease leading to the destruction of the tooth-supporting tissues. Current therapies are not always effective and this prevalent oral disease continues to be a significant health and economic burden. Early clinical studies have associated periodontitis with elevated complement activity. Consistently, subsequent genetic and pharmacological studies in rodents have implicated the central complement component C3 and downstream signaling pathways in periodontal host-microbe interactions that promote dysbiosis and inflammatory bone loss. This review discusses these mechanistic advances and moreover focuses on the compstatin family of C3 inhibitors as a novel approach to treat periodontitis. In this regard, local application of the current lead analog Cp40 was recently shown to block both inducible and naturally occurring periodontitis in non-human primates. These promising results from non-human primate studies and the parallel development of Cp40 for clinical use highlight the feasibility for developing an adjunctive, C3-targeted therapy for human periodontitis. |Animals [MESH] |Complement C3/metabolism [MESH] |Complement C5/metabolism [MESH] |Complement Inactivating Agents/*therapeutic use [MESH] |Drug Evaluation, Preclinical [MESH] |Dysbiosis/immunology/*therapy [MESH] |Humans [MESH] |Mouth/*immunology/microbiology [MESH] |Periodontitis/immunology/*therapy [MESH] |Primates [MESH] |Pyridones/*therapeutic use [MESH]Complement inhibition in pre-clinical models of periodontitis and pros(epmc).pdf DeepDyve Pubget Overpricing