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10.1186/2051-5960-2-53 http://scihub22266oqcxt.onion/10.1186/2051-5960-2-53 C4048455!4048455!24887075     free     free     free 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       Acta+Neuropathol+Commun 2014 ; 2 (ä): ä Nephropedia Template TP {{tp|p=24887075|t=2014. Complement activation in multiple sclerosis plaques: an immunohistochemical analysis |pdf=|usr=}}{{24887075}} gab.com Text Complement activation in multiple sclerosis plaques: an immunohistochemical analysis JO: Acta Neuropathol Commun http://www.kidney.de/pget.php?&tw=1&pmid=24887075 #FOAvip Introduction: Inflammation and complement activation are firmly implicated in the pathology of multiple sclerosis; however, the extent and nature of their involvement in specific pathological processes such as axonal damage, myelin loss and disease progression remains uncertain. This study aims to bring clarity to these questions. Results: We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive multiple sclerosis and 16 control donors, including 9 with central nervous system disease. Active, chronic active and chronic inactive multiple sclerosis plaques (35 in total) and non-plaque areas were examined.Multiple sclerosis plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, terminal complement complex) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite the absence of other evidence of ongoing inflammation. Complement staining was most apparent in plaque and peri-plaque but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. C1q staining was present in all plaques suggesting a dominant role for the classical pathway. Cellular staining for complement components was largely restricted to reactive astrocytes, often adjacent to clusters of microglia in close apposition to complement opsonised myelin and damaged axons. Conclusions: The findings demonstrate the ubiquity of complement involvement in multiple sclerosis, suggest a pathogenic role for complement contributing to cell, axon and myelin damage and make the case for targeting complement for multiple sclerosis monitoring and therapy. Electronic supplementary material: The online version of this article (doi:10.1186/2051-5960-2-53) contains supplementary material, which is available to authorized users. Twit Text FOAVip Complement activation in multiple sclerosis plaques: an immunohistochemical analysis ????Acta Neuropathol Commun http://www.kidney.de/pget.php?&tw=1&pmid=24887075 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24887075 #FOAvip English Wikipedia <ref>{{Cite pmid|24887075}}</ref> Complement activation in multiple sclerosis plaques: an immunohistochemical analysis #MMPMID24887075 Ingram G; Loveless S; Howell OW; Hakobyan S; Dancey B; Harris CL; Robertson NP; Neal JW; Morgan BP Acta Neuropathol Commun 2014[]; 2 (ä): ä PMID24887075show ga Introduction: Inflammation and complement activation are firmly implicated in the pathology of multiple sclerosis; however, the extent and nature of their involvement in specific pathological processes such as axonal damage, myelin loss and disease progression remains uncertain. This study aims to bring clarity to these questions. Results: We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive multiple sclerosis and 16 control donors, including 9 with central nervous system disease. Active, chronic active and chronic inactive multiple sclerosis plaques (35 in total) and non-plaque areas were examined.Multiple sclerosis plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, terminal complement complex) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite the absence of other evidence of ongoing inflammation. Complement staining was most apparent in plaque and peri-plaque but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. C1q staining was present in all plaques suggesting a dominant role for the classical pathway. Cellular staining for complement components was largely restricted to reactive astrocytes, often adjacent to clusters of microglia in close apposition to complement opsonised myelin and damaged axons. Conclusions: The findings demonstrate the ubiquity of complement involvement in multiple sclerosis, suggest a pathogenic role for complement contributing to cell, axon and myelin damage and make the case for targeting complement for multiple sclerosis monitoring and therapy. Electronic supplementary material: The online version of this article (doi:10.1186/2051-5960-2-53) contains supplementary material, which is available to authorized users. äComplement activation in multiple sclerosis plaques: an immunohistoche(epmc).pdf DeepDyve Pubget Overpricing