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10.1038/jcbfm.2014.154 http://scihub22266oqcxt.onion/10.1038/jcbfm.2014.154 C4269762!4269762!25160671     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cereb+Blood+Flow+Metab 2014 ; 34 (11): 1837-47 Nephropedia Template TP {{tp|p=25160671|t=2014. Bilirubin and its oxidation products damage brain white matter |pdf=|usr=}}{{25160671}} gab.com Text Bilirubin and its oxidation products damage brain white matter JO: J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=25160671 #FOAvip Brain injury after intracerebral hemorrhage (ICH) occurs in cortex and white matter and may be mediated by blood breakdown products, including hemoglobin and heme. Effects of blood breakdown products, bilirubin and bilirubin oxidation products, have not been widely investigated in adult brain. Here, we first determined the effect of bilirubin and its oxidation products on the structure and function of white matter in vitro using brain slices. Subsequently, we determined whether these compounds have an effect on the structure and function of white matter in vivo. In all, 0.5?mmol/L bilirubin treatment significantly damaged both the function and the structure of myelinated axons but not the unmyelinated axons in brain slices. Toxicity of bilirubin in vitro was prevented by dimethyl sulfoxide. Bilirubin oxidation products (BOXes) may be responsible for the toxicity of bilirubin. In in vivo experiments, unmyelinated axons were found more susceptible to damage from bilirubin injection. These results suggest that unmyelinated axons may have a major role in white-matter damage in vivo. Since bilirubin and BOXes appear in a delayed manner after ICH, preventing their toxic effects may be worth investigating therapeutically. Dimethyl sulfoxide or its structurally related derivatives may have a potential therapeutic value at antagonizing axonal damage after hemorrhagic stroke. Twit Text FOAVip Bilirubin and its oxidation products damage brain white matter ????J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=25160671 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25160671 #FOAvip English Wikipedia <ref>{{Cite pmid|25160671}}</ref> Bilirubin and its oxidation products damage brain white matter #MMPMID25160671 Lakovic K; Ai J; D'Abbondanza J; Tariq A; Sabri M; Alarfaj AK; Vasdev P; Macdonald RL J Cereb Blood Flow Metab 2014[Nov]; 34 (11): 1837-47 PMID25160671show ga Brain injury after intracerebral hemorrhage (ICH) occurs in cortex and white matter and may be mediated by blood breakdown products, including hemoglobin and heme. Effects of blood breakdown products, bilirubin and bilirubin oxidation products, have not been widely investigated in adult brain. Here, we first determined the effect of bilirubin and its oxidation products on the structure and function of white matter in vitro using brain slices. Subsequently, we determined whether these compounds have an effect on the structure and function of white matter in vivo. In all, 0.5?mmol/L bilirubin treatment significantly damaged both the function and the structure of myelinated axons but not the unmyelinated axons in brain slices. Toxicity of bilirubin in vitro was prevented by dimethyl sulfoxide. Bilirubin oxidation products (BOXes) may be responsible for the toxicity of bilirubin. In in vivo experiments, unmyelinated axons were found more susceptible to damage from bilirubin injection. These results suggest that unmyelinated axons may have a major role in white-matter damage in vivo. Since bilirubin and BOXes appear in a delayed manner after ICH, preventing their toxic effects may be worth investigating therapeutically. Dimethyl sulfoxide or its structurally related derivatives may have a potential therapeutic value at antagonizing axonal damage after hemorrhagic stroke. äBilirubin and its oxidation products damage brain white matter (epmc).pdf DeepDyve Pubget Overpricing