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10.1016/j.jceh.2014.07.006 http://scihub22266oqcxt.onion/10.1016/j.jceh.2014.07.006 C4442850!4442850!26041953     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Exp+Hepatol 2015 ; 5 (Suppl 1): S21-8 Nephropedia Template TP {{tp|p=26041953|t=2015. Neuroinflammation in Hepatic Encephalopathy: Mechanistic Aspects |pdf=|usr=}}{{26041953}} gab.com Text Neuroinflammation in Hepatic Encephalopathy: Mechanistic Aspects JO: J Clin Exp Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26041953 #FOAvip Hepatic encephalopathy (HE) is a major neurological complication of severe liver disease that presents in acute and chronic forms. While elevated brain ammonia level is known to be a major etiological factor in this disorder, recent studies have shown a significant role of neuroinflammation in the pathogenesis of both acute and chronic HE. This review summarizes the involvement of ammonia in the activation of microglia, as well as the means by which ammonia triggers inflammatory responses in these cells. Additionally, the role of ammonia in stimulating inflammatory events in brain endothelial cells (ECs), likely through the activation of the toll-like receptor-4 and the associated production of cytokines, as well as the stimulation of various inflammatory factors in ECs and in astrocytes, are discussed. This review also summarizes the inflammatory mechanisms by which activation of ECs and microglia impact on astrocytes leading to their dysfunction, ultimately contributing to astrocyte swelling/brain edema in acute HE. The role of microglial activation and its contribution to the progression of neurobehavioral abnormalities in chronic HE are also briefly presented. We posit that a better understanding of the inflammatory events associated with acute and chronic HE will uncover novel therapeutic targets useful in the treatment of patients afflicted with HE. Twit Text FOAVip Neuroinflammation in Hepatic Encephalopathy: Mechanistic Aspects ????J Clin Exp Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26041953 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26041953 #FOAvip English Wikipedia <ref>{{Cite pmid|26041953}}</ref> Neuroinflammation in Hepatic Encephalopathy: Mechanistic Aspects #MMPMID26041953 Jayakumar AR; Rama Rao KV; Norenberg MD J Clin Exp Hepatol 2015[Mar]; 5 (Suppl 1): S21-8 PMID26041953show ga Hepatic encephalopathy (HE) is a major neurological complication of severe liver disease that presents in acute and chronic forms. While elevated brain ammonia level is known to be a major etiological factor in this disorder, recent studies have shown a significant role of neuroinflammation in the pathogenesis of both acute and chronic HE. This review summarizes the involvement of ammonia in the activation of microglia, as well as the means by which ammonia triggers inflammatory responses in these cells. Additionally, the role of ammonia in stimulating inflammatory events in brain endothelial cells (ECs), likely through the activation of the toll-like receptor-4 and the associated production of cytokines, as well as the stimulation of various inflammatory factors in ECs and in astrocytes, are discussed. This review also summarizes the inflammatory mechanisms by which activation of ECs and microglia impact on astrocytes leading to their dysfunction, ultimately contributing to astrocyte swelling/brain edema in acute HE. The role of microglial activation and its contribution to the progression of neurobehavioral abnormalities in chronic HE are also briefly presented. We posit that a better understanding of the inflammatory events associated with acute and chronic HE will uncover novel therapeutic targets useful in the treatment of patients afflicted with HE. äNeuroinflammation in Hepatic Encephalopathy: Mechanistic Aspects (epmc).pdf DeepDyve Pubget Overpricing