Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1186/s40673-017-0073-7 http://scihub22266oqcxt.onion/10.1186/s40673-017-0073-7 C5609024!5609024!28944066     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cerebellum+Ataxias 2017 ; 4 (ä): ä Nephropedia Template TP {{tp|p=28944066|t=2017. Immune-mediated cerebellar ataxias: from bench to bedside |pdf=|usr=}}{{28944066}} gab.com Text Immune-mediated cerebellar ataxias: from bench to bedside JO: Cerebellum Ataxias http://www.kidney.de/pget.php?&tw=1&pmid=28944066 #FOAvip The cerebellum is a vulnerable target of autoimmunity in the CNS. The category of immune-mediated cerebellar ataxias (IMCAs) was recently established, and includes in particular paraneoplastic cerebellar degenerations (PCDs), gluten ataxia (GA) and anti-GAD65 antibody (Ab) associated-CA, all characterized by the presence of autoantibodies. The significance of onconeuronal autoantibodies remains uncertain in some cases. The pathogenic role of anti-GAD65Ab has been established both in vitro and in vivo, but a consensus has not been reached yet. Recent studies of anti-GAD65 Ab-associated CA have clarified that (1) autoantibodies are generally polyclonal and elicit pathogenic effects related to epitope specificity, and (2) the clinical course can be divided into two phases: a phase of functional disorder followed by cell death. These features provide the rationale for prompt diagnosis and therapeutic strategies. The concept ?Time is brain? has been completely underestimated in the field of immune ataxias. We now put forward the concept ?Time is cerebellum? to underline the importance of very early therapeutic strategies in order to prevent or stop the loss of neurons and synapses. The diagnosis of IMCAs should depend not only on Ab testing, but rather on a rapid and comprehensive assessment of the clinical/immune profile. Treatment should be applied during the period of preserved cerebellar reserve, and should encompass early removal of the conditions (such as remote primary tumors) or diseases that trigger the autoimmunity, followed by the combinations of various immunotherapies. Twit Text FOAVip Immune-mediated cerebellar ataxias: from bench to bedside ????Cerebellum Ataxias http://www.kidney.de/pget.php?&tw=1&pmid=28944066 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28944066 #FOAvip English Wikipedia <ref>{{Cite pmid|28944066}}</ref> Immune-mediated cerebellar ataxias: from bench to bedside #MMPMID28944066 Mitoma H; Manto M; Hampe CS Cerebellum Ataxias 2017[]; 4 (ä): ä PMID28944066show ga The cerebellum is a vulnerable target of autoimmunity in the CNS. The category of immune-mediated cerebellar ataxias (IMCAs) was recently established, and includes in particular paraneoplastic cerebellar degenerations (PCDs), gluten ataxia (GA) and anti-GAD65 antibody (Ab) associated-CA, all characterized by the presence of autoantibodies. The significance of onconeuronal autoantibodies remains uncertain in some cases. The pathogenic role of anti-GAD65Ab has been established both in vitro and in vivo, but a consensus has not been reached yet. Recent studies of anti-GAD65 Ab-associated CA have clarified that (1) autoantibodies are generally polyclonal and elicit pathogenic effects related to epitope specificity, and (2) the clinical course can be divided into two phases: a phase of functional disorder followed by cell death. These features provide the rationale for prompt diagnosis and therapeutic strategies. The concept ?Time is brain? has been completely underestimated in the field of immune ataxias. We now put forward the concept ?Time is cerebellum? to underline the importance of very early therapeutic strategies in order to prevent or stop the loss of neurons and synapses. The diagnosis of IMCAs should depend not only on Ab testing, but rather on a rapid and comprehensive assessment of the clinical/immune profile. Treatment should be applied during the period of preserved cerebellar reserve, and should encompass early removal of the conditions (such as remote primary tumors) or diseases that trigger the autoimmunity, followed by the combinations of various immunotherapies. äImmune-mediated cerebellar ataxias: from bench to bedside (epmc).pdf DeepDyve Pubget Overpricing