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10.1080/08916934.2018.1442442 http://scihub22266oqcxt.onion/10.1080/08916934.2018.1442442 C6036904!6036904 !29471675     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29471675 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 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\29471675 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Autoimmunity 2018 ; 51 (2 ): 53-61 Nephropedia Template TP {{tp|p=29471675 |t=2018. Alterations in nucleotide-binding oligomerization domain-2 expression, pathway activation, and cytokine production in Yao syndrome |pdf=|usr=}}{{29471675 }} gab.com Text Alterations in nucleotide-binding oligomerization domain-2 expression, pathway activation, and cytokine production in Yao syndrome JO: Autoimmunity http://www.kidney.de/pget.php?&tw=1&pmid=29471675 #FOAvip Yao syndrome (YAOS) is a systemic autoinflammatory disease (SAID), formerly termed nucleotide-binding oligomerization domain-2 (NOD2)-associated autoinflammatory disease. Due to the recent identification of YAOS, the molecular mechanisms underlying its disease pathogenesis are unclear. With specific NOD2 variants as characteristic genotypic features of YAOS, our study examined NOD2 expression, transcript splicing, signaling pathway activation, and cytokine profiles in peripheral blood mononuclear cells (PBMCs) from 10 YAOS patients and six healthy individuals. All participants were genotyped for NOD2 variants; all YAOS patients were heterozygous for the NOD2 IVS8(+158) variant (IVS8(+158)) and four patients also carried a concurrent NOD2 R702W variant (IVS8(+158)/R702W haplotype). Resembling other SAIDs, plasma levels of TNF?, IL-1?, IL-6, IFN?, and S100A12 were unaltered in YAOS patients. Intron-8 splicing of NOD2 transcripts was unaffected by carriage of NOD2 IVS8(+158). However, NOD2 transcript level and basal p38 mitogen-activated protein kinase (MAPK) activity were significantly elevated in PBMCs from IVS8(+158) YAOS patients. Moreover, these patients' cells had elevated basal IL-6 secretion that was enhanced by muramyl dipeptide (MDP) stimulation. Tocilizumab treatment of a YAOS IVS8(+158) patient resulted in marked clinical improvement. In contrast, MDP-stimulated NF-?B activity was uniquely suppressed in haplotype IVS8(+158)/R702W patients, as was TNF? secretion. Our study demonstrates for the first time that NOD2 expression and pathway activation are aberrant in YAOS, and specific NOD2 genotypes result in distinct NOD2 expression and cytokine profiles. These findings may also help select therapeutic strategies in the future. Twit Text FOAVip Alterations in nucleotide-binding oligomerization domain-2 expression, pathway activation, and cytokine production in Yao syndrome ????Autoimmunity http://www.kidney.de/pget.php?&tw=1&pmid=29471675 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29471675 #FOAvip English Wikipedia <ref>{{Cite pmid|29471675 }}</ref> Alterations in nucleotide-binding oligomerization domain-2 expression, pathway activation, and cytokine production in Yao syndrome #MMPMID29471675 McDonald C ; Shen M ; Johnson EE ; Kabi A ; Yao Q Autoimmunity 2018[Mar]; 51 (2 ): 53-61 PMID29471675 show ga Yao syndrome (YAOS) is a systemic autoinflammatory disease (SAID), formerly termed nucleotide-binding oligomerization domain-2 (NOD2)-associated autoinflammatory disease. Due to the recent identification of YAOS, the molecular mechanisms underlying its disease pathogenesis are unclear. With specific NOD2 variants as characteristic genotypic features of YAOS, our study examined NOD2 expression, transcript splicing, signaling pathway activation, and cytokine profiles in peripheral blood mononuclear cells (PBMCs) from 10 YAOS patients and six healthy individuals. All participants were genotyped for NOD2 variants; all YAOS patients were heterozygous for the NOD2 IVS8(+158) variant (IVS8(+158)) and four patients also carried a concurrent NOD2 R702W variant (IVS8(+158)/R702W haplotype). Resembling other SAIDs, plasma levels of TNF?, IL-1?, IL-6, IFN?, and S100A12 were unaltered in YAOS patients. Intron-8 splicing of NOD2 transcripts was unaffected by carriage of NOD2 IVS8(+158). However, NOD2 transcript level and basal p38 mitogen-activated protein kinase (MAPK) activity were significantly elevated in PBMCs from IVS8(+158) YAOS patients. Moreover, these patients' cells had elevated basal IL-6 secretion that was enhanced by muramyl dipeptide (MDP) stimulation. Tocilizumab treatment of a YAOS IVS8(+158) patient resulted in marked clinical improvement. In contrast, MDP-stimulated NF-?B activity was uniquely suppressed in haplotype IVS8(+158)/R702W patients, as was TNF? secretion. Our study demonstrates for the first time that NOD2 expression and pathway activation are aberrant in YAOS, and specific NOD2 genotypes result in distinct NOD2 expression and cytokine profiles. These findings may also help select therapeutic strategies in the future. |Adult [MESH] |Aged [MESH] |Antibodies, Monoclonal, Humanized/therapeutic use [MESH] |Cytokines/*blood [MESH] |Female [MESH] |Genetic Predisposition to Disease/*genetics [MESH] |Hereditary Autoinflammatory Diseases/drug therapy/*genetics/pathology [MESH] |Humans [MESH] |Interleukin-6/metabolism [MESH] |Leukocytes, Mononuclear/immunology [MESH] |Male [MESH] |Middle Aged [MESH] |Nod2 Signaling Adaptor Protein/*genetics [MESH] |Signal Transduction/genetics/immunology [MESH] |Young Adult [MESH]Alterations in nucleotide-binding oligomerization domain-2 expression,(epmc).pdf DeepDyve Pubget Overpricing