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10.3892/br.2017.966 http://scihub22266oqcxt.onion/10.3892/br.2017.966 C5590038!5590038 !28928970     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28928970 &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 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 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\28928970 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Biomed+Rep 2017 ; 7 (4 ): 325-330 Nephropedia Template TP {{tp|p=28928970 |t=2017. The role of hyperuricemia on vascular endothelium dysfunction |pdf=|usr=}}{{28928970 }} gab.com Text The role of hyperuricemia on vascular endothelium dysfunction JO: Biomed Rep http://www.kidney.de/pget.php?&tw=1&pmid=28928970 #FOAvip Hyperuricemia appears to be associated with an increased risk for cardiovascular disease and associated mortality. Population epidemiological data support a causal link between hyperuricemia and cardiovascular disease. Endothelium injury could be one of the potential mechanisms in hyperuricemia-induced cardiovascular disease. However, the specific role of uric acid (UA) in the impairment of vascular relaxation and its signal transduction pathway has not been examined. The authors investigated the role of UA on vascular relaxation, nitric oxide (NO) production and expression of proinflammatory cytokines. Brachial flow-mediated dilation and nitroglycerine-mediated dilation were measured by B-mode ultrasound with 10 megahertz linear-array transducer from 21 patients with hyperuricemia and 16 control subjects. Human umbilical vein endothelial cells (ECs) were incubated with UA (5-15 mg/dl) with or without nuclear factor (NF)-?B inhibitor II. Hyperuricemia inhibited brachial flow-mediated dilation. While UA significantly inhibited NO expression with time course- and dose- dependent manner in the cultured ECs, 10 mg/dl UA also increased expression of inflammation cytokine interleukin (IL)-6, IL-8 and tumor necrosis factor-? in vitro. These abnormalities were associated with UA-induced activation of transcription factor NF-?B. Furthermore, NF-?B inhibitor II prevented UA-induced reduction of NO and increased inflammation cytokines. These data suggested hyperuricemia-induced endothelium injury and vascular dysfunction by a reduction of NO and expression of inflammatory cytokines through the NF-?B pathway. Twit Text FOAVip The role of hyperuricemia on vascular endothelium dysfunction ????Biomed Rep http://www.kidney.de/pget.php?&tw=1&pmid=28928970 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28928970 #FOAvip English Wikipedia <ref>{{Cite pmid|28928970 }}</ref> The role of hyperuricemia on vascular endothelium dysfunction #MMPMID28928970 Zhen H ; Gui F Biomed Rep 2017[Oct]; 7 (4 ): 325-330 PMID28928970 show ga Hyperuricemia appears to be associated with an increased risk for cardiovascular disease and associated mortality. Population epidemiological data support a causal link between hyperuricemia and cardiovascular disease. Endothelium injury could be one of the potential mechanisms in hyperuricemia-induced cardiovascular disease. However, the specific role of uric acid (UA) in the impairment of vascular relaxation and its signal transduction pathway has not been examined. The authors investigated the role of UA on vascular relaxation, nitric oxide (NO) production and expression of proinflammatory cytokines. Brachial flow-mediated dilation and nitroglycerine-mediated dilation were measured by B-mode ultrasound with 10 megahertz linear-array transducer from 21 patients with hyperuricemia and 16 control subjects. Human umbilical vein endothelial cells (ECs) were incubated with UA (5-15 mg/dl) with or without nuclear factor (NF)-?B inhibitor II. Hyperuricemia inhibited brachial flow-mediated dilation. While UA significantly inhibited NO expression with time course- and dose- dependent manner in the cultured ECs, 10 mg/dl UA also increased expression of inflammation cytokine interleukin (IL)-6, IL-8 and tumor necrosis factor-? in vitro. These abnormalities were associated with UA-induced activation of transcription factor NF-?B. Furthermore, NF-?B inhibitor II prevented UA-induced reduction of NO and increased inflammation cytokines. These data suggested hyperuricemia-induced endothelium injury and vascular dysfunction by a reduction of NO and expression of inflammatory cytokines through the NF-?B pathway. äThe role of hyperuricemia on vascular endothelium dysfunction (epmc).pdf DeepDyve Pubget Overpricing