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10.1177/0271678X16669956 http://scihub22266oqcxt.onion/10.1177/0271678X16669956 C5094316!5094316!27634936     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27634936&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 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       J+Cereb+Blood+Flow+Metab 2016 ; 36 (11): 1865-71 Nephropedia Template TP {{tp|p=27634936|t=2016. Epidermal growth factor prevents oligomeric amyloid-? induced angiogenesis deficits in vitro |pdf=|usr=}}{{27634936}} gab.com Text Epidermal growth factor prevents oligomeric amyloid- induced angiogenesis deficits in vitro JO: J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=27634936 #FOAvip Cerebrovascular dysfunction is a critical component of Alzheimer?s disease (AD) pathogenesis. Oligomeric amyloid-?42 (oA?42) is considered a major contributor to AD progression. However, data are limited on the role of oA?42 in brain endothelial cell vessel degeneration/angiogenesis, including the interaction with angiogenic mediators. Thus, the current study determined the effect of oA?42 on angiogenesis in vitro, utilizing single brain endothelial cell cultures and triple cultures mimicking the microvascular unit (MVU: brain endothelial cells, astrocytes, and pericytes). oA?42 dose-dependently reduced angiogenesis and induced vessel disruption. Critically, epidermal growth factor prevented oA?42-induced deficits, implicating angiogenic pathways as potential therapeutics for AD. Twit Text FOAVip Epidermal growth factor prevents oligomeric amyloid- induced angiogenesis deficits in vitro ????J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=27634936 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27634936 #FOAvip English Wikipedia <ref>{{Cite pmid|27634936}}</ref> Epidermal growth factor prevents oligomeric amyloid-? induced angiogenesis deficits in vitro #MMPMID27634936 Koster KP; Thomas R; Morris AW; Tai LM J Cereb Blood Flow Metab 2016[Nov]; 36 (11): 1865-71 PMID27634936show ga Cerebrovascular dysfunction is a critical component of Alzheimer?s disease (AD) pathogenesis. Oligomeric amyloid-?42 (oA?42) is considered a major contributor to AD progression. However, data are limited on the role of oA?42 in brain endothelial cell vessel degeneration/angiogenesis, including the interaction with angiogenic mediators. Thus, the current study determined the effect of oA?42 on angiogenesis in vitro, utilizing single brain endothelial cell cultures and triple cultures mimicking the microvascular unit (MVU: brain endothelial cells, astrocytes, and pericytes). oA?42 dose-dependently reduced angiogenesis and induced vessel disruption. Critically, epidermal growth factor prevented oA?42-induced deficits, implicating angiogenic pathways as potential therapeutics for AD. äEpidermal growth factor prevents oligomeric amyloid-? induced angiogen(epmc).pdf DeepDyve Pubget Overpricing