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10.2176/nmc.ra.2014-0337 http://scihub22266oqcxt.onion/10.2176/nmc.ra.2014-0337 C4533330!4533330!25761423     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Neurol+Med+Chir+(Tokyo) 2015 ; 55 (3): 214-29 Nephropedia Template TP {{tp|p=25761423|t=2015. Molecular Mechanisms of the Formation and Progression of Intracranial Aneurysms |pdf=|usr=}}{{25761423}} gab.com Text Molecular Mechanisms of the Formation and Progression of Intracranial Aneurysms JO: Neurol Med Chir (Tokyo) http://www.kidney.de/pget.php?&tw=1&pmid=25761423 #FOAvip Until recently, only a little was understood about molecular mechanisms of the development of an intracranial aneurysm (IA). Recent advancements over the last decade in the field of genetics and molecular biology have provided us a wide variety of evidences supporting the notion that chronic inflammation is closely associated with the pathogenesis of IA development. In the field of genetics, large-scale Genome-wide association studies (GWAS) has identified some IA susceptible loci and genes related to cell cycle and endothelial function. Researches in molecular biology using human samples and animal models have revealed the common pathway of the initiation, progression, and rupture of IAs. IA formation begins with endothelial dysfunction followed by pathological remodeling with degenerative changes of vascular walls. Medical treatments inhibiting inflammatory cascades in IA development are likely to prevent IA progression and rupture. Statins and aspirin are expected to suppress IA progression by their anti-inflammatory effects. Decoy oligodeoxynucleotides (ODNs) inhibiting inflammatory transcription factors such as nuclear factor kappa-B (NF-?B) and Ets-1 are the other promising choice of the prevention of IA development. Further clarification of molecular mechanisms of the formation and progression of IAs will shed light to the pathogenesis of IA development and provide insight into novel diagnostic and therapeutic strategies for IAs. Twit Text FOAVip Molecular Mechanisms of the Formation and Progression of Intracranial Aneurysms ????Neurol Med Chir (Tokyo) http://www.kidney.de/pget.php?&tw=1&pmid=25761423 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25761423 #FOAvip English Wikipedia <ref>{{Cite pmid|25761423}}</ref> Molecular Mechanisms of the Formation and Progression of Intracranial Aneurysms #MMPMID25761423 KATAOKA H Neurol Med Chir (Tokyo) 2015[Mar]; 55 (3): 214-29 PMID25761423show ga Until recently, only a little was understood about molecular mechanisms of the development of an intracranial aneurysm (IA). Recent advancements over the last decade in the field of genetics and molecular biology have provided us a wide variety of evidences supporting the notion that chronic inflammation is closely associated with the pathogenesis of IA development. In the field of genetics, large-scale Genome-wide association studies (GWAS) has identified some IA susceptible loci and genes related to cell cycle and endothelial function. Researches in molecular biology using human samples and animal models have revealed the common pathway of the initiation, progression, and rupture of IAs. IA formation begins with endothelial dysfunction followed by pathological remodeling with degenerative changes of vascular walls. Medical treatments inhibiting inflammatory cascades in IA development are likely to prevent IA progression and rupture. Statins and aspirin are expected to suppress IA progression by their anti-inflammatory effects. Decoy oligodeoxynucleotides (ODNs) inhibiting inflammatory transcription factors such as nuclear factor kappa-B (NF-?B) and Ets-1 are the other promising choice of the prevention of IA development. Further clarification of molecular mechanisms of the formation and progression of IAs will shed light to the pathogenesis of IA development and provide insight into novel diagnostic and therapeutic strategies for IAs. äMolecular Mechanisms of the Formation and Progression of Intracranial (epmc).pdf DeepDyve Pubget Overpricing