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10.1152/ajprenal.00177.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00177.2014 C4101625!4101625!24829504     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 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 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2014 ; 307 (2): F183-94 Nephropedia Template TP {{tp|p=24829504|t=2014. Semaphorin 3A inactivation suppresses ischemia-reperfusion-induced inflammation and acute kidney injury |pdf=|usr=}}{{24829504}} gab.com Text Semaphorin 3A inactivation suppresses ischemia-reperfusion-induced inflammation and acute kidney injury JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24829504 #FOAvip Recent studies show that guidance molecules that are known to regulate cell migration during development may also play an important role in adult pathophysiologic states. One such molecule, semaphorin3A (sema3A), is highly expressed after acute kidney injury (AKI) in mice and humans, but its pathophysiological role is unknown. Genetic inactivation of sema3A protected mice from ischemia-reperfusion-induced AKI, improved tissue histology, reduced neutrophil infiltration, prevented epithelial cell apoptosis, and increased cytokine and chemokine excretion in urine. Pharmacological-based inhibition of sema3A receptor binding likewise protected against ischemia-reperfusion-induced AKI. In vitro, sema3A enhanced toll-like receptor 4-mediated inflammation in epithelial cells, macrophages, and dendritic cells. Moreover, administration of sema3A-treated, bone marrow-derived dendritic cells exacerbated kidney injury. Finally, sema3A augmented cisplatin-induced apoptosis in kidney epithelial cells in vitro via expression of DFFA-like effector a (cidea). Our data suggest that the guidance molecule sema3A exacerbates AKI via promoting inflammation and epithelial cell apoptosis. Twit Text FOAVip Semaphorin 3A inactivation suppresses ischemia-reperfusion-induced inflammation and acute kidney injury ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24829504 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24829504 #FOAvip English Wikipedia <ref>{{Cite pmid|24829504}}</ref> Semaphorin 3A inactivation suppresses ischemia-reperfusion-induced inflammation and acute kidney injury #MMPMID24829504 Ranganathan P; Jayakumar C; Mohamed R; Weintraub NL; Ramesh G Am J Physiol Renal Physiol 2014[Jul]; 307 (2): F183-94 PMID24829504show ga Recent studies show that guidance molecules that are known to regulate cell migration during development may also play an important role in adult pathophysiologic states. One such molecule, semaphorin3A (sema3A), is highly expressed after acute kidney injury (AKI) in mice and humans, but its pathophysiological role is unknown. Genetic inactivation of sema3A protected mice from ischemia-reperfusion-induced AKI, improved tissue histology, reduced neutrophil infiltration, prevented epithelial cell apoptosis, and increased cytokine and chemokine excretion in urine. Pharmacological-based inhibition of sema3A receptor binding likewise protected against ischemia-reperfusion-induced AKI. In vitro, sema3A enhanced toll-like receptor 4-mediated inflammation in epithelial cells, macrophages, and dendritic cells. Moreover, administration of sema3A-treated, bone marrow-derived dendritic cells exacerbated kidney injury. Finally, sema3A augmented cisplatin-induced apoptosis in kidney epithelial cells in vitro via expression of DFFA-like effector a (cidea). Our data suggest that the guidance molecule sema3A exacerbates AKI via promoting inflammation and epithelial cell apoptosis. äSemaphorin 3A inactivation suppresses ischemia-reperfusion-induced inf(epmc).pdf DeepDyve Pubget Overpricing