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10.1007/s00467-013-2590-9 http://scihub22266oqcxt.onion/10.1007/s00467-013-2590-9 C3925758!3925758!23949631     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Pediatr+Nephrol 2014 ; 29 (4): 537-41 Nephropedia Template TP {{tp|p=23949631|t=2014. Responses of Proximal Tubular Cells to Injury in Congenital Renal Disease: Fight or Flight |pdf=|usr=}}{{23949631}} gab.com Text Responses of Proximal Tubular Cells to Injury in Congenital Renal Disease: Fight or Flight JO: Pediatr Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=23949631 #FOAvip Most chronic kidney disease in children results from congenital or inherited disorders, which can be studied in mouse models. Following 2 weeks of unilateral ureteral obstruction (UUO) in the adult mouse, nephron loss is due to proximal tubular mitochondrial injury and cell death. In neonatal mice, proximal tubular cell death is delayed beyond 2 weeks of complete UUO, and release of partial UUO allows remodeling of remaining nephrons. Progressive cyst expansion develops in polycystic kidney disease (PKD), a common inherited renal disorder. The PCY mutant mouse (which develops late-onset PKD) develops thinning of the glomerulotubular junction in parallel with growth of cysts in adulthood. Renal insufficiency in nephropathic cystinosis, a rare inherited renal disorder, results from progressive tubular cystine accumulation. In the Ctns knock out mouse (a model of cystinosis), proximal tubular cells become flattened, with loss of mitochondria and thickening of tubular basement membrane. In each model, persistent obstructive or metabolic stress leads ultimately to the formation of atubular glomeruli. The initial ?fight? response (proximal tubular survival) switches to a ?flight? response (proximal tubular cell death) with ongoing oxidative injury and mitochondrial damage. Therapies should be directed at reducing proximal tubular mitochondrial oxidative injury to enhance repair and regeneration. Twit Text FOAVip Responses of Proximal Tubular Cells to Injury in Congenital Renal Disease: Fight or Flight ????Pediatr Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=23949631 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23949631 #FOAvip English Wikipedia <ref>{{Cite pmid|23949631}}</ref> Responses of Proximal Tubular Cells to Injury in Congenital Renal Disease: Fight or Flight #MMPMID23949631 Chevalier RL; Forbes MS; Galarreta CI; Thornhill BA Pediatr Nephrol 2014[Apr]; 29 (4): 537-41 PMID23949631show ga Most chronic kidney disease in children results from congenital or inherited disorders, which can be studied in mouse models. Following 2 weeks of unilateral ureteral obstruction (UUO) in the adult mouse, nephron loss is due to proximal tubular mitochondrial injury and cell death. In neonatal mice, proximal tubular cell death is delayed beyond 2 weeks of complete UUO, and release of partial UUO allows remodeling of remaining nephrons. Progressive cyst expansion develops in polycystic kidney disease (PKD), a common inherited renal disorder. The PCY mutant mouse (which develops late-onset PKD) develops thinning of the glomerulotubular junction in parallel with growth of cysts in adulthood. Renal insufficiency in nephropathic cystinosis, a rare inherited renal disorder, results from progressive tubular cystine accumulation. In the Ctns knock out mouse (a model of cystinosis), proximal tubular cells become flattened, with loss of mitochondria and thickening of tubular basement membrane. In each model, persistent obstructive or metabolic stress leads ultimately to the formation of atubular glomeruli. The initial ?fight? response (proximal tubular survival) switches to a ?flight? response (proximal tubular cell death) with ongoing oxidative injury and mitochondrial damage. Therapies should be directed at reducing proximal tubular mitochondrial oxidative injury to enhance repair and regeneration. äResponses of Proximal Tubular Cells to Injury in Congenital Renal Dise(epmc).pdf DeepDyve Pubget Overpricing