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10.14814/phy2.12257 http://scihub22266oqcxt.onion/10.14814/phy2.12257 C4387753!4387753!25602015     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Physiol+Rep 2015 ; 3 (1): ä Nephropedia Template TP {{tp|p=25602015|t=2015. Pregnant mice lacking indoleamine 2,3?dioxygenase exhibit preeclampsia phenotypes |pdf=|usr=}}{{25602015}} gab.com Text Pregnant mice lacking indoleamine 2,3 dioxygenase exhibit preeclampsia phenotypes JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=25602015 #FOAvip Preeclampsia is a cardiovascular disorder of late pregnancy that is, commonly characterized by hypertension, renal structural damage and dysfunction, and fetal growth restriction. Prevailing etiologic models of this disorder include T?cell dysfunction as an initiating cause of preeclampsia. Indoleamine 2,3?dioxygenase (IDO), an enzyme that mediates the conversion of tryptophan to kynurenine, has been linked to preeclampsia in humans, and is known to regulate T?cell activity and an endothelial?derived relaxing factor. To test the hypothesis that IDO is causally involved in the pathogenesis of preeclampsia, mice deficient for IDO (IDO?KO) were generated on a C57BL/6 background. IDO?KO and wild?type C57BL/6 mice were bred, and preeclampsia phenotypes were evaluated during pregnancy. Pregnant IDO?KO mice exhibited pathognomonic renal glomerular endotheliosis, proteinuria, pregnancy?specific endothelial dysfunction, intrauterine growth restriction, and mildly elevated blood pressure compared to wild?type mice. Together these findings highlight an important role for IDO in the generation of phenotypes typical of preeclampsia. Loss of IDO function may represent a risk factor for the development of preeclampsia. By extension, increased IDO activity, reductions in IDO reactants, or increases in IDO products may represent novel therapeutic approaches for this disorder. Twit Text FOAVip Pregnant mice lacking indoleamine 2,3 dioxygenase exhibit preeclampsia phenotypes ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=25602015 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25602015 #FOAvip English Wikipedia <ref>{{Cite pmid|25602015}}</ref> Pregnant mice lacking indoleamine 2,3?dioxygenase exhibit preeclampsia phenotypes #MMPMID25602015 Santillan MK; Pelham CJ; Ketsawatsomkron P; Santillan DA; Davis DR; Devor EJ; Gibson?Corley KN; Scroggins SM; Grobe JL; Yang B; Hunter SK; Sigmund CD Physiol Rep 2015[Jan]; 3 (1): ä PMID25602015show ga Preeclampsia is a cardiovascular disorder of late pregnancy that is, commonly characterized by hypertension, renal structural damage and dysfunction, and fetal growth restriction. Prevailing etiologic models of this disorder include T?cell dysfunction as an initiating cause of preeclampsia. Indoleamine 2,3?dioxygenase (IDO), an enzyme that mediates the conversion of tryptophan to kynurenine, has been linked to preeclampsia in humans, and is known to regulate T?cell activity and an endothelial?derived relaxing factor. To test the hypothesis that IDO is causally involved in the pathogenesis of preeclampsia, mice deficient for IDO (IDO?KO) were generated on a C57BL/6 background. IDO?KO and wild?type C57BL/6 mice were bred, and preeclampsia phenotypes were evaluated during pregnancy. Pregnant IDO?KO mice exhibited pathognomonic renal glomerular endotheliosis, proteinuria, pregnancy?specific endothelial dysfunction, intrauterine growth restriction, and mildly elevated blood pressure compared to wild?type mice. Together these findings highlight an important role for IDO in the generation of phenotypes typical of preeclampsia. Loss of IDO function may represent a risk factor for the development of preeclampsia. By extension, increased IDO activity, reductions in IDO reactants, or increases in IDO products may represent novel therapeutic approaches for this disorder. äPregnant mice lacking indoleamine 2,3?dioxygenase exhibit preeclampsia(epmc).pdf DeepDyve Pubget Overpricing