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10.1152/ajpregu.00052.2016 http://scihub22266oqcxt.onion/10.1152/ajpregu.00052.2016 C4967235!4967235 !27097659     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27097659 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Regul+Integr+Comp+Physiol 2016 ; 311 (1 ): R1-9 Nephropedia Template TP {{tp|p=27097659 |t=2016. Identifying immune mechanisms mediating the hypertension during preeclampsia |pdf=|usr=}}{{27097659 }} gab.com Text Identifying immune mechanisms mediating the hypertension during preeclampsia JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27097659 #FOAvip Preeclampsia (PE) is a pregnancy-associated disorder that affects 5-8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role. Twit Text FOAVip Identifying immune mechanisms mediating the hypertension during preeclampsia ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27097659 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27097659 #FOAvip English Wikipedia <ref>{{Cite pmid|27097659 }}</ref> Identifying immune mechanisms mediating the hypertension during preeclampsia #MMPMID27097659 LaMarca B ; Cornelius DC ; Harmon AC ; Amaral LM ; Cunningham MW ; Faulkner JL ; Wallace K Am J Physiol Regul Integr Comp Physiol 2016[Jul]; 311 (1 ): R1-9 PMID27097659 show ga Preeclampsia (PE) is a pregnancy-associated disorder that affects 5-8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role. |Adult [MESH] |Female [MESH] |Humans [MESH] |Hypertension, Pregnancy-Induced/*immunology/physiopathology [MESH] |Pre-Eclampsia/*immunology/physiopathology [MESH] |Pregnancy [MESH]Identifying immune mechanisms mediating the hypertension during preecl(epmc).pdf DeepDyve Pubget Overpricing