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10.3389/fendo.2015.00095 http://scihub22266oqcxt.onion/10.3389/fendo.2015.00095 C4464054!4464054!26124749     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       Front+Endocrinol+(Lausanne) 2015 ; 6 (ä): ä Nephropedia Template TP {{tp|p=26124749|t=2015. Molecular and Cellular Mechanisms of Aldosterone Producing Adenoma Development |pdf=|usr=}}{{26124749}} gab.com Text Molecular and Cellular Mechanisms of Aldosterone Producing Adenoma Development JO: Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=26124749 #FOAvip Primary aldosteronism (PA) is the most common form of secondary hypertension with an estimated prevalence of ~10% in referred patients. PA occurs as a result of a dysregulation of the normal mechanisms controlling adrenal aldosterone production. It is characterized by hypertension with low plasma renin and elevated aldosterone and often associated with hypokalemia. The two major causes of PA are unilateral aldosterone producing adenoma (APA) and bilateral adrenal hyperplasia, accounting together for ~95% of cases. In addition to the well-characterized effect of excess mineralocorticoids on blood pressure, high levels of aldosterone also have cardiovascular, renal, and metabolic consequences. Hence, long-term consequences of PA include increased risk of coronary artery disease, myocardial infarction, heart failure, and atrial fibrillation. Despite recent progress in the management of patients with PA, critical issues related to diagnosis, subtype differentiation, and treatment of non-surgically correctable forms still persist. A better understanding of the pathogenic mechanisms of the disease should lead to the identification of more reliable diagnostic and prognostic biomarkers for a more sensitive and specific screening and new therapeutic options. In this review, we will summarize our current knowledge on the molecular and cellular mechanisms of APA development. On one hand, we will discuss how various animal models have improved our understanding of the pathophysiology of excess aldosterone production. On the other hand, we will summarize the major advances made during the last few years in the genetics of APA due to transcriptomic studies and whole exome sequencing. The identification of recurrent and somatic mutations in genes coding for ion channels (KCNJ5 and CACNA1D) and ATPases (ATP1A1 and ATP2B3) allowed highlighting the central role of calcium signaling in autonomous aldosterone production by the adrenal. Twit Text FOAVip Molecular and Cellular Mechanisms of Aldosterone Producing Adenoma Development ????Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=26124749 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26124749 #FOAvip English Wikipedia <ref>{{Cite pmid|26124749}}</ref> Molecular and Cellular Mechanisms of Aldosterone Producing Adenoma Development #MMPMID26124749 Boulkroun S; Fernandes-Rosa FL; Zennaro MC Front Endocrinol (Lausanne) 2015[]; 6 (ä): ä PMID26124749show ga Primary aldosteronism (PA) is the most common form of secondary hypertension with an estimated prevalence of ~10% in referred patients. PA occurs as a result of a dysregulation of the normal mechanisms controlling adrenal aldosterone production. It is characterized by hypertension with low plasma renin and elevated aldosterone and often associated with hypokalemia. The two major causes of PA are unilateral aldosterone producing adenoma (APA) and bilateral adrenal hyperplasia, accounting together for ~95% of cases. In addition to the well-characterized effect of excess mineralocorticoids on blood pressure, high levels of aldosterone also have cardiovascular, renal, and metabolic consequences. Hence, long-term consequences of PA include increased risk of coronary artery disease, myocardial infarction, heart failure, and atrial fibrillation. Despite recent progress in the management of patients with PA, critical issues related to diagnosis, subtype differentiation, and treatment of non-surgically correctable forms still persist. A better understanding of the pathogenic mechanisms of the disease should lead to the identification of more reliable diagnostic and prognostic biomarkers for a more sensitive and specific screening and new therapeutic options. In this review, we will summarize our current knowledge on the molecular and cellular mechanisms of APA development. On one hand, we will discuss how various animal models have improved our understanding of the pathophysiology of excess aldosterone production. On the other hand, we will summarize the major advances made during the last few years in the genetics of APA due to transcriptomic studies and whole exome sequencing. The identification of recurrent and somatic mutations in genes coding for ion channels (KCNJ5 and CACNA1D) and ATPases (ATP1A1 and ATP2B3) allowed highlighting the central role of calcium signaling in autonomous aldosterone production by the adrenal. äMolecular and Cellular Mechanisms of Aldosterone Producing Adenoma Dev(epmc).pdf DeepDyve Pubget Overpricing