Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1161/CIRCRESAHA.113.301129 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.113.301129 C4112290!4112290!24951766     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 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Res 2014 ; 115 (1): 176-88 Nephropedia Template TP {{tp|p=24951766|t=2014. The Right Ventricle in Pulmonary Arterial Hypertension: Disorders of metabolism, angiogenesis and adrenergic signaling in right ventricular failure |pdf=|usr=}}{{24951766}} gab.com Text The Right Ventricle in Pulmonary Arterial Hypertension: Disorders of metabolism, angiogenesis and adrenergic signaling in right ventricular failure JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=24951766 #FOAvip The right ventricle (RV) is the major determinant of functional state and prognosis in pulmonary arterial hypertension (PAH). RV hypertrophy (RVH) triggered by pressure overload is initially compensatory but often leads to RV failure. Despite similar RV afterload and mass some patients develop adaptive RVH (concentric with retained RV function), whilst others develop maladaptive RVH, characterized by dilatation, fibrosis and RV failure. The differentiation of adaptive versus maladaptive RVH is imprecise but adaptive RVH is associated with better functional capacity and survival. At the molecular level, maladaptive RVH displays greater impairment of angiogenesis, adrenergic signaling and metabolism than adaptive RVH and these derangements often involve the left ventricle. Clinically, maladaptive RVH is characterized by increased NT-proBNP levels, troponin release, elevated catecholamine levels, RV dilatation and late gadolinium-enhancement on magnetic resonance imaging, increased 18fluorodeoxyglucose uptake on positron emission tomography and QTc prolongation on the electrocardiogram. In maladaptive RVH there is reduced inotrope responsiveness due to G-protein receptor kinase (GRK2)-mediated downregulation, desensitization and uncoupling of ?-adrenoreceptors. RV ischemia may result from capillary rarefaction and/or decreased right coronary artery perfusion pressure. Maladaptive RVH shares metabolic abnormalities with cancer including aerobic glycolysis (resulting from a FOXO1-mediated transcriptional upregulation of pyruvate dehydrogenase kinase, PDK), and glutaminolysis (reflecting ischemia-induced cMyc activation). Augmentation of glucose oxidation is beneficial in experimental RVH and can be achieved by inhibition of PDK, fatty acid oxidation, or glutaminolysis. Therapeutic targets in RV failure include chamber-specific abnormalities of metabolism, angiogenesis, adrenergic signaling and phosphodiesterase-5 expression. The ability to restore RV function in experimental models challenges the dogma that RV failure is irreversible without regression of pulmonary vascular disease. Twit Text FOAVip The Right Ventricle in Pulmonary Arterial Hypertension: Disorders of metabolism, angiogenesis and adrenergic signaling in right ventricular failure ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=24951766 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24951766 #FOAvip English Wikipedia <ref>{{Cite pmid|24951766}}</ref> The Right Ventricle in Pulmonary Arterial Hypertension: Disorders of metabolism, angiogenesis and adrenergic signaling in right ventricular failure #MMPMID24951766 Ryan JJ; Archer SL Circ Res 2014[Jun]; 115 (1): 176-88 PMID24951766show ga The right ventricle (RV) is the major determinant of functional state and prognosis in pulmonary arterial hypertension (PAH). RV hypertrophy (RVH) triggered by pressure overload is initially compensatory but often leads to RV failure. Despite similar RV afterload and mass some patients develop adaptive RVH (concentric with retained RV function), whilst others develop maladaptive RVH, characterized by dilatation, fibrosis and RV failure. The differentiation of adaptive versus maladaptive RVH is imprecise but adaptive RVH is associated with better functional capacity and survival. At the molecular level, maladaptive RVH displays greater impairment of angiogenesis, adrenergic signaling and metabolism than adaptive RVH and these derangements often involve the left ventricle. Clinically, maladaptive RVH is characterized by increased NT-proBNP levels, troponin release, elevated catecholamine levels, RV dilatation and late gadolinium-enhancement on magnetic resonance imaging, increased 18fluorodeoxyglucose uptake on positron emission tomography and QTc prolongation on the electrocardiogram. In maladaptive RVH there is reduced inotrope responsiveness due to G-protein receptor kinase (GRK2)-mediated downregulation, desensitization and uncoupling of ?-adrenoreceptors. RV ischemia may result from capillary rarefaction and/or decreased right coronary artery perfusion pressure. Maladaptive RVH shares metabolic abnormalities with cancer including aerobic glycolysis (resulting from a FOXO1-mediated transcriptional upregulation of pyruvate dehydrogenase kinase, PDK), and glutaminolysis (reflecting ischemia-induced cMyc activation). Augmentation of glucose oxidation is beneficial in experimental RVH and can be achieved by inhibition of PDK, fatty acid oxidation, or glutaminolysis. Therapeutic targets in RV failure include chamber-specific abnormalities of metabolism, angiogenesis, adrenergic signaling and phosphodiesterase-5 expression. The ability to restore RV function in experimental models challenges the dogma that RV failure is irreversible without regression of pulmonary vascular disease. äThe Right Ventricle in Pulmonary Arterial Hypertension: Disorders of m(epmc).pdf DeepDyve Pubget Overpricing