Publications by authors named "Tony Shaw"
Article Synopsis
- * Hypoxia-inducible factors (HIF) help the body respond to low oxygen levels and stimulate red blood cell production, but are regulated by prolyl hydroxylases (PHDs) that degrade them; inhibiting PHDs might mimic mild hypoxia and promote healthier erythropoiesis.
- * GSK1278863 is a new drug that inhibits PHDs, increasing EPO production effectively
Objective: We sought to identify changes in four-and-a-half LIM-protein 2 levels and location in human cardiomyocytes during the transition from compensated aortic stenosis to left ventricular failure. We also sought to characterize four-and-a-half LIM-protein 2 binding with the metabolic enzymes phosphofructokinase 2, adenylate kinase, and creatine kinase M isoform during this transition and their consequential subcellular localization in failing human ventricles.
Methods: Left ventricular biopsy specimens from selected patients undergoing aortic valve replacement for aortic stenosis were allocated to one of 2 groups: (1) nondilated with preserved left ventricular function (nonfailing group, n = 16) and (2) grossly dilated with poor left ventricular function (failing group, n = 15).
Objective: We identified changes in Jumonji (JARID2) expression in failing human hearts and determined its effects on expressions of atrial natriuretic factor (ANF), myosin light chain 2a (MLC2A), and alpha myosin heavy chain (MHCA), genes associated with both human heart failure and the fetal gene program.
Methods: Left ventricular outflow tract cardiac biopsy samples were taken from 31 patients with aortic valvular stenosis. Hearts were grouped according to left ventricular size and function: nonfailing hearts (undilated with good function) and failing hearts (dilated with poor function).
Objectives: We performed genetic investigations of cardiac troponin T (TNNT2) and troponin C (TNNC1) in 235 consecutive patients with idiopathic dilated cardiomyopathy (DCM) to evaluate prevalence of mutations and associated disease expression in affected families.
Background: Recently, mutations in sarcomeric genes have been reported in DCM. However, the prevalence, penetrance, and clinical significance of sarcomere gene mutations in large consecutive cohorts of DCM patients are poorly defined.