Zobrazeno 1 - 10
of 11
pro vyhledávání: '"Sarah J. Briston"'
Autor:
Chee Gee Liew, Nadia N Shah, Sarah J Briston, Ruth M Shepherd, Cheen Peen Khoo, Mark J Dunne, Harry D Moore, Karen E Cosgrove, Peter W Andrews
Publikováno v:
PLoS ONE, Vol 3, Iss 3, p e1783 (2008)
BACKGROUND:Human embryonic stem cells (HESC) readily differentiate into an apparently haphazard array of cell types, corresponding to all three germ layers, when their culture conditions are altered, for example by growth in suspension as aggregates
Externí odkaz:
https://doaj.org/article/c797fd1a21b54eddb11c832de0f19203
Autor:
Margaux A. Horn, David J. Greensmith, Helen K. Graham, Jessica D. Clarke, Mark C.S. Hall, Katharine M. Dibb, Sarah J. Briston, Andrew W. Trafford, Mark A. Richards
Publikováno v:
Journal of Molecular and Cellular Cardiology. 53:82-90
The incidence of heart failure (HF) increases with age. This study sought to determine whether aging exacerbates structural and functional remodeling of the myocardium in HF. HF was induced in young (~18months) and aged sheep (>8years) by right ventr
Autor:
Sarah J. Briston, Stephen C. O’Neill, David A. Eisner, Elizabeth F. Bode, C. L. Overend, Andrew W. Trafford
Publikováno v:
The Journal of Physiology. 589:4723-4729
Changes of the activity of the sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) affect the amplitude of the systolic Ca(2+) transient and thence cardiac contractility. This is thought to be due to alterations of SR Ca(2+) content. Recent work on mic
Autor:
Sarah J. Briston, Andrew W. Trafford, Mark A. Richards, Jessica D. Clarke, David A. Eisner, Jessica L. Caldwell, Margaux A. Horn, Katharine M. Dibb, Mark C.S. Hall, Helen K. Graham, David J. Greensmith
Publikováno v:
The Journal of Physiology. 589:1367-1382
Reduced inotropic responsiveness is characteristic of heart failure (HF). This study determined the cellular Ca2+ homeostatic and molecular mechanisms causing the blunted β-adrenergic (β-AR) response in HF.We induced HF by tachypacing in sheep; int
Autor:
Andrew W. Trafford, Sarah J. Briston
Publikováno v:
Journal of Molecular and Cellular Cardiology. 50:13-15
Autor:
Jessica D, Clarke, Jessica L, Caldwell, Margaux A, Horn, Elizabeth F, Bode, Mark A, Richards, Mark C S, Hall, Helen K, Graham, Sarah J, Briston, David J, Greensmith, David A, Eisner, Katharine M, Dibb, Andrew W, Trafford
Publikováno v:
Journal of Molecular and Cellular Cardiology
Heart failure (HF) is commonly associated with reduced cardiac output and an increased risk of atrial arrhythmias particularly during β-adrenergic stimulation. The aim of the present study was to determine how HF alters systolic Ca2 + and the respon
Publikováno v:
Biophysical Journal. 100(3)
The sarcoplasmic reticulum (SR) provides the majority of calcium to the systolic calcium transient. It is this rise in intracellular calcium that causes cardiac systole. The SR is, therefore, important for maintaining cardiac contractility. SR calciu
Autor:
David A. Eisner, Geir Christensen, Sarah J. Briston, William E. Louch, Andrew W. Trafford, Ivar Sjaastad, Leiv Øyehaug, Guro F. Jølle, Isma Manzoor, Mathis K. Stokke, Ole M. Sejersted
Publikováno v:
Cardiovascular research. 90(3)
Aims In this manuscript, we determined the roles of the sarcoendoplasmic reticulum Ca2+ ATPase 2 (SERCA2) and the ryanodine receptor (RyR) in Ca2+ wave development during β-adrenergic stimulation. Methods and results SERCA2 knockout mice (KO) were u
Autor:
David A. Eisner, Silvia G. Priori, Carlo Napolitano, Andrew W. Trafford, Sarah J. Briston, Takeshi Kashimura, Luigi Venetucci
Publikováno v:
Circulation research. 107(12)
Rationale: Mutations of the ryanodine receptor (RyR) cause catecholaminergic polymorphic ventricular tachycardia (CPVT). These mutations predispose to the generation of Ca waves and delayed afterdepolarizations during adrenergic stimulation. Ca waves
Autor:
Geir Christensen, Andrew W. Trafford, Ivar Sjaastad, Karina Hougen, Sarah J. Briston, William E. Louch, Ole M. Sejersted, Kristin B. Andersson, Mathis K. Stokke, David A. Eisner, Ulla H. Enger
Publikováno v:
Cardiovascular research. 86(1)
Aims To describe the overall role of reduced sarcoplasmic reticulum Ca2+ ATPase (SERCA2) for Ca2+ wave development. Methods and results SERCA2 knockout [ Serca2 flox/flox Tg(αMHC-MerCreMer); KO] mice allowing inducible cardiomyocyte-specific disrupt