Zobrazeno 1 - 10
of 18
pro vyhledávání: '"Donald Bers"'
Autor:
Bence Hegyi, Donald Bers
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 324:H338-H340
Autor:
Samuel Sossalla, Donald Bers
Publikováno v:
Circulation Research. 130:249-251
Autor:
Donald Bers
Publikováno v:
Nature Cardiovascular Research. 1:980-981
Autor:
Bence Hegyi, Donald Bers
Publikováno v:
Nature Cardiovascular Research. 1:408-409
Autor:
Huaxiao Yang, Alex C.Y. Chang, Helen M. Blau, Ning Ma, Karim Sallam, Donald Bers, Chi Keung Lam, Joe Zhang, June-Wha Rhee, Haodi Wu, Joseph C. Wu
Publikováno v:
Circulation Research. 123
Aims: Diastolic dysfunction (DD) is common among hypertrophic cardiomyopathy (HCM) patients, causing major morbidity and mortality. Yet its cellular mechanisms are not fully understood, and presently, there is no effective treatment. Patient-specific
Publikováno v:
The Journal of Physiology. 595:4131-4132
Ca2+ influx via the L-type Ca2+ channel Cav1.2 triggers our heartbeat. Perinatally and particularly at birth, angiotensin II is produced to augment necessary physiological changes in blood flow such as pulmonary perfusion. This article is protected b
Autor:
Donald Bers
The main aim of this monograph is to provide an overview of calcium regulation in cardiac muscle cells, particularly with respect to excitation-contraction coupling and the control of cardiac contractile force. It is my hope that this book will be us
Autor:
Feng lan, Andrew Lee, Ping Liang, Enrique Navarrete, Li Wang, Han Leng, Veronica Sanchez, Michelle Yen, Yongming Wang, Patricia Nguyen, Ning Sun, Oscar Abilez, Richard Lewis, Yoshinori Yamaguchi, Euan Ashley, Donald Bers, Robert Robbins, Michael Longaker, Joseph Wu
Publikováno v:
Circulation Research. 111
Background: Hypertrophic cardiomyopathy (HCM) is a prevalent familial cardiac disorder linked to development of heart failure, arrhythmia, and sudden cardiac death. Molecular genetic studies have demonstrated HCM is caused by mutations in genes encod
Publikováno v:
Circulation. 116
Background: Myocyte [Ca] i varies beat-to-beat and calmodulin (CaM) transduces Ca signals to regulate many cardiac functions (e.g. via CaM-dependent kinase, CaMKII, and calcineurin, CaN). We hypothesize that the different Ca-CaM affinities of CaMKII
Publikováno v:
Europe PubMed Central