Abstract

Stanford School of Medicine is a small, research-intensive medical school with a rich history of innovation and translation of biomedical science to the clinic and bedside. This proposal for a training program in translational myocardial biology reflects a multidisciplinary approach to research and education. The faculty are drawn from diverse departments around Campus and represent world renowned experts in their chosen fields. The cohesion of this group, which includes physiologists, molecular biologists, engineers, geneticists, and cardiologists has been fostered by the principal investigators in an environment which has for decades placed a high value on collaboration and which, over the course of the last several years, has been further strengthened through the founding of the Stanford Cardiovascular Institute. Faculty collaborate extensively, sharing lab equipment and techniques, co-mentoring trainees, and meeting quarterly to discuss future collaborations. In addition, the research groups come together weekly for a seminar series. This application seeks to underscore the proven success and productivity of this effort by putting at its center a training program for post doctoral scholars. In particular, the proposal reflects a commitment to rigorous scientific training by protecting a minimum period of three years. The commitment begins with a 'mentored'recruitment process, continues with a comprehensive approach to learning the scientific method, and extends well beyond the completion of the funded period with career development, help and advice to ensure our trainees'success as they enter into full time academic positions. As further testament to our dedication to rigorous training in the scientific method, MD trainees will be given the option to apply for an advanced degree in science (PhD) during which tuition would be paid by the School of Medicine.
Our aim i s to mentor the next generation of leaders in myocardial biology. Our commitment extends until our trainees fulfill this goal.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL094274-04
Application #
8470215
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Carlson, Drew E
Project Start
2010-07-01
Project End
2015-06-30
Budget Start
2013-07-01
Budget End
2014-06-30
Support Year
4
Fiscal Year
2013
Total Cost
$255,616
Indirect Cost
$26,564

  Institution

Name
Stanford University
Department
Pediatrics
Type
Schools of Medicine
DUNS #
009214214
City
Stanford
State
CA
Country
United States
Zip Code
94305

  Publications

Coronado, Michael; Fajardo, Giovanni; Nguyen, Kim et al. (2018) Physiological Mitochondrial Fragmentation Is a Normal Cardiac Adaptation to Increased Energy Demand. Circ Res 122:282-295
Goodyer, William R; Wu, Sean M (2018) Fates Aligned: Origins and Mechanisms of Ventricular Conduction System and Ventricular Wall Development. Pediatr Cardiol 39:1090-1098
Liang, Ping; Sallam, Karim; Wu, Haodi et al. (2016) Patient-Specific and Genome-Edited Induced Pluripotent Stem Cell-Derived Cardiomyocytes Elucidate Single-Cell Phenotype of Brugada Syndrome. J Am Coll Cardiol 68:2086-2096
Adhikari, Arjun S; Kooiker, Kristina B; Sarkar, Saswata S et al. (2016) Early-Onset Hypertrophic Cardiomyopathy Mutations Significantly Increase the Velocity, Force, and Actin-Activated ATPase Activity of Human ?-Cardiac Myosin. Cell Rep 17:2857-2864
Jung, Gwanghyun; Fajardo, Giovanni; Ribeiro, Alexandre J S et al. (2016) Time-dependent evolution of functional vs. remodeling signaling in induced pluripotent stem cell-derived cardiomyocytes and induced maturation with biomechanical stimulation. FASEB J 30:1464-79
Kojima, Yoko; Volkmer, Jens-Peter; McKenna, Kelly et al. (2016) CD47-blocking antibodies restore phagocytosis and prevent atherosclerosis. Nature 536:86-90
Woods, Christopher; Shang, Ching; Taghavi, Fouad et al. (2016) In Vivo Post-Cardiac Arrest Myocardial Dysfunction Is Supported by Ca2+/Calmodulin-Dependent Protein Kinase II-Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2. Circulation 134:961-977
Priest, James Rush; Gawad, Charles; Kahlig, Kristopher M et al. (2016) Early somatic mosaicism is a rare cause of long-QT syndrome. Proc Natl Acad Sci U S A 113:11555-11560
Homburger, Julian R; Green, Eric M; Caleshu, Colleen et al. (2016) Multidimensional structure-function relationships in human ?-cardiac myosin from population-scale genetic variation. Proc Natl Acad Sci U S A 113:6701-6
Miller, Clint L; Pjanic, Milos; Wang, Ting et al. (2016) Integrative functional genomics identifies regulatory mechanisms at coronary artery disease loci. Nat Commun 7:12092

Showing the most recent 10 out of 28 publications