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.
|Woods, Christopher E; 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 134:961-77|
|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|
|Sturzu, Anthony C; Rajarajan, Kuppusamy; Passer, Derek et al. (2015) Fetal Mammalian Heart Generates a Robust Compensatory Response to Cell Loss. Circulation 132:109-21|
|Serpooshan, Vahid; Sivanesan, Senthilkumar; Huang, Xiaoran et al. (2015) [Pyr1]-Apelin-13 delivery via nano-liposomal encapsulation attenuates pressure overload-induced cardiac dysfunction. Biomaterials 37:289-98|
|Dewey, Frederick E; Grove, Megan E; Pan, Cuiping et al. (2014) Clinical interpretation and implications of whole-genome sequencing. JAMA 311:1035-45|
|Priest, James R; Ceresnak, Scott R; Dewey, Frederick E et al. (2014) Molecular diagnosis of long QT syndrome at 10 days of life by rapid whole genome sequencing. Heart Rhythm 11:1707-13|
|Miller, Clint L; Haas, Ulrike; Diaz, Roxanne et al. (2014) Coronary heart disease-associated variation in TCF21 disrupts a miR-224 binding site and miRNA-mediated regulation. PLoS Genet 10:e1004263|
|Kojima, Yoko; Downing, Kelly; Kundu, Ramendra et al. (2014) Cyclin-dependent kinase inhibitor 2B regulates efferocytosis and atherosclerosis. J Clin Invest 124:1083-97|
|Snyder, Michael; Mias, George; Stanberry, Larissa et al. (2014) Metadata checklist for the integrated personal OMICS study: proteomics and metabolomics experiments. OMICS 18:81-5|
|Oikawa, Masayoshi; Wu, Meiping; Lim, Soyeon et al. (2013) Cyclic nucleotide phosphodiesterase 3A1 protects the heart against ischemia-reperfusion injury. J Mol Cell Cardiol 64:11-9|
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