Administrative Core: This core unit will be responsible for the overall administration and management of the Program Project. This core, which is responsible for four projects and four cores will be directed by Steven R. Houser, Ph.D., the Principal Investigator of the Program Project Grant. The Administrative core functions include: 1 .Overall scientific coordination of the research objectives of the Program Project Grant. This includes the review and recording of scientific progress made in all component projects and cores. 2. Follow and implement all guidelines for Program Project Grant, including administering the budget and subcontracts in accordance with all NIH, NHLBI and Temple University policies.3.Monitor ali expenditures for accuracy, fiscally responsibility for the projects and cores. 4. Facilitates and an-anges for interactions among the project leaders, direct collaboration with other institutions working in related areas. Arange, support and direct regular meetings of the Intemal and External Advisory Committee with the PPG investigators and core directors. S.Conduct and lead bi-weekly research data meetings that will be held for investigators, fellows, technicians and students involved in the projects and cores. Internet based meetings will be held so that all investigators at Cincinnati and at Jefferson can participate without having to travel to Temple. Core A will hold a bi-annual face to face meeting for all project core leaders and key personnel. 6.Support publication of new data resulting.from research projects. 7. Prepare annual reports and renewals for the Program Project Grant. This core will also be responsible for evaluation of progress of all portions of this PPG. This will be done in consultations with Intemal and Extemal advisory boards. The core will organize annual retreats so that students and fellows working on this project have an opportunity to present their work. This core will work with counterparts at collaborating Institutions to ensure progress is made at all sites.
This Core will be responsible for all administrative and management decisions related to this PPG. The goal of the program is to identify novel approaches to treat patients with ischemic heart disease, or other cardiac maladies that cause premature death and disability.
|Molkentin, Jeffery D (2014) Letter by Molkentin regarding article, "The absence of evidence is not evidence of absence: the pitfalls of Cre Knock-Ins in the c-Kit Locus". Circ Res 115:e21-3|
|Hullmann, Jonathan E; Grisanti, Laurel A; Makarewich, Catherine A et al. (2014) GRK5-mediated exacerbation of pathological cardiac hypertrophy involves facilitation of nuclear NFAT activity. Circ Res 115:976-85|
|van Berlo, Jop H; Kanisicak, Onur; Maillet, Marjorie et al. (2014) c-kit+ cells minimally contribute cardiomyocytes to the heart. Nature 509:337-41|
|Scimia, Maria C; Gumpert, Anna M; Koch, Walter J (2014) Cardiovascular gene therapy for myocardial infarction. Expert Opin Biol Ther 14:183-95|
|Davis, Jennifer; Molkentin, Jeffery D (2014) Myofibroblasts: trust your heart and let fate decide. J Mol Cell Cardiol 70:9-18|
|Correll, Robert N; Eder, Petra; Burr, Adam R et al. (2014) Overexpression of the Na+/K+ ATPase ?2 but not ?1 isoform attenuates pathological cardiac hypertrophy and remodeling. Circ Res 114:249-56|
|Duran, Jason M; Makarewich, Catherine A; Trappanese, Danielle et al. (2014) Sorafenib cardiotoxicity increases mortality after myocardial infarction. Circ Res 114:1700-12|
|Barr, Larry A; Makarewich, Catherine A; Berretta, Remus M et al. (2014) Imatinib activates pathological hypertrophy by altering myocyte calcium regulation. Clin Transl Sci 7:360-7|
|Makarewich, Catherine A; Zhang, Hongyu; Davis, Jennifer et al. (2014) Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction. Circ Res 115:567-80|
|Houser, Steven R (2014) Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias. Circ Res 114:1320-7; discussion 1327|
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