This Core unit will be responsible for the total administrative organization and the management of the Program Project. The Core will be directed by Walter J Koch, PhD, the overall PI of this Program Project as he has carried out this role through the first funding cycle of this award. He will be assisted in the adminsitration of Core A by Ms. Nora Baglivo who will share responsiblities as the PPG Administrative Assistant. In addition, as in the PPG through the first funding cycle, a PPG Administrator will also assist Dr. Koch in the overall admistration of this program. As in the first funding period, this will be Ms. Joanne Cortese. Together with Dr. Koch, they will be responsible for the organization of the Grant including financial budgeting. This is a strength of Ms. Cortese. The primary functions of this core will be the overall scientific coordination of the research goals of this PPG and assure compliance with all NIH, NHLBI and Temple University policies. Organization with include planning of monthly data meetings of all members of the PPG group and associated scientists and meetings of the internal (twice a year) and external advisory (once a year) committees and all travel associated with this PPG. Ms. Baglivo will also support with manuscript organization for studies from this PPG and also annual progress reports. Finally, Dr. Koch will also coordinate any biostatistical assistance and consulting needed with the Biostatistics Department of Temple University as there will be needed support for analysis of data generated in the various Projects. All Projects will utilize this Core evenly.

Public Health Relevance

This Core is responsible for the organization of all administrative and management needs of this Program Project and to ensure success of the primary goals to elucidate novel mechanisms involved in cardiac injury and repair. Success of the Program Project will uncover novel therapeutics effect to combat heart disease.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Program Projects (P01)
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Heart, Lung, and Blood Initial Review Group (HLBP)
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Temple University
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de Lucia, Claudio; Gambino, Giuseppina; Petraglia, Laura et al. (2018) Long-Term Caloric Restriction Improves Cardiac Function, Remodeling, Adrenergic Responsiveness, and Sympathetic Innervation in a Model of Postischemic Heart Failure. Circ Heart Fail 11:e004153
Tahrir, Farzaneh G; Shanmughapriya, Santhanam; Ahooyi, Taha Mohseni et al. (2018) Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes. J Cell Physiol 233:748-758
Myers, Valerie D; McClung, Joseph M; Wang, JuFang et al. (2018) The Multifunctional Protein BAG3: A Novel Therapeutic Target in Cardiovascular Disease. JACC Basic Transl Sci 3:122-131
Myers, Valerie D; Tomar, Dhanendra; Madesh, Muniswamy et al. (2018) Haplo-insufficiency of Bcl2-associated athanogene 3 in mice results in progressive left ventricular dysfunction, ?-adrenergic insensitivity, and increased apoptosis. J Cell Physiol 233:6319-6326
Borghetti, Giulia; von Lewinski, Dirk; Eaton, Deborah M et al. (2018) Diabetic Cardiomyopathy: Current and Future Therapies. Beyond Glycemic Control. Front Physiol 9:1514
Grisanti, Laurel A; Schumacher, Sarah M; Tilley, Douglas G et al. (2018) Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease. JACC Basic Transl Sci 3:550-562
de Lucia, Claudio; Eguchi, Akito; Koch, Walter J (2018) New Insights in Cardiac ?-Adrenergic Signaling During Heart Failure and Aging. Front Pharmacol 9:904
Grisanti, Laurel A; Thomas, Toby P; Carter, Rhonda L et al. (2018) Pepducin-mediated cardioprotection via ?-arrestin-biased ?2-adrenergic receptor-specific signaling. Theranostics 8:4664-4678
Cannavo, Alessandro; Koch, Walter J (2018) GRK2 as negative modulator of NO bioavailability: Implications for cardiovascular disease. Cell Signal 41:33-40
Yeh, Szu-Tsen; Zambrano, Cristina M; Koch, Walter J et al. (2018) PH domain leucine-rich repeat protein phosphatase 2 (PHLPP2) regulates G-protein-coupled receptor kinase 5 (GRK5)-induced cardiac hypertrophy in vitro. J Biol Chem 293:8056-8064

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