The program director, Dr. David P. Hajjar, will continue to assume overall responsibility for the scientific conduct of this program and he will set overall goals, acting with the advice of the Executive Committee of the PPG (the other principal investigators of each of the projects: Drs. Marcus, K. Hajjar, Hempstead, and Gross). Drs. D. Hajjar and K. Hajjar will coordinate the interchange of data and insure integration of results and planning. The investigators and staff from each project meet weekly for Research-in-Progress seminars. These meetings on Wednesdays at noon are currently structured so that a review of each project occurs regularly (usually every two months). Invited seminar speakers also participate, when possible, in these weekly conferences. The Administrative Core will provide financial management, including projected expenditures to the Principal Investigators at four month intervals from our financial data base. The Core will provide support services in the area of personnel. The Core will also assist the investigators in the preparation of their Animal and Human Rights Forms. At this time, the Executive Committee will meet to discuss fiscal matters, major issues involving space, new equipment needs, selection of outside speakers whose research presentations may help the individual projects, and any re-allocation of support, if necessary. The progress of the junior investigators and fellows will also be evaluated in bi-monthly intervals, as it relates to the PPG. Post-Doctoral fellows are also assigned to each project by Dr. D. Hajjar since he is Director of the NIH Training Program in Cardiovascular Biochemistry and Atherosclerosis (as he has been for the past 25 years) or by Dr. B. Hempstead, since she is the Director of her own NIH Training grant in Experimental Hematology.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL046403-20
Application #
8230891
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
2014-01-31
Budget Start
2011-02-01
Budget End
2013-01-31
Support Year
20
Fiscal Year
2011
Total Cost
$218,100
Indirect Cost
Name
Weill Medical College of Cornell University
Department
Type
DUNS #
060217502
City
New York
State
NY
Country
United States
Zip Code
10065
Ramakrishnan, Devi Prasadh; Hajj-Ali, Rula A; Chen, Yiliang et al. (2016) Extracellular Vesicles Activate a CD36-Dependent Signaling Pathway to Inhibit Microvascular Endothelial Cell Migration and Tube Formation. Arterioscler Thromb Vasc Biol 36:534-44
Hajjar, Katherine A (2015) The Biology of Annexin A2: From Vascular Fibrinolysis to Innate Immunity. Trans Am Clin Climatol Assoc 126:144-55
Abbott, Geoffrey W; Tai, Kwok-Keung; Neverisky, Daniel L et al. (2014) KCNQ1, KCNE2, and Na+-coupled solute transporters form reciprocally regulating complexes that affect neuronal excitability. Sci Signal 7:ra22
Dassah, Maryann; Almeida, Dena; Hahn, Rebecca et al. (2014) Annexin A2 mediates secretion of collagen VI, pulmonary elasticity and apoptosis of bronchial epithelial cells. J Cell Sci 127:828-44
Anastasia, Agustin; Deinhardt, Katrin; Wang, Shiyang et al. (2014) Trkb signaling in pericytes is required for cardiac microvessel stabilization. PLoS One 9:e87406
Hajjar, David P; Gotto Jr, Antonio M (2013) Biological relevance of inflammation and oxidative stress in the pathogenesis of arterial diseases. Am J Pathol 182:1474-81
Kennedy, David J; Chen, Yiliang; Huang, Wenxin et al. (2013) CD36 and Na/K-ATPase-?1 form a proinflammatory signaling loop in kidney. Hypertension 61:216-24
Zhou, Ming-Sheng; Chadipiralla, Kiranmai; Mendez, Armando J et al. (2013) Nicotine potentiates proatherogenic effects of oxLDL by stimulating and upregulating macrophage CD36 signaling. Am J Physiol Heart Circ Physiol 305:H563-74
Luo, Min; Hajjar, Katherine A (2013) Annexin A2 system in human biology: cell surface and beyond. Semin Thromb Hemost 39:338-46
Siao, Chia-Jen; Lorentz, Christina U; Kermani, Pouneh et al. (2012) ProNGF, a cytokine induced after myocardial infarction in humans, targets pericytes to promote microvascular damage and activation. J Exp Med 209:2291-305

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