CORE B: This Core supports the Projects in this application through three functions. These are: Function 1) to coordinate recruitment of PAH patients and controls, clinically evaluate enrollees and conduct sample collection;Function 2) establish and maintain a biospecimen repository and distribute its resources (serum, plasma, circulating cells, cultured fibroblasts, DNA, RNA, banked tissue samples) to Projects 1, 2 and 3 and to collaborators at Columbia and for other NIH funded investigators;Function 3) facilitate analysis of data, especially human data in Projects 1, 2 and 3. The idiopathic PAH patients will largely be drawn from our Center for Pulmonary Vascular Disease, a clinical center that has nearly 450 reference patients and has successfully participated in over 20 national clinical trials over the last decade. Controls will come from the Vanderbilt General Clinical Research Center bank (ResearchMatch.com) and from within families. We use a national specimen and survey company for offsite collection of specimens. HPAH patients will also be recruited from Columbia University through an ongoing collaboration with Dr. Wendy Chung who runs the PH genetics component of the Columbia PH group. In Function 2, blood, urine, fibroblasts, cells, DNA, RNA and tissue will be generated, processed and stored in the laboratories of the Pulmonary Circulation Genomics Center, the Vanderbilt DNA Resource Core and the laboratories of the Pulmonary Division. Management of the entire collection will be done by dedicated personnel using the comprehensive REDCap data base. We have a history of over 2 thousand total subjects in our database, including the Progeny Software used for genetic and family data, and can move DNA, RNA, data and materials reliably and accurately. Function 3 is the analysis of data created largely in Projects 1 and 2. The development and design of experiments has been aided by our Epidemiologist and Statistician who will be the statistical coordinator for the entire PPG, including powering, sample size, estimates, outcome measures, data check and quality control, application of appropriate biostatlstical tests depending on data sets and hypotheses. Thus statistical support is fully integrated into the design, conduct and analysis.
Pulmonary arterial hypertension (PAH) is elevated blood pressure in the lungs, which leads to right heart failure and death. No existing treatments are very effective. This Program Project Grant aims to develop new, more effective treatments based on interventions against the hormonal, metabolic, and signaling defects recently shown to form the molecular basis for disease. Core B supports these functions.
|Meoli, David F; Su, Yan Ru; Brittain, Evan L et al. (2018) The transpulmonary ratio of endothelin 1 is elevated in patients with preserved left ventricular ejection fraction and combined pre- and post-capillary pulmonary hypertension. Pulm Circ 8:2045893217745019|
|Yan, Ling; Cogan, Joy D; Hedges, Lora K et al. (2018) The Y Chromosome Regulates BMPR2 Expression via SRY: A Possible Reason ""Why"" Fewer Males Develop Pulmonary Arterial Hypertension. Am J Respir Crit Care Med 198:1581-1583|
|Whitaker, Morgan E; Nair, Vineet; Sinari, Shripad et al. (2018) Diabetes Mellitus Associates with Increased Right Ventricular Afterload and Remodeling in Pulmonary Arterial Hypertension. Am J Med 131:702.e7-702.e13|
|Hemnes, Anna R (2018) Using Omics to Understand and Treat Pulmonary Vascular Disease. Front Med (Lausanne) 5:157|
|Han, MeiLan K; Arteaga-Solis, Emilio; Blenis, John et al. (2018) Female Sex and Gender in Lung/Sleep Health and Disease. Increased Understanding of Basic Biological, Pathophysiological, and Behavioral Mechanisms Leading to Better Health for Female Patients with Lung Disease. Am J Respir Crit Care Med 198:850-858|
|Brittain, Evan L; Thennapan, Thennapan; Maron, Bradley A et al. (2018) Update in Pulmonary Vascular Disease 2016 and 2017. Am J Respir Crit Care Med 198:13-23|
|Suzuki, Toshio; Carrier, Erica J; Talati, Megha H et al. (2018) Isolation and characterization of endothelial-to-mesenchymal transition cells in pulmonary arterial hypertension. Am J Physiol Lung Cell Mol Physiol 314:L118-L126|
|Halliday, Stephen J; Xu, Meng; Thayer, Timothy E et al. (2018) Clinical and genetic associations with prostacyclin response in pulmonary arterial hypertension. Pulm Circ 8:2045894018800544|
|Hemnes, Anna R; Rathinasabapathy, Anandharajan; Austin, Eric A et al. (2018) A potential therapeutic role for angiotensin-converting enzyme 2 in human pulmonary arterial hypertension. Eur Respir J 51:|
|Gaskill, Christa F; Carrier, Erica J; Kropski, Jonathan A et al. (2017) Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction. J Clin Invest 127:2262-2276|
Showing the most recent 10 out of 56 publications