This Lung and cardiovascular Development and Disease Pathogenesis Training Program grant aims to provide advanced research training by supporting stipends for three pre-doctoral and for three post-doctoral candidates within the University of Cincinnati Graduate Programs. The training environment draws heavily upon established, integrated, innovative Graduate Programs focused to molecular, developmental, and cell biology research and benefits from related, NHLBI-supported research programs. The program brings together 30 distinguished, NIH-funded investigators experienced in using modern molecular, cellular, and gene targeting and transfer strategies to study the developmental biology of the lungs, heart, and blood and pathogenesis-based diagnostic and therapeutic discovery at Cincinnati Children's Medical Center and the University of Cincinnati College of Medicine. Program faculty have shared research interests and a long history of collaboration in basic and translational research. Major research themes include pathogenesis of pulmonary and cardiac disorders, gene expression, function, and regulation during lung development, injury, and repair, and development and evaluation of novel biomarkers, diagnostics, and therapies for lung diseases. Promising trainees engaged in pre- or post-doctoral training programs will be identified, recruited, and selected on a competitive basis. Pre-doctoral trainees will obtain their PhD degrees in either the Graduate Program in Developmental Biology, Immunobiology, Biomedical Sciences, or Pathobiology and Molecular Medicine;or the Department of Anatomy and Cell Biology, Molecular Genetics, or Biochemistry and Microbiology at the University of Cincinnati College of Medicine. Post-doctoral trainees may have an MD or PhD degree, or both. Special attention will be given to recruitment of minority individuals and candidates with an MD degree. Research training will include mentoring, career development, training in the responsible conduct of research, a course in Ethics in Research, research presentation skill development (all required), and various optional seminars and courses within the graduate programs in which training faculty participate. Two broad training focus areas are available: 1) pulmonary and cardiovascular development, injury and repair, and 2) pathogenesis-based lung and cardiovascular disease biomarkers, diagnostic, and therapeutics development. Trainees will attend regular research meetings and several pertinent seminar series. Program Administration will include the Principal Investigator, two Co-Principal Investigators, an Executive Committee, and External and internal Advisory Committees. The progress of each trainee, quality of mentors, and overall effectiveness of the program will be critically reviewed annually. Trainees will meet with their Mentor regularly, the Program Director twice yearly, and their Mentoring Committee annually. This T32 renewal application (Years 21-25) will permit us to continue a program with outstanding productivity in preparing new investigators with enhanced research training and competence in critical aspects of lung development and disease pathogenesis.
This renewal T32 grant application for a Lung and Cardiovascular Development and Disease Pathogenesis Training Program will continue support to recruit and train outstanding pre-doctoral and post-doctoral candidates, preparing them to advance discoveries that improve the diagnosis and treatment of lung diseases and to become the future research leaders in pulmonary research and medicine. This Program meets a critical national need to increase the quantity and quality of young investigators who can apply cellular, molecular, and genetic strategies to the study of lung, heart, and blood disorders. There is an ever-increasing loss of M.D. and Ph.D. candidates from academic-scientific careers at a time in which unparalleled opportunities exist to identify mechanisms of disease and to develop novel biomarkers, diagnostics, and treatment strategies to improve human health.
|Wagh, Purnima K; Gardner, Margaret A; Ma, Xiaolan et al. (2015) Cell- and developmental stage-specific Dicer1 ablation in the lung epithelium models cystic pleuropulmonary blastoma. J Pathol 236:41-52|
|Rankin, Scott A; Thi Tran, Hong; Wlizla, Marcin et al. (2015) A Molecular atlas of Xenopus respiratory system development. Dev Dyn 244:69-85|
|Kottyan, Leah C; Davis, Benjamin P; Sherrill, Joseph D et al. (2014) Genome-wide association analysis of eosinophilic esophagitis provides insight into the tissue specificity of this allergic disease. Nat Genet 46:895-900|
|Sutherland, Mardi J; Wang, Shuyun; Quinn, Malgorzata E et al. (2013) Zic3 is required in the migrating primitive streak for node morphogenesis and left-right patterning. Hum Mol Genet 22:1913-23|
|Mushaben, Elizabeth M; Hershey, Gurjit Khurana; Pauciulo, Michael W et al. (2012) Chronic allergic inflammation causes vascular remodeling and pulmonary hypertension in BMPR2 hypomorph and wild-type mice. PLoS One 7:e32468|
|Stoffers, Sara L; Meyer, Sara E; Grimes, H Leighton (2012) MicroRNAs in the midst of myeloid signal transduction. J Cell Physiol 227:525-33|
|Pattison, J Scott; Osinska, Hanna; Robbins, Jeffrey (2011) Atg7 induces basal autophagy and rescues autophagic deficiency in CryABR120G cardiomyocytes. Circ Res 109:151-60|
|Wissing, Erin R; Millay, Douglas P; Vuagniaux, Gregoire et al. (2010) Debio-025 is more effective than prednisone in reducing muscular pathology in mdx mice. Neuromuscul Disord 20:753-60|
|Weeks 2nd, James L; Corbin, Jackie D; Francis, Sharron H (2009) Interactions between cyclic nucleotide phosphodiesterase 11 catalytic site and substrates or tadalafil and role of a critical Gln-869 hydrogen bond. J Pharmacol Exp Ther 331:133-41|
|Lange, Alexander W; Keiser, Angela R; Wells, James M et al. (2009) Sox17 promotes cell cycle progression and inhibits TGF-beta/Smad3 signaling to initiate progenitor cell behavior in the respiratory epithelium. PLoS One 4:e5711|
Showing the most recent 10 out of 32 publications