The CHRCDA Program in the Department of Pediatrics at Duke University Medical Center is intended to foster the maturation of pediatric junior faculty into independent physician-scientists who are skilled in cutting-edge methods of laboratory research and who pursue long-term academic careers investigating important issues related to childhood diseases. This Program is based on a pool of outstanding candidates, a strong curriculum of didactic courses, experienced mentors who perform state-of-the-art laboratory research, and an excellent research environment. The Principal Investigator/Program Director and the Training Director will receive assistance from an Internal Advisory Board and an External Advisory Board in selecting scholars, reviewing the progress of scholars, and ensuring the optimal operation of the program. Four scholars will be supported each year and will be drawn from junior faculty in the Department of Pediatrics, with particular emphasis on recruitment of women and underrepresented minorities. The Program Faculty will be drawn from four broadly defined areas of research excellence, namely Developmental Biology, Cell Biology and Cell Signaling, Infection and Immunity, and Genetics, Genomics, and Metabolomics. The Program Faculty will include mentors from the Department of Pediatrics and from other departments at Duke University Medical Center, in all cases characterized by a strong track record in research, funding, and mentoring. Didactic courses will complement the laboratory research experiences and will include a four-lecture course on writing and a five-lecture course on Responsible Conduct of Research. The scholars will have access to all of the shared research facilities at Duke University, including core facilities of the NCI-funded Comprehensive Cancer Center, the Duke Institute for Genome Sciences and Policy, the Duke Center for Human Genome Variation, the Duke Center for Human Disease Modeling, the Duke Human Vaccine Institute, and the Duke Translational Medicine Institute, among others.
There is a paramount need for pediatricians who are skilled in modern scientific methods and have the background to develop novel approaches to the diagnosis, treatment, and prevention of childhood diseases. The proposed career development program will foster the maturation of talented pediatric junior faculty into independent investigators who use cutting-edge methods of laboratory research and who pursue long-term academic careers investigating important issues related to childhood diseases.
|Wang, Xiaoming; Bey, Alexandra L; Chung, Leeyup et al. (2014) Therapeutic approaches for shankopathies. Dev Neurobiol 74:123-35|
|Jiang, Yong-Hui; Ehlers, Michael D (2013) Modeling autism by SHANK gene mutations in mice. Neuron 78:8-27|
|Chinn, I K; Milner, J D; Scheinberg, P et al. (2013) Thymus transplantation restores the repertoires of forkhead box protein 3 (FoxP3)+ and FoxP3- T cells in complete DiGeorge anomaly. Clin Exp Immunol 173:140-9|
|Belyea, Brian C; Naini, Sarasija; Bentley, Rex C et al. (2011) Inhibition of the Notch-Hey1 axis blocks embryonal rhabdomyosarcoma tumorigenesis. Clin Cancer Res 17:7324-36|
|Chinn, Ivan K; Markert, M Louise (2011) Induction of tolerance to parental parathyroid grafts using allogeneic thymus tissue in patients with DiGeorge anomaly. J Allergy Clin Immunol 127:1351-5|
|MacIver, Nancie J; Blagih, Julianna; Saucillo, Donte C et al. (2011) The liver kinase B1 is a central regulator of T cell development, activation, and metabolism. J Immunol 187:4187-98|
|Chinn, Ivan K; Olson, John A; Skinner, Michael A et al. (2010) Mechanisms of tolerance to parental parathyroid tissue when combined with human allogeneic thymus transplantation. J Allergy Clin Immunol 126:814-820.e8|
|Naini, Sarasija; Etheridge, Katherine T; Adam, Stacey J et al. (2008) Defining the cooperative genetic changes that temporally drive alveolar rhabdomyosarcoma. Cancer Res 68:9583-8|
|Linardic, Corinne M (2008) PAX3-FOXO1 fusion gene in rhabdomyosarcoma. Cancer Lett 270:10-8|
|Idriss, Salim F; Bell, Jamie A (2008) Cardiac repolarization instability during normal postnatal development. J Electrocardiol 41:474-9|
Showing the most recent 10 out of 16 publications