The overall goal of the Pilot and Feasibility Program of the Digestive Health Center (DHC) is to promote digestive disease research by supporting innovative pilot projects that will lead to extramurally funded research and expansion of digestive disease research. The Program pursues this goal with three complementary aims: 1) To foster the career development of junior digestive disease investigators, 2) To encourage established investigators in other areas of biomedical research to extend their expertise to digestive disease research, and 3) To support highly focused new projects from established investigators exploring innovative new ideas that represent a significant departure from their funded research. The organization of the P/F Program aligns types of investigators with these aims (Type 1/?New,? Type 2/?Established New,? and Type 3/?Established?, respectively) according to well-established eligibility criteria. The DHC holds one P/F application process yearly, which undergoes scientific review by a panel of experts using the merit criteria used by NIH study sections, followed by a final review by the DHC External Advisory Board, who makes recommendation for funding of most meritorious research projects. With strong institutional support that supplements the DHC resources, the Program typically funds three awards of $50,000. The Program Director and Center Leadership provides awardees with mentorship opportunities. This program has been very successful, and Type 1/New awardees transitioned to independent investigator status with R01-level of funding. For the past 10 years, the Program invested approximately $1.6 million, which resulted >$34 million dollars in new grants, or a >22-fold return on the investment. Notably, P/F awardees have published 130 original papers and >90% remain engaged in digestive disease research.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
5P30DK078392-14
Application #
9951046
Study Section
Special Emphasis Panel (ZDK1)
Project Start
Project End
Budget Start
2020-06-01
Budget End
2021-05-31
Support Year
14
Fiscal Year
2020
Total Cost
Indirect Cost
Name
Cincinnati Children's Hospital Medical Center
Department
Type
DUNS #
071284913
City
Cincinnati
State
OH
Country
United States
Zip Code
45229
Jose, S; Abhyankar, M M; Mukherjee, A et al. (2018) Leptin receptor q223r polymorphism influences neutrophil mobilization after Clostridium difficile infection. Mucosal Immunol 11:947-957
Goodman, Michael Aaron; Arumugam, Paritha; Pillis, Devin Marie et al. (2018) Foamy Virus Vector Carries a Strong Insulator in Its Long Terminal Repeat Which Reduces Its Genotoxic Potential. J Virol 92:
Kim, Paul; Piraino, Giovanna; O'Connor, Michael et al. (2018) Metformin Exerts Beneficial Effects in Hemorrhagic Shock in An AMPK?1-Independent Manner. Shock 49:277-287
Lee, Kang Kug; McCauley, Heather A; Broda, Taylor R et al. (2018) Human stomach-on-a-chip with luminal flow and peristaltic-like motility. Lab Chip 18:3079-3085
D'Souza, Amber M; Jiang, Yanjun; Cast, Ashley et al. (2018) Gankyrin Promotes Tumor-Suppressor Protein Degradation to Drive Hepatocyte Proliferation. Cell Mol Gastroenterol Hepatol 6:239-255
Waddell, Amanda; Vallance, Jefferson E; Hummel, Amy et al. (2018) IL-33 Induces Murine Intestinal Goblet Cell Differentiation Indirectly via Innate Lymphoid Cell IL-13 Secretion. J Immunol :
Yang, Li; Mizuochi, Tatsuki; Shivakumar, Pranavkumar et al. (2018) Regulation of epithelial injury and bile duct obstruction by NLRP3, IL-1R1 in experimental biliary atresia. J Hepatol 69:1136-1144
Lee, Sanghoon; Zhou, Ping; Gupta, Anita et al. (2018) Reactive Ductules Are Associated With Angiogenesis and Tumor Cell Proliferation in Pediatric Liver Cancer. Hepatol Commun 2:1199-1212
Aihara, Eitaro; Medina-Candelaria, Neisha M; Hanyu, Hikaru et al. (2018) Cell injury triggers actin polymerization to initiate epithelial restitution. J Cell Sci 131:
Deshpande, Chandrika N; Ruwe, T Alex; Shawki, Ali et al. (2018) Calcium is an essential cofactor for metal efflux by the ferroportin transporter family. Nat Commun 9:3075

Showing the most recent 10 out of 543 publications