Accurate collection, storage and analysis of data have always been the foundation to successful rheumatic disease research. In many instances clinical data, such as laboratory data, that are necessary for research already exist, but an interface between the clinical system and research systems do not exist. This lack of interface often requires that these clinical data be manually entered into a research database. This method not only decreases efficiency, but manual data entry also increases the probability of data error. Rheumatic disease investigators are becoming increasingly collaborative and multi-disciplinary. This, combined with the continual and expanding flow of emergent technology that allows for the acquisition of large amounts of data, much of it on a longitudinal basis, and new data-storage and analytic methods, sets new demands and responsibilities on individual investigators. The Core will provide technical expertise, assistance and equipment to investigators in the research base whose studies require creation, migration, coordination, and maintenance and analysis of small and large data bases dedicated to pediatric rheumatology research. Specifically, the core will: Migrate current data and construct new data in a relational database so that longitudinal data collection, maintenance and analysis will become more effective. Migrate data to a relational database which, together with newly developed databases, will become Internet-based. Access to these data will be achieved through a secure world-wide-web based collection. Educate investigators throughout the research base about these services and provide them at reasonable cost. In the long-term, it is anticipated that as the core and its activities develop, its servers will become the basis for extensive interactions throughout the pediatric rheumatology research community will do so in a paperless, error-free approach.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
1P30AR047363-01
Application #
6447616
Study Section
Special Emphasis Panel (ZAR1)
Project Start
2001-03-15
Project End
2006-02-28
Budget Start
Budget End
Support Year
1
Fiscal Year
2001
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
Rydyznski, Carolyn E; Cranert, Stacey A; Zhou, Julian Q et al. (2018) Affinity Maturation Is Impaired by Natural Killer Cell Suppression of Germinal Centers. Cell Rep 24:3367-3373.e4
Carroll, Kaitlin R; Elfers, Eileen E; Stevens, Joseph J et al. (2018) Extending Remission and Reversing New-Onset Type 1 Diabetes by Targeted Ablation of Autoreactive T Cells. Diabetes 67:2319-2328
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:
Hinks, Anne; Marion, Miranda C; Cobb, Joanna et al. (2018) Brief Report: The Genetic Profile of Rheumatoid Factor-Positive Polyarticular Juvenile Idiopathic Arthritis Resembles That of Adult Rheumatoid Arthritis. Arthritis Rheumatol 70:957-962
Gupta, Varsha; Tangpricha, Vin; Yow, Eric et al. (2018) Analysis of relationships between 25-hydroxyvitamin D, parathyroid hormone and cathelicidin with inflammation and cardiovascular risk in subjects with paediatric systemic lupus erythematosus: an Atherosclerosis Prevention in Paediatric Lupus Erythematosus Lupus Sci Med 5:e000255
Rochman, Yrina; Dienger-Stambaugh, Krista; Richgels, Phoebe K et al. (2018) TSLP signaling in CD4+ T cells programs a pathogenic T helper 2 cell state. Sci Signal 11:
McIntosh, Laura A; Marion, Miranda C; Sudman, Marc et al. (2017) Genome-Wide Association Meta-Analysis Reveals Novel Juvenile Idiopathic Arthritis Susceptibility Loci. Arthritis Rheumatol 69:2222-2232
McCauley, Heather A; Chevrier, VĂ©ronique; Birnbaum, Daniel et al. (2017) De-repression of the RAC activator ELMO1 in cancer stem cells drives progression of TGF?-deficient squamous cell carcinoma from transition zones. Elife 6:
Litosh, Vladislav A; Rochman, Mark; Rymer, Jeffrey K et al. (2017) Calpain-14 and its association with eosinophilic esophagitis. J Allergy Clin Immunol 139:1762-1771.e7
Lages, Celine S; Simmons, Julia; Maddox, Avery et al. (2017) The dendritic cell-T helper 17-macrophage axis controls cholangiocyte injury and disease progression in murine and human biliary atresia. Hepatology 65:174-188

Showing the most recent 10 out of 214 publications