The Pediatric Rheumatology Tissue Repository (PRTR), a funded component of a PSO rheumatic disease core center, assists local and national investigators in specimen collection, processing, storage and distribution of biospecimens for rheumatic diseases-related studies. The principal functions of this core are: ? To collect, process and maintain biological specimens from patients with pediatric rheumatological and related musculoskeletal conditions as well as from relevant control populations for research purposes. Samples collected include blood, urine, synovial fluid, synovial tissue, hair and saliva. Products derived from these collections are suitable for genetic, genomic, proteomic, immunologic function and biomarker studies. ? To optimize the availability and potential for use of sample collections. Collection, processing and storage practices are optimized to meet current and future study needs and when possible standardized to be consistent with other national and international efforts. ? To provide high quality samples in an appropriate format for investigators conducting IRB-approved basic and translational studies in pediatric rheumatologic disease. Informatics solutions for sample storage documentation will allow accurate and appropriate use. Current systems have been optimized to allow information relative to consent, source of collection (study, extemal site, type of sample, etc), and specifics of handling/processing as well as prior use to be considered when accessing samples. Established practices of the PRTR for sample collection, processing shipping and training of clinical site personnel ensure that the scope of specimens needed for translational research projects are available. Thus, this unique resource is important to enabling definitive genomic and biological studies necessary to understand and define childhood rheumatic diseases.
Established practices of the PRTR for sample collection, processing shipping and training of clinical site personnel ensure that the scope of specimens needed for translational research projects are available. Thus, this unique resource is important to enabling definitive genomic and biological studies necessary to understand and define childhood rheumatic diseases.
|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:|
|Hinks, A; Bowes, J; Cobb, J et al. (2017) Fine-mapping the MHC locus in juvenile idiopathic arthritis (JIA) reveals genetic heterogeneity corresponding to distinct adult inflammatory arthritic diseases. Ann Rheum Dis 76:765-772|
|Ombrello, Michael J; Arthur, Victoria L; Remmers, Elaine F et al. (2017) Genetic architecture distinguishes systemic juvenile idiopathic arthritis from other forms of juvenile idiopathic arthritis: clinical and therapeutic implications. Ann Rheum Dis 76:906-913|
|Feldhoff, Lea M; Rueda, Cesar M; Moreno-Fernandez, Maria E et al. (2017) IL-1? induced HIF-1? inhibits the differentiation of human FOXP3+ T cells. Sci Rep 7:465|
|Lo, Yuan-Hung; Chung, Eunah; Li, Zhaohui et al. (2017) Transcriptional Regulation by ATOH1 and its Target SPDEF in the Intestine. Cell Mol Gastroenterol Hepatol 3:51-71|
Showing the most recent 10 out of 214 publications