The primary responsibility of the Patient Enrollment and Data Analysis Core (Core B) is to identify and recruit healthy lean control subjects as well as patients with type 2 diabetes and obesity for Projects 1-4 and provide specialized data analysis support for the University of Utah Molecular Medicine Translational Research Center in Thrombosis (U2M2-TRCT). A team of investigators with expertise in thrombosis and metabolic syndromes will lead Core B. This core also includes a clinical coordinator, database manager, and investigators with experience in statistics and bioinformatics. Core B will directly interact with Core C regarding isolation of human platelets from patients with metabolic syndromes and provide support for all four research projects. Patients enrolled through Project 3 will be identified and recruited by Core C using successful methods described in the Core description. The Core will utilize the University of Utah Clinical Center in Translational Science (CCTS) to enhance patient enrollment and study initiation. Core B will be responsible for entering patient data and management of the U-STAR (The Utah Study of Translational Science And Research Registry) database. In addition to recruiting, enrolling, and managing data, Core B will provide statistical and bioinformatics support for all of the projects. The statistics wing will provide sample size and power calculations, assist with study design, and analyze experimental data. The bioinformatics arm will provide support for the next-generation RNA-sequencing studies proposed by U2M2-TRCT investigators. This includes data interpretation, statistical support, and software development. The services provided by Core B, which is centrally located and readily available to all U2M2-TRCT participants, will ensure that enrollment goals are met and exceeded and that data analysis occurs seamlessly within the program.
Patients with type 2 diabetes, obesity, or the metabolic syndrome are at increased risk for blood clots (thrombosis) caused by cells called platelets. Our studies will determine how metabolic factors in the blood and tissues (the metabolic milieu), such as high glucose and lipids, make platelets more prone to induce thrombosis, providing new insights into the treatment and management of diabetes and obesity.
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|Morales-Ortíz, Jessica; Rondina, Matthew T; Brown, Samuel M et al. (2018) High Levels of Soluble Triggering Receptor Expressed on Myeloid Cells-Like Transcript (TLT)-1 Are Associated With Acute Respiratory Distress Syndrome. Clin Appl Thromb Hemost 24:1122-1127|
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|Cloutier, Nathalie; Allaeys, Isabelle; Marcoux, Genevieve et al. (2018) Platelets release pathogenic serotonin and return to circulation after immune complex-mediated sequestration. Proc Natl Acad Sci U S A 115:E1550-E1559|
|Manne, B K; Münzer, P; Badolia, R et al. (2018) PDK1 governs thromboxane generation and thrombosis in platelets by regulating activation of Raf1 in the MAPK pathway. J Thromb Haemost 16:1211-1225|
|Fidler, Trevor P; Rowley, Jesse W; Araujo, Claudia et al. (2017) Superoxide Dismutase 2 is dispensable for platelet function. Thromb Haemost 117:1859-1867|
|Manne, Bhanu K; Xiang, Shang Chun; Rondina, Matthew T (2017) Platelet secretion in inflammatory and infectious diseases. Platelets 28:155-164|
|Campbell, Robert A; Vieira-de-Abreu, Adriana; Rowley, Jesse W et al. (2017) Clots Are Potent Triggers of Inflammatory Cell Gene Expression: Indications for Timely Fibrinolysis. Arterioscler Thromb Vasc Biol 37:1819-1827|
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