The Translational and Research Skills Development Core (Core D) will be the primary vehicle by which the University of Utah Molecular MedicineTranslational Research Center in Thrombosis (U2M2-TRCT) trains young investigators. Core D will take advantage of existing infrastructure at the University of Utah and, in doing so, will provide a unique training environment for MD, PhD, and MD-PhD scientists at various career stages. This includes utilization of the University of Utah Clinical Center in Translational Science (CCTS), four T32 programs, a HHMI med-to-grad PhD scientist training program, the MD-PhD program, and the Medical Student Summer research program. All of these programs are directed or co-directed by U2M2-TRCT investigators. Core D will use this infrastructure to rigorously prepare young investigators for bench to-bedside research careers related to metabolism and/or thrombosis. The Core provides an in-depth and cohesive education program for all types of young invesfigators. This curriculum includes specialized classes that focus on metabolism and thrombosis. Core D also includes individualized mentoring with U2M2-TRCT established scientists that will introduce young investigators to the ins-and-outs of basic and translational research. A primary objective of Core D will be to help young investigators generate preliminary data for competitive grant applications. In parallel, the young investigators will participate in grant writing workshops and research-in-progress sessions that provide a platform for presentation and critique of research plans. The U2M2-TRCT program already includes several young and emerging investigators who participated in preparing this submission. These investigators have previously trained with U2M2-TRCT senior scientists, have successfully applied and received young investigator awards, and are well on their way to independent research careers. Core D will continue to provide a fertile environment that fosters the development of these investigators and other MD, PhD, and MD-PhD trainees who will enter the program over the next several years.
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.
|Koupenova, Milka; Vitseva, Olga; MacKay, Christopher R et al. (2014) Platelet-TLR7 mediates host survival and platelet count during viral infection in the absence of platelet-dependent thrombosis. Blood 124:791-802|
|Schubert, Sebastian; Weyrich, Andrew S; Rowley, Jesse W (2014) A tour through the transcriptional landscape of platelets. Blood 124:493-502|
|Clancy, Lauren; Freedman, Jane E (2014) New paradigms in thrombosis: novel mediators and biomarkers platelet RNA transfer. J Thromb Thrombolysis 37:12-6|
|Freedman, Jane E (2014) Inherited dysfunctional nitric oxide signaling and the pathobiology of atherothrombotic disease. Circ Res 114:1372-3|
|Major, Heather D; Campbell, Robert A; Silver, Robert M et al. (2014) Synthesis of sFlt-1 by platelet-monocyte aggregates contributes to the pathogenesis of preeclampsia. Am J Obstet Gynecol 210:547.e1-7|
|Madden, Jesse L; Drakos, Stavros G; Stehlik, Josef et al. (2014) Baseline red blood cell osmotic fragility does not predict the degree of post-LVAD hemolysis. ASAIO J 60:524-8|
|Shi, Dallas S; Smith, Matthew C P; Campbell, Robert A et al. (2014) Proteasome function is required for platelet production. J Clin Invest 124:3757-66|
|Chen, Karin; Coonrod, Emily M; Kumanovics, Attila et al. (2013) Germline mutations in NFKB2 implicate the noncanonical NF-*B pathway in the pathogenesis of common variable immunodeficiency. Am J Hum Genet 93:812-24|
|Franks, Zechariah; Campbell, Robert A; Vieira de Abreu, Adriana et al. (2013) Methicillin-resistant Staphylococcus aureus-induced thrombo-inflammatory response is reduced with timely antibiotic administration. Thromb Haemost 109:684-95|
|Freedman, Jane E; Tanriverdi, Kahraman (2013) Defining miRNA targets: balancing simplicity with complexity. Circulation 127:2075-7|