The focus for the George M. O'Brien Kidney Centers has been basic science investigation that has very successfully defined kidney structure, function and disease mechanisms. New technologies now provide opportunities to translate these remarkable basic science advances to the clinic in ways not previously imaginable. Advances in identification of genetic susceptibilities as well as the advent of the genome project and systems biology technologies set the stage for development of molecular maps that can be superimposed on traditional pathologic and functional descriptors so as to define diseases in a new way. These developments have important implications for definition of molecular markers that will allow accurate individualized prediction of outcome and response to therapy, and the identification of key pathways for therapeutic attack. The University of Michigan has developed and recruited expertise to help exploit these opportunities for people with kidney diseases. The realization of these opportunities requires collaborations between investigators world-wide for the collection of samples from well characterized individuals and populations, the application of technologies that facilitate information availability and exchange, the development and maintenance of databanks, and the integration of these technologies between human diseases, animals models, cellular systems and molecular signaling so as to define key pathways driving renal disease processes. Towards these goals the O'Brien Kidney Research Core Center at the University of Michigan will support four Cores: A. An Applied Systems Biology Core that has developed the platforms and infrastructure necessary to serve the integrative functions outlined above;B. A Clinical Phenotyping and Biobank Core that will collect the biosamples from affected characterized individuals;and C. An Applied Genetics Core that will perform mutational analysis for genotype/phenotype matching;D. A Basic Research Enhancement Core that will facilitate basic science development, integration and translation. These cores together with the Pilot and Feasibility Projects and Educational Enhancement Program in the Administrative Core will coordinate the grant, utilize the Cores and attract and support new talent into kidney research. The University of Michigan will provide $1,000,000 in supplemental support for the Center.
The aim i s to develop a structure which will serve local and national kidney investigators and the kidney community at large. Using web based tools, we will provide the basis for new understanding of disease-specific molecular pathology that can be used by every kidney investigator in the public and private sector world-wide.
|Bria, Carmen R M; Afshinnia, Farsad; Skelly, Patrick W et al. (2018) Asymmetrical flow field-flow fractionation for improved characterization of human plasma lipoproteins. Anal Bioanal Chem :|
|Troost, Jonathan P; Hawkins, Jennifer; Jenkins, Daniel R et al. (2018) Consent for Genetic Biobanking in a Diverse Multisite CKD Cohort. Kidney Int Rep 3:1267-1275|
|Zeng, Lixia; Mathew, Anna V; Byun, Jaeman et al. (2018) Myeloperoxidase-derived oxidants damage artery wall proteins in an animal model of chronic kidney disease-accelerated atherosclerosis. J Biol Chem 293:7238-7249|
|Mulder, Skander; Hamidi, Habib; Kretzler, Matthias et al. (2018) An integrative systems biology approach for precision medicine in diabetic kidney disease. Diabetes Obes Metab 20 Suppl 3:6-13|
|Duda, Marlena; Zhang, Hongjiu; Li, Hong-Dong et al. (2018) Brain-specific functional relationship networks inform autism spectrum disorder gene prediction. Transl Psychiatry 8:56|
|Afshinnia, Farsad; Rajendiran, Thekkelnaycke M; Wernisch, Stefanie et al. (2018) Lipidomics and Biomarker Discovery in Kidney Disease. Semin Nephrol 38:127-141|
|Jadoon, Adil; Mathew, Anna V; Byun, Jaeman et al. (2018) Gut Microbial Product Predicts Cardiovascular Risk in Chronic Kidney Disease Patients. Am J Nephrol 48:269-277|
|Mathew, Anna V; Li, Lei; Byun, Jaeman et al. (2018) Therapeutic Lifestyle Changes Improve HDL Function by Inhibiting Myeloperoxidase-Mediated Oxidation in Patients With Metabolic Syndrome. Diabetes Care 41:2431-2437|
|Skorecki, Karl L; Lee, Jessica H; Langefeld, Carl D et al. (2018) A null variant in the apolipoprotein L3 gene is associated with non-diabetic nephropathy. Nephrol Dial Transplant 33:323-330|
|Heinzel, Andreas; Kammer, Michael; Mayer, Gert et al. (2018) Validation of Plasma Biomarker Candidates for the Prediction of eGFR Decline in Patients With Type 2 Diabetes. Diabetes Care 41:1947-1954|
Showing the most recent 10 out of 178 publications