; Collaborative interactions between Investigators in the Section of Nephrology and the Department of Cellular and Molecular Physiology at Yale have historically provided much of the experimental evidence that underlies our current understanding of normal kidney function at the cellular, tubular and whole organ level. And yet, at a time when the development of increasingly sophisticated cell and molecular biology techniques has afforded scientists the ability to manipulate the genes and proteins that control these physiologic, processes, many of the investigators involved in these studies have not acquired the technical skills necessary to identify the mechanism(s) that underlie the phenotype that they uncover. The mission of the Yale O'Brien Kidney Center Renal Physiology and Phenotyping Core (Core A) is to utilize our unique expertise in the rigorous study and understanding of renal physiology to provide highly specialized phenotypic analysis of rodents at the systemic, whole kidney and/or individual nephron segment levels. By providing expertise and training in techniques such as tubule micropuncture, in vitro and in vivo microperfusion, determination of glomerular filtration rates and renal perfusion, and continuous blood pressure measurements. Core A is designed to allow investigators to accurately define the site, mechanism and impact of genetic and/or pharmacologic manipulations on cellular, organ, and whole animal physiology. To achieve this, the Yale O'Brien Kidney Center Renal Physiology and Phenotyping Core takes advantage of 2 major strengths: 1) the specialized equipment needed to provide phenotyping .services at the systemic, whole kidney, and individual nephron segment levels, and 2) experienced and skilled personnel capable of using that equipment to generate reliable and reproducible data that are required for thorough, accurate phenotypic analysis. During the previous funding period, this Core was heavily utilized by Investigators with 19 distinct services provided to more than 40 Investigators supporting studies in 32 manuscripts.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Center Core Grants (P30)
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Special Emphasis Panel (ZDK1-GRB-6 (M2))
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Braun, Daniela A; Schueler, Markus; Halbritter, Jan et al. (2016) Whole exome sequencing identifies causative mutations in the majority of consanguineous or familial cases with childhood-onset increased renal echogenicity. Kidney Int 89:468-75
Mulay, Shrikant Ramesh; Eberhard, Jonathan Nicodemos; Pfann, Victoria et al. (2016) Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice. Am J Physiol Renal Physiol :ajprenal.00488.2015
Knauf, Felix; Thomson, Robert B; Heneghan, John F et al. (2016) Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion. J Am Soc Nephrol :
Li, Yuanyuan; Tian, Xin; Ma, Ming et al. (2016) Deletion of ADP Ribosylation Factor-Like GTPase 13B Leads to Kidney Cysts. J Am Soc Nephrol 27:3628-3638
Schaub, Jennifer A; Parikh, Chirag R; TRIBE-AKI Consortium (2016) The Authors Reply. Kidney Int 89:1162-3
Reese, Peter P; Hall, Isaac E; Weng, Francis L et al. (2016) Associations between Deceased-Donor Urine Injury Biomarkers and Kidney Transplant Outcomes. J Am Soc Nephrol 27:1534-43
Guo, Xiaojia; Hollander, Lindsay; MacPherson, Douglas et al. (2016) Inhibition of renalase expression and signaling has antitumor activity in pancreatic cancer. Sci Rep 6:22996
Pema, Monika; Drusian, Luca; Chiaravalli, Marco et al. (2016) mTORC1-mediated inhibition of polycystin-1 expression drives renal cyst formation in tuberous sclerosis complex. Nat Commun 7:10786
Wang, Andrew; Huen, Sarah C; Luan, Harding H et al. (2016) Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation. Cell 166:1512-1525.e12
Stankewich, Michael C; Moeckel, Gilbert W; Ji, Lan et al. (2016) Isoforms of Spectrin and Ankyrin Reflect the Functional Topography of the Mouse Kidney. PLoS One 11:e0142687

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