; 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)
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Yale University
New Haven
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Besse, Whitney; Choi, Jungmin; Ahram, Dina et al. (2018) A noncoding variant in GANAB explains isolated polycystic liver disease (PCLD) in a large family. Hum Mutat 39:378-382
Hanberg, Jennifer S; Rao, Veena S; Ahmad, Tariq et al. (2018) Inflammation and cardio-renal interactions in heart failure: a potential role for interleukin-6. Eur J Heart Fail 20:933-934
Cassini, Marcelo F; Kakade, Vijayakumar R; Kurtz, Elizabeth et al. (2018) Mcp1 Promotes Macrophage-Dependent Cyst Expansion in Autosomal Dominant Polycystic Kidney Disease. J Am Soc Nephrol 29:2471-2481
Nadkarni, Girish N; Chauhan, Kinsuk; Verghese, Divya A et al. (2018) Plasma biomarkers are associated with renal outcomes in individuals with APOL1 risk variants. Kidney Int 93:1409-1416
Lausecker, Franziska; Tian, Xuefei; Inoue, Kazunori et al. (2018) Vinculin is required to maintain glomerular barrier integrity. Kidney Int 93:643-655
Knauf, Felix; Velazquez, Heino; Pfann, Victoria et al. (2018) Characterization of renal NaCl and oxalate transport in Slc26a6-/- mice. Am J Physiol Renal Physiol :
Silva, Luciane M; Jacobs, Damon T; Allard, Bailey A et al. (2018) Inhibition of Hedgehog signaling suppresses proliferation and microcyst formation of human Autosomal Dominant Polycystic Kidney Disease cells. Sci Rep 8:4985
Daga, Ankana; Majmundar, Amar J; Braun, Daniela A et al. (2018) Whole exome sequencing frequently detects a monogenic cause in early onset nephrolithiasis and nephrocalcinosis. Kidney Int 93:204-213
Mansour, Sherry G; Hall, Isaac E; Reese, Peter P et al. (2018) Reliability of deceased-donor procurement kidney biopsy images uploaded in United Network for Organ Sharing. Clin Transplant 32:e13441
Manfredo Vieira, S; Hiltensperger, M; Kumar, V et al. (2018) Translocation of a gut pathobiont drives autoimmunity in mice and humans. Science 359:1156-1161

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