; 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.
| Hall, Isaac E; Parikh, Chirag R; Schröppel, Bernd et al. (2018) Procurement Biopsy Findings Versus Kidney Donor Risk Index for Predicting Renal Allograft Survival. Transplant Direct 4:e373 |
| Luciano, Amelia K; Zhou, Wenping; Santana, Jeans M et al. (2018) CLOCK phosphorylation by AKT regulates its nuclear accumulation and circadian gene expression in peripheral tissues. J Biol Chem 293:9126-9136 |
| Greenberg, Jason H; Kakajiwala, Aadil; Parikh, Chirag R et al. (2018) Emerging biomarkers of chronic kidney disease in children. Pediatr Nephrol 33:925-933 |
| Cornec-Le Gall, Emilie; Olson, Rory J; Besse, Whitney et al. (2018) Monoallelic Mutations to DNAJB11 Cause Atypical Autosomal-Dominant Polycystic Kidney Disease. Am J Hum Genet 102:832-844 |
| Greenberg, Jason H; Zappitelli, Michael; Jia, Yaqi et al. (2018) Biomarkers of AKI Progression after Pediatric Cardiac Surgery. J Am Soc Nephrol 29:1549-1556 |
| 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 |
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