The Bioanalytical Core (Core C) serves the O'Brien Center community, both at UAB and UCSD and the extended research base by providing state-of-the-art bioenergetics, oxidative stress analysis and metabolite analysis support for acute kidney injury (AKI) research. Core C provides a comprehensive resource that includes optimized protocols and technology for bioanalytical analyses of oxidative stress and cellular bioenergetics, biomarkers of AKI, post-translational modifications, and changes in small molecule biochemistry. The services involve consultation, training in experimental design, recovery of samples suitable for analysis and assay performance. New services offered include unique techniques to determine mitochondrial bioenergetics, LC-mass spectrometry based assays for creatinine, F2-isoprostanes and citric acid cyle intermediates. State-of-the-art nanoLC-MS methods are being developed to perform both targeted and untargeted metabolomics and exosome analysis in clinical samples and from animal models of AKI. Core C has been successful in supporting the kidney research community. Since the inception of Core C, more than 8,500 assays have been performed for 48 principal investigators involving 56 projects. Of the 48 investigators, 44 were non-core personnel. The number of investigators using Core C each year is increasing, as is the annual publication rate. Core C has also supported the research efforts of 7 Pilot and Feasibility grant awardees. These combined efforts have been currently recognized in 23 peer-reviewed publications. The Core will participate in education and training of investigators providing hands-on experience and scientific interchange. A recurring feature from 2013-2017 will be an annual 4-day workshop for training in metabolomics (funded by NIGMS as part of the NIH Common Fund program in metabolomics). Finally, the Bioanalytical Core, in concert with the O'Brien Center leadership, will identify new bioanalytical needs of investigators and implement them for the Center.
Acute kidney injury is associated with severe consequences including death, prolonged hospitalization and can lead to chronic kidney disease. Core C of this Center provides investigators key resources required to enable a better understanding of the underlying mechanisms and determine best approaches to diagnose and manage this disease.
|Fu, Yiling; Gerasimova, Maria; Batz, Falk et al. (2015) PPAR? agonist-induced fluid retention depends on ?ENaC expression in connecting tubules. Nephron 129:68-74|
|Murray, Patrick T; Mehta, Ravindra L; Shaw, Andrew et al. (2014) Potential use of biomarkers in acute kidney injury: report and summary of recommendations from the 10th Acute Dialysis Quality Initiative consensus conference. Kidney Int 85:513-21|
|Wetta, Luisa A; Biggio, Joseph R; Cliver, Suzanne et al. (2014) Is midtrimester vitamin D status associated with spontaneous preterm birth and preeclampsia? Am J Perinatol 31:541-6|
|Wall, Stephanie B; Smith, M Ryan; Ricart, Karina et al. (2014) Detection of electrophile-sensitive proteins. Biochim Biophys Acta 1840:913-22|
|Virk-Baker, Mandeep K; Barnes, Stephen; Krontiras, Helen et al. (2014) S-(-)equol producing status not associated with breast cancer risk among low isoflavone-consuming US postmenopausal women undergoing a physician-recommended breast biopsy. Nutr Res 34:116-25|
|Andringa, Kelly K; Agarwal, Anupam (2014) Role of hypoxia-inducible factors in acute kidney injury. Nephron Clin Pract 127:70-4|
|Portilla, Didier (2014) Apoptosis, fibrosis and senescence. Nephron Clin Pract 127:65-9|
|Nourbakhsh, Noureddin; Singh, Prabhleen (2014) Role of renal oxygenation and mitochondrial function in the pathophysiology of acute kidney injury. Nephron Clin Pract 127:149-52|
|Kumar, Rajiv; Vallon, Volker (2014) Reduced renal calcium excretion in the absence of sclerostin expression: evidence for a novel calcium-regulating bone kidney axis. J Am Soc Nephrol 25:2159-68|
|Abdul Roda, Mojtaba; Sadik, Mariam; Gaggar, Amit et al. (2014) Targeting prolyl endopeptidase with valproic acid as a potential modulator of neutrophilic inflammation. PLoS One 9:e97594|
Showing the most recent 10 out of 177 publications