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Background. Delayed graft function (DGF) affects over 25% of deceased donor kidney transplants (DDKTs) and is associated with increased cost, worsened graft outcomes, and mortality. While approaches to preventing DGF have focused on minimizing cold ischemia, donor factors such as acute tubular injury can influence risk. There are currently no pharmacologic therapies to modify DGF risk or promote repair, in part due to our incomplete understanding of the biology of preimplantation tubular injury. Methods. We collected intraoperative, preimplantation kidney biopsies from 11 high-risk deceased donors and 10 living donors and followed transplant recipients for graft function. We performed quantitative high-dimensional histopathologic analysis using imaging mass cytometry to determine the cellular signatures that distinguished deceased and living donor biopsies as well as deceased donor biopsies which either did or did not progress to DGF. Results. We noted decreased tubular cells (P

BACKGROUND AND OBJECTIVE: Live-animal micro-computed tomography is a new and promising technique that can be used to quantify changes in bone volume for periodontal disease models. The major aim of this study was to develop the methodology of live-animal micro-computed tomography and to determine the effect of a novel secretory phospholipase A2 inhibitor on alveolar bone loss. MATERIAL AND METHODS: Periodontitis was induced in mice by oral infection with Porphyromonas gingivalis over a period of 13 wk, and live-animal micro-computed tomography scans were taken at different time-points to determine bone volume changes with disease progression. This enabled conclusions to be made as to when treatment was most likely to be effective. In addition, the model was used to investigate a novel drug, the secretory phospholipase A2 inhibitor, KHO64, and its potential ability to inhibit osteoclast bone resorption and treat periodontitis. RESULTS: The results from live-animal micro-computed tomography scans revealed greater, statistically significant, bone volume loss in diseased mice compared with normal mice (p < 0.05). This corresponded to a larger area from the cemento-enamel junction to the alveolar bone crest, as assessed by stereo imaging (p < 0.001). These techniques can therefore detect and quantify alveolar bone loss. Both methods revealed that KHO64 had no significant effect on the volume of bone resorption. CONCLUSION: Live-animal micro-computed tomography is a robust, reproducible technique that clearly demonstrates significant time-dependent changes in alveolar bone volume in a small-animal model of periodontitis. [ABSTRACT FROM AUTHOR]