Justin Zhang

Incidental findings in research with human participants may have implications for a person’s present health or future health outcomes. Current guidelines focus on methods for handling and reporting incidental findings from biological test data but incidental findings might also arise from non-biological tests. This article presents three examples in which the results from non-biological test data can be predictive of future disease and should be disclosed to research participants. It is intended to increase awareness and facilitate further discussion about the reporting of incidental findings from non-biological data.

Early detection of cancer and its precursors remains the best way to ensure patient survival and quality of life. Our specific aim is to test a multimodality approach to noninvasive diagnostics of oral premalignancy and malignancy. In the hamster cheek pouch model, in vivo optical coherence tomography and optical Doppler tomography map epithelial, subepithelial, and vascular change throughout carcinogenesis. In vivo multiwavelength multiphoton and second-harmonic generated fluorescence techniques provided parallel data on surface and subsurface tissue structure, specifically collagen presence and structure, cellular presence, and vasculature. Images are diagnosed by two blinded, prestandardized investigators using a scale from 0 to 6 for all modalities. After sacrifice, histopathology is evaluated on a scale of 0 to 6. Imaging data are reproducibly obtained with good accuracy. Carcinogenesis-related structural and vascular changes are clearly visible to tissue depths of 2 mm. Sensitivity and specificity compare well with conventional techniques. Our conclusions are that OCT/ODT and MPM/SHG are promising noninvasive in vivo diagnostic modalities for oral dysplasia and malignancy. © 2005 Society of Photo-Optical Instrumentation Engineers.

© 2015 The Authors.In the heart, augmented Ca 2+ fluxing drives contractility and ATP generation through mitochondrial Ca 2+ loading. Pathologic mitochondrial Ca 2+ overload with ischemic injury triggers mitochondrial permeability transition pore opening and cardiomyocyte death. Mitochondrial Ca 2+ uptake is primarily mediated by the mitochondrial Ca 2+ uniporter. Here, we generated mice with adult and cardiomyocyte-specific deletion of Mcu, which produced mitochondria refractory to acute Ca 2+ uptake, with impaired ATP production, and inhibited MPTP opening upon acute Ca 2+ challenge. Mice lacking Mcu inthe adult heart were also protected from acute ischemia-reperfusion injury. However, resting/basal mitochondrial Ca 2+ levels were normal in hearts of Mcu-deleted mice, and mitochondria lacking MCU eventually loaded with Ca 2+ after stress stimulation. Indeed, Mcu-deleted mice were unable to immediately sprint on a treadmill unless warmed up for 30min. Hence, MCU is a dedicated regulator of short-term mitochondrial Ca 2+ loading underlying a"fight-or-flight" response that acutely matches cardiac workload with ATP production.