Purpose In the last decade, there has been a great effort to bring mixed reality (MR) into the operating room to assist surgeons intraoperatively. However, progress towards this goal is still at an early stage. The aim of this paper is to propose a MR visualisation platform which projects multiple imaging modalities to assist intraoperative surgical guidance. Methodology In this work, a MR visualisation platform has been developed for the Microsoft HoloLens. The platform contains three visualisation components, namely a 3D organ model, volumetric data, and tissue morphology captured with intraoperative imaging modalities. Furthermore, a set of novel interactive functionalities have been designed including scrolling through volumetric data and adjustment of the virtual objects’ transparency. A pilot user study has been conducted to evaluate the usability of the proposed platform in the operating room. The participants were allowed to interact with the visualisation components and test the different functionalities. Each surgeon answered a questionnaire on the usability of the platform and provided their feedback and suggestions. Results The analysis of the surgeons’ scores showed that the 3D model is the most popular MR visualisation component and neurosurgery is the most relevant speciality for this platform. The majority of the surgeons found the proposed visualisation platform intuitive and would use it in their operating rooms for intraoperative surgical guidance. Our platform has several promising potential clinical applications, including vascular neurosurgery. Conclusion The presented pilot study verified the potential of the proposed visualisation platform and its usability in the operating room. Our future work will focus on enhancing the platform by incorporating the surgeons’ suggestions and conducting extensive evaluation on a large group of surgeons.

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Autophagy is an essential catabolic process that promotes clearance of surplus or damaged intracellular components 1 . As a recycling process, autophagy is also important for the maintenance of cellular metabolites during periods of starvation 2 . Loss of autophagy is sufficient to cause cell death in animal models and is likely to contribute to tissue degeneration in a number of human diseases including neurodegenerative and lysosomal storage disorders 3-7 . However, it remains unclear which of the many cellular functions of autophagy primarily underlies its role in cell survival. Here we have identified a critical role of autophagy in the maintenance of nicotinamide adenine dinucleotide (NAD + /NADH) levels. In respiring cells, loss of autophagy caused NAD(H) depletion resulting in mitochondrial membrane depolarisation and cell death. We also found that maintenance of NAD(H) is an evolutionary conserved function of autophagy from yeast to human cells. Importantly, cell death and reduced viability of autophagy-deficient animal models can be partially reversed by supplementation with an NAD(H) precursor. Our study provides a mechanistic link between autophagy and NAD(H) metabolism and suggests that boosting NAD(H) levels may be an effective intervention strategy to prevent cell death and tissue degeneration in human diseases associated with autophagy dysfunction.Macroautophagy, hereinafter autophagy, is a cellular trafficking pathway mediated by the formation of double-membraned vesicles called autophagosomes, which ultimately fuse with lysosomes, where their cargo is degraded. By sequestering and clearing dysfunctional cellular components, such as protein aggregates and damaged organelles, autophagy maintains cellular homeostasis whilst also providing metabolites and energy during periods of starvation. Studies using a range of laboratory models from yeast to mammals have established that autophagy is essential for cellular and organismal survival. For example, inducible knockout of core autophagy genes, such as Atg5, results in cell death and tissue degeneration in adult mice 3,8,9 . However, autophagy-deficient cells such as Atg5 -/mouse embryonic fibroblasts (MEFs) are viable in cell culture, which hinders in vitro studies of the mechanisms leading to cell death [8][9][10] . We hypothesized that this apparent discrepancy between the requirement for functional autophagy in vivo and in vitro could be due to a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis. Indeed, whilst differentiated cells with high energy demand, such as neurons, rely on aerobic ATP generation via OXPHOS, the abundance of glucose in standard cell culture conditions allows cells to generate sufficient levels of ATP via glycolysis. This decreased reliance on mitochondrial respiration could then mask an underlying viability defect 11 .A well-established strategy to reverse cellular reliance on energy generation via aerobic glycolysis and promote mitochondrial OXPHOS, is to replace glucose, the major carbon source in tissu...