Abstract-Properly handling parallax is important for video stabilization. Existing methods that achieve the aim require either 3D reconstruction or long feature trajectories to enforce the subspace or epipolar geometry constraints. In this paper, we present a robust and efficient technique that works on general videos. It achieves high-quality camera motion on videos where 3D reconstruction is difficult or long feature trajectories are not available. We represent each trajectory as a Bé zier curve and maintain the spatial relations between trajectories by preserving the original offsets of neighboring curves. Our technique formulates stabilization as a spatialtemporal optimization problem that finds smooth feature trajectories and avoids visual distortion. The Bé zier representation enables strong smoothness of each feature trajectory and reduces the number of variables in the optimization problem. We also stabilize videos in a streaming fashion to achieve scalability. The experiments show that our technique achieves high-quality camera motion on a variety of challenging videos that are difficult for existing methods.

Multipotent mesenchymal stem/stromal cells (MSCs) exhibit great potential for cell-based therapy. Proper epigenomic signatures in MSCs are important for the maintenance and the subsequent differentiation potential. The DNA methyltransferase 3-like (DNMT3L) that was mainly expressed in the embryonic stem (ES) cells and the developing germ cells plays an important role in shaping the epigenetic landscape. Here, we report the reduced colony forming ability and impaired in vitro osteogenesis in Dnmt3l-knockout-mice-derived MSCs (Dnmt3l KO MSCs). By comparing the transcriptome between undifferentiated Dnmt3l KO MSCs and the MSCs from the wild-type littermates, some of the differentially regulated genes (DEGs) were found to be associated with bone-morphology-related phenotypes. On the third day of osteogenic induction, differentiating Dnmt3l KO MSCs were enriched for genes associated with nucleosome structure, peptide binding and extracellular matrix modulation. Differentially expressed transposable elements in many subfamilies reflected the change of corresponding regional epigenomic signatures. Interestingly, DNMT3L protein is not expressed in cultured MSCs. Therefore, the observed defects in Dnmt3l KO MSCs are unlikely a direct effect from missing DNMT3L in this cell type; instead, we hypothesized them as an outcome of the pre-deposited epigenetic signatures from the DNMT3L-expressing progenitors. We observed that 24 out of the 107 upregulated DEGs in Dnmt3l KO MSCs were hypermethylated in their gene bodies of DNMT3L knock-down ES cells. Among these 24 genes, some were associated with skeletal development or homeostasis. However, we did not observe reduced bone development, or reduced bone density through aging in vivo. The stronger phenotype in vitro suggested the involvement of potential spreading and amplification of the pre-deposited epigenetic defects over passages, and the contribution of oxidative stress during in vitro culture. We demonstrated that transient deficiency of epigenetic co-factor in ES cells or progenitor cells caused compromised property in differentiating cells much later. In order to facilitate safer practice in cell-based therapy, we suggest more in-depth examination shall be implemented for cells before transplantation, even on the epigenetic level, to avoid long-term risk afterward.

Non-alcoholic fatty liver disease is associated with ageing, and impaired mitochondrial homeostasis is the main cause for hepatic ageing. Caloric restriction (CR) is a promising therapeutic approach to reduce fatty liver. The present study aimed to investigate the effect of early onset CR on decelerating the progression of ageing-related steatohepatitis. The potential mechanisms regarding to mitochondria were further evaluated. Eight-week-old C57BL/6 male mice (n = 21) were randomly divided into three groups, Young-AL (AL, ad libitum), Aged-AL, and Aged-CR (60% intake of AL). Mice were sacri ced at the age of 7 months (Young) or 20 months (Aged). Aged-AL mice displayed the greatest body weight, liver weight and liver relative weight among treatments. Ageing caused a great grade of steatosis, lipid peroxidation, in ammation, and brosis in the liver. Mega mitochondria with short, randomly organized crista were noticed in the aged liver. CR ameliorated these negative phenomena in aged liver. Ageing was accompanied with a lower level of hepatic ATP, while CR restored it. Mitochondrial-related protein expressions of respiratory chain complexes (NDUFB8 and SDHB), and ssion (DRP1) were suppressed in aged liver. Proteins related to mitochondrial biogenesis (TFAM), and fusion (MFN2) were upregulated in aged liver. CR reversed the expressions of SDHB, TFAM, DRP1, and MFN2 in aged liver. To conclude, early onset CR signi cantly prevented the negative effect of ageing-associated steatohepatitis, including lipid peroxidation, in ammation, steatosis and brosis. Moreover, CR eased ageing-associated energy de cit in liver partially via maintaining mitochondrial homeostasis.

Non-alcoholic fatty liver disease is associated with ageing, and impaired mitochondrial homeostasis is the main cause for hepatic ageing. Caloric restriction (CR) is a promising therapeutic approach to reduce fatty liver. The present study aimed to investigate the effect of early onset CR on decelerating the progression of ageing-related steatohepatitis. The potential mechanisms regarding to mitochondria were further evaluated. Eight-week-old C57BL/6 male mice (n = 21) were randomly divided into three groups, Young-AL (AL, ad libitum), Aged-AL, and Aged-CR (60% intake of AL). Mice were sacrificed at the age of 7 months (Young) or 20 months (Aged). Aged-AL mice displayed the greatest body weight, liver weight and liver relative weight among treatments. Ageing caused a great grade of steatosis, lipid peroxidation, inflammation, and fibrosis in the liver. Mega mitochondria with short, randomly organized crista were noticed in the aged liver. CR ameliorated these negative phenomena in aged liver. Ageing was accompanied with a lower level of hepatic ATP, while CR restored it. Mitochondrial-related protein expressions of respiratory chain complexes (NDUFB8 and SDHB), and fission (DRP1) were suppressed in aged liver. Proteins related to mitochondrial biogenesis (TFAM), and fusion (MFN2) were upregulated in aged liver. CR reversed the expressions of SDHB, TFAM, DRP1, and MFN2 in aged liver. To conclude, early onset CR significantly prevented the negative effect of ageing-associated steatohepatitis, including lipid peroxidation, inflammation, steatosis and fibrosis. Moreover, CR eased ageing-associated energy deficit in liver partially via maintaining mitochondrial homeostasis.