2,150 research outputs found

    MVG Mechanism: Differential Privacy under Matrix-Valued Query

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    Differential privacy mechanism design has traditionally been tailored for a scalar-valued query function. Although many mechanisms such as the Laplace and Gaussian mechanisms can be extended to a matrix-valued query function by adding i.i.d. noise to each element of the matrix, this method is often suboptimal as it forfeits an opportunity to exploit the structural characteristics typically associated with matrix analysis. To address this challenge, we propose a novel differential privacy mechanism called the Matrix-Variate Gaussian (MVG) mechanism, which adds a matrix-valued noise drawn from a matrix-variate Gaussian distribution, and we rigorously prove that the MVG mechanism preserves (ϵ,δ)(\epsilon,\delta)-differential privacy. Furthermore, we introduce the concept of directional noise made possible by the design of the MVG mechanism. Directional noise allows the impact of the noise on the utility of the matrix-valued query function to be moderated. Finally, we experimentally demonstrate the performance of our mechanism using three matrix-valued queries on three privacy-sensitive datasets. We find that the MVG mechanism notably outperforms four previous state-of-the-art approaches, and provides comparable utility to the non-private baseline.Comment: Appeared in CCS'1

    Oxytocin is an age-specific circulating hormone that is necessary for muscle maintenance and regeneration.

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    The regenerative capacity of skeletal muscle declines with age. Previous studies suggest that this process can be reversed by exposure to young circulation; however, systemic age-specific factors responsible for this phenomenon are largely unknown. Here we report that oxytocin--a hormone best known for its role in lactation, parturition and social behaviours--is required for proper muscle tissue regeneration and homeostasis, and that plasma levels of oxytocin decline with age. Inhibition of oxytocin signalling in young animals reduces muscle regeneration, whereas systemic administration of oxytocin rapidly improves muscle regeneration by enhancing aged muscle stem cell activation/proliferation through activation of the MAPK/ERK signalling pathway. We further show that the genetic lack of oxytocin does not cause a developmental defect in muscle but instead leads to premature sarcopenia. Considering that oxytocin is an FDA-approved drug, this work reveals a potential novel and safe way to combat or prevent skeletal muscle ageing

    Disruption of mesoderm formation during cardiac differentiation due to developmental exposure to 13-cis-retinoic acid.

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    13-cis-retinoic acid (isotretinoin, INN) is an oral pharmaceutical drug used for the treatment of skin acne, and is also a known teratogen. In this study, the molecular mechanisms underlying INN-induced developmental toxicity during early cardiac differentiation were investigated using both human induced pluripotent stem cells (hiPSCs) and human embryonic stem cells (hESCs). Pre-exposure of hiPSCs and hESCs to a sublethal concentration of INN did not influence cell proliferation and pluripotency. However, mesodermal differentiation was disrupted when INN was included in the medium during differentiation. Transcriptomic profiling by RNA-seq revealed that INN exposure leads to aberrant expression of genes involved in several signaling pathways that control early mesoderm differentiation, such as TGF-beta signaling. In addition, genome-wide chromatin accessibility profiling by ATAC-seq suggested that INN-exposure leads to enhanced DNA-binding of specific transcription factors (TFs), including HNF1B, SOX10 and NFIC, often in close spatial proximity to genes that are dysregulated in response to INN treatment. Altogether, these results identify potential molecular mechanisms underlying INN-induced perturbation during mesodermal differentiation in the context of cardiac development. This study further highlights the utility of human stem cells as an alternative system for investigating congenital diseases of newborns that arise as a result of maternal drug exposure during pregnancy
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