475 research outputs found

    A DNA Methylation Sensitive Nanopore Engineered from the phi29 Portal Protein GP10

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    Detection of Methylated DNA by Modified GP10 Nanopore

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    Secret Sharing Based on a Hard-on-Average Problem

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    The main goal of this work is to propose the design of secret sharing schemes based on hard-on-average problems. It includes the description of a new multiparty protocol whose main application is key management in networks. Its unconditionally perfect security relies on a discrete mathematics problem classiffied as DistNP-Complete under the average-case analysis, the so-called Distributional Matrix Representability Problem. Thanks to the use of the search version of the mentioned decision problem, the security of the proposed scheme is guaranteed. Although several secret sharing schemes connected with combinatorial structures may be found in the bibliography, the main contribution of this work is the proposal of a new secret sharing scheme based on a hard-on-average problem, which allows to enlarge the set of tools for designing more secure cryptographic applications

    Response to the letter by Udo Bonnet

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/153273/1/nmo13715_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/153273/2/nmo13715.pd

    Bringing Superheroes into the Fight against COVID-19 Misinformation

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    Over the past year, artists, doctors, medical professionals, and international agencies such as the World Health Organisation have been using comics to communicate the risks of the SARS-CoV2 virus. The visual economy and a near-universal language of lines, balloons, and panels in comics makes them well suited to disseminate epidemic-related information to children and adults

    Inorganic pyrophosphate generation by transforming growth factor-beta-1 is mainly dependent on ANK induction by Ras/Raf-1/extracellular signal-regulated kinase pathways in chondrocytes

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    ANK is a multipass transmembrane protein transporter thought to play a role in the export of intracellular inorganic pyrophosphate and so to contribute to the pathophysiology of chondrocalcinosis. As transforming growth factor-beta-1 (TGF-β1) was shown to favor calcium pyrophosphate dihydrate deposition, we investigated the contribution of ANK to the production of extracellular inorganic pyrophosphate (ePPi) by chondrocytes and the signaling pathways involved in the regulation of Ank expression by TGF-β1. Chondrocytes were exposed to 10 ng/mL of TGF-β1, and Ank expression was measured by quantitative polymerase chain reaction and Western blot. ePPi was quantified in cell supernatants. RNA silencing was used to define the respective roles of Ank and PC-1 in TGF-β1-induced ePPi generation. Finally, selective kinase inhibitors and dominant-negative/overexpression plasmid strategies were used to explore the contribution of several signaling pathways to Ank induction by TGF-β1. TGF-β1 strongly increased Ank expression at the mRNA and protein levels, as well as ePPi production. Using small interfering RNA technology, we showed that Ank contributed approximately 60% and PC-1 nearly 20% to TGF-β1-induced ePPi generation. Induction of Ank by TGF-β1 required activation of the extracellular signal-regulated kinase (ERK) pathway but not of p38-mitogen-activated protein kinase or of protein kinase A. In line with the general protein kinase C (PKC) inhibitor calphostin C, Gö6976 (a Ca2+-dependent PKC inhibitor) diminished TGF-β1-induced Ank expression by 60%, whereas a 10% inhibition was observed with rottlerin (a PKCδ inhibitor). These data suggest a regulatory role for calcium in TGF-β1-induced Ank expression. Finally, we demonstrated that the stimulatory effect of TGF-β1 on Ank expression was inhibited by the suppression of the Ras/Raf-1 pathway, while being enhanced by their constitutive activation. Transient overexpression of Smad 7, an inhibitory Smad, failed to affect the inducing effect of TGF-β1 on Ank mRNA level. These data show that TGF-β1 increases ePPi levels, mainly by the induction of the Ank gene, which requires activation of Ras, Raf-1, ERK, and Ca2+-dependent PKC pathways in chondrocytes
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