197 research outputs found

    An airdrop that preserves recipient privacy

    Get PDF
    A common approach to bootstrapping a new cryptocurrency is an airdrop, an arrangement in which existing users give away currency to entice new users to join. But current airdrops offer no recipient privacy: they leak which recipients have claimed the funds, and this information is easily linked to off-chain identities. In this work, we address this issue by defining a private airdrop and describing concrete schemes for widely-used user credentials, such as those based on ECDSA and RSA. Our private airdrop for RSA builds upon a new zero-knowledge argument of knowledge of the factorization of a committed secret integer, which may be of independent interest. We also design a private genesis airdrop that efficiently sends private airdrops to millions of users at once. Finally, we implement and evaluate. Our fastest implementation takes 40--180 ms to generate and 3.7--10 ms to verify an RSA private airdrop signature. Signatures are 1.8--3.3 kiB depending on the security parameter

    Very High Order Masking: Efficient Implementation and Security Evaluation

    Get PDF
    In this paper, we study the performances and security of recent masking algorithms specialized to parallel implementations in a 32-bit embedded software platform, for the standard AES Rijndael and the bitslice cipher Fantomas. By exploiting the excellent features of these algorithms for bitslice implementations, we first extend the recent speed records of Goudarzi and Rivain (presented at Eurocrypt 2017) and report realistic timings for masked implementations with 32 shares. We then observe that the security level provided by such implementations is uneasy to quantify with current evaluation tools. We therefore propose a new ``multi-model evaluation methodology which takes advantage of different (more or less abstract) security models introduced in the literature. This methodology allows us to both bound the security level of our implementations in a principled manner and to assess the risks of overstated security based on well understood parameters. Concretely, it leads us to conclude that these implementations withstand worst-case adversaries with >2^64 measurements under falsifiable assumptions

    Cytogenetic abnormalities and fragile-x syndrome in Autism Spectrum Disorder

    Get PDF
    BACKGROUND: Autism is a behavioral disorder with impaired social interaction, communication, and repetitive and stereotypic behaviors. About 5–10 % of individuals with autism have 'secondary' autism in which an environmental agent, chromosome abnormality, or single gene disorder can be identified. Ninety percent have idiopathic autism and a major gene has not yet been identified. We have assessed the incidence of chromosome abnormalities and Fragile X syndrome in a population of autistic patients referred to our laboratory. METHODS: Data was analyzed from 433 patients with autistic traits tested using chromosome analysis and/or fluorescence in situ hybridization (FISH) and/or molecular testing for fragile X syndrome by Southern and PCR methods. RESULTS: The median age was 4 years. Sex ratio was 4.5 males to 1 female [354:79]. A chromosome (cs) abnormality was found in 14/421 [3.33 %] cases. The aberrations were: 4/14 [28%] supernumerary markers; 4/14 [28%] deletions; 1/14 [7%] duplication; 3/14 [21%] inversions; 2/14 [14%] translocations. FISH was performed on 23 cases for reasons other than to characterize a previously identified cytogenetic abnormality. All 23 cases were negative. Fragile-X testing by Southern blots and PCR analysis found 7/316 [2.2 %] with an abnormal result. The mutations detected were: a full mutation (fM) and abnormal methylation in 3 [43 %], mosaic mutations with partial methylation of variable clinical significance in 3 [43%] and a permutation carrier [14%]. The frequency of chromosome and fragile-X abnormalities appears to be within the range in reported surveys (cs 4.8-1.7%, FRAX 2–4%). Limitations of our retrospective study include paucity of behavioral diagnostic information, and a specific clinical criterion for testing. CONCLUSIONS: Twenty-eight percent of chromosome abnormalities detected in our study were subtle; therefore a high resolution cytogenetic study with a scrutiny of 15q11.2q13, 2q37 and Xp23.3 region should be standard practice when the indication is autism. The higher incidence of mosaic fragile-X mutations with partial methylation compared to FRAXA positive population [50% vs 15–40%] suggests that faint bands and variations in the Southern band pattern may occur in autistic patients

    Prospects for the development of probiotics and prebiotics for oral applications

    Get PDF
    There has been a paradigm shift towards an ecological and microbial community-based approach to understanding oral diseases. This has significant implications for approaches to therapy and has raised the possibility of developing novel strategies through manipulation of the resident oral microbiota and modulation of host immune responses. The increased popularity of using probiotic bacteria and/or prebiotic supplements to improve gastrointestinal health has prompted interest in the utility of this approach for oral applications. Evidence now suggests that probiotics may function not only by direct inhibition of, or enhanced competition with, pathogenic micro-organisms, but also by more subtle mechanisms including modulation of the mucosal immune system. Similarly, prebiotics could promote the growth of beneficial micro-organisms that comprise part of the resident microbiota. The evidence for the use of pro or prebiotics for the prevention of caries or periodontal diseases is reviewed, and issues that could arise from their use, as well as questions that still need to be answered, are raised. A complete understanding of the broad ecological changes induced in the mouth by probiotics or prebiotics will be essential to assess their long-term consequences for oral health and disease

    Genomic and epigenetic evidence for oxytocin receptor deficiency in autism

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Autism comprises a spectrum of behavioral and cognitive disturbances of childhood development and is known to be highly heritable. Although numerous approaches have been used to identify genes implicated in the development of autism, less than 10% of autism cases have been attributed to single gene disorders.</p> <p>Methods</p> <p>We describe the use of high-resolution genome-wide tilepath microarrays and comparative genomic hybridization to identify copy number variants within 119 probands from multiplex autism families. We next carried out DNA methylation analysis by bisulfite sequencing in a proband and his family, expanding this analysis to methylation analysis of peripheral blood and temporal cortex DNA of autism cases and matched controls from independent datasets. We also assessed oxytocin receptor (OXTR) gene expression within the temporal cortex tissue by quantitative real-time polymerase chain reaction (PCR).</p> <p>Results</p> <p>Our analysis revealed a genomic deletion containing the oxytocin receptor gene, <it>OXTR </it>(MIM accession no.: 167055), previously implicated in autism, was present in an autism proband and his mother who exhibits symptoms of obsessive-compulsive disorder. The proband's affected sibling did not harbor this deletion but instead may exhibit epigenetic misregulation of this gene through aberrant gene silencing by DNA methylation. Further DNA methylation analysis of the CpG island known to regulate <it>OXTR </it>expression identified several CpG dinucleotides that show independent statistically significant increases in the DNA methylation status in the peripheral blood cells and temporal cortex in independent datasets of individuals with autism as compared to control samples. Associated with the increase in methylation of these CpG dinucleotides is our finding that <it>OXTR </it>mRNA showed decreased expression in the temporal cortex tissue of autism cases matched for age and sex compared to controls.</p> <p>Conclusion</p> <p>Together, these data provide further evidence for the role of OXTR and the oxytocin signaling pathway in the etiology of autism and, for the first time, implicate the epigenetic regulation of <it>OXTR </it>in the development of the disorder.</p> <p>See the related commentary by Gurrieri and Neri: <url>http://www.biomedcentral.com/1741-7015/7/63</url></p

    Socioeconomic mobility and talent utilization of workers from poorer backgrounds: The overlooked importance of within-organization dynamics

    Get PDF
    Socioeconomic mobility, or the ability of individuals to improve their socioeconomic standing through merit-based contributions, is a fundamental ideal of modern societies. The key focus of societal efforts to ensure socioeconomic mobility has been on the provision of educational opportunities. We review evidence that even with the same education and job opportunities, being born into a poorer family undermines socioeconomic mobility due to processes occurring within organizations. The burden of poorer background might, ceteris paribus, be economically comparable to the gender gap. We argue that in the societal and scientific effort to promote socioeconomic mobility, the key context in which mobility is supposed to happen—organizations—as well as the key part of the life of people striving toward socioeconomic advancement—that as working adults—have been overlooked. We integrate the organizational literature pointing to key within-organizational processes impacting objective (socioeconomic) success with research, some emergent in organizational sciences and some disciplinary, on when, why, and how people from poorer backgrounds behave or are treated by others in the relevant situations. Integrating these literatures generates a novel and useful framework for identifying issues people born into poorer families face as employees, systematizes extant evidence and makes it more accessible to organizational scientists, and allows us to lay the agenda for future organizational scholarshi

    Evolution of Thrombosis of the Vein of Galen in Sickle Cell Disease

    No full text
    PubMedID: 8505485[No abstract available
    • 

    corecore