274 research outputs found

    Coarse-grained simulations of flow-induced nucleation in semi-crystalline polymers

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    We perform kinetic Monte Carlo simulations of flow-induced nucleation in polymer melts with an algorithm that is tractable even at low undercooling. The configuration of the non-crystallized chains under flow is computed with a recent non-linear tube model. Our simulations predict both enhanced nucleation and the growth of shish-like elongated nuclei for sufficiently fast flows. The simulations predict several experimental phenomena and theoretically justify a previously empirical result for the flow-enhanced nucleation rate. The simulations are highly pertinent to both the fundamental understanding and process modeling of flow-induced crystallization in polymer melts.Comment: 17 pages, 6 eps figure

    Affiliation-Hiding Authentication with Minimal Bandwidth Consumption

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    Part 3: Lightweight AuthenticationInternational audienceAffiliation-Hiding Authentication (AHA) protocols have the seemingly contradictory property of enabling users to authenticate each other as members of certain groups, without revealing their affiliation to group outsiders. Of particular interest in practice is the group-discovering variant, which handles multiple group memberships per user. Corresponding solutions were only recently introduced, and have two major drawbacks: high bandwidth consumption (typically several kilobits per user and affiliation), and only moderate performance in scenarios of practical application.While prior protocols have O(n2) time complexity, where n denotes the number of affiliations per user, we introduce a new AHA protocol running in O(nlogn) time. In addition, the bandwidth consumed is considerably reduced. We consider these advances a major step towards deployment of privacy-preserving methods in constraint devices, like mobile phones, to which the economization of these resources is priceless

    Treatment algorithm for infants diagnosed with spinal muscular atrophy through newborn screening

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    Spinal muscular atrophy (SMA) is an autosomal recessive disease characterized by the degeneration of alpha motor neurons in the spinal cord, leading to muscular atrophy. SMA is caused by deletions or mutations in the survival motor neuron 1 gene (SMN1). In humans, a nearly identical copy gene, SMN2, is present. Because SMN2 has been shown to decrease disease severity in a dose-dependent manner, SMN2 copy number is predictive of disease severity. To develop a treatment algorithm for SMA-positive infants identified through newborn screening based upon SMN2 copy number. A working group comprised of 15 SMA experts participated in a modified Delphi process, moderated by a neutral third-party expert, to develop treatment guidelines. The overarching recommendation is that all infants with two or three copies of SMN2 should receive immediate treatment (n = 13). For those infants in which immediate treatment is not recommended, guidelines were developed that outline the timing and appropriate screens and tests to be used to determine the timing of treatment initiation. The identification SMA affected infants via newborn screening presents an unprecedented opportunity for achievement of maximal therapeutic benefit through the administration of treatment pre-symptomatically. The recommendations provided here are intended to help formulate treatment guidelines for infants who test positive during the newborn screening process

    TMPS: Ticket-Mediated Password Strengthening

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    We introduce the notion of Ticket-Mediated Password Strengthening (TMPS), a technique for allowing users to derive keys from passwords while imposing a strict limit on the number of guesses of their password any attacker can make, and strongly protecting the users\u27 privacy. We describe the security requirements of TMPS, and then a set of efficient and practical protocols to implement a TMPS scheme, requiring only hash functions, CCA2-secure encryption, and blind signatures. We provide several variant protocols, including an offline symmetric-only protocol that uses a local trusted computing environment, and online variants that use group signatures or stronger trust assumptions instead of blind signatures. We formalize the security of our scheme by defining an ideal functionality in the Universal Composability (UC) framework, and by providing game-based definitions of security. We prove that our protocol realizes the ideal functionality in the random oracle model (ROM) under adaptive corruptions with erasures, and prove that security with respect to the ideal/real definition implies security with respect to the game-based definitions

    Security and Efficiency Analysis of the Hamming Distance Computation Protocol Based on Oblivious Transfer

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    open access articleBringer et al. proposed two cryptographic protocols for the computation of Hamming distance. Their first scheme uses Oblivious Transfer and provides security in the semi-honest model. The other scheme uses Committed Oblivious Transfer and is claimed to provide full security in the malicious case. The proposed protocols have direct implications to biometric authentication schemes between a prover and a verifier where the verifier has biometric data of the users in plain form. In this paper, we show that their protocol is not actually fully secure against malicious adversaries. More precisely, our attack breaks the soundness property of their protocol where a malicious user can compute a Hamming distance which is different from the actual value. For biometric authentication systems, this attack allows a malicious adversary to pass the authentication without knowledge of the honest user's input with at most O(n)O(n) complexity instead of O(2n)O(2^n), where nn is the input length. We propose an enhanced version of their protocol where this attack is eliminated. The security of our modified protocol is proven using the simulation-based paradigm. Furthermore, as for efficiency concerns, the modified protocol utilizes Verifiable Oblivious Transfer which does not require the commitments to outputs which improves its efficiency significantly

    Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable

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    Background: Paroxysmal extreme pain disorder (PEPD) is an autosomal dominant painful neuropathy with many, but not all, cases linked to gain-of-function mutations in SCN9A which encodes voltage-gated sodium channel Nav1.7. Severe pain episodes and skin flushing start in infancy and are induced by perianal probing or bowl movement, and pain progresses to ocular and mandibular areas with age. Carbamazepine has been effective in relieving symptoms, while other drugs including other anti-epileptics are less effective. Results: Sequencing of SCN9A coding exons from an English patient, diagnosed with PEPD, has identified a methionine 1627 to lysine (M1627K) substitution in the linker joining segments S4 and S5 in domain IV. We confirm that M1627K depolarizes the voltage-dependence of fast-inactivation without substantially altering activation or slow-inactivation, and inactivates from the open state with slower kinetics. We show here that M1627K does not alter development of closed-state inactivation, and that M1627K channels recover from fast-inactivation faster than wild type channels, and produce larger currents in response to a slow ramp stimulus. Using current-clamp recordings, we also show that the M1627K mutant channel reduces the threshold for single action potentials in DRG neurons and increases the number of action potentials in response to graded stimuli. Conclusion: M1627K mutation was previously identified in a sporadic case of PEPD from France, and we now report it in an English family. We confirm the initial characterization of mutant M1627K effect on fast-inactivation of Nav1.7 and extend the analysis to other gating properties of the channel. We also show that M1627K mutant channels render DRG neurons hyperexcitable. Our new data provide a link between altered channel biophysics and pain in PEPD patients
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