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Marca tip. ao finalOs impresores constan nos colofóns dos t. 2 e 3: "per Ioannem Hervagium" e 5: "per Hier. Frobenium et Nic. Episcopium"Sign.: a-t\p6\s, v\p4\s ; [alfa]-[beta]\p6\s, a-z\p6\s, A-K\p6\s, L-M\p8\sÍndices con portadilla propiaTexto a dúas colApostilas marxinai

Practical Improvements of Profiled Side-Channel Attacks on a Hardware Crypto-Accelerator

Abstract. This article investigates the relevance of the theoretical frame-work on profiled side-channel attacks presented by F.-X. Standaert et al. at Eurocrypt 2009. The analyses consist in a case-study based on side-channel measurements acquired experimentally from a hardwired crypto-graphic accelerator. Therefore, with respect to previous formal analyses carried out on software measurements or on simulated data, the inves-tigations we describe are more complex, due to the underlying chip’s architecture and to the large amount of algorithmic noise. In this dif-ficult context, we show however that with an engineer’s mindset, two techniques can greatly improve both the off-line profiling and the on-line attack. First, we explore the appropriateness of different choices for the sensitive variables. We show that a skilled attacker aware of the regis-ter transfers occurring during the cryptographic operations can select the most adequate distinguisher, thus increasing its success rate. Sec-ond, we introduce a method based on the thresholding of leakage data to accelerate the profiling or the matching stages. Indeed, leveraging on an engineer’s common sense, it is possible to visually foresee the shape of some eigenvectors thereby anticipating their estimation towards their asymptotic value by authoritatively zeroing weak components containing mainly non-informational noise. This method empowers an attacker, in that it saves traces when converging towards correct values of the secret. Concretely, we demonstrate a 5 times speed-up in the on-line phase of the attack.

Efficient template attacks

This is the accepted manuscript version. The final published version is available from http://link.springer.com/chapter/10.1007/978-3-319-08302-5_17.Template attacks remain a powerful side-channel technique to eavesdrop on tamper-resistant hardware. They model the probability distribution of leaking signals and noise to guide a search for secret data values. In practice, several numerical obstacles can arise when implementing such attacks with multivariate normal distributions. We propose efficient methods to avoid these. We also demonstrate how to achieve significant performance improvements, both in terms of information extracted and computational cost, by pooling covariance estimates across all data values. We provide a detailed and systematic overview of many different options for implementing such attacks. Our experimental evaluation of all these methods based on measuring the supply current of a byte-load instruction executed in an unprotected 8-bit microcontroller leads to practical guidance for choosing an attack algorithm.Omar Choudary is a recipient of the Google Europe Fellowship in Mobile Security, and this research is supported in part by this Google Fellowship

Revisiting protein aggregation as pathogenic in sporadic Parkinson and Alzheimer diseases.

The gold standard for a definitive diagnosis of Parkinson disease (PD) is the pathologic finding of aggregated α-synuclein into Lewy bodies and for Alzheimer disease (AD) aggregated amyloid into plaques and hyperphosphorylated tau into tangles. Implicit in this clinicopathologic-based nosology is the assumption that pathologic protein aggregation at autopsy reflects pathogenesis at disease onset. While these aggregates may in exceptional cases be on a causal pathway in humans (e.g., aggregated α-synuclein in SNCA gene multiplication or aggregated β-amyloid in APP mutations), their near universality at postmortem in sporadic PD and AD suggests they may alternatively represent common outcomes from upstream mechanisms or compensatory responses to cellular stress in order to delay cell death. These 3 conceptual frameworks of protein aggregation (pathogenic, epiphenomenon, protective) are difficult to resolve because of the inability to probe brain tissue in real time. Whereas animal models, in which neither PD nor AD occur in natural states, consistently support a pathogenic role of protein aggregation, indirect evidence from human studies does not. We hypothesize that (1) current biomarkers of protein aggregates may be relevant to common pathology but not to subgroup pathogenesis and (2) disease-modifying treatments targeting oligomers or fibrils might be futile or deleterious because these proteins are epiphenomena or protective in the human brain under molecular stress. Future precision medicine efforts for molecular targeting of neurodegenerative diseases may require analyses not anchored on current clinicopathologic criteria but instead on biological signals generated from large deeply phenotyped aging populations or from smaller but well-defined genetic-molecular cohorts

Insulin but not phorbol ester treatment increases phosphorylation of vinculin by protein kinase C in BC3H-1 myocytes

AbstractInsulin was found to increase protein kinase C activity in BC3H-1 myocytes as determined by in vitro phosphorylation of both a lysine-rich histone fraction (histone III-S) and vinculin. TPA treatment for 20 min or 18 h provoked an apparent loss of histone-directed but not vinculin-directed phosphorylation by cytosolic C-kinase. Thus, chronic TPA-induced ‘desensitization’ or ‘depletion’ of cellular protein kinase C is more apparent than real, and is not a valid means for evaluating the role of C-kinase in hormone action

Basic Science in Movement Disorders: Fueling the Engine of Translation into Clinical Practice

\ua9 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. Basic Science is crucial for the advancement of clinical care for Movement Disorders. Here, we provide brief updates on how basic science is important for understanding disease mechanisms, disease prevention, disease diagnosis, development of novel therapies and to establish the basis for personalized medicine. We conclude the viewpoint by a call to action to further improve interactions between clinician and basic scientists. \ua9 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society