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

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

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

Impact of Fatty-Acid Labeling of Bacillus subtilis Membranes on the Cellular Lipidome and Proteome

Developing cultivation methods that yield chemically and isotopically defined fatty acid (FA) compositions within bacterial cytoplasmic membranes establishes an in vivo experimental platform to study membrane biophysics and cell membrane regulation using novel approaches. Yet before fully realizing the potential of this method, it is prudent to understand the systemic changes in cells induced by the labeling procedure itself. In this work, analysis of cellular membrane compositions was paired with proteomics to assess how the proteome changes in response to the directed incorporation of exogenous FAs into the membrane of Bacillus subtilis. Key findings from this analysis include an alteration in lipid headgroup distribution, with an increase in phosphatidylglycerol lipids and decrease in phosphatidylethanolamine lipids, possibly providing a fluidizing effect on the cell membrane in response to the induced change in membrane composition. Changes in the abundance of enzymes involved in FA biosynthesis and degradation are observed; along with changes in abundance of cell wall enzymes and isoprenoid lipid production. The observed changes may influence membrane organization, and indeed the well-known lipid raft-associated protein flotillin was found to be substantially down-regulated in the labeled cells – as was the actin-like protein MreB. Taken as a whole, this study provides a greater depth of understanding for this important cell membrane experimental platform and presents a number of new connections to be explored in regard to modulating cell membrane FA composition and its effects on lipid headgroup and raft/cytoskeletal associated proteins

Lipid bilayer thickness determines cholesterol's location in model membranes

Cholesterol is an essential biomolecule of animal cell membranes, and an important precursor for the biosynthesis of certain hormones and vitamins. It is also thought to play a key role in cell signaling processes associated with functional plasma membrane microdomains (domains enriched in cholesterol), commonly referred to as rafts. In all of these diverse biological phenomena, the transverse location of cholesterol in the membrane is almost certainly an important structural feature. Using a combination of neutron scattering and solid-state 2H NMR, we have determined the location and orientation of cholesterol in phosphatidylcholine (PC) model membranes having fatty acids of different lengths and degrees of unsaturation. The data establish that cholesterol reorients rapidly about the bilayer normal in all the membranes studied, but is tilted and forced to span the bilayer midplane in the very thin bilayers. The possibility that cholesterol lies flat in the middle of bilayers, including those made from PC lipids containing polyunsaturated fatty acids (PUFAs), is ruled out. These results support the notion that hydrophobic thickness is the primary determinant of cholesterol's location in membranes

Correction to: A randomized controlled trial of an intervention delivered by mobile phone app instant messaging to increase the acceptability of effective contraception among young people in Tajikistan.

After publication of the original article [1], it came to the authors' attention that there is a typo in the Results section