Constructing TI-Friendly Substitution Boxes Using Shift-Invariant Permutations

The threat posed by side channels requires ciphers that can be efficiently protected in both software and hardware against such attacks. In this paper, we proposed a novel Sbox construction based on iterations of shift-invariant quadratic permutations and linear diffusions. Owing to the selected quadratic permutations, all of our Sboxes enable uniform 3-share threshold implementations, which provide first order SCA protections without any fresh randomness. More importantly, because of the shift-invariant property, there are ample implementation trade-offs available, in software as well as hardware. We provide implementation results (software and hardware) for a four-bit and an eight-bit Sbox, which confirm that our constructions are competitive and can be easily adapted to various platforms as claimed. We have successfully verified their resistance to first order attacks based on real acquisitions. Because there are very few studies focusing on software-based threshold implementations, our software implementations might be of independent interest in this regard

A multi-targeted approach to suppress tumor-promoting inflammation

Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-κB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes

Amplification of a Zygosaccharomyces bailii DNA Segment in Wine Yeast Genomes by Extrachromosomal Circular DNA Formation

We recently described the presence of large chromosomal segments resulting from independent horizontal gene transfer (HGT) events in the genome of Saccharomyces cerevisiae strains, mostly of wine origin. We report here evidence for the amplification of one of these segments, a 17 kb DNA segment from Zygosaccharomyces bailii, in the genome of S. cerevisiae strains. The copy number, organization and location of this region differ considerably between strains, indicating that the insertions are independent and that they are post-HGT events. We identified eight different forms in 28 S. cerevisiae strains, mostly of wine origin, with up to four different copies in a single strain. The organization of these forms and the identification of an autonomously replicating sequence functional in S. cerevisiae, strongly suggest that an extrachromosomal circular DNA (eccDNA) molecule serves as an intermediate in the amplification of the Z. bailii region in yeast genomes. We found little or no sequence similarity at the breakpoint regions, suggesting that the insertions may be mediated by nonhomologous recombination. The diversity between these regions in S. cerevisiae represents roughly one third the divergence among the genomes of wine strains, which confirms the recent origin of this event, posterior to the start of wine strain expansion. This is the first report of a circle-based mechanism for the expansion of a DNA segment, mediated by nonhomologous recombination, in natural yeast populations

Lightweight Authenticated Encryption Mode Suitable for Threshold Implementation

This paper proposes tweakable block cipher (TBC) based modes $\mathsf{PFB\_Plus}$ and $\mathsf{PFB}\omega$ that are efficient in threshold implementations (TI). Let $t$ be an algebraic degree of a target function, e.g.~$t=1$ (resp.~$t>1$) for linear (resp.~non-linear) function. The $d$-th order TI encodes the internal state into $d t + 1$ shares. Hence, the area size increases proportionally to the number of shares. This implies that TBC based modes can be smaller than block cipher (BC) based modes in TI because TBC requires $s$-bit block to ensure $s$-bit security, e.g. \textsf{PFB} and \textsf{Romulus}, while BC requires $2s$-bit block. However, even with those TBC based modes, the minimum we can reach is 3 shares of $s$-bit state with $t=2$ and the first-order TI ($d=1$). Our first design $\mathsf{PFB\_Plus}$ aims to break the barrier of the $3s$-bit state in TI. The block size of an underlying TBC is $s/2$ bits and the output of TBC is linearly expanded to $s$ bits. This expanded state requires only 2 shares in the first-order TI, which makes the total state size $2.5s$ bits. We also provide rigorous security proof of $\mathsf{PFB\_Plus}$. Our second design $\mathsf{PFB}\omega$ further increases a parameter $\omega$: a ratio of the security level $s$ to the block size of an underlying TBC. We prove security of $\mathsf{PFB}\omega$ for any $\omega$ under some assumptions for an underlying TBC and for parameters used to update a state. Next, we show a concrete instantiation of $\mathsf{PFB\_Plus}$ for 128-bit security. It requires a TBC with 64-bit block, 128-bit key and 128-bit tweak, while no existing TBC can support it. We design a new TBC by extending \textsf{SKINNY} and provide basic security evaluation. Finally, we give hardware benchmarks of $\mathsf{PFB\_Plus}$ in the first-order TI to show that TI of $\mathsf{PFB\_Plus}$ is smaller than that of \textsf{PFB} by more than one thousand gates and is the smallest within the schemes having 128-bit security

Leukocyte Telomere Length in Major Depression: Correlations with Chronicity, Inflammation and Oxidative Stress - Preliminary Findings

Depression is associated with an unusually high rate of aging-related illnesses and early mortality. One aspect of “accelerated aging” in depression may be shortened leukocyte telomeres. When telomeres critically shorten, as often occurs with repeated mitoses or in response to oxidation and inflammation, cells may die. Indeed, leukocyte telomere shortening predicts early mortality and medical illnesses in non-depressed populations. We sought to determine if leukocyte telomeres are shortened in Major Depressive Disorder (MDD), whether this is a function of lifetime depression exposure and whether this is related to putative mediators, oxidation and inflammation.Leukocyte telomere length was compared between 18 unmedicated MDD subjects and 17 controls and was correlated with lifetime depression chronicity and peripheral markers of oxidation (F2-isoprostane/Vitamin C ratio) and inflammation (IL-6). Analyses were controlled for age and sex.The depressed group, as a whole, did not differ from the controls in telomere length. However, telomere length was significantly inversely correlated with lifetime depression exposure, even after controlling for age (p<0.05). Average telomere length in the depressed subjects who were above the median of lifetime depression exposure (≥9.2 years' cumulative duration) was 281 base pairs shorter than that in controls (p<0.05), corresponding to approximately seven years of “accelerated cell aging.” Telomere length was inversely correlated with oxidative stress in the depressed subjects (p<0.01) and in the controls (p<0.05) and with inflammation in the depressed subjects (p<0.05).These preliminary data indicate that accelerated aging at the level of leukocyte telomeres is proportional to lifetime exposure to MDD. This might be related to cumulative exposure to oxidative stress and inflammation in MDD. This suggest that telomere shortening does not antedate depression and is not an intrinsic feature. Rather, telomere shortening may progress in proportion to lifetime depression exposure

NimbleAI: towards neuromorphic sensing-processing 3D-integrated chips

Computer Systems, Imagery and Medi