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

Computer Systems, Imagery and Medi

The First Thorough Side-Channel Hardware Trojan

Hardware Trojans have gained high attention in academia, industry and by government agencies. The effective detection mechanisms and countermeasures against such malicious designs are only possible when there is a deep understanding of how hardware Trojans can be built in practice. In this work, we present a mechanism which shows how easily a stealthy hardware Trojan can be inserted in a provably-secure side-channel analysis protected implementation. Once the Trojan is triggered, the malicious design exhibits exploitable side-channel leakage leading to successful key recovery attacks. Such a Trojan does not add or remove any logic (even a single gate) to the design which makes it very hard to detect. In ASIC platforms, it is indeed inserted by subtle manipulations at the sub-transistor level to modify the parameters of a few transistors. The same is applicable on FPGA applications by changing the routing of particular signals, leading to null resource utilization overhead. The underlying concept is based on a secure masked hardware implementation which does not exhibit any detectable leakage. However, by running the device at a particular clock frequency one of the requirements of the underlying masking scheme is not fulfilled anymore, i.e., the Trojan is triggered, and the device\u27s side-channel leakage can be exploited. Although as a case study we show an application of our designed Trojan on an FPGA-based threshold implementation of the PRESENT cipher, our methodology is a general approach and can be applied on any similar circuit

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

Mutations of IDH1 and IDH2 genes in early and accelerated phases of myelodysplastic syndromes and MDS/myeloproliferative neoplasms.

International audienc