FourQ on Embedded Devices with Strong Countermeasures Against Side-Channel Attacks

This work deals with the energy-efficient, high-speed and high-security implementation of elliptic curve scalar multiplication, elliptic curve Diffie-Hellman (ECDH) key exchange and elliptic curve digital signatures on embedded devices using FourQ and incorporating strong countermeasures to thwart a wide variety of side-channel attacks. First, we set new speed records for constant-time curve-based scalar multiplication, DH key exchange and digital signatures at the 128-bit security level with implementations targeting 8, 16 and 32-bit microcontrollers. For example, our software computes a static ECDH shared secret in 6.9 million cycles (or 0.86 seconds @8MHz) on a low-power 8-bit AVR microcontroller which, compared to the fastest Curve25519 and genus-2 Kummer implementations on the same platform, offers 2x and 1.4x speedups, respectively. Similarly, it computes the same operation in 496 thousand cycles on a 32-bit ARM Cortex-M4 microcontroller, achieving a factor-2.9 speedup when compared to the fastest Curve25519 implementation targeting the same platform. A similar speed performance is observed in the case of digital signatures. Second, we engineer a set of side-channel countermeasures taking advantage of FourQ\u27s rich arithmetic and propose a secure implementation that offers protection against a wide range of sophisticated side-channel attacks, including differential power analysis (DPA). Despite the use of strong countermeasures, the experimental results show that our FourQ software is still efficient enough to outperform implementations of Curve25519 that only protect against timing attacks. Finally, we perform a differential power analysis evaluation of our software running on an ARM Cortex-M4, and report that no leakage was detected with up to 10 million traces. These results demonstrate the potential of deploying FourQ on low-power applications such as protocols for the Internet of Things

IMPROVING FINANCIAL INCLUSION: TOWARDS A CRITICAL FINANCIAL EDUCATION FRAMEWORK

ABSTRACT Empirical research suggests that financial inclusion initiatives - such as facilitating access to financial resources or providing microcredit - are alone not enough to lower socioeconomic disparities. In this article, we adopt a critical stance as a guide for our empirical investigation. Our aim is to propose a financial education framework, tailored to low-income micro-entrepreneurs, that embraces new information and communication technologies (ICTs) and seeks to improve financial inclusion and social emancipation. This empirical study was conducted in an Amazonian municipality in Brazil where recent access to ICTs has brought about important and varied socioeconomic changes. Results show that ICT-supported and tailored critical financial education can play a dual role: on the one hand, access to financial education might decrease the effects of generative mechanisms on global/local tensions, triggered by standardized ICT applications; on the other hand, such access might increase financial inclusion and social transformation through the integration of guiding principles into financial education programs

APOE status modulates the changes in network connectivity induced by brain stimulation in non-demented elders

Correction: https://doi.org/10.1371/annotation/fe36cdbc-5ad0-40d4-8289-fe78d2011ca4Behavioral consequences of a brain insult represent an interaction between the injury and the capacity of the rest of the brain to adapt to it. We provide experimental support for the notion that genetic factors play a critical role in such adaptation. We induced a controlled brain disruption using repetitive transcranial magnetic stimulation (rTMS) and show that APOE status determines its impact on distributed brain networks as assessed by functional MRI (fMRI).Twenty non-demented elders exhibiting mild memory dysfunction underwent two fMRI studies during face-name encoding tasks (before and after rTMS). Baseline task performance was associated with activation of a network of brain regions in prefrontal, parietal, medial temporal and visual associative areas. APOE ε4 bearers exhibited this pattern in two separate independent components, whereas ε4-non carriers presented a single partially overlapping network. Following rTMS all subjects showed slight ameliorations in memory performance, regardless of APOE status. However, after rTMS APOE ε4-carriers showed significant changes in brain network activation, expressing strikingly similar spatial configuration as the one observed in the non-carrier group prior to stimulation. Similarly, activity in areas of the default-mode network (DMN) was found in a single component among the ε4-non bearers, whereas among carriers it appeared disaggregated in three distinct spatiotemporal components that changed to an integrated single component after rTMS. Our findings demonstrate that genetic background play a fundamental role in the brain responses to focal insults, conditioning expression of distinct brain networks to sustain similar cognitive performance

Jacobian Coordinates on Genus 2 Curves

Abstract. This paper presents a new projective coordinate system and new explicit algorithms which together boost the speed of arithmetic in the divisor class group of genus 2 curves. The proposed formulas generalise the use of Jacobian coordinates on elliptic curves, and their application improves the speed of performing cryptographic scalar multiplications in Jacobians of genus 2 curves over prime fields by an approximate factor of 1.25x. For example, on a single core of an Intel Core i7-3770M (Ivy Bridge), we show that replacing the previous best formulas with our new set improves the cost of generic scalar multiplications from 243,000 to 195,000 cycles, and drops the cost of specialised GLV-style scalar multiplications from 166,000 to 129,000 cycles

Whitepaper: Defining and investigating cognitive reserve, brain reserve, and brain maintenance

Several concepts, which in the aggregate get might be used to account for \u201cresilience\u201d against age- and disease-related changes, have been the subject of much research. These include brain reserve, cognitive reserve, and brain maintenance. However, different investigators have use these terms in different ways, and there has never been an attempt to arrive at consensus on the definition of these concepts. Furthermore, there has been confusion regarding the measurement of these constructs and the appropriate ways to apply them to research. Therefore the reserve, resilience, and protective factors professional interest area, established under the auspices of the Alzheimer's Association, established a whitepaper workgroup to develop consensus definitions for cognitive reserve, brain reserve, and brain maintenance. The workgroup also evaluated measures that have been used to implement these concepts in research settings and developed guidelines for research that explores or utilizes these concepts. The workgroup hopes that this whitepaper will form a reference point for researchers in this area and facilitate research by supplying a common language

Whitepaper: Defining and investigating cognitive reserve, brain reserve, and brain maintenance

Several concepts, which in the aggregate get might be used to account for “resilience” against age- and disease-related changes, have been the subject of much research. These include brain reserve, cognitive reserve, and brain maintenance. However, different investigators have use these terms in different ways, and there has never been an attempt to arrive at consensus on the definition of these concepts. Furthermore, there has been confusion regarding the measurement of these constructs and the appropriate ways to apply them to research. Therefore the reserve, resilience, and protective factors professional interest area, established under the auspices of the Alzheimer's Association, established a whitepaper workgroup to develop consensus definitions for cognitive reserve, brain reserve, and brain maintenance. The workgroup also evaluated measures that have been used to implement these concepts in research settings and developed guidelines for research that explores or utilizes these concepts. The workgroup hopes that this whitepaper will form a reference point for researchers in this area and facilitate research by supplying a common language. © 2019 the Alzheimer's Associatio

The Inflammatory Marker YKL-40 Is Elevated in Cerebrospinal Fluid from Patients with Alzheimer’s but Not Parkinson’s Disease or Dementia with Lewy Bodies

<div><p>A major difference in the revised diagnostic criteria for Alzheimer’s disease (AD) is the incorporation of biomarkers to support a clinical diagnosis and allow the identification of preclinical AD due to AD neuropathological processes. However, AD-specific fluid biomarkers which specifically distinguish clinical AD dementia from other dementia disorders are still missing. Here we aimed to evaluate the disease-specificity of increased YKL-40 levels in cerebrospinal fluid (CSF) from AD patients with mild to moderate dementia (n = 49) versus Parkinson’s disease (PD) (n = 61) and dementia with Lewy bodies (DLB) patients (n = 36), and non-demented controls (n = 44). Second we aimed to investigate whether altered YKL-40 levels are associated with CSF levels of other inflammation-associated molecules. When correcting for age, AD patients exhibited 21.3%, 27.7% and 38.8% higher YKL-40 levels compared to non-demented controls (p = 0.0283), DLB (p = 0.0027) and PD patients (p<0.0001). The AD-associated increase in YKL-40 was not associated with CSF P-tau, T-tau or Aβ42. No relationship between increased YKL-40 and levels of the astrocytic marker glial-fibrillary acidic protein (GFAP), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and interferon gamma-induced protein 10 (IP-10) could be identified. Our results confirm previous reports of an age-associated increased in CSF YKL-40 levels and further demonstrate increased CSF YKL-40 in AD patients versus non-demented controls and patients with DLB or PD. The increase in YKL-40 levels in the AD patients was unrelated to the established CSF AD biomarkers and the inflammatory markers GFAP, MCP-1, IP-10 and IL-8, proposing YKL-40 as a marker of yet to be identified AD-related pathological processes.</p></div