Abstract. Public-key cryptography based on the "ring-variant" of the Learning with Errors (ring-LWE) problem is both efficient and believed to remain secure in a post-quantum world. In this paper, we introduce a carefully-optimized implementation of a ring-LWE encryption scheme for 8-bit AVR processors like the ATxmega128. Our research contributions include several optimizations for the Number Theoretic Transform (NTT) used for polynomial multiplication. More concretely, we describe the Move-and-Add (MA) and the Shift-Add-Multiply-Subtract-Subtract (SAMS2) technique to speed up the performance-critical multiplication and modular reduction of coefficients, respectively. We take advantage of incompletely-reduced intermediate results to minimize the total number of reduction operations and use a special coefficient-storage method to decrease the RAM footprint of NTT multiplications. In addition, we propose a byte-wise scanning strategy to improve the performance of a discrete Gaussian sampler based on the Knuth-Yao random walk algorithm. For medium-term security, our ring-LWE implementation needs 590 k, 672 k, and 276 k clock cycles for key-generation, encryption, and decryption, respectively. On the other hand, for long-term security, the execution time of key-generation, encryption, and decryption amount to 2.2 M, 2.6 M, and 686 k cycles, respectively. These results set new speed records for ring-LWE encryption on an 8-bit processor and outperform related RSA and ECC implementations by an order of magnitude.

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Abstract. This work deals with the energy-efficient, high-speed and high-security implementation of elliptic curve scalar multiplication and elliptic curve Diffie-Hellman (ECDH) key exchange 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 and DH key exchange 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. Second, we engineer a set of side-channel countermeasures taking advantage of FourQ's rich arithmetic and propose a secure implementation that offers protection against a wide range of sophisticated side-channel 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 IoT.

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Osteoclasts are multinucleated cells that play a crucial role in bone resorption, and are formed by the fusion of mononuclear osteoclasts derived from osteoclast precursors of the macrophage lineage. Compounds that specifically target functional osteoclasts would be ideal candidates for anti-resorptive agents for clinical applications. In the present study, we investigated the effects of luteolin, a flavonoid, on the regulation of receptor activator of nuclear factorjB ligand (RANKL)-induced osteoclastogenesis, functions and signaling pathway. Addition of luteolin to a coculture system of mouse bone marrow cells and ST2 cells in the presence of 10 -8 M 1a,25(OH) 2 D 3 caused significant inhibition of osteoclastogenesis. Luteolin had no effects on the 1a,25(OH) 2 D 3 -induced expressions of RANKL, osteoprotegerin and macrophage colony-stimulating factor mRNAs. Next, we examined the direct effects of luteolin on osteoclast precursors using bone marrow macrophages and RAW264.7 cells. Luteolin completely inhibited RANKL-induced osteoclast formation. Moreover, luteolin inhibited the bone resorption by mature osteoclasts accompanied by the disruption of their actin rings, and these effects were reversely induced by the disruption of the actin rings in mature osteoclasts. Finally, we found that luteolin inhibited RANKLinduced osteoclastogenesis through the suppression of ATF2, downstream of p38 MAPK and nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) expression, respectively. Taken together, the present results indicate that naturally occurring luteolin has inhibitory activities toward both osteoclast differentiation and functions through inhibition of RANKL-induced signaling pathway as well as actin ring disruption, respectively.