Modal parameter estimation in the presence of non-linearities

This paper investigates the use of time-frequency techniques to assist in the estimation of power system modes which are resolvable by a Digital Fourier Transform (DFT). The limitations of linear estimation techniques in the presence of large disturbances which excite system non-linearities, particularly the swing equation non-linearity are shown. Where a nonlinearity manifests itself as time varying modal frequencies the Wigner-Ville Distribution (WVD) is used to describe the variation in modal frequencies and construct a window over which standard linear estimation techniques can be used. The error obtained even in the presence of multiple resolvable modes is better than 2%.

Automated proofs for Diffie–Hellman–based key exchanges

We present an automated verification method for security of Diffie–Hellman–based key exchange protocols. The method includes a Hoare-style logic and syntactic checking. The method is applied to protocols in a simplified version of the Bellare–Rogaway–Pointcheval model (2000). The security of the protocol in the complete model can be established automatically by a modular proof technique of Kudla and Paterson (2005).

Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture

Bone mineral density (BMD) is the most widely used predictor of fracture risk. We performed the largest meta-analysis to date on lumbar spine and femoral neck BMD, including 17 genome-wide association studies and 32,961 individuals of European and east Asian ancestry. We tested the top BMD-associated markers for replication in 50,933 independent subjects and for association with risk of low-trauma fracture in 31,016 individuals with a history of fracture (cases) and 102,444 controls. We identified 56 loci (32 new) associated with BMD at genome-wide significance (P < 5 × 10−8). Several of these factors cluster within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways. However, we also discovered loci that were localized to genes not known to have a role in bone biology. Fourteen BMD-associated loci were also associated with fracture risk (P < 5 × 10−4, Bonferroni corrected), of which six reached P < 5 × 10−8, including at 18p11.21 (FAM210A), 7q21.3 (SLC25A13), 11q13.2 (LRP5), 4q22.1 (MEPE), 2p16.2 (SPTBN1) and 10q21.1 (DKK1). These findings shed light on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility.