Geometry, kinematics and rates of deformation in a normal fault segment boundary, central Greece

The geometry, kinematics and rates of deformation within a fault segment boundary between the ends of two major active normal fault segments have been investigated through examination of a faulted 126 ka marine terrace. Slip‐vector azimuths defined by striations on the faults indicate N‐S extension on c. E‐W faults, sub‐parallel to those from earthquake focal mechanisms, together with significant and contemporaneous E‐W extension on c. N‐S faults. Summed rates of E‐W extension along a c. 550 m transect (0.17 mm/yr) are comparable with those for N‐S extension (0.20 mm/yr) along a c. 350 m transect. Our observations show that distributed non‐plane strain extension occurs in fault segment boundaries and this should be noted when studying fault‐tip fracture toughness and regional deformation rates

Genetic variants near TIMP3 and high-density lipoprotein–associated loci influence susceptibility to age-related macular degeneration

We executed a genome-wide association scan for age-related macular degeneration (AMD) in 2,157 cases and 1,150 controls. Our results validate AMD susceptibility loci near CFH (P < 10−75), ARMS2 (P < 10−59), C2/CFB (P < 10−20), C3 (P < 10−9), and CFI (P < 10−6). We compared our top findings with the Tufts/Massachusetts General Hospital genome-wide association study of advanced AMD (821 cases, 1,709 controls) and genotyped 30 promising markers in additional individuals (up to 7,749 cases and 4,625 controls). With these data, we identified a susceptibility locus near TIMP3 (overall P = 1.1 × 10−11), a metalloproteinase involved in degradation of the extracellular matrix and previously implicated in early-onset maculopathy. In addition, our data revealed strong association signals with alleles at two loci (LIPC, P = 1.3 × 10−7; CETP, P = 7.4 × 10−7) that were previously associated with high-density lipoprotein cholesterol (HDL-c) levels in blood. Consistent with the hypothesis that HDL metabolism is associated with AMD pathogenesis, we also observed association with AMD of HDL-c—associated alleles near LPL (P = 3.0 × 10−3) and ABCA1 (P = 5.6 × 10−4). Multilocus analysis including all susceptibility loci showed that 329 of 331 individuals (99%) with the highest-risk genotypes were cases, and 85% of these had advanced AMD. Our studies extend the catalog of AMD associated loci, help identify individuals at high risk of disease, and provide clues about underlying cellular pathways that should eventually lead to new therapies