Influence of the Fermi Surface Morphology on the Magnetic Field-Driven Vortex Lattice Structure Transitions in YBa2_{2}Cu3_{3}O7−δ:δ=_{7-\delta}:\delta=0, 0.15

We report small-angle neutron scattering measurements of the vortex lattice (VL) structure in single crystals of the lightly underdoped cuprate superconductor YBa2Cu3O6.85. At 2 K, and for fields of up to 16 T applied parallel to the crystal c-axis, we observe a sequence of field-driven and first-order transitions between different VL structures. By rotating the field away from the c-axis, we observe each structure transition to shift to either higher or lower field dependent on whether the field is rotated towards the [100] or [010] direction. We use this latter observation to argue that the Fermi surface morphology must play a key role in the mechanisms that drive the VL structure transitions. Furthermore, we show this interpretation is compatible with analogous results obtained previously on lightly overdoped YBa2Cu3O7. In that material, it has long-been suggested that the high field VL structure transition is driven by the nodal gap anisotropy. In contrast, the results and discussion presented here bring into question the role, if any, of a nodal gap anisotropy on the VL structure transitions in both YBa2Cu3O6.85 and YBa2Cu3O7

Towards generalized data reduction on a time-of-flight neutron reflectometer

The calculation of neutron reflectivity from raw time-of-flight data including instrumental corrections and an improved resolution calculation is presented. The theoretical calculations are compared with experimental data measured on the vertical sample plane reflectometer D17 and the horizontal sample plane reflectometer FIGARO at the Institut Laue–Langevin (ILL), Grenoble, France. This article comprises the mathematical body of the time-of-flight reflectivity data-reduction software COSMOS which is used on D17 and FIGARO.</jats:p

Hexagonal and Square Flux Line Lattices in CeCoIn5

Using small-angle neutron scattering, we have imaged the magnetic flux line lattice (FLL) in the d-wave heavy-fermion superconductor CeCoIn5. At low fields we find a hexagonal FLL. Around 0.6 T this undergoes what is very likely a first-order transition to square symmetry, with the nearest neighbors oriented along the gap node directions. This orientation of the square FLL is consistent with theoretical predictions based on the d-wave order parameter symmetry.Comment: 4 pages, 3 figs (1 color

The conservation status of the world's freshwater molluscs

With the biodiversity crisis continuing unchecked, we need to establish levels and drivers of extinction risk, and reassessments over time, to effectively allocate conservation resources and track progress towards global conservation targets. Given that threat appears particularly high in freshwaters, we assessed the extinction risk of 1428 randomly selected freshwater molluscs using the IUCN Red List Categories and Criteria, as part of the Sampled Red List Index project. We show that close to one-third of species in our sample are estimated to be threatened with extinction, with highest levels of threat in the Nearctic, Palearctic and Australasia and among gastropods. Threat levels were higher in lotic than lentic systems. Pollution (chemical and physical) and the modification of natural systems (e.g. through damming and water abstraction) were the most frequently reported threats to freshwater molluscs, with some regional variation. Given that we found little spatial congruence between species richness patterns of freshwater molluscs and other freshwater taxa, apart from crayfish, new additional conservation priority areas emerged from our study. We discuss the implications of our findings for freshwater mollusc conservation, the adequacy of a sampled approach and important next steps to estimate trends in freshwater mollusc extinction risk over time

Oncogenic PIK3CA induces centrosome amplification and tolerance to genome doubling

Mutations in PIK3CA are very frequent in cancer and lead to sustained PI3K pathway activation. The impact of acute expression of mutant PIK3CA during early stages of malignancy is unknown. Using a mouse model to activate the Pik3ca H1047R hotspot mutation in the heterozygous state from its endogenous locus, we here report that mutant Pik3ca induces centrosome amplification in cultured cells (through a pathway involving AKT, ROCK and CDK2/Cyclin E-nucleophosmin) and in mouse tissues, and increased in vitro cellular tolerance to spontaneous genome doubling. We also present evidence that the majority of PIK3CA H1047R mutations in the TCGA breast cancer cohort precede genome doubling. These previously unappreciated roles of PIK3CA mutation show that PI3K signalling can contribute to the generation of irreversible genomic changes in cancer. While this can limit the impact of PI3K-targeted therapies, these findings also open the opportunity for therapeutic approaches aimed at limiting tumour heterogeneity and evolution

De Novo Truncating Mutations in WASF1 Cause Intellectual Disability with Seizures.

Next-generation sequencing has been invaluable in the elucidation of the genetic etiology of many subtypes of intellectual disability in recent years. Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WAS protein family member 1 (WASF1) in five unrelated individuals with moderate to profound intellectual disability with autistic features and seizures. WASF1, also known as WAVE1, is part of the WAVE complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three variants are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using fibroblast cells from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 cause a rare form of intellectual disability