Effect of Fibrin Glue on the Biomechanical Properties of Human Descemet's Membrane

10.1371/journal.pone.0037456PLoS ONE75

High- K three-quasiparticle isomers in the proton-rich nucleus 129 Nd

Three three-quasiparticle isomers, one at an excitation energy of 2.3 MeV with T1/2=0.48(4)μs, and two shorter-lived with unknown half-lives at slightly lower energies have been identified in Nd129 using the MARA + JUROGAM 3 setup and the recoil tagging technique. All three isomers present decay patterns characteristic of high-K isomers. The known 6.7 s β-decaying isomer previously assigned to the 5/2+ level is now assigned to the new 7/2- ground state. A new low-spin 5/2+ isomeric state with a half-life of a few tens of nanoseconds has been identified, while a previously known 2.6 s β-decay activity was assigned to the band head of the ν1/2+[411] band. The transitions depopulating the high-K isomers to low-lying states also establish the relative energies of three low-lying one-quasiparticle bands, leading to a new spin-parity assignment of 7/2- to the ground state of Nd129. The partial half-lives of the depopulating transitions suggest spin-parities 21/2+, 19/2+, and 17/2+ for the three high-K isomers. The properties of the band built on the 21/2+ isomeric state suggest a one neutron-two proton configuration. Based on the results of extensive calculations with different models, we also assign one neutron-two proton configurations to the 19/2+ and 17/2+ isomeric states. The assigned configurations of the 17/2+ and 21/2+ isomeric states involve the π9/2+[404] orbital, which is identified in three-quasiparticle bands of proton-rich A≈130 nuclei

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe