238 research outputs found
Effect of Interfacial Bonds on the Morphology of InAs QDs Grown on GaAs (311) B and (100) Substrates
The morphology and transition thickness (tc) for InAs quantum dots (QDs) grown on GaAs (311) B and (100) substrates were investigated. The morphology varies with the composition of buffer layer and substrate orientation. Andtcdecreased when the thin InGaAs was used as a buffer layer instead of the GaAs layer on (311) B substrates. For InAs/(In)GaAs QDs grown on high miller index surfaces, both the morphology andtccan be influenced by the interfacial bonds configuration. This indicates that buffer layer design with appropriate interfacial bonds provides an approach to adjust the morphologies of QDs grown on high miller surfaces
Tissue engineering rib with the incorporation of biodegradable polymer cage and BMSCs/decalcified bone: an experimental study in a canine model
A Bi-layer Composite Film Based on TiO2 Hollow Spheres, P25, and Multi-walled Carbon Nanotubes for Efficient Photoanode of Dye-sensitized Solar Cell
Characteristics of clinical studies of summer acupoint herbal patching: a bibliometric analysis
Epigenetics and male reproduction: the consequences of paternal lifestyle on fertility, embryo development, and children lifetime health
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
DNA sequence polymorphism of the Rhg4 candidate gene conferring resistance to soybean cyst nematode in Chinese domesticated and wild soybeans
The measurement of wind erosion through field survey and remote sensing: a case study of the Mu Us Desert, China
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