Slip-Flow and Heat Transfer of a Non-Newtonian Nanofluid in a Microtube

The slip-flow and heat transfer of a non-Newtonian nanofluid in a microtube is theoretically studied. The power-law rheology is adopted to describe the non-Newtonian characteristics of the flow, in which the fluid consistency coefficient and the flow behavior index depend on the nanoparticle volume fraction. The velocity profile, volumetric flow rate and local Nusselt number are calculated for different values of nanoparticle volume fraction and slip length. The results show that the influence of nanoparticle volume fraction on the flow of the nanofluid depends on the pressure gradient, which is quite different from that of the Newtonian nanofluid. Increase of the nanoparticle volume fraction has the effect to impede the flow at a small pressure gradient, but it changes to facilitate the flow when the pressure gradient is large enough. This remarkable phenomenon is observed when the tube radius shrinks to micrometer scale. On the other hand, we find that increase of the slip length always results in larger flow rate of the nanofluid. Furthermore, the heat transfer rate of the nanofluid in the microtube can be enhanced due to the non-Newtonian rheology and slip boundary effects. The thermally fully developed heat transfer rate under constant wall temperature and constant heat flux boundary conditions is also compared

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