Modified Bautista–Manero (MBM) modelling for hyperbolic contraction–expansion flows

In this study, modelling of network-structured material flow is considered through a rounded-corner, hyperbolic 4:1:4 contraction-expansion geometry, under axisymmetric configuration. Three representative constitutive models are adopted to represent networked behaviour and to investigate the flow of wormlike micellar fluids in this context. This includes the MBM model (for base thixotropic properties), some newly proposed micellar models (NM_τp & NM_T; for advanced thixotropic modelling), and the EPPT model (for contrast against non-thixotropic properties). In this configuration, emphasis is placed upon interpretation of flow behaviour for these constitutive models, against their response in simple rheometrical flows. To best determine the factors that contribute to epd-prediction, current findings have also been contrasted against those reported earlier in Lopez-Aguilar et al. [1], for the counterpart abrupt rounded-corner, axisymmetric 4:1:4 contraction-expansion flow

Genomic and Transcriptional Alterations in Lung Adenocarcinoma in Relation to EGFR and KRAS Mutation Status

Introduction: In lung adenocarcinoma, the mutational spectrum is dominated by EGFR and KRAS mutations. Improved knowledge about genomic and transcriptional alterations in and between mutation-defined subgroups may identify genes involved in disease development or progression. Methods: Genomic profiles from 457 adenocarcinomas, including 113 EGFR-mutated, 134 KRAS-mutated and 210 EGFR and KRAS-wild type tumors (EGFRwt/KRASwt), and gene expression profiles from 914 adenocarcinomas, including 309 EGFR-mutated, 192 KRAS-mutated, and 413 EGFRwt/KRASwt tumors, were assembled from different repositories. Genomic and transcriptional differences between the three mutational groups were analyzed by both supervised and unsupervised methods. Results: EGFR-mutated adenocarcinomas displayed a larger number of copy number alterations and recurrent amplifications, a higher fraction of total loss-of-heterozygosity, higher genomic complexity, and a more distinct expression pattern than EGFR-wild type adenocarcinomas. Several of these differences were also consistent when the three mutational groups were stratified by stage, gender and smoking status. Specific copy number alterations were associated with mutation status, predominantly including regions of gain with the highest frequency in EGFR-mutated tumors. Differential regions included both large and small regions of gain on 1p, 5q34-q35.3, 7p, 7q11.21, 12p12.1, 16p, and 21q, and losses on 6q16.3-q21, 8p, and 9p, with 20-40% frequency differences between the mutational groups. Supervised gene expression analyses identified 96 consistently differentially expressed genes between the mutational groups, and together with unsupervised analyses these analyses highlighted the difficulty in broadly resolving the three mutational groups into distinct transcriptional entities. Conclusions: We provide a comprehensive overview of the genomic and transcriptional landscape in lung adenocarcinoma stratified by EGFR and KRAS mutations. Our analyses suggest that the overall genomic and transcriptional landscape of lung adenocarcinoma is affected, but only to a minor extent, by EGFR and KRAS mutation status