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- Yoshizawa, A., et al.
(author)
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A Reynolds-averaged turbulence modelling approach to the maintenance of the Venus superrotation
- 2013
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In: Geophysical and Astrophysical Fluid Dynamics. - : Informa UK Limited. - 0309-1929 .- 1029-0419. ; 107:6, s. 614-639
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Journal article (peer-reviewed)abstract
- A maintenance mechanism of an approximately linear velocity profile of the Venus zonal flow or superrotation is explored, with the aid of a Reynolds-averaged turbulence modelling approach. The basic framework is similar to that of Gierasch (Meridional circulation and maintenance of the Venus atmospheric rotation. J. Atmos. Sci. 1975, 32, 1038-1044) in the sense that the mechanism is examined under a given meridional circulation. The profile mimicking the observations of the flow is initially assumed, and its maintenance mechanism in the presence of turbulence effects is investigated from a viewpoint of the suppression of energy cascade. In the present work, the turbulent viscosity is regarded as an indicator of the intensity of the cascade. A novelty of this formalism is the use of the isotropic turbulent viscosity based on a non-local time scale linked to a large-scale flow structure. The mechanism is first discussed qualitatively. On the basis of these discussions, the two-dimensional numerical simulation of the proposed model is performed, with an initially assumed superrotation, and the fast zonal flow is shown to be maintained, compared with the turbulent viscosity lacking the non-local time scale. The relationship of the present model with the current general circulation model simulation is discussed in light of a crucial role of the vertical viscosity.
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- Ding, Li, et al.
(author)
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Somatic mutations affect key pathways in lung adenocarcinoma
- 2008
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In: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 455:7216, s. 1069-1075
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Journal article (peer-reviewed)abstract
- Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.
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