805 research outputs found

    On the formation of cyclones and anticyclones in a rotating fluid

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    It is commonly observed that the columnar vortices that dominate the large scales in homogeneous, rapidly rotating turbulence are predominantly cyclonic. This has prompted us to ask how this asymmetry arises. To provide a partial answer to this we look at the process of columnar vortex formation in a rotating fluid and, in particular, we examine how a localized region of swirl (an eddy) can convert itself into a columnar structure by inertial wave propagation. We show that, when the Rossby number (Ro) is small, the vortices evolve into columnar eddies through the radiation of linear inertial waves. When the Rossby number is large, on the other hand, no such column is formed. Rather, the eddy bursts radially outward under the action of the centrifugal force. There is no asymmetry between cyclonic and anticyclonic eddies for these two regimes. However, cyclones and anticyclones behave differently in the intermediate regime of Ro~1. Here we find that the transition from columnar vortex formation to radial bursting occurs at lower values of Ro for anticyclones, with the transition for anticyclones occurring at Ro~0.5, and that for cyclones at Ro~2. Thus, in a homogeneous turbulence experiment conducted at, say, Ro=1, we would expect to see more cyclones than anticyclones. The reason for this asymmetry at Ro~1 is explained

    The decay of Batchelor and Saffman rotating turbulence

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    The decay rate of isotropic and homogeneous turbulence is known to be affected by the large-scale spectrum of the initial perturbations, associated with at least two cannonical self-preserving solutions of the von K\'arm\'an-Howarth equation: the so-called Batchelor and Saffman spectra. The effect of long-range correlations in the decay of anisotropic flows is less clear, and recently it has been proposed that the decay rate of rotating turbulence may be independent of the large-scale spectrum of the initial perturbations. We analyze numerical simulations of freely decaying rotating turbulence with initial energy spectra ∼k4\sim k^4 (Batchelor turbulence) and ∼k2\sim k^2 (Saffman turbulence) and show that, while a self-similar decay cannot be identified for the total energy, the decay is indeed affected by long-range correlations. The decay of two-dimensional and three-dimensional modes follows distinct power laws in each case, which are consistent with predictions derived from the anisotropic von K\'arm\'an-Howarth equation, and with conservation of anisotropic integral quantities by the flow evolution

    The decay of turbulence in rotating flows

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    We present a parametric space study of the decay of turbulence in rotating flows combining direct numerical simulations, large eddy simulations, and phenomenological theory. Several cases are considered: (1) the effect of varying the characteristic scale of the initial conditions when compared with the size of the box, to mimic "bounded" and "unbounded" flows; (2) the effect of helicity (correlation between the velocity and vorticity); (3) the effect of Rossby and Reynolds numbers; and (4) the effect of anisotropy in the initial conditions. Initial conditions include the Taylor-Green vortex, the Arn'old-Beltrami-Childress flow, and random flows with large-scale energy spectrum proportional to k4k^4. The decay laws obtained in the simulations for the energy, helicity, and enstrophy in each case can be explained with phenomenological arguments that separate the decay of two-dimensional from three-dimensional modes, and that take into account the role of helicity and rotation in slowing down the energy decay. The time evolution of the energy spectrum and development of anisotropies in the simulations are also discussed. Finally, the effect of rotation and helicity in the skewness and kurtosis of the flow is considered.Comment: Sections reordered to address comments by referee

    p16 mutations/deletions are not frequent events in prostate cancer.

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    Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene involved in a wide variety of human cancers. To investigate the frequency of p16INK mutations/deletions in prostate cancer, we screened 20 primary prostate tumours and four established cell lines by polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) analysis for exon 1 and exon 2. In contrast to most previous reports, no homozygous deletions were found in prostate cancer cell lines, but one cell line (DU145) has revealed to a mutation at codon 76. Only two SSCP shifts were detected in primary tumours: one of them corresponds to a mutation at codon 55 and the other one probably corresponds to a polymorphism. These data suggest that mutation of the p16INK4 gene is not a frequent genetic alteration implicated in prostate cancer development
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