640 research outputs found
Towards higher order lattice Boltzmann schemes
In this contribution we extend the Taylor expansion method proposed
previously by one of us and establish equivalent partial differential equations
of DDH lattice Boltzmann scheme at an arbitrary order of accuracy. We derive
formally the associated dynamical equations for classical thermal and linear
fluid models in one to three space dimensions. We use this approach to adjust
relaxation parameters in order to enforce fourth order accuracy for thermal
model and diffusive relaxation modes of the Stokes problem. We apply the
resulting scheme for numerical computation of associated eigenmodes and compare
our results with analytical references
On the Three-dimensional Central Moment Lattice Boltzmann Method
A three-dimensional (3D) lattice Boltzmann method based on central moments is
derived. Two main elements are the local attractors in the collision term and
the source terms representing the effect of external and/or self-consistent
internal forces. For suitable choices of the orthogonal moment basis for the
three-dimensional, twenty seven velocity (D3Q27), and, its subset, fifteen
velocity (D3Q15) lattice models, attractors are expressed in terms of
factorization of lower order moments as suggested in an earlier work; the
corresponding source terms are specified to correctly influence lower order
hydrodynamic fields, while avoiding aliasing effects for higher order moments.
These are achieved by successively matching the corresponding continuous and
discrete central moments at various orders, with the final expressions written
in terms of raw moments via a transformation based on the binomial theorem.
Furthermore, to alleviate the discrete effects with the source terms, they are
treated to be temporally semi-implicit and second-order, with the implicitness
subsequently removed by means of a transformation. As a result, the approach is
frame-invariant by construction and its emergent dynamics describing fully 3D
fluid motion in the presence of force fields is Galilean invariant. Numerical
experiments for a set of benchmark problems demonstrate its accuracy.Comment: 55 pages, 8 figure
Three-dimensional lattice-Boltzmann simulations of critical spinodal decomposition in binary immiscible fluids
We use a modified Shan-Chen, noiseless lattice-BGK model for binary
immiscible, incompressible, athermal fluids in three dimensions to simulate the
coarsening of domains following a deep quench below the spinodal point from a
symmetric and homogeneous mixture into a two-phase configuration. We find the
average domain size growing with time as , where increases
in the range , consistent with a crossover between
diffusive and hydrodynamic viscous, , behaviour. We find
good collapse onto a single scaling function, yet the domain growth exponents
differ from others' works' for similar values of the unique characteristic
length and time that can be constructed out of the fluid's parameters. This
rebuts claims of universality for the dynamical scaling hypothesis. At early
times, we also find a crossover from to in the scaled structure
function, which disappears when the dynamical scaling reasonably improves at
later times. This excludes noise as the cause for a behaviour, as
proposed by others. We also observe exponential temporal growth of the
structure function during the initial stages of the dynamics and for
wavenumbers less than a threshold value.Comment: 45 pages, 18 figures. Accepted for publication in Physical Review
Variational Principles for Stellar Structure
The four equations of stellar structure are reformulated as two alternate
pairs of variational principles. Different thermodynamic representations lead
to the same hydromechanical equations, but the thermal equations require, not
the entropy, but the temperature as the thermal field variable. Our treatment
emphasizes the hydrostatic energy and the entropy production rate of luminosity
produced and transported. The conceptual and calculational advantages of
integral over differential formulations of stellar structure are discussed
along with the difficulties in describing stellar chemical evolution by
variational principles.Comment: 28 pages, LaTeX, requires AASTeX, 1 PostScript figure, revisions:
erratum; accepted by Astrophysical Journa
Cytoplasmic PML promotes TGF-β-associated epithelial–mesenchymal transition and invasion in prostate cancer
Epithelial–mesenchymal transition (EMT) is a key event that is involved in the invasion and dissemination of cancer cells. Although typically considered as having tumour-suppressive properties, transforming growth factor (TGF)-β signalling is altered during cancer and has been associated with the invasion of cancer cells and metastasis. In this study, we report a previously unknown role for the cytoplasmic promyelocytic leukaemia (cPML) tumour suppressor in TGF-β signalling-induced regulation of prostate cancer-associated EMT and invasion. We demonstrate that cPML promotes a mesenchymal phenotype and increases the invasiveness of prostate cancer cells. This event is associated with activation of TGF-β canonical signalling pathway through the induction of Sma and Mad related family 2 and 3 (SMAD2 and SMAD3) phosphorylation. Furthermore, the cytoplasmic localization of promyelocytic leukaemia (PML) is mediated by its nuclear export in a chromosomal maintenance 1 (CRM1)-dependent manner. This was clinically tested in prostate cancer tissue and shown that cytoplasmic PML and CRM1 co-expression correlates with reduced disease-specific survival. In summary, we provide evidence of dysfunctional TGF-β signalling occurring at an early stage in prostate cancer. We show that this disease pathway is mediated by cPML and CRM1 and results in a more aggressive cancer cell phenotype. We propose that the targeting of this pathway could be therapeutically exploited for clinical benefit
Prehistory of Transit Searches
Nowadays the more powerful method to detect extrasolar planets is the transit
method. We review the planet transits which were anticipated, searched, and the
first ones which were observed all through history. Indeed transits of planets
in front of their star were first investigated and studied in the solar system.
The first observations of sunspots were sometimes mistaken for transits of
unknown planets. The first scientific observation and study of a transit in the
solar system was the observation of Mercury transit by Pierre Gassendi in 1631.
Because observations of Venus transits could give a way to determine the
distance Sun-Earth, transits of Venus were overwhelmingly observed. Some
objects which actually do not exist were searched by their hypothetical
transits on the Sun, as some examples a Venus satellite and an infra-mercurial
planet. We evoke the possibly first use of the hypothesis of an exoplanet
transit to explain some periodic variations of the luminosity of a star, namely
the star Algol, during the eighteen century. Then we review the predictions of
detection of exoplanets by their transits, those predictions being sometimes
ancient, and made by astronomers as well as popular science writers. However,
these very interesting predictions were never published in peer-reviewed
journals specialized in astronomical discoveries and results. A possible
transit of the planet beta Pic b was observed in 1981. Shall we see another
transit expected for the same planet during 2018? Today, some studies of
transits which are connected to hypothetical extraterrestrial civilisations are
published in astronomical refereed journals. Some studies which would be
classified not long ago as science fiction are now considered as scientific
ones.Comment: Submiited to Handbook of Exoplanets (Springer
SUMO chain formation is required for response to replication arrest in S. pombe
SUMO is a ubiquitin-like protein that is post-translationally attached to one or more lysine residues on target proteins. Despite having only 18% sequence identity with ubiquitin, SUMO contains the conserved betabetaalphabetabetaalphabeta fold present in ubiquitin. However, SUMO differs from ubiquitin in having an extended N-terminus. In S. pombe the N-terminus of SUMO/Pmt3 is significantly longer than those of SUMO in S. cerevisiae, human and Drosophila. Here we investigate the role of this N-terminal region. We have used two dimensional gel electrophoresis to demonstrate that S. pombe SUMO/Pmt3 is phosphorylated, and that this occurs on serine residues at the extreme N-terminus of the protein. Mutation of these residues (in pmt3-1) results in a dramatic reduction in both the levels of high Mr SUMO-containing species and of total SUMO/Pmt3, indicating that phosphorylation of SUMO/Pmt3 is required for its stability. Despite the significant reduction in high Mr SUMO-containing species, pmt3-1 cells do not display an aberrant cell morphology or sensitivity to genotoxins or stress. Additionally, we demonstrate that two lysine residues in the N-terminus of S. pombe SUMO/Pmt3 (K14 and K30) can act as acceptor sites for SUMO chain formation in vitro. Inability to form SUMO chains results in aberrant cell and nuclear morphologies, including stretched and fragmented chromatin. SUMO chain mutants are sensitive to the DNA synthesis inhibitor, hydroxyurea (HU), but not to other genotoxins, such as UV, MMS or CPT. This implies a role for SUMO chains in the response to replication arrest in S. pomb
Placental syncytiotrophoblast constitutes a major barrier to vertical transmission of Listeria monocytogenes.
Listeria monocytogenes is an important cause of maternal-fetal infections and serves as a model organism to study these important but poorly understood events. L. monocytogenes can infect non-phagocytic cells by two means: direct invasion and cell-to-cell spread. The relative contribution of each method to placental infection is controversial, as is the anatomical site of invasion. Here, we report for the first time the use of first trimester placental organ cultures to quantitatively analyze L. monocytogenes infection of the human placenta. Contrary to previous reports, we found that the syncytiotrophoblast, which constitutes most of the placental surface and is bathed in maternal blood, was highly resistant to L. monocytogenes infection by either internalin-mediated invasion or cell-to-cell spread. Instead, extravillous cytotrophoblasts-which anchor the placenta in the decidua (uterine lining) and abundantly express E-cadherin-served as the primary portal of entry for L. monocytogenes from both extracellular and intracellular compartments. Subsequent bacterial dissemination to the villous stroma, where fetal capillaries are found, was hampered by further cellular and histological barriers. Our study suggests the placenta has evolved multiple mechanisms to resist pathogen infection, especially from maternal blood. These findings provide a novel explanation why almost all placental pathogens have intracellular life cycles: they may need maternal cells to reach the decidua and infect the placenta
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