113 research outputs found
Scaling of acceleration in locally isotropic turbulence
The variances of the fluid-particle acceleration and of the pressure-gradient
and viscous force are given. The scaling parameters for these variances are
velocity statistics measureable with a single-wire anemometer. For both high
and low Reynolds numbers, asymptotic scaling formulas are given; these agree
quantitatively with DNS data. Thus, the scaling can be presumed known for all
Reynolds numbers. Fluid-particle acceleration variance does not obey K41
scaling at any Reynolds number; this is consistent with recent experimental
data. The non-dimensional pressure-gradient variance named lambda-sub{T}
/lambda-sub{P} is shown to be obsolete.Comment: in press, J. Fluid Mech.; 7pages, 2 figure
Equations relating structure functions of all orders
The hierarchy of exact equations is given that relates two-spatial-point
velocity structure functions of arbitrary order with other statistics. Because
no assumption is used, the exact statistical equations can apply to any flow
for which the Navier-Stokes equations are accurate, and they apply no matter
how small the number of samples in the ensemble. The exact statistical
equations can be used to verify DNS computations and to detect their
limitations. For example,if DNS data are used to evaluate the exact statistical
equations, then the equations should balance to within numerical precision,
otherwise a computational problem is indicated. The equations allow
quantification of the approach to local homogeneity and to local isotropy.
Testing the balance of the equations allows detection of scaling ranges for
quantification of scaling-range exponents. The second-order equations lead to
Kolmogorov's equation. All higher-order equations contain a statistic composed
of one factor of the two-point difference of the pressure gradient multiplied
by factors of velocity difference. Investigation of this
pressure-gradient-difference statistic can reveal much about two issues: 1)
whether or not different components of the velocity structure function of given
order have differing exponents in the inertial range, and 2) the increasing
deviation of those exponents from Kolmogorov scaling as the order increases.
Full disclosure of the mathematical methods is in
xxx.lanl.gov/list/physics.flu-dyn/0102055.Comment: The Laplacians of structure functions in Table 1 are herein correct
and extended to order 8, but were incorrect in the journal publication JFM
2001, 8 pages, no figures. arXiv admin note: text overlap with
arXiv:physics/010205
Exact Second-Order Structure-Function Relationships
Equations that follow from the Navier-Stokes equation and incompressibility
but with no other approximations are "exact.". Exact equations relating second-
and third-order structure functions are studied, as is an exact
incompressibility condition on the second-order velocity structure function.
Opportunities for investigations using these equations are discussed. Precisely
defined averaging operations are required to obtain exact averaged equations.
Ensemble, temporal, and spatial averages are all considered because they
produce different statistical equations and because they apply to theoretical
purposes, experiment, and numerical simulation of turbulence. Particularly
simple exact equations are obtained for the following cases: i) the trace of
the structure functions, ii) DNS that has periodic boundary conditions, and
iii) an average over a sphere in r-space. The last case (iii) introduces the
average over orientations of r into the structure function equations. The
energy dissipation rate appears in the exact trace equation without averaging,
whereas in previous formulations energy dissipation rate appears after
averaging and use of local isotropy. The trace mitigates the effect of
anisotropy in the equations, thereby revealing that the trace of the
third-order structure function is expected to be superior for quantifying
asymptotic scaling laws. The orientation average has the same property.Comment: no figure
Length Scales of Acceleration for Locally Isotropic Turbulence
Length scales are determined that govern the behavior at small separations of
the correlations of fluid-particle acceleration, viscous force, and pressure
gradient. The length scales and an associated universal constant are quantified
on the basis of published data. The length scale governing pressure spectra at
high wave numbers is discussed. Fluid-particle acceleration correlation is
governed by two length scales; one arises from the pressure gradient, the other
from the viscous force.Comment: 2 figures, 4 pages. Physical Review Letters, accepted August 200
Opportunities for use of exact statistical equations
Exact structure function equations are an efficient means of obtaining
asymptotic laws such as inertial range laws, as well as all measurable effects
of inhomogeneity and anisotropy that cause deviations from such laws. "Exact"
means that the equations are obtained from the Navier-Stokes equation or other
hydrodynamic equations without any approximation. A pragmatic definition of
local homogeneity lies within the exact equations because terms that explicitly
depend on the rate of change of measurement location appear within the exact
equations; an analogous statement is true for local stationarity. An exact
definition of averaging operations is required for the exact equations. Careful
derivations of several inertial range laws have appeared in the literature
recently in the form of theorems. These theorems give the relationships of the
energy dissipation rate to the structure function of acceleration increment
multiplied by velocity increment and to both the trace of and the components of
the third-order velocity structure functions. These laws are efficiently
derived from the exact velocity structure function equations. In some respects,
the results obtained herein differ from the previous theorems. The
acceleration-velocity structure function is useful for obtaining the energy
dissipation rate in particle tracking experiments provided that the effects of
inhomogeneity are estimated by means of displacing the measurement location.Comment: accepted by Journal of Turbulenc
Cancer-associated fibroblast exosomes regulate survival and proliferation of pancreatic cancer cells
Cancer associated fibroblasts (CAFs) comprise the majority of the tumor bulk of pancreatic adenocarcinomas (PDACs). Current efforts to eradicate these tumors focus predominantly on targeting the proliferation of rapidly growing cancer epithelial cells. We know that this is largely ineffective with resistance arising in most tumors following exposure to chemotherapy. Despite the long-standing recognition of the prominence of CAFs in PDAC, the effect of chemotherapy on CAFs and how they may contribute to drug resistance in neighboring cancer cells is not well characterized. Here we show that CAFs exposed to chemotherapy play an active role in regulating the survival and proliferation of cancer cells. We found that CAFs are intrinsically resistant to gemcitabine, the chemotherapeutic standard of care for PDAC. Further, CAFs exposed to gemcitabine significantly increase the release of extracellular vesicles called exosomes. These exosomes increased chemoresistance-inducing factor, Snail, in recipient epithelial cells and promote proliferation and drug resistance. Finally, treatment of gemcitabine-exposed CAFs with an inhibitor of exosome release, GW4869, significantly reduces survival in co-cultured epithelial cells, signifying an important role of CAF exosomes in chemotherapeutic drug resistance. Collectively, these findings show the potential for exosome inhibitors as treatment options alongside chemotherapy for overcoming PDAC chemoresistance
Selective Evolution of Stromal Mesenchyme with p53 Loss in Response to Epithelial Tumorigenesis
Our understanding of cancer has largely come from the analysis of aberrations within the tumor cell population. Yet it is increasingly clear that the tumor microenvironment can significantly influence tumorigenesis. For example, the mesenchyme can support the growth of tumorigenic epithelium. However, whether fibroblasts are subject to genetic/epigenetic changes as a result of selective pressures conferred by oncogenic stress in the epithelium has not been experimentally assessed. Recent analyses of some human carcinomas have shown tumor-suppressor gene mutations within the stroma, suggesting that the interplay among multiple cell types can select for aberrations nonautonomously during tumor progression. We demonstrate that this indeed occurs in a mouse model of prostate cancer where epithelial cell cycle disruption via cell-specific inhibition of pRb function induces a paracrine p53 response that suppresses fibroblast proliferation in associated stroma. This interaction imposes strong selective pressure yielding a highly proliferative mesenchyme that has undergone p53 loss
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