2,007 research outputs found
Saturation-Dependence of Dispersion in Porous Media
In this study, we develop a saturation-dependent treatment of dispersion in
porous media using concepts from critical path analysis, cluster statistics of
percolation, and fractal scaling of percolation clusters. We calculate spatial
solute distributions as a function of time and calculate arrival time
distributions as a function of system size. Our previous results correctly
predict the range of observed dispersivity values over ten orders of magnitude
in experimental length scale, but that theory contains no explicit dependence
on porosity or relative saturation. This omission complicates comparisons with
experimental results for dispersion, which are often conducted at saturation
less than 1. We now make specific comparisons of our predictions for the
arrival time distribution with experiments on a single column over a range of
saturations. This comparison suggests that the most important predictor of such
distributions as a function of saturation is not the value of the saturation
per se, but the applicability of either random or invasion percolation models,
depending on experimental conditions
The Fantastic Four: A plug 'n' play set of optimal control pulses for enhancing nmr spectroscopy
We present highly robust, optimal control-based shaped pulses designed to
replace all 90{\deg} and 180{\deg} hard pulses in a given pulse sequence for
improved performance. Special attention was devoted to ensuring that the pulses
can be simply substituted in a one-to-one fashion for the original hard pulses
without any additional modification of the existing sequence. The set of four
pulses for each nucleus therefore consists of 90{\deg} and 180{\deg}
point-to-point (PP) and universal rotation (UR) pulses of identical duration.
These 1 ms pulses provide uniform performance over resonance offsets of 20 kHz
(1H) and 35 kHz (13C) and tolerate reasonably large radio frequency (RF)
inhomogeneity/miscalibration of (+/-)15% (1H) and (+/-)10% (13C), making them
especially suitable for NMR of small-to-medium-sized molecules (for which
relaxation effects during the pulse are negligible) at an accessible and widely
utilized spectrometer field strength of 600 MHz. The experimental performance
of conventional hard-pulse sequences is shown to be greatly improved by
incorporating the new pulses, each set referred to as the Fantastic Four
(Fanta4).Comment: 28 pages, 19 figure
Localization dynamics of fluids in random confinement
The dynamics of two-dimensional fluids confined within a random matrix of
obstacles is investigated using both colloidal model experiments and molecular
dynamics simulations. By varying fluid and matrix area fractions in the
experiment, we find delocalized tracer particle dynamics at small matrix area
fractions and localized motion of the tracers at high matrix area fractions. In
the delocalized region, the dynamics is subdiffusive at intermediate times, and
diffusive at long times, while in the localized regime, trapping in finite
pockets of the matrix is observed. These observations are found to agree with
the simulation of an ideal gas confined in a weakly correlated matrix. Our
results show that Lorentz gas systems with soft interactions are exhibiting a
smoothening of the critical dynamics and consequently a rounded
delocalization-to-localization transition.Comment: 5 pages, 3 figure
Broadband 180 degree universal rotation pulses for NMR spectroscopy designed by optimal control
Broadband inversion pulses that rotate all magnetization components 180
degrees about a given fixed axis are necessary for refocusing and mixing in
high-resolution NMR spectroscopy. The relative merits of various methodologies
for generating pulses suitable for broadband refocusing are considered. The de
novo design of 180 degree universal rotation pulses using optimal control can
provide improved performance compared to schemes which construct refocusing
pulses as composites of existing pulses. The advantages of broadband universal
rotation by optimized pulses (BURBOP) are most evident for pulse design that
includes tolerance to RF inhomogeneity or miscalibration. We present new
modifications of the optimal control algorithm that incorporate symmetry
principles and relax conservative limits on peak RF pulse amplitude for short
time periods that pose no threat to the probe. We apply them to generate a set
of pulses suitable for widespread use in Carbon-13 spectroscopy on the majority
of available probes
Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment.
Increasing evidence points to an important role for neutrophils in participating in the pathogenesis of the human demyelinating disease MS and the animal model EAE. Therefore, a better understanding of the signals controlling migration of neutrophils as well as evaluating the role of these cells in demyelination is important to define cellular components that contribute to disease in MS patients. In this study, we examined the functional role of the chemokine CXCL1 in contributing to neuroinflammation and demyelination in EAE. Using transgenic mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within glial fibrillary acidic protein-positive cells, we have shown that sustained CXCL1 expression within the CNS increased the severity of clinical and histologic disease that was independent of an increase in the frequency of encephalitogenic Th1 and Th17 cells. Rather, disease was associated with enhanced recruitment of CD11b+ Ly6G+ neutrophils into the spinal cord. Targeting neutrophils resulted in a reduction in demyelination arguing for a role for these cells in myelin damage. Collectively, these findings emphasize that CXCL1-mediated attraction of neutrophils into the CNS augments demyelination suggesting that this signaling pathway may offer new targets for therapeutic intervention
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Disrupted CXCR2 Signaling in Oligodendroglia Lineage Cells Enhances Myelin Repair in a Viral Model of Multiple Sclerosis.
CXCR2 is a chemokine receptor expressed on oligodendroglia that has been implicated in the pathogenesis of neuroinflammatory demyelinating diseases as well as enhancement of the migration, proliferation, and myelin production by oligodendroglia. Using an inducible proteolipid protein (Plp) promoter-driven Cre-loxP recombination system, we were able to assess how timed ablation of Cxcr2 in oligodendroglia affected disease following intracranial infection with the neurotropic JHM strain of mouse hepatitis virus (JHMV). Generation of Plp-Cre-ER(T)::Cxcr2flox/flox transgenic mice (termed Cxcr2-CKO mice) allows for Cxcr2 to be silenced in oligodendrocytes in adult mice following treatment with tamoxifen. Ablation of oligodendroglia Cxcr2 did not influence clinical severity in response to intracranial infection with JHMV. Infiltration of activated T cells or myeloid cells into the central nervous system (CNS) was not affected, nor was the ability to control viral infection. In addition, the severity of demyelination was similar between tamoxifen-treated mice and vehicle-treated controls. Notably, deletion of Cxcr2 resulted in increased remyelination, as assessed by g-ratio (the ratio of the inner axonal diameter to the total outer fiber diameter) calculation, compared to that in vehicle-treated control mice. Collectively, our findings argue that CXCR2 signaling in oligodendroglia is dispensable with regard to contributing to neuroinflammation, but its deletion enhances remyelination in a preclinical model of the human demyelinating disease multiple sclerosis (MS).IMPORTANCE Signaling through the chemokine receptor CXCR2 in oligodendroglia is important for developmental myelination in rodents, while chemical inhibition or nonspecific genetic deletion of CXCR2 appears to augment myelin repair in animal models of the human demyelinating disease multiple sclerosis (MS). To better understand the biology of CXCR2 signaling on oligodendroglia, we generated transgenic mice in which Cxcr2 is selectively ablated in oligodendroglia upon treatment with tamoxifen. Using a viral model of neuroinflammation and demyelination, we demonstrate that genetic silencing of CXCR2 on oligodendroglia did not affect clinical disease, neuroinflammation, or demyelination, yet there was increased remyelination. These findings support and extend previous findings suggesting that targeting CXCR2 may offer a therapeutic avenue for enhancing remyelination in patients with demyelinating diseases
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