13,347 research outputs found
Exact phase diagrams for an Ising model on a two-layer Bethe lattice
Using an iteration technique, we obtain exact expressions for the free energy
and the magnetization of an Ising model on a two - layer Bethe lattice with
intralayer coupling constants J1 and J2 for the first and the second layer,
respectively, and interlayer coupling constant J3 between the two layers; the
Ising spins also couple with external magnetic fields, which are different in
the two layers. We obtain exact phase diagrams for the system.Comment: 24 pages, 2 figures. To be published in Phys. Rev. E 59, Issue 6,
199
Geometry, thermodynamics, and finite-size corrections in the critical Potts model
We establish an intriguing connection between geometry and thermodynamics in
the critical q-state Potts model on two-dimensional lattices, using the q-state
bond-correlated percolation model (QBCPM) representation. We find that the
number of clusters of the QBCPM has an energy-like singularity for q different
from 1, which is reached and supported by exact results, numerical simulation,
and scaling arguments. We also establish that the finite-size correction to the
number of bonds, has no constant term and explains the divergence of related
quantities as q --> 4, the multicritical point. Similar analyses are applicable
to a variety of other systems.Comment: 12 pages, 6 figure
Anosmin-1 modulates fibroblast growth factor receptor 1 signaling in human gonadotropin-releasing hormone olfactory neuroblasts through a heparan sulfate-dependent mechanism
Finite-size corrections for logarithmic representations in critical dense polymers
We study (analytic) finite-size corrections in the dense polymer model on the
strip by perturbing the critical Hamiltonian with irrelevant operators
belonging to the tower of the identity. We generalize the perturbation
expansion to include Jordan cells, and examine whether the finite-size
corrections are sensitive to the properties of indecomposable representations
appearing in the conformal spectrum, in particular their indecomposability
parameters. We find, at first order, that the corrections do not depend on
these parameters nor even on the presence of Jordan cells. Though the
corrections themselves are not universal, the ratios are universal and
correctly reproduced by the conformal perturbative approach, to first order.Comment: 5 pages, published versio
Exact Ampitude Ratio and Finite-Size Corrections for the M x N Square Lattice Ising Model The :
Let f, U and C represent, respectively, the free energy, the internal energy
and the specific heat of the critical Ising model on the square M x N lattice
with periodic boundary conditions. We find that N f and U are well-defined odd
function of 1/N. We also find that ratios of subdominant (N^(-2 i - 1))
finite-size corrections amplitudes for the internal energy and the specific
heat are constant. The free energy and the internal energy at the critical
point are calculated asymtotically up to N^(-5) order, and the specific heat up
to N^(-3) order.Comment: 18 pages, 4 figures, to be published in Phys. Rev. E 65, 1 February
200
Hepatitis B virus X gene in the development of hepatocellular carcinoma
Key Messages 1. Deletion of the 3’end of the hepatitis B virus X gene (HBx) was frequently detected in clinical hepatocellular carcinoma (HCC) samples. 2. In vivo animal tumour xenograft experiments demonstrated the tumourigenic ability of the C-terminal truncated HBx. 3. cDNA microarray study suggested that the C-terminal truncated HBx played a critical role in the HCC development via activation of cell proliferation and inhibition of apoptosis.published_or_final_versio
The 6-vertex model of hydrogen-bonded crystals with bond defects
It is shown that the percolation model of hydrogen-bonded crystals, which is
a 6-vertex model with bond defects, is completely equivalent with an 8-vertex
model in an external electric field. Using this equivalence we solve exactly a
particular 6-vertex model with bond defects. The general solution for the
Bethe-like lattice is also analyzed.Comment: 13 pages, 6 figures; added references for section
Moxifloxacin Replacement in Contemporary Tuberculosis Drug Regimens Is Ineffective against Persistent Mycobacterium tuberculosis in the Cornell Mouse Model
Tuberculosis (TB) caused by Mycobacterium tuberculosis remains a leading killer worldwide, and disease control is hampered by ineffective control of persistent infections. Substitution of moxifloxacin for isoniazid or ethambutol in standard TB regimens reduces treatment duration and relapse rates in animal studies and four-month regimens were not non-inferior in clinical trials. Resuscitation promoting factor (RPF) dependent bacilli have recently been implicated in M. tuberculosis persistence. We aimed to investigate the therapeutic effects of moxifloxacin substitution in the standard drug regimen for eradicating colony forming count (CFU) positive and RPF-dependent persistent M. tuberculosis using the Cornell murine model. M. tuberculosis infected mice were treated with regimens in which either isoniazid or ethambutol were replaced by moxifloxacin to the standard regimen. The efficacy of the regimens was compared to the standard regimen for bacterial CFU count elimination and removal of persistent tubercle bacilli evaluated using culture filtrate (CF) derived from M. tuberculosis strain H37Rv. We also measured disease relapse rates. Moxifloxacin-isoniazid substituted regimen achieved total organ CFU count clearance at 11 weeks post-treatment, faster than standard regimen (14 weeks), and with a 34% lower relapse rate. Moxifloxacin-ethambutol substituted regimen was similar to standard regimens in these regards. Importantly, neither moxifloxacin-substituted regimens nor the standard regimen could remove CF-dependent persistent bacilli. Evaluation of CF-dependent persistent M. tuberculosis requires confirmation in human studies, and has implications in future drug design, testing and clinical applications
Defining dormancy in mycobacterial disease.
Tuberculosis remains a threat to global health and recent attempts to shorten therapy have not succeeded mainly due to cases of clinical relapse. This has focussed attention on the importance of "dormancy" in tuberculosis. There are a number of different definitions of the term and a similar multiplicity of different in vitro and in vivo models. The danger with this is the implicit assumption of equivalence between the terms and models, which will make even more difficult to unravel this complex conundrum. In this review we summarise the main models and definitions and their impact on susceptibility of Mycobacterium tuberculosis. We also suggest a potential nomenclature for debate. Dormancy researchers agree that factors underpinning this phenomenon are complex and nuanced. If we are to make progress we must agree the terms to be used and be consistent in using them
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