4,279 research outputs found
Berry's phase in the multimode Peierls states
It is shown that Berry's phase associated with the adiabatic change of local
variables in the Hamiltonian can be used to characterize the multimode Peierls
state, which has been proposed as a new type of the ground state of the
two-dimensional(2D) systems with the electron-lattice interaction.Comment: 2 pages, 2 figure
Universal mechanism of discontinuity of commensurate-incommensurate transitions in three-dimensional solids: Strain dependence of soliton self-energy
We show that there exists a universal mechanism of long-range soliton
attraction in three-dimensional solids and, therefore, of discontinuity of any
commensurate-incommensurate (C-IC) phase transition. This mechanism is due to
the strain dependence of the soliton self-energy and specific features of the
solid-state elasticity. The role of this mechanism is studied in detail for a
class of C-IC transitions where the IC modulation is one-dimensional, the
anisotropy in the order parameter space is small, and the symmetry of the
systems allows the existence of the Lifshitz invariant. Two other mechanisms of
soliton attraction are operative here but the universal mechanism considered in
this paper is found to be the most important one in some cases. Comparison with
the most extensively studied C-IC transition in shows that the
experimentally observed thermal anomalies can be understood as a result of the
smearing of the theoretically predicted discontinuous transition.Comment: 8 pages (extended version, title changed
Isolation of Salmonella mutants resistant to the inhibitory effect of Salicylidene acylhydrazides on flagella-mediated motility.
Salicylidene acylhydrazides identified as inhibitors of virulence-mediating type III secretion systems (T3SSs) potentially target their inner membrane export apparatus. They also lead to inhibition of flagellar T3SS-mediated swimming motility in Salmonella enterica serovar. Typhimurium. We show that INP0404 and INP0405 act by reducing the number of flagella/cell. These molecules still inhibit motility of a Salmonella ΔfliH-fliI-fliJ/flhB((P28T)) strain, which lacks three soluble components of the flagellar T3S apparatus, suggesting that they are not the target of this drug family. We implemented a genetic screen to search for the inhibitors' molecular target(s) using motility assays in the ΔfliH-fliI/flhB((P28T)) background. Both mutants identified were more motile than the background strain in the absence of the drugs, although HM18 was considerably more so. HM18 was more motile than its parent strain in the presence of both drugs while DI15 was only insensitive to INP0405. HM18 was hypermotile due to hyperflagellation, whereas DI15 was not hyperflagellated. HM18 was also resistant to a growth defect induced by high concentrations of the drugs. Whole-genome resequencing of HM18 indicated two alterations within protein coding regions, including one within atpB, which encodes the inner membrane a-subunit of the F(O)F(1)-ATP synthase. Reverse genetics indicated that the alteration in atpB was responsible for all of HM18's phenotypes. Genome sequencing of DI15 uncovered a single A562P mutation within a gene encoding the flagellar inner membrane protein FlhA, the direct role of which in mediating drug insensitivity could not be confirmed. We discuss the implications of these findings in terms of T3SS export apparatus function and drug target identification.Funding: IMA and XL were supported by Wellcome Trust Project Grant 088266 to IMA and AJB. AKJV was funded by an E.C. Marie Curie postdoctoral fellowship (MEIF-CT-2005-023694) and an EMBO short-term fellowship (244-2007). XL was supported additionally by Wellcome Trust Project Grant 088231 to AJB and KN. DR was supported by a University of Bristol Centenary Postgraduate Studentship. This work was also supported in part by MRC project grants G0701243 and MR-J002097-1 to AJB and AJB and KN, respectively, and by Grants-in-Aid for Scientific Research (22570161 and 23121516 to TM, and 21227006 to KN) and Targeted Proteins Research Program from the Ministry of Education, Culture, Sports, Science and Technology of Japan and by Takeda Science Foundation (to TM). YVM is a Research Fellow of the Japanese Society for the Promotion of Science. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in immunodeficient hosts.
The inhibition of death-receptor apoptosis is a conserved viral function. The murine cytomegalovirus (MCMV) gene M36 is a sequence and functional homologue of the human cytomegalovirus gene UL36, and it encodes an inhibitor of apoptosis that binds to caspase-8, blocks downstream signaling and thus contributes to viral fitness in macrophages and in vivo. Here we show a direct link between the inability of mutants lacking the M36 gene (ΔM36) to inhibit apoptosis, poor viral growth in macrophage cell cultures and viral in vivo fitness and virulence. ΔM36 grew poorly in RAG1 knockout mice and in RAG/IL-2-receptor common gamma chain double knockout mice (RAGγC(-/-)), but the depletion of macrophages in either mouse strain rescued the growth of ΔM36 to almost wild-type levels. This was consistent with the observation that activated macrophages were sufficient to impair ΔM36 growth in vitro. Namely, spiking fibroblast cell cultures with activated macrophages had a suppressive effect on ΔM36 growth, which could be reverted by z-VAD-fmk, a chemical apoptosis inhibitor. TNFα from activated macrophages synergized with IFNγ in target cells to inhibit ΔM36 growth. Hence, our data show that poor ΔM36 growth in macrophages does not reflect a defect in tropism, but rather a defect in the suppression of antiviral mediators secreted by macrophages. To the best of our knowledge, this shows for the first time an immune evasion mechanism that protects MCMV selectively from the antiviral activity of macrophages, and thus critically contributes to viral pathogenicity in the immunocompromised host devoid of the adaptive immune system
Odor pleasantness modulates functional connectivity in the olfactory hedonic processing network
Olfactory hedonic evaluation is the primary dimension of olfactory perception and thus central to our sense of smell. It involves complex interactions between brain regions associated with sensory, affective and reward processing. Despite a recent increase in interest, several aspects of olfactory hedonic evaluation remain ambiguous: uncertainty surrounds the communication between, and interaction among, brain areas during hedonic evaluation of olfactory stimuli with different levels of pleasantness, as well as the corresponding supporting oscillatory mechanisms. In our study we investigated changes in functional interactions among brain areas in response to odor stimuli using electroencephalography (EEG). To this goal, functional connectivity networks were estimated based on phase synchronization between EEG signals using the weighted phase lag index (wPLI). Graph theoretic metrics were subsequently used to quantify the resulting changes in functional connectivity of relevant brain regions involved in olfactory hedonic evaluation. Our results indicate that odor stimuli of different hedonic values evoke significantly different interaction patterns among brain regions within the olfactory cortex, as well as in the anterior cingulate and orbitofrontal cortices. Furthermore, significant hemispheric laterality effects have been observed in the prefrontal and anterior cingulate cortices, specifically in the beta ((13–30) Hz) and gamma ((30–40) Hz) frequency band
Ising Universality in Three Dimensions: A Monte Carlo Study
We investigate three Ising models on the simple cubic lattice by means of
Monte Carlo methods and finite-size scaling. These models are the spin-1/2
Ising model with nearest-neighbor interactions, a spin-1/2 model with
nearest-neighbor and third-neighbor interactions, and a spin-1 model with
nearest-neighbor interactions. The results are in accurate agreement with the
hypothesis of universality. Analysis of the finite-size scaling behavior
reveals corrections beyond those caused by the leading irrelevant scaling
field. We find that the correction-to-scaling amplitudes are strongly dependent
on the introduction of further-neighbor interactions or a third spin state. In
a spin-1 Ising model, these corrections appear to be very small. This is very
helpful for the determination of the universal constants of the Ising model.
The renormalization exponents of the Ising model are determined as y_t = 1.587
(2), y_h = 2.4815 (15) and y_i = -0.82 (6). The universal ratio Q =
^2/ is equal to 0.6233 (4) for periodic systems with cubic symmetry.
The critical point of the nearest-neighbor spin-1/2 model is K_c=0.2216546
(10).Comment: 25 pages, uuencoded compressed PostScript file (to appear in Journal
of Physics A
Improved high-temperature expansion and critical equation of state of three-dimensional Ising-like systems
High-temperature series are computed for a generalized Ising model with
arbitrary potential. Two specific ``improved'' potentials (suppressing leading
scaling corrections) are selected by Monte Carlo computation. Critical
exponents are extracted from high-temperature series specialized to improved
potentials, achieving high accuracy; our best estimates are:
, , , ,
. By the same technique, the coefficients of the small-field
expansion for the effective potential (Helmholtz free energy) are computed.
These results are applied to the construction of parametric representations of
the critical equation of state. A systematic approximation scheme, based on a
global stationarity condition, is introduced (the lowest-order approximation
reproduces the linear parametric model). This scheme is used for an accurate
determination of universal ratios of amplitudes. A comparison with other
theoretical and experimental determinations of universal quantities is
presented.Comment: 65 pages, 1 figure, revtex. New Monte Carlo data by Hasenbusch
enabled us to improve the determination of the critical exponents and of the
equation of state. The discussion of several topics was improved and the
bibliography was update
Evidence for the η_b(1S) Meson in Radiative Υ(2S) Decay
We have performed a search for the η_b(1S) meson in the radiative decay of the Υ(2S) resonance using a sample of 91.6 × 10^6 Υ(2S) events recorded with the BABAR detector at the PEP-II B factory at the SLAC National Accelerator Laboratory. We observe a peak in the photon energy spectrum at E_γ = 609.3^(+4.6)_(-4.5)(stat)±1.9(syst) MeV, corresponding to an η_b(1S) mass of 9394.2^(+4.8)_(-4.9)(stat) ± 2.0(syst) MeV/c^2. The branching fraction for the decay Υ(2S) → γη_b(1S) is determined to be [3.9 ± 1.1(stat)^(+1.1)_(-0.9)(syst)] × 10^(-4). We find the ratio of branching fractions B[Υ(2S) → γη_b(1S)]/B[Υ(3S) → γη_b(1S)]= 0.82 ± 0.24(stat)^(+0.20)_(-0.19)(syst)
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