62 research outputs found
Many-body localization in a quantum simulator with programmable random disorder
When a system thermalizes it loses all local memory of its initial
conditions. This is a general feature of open systems and is well described by
equilibrium statistical mechanics. Even within a closed (or reversible) quantum
system, where unitary time evolution retains all information about its initial
state, subsystems can still thermalize using the rest of the system as an
effective heat bath. Exceptions to quantum thermalization have been predicted
and observed, but typically require inherent symmetries or noninteracting
particles in the presence of static disorder. The prediction of many-body
localization (MBL), in which disordered quantum systems can fail to thermalize
in spite of strong interactions and high excitation energy, was therefore
surprising and has attracted considerable theoretical attention. Here we
experimentally generate MBL states by applying an Ising Hamiltonian with
long-range interactions and programmably random disorder to ten spins
initialized far from equilibrium. We observe the essential signatures of MBL:
memory retention of the initial state, a Poissonian distribution of energy
level spacings, and entanglement growth in the system at long times. Our
platform can be scaled to higher numbers of spins, where detailed modeling of
MBL becomes impossible due to the complexity of representing such entangled
quantum states. Moreover, the high degree of control in our experiment may
guide the use of MBL states as potential quantum memories in naturally
disordered quantum systems.Comment: 9 pages, 9 figure
Disorder Effects on Exciton-Polariton Condensates
The impact of a random disorder potential on the dynamical properties of Bose
Einstein condensates is a very wide research field. In microcavities, these
studies are even more crucial than in the condensates of cold atoms, since
random disorder is naturally present in the semiconductor structures. In this
chapter, we consider a stable condensate, defined by a chemical potential,
propagating in a random disorder potential, like a liquid flowing through a
capillary. We analyze the interplay between the kinetic energy, the
localization energy, and the interaction between particles in 1D and 2D
polariton condensates. The finite life time of polaritons is taken into account
as well. In the first part, we remind the results of [G. Malpuech et al. Phys.
Rev. Lett. 98, 206402 (2007).] where we considered the case of a static
condensate. In that case, the condensate forms either a glassy insulating phase
at low polariton density (strong localization), or a superfluid phase above the
percolation threshold. We also show the calculation of the first order spatial
coherence of the condensate versus the condensate density. In the second part,
we consider the case of a propagating non-interacting condensate which is
always localized because of Anderson localization. The localization length is
calculated in the Born approximation. The impact of the finite polariton life
time is taken into account as well. In the last section we consider the case of
a propagating interacting condensate where the three regimes of strong
localization, Anderson localization, and superfluid behavior are accessible.
The localization length is calculated versus the system parameters. The
localization length is strongly modified with respect to the non-interacting
case. It is infinite in the superfluid regime whereas it is strongly reduced if
the fluid flows with a supersonic velocity.Comment: chapter for a book "Exciton Polaritons in Microcavities: New
Frontiers" by Springer (2012), the original publication is available at
http://www.springerlink.co
Response of Methicillin-Resistant Staphylococcus aureus to Amicoumacin A
Amicoumacin A exhibits strong antimicrobial activity against methicillin-resistant Staphylococcus aureus (MRSA), hence we sought to uncover its mechanism of action. Genome-wide transcriptome analysis of S. aureus COL in response to amicoumacin A showed alteration in transcription of genes specifying several cellular processes including cell envelope turnover, cross-membrane transport, virulence, metabolism, and general stress response. The most highly induced gene was lrgA, encoding an antiholin-like product, which is induced in cells undergoing a collapse of Δψ. Consistent with the notion that LrgA modulates murein hydrolase activity, COL grown in the presence of amicoumacin A showed reduced autolysis, which was primarily caused by lower hydrolase activity. To gain further insight into the mechanism of action of amicoumacin A, a whole genome comparison of wild-type COL and amicoumacin A-resistant mutants isolated by a serial passage method was carried out. Single point mutations generating codon substitutions were uncovered in ksgA (encoding RNA dimethyltransferase), fusA (elongation factor G), dnaG (primase), lacD (tagatose 1,6-bisphosphate aldolase), and SACOL0611 (a putative glycosyl transferase). The codon substitutions in EF-G that cause amicoumacin A resistance and fusidic acid resistance reside in separate domains and do not bring about cross resistance. Taken together, these results suggest that amicoumacin A might cause perturbation of the cell membrane and lead to energy dissipation. Decreased rates of cellular metabolism including protein synthesis and DNA replication in resistant strains might allow cells to compensate for membrane dysfunction and thus increase cell survivability
Baseline and stress-induced levels of corticosterone in male and female Afrotropical and European temperate stonechats during breeding
Species concepts and speciation factors in cyanobacteria, with connection to the problems of diversity and classification
Insight change in psychosis: relationship with neurocognition, social cognition, clinical symptoms and phase of illness
Phosphoinositide metabolism links cGMP-dependent protein kinase G to essential Ca²⁺ signals at key decision points in the life cycle of malaria parasites
This work was funded by grants from the Wellcome Trust (WT098051 and 079643/Z/06/Z) and the Medical Research Council (G0501670) to OB, a Wellcome Trust project grant to DB (WT094752), a Wellcome Trust Grant (WT093228) to TKS, a Marie Curie Fellowship (PIEF-GA-2008-220180) to SS, and a Marie Curie Fellowship (PIEF-GA-2009-253899) and an EMBO Long Term Fellowship (ALTF 45-2009) to MBr. C2 was synthesised and kindly provided by Katy Kettleborough and colleagues at MRC Technology through an MRC grant to DB (G10000779).Many critical events in the Plasmodium life cycle rely on the controlled release of Ca2+ from intracellular stores to activate stage-specific Ca2+-dependent protein kinases. Using the motility of Plasmodium berghei ookinetes as a signalling paradigm, we show that the cyclic guanosine monophosphate (cGMP)-dependent protein kinase, PKG, maintains the elevated level of cytosolic Ca2+ required for gliding motility. We find that the same PKG-dependent pathway operates upstream of the Ca2+ signals that mediate activation of P. berghei gametocytes in the mosquito and egress of Plasmodium falciparum merozoites from infected human erythrocytes. Perturbations of PKG signalling in gliding ookinetes have a marked impact on the phosphoproteome, with a significant enrichment of in vivo regulated sites in multiple pathways including vesicular trafficking and phosphoinositide metabolism. A global analysis of cellular phospholipids demonstrates that in gliding ookinetes PKG controls phosphoinositide biosynthesis, possibly through the subcellular localisation or activity of lipid kinases. Similarly, phosphoinositide metabolism links PKG to egress of P. falciparum merozoites, where inhibition of PKG blocks hydrolysis of phosphatidylinostitol (4,5)-bisphosphate. In the face of an increasing complexity of signalling through multiple Ca2+ effectors, PKG emerges as a unifying factor to control multiple cellular Ca2+ signals essential for malaria parasite development and transmission.Publisher PDFPeer reviewe
Conserved relationship between psbH and petBD genes: presence of a shared upstream element in Prochlorothrix hollandica
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