904 research outputs found
Interplay between Zeeman Coupling and Swap Action in Spin-based Quantum Computer Models: Error Correction in Inhomogeneous Magnetic Fields
We consider theoretically the interplay between Zeeman coupling and
exchange-induced swap action in spin-based quantum dot quantum computer models
in the presence of inhomogeneous magnetic fields, which are invariably present
in real systems. We estimate quantitatively swap errors caused by the
inhomogeneous field, establishing that error correction would, in principle, be
possible in the presence of non-uniform magnetic fields in realistic
structures.Comment: Revised version. To appear in Phys. Rev. Let
Decoherence by engineered quantum baths
We introduce, and determine decoherence for, a wide class of non-trivial
quantum spin baths which embrace Ising, XY and Heisenberg universality classes
coupled to a two-level system. For the XY and Ising universality classes we
provide an exact expression for the decay of the loss of coherence beyond the
case of a central spin coupled uniformly to all the spins of the baths which
has been discussed so far in the literature. In the case of the Heisenberg spin
bath we study the decoherence by means of the time-dependent density matrix
renormalization group. We show how these baths can be engineered, by using
atoms in optical lattices.Comment: 4 pages, 4 figure
Quantum Computing
Quantum mechanics---the theory describing the fundamental workings of
nature---is famously counterintuitive: it predicts that a particle can be in
two places at the same time, and that two remote particles can be inextricably
and instantaneously linked. These predictions have been the topic of intense
metaphysical debate ever since the theory's inception early last century.
However, supreme predictive power combined with direct experimental observation
of some of these unusual phenomena leave little doubt as to its fundamental
correctness. In fact, without quantum mechanics we could not explain the
workings of a laser, nor indeed how a fridge magnet operates. Over the last
several decades quantum information science has emerged to seek answers to the
question: can we gain some advantage by storing, transmitting and processing
information encoded in systems that exhibit these unique quantum properties?
Today it is understood that the answer is yes. Many research groups around the
world are working towards one of the most ambitious goals humankind has ever
embarked upon: a quantum computer that promises to exponentially improve
computational power for particular tasks. A number of physical systems,
spanning much of modern physics, are being developed for this task---ranging
from single particles of light to superconducting circuits---and it is not yet
clear which, if any, will ultimately prove successful. Here we describe the
latest developments for each of the leading approaches and explain what the
major challenges are for the future.Comment: 26 pages, 7 figures, 291 references. Early draft of Nature 464, 45-53
(4 March 2010). Published version is more up-to-date and has several
corrections, but is half the length with far fewer reference
Quantum entanglement and disentanglement of multi-atom systems
We present a review of recent research on quantum entanglement, with special
emphasis on entanglement between single atoms, processing of an encoded
entanglement and its temporary evolution. Analysis based on the density matrix
formalism are described. We give a simple description of the entangling
procedure and explore the role of the environment in creation of entanglement
and in disentanglement of atomic systems. A particular process we will focus on
is spontaneous emission, usually recognized as an irreversible loss of
information and entanglement encoded in the internal states of the system. We
illustrate some certain circumstances where this irreversible process can in
fact induce entanglement between separated systems. We also show how
spontaneous emission reveals a competition between the Bell states of a two
qubit system that leads to the recently discovered "sudden" features in the
temporal evolution of entanglement. An another problem illustrated in details
is a deterministic preparation of atoms and atomic ensembles in long-lived
stationary squeezed states and entangled cluster states. We then determine how
to trigger the evolution of the stable entanglement and also address the issue
of a steered evolution of entanglement between desired pairs of qubits that can
be achieved simply by varying the parameters of a given system.Comment: Review articl
Caribbean Corals in Crisis: Record Thermal Stress, Bleaching, and Mortality in 2005
BACKGROUND The rising temperature of the world's oceans has become a major threat to coral reefs globally as the severity and frequency of mass coral bleaching and mortality events increase. In 2005, high ocean temperatures in the tropical Atlantic and Caribbean resulted in the most severe bleaching event ever recorded in the basin. METHODOLOGY/PRINCIPAL FINDINGS Satellite-based tools provided warnings for coral reef managers and scientists, guiding both the timing and location of researchers' field observations as anomalously warm conditions developed and spread across the greater Caribbean region from June to October 2005. Field surveys of bleaching and mortality exceeded prior efforts in detail and extent, and provided a new standard for documenting the effects of bleaching and for testing nowcast and forecast products. Collaborators from 22 countries undertook the most comprehensive documentation of basin-scale bleaching to date and found that over 80% of corals bleached and over 40% died at many sites. The most severe bleaching coincided with waters nearest a western Atlantic warm pool that was centered off the northern end of the Lesser Antilles. CONCLUSIONS/SIGNIFICANCE Thermal stress during the 2005 event exceeded any observed from the Caribbean in the prior 20 years, and regionally-averaged temperatures were the warmest in over 150 years. Comparison of satellite data against field surveys demonstrated a significant predictive relationship between accumulated heat stress (measured using NOAA Coral Reef Watch's Degree Heating Weeks) and bleaching intensity. This severe, widespread bleaching and mortality will undoubtedly have long-term consequences for reef ecosystems and suggests a troubled future for tropical marine ecosystems under a warming climate.This work was partially supported by salaries from the NOAA Coral Reef Conservation Program to the NOAA Coral Reef Conservation Program authors. NOAA provided funding to Caribbean ReefCheck investigators to undertake surveys of bleaching and mortality. Otherwise, no funding from outside authors' institutions was necessary for the undertaking of this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
Critical Roles of the WASP N-Terminal Domain and Btk in LPS-Induced Inflammatory Response in Macrophages
While Wiskott-Aldrich syndrome protein (WASP) plays critical roles in TCR signaling as an adaptor molecule, how it transduces innate immune signals remains to be elucidated. To investigate the roles of WASP in innate immune cells, we established bone marrow-derived macrophage (BMDM) cell lines from WASP15 transgenic (Tg) mice overexpressing the WASP N-terminal region (exons 1–5). Upon LPS stimulation, WASP15 Tg BMDM cell lines produce lower levels of inflammatory cytokines, such as TNF-α, IL-6, and IL-12p40 than the wild-type BMDM cell line. In addition, the production of nitric oxide by WASP15 Tg BMDM cells in response to LPS and IFN-γ was significantly impaired. Furthermore, we uncovered that the WASP N-terminal domain associates with the Src homology (SH) 3 domain of Bruton's tyrosine kinase (Btk). Overexpression of the WASP N-terminal domain diminishes the extent of tyrosine phosphorylation of endogenous WASP in WASP15 Tg BMDM cells, possibly by interfering with the specific binding between endogenous WASP and Btk during LPS signaling. These observations strongly suggest that the interaction between WASP N-terminal domain and Btk plays important roles in the LPS signaling cascade in innate immunity
Micro-Environmental Mechanical Stress Controls Tumor Spheroid Size and Morphology by Suppressing Proliferation and Inducing Apoptosis in Cancer Cells
Compressive mechanical stress produced during growth in a confining matrix limits the size of tumor spheroids, but little is known about the dynamics of stress accumulation, how the stress affects cancer cell phenotype, or the molecular pathways involved.We co-embedded single cancer cells with fluorescent micro-beads in agarose gels and, using confocal microscopy, recorded the 3D distribution of micro-beads surrounding growing spheroids. The change in micro-bead density was then converted to strain in the gel, from which we estimated the spatial distribution of compressive stress around the spheroids. We found a strong correlation between the peri-spheroid solid stress distribution and spheroid shape, a result of the suppression of cell proliferation and induction of apoptotic cell death in regions of high mechanical stress. By compressing spheroids consisting of cancer cells overexpressing anti-apoptotic genes, we demonstrate that mechanical stress-induced apoptosis occurs via the mitochondrial pathway.Our results provide detailed, quantitative insight into the role of micro-environmental mechanical stress in tumor spheroid growth dynamics, and suggest how tumors grow in confined locations where the level of solid stress becomes high. An important implication is that apoptosis via the mitochondrial pathway, induced by compressive stress, may be involved in tumor dormancy, in which tumor growth is held in check by a balance of apoptosis and proliferation
The Anti-Apoptotic Bcl-xL Protein, a New Piece in the Puzzle of Cytochrome C Interactome
A structural model of the adduct between human cytochrome c and the human
anti-apoptotic protein Bcl-xL, which defines the protein-protein
interaction surface, was obtained from solution NMR chemical shift perturbation
data. The atomic level information reveals key intermolecular contacts
identifying new potentially druggable areas on cytochrome c and
Bcl-xL. Involvement of residues on cytochrome c other than those
in its complexes with electron transfer partners is apparent. Key differences in
the contact area also exist between the Bcl-xL adduct with the Bak
peptide and that with cytochrome c. The present model provides insights to the
mechanism by which cytochrome c translocated to cytosol can be intercepted, so
that the apoptosome is not assembled
Selective regulation of IP3-receptor-mediated Ca2+ signaling and apoptosis by the BH4 domain of Bcl-2 versus Bcl-Xl
Antiapoptotic B-cell lymphoma 2 (Bcl-2) targets the inositol 1,4,5-trisphosphate receptor (IP3R) via its BH4 domain, thereby suppressing IP3R Ca2+-flux properties and protecting against Ca2+-dependent apoptosis. Here, we directly compared IP3R inhibition by BH4-Bcl-2 and BH4-Bcl-Xl. In contrast to BH4-Bcl-2, BH4-Bcl-Xl neither bound the modulatory domain of IP3R nor inhibited IP3-induced Ca2+ release (IICR) in permeabilized and intact cells. We identified a critical residue in BH4-Bcl-2 (Lys17) not conserved in BH4-Bcl-Xl (Asp11). Changing Lys17 into Asp in BH4-Bcl-2 completely abolished its IP3R-binding and -inhibitory properties, whereas changing Asp11 into Lys in BH4-Bcl-Xl induced IP3R binding and inhibition. This difference in IP3R regulation between BH4-Bcl-2 and BH4-Bcl-Xl controls their antiapoptotic action. Although both BH4-Bcl-2 and BH4-Bcl-Xl had antiapoptotic activity, BH4-Bcl-2 was more potent than BH4-Bcl-Xl. The effect of BH4-Bcl-2, but not of BH4-Bcl-Xl, depended on its binding to IP(3)Rs. In agreement with the IP3R-binding properties, the antiapoptotic activity of BH4-Bcl-2 and BH4-Bcl-Xl was modulated by the Lys/Asp substitutions. Changing Lys17 into Asp in full-length Bcl-2 significantly decreased its binding to the IP3R, its ability to inhibit IICR and its protection against apoptotic stimuli. A single amino-acid difference between BH4-Bcl-2 and BH4-Bcl-Xl therefore underlies differential regulation of IP(3)Rs and Ca2+-driven apoptosis by these functional domains. Mutating this residue affects the function of Bcl-2 in Ca2+ signaling and apoptosis
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