158 research outputs found
Ground states of unfrustrated spin Hamiltonians satisfy an area law
We show that ground states of unfrustrated quantum spin-1/2 systems on
general lattices satisfy an entanglement area law, provided that the
Hamiltonian can be decomposed into nearest-neighbor interaction terms which
have entangled excited states. The ground state manifold can be efficiently
described as the image of a low-dimensional subspace of low Schmidt measure,
under an efficiently contractible tree-tensor network. This structure gives
rise to the possibility of efficiently simulating the complete ground space
(which is in general degenerate). We briefly discuss "non-generic" cases,
including highly degenerate interactions with product eigenbases, using a
relationship to percolation theory. We finally assess the possibility of using
such tree tensor networks to simulate almost frustration-free spin models.Comment: 14 pages, 4 figures, small corrections, added a referenc
A human coronavirus responsible for the common cold massively kills dendritic cells but not monocytes
Copyright @ 2012, American Society for Microbiology.Human coronaviruses are associated with upper respiratory tract infections that occasionally spread to the lungs and other organs. Although airway epithelial cells represent an important target for infection, the respiratory epithelium is also composed of an elaborate network of dendritic cells (DCs) that are essential sentinels of the immune system, sensing pathogens and presenting foreign antigens to T lymphocytes. In this report, we show that in vitro infection by human coronavirus 229E (HCoV-229E) induces massive cytopathic effects in DCs, including the formation of large syncytia and cell death within only few hours. In contrast, monocytes are much more resistant to infection and cytopathic effects despite similar expression levels of CD13, the membrane receptor for HCoV-229E. While the differentiation of monocytes into DCs in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4 requires 5 days, only 24 h are sufficient for these cytokines to sensitize monocytes to cell death and cytopathic effects when infected by HCoV-229E. Cell death induced by HCoV-229E is independent of TRAIL, FasL, tumor necrosis factor alpha, and caspase activity, indicating that viral replication is directly responsible for the observed cytopathic effects. The consequence of DC death at the early stage of HCoV-229E infection may have an impact on the early control of viral dissemination and on the establishment of long-lasting immune memory, since people can be reinfected multiple times by HCoV-229E
Elevated miR-499 Levels Blunt the Cardiac Stress Response
The heart responds to myriad stresses by well-described transcriptional responses that involve long-term changes in gene expression as well as more immediate, transient adaptations. MicroRNAs quantitatively regulate mRNAs and thus may affect the cardiac transcriptional output and cardiac function. Here we investigate miR-499, a microRNA embedded within a ventricular-specific myosin heavy chain gene, which is expressed in heart and skeletal muscle.We assessed miR-499 expression in human tissue to confirm its potential relevance to human cardiac gene regulation. Using a transgenic mouse model, we found that elevated miR-499 levels caused cellular hypertrophy and cardiac dysfunction in a dose-dependent manner. Global gene expression profiling revealed altered levels of the immediate early stress response genes (Egr1, Egr2 and Fos), ß-myosin heavy chain (Myh7), and skeletal muscle actin (Acta1). We verified the effect of miR-499 on the immediate early response genes by miR-499 gain- and loss-of-function in vitro. Consistent with a role for miR-499 in blunting the response to cardiac stress, asymptomatic miR-499-expressing mice had an impaired response to pressure overload and accentuated cardiac dysfunction.Elevated miR-499 levels affect cardiac gene expression and predispose to cardiac stress-induced dysfunction. miR-499 may titrate the cardiac response to stress in part by regulating the immediate early gene response
Epigenetic modifications in cardiovascular disease
Epigenetics represents a phenomenon of altered heritable phenotypic expression of genetic information occurring without changes in DNA sequence. Epigenetic modifications control embryonic development, differentiation and stem cell (re)programming. These modifications can be affected by exogenous stimuli (e.g., diabetic milieu, smoking) and oftentimes culminate in disease initiation. DNA methylation has been studied extensively and represents a well-understood epigenetic mechanism. During this process cytosine residues preceding a guanosine in the DNA sequence are methylated. CpG-islands are short-interspersed DNA sequences with clusters of CG sequences. The abnormal methylation of CpG islands in the promoter region of genes leads to a silencing of genetic information and finally to alteration of biological function. Emerging data suggest that these epigenetic modifications also impact on the development of cardiovascular disease. Histone modifications lead to the modulation of the expression of genetic information through modification of DNA accessibility. In addition, RNA-based mechanisms (e.g., microRNAs and long non-coding RNAs) influence the development of disease. We here outline the recent work pertaining to epigenetic changes in a cardiovascular disease setting
Phase transition in Random Circuit Sampling
Quantum computers hold the promise of executing tasks beyond the capability
of classical computers. Noise competes with coherent evolution and destroys
long-range correlations, making it an outstanding challenge to fully leverage
the computation power of near-term quantum processors. We report Random Circuit
Sampling (RCS) experiments where we identify distinct phases driven by the
interplay between quantum dynamics and noise. Using cross-entropy benchmarking,
we observe phase boundaries which can define the computational complexity of
noisy quantum evolution. We conclude by presenting an RCS experiment with 70
qubits at 24 cycles. We estimate the computational cost against improved
classical methods and demonstrate that our experiment is beyond the
capabilities of existing classical supercomputers
Non-Abelian braiding of graph vertices in a superconducting processor
Indistinguishability of particles is a fundamental principle of quantum
mechanics. For all elementary and quasiparticles observed to date - including
fermions, bosons, and Abelian anyons - this principle guarantees that the
braiding of identical particles leaves the system unchanged. However, in two
spatial dimensions, an intriguing possibility exists: braiding of non-Abelian
anyons causes rotations in a space of topologically degenerate wavefunctions.
Hence, it can change the observables of the system without violating the
principle of indistinguishability. Despite the well developed mathematical
description of non-Abelian anyons and numerous theoretical proposals, the
experimental observation of their exchange statistics has remained elusive for
decades. Controllable many-body quantum states generated on quantum processors
offer another path for exploring these fundamental phenomena. While efforts on
conventional solid-state platforms typically involve Hamiltonian dynamics of
quasi-particles, superconducting quantum processors allow for directly
manipulating the many-body wavefunction via unitary gates. Building on
predictions that stabilizer codes can host projective non-Abelian Ising anyons,
we implement a generalized stabilizer code and unitary protocol to create and
braid them. This allows us to experimentally verify the fusion rules of the
anyons and braid them to realize their statistics. We then study the prospect
of employing the anyons for quantum computation and utilize braiding to create
an entangled state of anyons encoding three logical qubits. Our work provides
new insights about non-Abelian braiding and - through the future inclusion of
error correction to achieve topological protection - could open a path toward
fault-tolerant quantum computing
Measurement-induced entanglement and teleportation on a noisy quantum processor
Measurement has a special role in quantum theory: by collapsing the
wavefunction it can enable phenomena such as teleportation and thereby alter
the "arrow of time" that constrains unitary evolution. When integrated in
many-body dynamics, measurements can lead to emergent patterns of quantum
information in space-time that go beyond established paradigms for
characterizing phases, either in or out of equilibrium. On present-day NISQ
processors, the experimental realization of this physics is challenging due to
noise, hardware limitations, and the stochastic nature of quantum measurement.
Here we address each of these experimental challenges and investigate
measurement-induced quantum information phases on up to 70 superconducting
qubits. By leveraging the interchangeability of space and time, we use a
duality mapping, to avoid mid-circuit measurement and access different
manifestations of the underlying phases -- from entanglement scaling to
measurement-induced teleportation -- in a unified way. We obtain finite-size
signatures of a phase transition with a decoding protocol that correlates the
experimental measurement record with classical simulation data. The phases
display sharply different sensitivity to noise, which we exploit to turn an
inherent hardware limitation into a useful diagnostic. Our work demonstrates an
approach to realize measurement-induced physics at scales that are at the
limits of current NISQ processors
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