Thermalization in a 1D Rydberg gas: validity of the microcanonical ensemble hypothesis

We question the microcanonical hypothesis, often made to account for the thermalization of complex closed quantum systems, on the specific example of a chain of two-level atoms optically driven by a resonant laser beam and strongly interacting via Rydberg-Rydberg dipole-dipole interactions. Along its (necessarily unitary) evolution, this system is indeed expected to thermalize, i.e. observables, such as the number of excitations, stop oscillating and reach equilibrium-like expectation values. The latter are often calculated through assuming the system can be effectively described by a thermal-like microcanonical state. Here, we compare the distribution of excitations in the chain calculated either according to the microcanonical assumption or through direct exact numerical simulation. This allows us to show the limitations of the thermal equilibrium hypothesis and precise its applicability conditions.Comment: v2: Add comparison with Bettelli et al.'s Monte-Carlo simulation (App. A) + typo correctio

Toward an architecture for quantum programming

It is becoming increasingly clear that, if a useful device for quantum computation will ever be built, it will be embodied by a classical computing machine with control over a truly quantum subsystem, this apparatus performing a mixture of classical and quantum computation. This paper investigates a possible approach to the problem of programming such machines: a template high level quantum language is presented which complements a generic general purpose classical language with a set of quantum primitives. The underlying scheme involves a run-time environment which calculates the byte-code for the quantum operations and pipes it to a quantum device controller or to a simulator. This language can compactly express existing quantum algorithms and reduce them to sequences of elementary operations; it also easily lends itself to automatic, hardware independent, circuit simplification. A publicly available preliminary implementation of the proposed ideas has been realized using the C++ language.Comment: 23 pages, 5 figures, A4paper. Final version accepted by EJPD ("swap" replaced by "invert" for Qops). Preliminary implementation available at: http://sra.itc.it/people/serafini/quantum-computing/qlang.htm

Entanglement as a signature of quantum chaos

We explore the dynamics of entanglement in classically chaotic systems by considering a multiqubit system that behaves collectively as a spin system obeying the dynamics of the quantum kicked top. In the classical limit, the kicked top exhibits both regular and chaotic dynamics depending on the strength of the chaoticity parameter $\kappa$ in the Hamiltonian. We show that the entanglement of the multiqubit system, considered for both bipartite and pairwise entanglement, yields a signature of quantum chaos. Whereas bipartite entanglement is enhanced in the chaotic region, pairwise entanglement is suppressed. Furthermore, we define a time-averaged entangling power and show that this entangling power changes markedly as $\kappa$ moves the system from being predominantly regular to being predominantly chaotic, thus sharply identifying the edge of chaos. When this entangling power is averaged over initial states, it yields a signature of global chaos. The qualitative behavior of this global entangling power is similar to that of the classical Lyapunov exponent.Comment: 8 pages, 8 figure

Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease

Celiac disease (CD) is an autoimmune enteropathy induced by the ingestion of gluten in genetically predisposed individuals who carry the HLA-DQ2 or -DQ8 alleles. The immune response is abnormal in celiac disease with small intestinal epithelial damage via CD8+CD4- intraepithelial lymphocytes. The etiology is multifactorial involving genetic and environmental factors, an abnormal immune response, and intestinal dysbiosis. The innate and acquired T-cell mediated immunity play important roles in the pathogenesis of this disease, particularly CD4+ Th17 cells, which have been shown to have critical functions in host defense against bacterial pathogens and in the inflammatory responses to deamidated gluten peptides. We review what is known about the interaction between immune system and intestinal microbiota in the pathogenesis of celiac disease

On the optimality of individual entangling-probe attacks against BB84 quantum key distribution

It is shown that an existing method to study ideal individual attacks on the BB84 QKD protocol using error discard can be adapted to reconciliation with error correction, and that an optimal attack can be explicitly found. Moreover, this attack fills Luetkenhaus bound, independently of whether error positions are leaked to Eve, proving that it is tight. In addition, we clarify why the existence of such optimal attacks is not in contradiction with the established ``old-style'' theory of BB84 individual attacks, as incorrectly suggested recently in a news feature.Comment: 12 pages, 3 figure

IL-6 controls susceptibility to helminth infection by impeding Th2 responsiveness and altering the Treg phenotype in vivo

IL-6 plays a pivotal role in favoring T-cell commitment toward a Th17 cell rather than Treg-cell phenotype, as established through in vitro model systems. We predicted that in the absence of IL-6, mice infected with the gastrointestinal helminth Heligmosomoides polygyrus would show reduced Th17-cell responses, but also enhanced Treg-cell activity and consequently greater susceptibility. Surprisingly, worm expulsion was markedly potentiated in IL-6-deficient mice, with significantly stronger adaptive Th2 responses in both IL-6−/− mice and BALB/c recipients of neutralizing anti-IL-6 monoclonal Ab. Although IL-6-deficient mice showed lower steady-state Th17-cell levels, IL-6-independent Th17-cell responses occurred during in vivo infection. We excluded the Th17 response as a factor in protection, as Ab neutralization did not modify immunity to H. polygyrus infection in BALB/c mice. Resistance did correlate with significant changes to the associated Treg-cell phenotype however, as IL-6-deficient mice displayed reduced expression of Foxp3, Helios, and GATA-3, and enhanced production of cytokines within the Treg-cell population. Administration of an anti-IL-2:IL-2 complex boosted Treg-cell proportions in vivo, reduced adaptive Th2 responses to WT levels, and fully restored susceptibility to H. polygyrus in IL-6-deficient mice. Thus, in vivo, IL-6 limits the Th2 response, modifies the Treg-cell phenotype, and promotes host susceptibility following helminth infection

Tolerance without clonal expansion: Self-antigen-expressing B cells program self-reactive T cells for future deletion

B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by ablation of conventional self-reactive T cells