A Factorization Law for Entanglement Decay

We present a simple and general factorization law for quantum systems shared by two parties, which describes the time evolution of entanglement upon passage of either component through an arbitrary noisy channel. The robustness of entanglement-based quantum information processing protocols is thus easily and fully characterized by a single quantity.Comment: 4 pages, 5 figure

Degos disease – malignant atrophic papulosis or cutaneointestinal lethal syndrome: rarity of the disease

Background: Degos disease is a very rare syndrome with a rare type of multisystem vasculopathy of unknown cause that affects the skin, gastrointestinal tract, and central nervous system. Other organs such as the kidneys, lungs, pleura, liver, heart, and eyes, can also be involved. Objective: To highlight the incidence of Degos disease with regard to age and sex, discuss the necessity of its accurate and early diagnosis, and demonstrate the most current techniques for its diagnosis; to discuss whether early therapeutic intervention can impact patient prognosis; and to present a literature review about this disease. Design: With a retrospective, observational, nonrandomized trial, we described the evolution of the different forms of Degos disease and referenced the literature. Data sources Research on rare documented cases in the literature, including two cases of potentially lethal form of the disease involving the skin and gastrointestinal system and, possibly, the lungs, kidneys, and central nervous system. A case of the benign form of the disease involving the skin was observed by the authors. Main outcome measures Differences between outcomes in patients with the cutaneointestinal form and skin-only form of the disease. There was one fatal outcome. We reviewed possible new approaches to diagnosis and treatment. Results: The study demonstrated the rapid evolution of the aggressive and malignant form of the disease. It also described newly accessible Phase I diagnostic tools being currently researched as well as new therapeutic approaches. Limitation The rarity of the disease, with only eleven cases throughout the literature. Conclusion: The gastrointestinal form of Degos disease can be lethal. Its vascular etiology has finally been confirmed; however, new and more accurate early diagnostic modalities need to be developed. There are new therapeutic possibilities, but the studies of them are still in the early stages and have not yet shown the full effectiveness of these new therapies

Tricritical Points in the Sherrington-Kirkpatrick Model in the Presence of Discrete Random Fields

The infinite-range-interaction Ising spin glass is considered in the presence of an external random magnetic field following a trimodal (three-peak) distribution. The model is studied through the replica method and phase diagrams are obtained within the replica-symmetry approximation. It is shown that the border of the ferromagnetic phase may present first-order phase transitions, as well as tricritical points at finite temperatures. Analogous to what happens for the Ising ferromagnet under a trimodal random field, it is verified that the first-order phase transitions are directly related to the dilution in the fields (represented by $p_{0}$). The ferromagnetic boundary at zero temperature also exhibits an interesting behavior: for $0<p_{0}<p_{0}^{*} \approx 0.30856$, a single tricritical point occurs, whereas if $p_{0}>p_{0}^{*}$ the critical frontier is completely continuous; however, for $p_{0}=p_{0}^{*}$, a fourth-order critical point appears. The stability analysis of the replica-symmetric solution is performed and the regions of validity of such a solution are identified; in particular, the Almeida-Thouless line in the plane field versus temperature is shown to depend on the weight $p_{0}$.Comment: 23pages, 7 ps figure

Universality of the Lyapunov regime for the Loschmidt echo

The Loschmidt echo (LE) is a magnitude that measures the sensitivity of quantum dynamics to perturbations in the Hamiltonian. For a certain regime of the parameters, the LE decays exponentially with a rate given by the Lyapunov exponent of the underlying classically chaotic system. We develop a semiclassical theory, supported by numerical results in a Lorentz gas model, which allows us to establish and characterize the universality of this Lyapunov regime. In particular, the universality is evidenced by the semiclassical limit of the Fermi wavelength going to zero, the behavior for times longer than Ehrenfest time, the insensitivity with respect to the form of the perturbation and the behavior of individual (non-averaged) initial conditions. Finally, by elaborating a semiclassical approximation to the Wigner function, we are able to distinguish between classical and quantum origin for the different terms of the LE. This approach renders an understanding for the persistence of the Lyapunov regime after the Ehrenfest time, as well as a reinterpretation of our results in terms of the quantum--classical transition.Comment: 33 pages, 17 figures, uses Revtex

Glucocorticoid Regulation of Astrocytic Fate and Function

Glial loss in the hippocampus has been suggested as a factor in the pathogenesis of stress-related brain disorders that are characterized by dysregulated glucocorticoid (GC) secretion. However, little is known about the regulation of astrocytic fate by GC. Here, we show that astrocytes derived from the rat hippocampus undergo growth inhibition and display moderate activation of caspase 3 after exposure to GC. Importantly, the latter event, observed both in situ and in primary astrocytic cultures is not followed by either early- or late-stage apoptosis, as monitored by stage I or stage II DNA fragmentation. Thus, unlike hippocampal granule neurons, astrocytes are resistant to GC-induced apoptosis; this resistance is due to lower production of reactive oxygen species (ROS) and a greater buffering capacity against the cytotoxic actions of ROS. We also show that GC influence hippocampal cell fate by inducing the expression of astrocyte-derived growth factors implicated in the control of neural precursor cell proliferation. Together, our results suggest that GC instigate a hitherto unknown dialog between astrocytes and neural progenitors, adding a new facet to understanding how GC influence the cytoarchitecture of the hippocampus

Characterization of the genetic diversity of Mycobacterium tuberculosis in São Paulo city, Brazil

<p>Abstract</p> <p>Background</p> <p>Tuberculosis is a major health problem in São Paulo, Brazil, which is the most populous and one of the most cosmopolitan cities in South America. To characterize the genetic diversity of <it>Mycobacterium tuberculosis </it>in the population of this city, the genotyping techniques of spoligotyping and MIRU were applied to 93 isolates collected in two consecutive years from 93 different tuberculosis patients residing in São Paulo city and attending the Clemente Ferreira Institute (the reference clinic for the treatment of tuberculosis).</p> <p>Findings</p> <p>Spoligotyping generated 53 different spoligotype patterns. Fifty-one isolates (54.8%) were grouped into 13 spoligotyping clusters. Seventy- two strains (77.4%) showed spoligotypes described in the international databases (SpolDB4, SITVIT), and 21 (22.6%) showed unidentified patterns. The most frequent spoligotype families were Latin American Mediterranean (LAM) (26 isolates), followed by the T family (24 isolates) and Haarlem (H) (11 isolates), which together accounted for 65.4% of all the isolates. These three families represent the major genotypes found in Africa, Central America, South America and Europe. Six Spoligo-International-types (designated SITs by the database) comprised 51.8% (37/72) of all the identified spoligotypes (SIT53, SIT50, SIT42, SIT60, SIT17 and SIT1). Other SITs found in this study indicated the great genetic diversity of <it>M. tuberculosis</it>, reflecting the remarkable ethnic diversity of São Paulo city inhabitants. The MIRU technique was more discriminatory and did not identify any genetic clusters with 100% similarity among the 93 isolates. The allelic analysis showed that MIRU loci 26, 40, 23 and 10 were the most discriminatory. When MIRU and spoligotyping techniques were combined, all isolates grouped in the 13 spoligotyping clusters were separated.</p> <p>Conclusions</p> <p>Our data indicated the genomic stability of over 50% of spoligotypes identified in São Paulo and the great genetic diversity of <it>M. tuberculosis </it>isolates in the remaining SITs, reflecting the large ethnic mix of the São Paulo city inhabitants. The results also indicated that in this city, <it>M. tuberculosis </it>isolates acquired drug resistance independently of genotype and that resistance was more dependent on the selective pressure of treatment failure and the environmental circumstances of patients.</p

A multi-targeted approach to suppress tumor-promoting inflammation

Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-κB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes