Local aspects of disentanglement induced by spontaneous emission

We consider spontaneous emission of two two-level atoms interacting with vacuum fluctuations. We study the process of disentanglement in this system and show the possibility of changing disentanglement time by local operations.Comment: 7 pages, 2 figure

Long-distance quantum communication over noisy networks without long-time quantum memory

The problem of sharing entanglement over large distances is crucial for implementations of quantum cryptography. A possible scheme for long-distance entanglement sharing and quantum communication exploits networks whose nodes share Einstein-Podolsky-Rosen (EPR) pairs. In Perseguers et al. [Phys. Rev. A 78, 062324 (2008)] the authors put forward an important isomorphism between storing quantum information in a dimension $D$ and transmission of quantum information in a $D+1$-dimensional network. We show that it is possible to obtain long-distance entanglement in a noisy two-dimensional (2D) network, even when taking into account that encoding and decoding of a state is exposed to an error. For 3D networks we propose a simple encoding and decoding scheme based solely on syndrome measurements on 2D Kitaev topological quantum memory. Our procedure constitutes an alternative scheme of state injection that can be used for universal quantum computation on 2D Kitaev code. It is shown that the encoding scheme is equivalent to teleporting the state, from a specific node into a whole two-dimensional network, through some virtual EPR pair existing within the rest of network qubits. We present an analytic lower bound on fidelity of the encoding and decoding procedure, using as our main tool a modified metric on space-time lattice, deviating from a taxicab metric at the first and the last time slices.Comment: 15 pages, 10 figures; title modified; appendix included in main text; section IV extended; minor mistakes remove

Quantum Computation with Generalized Binomial States in Cavity Quantum Electrodynamics

We study universal quantum computation in the cavity quantum electrodynamics (CQED) framework exploiting two orthonormal two-photon generalized binomial states as qubit and dispersive interactions of Rydberg atoms with high-$Q$ cavities. We show that an arbitrary qubit state may be generated and that controlled-NOT and 1-qubit rotation gates can be realized via standard atom-cavity interactions.Comment: 7 pages, 3 figure

Modelling and Simulation of Asynchronous Real-Time Systems using Timed Rebeca

In this paper we propose an extension of the Rebeca language that can be used to model distributed and asynchronous systems with timing constraints. We provide the formal semantics of the language using Structural Operational Semantics, and show its expressiveness by means of examples. We developed a tool for automated translation from timed Rebeca to the Erlang language, which provides a first implementation of timed Rebeca. We can use the tool to set the parameters of timed Rebeca models, which represent the environment and component variables, and use McErlang to run multiple simulations for different settings. Timed Rebeca restricts the modeller to a pure asynchronous actor-based paradigm, where the structure of the model represents the service oriented architecture, while the computational model matches the network infrastructure. Simulation is shown to be an effective analysis support, specially where model checking faces almost immediate state explosion in an asynchronous setting.Comment: In Proceedings FOCLASA 2011, arXiv:1107.584

The phenotypic presentation of adult individuals with SLC6A1-related neurodevelopmental disorders

Epilepsy; Intellectual disability; Neurodevelopmental disordersEpilepsia; Discapacidad intelectual; Trastornos del neurodesarrolloEpilèpsia; Discapacitat intel·lectual; Trastorns del neurodesenvolupamentIntroduction: SLC6A1 is one of the most common monogenic causes of epilepsy and is a well-established cause of neurodevelopmental disorders. SLC6A1-neurodevelopmental disorders have a consistent phenotype of mild to severe intellectual disability (ID), epilepsy, language delay and behavioral disorders. This phenotypic description is mainly based on knowledge from the pediatric population. Method: Here, we sought to describe patients with SLC6A1 variants and age above 18 years through the ascertainment of published and unpublished patients. Unpublished patients were ascertained through international collaborations, while previously published patients were collected through a literature search. Results: A total of 15 adult patients with SLC6A1 variants were included. 9/13 patients had moderate to severe ID (data not available in two). Epilepsy was prevalent (11/15) with seizure types such as absence, myoclonic, atonic, and tonic–clonic seizures. Epilepsy was refractory in 7/11, while four patients were seizure free with lamotrigine, valproate, or lamotrigine in combination with valproate. Language development was severely impaired in five patients. Behavioral disorders were reported in and mainly consisted of autism spectrum disorders and aggressive behavior. Schizophrenia was not reported in any of the patients. Discussion: The phenotype displayed in the adult patients presented here resembled that of the pediatric cohort with ID, epilepsy, and behavioral disturbances, indicating that the phenotype of SLC6A1-NDD is consistent over time. Seizures were refractory in >60% of the patients with epilepsy, indicating the lack of targeted treatment in SLC6A1-NDDs. With increased focus on repurposing drugs and on the development of new treatments, hope is that the outlook reflected here will change over time. ID appeared to be more severe in the adult patients, albeit this might reflect a recruitment bias, where only patients seen in specialized centers were included or it might be a feature of the natural history of SLC6A1-NDDs. This issue warrants to be explored in further studies in larger cohorts

The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity

Summary: Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in plasma high-density lipoproteins. S1P is a bioactive lipid interacting with five receptors (S1P1–5). We show that lack of apoM in mice increases the amount of brown adipose tissue (BAT), accelerates the clearance of postprandial triglycerides, and protects against diet-induced obesity (i.e., a phenotype similar to that induced by cold exposure or β3-adrenergic stimulation). Moreover, the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism. : Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in lipoproteins. Christoffersen et al. show that lack of apoM in mice increases the amount of brown adipose tissue, accelerates the turnover of fat, and protects against obesity. The results reveal a link between the apoM/S1P axis and energy metabolism. Keywords: apolipoproteins, sphingolipids, sphingosine-1-phosphate, lipoproteins, lipid metabolism, triglyceride, brown adipose tissue, apo

A Placebo-Controlled Study on the Effects of the Glucagon-Like Peptide-1 Mimetic, Exenatide, on Insulin Secretion, Body Composition and Adipokines in Obese, Client-Owned Cats

Glucagon-like Peptide-1 mimetics increase insulin secretion and reduces body weight in humans. In lean, healthy cats, short-term treatment has produced similar results, whereas the effect in obese cats or with extended duration of treatment is unknown. Here, prolonged (12 weeks) treatment with the Glucagon-like Peptide-1 mimetic, exenatide, was evaluated in 12 obese, but otherwise healthy, client-owned cats. Cats were randomized to exenatide (1.0 μg/kg) or placebo treatment twice daily for 12 weeks. The primary endpoint was changes in insulin concentration; the secondary endpoints were glucose homeostasis, body weight, body composition as measured by dual-energy x-ray absorptiometry and overall safety. An intravenous glucose tolerance test (1 g/kg body weight) was conducted at week 0 and week 12. Exenatide did not change the insulin concentration, plasma glucose concentration or glucose tolerance (P>0.05 for all). Exenatide tended to reduce body weight on continued normal feeding. Median relative weight loss after 12 weeks was 5.1% (range 1.7 to 8.4%) in the exenatide group versus 3.2% (range -5.3 to 5.7%) in the placebo group (P = 0.10). Body composition and adipokine levels were unaffected by exenatide (P>0.05). Twelve weeks of exenatide was well-tolerated, with only two cases of mild, self-limiting gastrointestinal signs and a single case of mild hypoglycemia. The long-term insulinotropic effect of exenatide appeared less pronounced in obese cats compared to previous short-term studies in lean cats. Further investigations are required to fully elucidate the effect on insulin secretion, glucose tolerance and body weight in obese cats