Classical communication and non-classical fidelity of quantum teleportation

In quantum teleportation, the role of entanglement has been much discussed. It is known that entanglement is necessary for achieving non-classical teleportation fidelity. Here we focus on the amount of classical communication that is necessary to obtain non-classical fidelity in teleportation. We quantify the amount of classical communication that is sufficient for achieving non-classical fidelity for two independent 1-bit and single 2-bits noisy classical channels. It is shown that on average 0.208 bits of classical communication is sufficient to get non-classical fidelity. We also find the necessary amount of classical communication in case of isotropic transformation. Finally we study how the amount of sufficient classical communication increases with weakening of entanglement used in the teleportation process.Comment: Accepted in Quantum Info. Proces

Chemical concentration map building through bacterial foraging optimization based search algorithm by mobile robots

In this article we present implementation of Bacterial Foraging Optimization algorithm inspired search by multiple robots in an unknown area in order to find the region with highest chemical gas concentration as well as to build the chemical gas concentration map. The searching and map building tasks are accomplished by using mobile robots equipped with smart transducers for gas sensing called "KheNose". Robots perform the search autonomously via bacterial chemotactic behavior. Moreover, simultaneously the robots send their sensor readings of the chemical concentration and their position data to a remote computer (a base station), where the data is combined, interpolated, and filtered to form an real-time map of the chemical gas concentration in the environment. ©2010 IEEE

Fungal Recognition Enhances Mannose Receptor Shedding Through Dectin-1 Engagement

The mannose receptor (MR) is an endocytic type I membrane molecule with a broad ligand specificity that is involved in both hemostasis and pathogen recognition. Membrane-anchored MRis cleaved by a metalloproteinase into functional soluble MR (sMR) composed of the extracellular domains of intact MR. Although sMR production was initially considered a constitutive process, enhanced MR shedding has been observed in response to the fungal pathogen Pneumocystis carinii. In this work, we have investigated the mechanism mediating enhanced MR shedding in response to fungi. We show that other fungal species, including Candida albicans and Aspergillus fumigatus, together with zymosan, a preparation of the cell wall of Saccharomyces cerevisiae, mimic the effect of P. carinii on sMR production and that this effect takes place mainly through β-glucan recognition. Additionally, we demonstrate that MR cleavage in response to C. albicans and bioactive particulate β-glucan requires expression of dectin-1. Our data, obtained using specific inhibitors, are consistent with the canonical Syk-mediated pathway triggered by dectin-1 being mainly responsible for inducing MR shedding, with Raf-1 being partially involved. As in the case of steady-state conditions, MR shedding in response to C. albicans and β-glucan particles requires metalloprotease activity. The induction of MR shedding by dectin-1 has clear implications for the role of MR in fungal recognition, as sMR was previously shown to retain the ability to bind fungal pathogens and can interact with numerous host molecules, including lysosomal hydrolases. Thus, MR cleavage could also impact on the magnitude of inflammation during fungal infection

State Transitions and the Continuum Limit for a 2D Interacting, Self-Propelled Particle System

We study a class of swarming problems wherein particles evolve dynamically via pairwise interaction potentials and a velocity selection mechanism. We find that the swarming system undergoes various changes of state as a function of the self-propulsion and interaction potential parameters. In this paper, we utilize a procedure which, in a definitive way, connects a class of individual-based models to their continuum formulations and determine criteria for the validity of the latter. H-stability of the interaction potential plays a fundamental role in determining both the validity of the continuum approximation and the nature of the aggregation state transitions. We perform a linear stability analysis of the continuum model and compare the results to the simulations of the individual-based one

PTEN and DNA-PK determine sensitivity and recovery in response to WEE1 inhibition in human breast cancer

Inhibition of WEE1 kinase by AZD1775 has shown promising results in clinical cancer trials, but markers predicting AZD1775 response are lacking. Here we analysed AZD1775 response in a panel of human breast cancer (BC) cell lines by global proteome/transcriptome profiling and identified two groups of basal-like BC (BLBCs): ‘PTEN low’ BLBCs were highly sensitive to AZD1775 and failed to recover following removal of AZD1775, while ‘PTEN high’ BLBCs recovered. AZD1775 induced phosphorylation of DNA-PK, protecting cells from replication-associated DNA damage and promoting cellular recovery. Deletion of DNA-PK or PTEN, or inhibition of DNA-PK sensitized recovering BLBCs to AZD1775 by abrogating replication arrest, allowing replication despite DNA damage. This was linked to reduced CHK1 activation, increased cyclin E levels and apoptosis. In conclusion, we identified PTEN and DNA-PK as essential regulators of replication checkpoint arrest in response to AZD1775 and defined PTEN as a promising biomarker for efficient WEE1 cancer therapy

The future of research in an artificial intelligence-driven world

Current and future developments in artificial intelligence (AI) systems have the capacity to revolutionize the research process for better or worse. On the one hand, AI systems can serve as collaborators as they help streamline and conduct our research. On the other hand, such systems can also become our adversaries when they impoverish our ability to learn as theorists, or when they lead us astray through inaccurate, biased, or fake information. No matter which angle is considered, and whether we like it or not, AI systems are here to stay. In this curated discussion, we raise questions about human centrality and agency in the research process, and about the multiple philosophical and practical challenges we are facing now and ones we will face in the future

PloS one

Systemic lupus erythematosus is a polymorphic and multigenic inflammatory autoimmune disease. Cyclic AMP (cAMP) modulates inflammation and the inhibition of cyclic nucleotide phosphodiesterase type 4 (PDE4), which specifically hydrolyzes cAMP, inhibits TNFalpha secretion. This study was aimed at investigating the evolution of PDE activity and expression levels during the course of the disease in MRL/lpr lupus-prone mice, and to evaluate in these mice the biological and clinical effects of treatments with pentoxifylline, denbufylline and NCS 613 PDE inhibitors. This study reveals that compared to CBA/J control mice, kidney PDE4 activity of MRL/lpr mice increases with the disease progression. Furthermore, it showed that the most potent and selective PDE4 inhibitor NCS 613 is also the most effective molecule in decreasing proteinuria and increasing survival rate of MRL/lpr mice. NCS 613 is a potent inhibitor, which is more selective for the PDE4C subtype (IC(50) = 1.4 nM) than the other subtypes (PDE4A, IC(50) = 44 nM; PDE4B, IC(50) = 48 nM; and PDE4D, IC(50) = 14 nM). Interestingly, its affinity for the High Affinity Rolipram Binding Site is relatively low (K(i) = 148 nM) in comparison to rolipram (K(i) = 3 nM). Finally, as also observed using MRL/lpr peripheral blood lymphocytes (PBLs), NCS 613 inhibits basal and LPS-induced TNFalpha secretion from PBLs of lupus patients, suggesting a therapeutic potential of NCS 613 in systemic lupus. This study reveals that PDE4 represent a potential therapeutic target in lupus disease