Directed quantum communication

We raise the question whether there is a way to characterize the quantum information transport properties of a medium or material. For this analysis the special features of quantum information have to be taken into account. We find that quantum communication over an isotropic medium, as opposed to classical information transfer, requires the transmitter to direct the signal towards the receiver. Furthermore, for large classes of media there is a threshold, in the sense that `sufficiently much' of the signal has to be collected. Therefore, the medium's capacity for quantum communication can be characterized in terms of how the size of the transmitter and receiver has to scale with the transmission distance to maintain quantum information transmission. To demonstrate the applicability of this concept, an n-dimensional spin lattice is considered, yielding a sufficient scaling of d^(n/3) with the distance d

Impossibility of Growing Quantum Bit Commitments

Quantum key distribution (QKD) is often, more correctly, called key growing. Given a short key as a seed, QKD enables two parties, connected by an insecure quantum channel, to generate a secret key of arbitrary length. Conversely, no key agreement is possible without access to an initial key. Here, we consider another fundamental cryptographic task, commitments. While, similar to key agreement, commitments cannot be realized from scratch, we ask whether they may be grown. That is, given the ability to commit to a fixed number of bits, is there a way to augment this to commitments to strings of arbitrary length? Using recently developed information-theoretic techniques, we answer this question to the negative.Comment: 10 pages, minor change

In silico labeling reveals the time-dependent label half-life and transit-time in dynamical systems

Background: Mathematical models of dynamical systems facilitate the computation of characteristic properties that are not accessible experimentally. In cell biology, two main properties of interest are (1) the time-period a protein is accessible to other molecules in a certain state - its half-life - and (2) the time it spends when passing through a subsystem - its transit-time. We discuss two approaches to quantify the half-life, present the novel method of in silico labeling, and introduce the label half-life and label transit-time. The developed method has been motivated by laboratory tracer experiments. To investigate the kinetic properties and behavior of a substance of interest, we computationally label this species in order to track it throughout its life cycle. The corresponding mathematical model is extended by an additional set of reactions for the labeled species, avoiding any double-counting within closed circuits, correcting for the influences of upstream fluxes, and taking into account combinatorial multiplicity for complexes or reactions with several reactants or products. A profile likelihood approach is used to estimate confidence intervals on the label half-life and transit-time. Results: Application to the JAK-STAT signaling pathway in Epo-stimulated BaF3-EpoR cells enabled the calculation of the time-dependent label half-life and transit-time of STAT species. The results were robust against parameter uncertainties. Conclusions: Our approach renders possible the estimation of species and label half-lives and transit-times. It is applicable to large non-linear systems and an implementation is provided within the PottersWheel modeling framework (http://www.potterswheel.de)

Directed quantum communication

We address the question of whether there is a way of characterizing the quantum information transport properties of a medium or material. For this analysis, the special features of quantum information have to be taken into account. We find that quantum communication over an isotropic medium, as opposed to classical information transfer, requires the transmitter to direct the signal toward the receiver. Furthermore, for large classes of media there is a threshold, in the sense that 'sufficiently much' of the signal has to be collected. Therefore, the medium's capacity for quantum communication can be characterized in terms of how the sizes of the transmitter and receiver have to scale with the transmission distance to maintain quantum information transmission. To demonstrate the applicability of this concept, an n-dimensional spin lattice is considered, yielding a sufficient scaling of δn/3 with the distance δ.ISSN:1367-263

Theoretical and experimental analysis links isoform- specific ERK signalling to cell fate decisions

Cell fate decisions are regulated by the coordinated activation of signalling pathways such as the extracellular signal-regulated kinase (ERK) cascade, but contributions of individual kinase isoforms are mostly unknown. By combining quantitative data from erythropoietin-induced pathway activation in primary erythroid progenitor (colony-forming unit erythroid stage, CFU-E) cells with mathematical modelling, we predicted and experimentally confirmed a distributive ERK phosphorylation mechanism in CFU-E cells. Model analysis showed bow-tie-shaped signal processing and inherently transient signalling for cytokine-induced ERK signalling. Sensitivity analysis predicted that, through a feedback-mediated process, increasing one ERK isoform reduces activation of the other isoform, which was verified by protein over-expression. We calculated ERK activation for biochemically not addressable but physiologically relevant ligand concentrations showing that double-phosphorylated ERK1 attenuates proliferation beyond a certain activation level, whereas activated ERK2 enhances proliferation with saturation kinetics. Thus, we provide a quantitative link between earlier unobservable signalling dynamics and cell fate decisions.Not SpecifiedDeposited by bulk impor

Modeled integrated responses of ppERK1 and ppERK2 of normal and elevated ERK1 and ERK2 levels (Figure 5b)

The present dataset contain source data for Figure 5b from Schilling et al., 2009. Cell fate decisions are regulated by the coordinated activation of signalling pathways such as the extracellular signal-regulated kinase (ERK) cascade, but contributions of individual kinase isoforms are mostly unknown. The authors combined quantitative data from erythropoietin-induced pathway activation in primary erythroid progenitor (colony-forming unit erythroid stage, CFU-E) cells with mathematical modelling, in order to predict and experimentally confirmed a distributive ERK phosphorylation mechanism in CFU-E cells. The authors found evidences that double-phosphorylated ERK1 attenuates proliferation beyond a certain activation level, whereas activated ERK2 enhances proliferation with saturation kinetics. They show integrated responses of double-phosphorylated ERK1 and ERK2 that were calculated for different Epo concentrations for the original model as well as for models with elevated ERK1 or ERK2 levels

Phosphorylation levels of JAK2 after addition of increasing Epo-concentrations: experimental data (Figure 5a)

The present dataset data contain source data for Figure 5a from Schilling et al., 2009. Cell fate decisions are regulated by the coordinated activation of signalling pathways such as the extracellular signal-regulated kinase (ERK) cascade, but contributions of individual kinase isoforms are mostly unknown. The authors combined quantitative data from erythropoietin-induced pathway activation in primary erythroid progenitor (colony-forming unit erythroid stage, CFU-E) cells with mathematical modelling, in order to predict and experimentally confirmed a distributive ERK phosphorylation mechanism in CFU-E cells. The authors found evidences that double-phosphorylated ERK1 attenuates proliferation beyond a certain activation level, whereas activated ERK2 enhances proliferation with saturation kinetics. CFU-E cells were stimulated with the indicated Epo concentrations for 7 min and phosphorylation levels were determined by quantitative immunoblotting

Phosphorylation levels of JAK2 after addition of increasing Epo-concentrations: model approach (Figure 5a)

The present dataset contain source data for Figure 5a from Schilling et al., 2009. Cell fate decisions are regulated by the coordinated activation of signalling pathways such as the extracellular signal-regulated kinase (ERK) cascade, but contributions of individual kinase isoforms are mostly unknown. The authors combined quantitative data from erythropoietin-induced pathway activation in primary erythroid progenitor (colony-forming unit erythroid stage, CFU-E) cells with mathematical modelling, in order to predict and experimentally confirmed a distributive ERK phosphorylation mechanism in CFU-E cells. The authors found evidences that double-phosphorylated ERK1 attenuates proliferation beyond a certain activation level, whereas activated ERK2 enhances proliferation with saturation kinetics. Phosphorylation levels of JAK2 at 7 min after stimulation for Epo concentrations ranging from 0.1 to 1000 U/ml were simulated

Proliferation of retrovirally transduced CFU-E cells after incubation with increasing Epo-concentration (Figure 5c)

Data contain source data for Figure 5c from Schilling et al., 2009. Cell fate decisions are regulated by the coordinated activation of signalling pathways such as the extracellular signal-regulated kinase (ERK) cascade, but contributions of individual kinase isoforms are mostly unknown. The authors combined quantitative data from erythropoietin-induced pathway activation in primary erythroid progenitor (colony-forming unit erythroid stage, CFU-E) cells with mathematical modelling, in order to predict and experimentally confirmed a distributive ERK phosphorylation mechanism in CFU-E cells. The authors found evidences that double-phosphorylated ERK1 attenuates proliferation beyond a certain activation level, whereas activated ERK2 enhances proliferation with saturation kinetics. Retrovirally transduced CFU-E cells were incubated with increasing Epo concentrations for 14 h and proliferation was measured by [3H]-thymidine incorporation

Soil structure is an important omission in Earth System Models.

Most soil hydraulic information used in Earth System Models (ESMs) is derived from pedo-transfer functions that use easy-to-measure soil attributes to estimate hydraulic parameters. This parameterization relies heavily on soil texture, but overlooks the critical role of soil structure originated by soil biophysical activity. Soil structure omission is pervasive also in sampling and measurement methods used to train pedotransfer functions. Here we show how systematic inclusion of salient soil structural features of biophysical origin affect local and global hydrologic and climatic responses. Locally, including soil structure in models significantly alters infiltration-runoff partitioning and recharge in wet and vegetated regions. Globally, the coarse spatial resolution of ESMs and their inability to simulate intense and short rainfall events mask effects of soil structure on surface fluxes and climate. Results suggest that although soil structure affects local hydrologic response, its implications on global-scale climate remains elusive in current ESMs