Undoing a weak quantum measurement of a solid-state qubit

We propose an experiment which demonstrates the undoing of a weak continuous measurement of a solid-state qubit, so that any unknown initial state is fully restored. The undoing procedure has only a finite probability of success because of the non-unitary nature of quantum measurement, though it is accompanied by a clear experimental indication of whether or not the undoing has been successful. The probability of success decreases with increasing strength of the measurement, reaching zero for a traditional projective measurement. Measurement undoing (``quantum un-demolition'') may be interpreted as a kind of a quantum eraser, in which the information obtained from the first measurement is erased by the second measurement, which is an essential part of the undoing procedure. The experiment can be realized using quantum dot (charge) or superconducting (phase) qubits.Comment: 5 page

Improved fidelity of triggered entangled photons from single quantum dots

We demonstrate the on-demand emission of polarisation-entangled photon pairs from the biexciton cascade of a single InAs quantum dot embedded in a GaAs/AlAs planar microcavity. Improvements in the sample design blue shifts the wetting layer to reduce the contribution of background light in the measurements. Results presented show that >70% of the detected photon pairs are entangled. The high fidelity of the (|HxxHx>+|VxxVx>)/2^0.5 state that we determine is sufficient to satisfy numerous tests for entanglement. The improved quality of entanglement represents a significant step towards the realisation of a practical quantum dot source compatible with applications in quantum information.Comment: 9 pages. Paper is available free of charge at http://www.iop.org/EJ/abstract/1367-2630/8/2/029/, see also 'A semiconductor source of triggered entangled photon pairs', R. M. Stevenson et al., Nature 439, 179 (2006

High speed quantum gates with cavity quantum electrodynamics

Cavity quantum electrodynamic schemes for quantum gates are amongst the earliest quantum computing proposals. Despite continued progress, and the dramatic recent demonstration of photon blockade, there are still issues with optimal coupling and gate operation involving high-quality cavities. Here we show dynamic control techniques that allow scalable cavity-QED based quantum gates, that use the full bandwidth of the cavities. When applied to quantum gates, these techniques allow an order of magnitude increase in operating speed, and two orders of magnitude reduction in cavity Q, over passive cavity-QED architectures. Our methods exploit Stark shift based Q-switching, and are ideally suited to solid-state integrated optical approaches to quantum computing.Comment: 4 pages, 3 figures, minor revision

Quantum information processing using quasiclassical electromagnetic interactions between qubits and electrical resonators

Electrical resonators are widely used in quantum information processing, by engineering an electromagnetic interaction with qubits based on real or virtual exchange of microwave photons. This interaction relies on strong coupling between the qubits' transition dipole moments and the vacuum fluctuations of the resonator in the same manner as cavity quantum electrodynamics (QED), and has consequently come to be called 'circuit QED' (cQED). Great strides in the control of quantum information have already been made experimentally using this idea. However, the central role played by photon exchange induced by quantum fluctuations in cQED does result in some characteristic limitations. In this paper, we discuss an alternative method for coupling qubits electromagnetically via a resonator, in which no photons are exchanged, and where the resonator need not have strong quantum fluctuations. Instead, the interaction can be viewed in terms of classical, effective 'forces' exerted by the qubits on the resonator, and the resulting resonator dynamics used to produce qubit entanglement are purely classical in nature. We show how this type of interaction is similar to that encountered in the manipulation of atomic ion qubits, and we exploit this analogy to construct two-qubit entangling operations that are largely insensitive to thermal or other noise in the resonator, and to its quality factor. These operations are also extensible to larger numbers of qubits, allowing interactions to be selectively generated among any desired subset of those coupled to a single resonator. Our proposal is potentially applicable to a variety of physical qubit modalities, including superconducting and semiconducting solid-state qubits, trapped molecular ions, and possibly even electron spins in solids.United States. Dept. of Defense. Assistant Secretary of Defense for Research & Engineering (United States. Air Force Contract FA8721-05-C-0002

Identification of Basophils as a Major Source of Hepatocyte Growth Factor in Chronic Myeloid Leukemia: A Novel Mechanism of BCR-ABL1-Independent Disease Progression

AbstractChronic myeloid leukemia (CML) is a hematopoietic neoplasm characterized by the Philadelphia chromosome and the related BCR-ABL1 oncoprotein. Acceleration of CML is usually accompanied by basophilia. Several proangiogenic molecules have been implicated in disease acceleration, including the hepatocyte growth factor (HGF). However, little is known so far about the cellular distribution and function of HGF in CML. We here report that HGF is expressed abundantly in purified CML basophils and in the basophil-committed CML line KU812, whereas all other cell types examined expressed only trace amounts of HGF or no HGF. Interleukin 3, a major regulator of human basophils, was found to promote HGF expression in CML basophils. By contrast, BCR-ABL1 failed to induce HGF synthesis in CML cells, and imatinib failed to inhibit expression of HGF in these cells. Recombinant HGF as well as basophil-derived HGF induced endothelial cell migration in a scratch wound assay, and these effects of HGF were reverted by an anti-HGF antibody as well as by pharmacologic c-Met inhibitors. In addition, anti-HGF and c-Met inhibitors were found to suppress the spontaneous growth of KU812 cells, suggesting autocrine growth regulation. Together, HGF is a BCR-ABL1-independent angiogenic and autocrine growth regulator in CML. Basophils are a unique source of HGF in these patients and may play a more active role in disease-associated angiogenesis and disease progression than has so far been assumed. Our data also suggest that HGF and c-Met are potential therapeutic targets in CML

Expression and Functions of the Vascular Endothelial Growth Factors and Their Receptors in Human Basophils

Abstract Angiogenesis is a multistep complex phenomenon critical for several inflammatory and neoplastic disorders. Basophils, normally confined to peripheral blood, can infiltrate the sites of chronic inflammation. In an attempt to obtain insights into the mechanism(s) underlying human basophil chemotaxis and its role in inflammation, we have characterized the expression and function of vascular endothelial growth factors (VEGFs) and their receptors in these cells. Basophils express mRNA for three isoforms of VEGF-A (121, 165, and 189) and two isoforms of VEGF-B (167 and 186). Peripheral blood and basophils in nasal polyps contain VEGF-A localized in secretory granules. The concentration of VEGF-A in basophils was 144.4 ± 10.8 pg/106 cells. Immunologic activation of basophils induced the release of VEGF-A. VEGF-A (10–500 ng/ml) induced basophil chemotaxis. Supernatants of activated basophils induced an angiogenic response in the chick embryo chorioallantoic membrane that was inhibited by an anti-VEGF-A Ab. The tyrosine kinase VEGFR-2 (VEGFR-2/KDR) mRNA was expressed in basophils. These cells also expressed mRNA for the soluble form of VEGFR-1 and neuropilin (NRP)1 and NRP2. Flow cytometric analysis indicated that basophils express epitopes recognized by mAbs against the extracellular domains of VEGFR-2, NRP1, and NRP2. Our data suggest that basophils could play a role in angiogenesis and inflammation through the expression of several forms of VEGF and their receptors

Innate and adaptive T cells in asthmatic patients: relationship to severity and disease mechanisms

BackgroundAsthma is a chronic inflammatory disease involving diverse cells and mediators whose interconnectivity and relationships to asthma severity are unclear.ObjectiveWe performed a comprehensive assessment of TH17 cells, regulatory T cells, mucosal-associated invariant T (MAIT) cells, other T-cell subsets, and granulocyte mediators in asthmatic patients.MethodsSixty patients with mild-to-severe asthma and 24 control subjects underwent detailed clinical assessment and provided induced sputum, endobronchial biopsy, bronchoalveolar lavage, and blood samples. Adaptive and invariant T-cell subsets, cytokines, mast cells, and basophil mediators were analyzed.ResultsSignificant heterogeneity of T-cell phenotypes was observed, with levels of IL-13–secreting T cells and type 2 cytokines increased at some, but not all, asthma severities. TH17 cells and ??-17 cells, proposed drivers of neutrophilic inflammation, were not strongly associated with asthma, even in severe neutrophilic forms. MAIT cell frequencies were strikingly reduced in both blood and lung tissue in relation to corticosteroid therapy and vitamin D levels, especially in patients with severe asthma in whom bronchoalveolar lavage regulatory T-cell numbers were also reduced. Bayesian network analysis identified complex relationships between pathobiologic and clinical parameters. Topological data analysis identified 6 novel clusters that are associated with diverse underlying disease mechanisms, with increased mast cell mediator levels in patients with severe asthma both in its atopic (type 2 cytokine–high) and nonatopic forms.ConclusionThe evidence for a role for TH17 cells in patients with severe asthma is limited. Severe asthma is associated with a striking deficiency of MAIT cells and high mast cell mediator levels. This study provides proof of concept for disease mechanistic networks in asthmatic patients with clusters that could inform the development of new therapies

High-performance diamond-based single-photon sources for quantum communication

Quantum communication places stringent requirements on single-photon sources. Here we report a theoretical study of the cavity Purcell enhancement of two diamond point defects, the nickel-nitrogen (NE8) and silicon-vacancy (SiV) centers, for high-performance, near on-demand single-photon generation. By coupling the centers strongly to high-finesse optical photonic-bandgap cavities with modest quality factor Q = O(10^4) and small mode volume V = O(\lambda^3), these system can deliver picosecond single-photon pulses at their zero-phonon lines with probabilities of 0.954 (NE8) and 0.812 (SiV) under a realistic optical excitation scheme. The undesirable blinking effect due to transitions via metastable states can also be suppressed with O(10^{-4}) blinking probability. We analyze the application of these enhanced centers, including the previously-studied cavity-enhanced nitrogen-vacancy (NV) center, to long-distance BB84 quantum key distribution (QKD) in fiber-based, open-air terrestrial and satellite-ground setups. In this comparative study, we show that they can deliver performance comparable with decoy state implementation with weak coherent sources, and are most suitable for open-air communication.Comment: 12 pages, 6 figures, 3 tables, revisions to excitation parameter

Age-specific trends in cardiovascular mortality rates in the Netherlands between 1980 and 2009

Recent analyses suggest the decline in coronary heart disease mortality rates is slowing in younger age groups in countries such as the US and the UK. This work aimed to analyse recent trends in cardiovascular mortality rates in the Netherlands. Analysis was of annual all circulatory, ischaemic heart disease (IHD), and cerebrovascular disease mortality rates between 1980 and 2009 for the Netherlands. Data were stratified by sex and 10-year age group (age 35–85+). The annual rate of change and significant changes in the trend were identified using joinpoint Poisson regression. For almost all age and sex groups examined the rate of IHD and cerebrovascular disease mortality in the Netherlands has more than halved between 1980 and 2009. The decline in mortality from both IHD and cerebrovascular disease is continuing for all ages and sex groups, with anacceleration in the decline apparent from the late 1990s/early 2000s. The decline in age-specific all circulatory, coronary heart disease and cerebrovascular disease mortality rates continues for all age and sex groups in the Netherlands