Testing the photon-number statistics of a quantum key distribution light source.

A commonly held tenet is that lasers well above threshold emit photons in a coherent state, which follow Poissonian statistics when measured in photon number. This feature is often exploited to build quantum-based random number generators or to derive the secure key rate of quantum key distribution systems. Hence the photon number distribution of the light source can directly impact the randomness and the security distilled from such devices. Here, we propose a method based on measuring correlation functions to experimentally characterize a light source's photon statistics and use it in the estimation of a quantum key distribution system's key rate. This promises to be a useful tool for the certification of quantum-related technologies.

Antithrombotic use following transient ischaemic attack or ischaemic stroke among older Australians with atrial fibrillation.

Hospital audits may underestimate anticoagulant use among acute ischaemic stroke patients with atrial fibrillation (AF), as treatment may commence after discharge. To account for this, antithrombotic use in the 4 months after hospitalisation for transient ischaemic attack or ischaemic stroke among AF patients was assessed using claims data. Results suggest that treatment may be commenced soon after discharge and should be considered when assessing prevalence of use.

Coherent dynamics of a telecom-wavelength entangled photon source.

Quantum networks can interconnect remote quantum information processors, allowing interaction between different architectures and increasing net computational power. Fibre-optic telecommunications technology offers a practical platform for routing weakly interacting photonic qubits, allowing quantum correlations and entanglement to be established between distant nodes. Although entangled photons have been produced at telecommunications wavelengths using spontaneous parametric downconversion in nonlinear media, as system complexity increases their inherent excess photon generation will become limiting. Here we demonstrate entangled photon pair generation from a semiconductor quantum dot at a telecommunications wavelength. Emitted photons are intrinsically anti-bunched and violate Bell's inequality by 17 standard deviations High-visibility oscillations of the biphoton polarization reveal the time evolution of the emitted state with exceptional clarity, exposing long coherence times. Furthermore, we introduce a method to evaluate the fidelity to a time-evolving Bell state, revealing entanglement between photons emitted up to 5 ns apart, exceeding the exciton lifetime.

Fabrication and characterization of gold nano-wires templated on virus-like arrays of tobacco mosaic virus coat proteins.

The rod-shaped plant virus tobacco mosaic virus (TMV) is widely used as a nano-fabrication template, and chimeric peptide expression on its major coat protein has extended its potential applications. Here we describe a simple bacterial expression system for production and rapid purification of recombinant chimeric TMV coat protein carrying C-terminal peptide tags. These proteins do not bind TMV RNA or form disks at pH 7. However, they retain the ability to self-assemble into virus-like arrays at acidic pH. C-terminal peptide tags in such arrays are exposed on the protein surface, allowing interaction with target species. We have utilized a C-terminal His-tag to create virus coat protein-templated nano-rods able to bind gold nanoparticles uniformly. These can be transformed into gold nano-wires by deposition of additional gold atoms from solution, followed by thermal annealing. The resistivity of a typical annealed wire created by this approach is significantly less than values reported for other nano-wires made using different bio-templates. This expression construct is therefore a useful additional tool for the creation of chimeric TMV-like nano-rods for bio-templating.

Indistinguishable entangled photons generated by a light-emitting diode.

A linear optical quantum computer relies on interference between photonic qubits for logic, and entanglement for near-deterministic operation. Here we measure the interference and entanglement properties of photons emitted by a quantum dot embedded within a light-emitting diode. We show that pairs of simultaneously generated photons are entangled, and indistinguishable from subsequently generated photons. We measure entanglement fidelity of 0.87 and two-photon-interference visibility of 0.60 ± 0.05. The visibility, limited by detector jitter, could be improved by optical cavity designs.

Investigation of dentinal tubule occlusion using FIB-SEM milling and EDX.

OBJECTIVE: The aim of this study was to evaluate in vitro the dentin tubule occluding effect of an 8% strontium acetate dentifrice (Sensodyne Rapid Relief) compared to patent dentin tubules using modern sample preparation, imaging, and analysis techniques. METHODS: Etched dentin discs, either untreated or treated with the dentifrice, were analyzed by preparing cross-sections using focused ion beam scanning electron microscopy (FIB-SEM) milling, and the strontium presence mapped using energy dispersive X-ray spectroscopy (EDX). RESULTS: Surface imaging showed the dentifrice had coated the treated sample. Sub-surface information gained by preparing longitudinal cross-sections of the treated samples showed the tubule openings to be plugged, and EDX mapping of the cross-section confirmed enhanced strontium levels within the tubules several microns below the treatment surface. CONCLUSION: The combination of modern sample preparation, imaging, and analysis techniques employed in this study has shown that the 8% strontium acetate dentifrice occludes dentin tubules. EDX analysis has shown the presence of strontium within the dentin tubules, with elemental maps illustrating how the strontium has been incorporated into the dentin.

Prasugrel vs. clopidogrel for cytochrome P450 2C19-genotyped subgroups: integration of the TRITON-TIMI 38 trial data.

BACKGROUND: Prasugrel is a newly marketed antiplatelet drug with improved cardiac outcomes as compared with clopidogrel for acute coronary syndromes involving percutaneous coronary intervention (PCI). Analysis of a subset of the TRITON-TIMI 38 trial demonstrated that cytochrome P450 2C19 (CYP2C19) reduced-function genotypes are associated with differential clinical responses to clopidogrel, but not prasugrel. Whether the CYP2C19 genotype has the potential to influence clinical choice of these drugs prior to PCI for individuals with unstable angina or non-ST segment elevation myocardial infarction is currently uncertain. METHODS AND RESULTS: An exploratory, secondary analysis was undertaken to estimate the clinical benefit of prasugrel over clopidogrel in subgroups defined by CYP2C19 genotype, by integrating the published results of the genetic substudy and the overall TRITON-TIMI 38 trial. Individuals with a CYP2C19 reduced-metabolizer genotype were estimated to have a substantial reduction in the risk of the composite primary outcome (cardiovascular death, myocardial infarction, or stroke) with prasugrel as compared with clopidogrel [relative risk (RR) 0.57; 95% confidence interval (CI) 0.39-0.83]. For CYP2C19 extensive metabolizers (∼70% of the population), however, the composite outcome risks with prasugrel and clopidogrel were not substantially different (RR 0.98; 95% CI 0.80-1.20). CONCLUSIONS: Integration of the TRITON-TIMI 38 data suggests that the CYP2C19 genotype can discriminate between individuals who receive extensive benefit from using prasugrel instead of clopidogrel, and individuals with comparable clinical outcomes with prasugrel and clopidorel. Thus, CYP2C19 genotyping has the potential to guide the choice of antiplatelet therapy, and further research is warranted to validate this estimate.

Single-photon emitting diode based on a quantum dot in a micro-pillar.

We have fabricated a single-photon emitting diode based on a quantum dot in a micro-pillar cavity. By temperature tuning the dot emission into resonance with the cavity mode we see an enhancement in the collected photon intensity at 40 K. We perform autocorrelation measurements on the electroluminescence at fixed bias, observing photon anti-bunching. Due to the low resistance and capacitance of our device we can inject current pulses shorter than the lifetime of the quantum state, producing single-photon emission with g((2))(0) = 0.17.

Reduction in myocardial neutrophil accumulation and infarct size following administration of thromboxane inhibitor U-63,557A.

We examined the effects of a new selective thromboxane A2 (TXA2) synthetase inhibitor, U-63,557A, on myocardial infarct size 48 hours following left coronary ligation in rats. With a single 8 mg/kg dose of U-63,557A (furegrelate) administered prior to coronary ligation, platelet aggregation and serum TXA2 formation declined significantly (p less than 0.02) for up to 48 hours. Myocardial infarct size, as measured by planimetry of serial left ventricular sections, was decreased from 44 +/- 3% (saline-treated control rats) to 34 +/- 4% (p less than 0.05). Left ventricular creatine kinase (CK) following coronary ligation was also preserved in U-63,557A vs saline-treated control animals (p less than 0.05). These beneficial effects of U-63,557A were not accompanied by reduction in the indices of myocardial oxygen demand (heart rate and arterial pressure). Furthermore, neutrophil accumulation in the infarcted myocardium was significantly decreased by U-63,557A (26 +/- 6 vs 96 +/- 3/high-power field [p less than 0.01]). These data suggest that administration of a single dose of selective TXA2 synthetase inhibitor prior to coronary ligation modulates platelet function for up to 48 hours and reduces the extent of myocardial injury, which may, in part, relate to decrease in neutrophil accumulation.

Inhibition of human platelet and neutrophil function by piriprost (U-60,257).

Platelets and neutrophils are important in determining the extent of myocardial injury following coronary occlusion. The detrimental effects of these blood elements are mediated in part via release of arachidonate metabolites and oxidative species. A new selective inhibitor of leukotriene formation, piriprost (U-60,257), has been observed to decrease both neutrophil accumulation in the myocardium and infarct size following coronary ligation in experimental animals. Since piriprost may have clinical use, we examined its effects on human platelet and neutrophil functions. This compound was found to exert potent inhibitory effects on epinephrine-induced human platelet aggregation and TXA2 biosynthesis (IC50 0.04 microM). Piriprost also inhibited human neutrophil chemotaxis, oxidative species release, aggregation, and LTB4 synthesis with IC50 of 0.1, 0.04, 10 and 14 microM, respectively. Thus, piriprost inhibits a variety of human platelet and neutrophil functions. Because of its suppressive effects on human platelet and neutrophil functions and protective effects in experimental myocardial infarction, this agent may have clinical applications.

Effect of human tumor cells on platelet aggregation: potential relevance to pattern of metastasis.

Tumor metastasis may be facilitated by interaction of tumor cells with platelets. It is not known, however, whether solid tumors which have predisposition to pulmonary metastasis affect platelets differently than lymphoid tumors, which rarely spread to lungs. We therefore examined the effects of cultured osteogenic sarcoma (MG-63, U2-OS), as well as leukemia (NALM-16, LAZ-221, K-562) and lymphoma (RAJI, MOlt 4) cells, on human platelet aggregation. Human osteogenic sarcoma (MG-63) cells alone induced platelet aggregation, whereas U2-OS cells induced platelet aggregation only after preincubation of platelets with subthreshold concentrations of epinephrine. In contrast, neither leukemia nor lymphoma cells affected platelet aggregation. These observations suggest that the platelet proaggregatory potential of tumor cells is variable and that the platelet stimulatory effects of osteogenic sarcoma cells may relate to their high risk of pulmonary metastasis.

Spontaneous platelet aggregation: observations on potential mechanisms.

We identified SPA in three young apparently healthy women. SPA was associated with release of TXA2 and was only partially inhibited by ADP-inhibitor apyrase and alpha 2-adrenoceptor blocker yohimbine. In vitro incubation of aspirin (90 micrograms/ml) or selective TXA2 synthetase inhibitor OKY-046 (0.1 uM) with platelet rich plasma (PRP) did not abolish SPA, although platelet generation of TXA2 was markedly inhibited. In contrast, oral administration of large amounts of aspirin in one subject or in vitro incubation of PRP with TXA2 -endoperoxide receptor blocker SQ 29,548 (20-100 nM) significantly inhibited SPA. These studies suggest that SPA is associated with TXA2 release. Since TXA2 -endoperoxide receptor blocker completely abolishes the secondary wave, agents like this may be of therapeutic value in individuals with SPA and evidence of tissue ischemia.

Effects of thromboxane A2 inhibition on osteogenic sarcoma cell-induced platelet aggregation.

There is evidence that tumors may stimulate platelet aggregation, causing release of thromboxane A2. Thromboxane A2 may potentiate tumor metastasis by stimulating tumor cell growth and proliferation and by enhancing platelet-tumor cell aggregate formation. Despite potential significance of thromboxane A2 in tumor metastasis, agents which inhibit thromboxane A2 synthesis have not been uniformly effective in reducing tumor metastasis. We, therefore, evaluated the effects of a thromboxane A2 receptor antagonist SQ-29,548 compared to those of a thromboxane A2 synthetase inhibitor OKY-046 on osteogenic sarcoma-induced platelet aggregation and thromboxane A2 release. Osteogenic sarcoma cells added to platelet-rich plasma caused complete and irreversible platelet aggregation as well as thromboxane A2 release. Preincubation of platelet-rich plasma with SQ-29,548 (2 to 20 nM) decreased platelet aggregation induced by tumor cells, but it had no effect on thromboxane A2 release. In contrast, preincubation of platelet-rich plasma with OKY-046 (0.1 to 10 microM) had no effect on platelet aggregation despite a decrease in thromboxane A2 synthesis. These results suggest that thromboxane A2 receptor blockers, rather than synthetase inhibitors, may prevent tumor cell-induced platelet aggregation.