Electric-field controlled spin reversal in a quantum dot with ferromagnetic contacts

Manipulation of the spin-states of a quantum dot by purely electrical means is a highly desirable property of fundamental importance for the development of spintronic devices such as spin-filters, spin-transistors and single-spin memory as well as for solid-state qubits. An electrically gated quantum dot in the Coulomb blockade regime can be tuned to hold a single unpaired spin-1/2, which is routinely spin-polarized by an applied magnetic field. Using ferromagnetic electrodes, however, the properties of the quantum dot become directly spin-dependent and it has been demonstrated that the ferromagnetic electrodes induce a local exchange-field which polarizes the localized spin in the absence of any external fields. Here we report on the experimental realization of this tunneling-induced spin-splitting in a carbon nanotube quantum dot coupled to ferromagnetic nickel-electrodes. We study the intermediate coupling regime in which single-electron states remain well defined, but with sufficiently good tunnel-contacts to give rise to a sizable exchange-field. Since charge transport in this regime is dominated by the Kondo-effect, we can utilize this sharp many-body resonance to read off the local spin-polarization from the measured bias-spectroscopy. We show that the exchange-field can be compensated by an external magnetic field, thus restoring a zero-bias Kondo-resonance, and we demonstrate that the exchange-field itself, and hence the local spin-polarization, can be tuned and reversed merely by tuning the gate-voltage. This demonstrates a very direct electrical control over the spin-state of a quantum dot which, in contrast to an applied magnetic field, allows for rapid spin-reversal with a very localized addressing.Comment: 19 pages, 11 figure

Cardiothoracic CT: one-stop-shop procedure? Impact on the management of acute pulmonary embolism

In the treatment of pulmonary embolism (PE) two groups of patients are traditionally identified, namely the hemodynamically stable and instable groups. However, in the large group of normotensive patients with PE, there seems to be a subgroup of patients with an increased risk of an adverse outcome, which might benefit from more aggressive therapy than the current standard therapy with anticoagulants. Risk stratification is a commonly used method to define subgroups of patients with either a high or low risk of an adverse outcome. In this review the clinical parameters and biomarkers of myocardial injury and right ventricular dysfunction (RVD) that have been suggested to play an important role in the risk stratification of PE are described first. Secondly, the use of more direct imaging techniques like echocardiography and CT in the assessment of RVD are discussed, followed by a brief outline of new imaging techniques. Finally, two risk stratification models are proposed, combining the markers of RVD with cardiac biomarkers of ischemia to define whether patients should be admitted to the intensive care unit (ICU) and/or be given thrombolysis, admitted to the medical ward, or be safely treated at home with anticoagulant therapy

Treatment of acute venous thromboembolism with dabigatran or warfarin and pooled analysis.

Dabigatran and warfarin have been compared for the treatment of acute venous thromboembolism (VTE) in a previous trial. We undertook this study to extend those findings. METHODS AND RESULTS: In a randomized, double-blind, double-dummy trial of 2589 patients with acute VTE treated with low-molecular-weight or unfractionated heparin for 5 to 11 days, we compared dabigatran 150 mg twice daily with warfarin. The primary outcome, recurrent symptomatic, objectively confirmed VTE and related deaths during 6 months of treatment occurred in 30 of the 1279 dabigatran patients (2.3%) compared with 28 of the 1289 warfarin patients (2.2%; hazard ratio, 1.08; 95% confidence interval [CI], 0.64-1.80; absolute risk difference, 0.2%; 95% CI, -1.0 to 1.3; P<0.001 for the prespecified noninferiority margin for both criteria). The safety end point, major bleeding, occurred in 15 patients receiving dabigatran (1.2%) and in 22 receiving warfarin (1.7%; hazard ratio, 0.69; 95% CI, 0.36-1.32). Any bleeding occurred in 200 dabigatran (15.6%) and 285 warfarin (22.1%; hazard ratio, 0.67; 95% CI, 0.56-0.81) patients. Deaths, adverse events, and acute coronary syndromes were similar in both groups. Pooled analysis of this study RE-COVER II and the RE-COVER trial gave hazard ratios for recurrent VTE of 1.09 (95% CI, 0.76-1.57), for major bleeding of 0.73 (95% CI, 0.48-1.11), and for any bleeding of 0.70 (95% CI, 0.61-0.79). CONCLUSION: Dabigatran has similar effects on VTE recurrence and a lower risk of bleeding compared with warfarin for the treatment of acute VTE