19 research outputs found

    Robust quantum state transfer using tunable couplers

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    We analyze the transfer of a quantum state between two resonators connected by a superconducting transmission line. Nearly perfect state-transfer efficiency can be achieved by using adjustable couplers and destructive interference to cancel the back-reflection into the transmission line at the receiving coupler. We show that the transfer protocol is robust to parameter variations affecting the transmission amplitudes of the couplers. We also show that the effects of the Gaussian filtering, pulse-shape noise, and multiple reflections on the transfer efficiency are insignificant. However, the transfer protocol is very sensitive to frequency mismatch between the two resonators. Moreover, the tunable coupler we considered produces time-varying frequency detuning caused by the changing coupling. This detuning requires an active frequency compensation with an accuracy better than 90% to yield the transfer efficiency above 99%

    Selective propene oligomerization with nickel(II)-based metal-organic frameworks

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    Two Ni2+-containing metal-organic frameworks, Ni 2(dobdc) and Ni2(dobpdc), are shown to be active for the oligomerization of propene in the gas phase. The metal-organic frameworks exhibit activity comparable to Ni2+-exchanged aluminosilicates but maintain high selectivity for linear oligomers. Thus, these frameworks should enable the high yielding synthesis of linear propene oligomers for use in detergent and diesel fuel applications. © 2014 American Chemical Society

    Dihydropyridine Ca(2+) channel antagonists and agonists block Kv4.2, Kv4.3 and Kv1.4 K(+) channels expressed in HEK293 cells

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    1. We have determined the molecular basis of nicardipine-induced block of cardiac transient outward K(+) currents (I(to)). Inhibition of I(to) was studied using cloned voltage-dependent K(+) channels (Kv) channels, rat Kv4.3L, Kv4.2, and Kv1.4, expressed in human embryonic kindey cell line 293 (HEK293) cells. 2. Application of the dihydropyridine Ca(2+) channel antagonist, nicardipine, accelerated the inactivation rate and reduced the peak amplitude of Kv4.3L currents in a concentration-dependent manner (IC(50): 0.42 μM). The dihydropyridine (DHP) Ca(2+) channel agonist, Bay K 8644, also blocked this K(+) current (IC(50): 1.74 μM). 3. Nicardipine (1 μM) slightly, but significantly, shifted the voltage dependence of activation and steady-state inactivation to more negative potentials, and also slowed markedly the recovery from inactivation of Kv4.3L currents. 4. Coexpression of K(+) channel-interacting protein 2 (KChIP2) significantly slowed the inactivation of Kv4.3L currents as expected. However, the features of DHP-induced block of K(+) current were not substantially altered. 5. Nicardipine exhibited similar block of Kv1.4 and Kv4.2 channels stably expressed in HEK293 cells; IC(50)'s were 0.80 and 0.62 μM, respectively. 6. Thus, at submicromolar concentrations, DHP Ca(2+) antagonist and agonist inhibit Kv4.3L and have similar inhibiting effects on other components of cardiac I(to), Kv4.2 and Kv1.4
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