Holographic Storage of Biphoton Entanglement

Coherent and reversible storage of multi-photon entanglement with a multimode quantum memory is essential for scalable all-optical quantum information processing. Although single photon has been successfully stored in different quantum systems, storage of multi-photon entanglement remains challenging because of the critical requirement for coherent control of photonic entanglement source, multimode quantum memory, and quantum interface between them. Here we demonstrate a coherent and reversible storage of biphoton Bell-type entanglement with a holographic multimode atomic-ensemble-based quantum memory. The retrieved biphoton entanglement violates Bell's inequality for 1 microsecond storage time and a memory-process fidelity of 98% is demonstrated by quantum state tomography.Comment: 5 pages, 4 figures, accepted by Phys. Rev. Let

Characteristics of DSSC Panels with Silicone Encapsulant

Dye-sensitized solar cells (DSSC) allow light transmission and the application of various colors that make them especially suitable for building-integrated PV (BIPV) application. In order to apply DSSC modules to windows, the module has to be panelized: a DSSC module should be protected with toughened glass on the entire surface. Up to the present, it seems to be common to use double glazing with DSSC modules, with air gaps between the glass pane and the DSSC modules. Few studies have been conducted on the characteristics of various glazing methods with DSSC modules. This paper proposes a paneling method that uses silicone encapsulant, analyzing the performance through experimentation. Compared to a multilayered DSSC panel with an air gap, the encapsulant-applied panel showed 6% higher light transmittance and 7% higher electrical efficiency. The encapsulant also prevented electrolyte leakage by strengthening the seals in the DSSC module

Src kinase up-regulates the ERK cascade through inactivation of protein phosphatase 2A following cerebral ischemia

<p>Abstract</p> <p>Background</p> <p>The regulation of protein phosphorylation requires a balance in the activity of protein kinases and protein phosphatases. Our previous data indicates that Src can increase ERK activity through Raf kinase in response to ischemic stimuli. This study examined the molecular mechanisms by which Src activates ERK cascade through protein phosphatases following cerebral ischemia.</p> <p>Results</p> <p>Ischemia-induced Src activation is followed by phosphorylation of PP2A at Tyr307 leading to its inhibition in the rat hippocampus. SU6656, a Src inhibitor, up-regulates PP2A activity, resulting in a significant decreased activity in ERK and its targets, CREB and ERα. In addition, the PP2A inhibitor, cantharidin, led to an up-regulation of ERK activity and was able to counteract Src inhibition during ischemia.</p> <p>Conclusion</p> <p>Src induces up-regulation of ERK activity and its target transcription factors, CREB and ERα, through attenuation of PP2A activity. Therefore, activation of ERK is the result of a crosstalk between two pathways, Raf-dependent positive regulators and PP2A-dependent negative regulators.</p