Analysis of a single-atom dipole trap

We describe a simple experimental technique which allows to store a single Rubidium 87 atom in an optical dipole trap. Due to light-induced two-body collisions during the loading stage of the trap the maximum number of captured atoms is locked to one. This collisional blockade effect is confirmed by the observation of photon anti-bunching in the detected fluorescence light. The spectral properties of single photons emitted by the atom were studied with a narrow-band scanning cavity. We find that the atomic fluorescence spectrum is dominated by the spectral width of the exciting laser light field. In addition we observe a spectral broadening of the atomic fluorescence light due to the Doppler effect. This allows us to determine the mean kinetic energy of the trapped atom corresponding to a temperature of 105 micro Kelvin. This simple single-atom trap is the key element for the generation of atom-photon entanglement required for future applications in quantum communication and a first loophole-free test of Bell's inequality.Comment: Version 2; formula in equ. 3 correcte

Towards a loophole-free test of Bell's inequality with entangled pairs of neutral atoms

Experimental tests of Bell's inequality allow to distinguish quantum mechanics from local hidden variable theories. Such tests are performed by measuring correlations of two entangled particles (e.g. polarization of photons or spins of atoms). In order to constitute conclusive evidence, two conditions have to be satisfied. First, strict separation of the measurement events in the sense of special relativity is required ("locality loophole"). Second, almost all entangled pairs have to be detected (for particles in a maximally entangled state the required detector efficiency is 82.8%), which is hard to achieve experimentally ("detection loophole"). By using the recently demonstrated entanglement between single trapped atoms and single photons it becomes possible to entangle two atoms at a large distance via entanglement swapping. Combining the high detection efficiency achieved with atoms with the space-like separation of the atomic state detection events, both loopholes can be closed within the same experiment. In this paper we present estimations based on current experimental achievements which show that such an experiment is feasible in future.Comment: 6 pages, 3 figures, to be published in Advanced Science Letter

Keratinocyte-intrinsic BCL10/MALT1 activity initiates and amplifies psoriasiform skin inflammation

Psoriasis is a chronic inflammatory skin disease arising from poorly defined pathological cross-talk between keratinocytes and the immune system. BCL10 (B cell lymphoma/leukemia 10) and MALT1 (mucosa-associated lymphoid tissue lymphoma translocation protein 1) are ubiquitously expressed inflammatory signaling proteins that can interact with the psoriasis susceptibility factor CARD14, but their functions in psoriasis are insufficiently understood. We report that although keratinocyte-intrinsic BCL10/MALT1 deletions completely rescue inflammatory skin pathology triggered by germline Card14 gain-of-function mutation in mice, the BCL10/MALT1 signalosome is unexpectedly not involved in the CARD14-dependent interleukin-17 receptor (IL-17R) proximal pathway. Instead, it plays a more pleiotropic role by amplifying keratinocyte responses to a series of inflammatory cytokines, including IL-17A, IL-1 beta, and TNF. Moreover, selective keratinocyte-intrinsic activation of BCL10/MALT1 signaling with an artificial engager molecule is sufficient to initiate lymphocyte-mediated psoriasiform skin inflammation, and aberrant BCL10/MALT1 activity is frequently detected in the skin of human sporadic psoriasis. Together, these results establish that BCL10/MALT1 signalosomes can act as initiators and crucial amplifiers of psoriatic skin inflammation and indicate a critical function for this complex in sporadic psoriasis

Strong Coupling between Single Atoms and Nontransversal Photons

Light is often described as a fully transverse-polarized wave, i.e., with an electric field vector that is orthogonal to the direction of propagation. However, light confined in dielectric structures such as optical waveguides or whispering-gallery-mode microresonators can have a strong longitudinal polarization component. Here, using single Rb-85 atoms strongly coupled to a whispering-gallery-mode microresonator, we experimentally and theoretically demonstrate that the presence of this longitudinal polarization fundamentally alters the interaction between light and matter

Chiral quantum optics

At the most fundamental level, the interaction between light and matter is manifested by the emission and absorption of single photons by single quantum emitters. Controlling light--matter interaction is the basis for diverse applications ranging from light technology to quantum--information processing. Many of these applications are nowadays based on photonic nanostructures strongly benefitting from their scalability and integrability. The confinement of light in such nanostructures imposes an inherent link between the local polarization and propagation direction of light. This leads to {\em chiral light--matter interaction}, i.e., the emission and absorption of photons depend on the propagation direction and local polarization of light as well as the polarization of the emitter transition. The burgeoning research field of {\em chiral quantum optics} offers fundamentally new functionalities and applications both for single emitters and ensembles thereof. For instance, a chiral light--matter interface enables the realization of integrated non--reciprocal single--photon devices and deterministic spin--photon interfaces. Moreover, engineering directional photonic reservoirs opens new avenues for constructing complex quantum circuits and networks, which may be applied to simulate a new class of quantum many--body systems

Haematological effects of oral administration of bitopertin, a glycine transport inhibitor, in patients with non‐transfusion‐dependent β‐thalassaemia

Bitopertin is a small molecule selective inhibitor of glycine transporter 1 (GlyT1), initially developed to increase brain extracellular levels of glycine in the vicinity of neuronal N-methyl-D-aspartate receptors for the treatment of schizophrenia. GlyT1, the pharmacological target of bitopertin, is also present as a transmembrane transporter in erythroid cells1 and accounts for 50–55% of glycine uptake in human red blood cells (RBCs).2, 3 Erythroid GlyT1 inhibition by bitopertin leads to reduced intracellular glycine availability, interfering with the first step of haem synthesis, in which 5-aminolevulinate synthase catalyses the condensation reaction between glycine and succinyl-coenzyme A, forming 5-aminolevulinic acid.