Experimental Quantum Communication without a Shared Reference Frame

We present an experimental realization of a robust quantum communication scheme [Phys. Rev. Lett. 93, 220501 (2004)] using pairs of photons entangled in polarization and time. Our method overcomes errors due to collective rotation of the polarization modes (e.g., birefringence in optical fiber or misalignment), is insensitive to the phase's fluctuation of the interferometer, and does not require any shared reference frame including time reference, except the need to label different photons. The practical robustness of the scheme is further shown by implementing a variation of the Bennett-Brassard 1984 quantum key distribution protocol over 1 km optical fiber.Comment: 4 pages, 4 figure

Distributed coherent manipulation of qutrits by virtual excitation processes

We propose a scheme for the deterministic coherent manipulation of two atomic qutrits, trapped in separate cavities coupled through a short optical fibre or optical resonator. We study such a system in the regime of dispersive atom-field interactions, where the dynamics of atoms, cavities and fibre operates through virtual population of both the atomic excited states and photonic states in the cavities and fibre. We show that the resulting effective dynamics allows for the creation of robust qutrit entanglement, and thoroughly investigate the influence of imperfections and dissipation, due to atomic spontaneous emission and photon leakage, on the entanglement of the two qutrits state.Comment: 15 pages, 4 figure

Experimental quantum "Guess my Number" protocol using multiphoton entanglement

We present an experimental demonstration of a modified version of the entanglement-assisted "Guess my Number" protocol for the reduction of communication complexity among three separated parties. The results of experimental measurements imply that the separated parties can compute a function of distributed inputs by exchanging less classical information than by using any classical strategy. And the results also demonstrate the advantages of entanglement-enhanced communication, which is very close to quantum communication. The advantages are based on the properties of Greenberger-Horne-Zeilinger states.Comment: 4 pages, 2 figure

A laser-induced mouse model with long-term intraocular pressure elevation

Purpose: To develop and characterize a mouse model with intraocular pressure (IOP) elevation after laser photocoagulation on the trabecular meshwork (TM), which may serve as a model to investigate the potential of stem cell-based therapies for glaucoma. Methods: IOP was measured in 281 adult C57BL/6 mice to determine normal IOP range. IOP elevation was induced unilaterally in 50 adult mice, by targeting the TM through the limbus with a 532-nm diode laser. IOP was measured up to 24 weeks post-treatment. The optic nerve damage was detected by electroretinography and assessed by semiautomatic counting of optic nerve axons. Effects of laser treatment on the TM were evaluated by histology, immunofluorescence staining, optical coherence tomography (OCT) and transmission electron microscopy (TEM). Results: The average IOP of C57BL/6 mice was 14.5±2.6 mmHg (Mean ±SD). After laser treatment, IOP averaged above 20 mmHg throughout the follow-up period of 24 weeks. At 24 weeks, 57% of treated eyes had elevated IOP with the mean IOP of 22.5±2.5 mmHg (Mean ±SED). The difference of average axon count (59.0%) between laser treated and untreated eyes was statistically significant. Photopic negative response (PhNR) by electroretinography was significantly decreased. CD45+ inflammatory cells invaded the TM within 1 week. The expression of SPARC was increased in the TM from 1 to 12 weeks. Histology showed the anterior chamber angle open after laser treatment. OCT indicated that most of the eyes with laser treatment had no synechia in the anterior chamber angles. TEM demonstrated disorganized and compacted extracellular matrix in the TM. Conclusions: An experimental murine ocular hypertension model with an open angle and optic nerve axon loss was produced with laser photocoagulation, which could be used to investigate stem cell-based therapies for restoration of the outflow pathway integrity for ocular hypertension or glaucoma. Copyright

Z0Z_0 Boson Decays to Bc(∗)B^{(*)}_c Meson and Its Uncertainties

The programming new $e^{+}e^-$ collider with high luminosity shall provide another useful platform to study the properties of the doubly heavy $B_c$ meson in addition to the hadronic colliders as LHC and TEVATRON. Under the `New Trace Amplitude Approach', we calculate the production of the spin-singlet $B_c$ and the spin-triplet $B^*_c$ mesons through the $Z^0$ boson decays, where uncertainties for the production are also discussed. Our results show $\Gamma_{(^1S_0)}= 81.4^{+102.1}_{-40.5}$ KeV and $\Gamma_{(^3S_1)}=116.4^{+163.9}_{-62.8}$ KeV, where the errors are caused by varying $m_b$ and $m_c$ within their reasonable regions.Comment: 11 pages, 5 figures, 2 tables. To be published in Eur.Phys.J.

Radiation-induced Assembly of Rad51 and Rad52 Recombination Complex Requires ATM and c-Abl

Cells from individuals with the recessive cancer-prone disorder ataxia telangiectasia (A-T) are hypersensitive to ionizing radiation (I-R). ATM (mutated in A-T) is a protein kinase whose activity is stimulated by I-R. c-Abl, a nonreceptor tyrosine kinase, interacts with ATM and is activated by ATM following I-R. Rad51 is a homologue of bacterial RecA protein required for DNA recombination and repair. Here we demonstrate that there is an I-R-induced Rad51 tyrosine phosphorylation, and this induction is dependent on both ATM and c-Abl. ATM, c-Abl, and Rad51 can be co-immunoprecipitated from cell extracts. Consistent with the physical interaction, c-Abl phosphorylates Rad51 in vitro and in vivo. In assays using purified components, phosphorylation of Rad51 by c-Abl enhances complex formation between Rad51 and Rad52, which cooperates with Rad51 in recombination and repair. After I-R, an increase in association between Rad51 and Rad52 occurs in wild-type cells but not in cells with mutations that compromise ATM or c-Abl. Our data suggest signaling mediated through ATM, and c-Abl is required for the correct post-translational modification of Rad51, which is critical for the assembly of Rad51 repair protein complex following I-R