A Possibility of Search for New Physics at LHCb

It is interesting to search for new physics beyond the standard model at LHCb. We suggest that weak decays of doubly charmed baryon such as $\Xi_{cc}(3520)^+, \Xi_{cc}^{++}$ to charmless final states would be a possible signal for new physics. In this work, we consider two models, i.e. the unparticle and $Z'$ as examples to study such possibilities. We also discuss the cases for $\Xi^0_{bb}, \Xi_{bb}^-$ which have not been observed yet, but one can expect to find them when LHCb begins running. Our numerical results show that these two models cannot result in sufficiently large decay widths, therefore if such modes are observed at LHCb, there must be a new physics other than the unparticle or $Z'$ models.Comment: 7 pages, 3 figures, 1 table. More references and discussion adde

Steady Bell state generation via magnon-photon coupling

We show that parity-time ($\mathcal{PT}$) symmetry can be spontaneously broken in the recently reported energy level attraction of magnons and cavity photons. In the $\mathcal{PT}$-broken phase, magnon and photon form a high-fidelity Bell state with maximum entanglement. This entanglement is steady and robust against the perturbation of environment, in contrast to the general wisdom that expects instability of the hybridized state when the symmetry is broken. This anomaly is further understood by the compete of non-Hermitian evolution and particle number conservation of the hybridized system. As a comparison, neither $\mathcal{PT}$-symmetry broken nor steady magnon-photon entanglement is observed inside the normal level repulsion case. Our results may open a novel window to utilize magnon-photon entanglement as a resource for quantum technologies.Comment: 5 pages, 4 figure

4-(4-Nitro­benzene­sulfonamido)pyridinium trichloro­acetate

In the title compound, C11H10N3O4S+·C2Cl3O2 −, the benzene ring forms an angle of 85.21 (13)° with the pyridinium ring. The nitro group is nearly coplanar with its attached benzene ring [dihedral angle = 3.68 (12)°]. In the crystal structure, strong N—H⋯O hydrogen bonds link the ion-pairs. The packing is further consolidated by weak C—H⋯O inter­ations

Creating One-dimensional Nanoscale Periodic Ripples in a Continuous Mosaic Graphene Monolayer

In previous studies, it proved difficult to realize periodic graphene ripples with wavelengths of few nanometers. Here we show that one-dimensional periodic graphene ripples with wavelengths from 2 nm to tens of nanometers can be implemented in the intrinsic areas of a continuous mosaic, locally N-doped, graphene monolayer by simultaneously using both the thermal strain engineering and the anisotropic surface stress of Cu substrate. Our result indicates that the constraint imposed at the boundaries between the intrinsic and the N-doped regions play a vital role in creating these 1D ripples. We also demonstrate that the observed rippling modes are beyond the descriptions of continuum mechanics due to the decoupling of graphene bending and tensional deformations. Scanning tunneling spectroscopy measurements indicate that the nanorippling generates a periodic electronic superlattice and opens a zero-energy gap of about 130 meV in graphene. This result may pave a facile way for tailoring the structures and electronic properties of graphene.Comment: 4 Figures, to appear in Phys. Rev. Let

Dexmedetomidine post-treatment attenuates cardiac ischaemia/reperfusion injury by inhibiting apoptosis through HIF-1α signalling.

Hypoxia-inducible factor 1α (HIF-1α) plays a critical role in the apoptotic process during cardiac ischaemia/reperfusion (I/R) injury. This study aimed to investigate whether post-treatment with dexmedetomidine (DEX) could protect against I/R-induced cardiac apoptosis in vivo and in vitro via regulating HIF-1α signalling pathway. Rat myocardial I/R was induced by occluding the left anterior descending artery for 30 minutes followed by 6-hours reperfusion, and cardiomyocyte hypoxia/reoxygenation (H/R) was induced by oxygen-glucose deprivation for 6 hours followed by 3-hours reoxygenation. Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1α and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Conversely, the HIF-1α prolyl hydroxylase-2 inhibitor IOX2 partly blocked DEX-mediated cardioprotection both in vivo and in vitro. Mechanistically, DEX down-regulated HIF-1α expression at the post-transcriptional level and inhibited the transcriptional activation of the target gene BNIP3. Post-treatment with DEX protects against cardiac I/R injury in vivo and H/R injury in vitro. These effects are, at least in part, mediated via the inhibition of cell apoptosis by targeting HIF-1α signalling