Enhancing optical delay using cross-Kerr nonlinearity in Rydberg atoms.

A scheme to enhance the optical delay in Rydberg atoms is proposed. In the linear case, the optical delay in a four-level system can be significantly enhanced compared to that of the three-level system. However, the width of the transparent window will decrease with an increase in the optical delay. In the nonlinear case, the nonlinear dispersion becomes steep around the transparency window. The enhanced cross-Kerr nonlinearity mainly contributes to the effective dispersion, which dramatically increases the optical delay. The simulation result shows that the optical delay of the system could be enhanced tens of times; moreover, the wide transparency window remains. So the delay-bandwidth product could be significantly improved due to nonlinear dispersion. We further examine Gaussian pulse propagation in the Rydberg atoms.

THz white light cavity with nonlinear dispersion in graphene.

A white light cavity (WLC) scheme is proposed to achieve broadband response in the terahertz (THz) region by enhanced nonlinear dispersion in a magnetized graphene system. In the weak probe field limit, the cavity linewidth is narrowed due to electromagnetically induced transparency, and then it becomes nearly as broad as the empty-cavity linewidth under the condition of Autler-Towns splitting. It is interesting to find that the cavity linewidth can be further broadened by enhanced nonlinear dispersion. The simulation result shows that the response range of the cavity is from 6.273 THz to 6.308 THz under the given condition, which is nearly 11 times larger than the empty-cavity linewidth. Furthermore, the improvement in cavity transmission and the response of WLC at different frequencies are investigated.

MicroRNA-29b-3p Targets SPARC Gene to Protect Cardiocytes against Autophagy and Apoptosis in Hypoxic-Induced H9c2 Cells.

MicroRNAs participate in the regulation of abnormal cardiomyocyte apoptosis and autophagy, which leads to heart failure (HF). Lower miR-29b-3p levels were found in HF patients in this study. However, the role of miR-29b-3p in the molecular pathogenesis of HF remains unclear. Hypoxia-stimulated H9c2 cells were used an in vitro model of HF. It was found that hypoxia stimulation decreased the miR-29b-3p expression and enhanced cell apoptosis and autophagy response in H9c2 cells. While the effects of hypoxia on cell apoptosis and autophagy were reversed by miR-29b-3p transfection, especially 100 nM. The secreted protein acidic and rich in cysteine (SPARC), predicted as a direct target of miR-29b-3p, aggravated the hypoxia-induced cells apoptosis, autophagy, and TGFß1/Smad3 activation. While the changes were dramatically reversed by miR-29b-3p. Taken together, our data suggest that miR-29b-3p plays an important role in the progression of HF through targeting SPARC and regulating TGFß1/Smad3 pathway.