Photon blockade by enhancing coupling via a nonlinear medium.

A significantly low value of the single-photon coupling constant is a major challenge in the creation of a single-photon source via photon blockade. Here, we propose a photon blockade scheme composed of a weakly second-order nonlinear medium with an optical parametric amplification in a low-frequency cavity. Unlike the traditional weakly coupled system, the effective coupling strength in the proposed scheme can be significantly higher than the decay rate of the cavity mode. This can be achieved by adjusting the squeezing parameter even if the original coupling strength is weak. The thermal noise of the squeezed cavity mode can be suppressed by a squeezed vacuum field. Using a probability amplitude method, we obtain the optimal condition of photon blockade in the steady-state. By solving the master equation numerically in the steady-state, a strong photon antibunching effect that is consistent with the optimal conditions can be obtained in the cavity with low frequency. Besides, the photon blockade phenomenon and cross-correlation of two cavities can be significantly enhanced under a specific squeezing parameter. Our results may be useful for future studies on the characteristics of photon statistics.

Ground-state cooling of mechanical oscillator via quadratic optomechanical coupling with two coupled optical cavities.

We present a scheme for the electromagnetically induced transparency (EIT)-like nonlinear ground-state cooling in a double-cavity optomechanical system in which an optical cavity mode is coupled parametrically to the square of the position of a mechanical oscillator, an additional auxiliary cavity is coupled to the optomechanical cavity. The optimum cooling conditions is derived, based on which the heating process can be well suppressed and the mechanical resonator can be cooled with an optimal effect to near its ground state through EIT-like cooling mechanism even in unresolved sideband regime. It is demonstrated by numerical simulations that not only the average phonon number of steady state is lower than that of single-cavity optomechanical system, but also the cooling rate is greatly faster than that of the linear optomechanical coupling due to the two-phonon cooling process in the quadratic coupling. Also, the ground-state cooling is achievable even with a relatively weak quadratic coupling strengthby tunning the coupling between two cavities to reach the optimum cooling conditions, thus provides an solution for overcoming the limitations of weak quadratic coupling rate in experiments. The proposed approach provides a platform for quantum manipulation of macroscopic mechanical devices beyond the resolved sideband limit and linear coupling regime.

MiR-223 regulates proliferation and apoptosis of IL-22-stimulated HaCat human keratinocyte cell lines via the PTEN/Akt pathway.

Psoriasis, a chronic inflammatory skin disorder disease, is closely associated with hyperproliferation of keratinocytes. Upregulated miR-223 has been found in peripheral blood mononuclear cells from patients with psoriasis and from psoriatic skin. However, its role in keratinocytes remains unknown. We thus aimed to investigate the function of miR-223 in psoriasis. Interleukin-22 (IL-22) is a crucial keratinocyte trigger in the T-cell-mediated immune response to psoriasis. We found miR-223 to be overexpressed in psoriatic lesions and in IL-22-stimulated HaCaT cells. HaCaT cells then were transfected with a miR-223 mimic or inhibitor to overexpress or inhibit expression of miR-223, respectively. A Cell Counting Kit-8 assay revealed that miR-223 overexpression promoted and miR-223 downregulation inhibited proliferation in IL-22-stimulated HaCaT cells. Flow cytometry analysis certified that miR-223 overexpression decreased HaCaT cell apoptosis, whereas miR-223 downregulation increased it. A dual-luciferase reporter assay demonstrated that miR-223 directly targeted the phosphatase and tensin homolog (PTEN) gene. MiR-223 also negatively regulated mRNA and protein expression of PTEN and modulated the PTEN/Akt pathway in IL-22-stimulated HaCaT cells. PTEN silencing attenuated the activity of the miR-223 inhibitor in these cells via the PTEN/Akt pathway. Overall, the results showed that miR-223 increased proliferation and inhibited apoptosis of IL-22-stimulated keratinocytes via the PTEN/Akt pathway.