Deflecting and routing nematicons via orientation programmable liquid crystal array.

By designing a liquid crystal cell with comb electrode structure, the alignment modulation of nematic liquid crystal in the cell can be realized after the electric field is applied. In different orientation regions, the incident laser beam can deflect at different angles. At the same time, by changing the incident angle of the laser beam, the reflection modulation of the laser beam on the interface of the liquid crystal molecular orientation change can be realized. Based on the above discussion, we then demonstrate the modulation of liquid crystal molecular orientation arrays on nematicon pairs. In different orientation regions of liquid crystal molecules, nematicon pairs can exhibit various combinations of deflections, and these deflection angles are modulable under external fields. Deflection and modulation of nematicon pairs have potential applications in optical routing and optical communication.

Ultra-broadband holography in visible and infrared regions with full-polarization nondispersive response.

Holography is promising to fully record and reconstruct the fundamental properties of light, while the limitations of working bandwidth, allowed polarization states, and dispersive response impede further advances in the integration level and functionality. Here, we propose an ultra-broadband holography based on twisted nematic liquid crystals (TNLCs), which can efficiently work in both the visible and infrared regions with a working spectrum of over 1000 nm. The underlying physics is that the electric field vector of light through TNLCs can be parallelly manipulated in the broad spectral range, thus enabling to build the ultra-broadband TNLC hologram by dynamic photopatterning. Furthermore, by introducing a simple nematic liquid crystal (NLC) element, the cascaded device allows for an excellent nondispersive polarization-maintaining performance that can adapt to full-polarization incidence. We expect our proposed methodology of holography may inspire new avenues for usages in polarization imaging, augmented/virtual reality display, and optical encryption.

Glycyrretinic acid blocks cardiac sodium channels expressed in Xenopus oocytes.

ETHNOPHARMACOLOGICAL RELEVANCE: Licorice has been used to treat many ailments including cardiovascular disorders in China for long time. Recent studies have shown that the cardiac actions of licorice have been attributed to its active component, glycyrretinic acid (GA). However, its mechanism remains poorly understood. AIM OF THE STUDY: The effects of GA on the cardiac sodium currents (I(Na)), L-type calcium currents (I(Ca,L)) and hyperpolarization-activated inward currents (I(f)) were investigated. MATERIALS AND METHODS: Human isoforms of wild-type and DeltaKPQ-mutant type sodium channels were expressed in Xenopus oocytes, and the resulting currents (peak and late I(Na)) were recorded using a two-microelectrode voltage-clamp technique. A perforated patch clamp technique was employed to record I(Ca,L) and I(f) from isolated rabbit sinoatrial node pacemaker cells. RESULTS: GA inhibited peak I(Na) (33% at 90 microM) and late I(Na) (72% at 90 microM), but caused no significant effects on I(Ca,L) and I(f). CONCLUSION: GA blocked cardiac sodium currents, particularly late I(Na.) Our findings might help to understand the traditional use of licorice in the treatment of cardiovascular disorders, because reduction of sodium currents (particularly late I(Na)) would be expected to provide protection from Na(+)-induced Ca(2+) overload and cell damage.

The role of hERG1 K+ channels and a functional link between hERG1 K+ channels and SDF-1 in acute leukemic cell migration.

Stromal cell-derived factor-1 (SDF-1) and its unique receptor, CXCR4, regulate stem/progenitor cell migration and retention in the bone marrow and are required for hematopoiesis. Recent studies found that hERG1 K(+) channels were important regulators of tumor cell migration. In this study, we investigated whether SDF-1 induced acute leukemic cell migration associated with hERG1 K(+) channels. Our results showed that E-4031, a specific hERG1 K(+) channels inhibitor, significantly blocked SDF-1-induced migration of leukemic cell lines, primary acute leukemic cells, leukemic stem cells and HEK293T cells transfected with herg-pEGFP. The migration of phenotypically recognizable subsets gave the indication that lymphoblastic leukemic cells were inhibited more than myeloid cells while in the presence of E-4031 which maybe associated with herg expression. SDF-1 increased hERG1 K(+) current expressed in oocytes and HEK293T cells transfected with herg-pEGFP. There were no significant changes of CXCR4 expression on both HL-60 cells and primary leukemic cells regardless if untreated or treated with E-4031 for 24 h (P>0.05). The hERG1 K(+) current increased by SDF-1 might contribute to the mechanism of SDF-1-induced leukemic cell migration. The data suggested that hERG1 K(+) channels functionally linked to cell migration induced by SDF-1.