ABSTRACT
High harmonic generation (HHG) with longitudinal optical orbital angular momentum has attracted much attention over the past decade. Here, we present the first study on the HHG with transverse orbital angular momentum driven by the spatiotemporal optical vortex (STOV) pulses. We show that the produced spatial-resolved harmonic spectra reveal unique structures, such as the spatially spectral tilt and the fine interference patterns. We show these spatiospectral structures originate from both the macroscopic and microscopic effect of spatiotemporal optical singularity in HHG. Employing two-color counterspin and countervorticity STOV pulses, we further discuss a robust method to control the spatiotemporal topological charge and spectral structure of high-order harmonics. The conservation rule of photon transverse orbital angular momentum in HHG process is also discussed when mixing with photon spin angular momenta.
ABSTRACT
Angiotensin II (Ang II) has been proven to induce epithelial-mesenchymal transition (EMT). The aim of the present study was to determine the role of microRNA-29b (miR-29b) during Ang II-induced EMT. For this purpose, we used spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rats. The levels of Ang II and its receptor in the kidneys of the SHRs are significantly higher than those in the age-matched WKY rats. As shown by RT-qPCR, the expression of miR-29b in the renal cortex was lower in the SHRs than in the WKY rats. For in vitro experiments, NRK-52E renal tubular epithelial cells were treated with 10(-7) M Ang II; we found that the expression of miR-29b was decreased in the cells treated with Ang II. In addition, transfection of the NRK-52E cells with miR-29b inhibitor led to the downregulation of miR-29b in these cells, and increased the expression of transforming growth factor (TGF)-ß, α-smooth muscle actin (α-SMA) and collagen I (Col I). Similar results were observed with the induction of Ang II expression in the NRK-52E cells. By contrast, the upregulation of miR-29b by transfection with miR-29b mimics inhibited the overexpression of these genes induced by Ang II. These results suggest that miR-29b plays an important role in Ang II-induced EMT.
