Anti-APLN (full length) polyclonal antibody

We propose a general routine, Genetic-Simulated Annealing method (GSA) for the optimal design of quasi-phase matched (QPM) non-uniform grating. Here this method is applied to the design of the flat broadened wavelength conversion bandwidth of 40-mm aperiodically poled lithium niobate (APLN) based on difference-frequency generation (DFG). The flat conversion bandwidth of APLN is broadened from the original 65 nm in a 40-mm periodically poled lithium niobate (PPLN) to the pre-designated 130 nm in a 40-mm APLN, which conversion efficiency is 6.7 dB higher than that of 12.4-mm PPLN under the same conversion bandwidth.

Pulmonary arterial hypertension (PAH) is characterized by vascular remodeling associated with obliteration of pulmonary arterioles and formation of plexiform lesions composed of hyperproliferative endothelial and vascular smooth-muscle cells. Here we describe a microRNA (miRNA)-dependent association between apelin (APLN) and fibroblast growth factor 2 (FGF2) signaling in pulmonary artery endothelial cells (PAECs). APLN deficiency in these cells led to increased expression of FGF2 and its receptor FGFR1 as a consequence of decreased expression of miR-424 and miR-503, which directly target FGF2 and FGFR1. miR-424 and miR-503 were downregulated in PAH, exerted antiproliferative effects in PAECs and inhibited the capacity of PAEC-conditioned medium to induce the proliferation of pulmonary artery smooth-muscle cells. Reconstitution of miR-424 and miR-503 in vivo ameliorated pulmonary hypertension in experimental models. These studies identify an APLN-dependent miRNA-FGF signaling axis needed for the maintenance of pulmonary vascular homeostasis.