Restoring atmospheric-turbulence-degraded images.

Image data experiences geometric distortions and spatial-temporal varying blur due to the strong effects of random spatial and temporal variations in the optical refractive index of the communication path. Simultaneously removing these effects from an image is a challenging task. An efficient approach is proposed in this paper to address this problem. The approach consists of four steps. First, a frame selection strategy is employed by proposing an unsupervised k-means clustering technique. Second, a B-spline-based nonrigid image registration is carried out to suppress geometric distortions. Third, a spatiotemporal kernel regression is proposed by introducing the local sharp patch concept to fuse the registered frame sequences into an image. Finally, a blind deconvolution technique is employed to deblur the fused image. Experiments are carried out with synthetic and real-world turbulence-degraded data by implementing the proposed method and two recently reported methods. The proposed method demonstrates significant improvement over the two reported methods in terms of alleviating blur and distortions, as well as improving visual quality.

Ginsenoside Rg1 reduces aldosterone-induced autophagy via the AMPK/mTOR pathway in NRK-52E cells.

Aldosterone is a steroid hormone secreted from the adrenal cortex, which regulates blood pressure. Higher concentrations of aldosterone can cause several diseases, including hypertension, diabetic nephropathy and chronic kidney disease. Previous reports have demonstrated that aldosterone has a pathogenic role in renal injury via reactive oxygen species (ROS), which involves the regulation of autophagy. However, whether aldosterone can induce autophagy in renal tubular cells remains to be elucidated. In the present study, elevated autophagy was observed in rat renal tubular NRK-52E cells exposed to aldosterone, which was demonstrated by the increased number of autophagosomes, conversion of LC3-I to LC3-II and the expression of Beclin-1. The enhanced autophagy was accompanied by increased production of intracellular ROS, which was reversed by N-acetylcysteine, a specific inhibitor of ROS signaling. Furthermore, treatment with ginsenoside Rg1 reduced the aldosterone-induced autophagy and production of ROS, possibly through reducing the phosphorylation of AMPK and preserving mTOR activity. These findings demonstrated that aldosterone promoted ROS generation and increased autophagy in the NRK-52E cells. Ginsenoside Rg1 effectively relieved aldosterone-induced oxidative stress and abnormal autophagy, suggesting that Rg1 may be used as a potential therapeutic drug to inhibit the renal injury, which is induced by aldosterone.