Neutrophil extracellular traps (NETs), the product of NETosis, is found to localize pathogens and crystals in immune response. Recent studies have found that excessive NETs lead to disease conditions such as diabetes and its complications like diabetic retinopathy (DR). However, the correlation between NETs and high glucose or DR remains unclear. Here, we found NETs level was significantly increased in the serum of diabetic patients, especially in proliferation diabetic retinopathy (PDR) patients. High glucose dramatically increased NETs production in diabetic individuals with time prolonging. The activation of NADPH oxidase was involved in the NETs process which is triggered by high glucose. Moreover, we verified the infiltration of neutrophils in the eyes and adhesion to vascular endothelial cells in diabetic rat models. NETs formation was observed in the vitreous bodies and retinas of diabetic individuals, which indicates NETs may play a role in the pathogenesis of diabetic retinopathy. Furthermore, anti-VEGF therapy downregulates NETs production indicating that NADPH oxidase-derived ROS may be another signaling pathway involved in anti-VEGF therapy.

Inspired by natural creatures, the development of a device that collects water from fog represents an important research direction.

A computational auditory nerve (AN) model was developed for use in modeling psychophysical experiments with normal and impaired human listeners. In this phenomenological model, many physiologically vulnerable response properties associated with the cochlear amplifier are represented by a single nonlinear control mechanism, including the effects of level-dependent tuning, compression, level-dependent phase, suppression, and fast nonlinear dynamics on the responses of high, medium, and low spontaneous-rate (SR) AN fibers. Several model versions are described that can be used to evaluate the relative effects of these nonlinear properties.

The present results suggest that miR-155 expression is decreased in active BD but not in VKH patients. Downregulated miR-155 may be involved in BD pathogenesis by targeting TAB2.