Nickel-vanadium layered double hydroxide for a mid-infrared 2 µm Tm:YAG ceramic ultrafast laser.

In this study, a nickel-vanadium layered double hydroxide (NiV-LDH) nanosheet was prepared as a saturable absorber (SA) by liquid phase exfoliation and a drop-coating method. The microstructure and optical transmission properties of the obtained NiV-LDH nanosheet were then systematically studied. An "X"-type fold cavity was designed to evaluate the ultrafast laser modulation performance of the NiV-LDH nanosheet with a Tm:YAG ceramic gain medium. A stable passively Q-switched mode-locked (QML) pulse centered at 2011.6 nm has successfully been realized, with a repetition frequency of 145 MHz and a pulse duration of 320 ps. To the best of our knowledge, this is the first time that the LDH has been used as an SA in a mid-infrared range ultrafast laser.

Diosmetin attenuates oxidative stress-induced damage to lens epithelial cells via the mitogen-activated protein kinase (MAPK) pathway.

Cataract is a global ophthalmic disease that blinds the eye, and oxidative stress is one of its primary causes. Apoptosis of lens epithelial cells (LECs) is considered the major cytological basis of many cataracts except congenital cataracts. The purpose of this study was to investigate whether diosmetin could reduce oxidative stress-induced damage to LECs, and explore its regulatory pathway. Lens epithelial cell line SRA01/04 was used as the object of study. Using ultraviolet B (UVB) and hydrogen peroxide (H2O2) as sources of oxidative stress, the protective effects of diosmetin at different concentrations on cells were investigated, including inhibition of proliferation, apoptosis, and oxidative stress. Molecular docking was then used to predict the target proteins and validation was performed at the cellular and protein levels. The oxidative stress of SRA01/04 was induced by UVB and H2O2, and inhibition of proliferation and apoptosis were observed. Here, diosmetin has a dose-dependent cell-protecting effect. This effect is achieved by targeting the MEK2 protein and inhibiting the MAPK signaling. In conclusion, diosmetin reduces H2O2- and UVB-induced inhibition of SRA01/04 proliferation and apoptosis by reducing oxidative stress-induced activation of the MAPK pathway.