[Research progress of PD-L1 in inflammatory lung diseases].

Programmed death-ligand 1 (PD-L1) is important in maintaining central and peripheral immune tolerance in normal tissues, mediating tumor immune escape and keeping the balance between anti- and pro-inflammatory responses. Inflammation plays an important role in inflammatory lung diseases. This article reviews the research progress and potential clinical value of PD-L1 in inflammatory lung diseases, including acute lung injury, chronic obstructive pulmonary disease, asthma and idiopathic pulmonary fibrosis.

U-Shaped Tube Based Liquid-Solid Triboelectric Nanogenerator for Harvesting Unutilized Compressed Air Energy.

Due to a lack of technologies that harvest green and sustainable energy, unutilized compressed air energy during the operation of pneumatic systems is wasted. Liquid-solid triboelectric nano-generators (L-S TENGs) have been widely used as an advanced technology with broad development prospects due to their advantages of a simple structure and long service life. Among them, liquid-solid triboelectric nanogenerators with tube structures have great potential for coupling multiple physical effects and integrating them into a single device. Herein, a U-shaped tube triboelectric nanogenerator composed of fluorinated ethylene propylene (FEP) and copper foil (UFC-TENG) is proposed to directly harvest unutilized compressed air energy. The UFC-TENG can collect unutilized compressed air energy with a stable peak voltage and current of approximately 33 V and 0.25 µA, respectively. When the alternating frequency of the liquid is 0.9 Hz, the unutilized compressed air can drive the UFC-TENG unit with an inner diameter of 12 mm, achieving a maximum output power of 3.93 µW at an external load resistance of 90 MΩ. The UFC-TENG is a novel driving method for L-S TENGs and demonstrates the promising potential of TENGs in the harvesting of unutilized compressed air energy in pneumatic systems.

CORO1A regulates lipoprotein uptake in Leydig cells exposed to cadmium.

Cadmium (Cd) is one of the most common environmental pollutants, which has a long biological half-life. Maternal Cd-exposure in the natural environment causes steroidogenesis defects resulting in spermatogenesis disorder in male offspring. For better understanding its underlying mechanism, we have employed iTRAQ to screen the differentially expressed protein and found that the expression of CORO1A and Cofilin 1 was up-regulated approximately 2 fold in Leydig cells of maternal Cd-exposure offspring. As the major source of steroid hormone, cholesterol is transported to cells via receptor-mediated endocytosis which relies on the remodel of cytoskeleton, then stores in lipid droplets (LDs). However, few studies have focused on the role of cytoskeleton in abnormal steroidogenesis. This study was performed to explore the role of CORO1A in androgen deficiency caused by Cd exposure and its involvement of low-density lipoprotein (LDL) uptake and effects on LDs. We found that Cd resulted in the up-regulation of CORO1A and Cofilin 1, and down-regulation of Profilin 1 in the testis of male offspring with maternal exposure. The structure of filamentous actin was broken, disordered and even crumpled up in Cd-treated R2C cells. F-actin disassembly led to a low uptake of LDL with a reduced number of LDs, followed by decreased total cholesterol and low progesterone production. When CORO1A was silenced, the expression of Cofilin 1 was down-regulated and Profilin 1 was up-regulated in Cd-treated R2C cells. The filamentous actin was rescued and the integrated cytoskeleton prompted LDL uptake, which resulted in the increased total cholesterol and high progesterone production. These findings highlight the crucial role of CORO1A as a cytoskeleton regulatory protein in steroidogenesis, which may help to better understand Cd-induced steroid hormone deficiency in children.