Polylactide (PLA) was plasticized by polyethylene glycols (PEGs) with five different molecular weights (M w = 200-20,000 g/mol). The effects of content and molecular weight of PEG on the crystallization and impact properties of PLA were studied by wide-angle X-ray diffraction, differential scanning calorimetry, scanning electron microscopy, transmission electron microscopy, and V-notched impact tests, respectively. The results revealed that PEG-10,000 could significantly improve the crystallization capacity and impact toughness of PLA. When the PEG-10,000 content ranged from 0 to 20 wt%, the increases in both V-notched Izod and Charpy impact strengths of PLA/PEG-10,000 blends were 206.10% and 137.25%, respectively. Meanwhile, the crystallinity of PLA/PEG-10,000 blends increased from 3.95% to 43.42%. For 10 wt% PEG content, the crystallization and impact properties of PLA/PEG blends mainly depended upon PEG molecular weight. With increasing the M w of PEG, the crystallinity and impact strength of PLA/PEG blends first decreased and then increased. The introduction of PEG reduced the intermolecular force and enhanced the mobility of PLA chains, thus improving the crystallization capacity and flexibility of PLA.
The activation of ferroptosis is a new effective way to treat drug-resistant solid tumors. Ferroptosis is an iron-mediated form of cell death caused by the accumulation of lipid peroxides. The intracellular imbalance between oxidant and antioxidant due to the abnormal expression of multiple redox active enzymes will promote the produce of reactive oxygen species (ROS). So far, a few pathways and regulators have been discovered to regulate ferroptosis. In particular, the cystine/glutamate antiporter (System Xc−), glutathione peroxidase 4 (GPX4) and glutathione (GSH) (System Xc−/GSH/GPX4 axis) plays a key role in preventing lipid peroxidation-mediated ferroptosis, because of which could be inhibited by blocking System Xc−/GSH/GPX4 axis. This review aims to present the current understanding of the mechanism of ferroptosis based on the System Xc−/GSH/GPX4 axis in the treatment of drug-resistant solid tumors.
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