No abstract

Despite the high expectation of deformable and see-through displays for future ubiquitous society, current light-emitting diodes (LEDs) fail to meet the desired mechanical and optical properties, mainly because of the fragile transparent conducting oxides and opaque metal electrodes. Here, by introducing a highly conductive nanofibrillated conducting polymer (CP) as both deformable transparent anode and cathode, ultraflexible and see-through polymer LEDs (PLEDs) are demonstrated. The CP-based PLEDs exhibit outstanding dual-side light-outcoupling performance with a high optical transmittance of 75% at a wavelength of 550 nm and with an excellent mechanical durability of 9% bending strain. Moreover, the CP-based PLEDs fabricated on 4 µm thick plastic foils with all-solution processing have extremely deformable and foldable light-emitting functionality. This approach is expected to open a new avenue for developing wearable and attachable transparent displays.

Ferroptosis is a regulated form of cell death driven by the lethal accumulation of lipid peroxides in cell membranes. Several regulators of ferroptosis have been identified using cancer cell lines. However, the cellular pathways of ferroptosis in neurons remain poorly characterized. In this study, we used a mouse embryonic stem cell‐derived motor neuron model to investigate how motor neurons respond to ferroptosis inducers. Pharmacological and genetic inhibition of glutathione peroxidase 4 (GPx4) induced ferroptosis in motor neurons, while system xc− inhibition by erastin had no effect. RNA‐seq analysis showed that the expression levels of several genes were altered during RSL3‐induced ferroptosis. Subsequent bioinformatic analysis revealed alterations in several biological pathways during ferroptosis, including synaptogenesis and calcium signaling. Finally, we found that edaravone, an FDA‐approved drug for treating amyotrophic lateral sclerosis (ALS) disease, rescued motor neurons from RSL3‐induced ferroptosis. Our data highlight the crucial role of GPx4 in ferroptosis regulation and demonstrate that stem cell‐derived motor neuron culture is a valuable model to study ferroptosis at the single‐cell level in a neuronal context.