Anisotropic crystal growth in blue phase I transitioned from a uniformly oriented cholesteric phase.

Phase transitions in blue phase liquid crystals (BPLCs) have attracted significant attention from the technical perspective of BP orientation control and the theoretical perspective of analogs with crystalline solids. The phase transition phenomena in BPs significantly depend on the phase state before the transition. In this study, we focused on the cholesteric (Ch)-BPI phase transition and found that BPI crystals exhibited a square shape upon the phase transition from the uniformly oriented Ch phase to the BPI phase. This square crystal shape was common across three BPLC materials with different elastic constants, and the shape reflected the crystal axis. The in-plane crystal orientation correlates with the easy axis on the substrate surface, suggesting that the [011] axis tends to coincide with the easy axis. However, the easy axis has little effect on the crystal growth rate. Furthermore, scratches on the substrate surface promoted nucleation. Based on this behavior, it was demonstrated that the nucleation position and density could be controlled by intentionally disturbing the Ch orientation by locally changing the easy axis using photoalignment. This study focused on the anisotropic crystal growth of BPI, providing interesting insights into LC phase transitions and soft matter crystal growth. In addition, it offers techniques for the fabrication of large BPI crystals, contributing to the enhanced electrical and optical performances of BPLC devices.

Slanted Structure of Blue Phase II Self-Aligned on One-Dimensional Patterned Surfaces.

Orientation analysis of liquid crystal (LC) devices is important for understanding and controlling light propagation behavior in these devices. Blue phases (BPs)─unique LC phases that self-organize into three-dimensional helical structures─are candidate materials for LC-based reflective diffractors. We realized BPII deflectors with large diffraction angles using one-dimensional surface alignment patterns. We analyzed the BPII lattice arrangement in the deflector based on Bragg reflections and demonstrated that the lattice structure was slanted with respect to the substrate, which was confirmed using transmission electron microscopy. In addition, we calculated the similarity between the alignment pattern on the substrate surface and the director arrangement of BPII near the interface, confirming that the structure observed experimentally matched the most probable calculated structure. Thus, this study contributes to the optical design of BPII deflectors and provides information on the orientation mechanism in high-order self-organizing soft matter structures.

Ferroptosis model system by the re-expression of BACH1.

Ferroptosis is a regulated cell death induced by iron-dependent lipid peroxidation. The heme-responsive transcription factor BTB and CNC homology 1 (BACH1) promotes ferroptosis by repressing the transcription of genes involved in glutathione (GSH) synthesis and intracellular labile iron metabolism, which are key regulatory pathways in ferroptosis. We found that BACH1 re-expression in Bach1-/- immortalized mouse embryonic fibroblasts (iMEFs) can induce ferroptosis upon 2-mercaptoethanol removal, without any ferroptosis inducers. In these iMEFs, GSH synthesis was reduced, and intracellular labile iron levels were increased upon BACH1 re-expression. We used this system to investigate whether the major ferroptosis regulators glutathione peroxidase 4 (Gpx4) and apoptosis-inducing factor mitochondria-associated 2 (Aifm2), the gene for ferroptosis suppressor protein 1, are target genes of BACH1. Neither Gpx4 nor Aifm2 was regulated by BACH1 in the iMEFs. However, we found that BACH1 represses AIFM2 transcription in human pancreatic cancer cells. These results suggest that the ferroptosis regulators targeted by BACH1 may vary across different cell types and animal species. Furthermore, we confirmed that the ferroptosis induced by BACH1 re-expression exhibited a propagating effect. BACH1 re-expression represents a new strategy for inducing ferroptosis after GPX4 or system Xc- suppression and is expected to contribute to future ferroptosis research.