Unipolar resistance switching (RS) in TiO2 thin films originates from the repeated formation and rupture of the Magnéli phase conducting filaments through repeated nano-scale phase transitions. By applying the Johnson-Mehl-Avrami (JMA) type kinetic model to the careful analysis on the evolution of transient current in a pulse-switching, it was possible to elucidate the material specific evolution of the Magnéli phase filament. This methodology was applied to the two types of TiO2 films grown by plasma-enhanced atomic layer deposition (PEALD) and sputtering. These two samples have structurally and electrically distinctive properties: PEALD film exhibited high variability in switching parameters and required an electroforming while sputtered film showed higher uniformity without distinct electroforming process. The JMA-type kinetic analysis of the RS behaviors revealed that the rejuvenation of the filament is accomplished by repeated one-dimensional nucleation followed by a two-dimensional growth in PEALD samples, whereas one-dimensional nucleation-free mechanism dominates in sputtered films.

Cytoplasmic accumulation of TDP-43 in motor neurons is the most prominent pathological feature in amyotrophic lateral sclerosis (ALS). A feedback cycle between nucleocytoplasmic transport (NCT) defect and TDP-43 aggregation was shown to contribute to accumulation of TDP-43 in the cytoplasm. However, little is known about cellular factors that can control the activity of NCT, thereby affecting TDP-43 accumulation in the cytoplasm. Here, we identified via FRAP and optogenetics cytosolic calcium as a key cellular factor controlling NCT of TDP-43. Dynamic and reversible changes in TDP-43 localization were observed in Drosophila sensory neurons during development. Genetic and immunohistochemical analyses identified the cytosolic calcium-Calpain-A-Importin α3 pathway as a regulatory mechanism underlying NCT of TDP-43. In C9orf72 ALS fly models, upregulation of the pathway activity by increasing cytosolic calcium reduced cytoplasmic accumulation of TDP-43 and mitigated behavioral defects. Together, these results suggest the calcium-Calpain-A-Importin α3 pathway as a potential therapeutic target of ALS.