The morphological evolution of thin composite films based on poly(3-hexylthiophene) (P3HT) and [6,6]-phenyl C 61 butyric acid methyl ester (PCBM) upon annealing has been studied by means of transmission electron microscopy (TEM), scanning near-field optical microscopy (SNOM), and confocal Raman microscopy. This system currently is the most promising candidate for high-performance polymer solar cells. TEM bright field and SNOM topography measurements show that segregation and large-scale crystallization of PCBM take place upon thermal annealing. Additional SNOM optical absorbance measurements using laser irradiation sources with two different wavelengths in the visible light range and Raman microscopy are able to detect the component distribution within the thin composite film, which in detail demonstrates high diffusive mobility of PCBM upon annealing.

Recent studies have reported the role of Wnt/β-catenin signaling in hair cell (HC) development, regeneration, and differentiation in the mouse cochlea; however, the role of Wnt/β-catenin signaling in HC protection remains unknown. In this study, we took advantage of transgenic mice to specifically knockout or overactivate the canonical Wnt signaling mediator β-catenin in HCs, which allowed us to investigate the role of Wnt/β-catenin signaling in protecting HCs against neomycin-induced damage. We first showed that loss of β-catenin in HCs made them more vulnerable to neomycin-induced injury, while constitutive activation of β-catenin in HCs reduced HC loss both in vivo and in vitro. We then showed that loss of β-catenin in HCs increased caspase-mediated apoptosis induced by neomycin injury, while β-catenin overexpression inhibited caspase-mediated apoptosis. Finally, we demonstrated that loss of β-catenin in HCs led to increased expression of forkhead box O3 transcription factor (Foxo3) and Bim along with decreased expression of antioxidant enzymes; thus, there were increased levels of reactive oxygen species (ROS) after neomycin treatment that might be responsible for the increased aminoglycoside sensitivity of HCs. In contrast, β-catenin overexpression reduced Foxo3 and Bim expression and ROS levels, suggesting that β-catenin is protective against neomycin-induced HC loss. Our findings demonstrate that Wnt/β-catenin signaling has an important role in protecting HCs against neomycin-induced HC loss and thus might be a new therapeutic target for the prevention of HC death.