Relaxor ferroelectric polymers exhibit high k at their structural phase transition around room temperature. They are particularly attractive as gate dielectric in organic field effect transistor (OFET). Nevertheless, their applications are limited due to their low thermal stability. A polymer blend system with a high and thermally stable dielectric constant is demonstrated by mixing terpolymer poly(vinylidene fluoride‐trifluoroethylene‐chlorofluorethylene) P(VDF‐ter‐TrFE‐ter‐CFE) with copolymer poly(vinylidene fluoride‐trifluoroethylene) P(VDF‐co‐TrFE). PVDF‐based blends of various compositions are characterized by dielectric spectroscopy, differential scanning calorimetry (DSC), infrared spectroscopy, small and wide angle X‐ray scattering (SAXS and WAXS), and atomic force microscopy (AFM) in order to investigate the relationship between morphology and crystallization of the blend and their dielectric properties. An optimized blend of P(VDF‐ter‐TrFE‐ter‐CFE) [55/37/8] and P(VDF‐co‐TrFE) [46/54] at a ratio of 70/30 is found to exhibit a quasi‐constant dielectric constant of 40 ± 2 over a wide temperature range (20–80 °C). Furthermore, electrical characteristics of the PVDF‐blend‐based gate dielectric OFET show further thermal stability in comparison to OFET based on high‐k terpolymer P(VDF‐ter‐TrFE‐ter‐CFE) [55/37/8]. An improvement of their drain current stability by up to 60% is demonstrated at 60 °C. These findings enable broader applications of fluoropolymers in organic electronics.

Development of the teeth requires complex signaling interactions between the mesenchyme and the epithelium mediated by multiple pathways. For example, canonical WNT signaling is essential to many aspects of odontogenesis, and inhibiting this pathway blocks tooth development at an early stage. R-spondins (RSPOs) are secreted proteins, and they mostly augment WNT signaling. Although RSPOs have been shown to play important roles in the development of many organs, their role in tooth development is unclear. A previous study reported that mutating Rspo2 in mice led to supernumerary lower molars, while teeth forming at the normal positions showed no significant anomalies. Because multiple Rspo genes are expressed in the orofacial region, it is possible that the relatively mild phenotype of Rspo2 mutants is due to functional compensation by other RSPO proteins. We found that inactivating Rspo3 in the craniofacial mesenchyme caused the loss of lower incisors, which did not progress beyond the bud stage. A simultaneous deletion of Rspo2 and Rspo3 caused severe disruption of craniofacial development from early stages, which was accompanied with impaired development of all teeth. Together, these results indicate that Rspo3 is an important regulator of mammalian dental and craniofacial development.

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