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To realize the advanced thin-film transistors (TFTs), high-carrier-mobility semiconductor films on insulator structures should be fabricated with low-temperature processing conditions (≤500 °C). To achieve this, we investigated the solid-phase crystallization of amorphous-GeSn films on insulating substrates under a wide range of Sn concentrations (0%–20%), film thicknesses (30–500 nm), and annealing temperatures (380–500 °C). Our results reveal that a Sn concentration close to the solid solubility of Sn in Ge (∼2%) is effective in increasing the grain-size of poly-GeSn. In addition, we discovered that the carrier mobility depends on the film thickness, where the mobilities are determined by the counterbalance between two different carrier scattering mechanisms. Here, vacancy-related defects dominate the carrier scattering near the insulating substrates (≤∼120 nm), and grain-size determined by bulk nucleation dominates the grain-boundary scattering of thick films (≥∼200 nm). Consequently, we obtained the maximum mobilities in samples with a Sn concentration of 2% and a film thickness of 200 nm. The effect of increasing the grain-size of poly-GeSn by lowering the annealing temperature was also clarified. By combining these results, a very high carrier mobility of 320 cm2/Vs was obtained at a low temperature of 380 °C. This mobility is about 2.5 times as high as previously reported data for Ge and GeSn films grown at low temperatures (≤500 °C). Our technique therefore opens up the possibility of high-speed TFTs for use in the next generation of electronics.

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Background and Purpose-Cerebral vasospasm is one of the major complications of subarachnoid hemorrhage (SAH). Its pathogenesis still remains elusive, and effective therapeutic strategies are yet to be established. We investigated the role of proteinase-activated receptor-1 (PAR1) in the hypercontractile state in SAH. Methods-Rabbit double hemorrhage model was used as a model of SAH. The contractile response to thrombin and the PAR1 expression were evaluated in the isolated rings of basilar artery. Results-Thrombin exhibited only a minor contractile effect in the control, whereas it induced augmented contractions in SAH. The expression of PAR1 was upregulated in SAH. Intracisternal injection of PAR1 antagonist E5555 prevented the enhancement of the contractile responses to thrombin in SAH. The maximal prevention was obtained with 2 g/kg weight/injection. The contractile responses to K ϩ depolarization or endothelin-1 remained unaffected. The upregulation of PAR1 was also prevented by E5555 (2 g/kg weight/injection) to a level similar to that seen in the control. Ex vivo treatment with E5555 (1 mol/L) inhibited the contraction induced by thrombin, whereas it had little effect on the contraction induced by K ϩ depolarization or endothelin-1, in the basilar artery of SAH. E5555 also inhibited the [Ca 2ϩ ] i elevation induced by thrombin, but not trypsin, in cultured smooth muscle cells. Conclusions-PAR1 plays a critical role in upregulating PAR1 itself, thereby enhancing the contractile response to thrombin in SAH. PAR1 could thus be a therapeutic target. However, the usefulness of PAR1 antagonist remains to be investigated in vivo. (Stroke. 2007;38:3259-3265.)