ABSTRACT
HfO2 shows promise for emerging ferroelectric and resistive switching (RS) memory devices owing to its excellent electrical properties and compatibility with complementary metal oxide semiconductor technology based on mature fabrication processes such as atomic layer deposition. Oxygen vacancy (Vo), which is the most frequently observed intrinsic defect in HfO2-based films, determines the physical/electrical properties and device performance. Vo influences the polymorphism and the resulting ferroelectric properties of HfO2. Moreover, the switching speed and endurance of ferroelectric memories are strongly correlated to the Vo concentration and redistribution. They also strongly influence the device-to-device and cycle-to-cycle variability of integrated circuits based on ferroelectric memories. The concentration, migration, and agglomeration of Vo form the main mechanism behind the RS behavior observed in HfO2, suggesting that the device performance and reliability in terms of the operating voltage, switching speed, on/off ratio, analog conductance modulation, endurance, and retention are sensitive to Vo. Therefore, the mechanism of Vo formation and its effects on the chemical, physical, and electrical properties in ferroelectric and RS HfO2 should be understood. This study comprehensively reviews the literature on Vo in HfO2 from the formation and influencing mechanism to material properties and device performance. This review contributes to the synergetic advances of current knowledge and technology in emerging HfO2-based semiconductor devices.
ABSTRACT
Bone morphogenic protein-4 (BMP-4), one of TGF-ß superfamily, is involved in bone and cartilage development, specifically tooth and bone fracture repair. In the present study, the role of protein kinase C (PKC) was investigated in BMP-4-induced differentiation of osteoblast-like MC3T3-E1 cells. PKC inhibitor UCN-01 significantly attenuated the synthesis of osteocalcin, a marker of mature osteoblast phenotype, in a dose-dependent manner as well as blocked osteroblastic differentiation and mineralization in BMP-4-treated MC3T3-E1 cells. Also, UCN-01 suppressed vascular endothelial growth factor (VEGF) production in BMP-4-treated MC3T3-E1 cells. In addition, UCN-01 remarkably suppressed BMP-4-activated PKC ßII and PKC δ/θ of PKC family proteins by Western blotting. Consistently, 2-dimensional electrophoresis (2-DE) immunoblotting revealed that UCN-01 inhibited the BMP-4-induced activation of PKC subfamilies in MC3T3-E1 cells. Taken together, our findings suggest that PKC ßII and PKC δ/θ mediate BMP-4-induced osteoblastic differentiation.
