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This paper describes a drastic enhancement of the effective coupling factor by mass loading in layered surface acoustic wave (SAW) device structures such as the ScAlN film/Si substrate structure. This phenomenon occurs when the piezoelectric layer exhibits a high acoustic wave velocity. The mass loading decreases the SAW velocity and causes SAW energy confinement close to the top surface where an interdigital transducer is placed. It is shown that this phenomenon is obvious even when an amorphous SiO2 film is deposited on the top surface for temperature compensation. This enhancement was also found in various combinations of electrode, piezoelectric layer, and/or substrate materials. The existence of this phenomenon was verified experimentally using the ScAlN film/Si substrate structure.

A layered structure of aluminum nitride (AlN)/silicon dioxide (SiO)/cubic silicon carbide with embedded electrodes, which enables the growth of high-quality AlN thin films, is proposed and studied. The phase velocity, coupling factor, and temperature coefficient of frequency (TCF) of surface acoustic waves in the proposed structure have been investigated using the finite-element method. The simulation results show that a high velocity of 5485 m/s and a large effective coupling factor ( K) of 1.45% can be simultaneously obtained for the first mode. The dramatic enhanced K of 10.5% is also obtainable on the proposed structure employing Sc0.4Al0.6N thin film. Besides, the excellent zero TCF is also achieved without deteriorating the coupling factor by adding an amorphous SiO overlay.

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It is known that cadmium (Cd) induces cytotoxicity in hepatocytes; however, the underlying mechanism is unclear. Here, we studied the molecular mechanisms of Cd-induced hepatotoxicity in rat liver cells (BRL 3A) and in vivo. We observed that Cd treatment was associated with a time- and concentration-dependent decrease in the cell index (CI) of BRL 3A cells and cellular organelle ultrastructure injury in the rat liver. Meanwhile, Cd treatment resulted in the inhibition of gap junction intercellular communication (GJIC) and activation of mitogen-activated protein kinase (MAPK) pathways. Gap junction blocker 18-β-glycyrrhetinic acid (GA), administered in combination with Cd, exacerbated cytotoxic injury in BRL 3A cells; however, GA had a protective effect on healthy cells co-cultured with Cd-exposed cells in a co-culture system. Cd-induced cytotoxic injury could be attenuated by co-treatment with an extracellular signal-regulated kinase (ERK) inhibitor (U0126) and a p38 inhibitor (SB202190) but was not affected by co-treatment with a c-Jun N-terminal kinase (JNK) inhibitor (SP600125). These results indicate that ERK and p38 play critical roles in Cd-induced hepatotoxicity and mediate the function of gap junctions. Moreover, MAPKs induce changes in GJIC by controlling connexin gene expression, while GJIC has little effect on the Cd-induced activation of MAPK pathways. Collectively, our study has identified a possible mechanistic pathway of Cd-induced hepatotoxicity in vitro and in vivo, and identified the participation of GJIC and MAPK-mediated pathways in Cd-induced hepatotoxicity. Furthermore, we have shown that salidroside may be a functional chemopreventative agent that ameliorates the negative effects of Cd via GJIC and MAPK pathways.

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