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The resistive switching evolution of NiO/AlO in Pt/NiO/AlO/n-Si structure was investigated with postannealing time. When increasing the postannealing time, larger voltage/current is needed to turn on/turn off the structure, respectively. Large memory resistance window can be obtained by the interface modulation of NiO/AlO. For the fresh structure, the low resistance state (LRS) obeys Ohmic conduction mechanism and the high resistance state (HRS) fits Poole-Frenkel-like behavior. With the postannealing time increase, the reaction between NiO and AlO occurs. Finally, the Pt/Ni-Al-O/n-Si structure forms. Schottky emission mechanism has dominated in the HRS, while the LRS shows Poole-Frenkel-like behavior. [ABSTRACT FROM AUTHOR]

The homeodomain transcription factor distal-less homeobox 3 gene (DLX3) is required for hair, tooth and skeletal development. DLX3 mutations have been found to be responsible for Tricho-Dento-Osseous (TDO) syndrome, characterized by kinky hair, thin-pitted enamel and increased bone density. Here we show that the DLX3 mutation (c.533 A>G; Q178R) attenuates osteogenic potential and senescence of bone mesenchymal stem cells (BMSCs) isolated from a TDO patient, providing a molecular explanation for abnormal increased bone density. Both DLX3 mutations (c.533 A>G and c.571_574delGGGG) delayed cellular senescence when they were introduced into pre-osteoblastic cells MC3T3-E1. Furthermore, the attenuated skeletal aging and bone loss in DLX3 (Q178R) transgenic mice not only reconfirmed that DLX3 mutation (Q178R) delayed cellular senescence, but also prevented aging-mediated bone loss. Taken together, these results indicate that DLX3 mutations act as a loss of function in senescence. The delayed senescence of BMSCs leads to increased bone formation by compensating decreased osteogenic potentials with more generations and extended functional lifespan. Our findings in the rare human genetic disease unravel a novel mechanism of DLX3 involving the senescence regulation of bone formation. [ABSTRACT FROM AUTHOR]