Stabilizing resistive random access memory by constructing an oxygen reservoir with analyzed state distribution.

In this paper, the instability mechanism of resistive random access memory (RRAM) was investigated, and a technique was developed to stabilize the distribution of high resistance states (HRS) and better concentrate the set voltage. Due to the accumulation of oxygen, an interface-type switching characteristic was observed on the I-V curves beneath the filament-type switching behavior. In this work, the interface-type switching characteristic is used to fit the natural distribution of HRS as an analysis of the instability mechanism. According to the results, the HRS distribution is attributed to the accumulation of excess oxygen ions left from the lower oxygen content and oxygen vacancy recombination during the reset process. The proposed solution with simple plasma treatment, can create an excess oxygen reservoir by changing the surface topography of the electrode to store the surplus oxygen ions from the reset process, eliminating the oxygen accumulation effect and further improving the device stability.

The antileukemia activity of natural product HQ17(3) is possibly associated with downregulation of miR-17-92 cluster.

The compound 10'(Z),13'(E),15'(E)-heptadecatrienylhydroquinone [HQ17(3)] was purified from the sap of the lacquer tree Rhus succedanea. HQ17(3) has cytotoxic effect on cancer cells and can inhibit topoisomerase (topo) IIα activity. We treated various cancer cells with different doses of HQ17(3) and found that leukemia cells were most sensitive to HQ17(3). After analysis of microRNA (miRNA) profiling, we found that treatment with HQ17(3) caused downregulation of miR-17-92 cluster in some leukemia cells. These changes partially restored the normal levels from leukemia-specific miRNA expression signature. Messenger RNAs of tumor suppressor proteins, such as pRB, PTEN, and Dicer, are targets of miR-17-92 cluster. Their protein levels were increased after the treatment. c-Myc is a regulatory protein for miR-17-92 gene. Similar to topo IIα, we found that c-Myc decreased its activity after the HQ17(3) treatment, which may explain the downregulation of miR-17-92 cluster. Combined with 5-fluorouracil, NaAsO2, or ABT-737, HQ17(3) elicited additive inhibitory effects on leukemia cells. In conclusion, the high sensitivity of leukemia cells to HQ17(3) may be associated with the reduction of topo IIα and c-Myc activities, as well as with the downregulation of the miR-17-92 cluster expression.