The rectifying properties in dipyrimidinyl-diphenyl co-oligomer diodes with asymmetric anchoring groups were investigated using density functional theory combined with the nonequilibrium Green’s function method. Effects of asymmetric interfaces caused by both the anchoring groups and/or contact geometries of electrodes have been investigated. Our results showed that the rectifying behavior of the co-oligomer diode could be reversed or largely enhanced by adjusting asymmetric anchoring groups. Whether the asymmetric contact geometries play a positive or negative role in improving the rectifying behavior is closely related to each molecular diode. The mechanism of modulation was analyzed in terms of molecular projected self-consistent Hamiltonian states and transmission spectra. The theoretical simulations are helpful for understanding recent experimental results [Lee et al. Langmuir 2009, 25, 1495 and Hihath et al. ACS Nano 2011, 5, 8331]. Moreover, the mechanism of the rectification only due to the electrode asymmetry was explained, and a single-molecule diode with significant rectifying behaviors has been theoretically designed.

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TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell proliferation, migration and invasion. Silencing TMED2 inhibited ovarian cancer growth in mice. Silencing TMED2 inhibited IGF2/IGF1R/PI3K/Akt pathway. In agreement, ectopically expressed TMED2 activated IGF2/IGF1R/PI3K/Akt pathway. Mechanistic study revealed that TMED2 directly binds to AKT2, thereby facilitating its phosphorylation. We also found that TMED2 increased IGF1R expression by competing for miR-30a. Thus, TMED2 is oncogenic and a potential target for epithelial ovarian cancer therapy.

Roflumilast enhanced DDP sensitivity and reversed the DDP resistance of ovarian cancer cells via activation of cAMP/PKA/CREB pathway and upregulation of the downstream FtMt expression, which has great promise in clinical treatment.