Oxidation of layered P3-Na0.6(Li0.2Mn0.8)O2 by electrochemical removal of Na+ introduces holes into the O-2p bands at 4.2 V, but the voltage plateau fades on cycling.
Recent studies have emphasized causative links between aberrant microRNA expression patterns and cancer progression. miR-183 is dysregulated in certain types of human cancers. The expression pattern, clinical significance, and biological role of miR-183 in osteosarcoma, however, remain largely undefined. In this paired analysis, we found that miR-183 was markedly down-regulated in osteosarcoma cells and tissues compared with matching normal bone tissues using RT-qPCR. Statistical analyses revealed that the expression levels of miR-183 significantly correlated with lung metastasis as well as with local recurrence of osteosarcoma. miR-183 expression was inversely correlated with Ezrin mRNA and protein expression levels in osteosarcoma cells as well as in a subset of primary osteosarcoma. Ectopically expressed miR-183 inhibited migratory and invasive abilities of osteosarcoma cells, whereas knockdown of endogenous miR-183 significantly enhanced these abilities. Using a luciferase reporter carrying the 3'-untranslated region (3'-UTR) of Ezrin, we identified Ezrin as a direct target of miR-183. Moreover, ectopic expression of Ezrin could significantly rescue miR-183-suppressed migration and invasion. Of interest, suppression of Ezrin by miR-183 caused a reduction of phosphorylated p44/42 (p-p44/42). Finally, suppression of Ezrin by RNAi mimicked miR-183 action in the suppression of migration and invasion, which was associated with down-regulation of p-p44/42. Taken together, these results suggest that as a tumor suppressor miRNA, miR-183 plays an important role in the aggressiveness of osteosarcoma.
In conclusion, we have demonstrated a hybrid-memory device where information can be introduced optically and can be extracted or erased electrically. We expect much improved performance, in terms of retention, stability, and operating voltages upon introducing intentional electron-trapping centers in dilute proportions in the semiconducting-polymer matrix, along with optimization of geometrical parameters. ExperimentalThe top-contact geometry, as shown in Figure 1a, was used to fabricate the polymer field-effect transistor devices based on poly(3-hexylthiophene) (P3HT) [7]. Regioregular P3HT was obtained from Aldrich Inc., and was re-purified using standard procedures (re-precipitation method). Our samples and devices were handled in a glove box (MBraun, Inc.), and stringent procedures were observed to ensure the quality of the devices. A transparent water-soluble dielectric (polyvinyl alcohol, e » 8) layer with a thickness of 0.5 lm was spincoated on top of an aluminum-coated glass substrate. The dielectric surface was then treated using standard established procedures using hexamethyldisilazane. A layer of regioregular P3HT (thickness » 150 nm) was spin-coated (1500 rpm) from chloroform solution on the insulator under an inert atmosphere, followed by a thermal treatment under vacuum at 60 C for 24 h. The drain and source electrodes with a separation of 25±40 lm (L) and width of 2 mm (W) were deposited by thermal evaporation of gold using a shadow mask. All the experiments were performed under vacuum (10 ±1 Pa).
Background:Recent studies have reported miR-145 dysregulated in colorectal cancer (CRC). In this study, miR-145 profiles were compared between CRC and corresponding non-tumour tissues.Methods:The expression levels of miR-145 were analysed in CRC cell lines and tumour tissues by real-time PCR. A luciferase reporter assay confirmed direct targets. The functional effects of miR-145 were examined in transfected CRC cells in vitro and in vivo using established assays.Results:Downregulation of miR-145 was detected in most primary CRC tumours, and was significantly correlated with a more aggressive phenotype of CRC in patients. In CRC cell lines, ectopic overexpression of miR-145 inhibited cell proliferation, motility and invasion in vitro. Stable overexpression of miR-145 suppressed tumour growth and pulmonary metastasis in vivo. Further studies indicated that miR-145 may directly interact with the 3′-untranslated region (3′-UTR) of Fascin-1 messenger RNA (mRNA), downregulating its mRNA and protein expression levels. In clinical specimens, Fascin-1 expression was negatively correlated with miR-145 expression.Conclusions:MiR-145 has a critical role in the inhibition of invasive and metastatic capacities of CRC, probably through directly targeting Fascin-1. This miRNA may be involved in the development and progression of CRC.
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