RESUMEN
The topic of superconductivity in strongly disordered materials has attracted significant attention. These materials appear to be rather promising for fabrication of various nanoscale devices such as bolometers and transition edge sensors of electromagnetic radiation. The vividly debated subject of intrinsic spatial inhomogeneity responsible for the non-Bardeen-Cooper-Schrieffer relation between the superconducting gap and the pairing potential is crucial both for understanding the fundamental issues of superconductivity in highly disordered superconductors, and for the operation of corresponding nanoelectronic devices. Here we report an experimental study of the electron transport properties of narrow NbN nanowires with effective cross sections of the order of the debated inhomogeneity scales. The temperature dependence of the critical current follows the textbook Ginzburg-Landau prediction for the quasi-one-dimensional superconducting channel I c â¼ (1-T/T c)3/2. We find that conventional models based on the the phase slip mechanism provide reasonable fits for the shape of R(T) transitions. Better agreement with R(T) data can be achieved assuming the existence of short 'weak links' with slightly reduced local critical temperature T c. Hence, one may conclude that an 'exotic' intrinsic electronic inhomogeneity either does not exist in our structures, or, if it does exist, it does not affect their resistive state properties, or does not provide any specific impact distinguishable from conventional weak links.
RESUMEN
Although the Mdm2/p53 interaction has been well documented, it is not clear whether there are new microRNAs participating in this regulatory network. Here, we provide evidence that miR-509-5p, which is downregulated in a subset of newly diagnosed cervical cancer and hepatocellular carcinoma tissues compared with the adjacent nontumor tissue, can be activated by p53 through binding the promoter of miR-509-5p and it suppresses the growth and invasion/migration of cervical cancer and hepatoma cells by regulating apoptosis and the G1/S-phase transition of cell cycle. Furthermore, Mdm2 was identified to be a target of miR-509-5p by targeting its 3'-UTR. Restoration of Mdm2 abrogated the cell phenotypes induced by miR-509-5p. Moreover, ectopic expression of miR-509-5p in HeLa and QGY-7703 cells repressed the expression of Mdm2, subsequently enhancing its p53-activating effects. These results suggest that miR-509-5p is a new regulator of Mdm2/p53 pathway and may play a key role in cancer development.