Critical Temperature in Bulk Ultrafine-Grained Superconductors of Nb, V, and Ta Processed by High-Pressure Torsion

This overview describes the progressive results of the superconducting critical temperature in bulk nanostructured metals (niobium, vanadium and tantalum) processed by high-pressure torsion (HPT). Bulk nanostructured superconductors provide a new route to control superconducting property, because ultrafine-grain structures with a high density of grain boundaries, dislocations, and other crystalline defects modify the superconducting order parameter. The critical temperature Tc in Nb increases with the evolution of grain refinement owing to the quantum confinement of electrons in ultrafine grains. In V and Ta, however, Tc decreases at a certain HPT revolution number (i.e. at certain strain levels). The different behaviour of Tc in the three materials is explained by the competition effect between the quantum size effect and disorder effect; these effects are characterized by the parameters of grain size, electron mean free path, and superconducting coherence length

Critical Temperature in Bulk Ultrafine-Grained Superconductors of Nb, V, and Ta Processed by High-Pressure Torsion

This overview describes the progressive results of the superconducting critical temperature in bulk nanostructured metals (niobium, vanadium and tantalum) processed by high-pressure torsion (HPT). Bulk nanostructured superconductors provide a new route to control superconducting property, because ultrafine-grain structures with a high density of grain boundaries, dislocations, and other crystalline defects modify the superconducting order parameter. The critical temperature Tc in Nb increases with the evolution of grain refinement owing to the quantum confinement of electrons in ultrafine grains. In V and Ta, however, Tc decreases at a certain HPT revolution number (i.e. at certain strain levels). The different behaviour of Tc in the three materials is explained by the competition effect between the quantum size effect and disorder effect; these effects are characterized by the parameters of grain size, electron mean free path, and superconducting coherence length

Copper-transporting P-Type ATPase, ATP7A, confers multidrug resistance and its expression is related to resistance to SN-38 in clinical colon cancer

We and others have shown that the copper transporters ATP7A and ATP7B play a role in cellular resistance to cisdiaminedichloroplatinum (II) (CDDP).&nbsp; In this study, we found that ATP7A transfection of Chinese hamster ovary&nbsp; cells (CHOK1) and fibroblasts isolated from Menkes disease patients&nbsp; enhanced resistance not only to CDDP but also to various anticancer drugs, such as vincristine, paclitaxel, 7-ethyl-10- hydroxy-camptothecin (SN-38),&nbsp; etoposide, doxorubicin, mitoxantron, and 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11). ATP7A preferentially localizeddoxorubicin fluorescence to the Golgi apparatus in contrast to the more intense nuclear staining of doxorubicin in the parental cells. Brefeldin A&nbsp;&nbsp; partially and monensin completely altered the distribution of doxorubicin to the nuclei in the ATP7A-expressing cells. ATP7A expression also enhanced the efflux rates of doxorubicin and SN-38 from cells and increased the uptake of SN-38 in membrane vesicles. These findings strongly suggested that&nbsp;&nbsp; ATP7A confers multidrug resistance to the cells by compartmentalizing drugs in the Golgi apparatus and by enhancing efflux of these drugs, and the trans-Golgi network has an important role of ATP7A-related drug resistance. ATP7A was expressed in 8 of 34 (23.5%) clinical colon cancer specimens but not in the adjacent normal epithelium. Using the histoculture drug response assay that is useful for the prediction of drug sensitivity of clinical cancers, ATP7A-expressing colon cancer cells were significantly more&nbsp; resistant to SN-38 than ATP7Anegative cells. Thus, ATP7A confers&nbsp; resistance to various anticancer agents on cancer cells and might be a good index of drug resistance in clinical colon cancers.<br /