It is feasible and safe to perform PD using the Da Vinci robot-assisted surgical system; patients recovered faster postoperatively with less blood loss during surgery.
We fabricated (Ba,K)Fe 2 As 2 superconducting wires and tapes using the powder-in-tube method and hot isostatic pressing (HIP). HIP wires and tapes showed a high value of transport critical current density (J c ) exceeding 100 kAcm −2 at T=4.2 K and the self-field. Transport J c in the HIP wire reached 38 kAcm −2 in a high magnetic field of 100 kOe. This value is almost twice larger than the previous highest value of J c among round wires using iron-based superconductors. Enhancement of J c in the wires and tapes was caused by improvement of the drawing process, which caused degradation of the core, formation of microcracks, weak links between grains, and random orientation of grains. Details of the effect of the improved fabrication processes on the J c are discussed. Keywords: superconducting wires and tapes, (Ba,K)Fe 2 As 2 , critical current density, powder-intube (PIT), hot isostatic pressing (HIP)
Abstract. In this paper, we systematically study the electron doping effect in a new BiS 2 -based system Sr 1−x La x FBiS 2 (0 ≤ x ≤ 0.7) through multiple techniques of X-ray diffraction, electrical transport, magnetic susceptibility, and Hall effect measurements. The parent compound SrFBiS 2 is found to possess a semiconducting-like ground state, with thermally activation energy E g ∼ 38 meV. By the partial substitution of La for Sr, superconductivity emerges when x > 0.3, reaching its maximal superconducting transition temperature T c ∼ 3.5 K at x = 0.55. In the normal state of superconducting samples, it is clearly seen that there exists a crossover from metallic to semiconducting state below a temperature T min , which shifts to lower temperatures with increasing La content. Based on these measurements, the associated electronic phase diagram of Sr 1−x La x FBiS 2 system has thus been established.
FXYD6, FXYD domain containing ion transport regulator 6, has been reported to affect the activity of Na+/K+-ATPase and be associated with mental diseases. Here, we demonstrate that FXYD6 is up-regulated in hepatocellular carcinoma (HCC) and enhances the migration and proliferation of HCC cells. Up-regulation of FXYD6 not only positively correlates with the increase of Na+/K+-ATPase but also coordinates with the activation of its downstream Src-ERK signaling pathway. More importantly, blocking FXYD6 by its functional antibody significantly inhibits the growth potential of the xenografted HCC tumors in mice, indicating that FXYD6 represents a potential therapeutic target toward HCC. Altogether, our results establish a critical role of FXYD6 in HCC progression and suggest that the therapy targeting FXYD6 can benefit the clinical treatment toward HCC patients.Electronic supplementary materialThe online version of this article (doi:10.1007/s13238-014-0045-0) contains supplementary material, which is available to authorized users.
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