Motivated by the recent observation and argument on a large half-quantum vortex (HQV) pair connencted by a Kibble wall in superfluid 3 He in nematic aerogels, we numerically study to what extent a huge HQV pair can intrinsically occur with no pinning effect due to the aerogel structure in the polar-distorted B (PdB) phase of superfluid 3 He. By fully examining the impurity-scattering induced pairing vertex, the emergence of Anderson's Theorem in the p-wave superfluid is verified in the two opposite limits, the isotropic and strongly anisotropic limits. Solving numerically the resulting Ginzburg-Landau (GL) free energy in the weak-coupling approximation and by taking account of the Fermi-liquid (FL) corrected gradient terms, the anisotropy dependence of the vortex structure minimizing the free energy is examined. It is found that, close to the transition between the polar and PdB phases, an interplay of the strong anisotropy and the FL correction makes emergence of a large HQV pair in the PdB phase possible, and that, nevertheless, such a large pair easily shrinks deep in the PdB phase, indicating that a pinning effect due to the aerogel structure is necessary in order to keep a large pair size there. The obtained result indicates the validity of the London limit for describing the vortex structure, and a consistency with the picture based on the NMR measurement is discussed.PACS numbers:
Many genes responsible for Malignant mesothelioma (MM) have been identified as tumor suppressor genes and it is difficult to target these genes directly at a molecular level. We searched for the gene which showed synthetic lethal phenotype with LATS2, one of the MM causative genes and one of the kinases in the Hippo pathway. Here we showed that knockdown of SMG6 results in synthetic lethality in LATS2-inactivated cells. We found that this synthetic lethality required the nuclear translocation of YAP1 and TAZ. Both are downstream factors of the Hippo pathway. We also demonstrated that this synthetic lethality did not require SMG6 in nonsense-mediated mRNA decay (NMD) but in regulating telomerase reverse transcriptase (TERT) activity. In addition, the RNA-dependent DNA polymerase (RdDP) activity of TERT was required for this synthetic lethal phenotype. We confirmed the inhibitory effects of LATS2 and SMG6 on cell proliferation in vivo. The result suggests an interaction between the Hippo and TERT signaling pathways. We also propose that SMG6 and TERT are novel molecular target candidates for LATS2-inactivated cancers such as MM.
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