Superfluid density in the slave-boson theory

Despite of the success of the slave-boson theory in capturing qualitative physics of high-temperature superconductors like cuprates, it fails to reproduce the correct temperature-dependent behavior of superfluid density, let alone the independence of the linear temperature term on doping in the underdoped regimes of hole-doped cuprate, a common experimental observation in different cuprates. It remains puzzling up to now in spite of intensive theoretical efforts. For electron-doped case, even qualitative treatment is not reported at present time. Here we revisit these problems and provide an alternative superfluid density formulation by using the London relation instead of employing the paramagnetic current-current correlation function. The obtained formula, on the one hand, provides the correct temperature-dependent behavior of the superfluid density in the whole temperature regime, on the other hand, makes the doping dependence of the linear temperature term substantially weaken and a possible interpretation for its independence on doping is proposed. As an application, electron-doped cuprate is studied, whose result qualitatively agrees with existing experiments and successfully explains the origin of $d$- to anisotropic $s$-wave transition across the optimal doping. Our result remedies some failures of the slave-boson theory as employed to calculate superfluid density in cuprates and may be useful in the understanding of the related physics in other strongly correlated systems, e.g. Na$_{x}$CoO$_{2}$$\cdot$yH$_{2}$O and certain iron-based superconductors with dominating local magnetic exchange interaction.Comment: 7 pages, 4 figure

LARP7 suppresses P-TEFb activity to inhibit breast cancer progression and metastasis.

Transcriptional elongation by RNA polymerase (Pol) II is essential for gene expression during cell growth and differentiation. The positive transcription elongation factor b (P-TEFb) stimulates transcriptional elongation by phosphorylating Pol II and antagonizing negative elongation factors. A reservoir of P-TEFb is sequestered in the inactive 7SK snRNP where 7SK snRNA and the La-related protein LARP7 are required for the integrity of this complex. Here, we show that P-TEFb activity is important for the epithelial-mesenchymal transition (EMT) and breast cancer progression. Decreased levels of LARP7 and 7SK snRNA redistribute P-TEFb to the transcriptionally active super elongation complex, resulting in P-TEFb activation and increased transcription of EMT transcription factors, including Slug, FOXC2, ZEB2, and Twist1, to promote breast cancer EMT, invasion, and metastasis. Our data provide the first demonstration that the transcription elongation machinery plays a key role in promoting breast cancer progression by directly controlling the expression of upstream EMT regulators