We study the classical spectrum of string theory on AdS 5 × S 5 in the Hofman-Maldacena limit. We find a family of classical solutions corresponding to Giant Magnons with two independent angular momenta on S 5 . These solutions are related via Pohlmeyer's reduction procedure to the charged solitons of the Complex sine-Gordon equation. The corresponding string states are dual to BPS boundstates of many magnons in the spin-chain description of planar N = 4 SUSY Yang-Mills.The exact dispersion relation for these states is obtained from a purely classical calculation in string theory.

We prove a duality, recently conjectured in arXiv:1103.5726, which relates the F-terms of supersymmetric gauge theories defined in two and four dimensions respectively. The proof proceeds by a saddle point analysis of the four-dimensional partition function in the Nekrasov-Shatashvili limit. At special quantized values of the Coulomb branch moduli, the saddle point condition becomes the Bethe Ansatz Equation of the SL(2) Heisenberg spin chain which coincides with the F-term equation of the dual two-dimensional theory. The on-shell values of the superpotential in the two theories are shown to coincide in corresponding vacua. We also identify two-dimensional duals for a large set of quiver gauge theories in four dimensions and generalize our proof to these cases.

We study the scattering of magnon boundstates in the spin-chain description of planar N = 4 SUSY Yang-Mills. Starting from the conjectured exact S-matrix for magnons in the SU (2) sector, we calculate the corresponding S-matrix for boundstates with an arbitrary number of constituent magnons. The resulting expression has an interesting analytic structure with both simple and double poles. We also calculate the semiclassical S-matrix for the scattering of the corresponding excitations on the string worldsheet known as Dyonic Giant Magnons. We find precise agreement with the magnon boundstate S-matrix in the limit of large 't Hooft coupling.

The contribution of long noncoding RNAs (lncRNAs) to pancreatic cancer progression and the regulatory mechanisms of their expression are attractive areas. In the present study, the overexpression of lncRNA-BX111887 (BX111) in pancreatic cancer tissues was detected by microarray and further validated in a cohort of pancreatic cancer tissues. We further demonstrated that knockdown or overexpression of BX111 dramatically repressed or enhanced proliferation and invasion of pancreatic cancer cells. Mechanically, BX111 activated transcription of ZEB1, a key regulator for epithelia-mesenchymal transition (EMT), via recruiting transcriptional factor Y-box protein (YB1) to its promoter region. Moreover, we revealed that BX111 transcription was induced by hypoxia-inducible factor (HIF-1α) in response to hypoxia. In addition, BX111 contributed to the hypoxia-induced EMT of pancreatic cells by regulating expression of ZEB1 and its downstream proteins E-cadherin and MMP2. Coincidence with in vitro results, BX111 depletion effectively inhibited growth and metastasis of xenograft tumor in vivo. The clinical samples of pancreatic cancer further confirmed a positive association between BX111 and ZEB1. Moreover, high BX111 expression was correlated with late TNM stage, lymphatic invasion and distant metastasis, as well as short overall survival time in patients. Taken together, our findings implicate a hypoxia-induced lncRNA contributes to metastasis and progression of pancreatic cancer, and suggest BX111 might be applied as a potential biomarker and therapeutic target for pancreatic cancer.