1,419 research outputs found

    Little String Amplitudes (and the Unreasonable Effectiveness of 6D SYM)

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    We study tree level scattering amplitudes of four massless states in the double scaled little string theory, and compare them to perturbative loop amplitudes in six-dimensional super-Yang-Mills theory. The little string amplitudes are computed from correlators in the cigar coset CFT and in N=2 minimal models. The results are expressed in terms of integrals of conformal blocks and evaluated numerically in the alpha' expansion. We find striking agreements with up to 2-loop scattering amplitudes of massless gluons in 6D SU(k) SYM at a Z_k invariant point on the Coulomb branch. We comment on the issue of UV divergence at higher loop orders in the gauge theory and discuss the implication of our results.Comment: 58 pages, 5 figures, 3 tables, comments added, references adde

    Topological Defect Lines and Renormalization Group Flows in Two Dimensions

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    We consider topological defect lines (TDLs) in two-dimensional conformal field theories. Generalizing and encompassing both global symmetries and Verlinde lines, TDLs together with their attached defect operators provide models of fusion categories without braiding. We study the crossing relations of TDLs, discuss their relation to the 't Hooft anomaly, and use them to constrain renormalization group flows to either conformal critical points or topological quantum field theories (TQFTs). We show that if certain non-invertible TDLs are preserved along a RG flow, then the vacuum cannot be a non-degenerate gapped state. For various massive flows, we determine the infrared TQFTs completely from the consideration of TDLs together with modular invariance.Comment: 101 pages, 63 figures, 2 tables; v3: minor changes, added footnotes and references, published versio

    Deformations with maximal supersymmetries part 2: off-shell formulation

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    Continuing our exploration of maximally supersymmetric gauge theories (MSYM) deformed by higher dimensional operators, in this paper we consider an off-shell approach based on pure spinor superspace and focus on constructing supersymmetric deformations beyond the first order. In particular, we give a construction of the Batalin-Vilkovisky action of an all-order non-Abelian Born-Infeld deformation of MSYM in the non-minimal pure spinor formalism. We also discuss subtleties in the integration over the pure spinor superspace and the relevance of Berkovits-Nekrasov regularization.Kavli Institute for Theoretical Physics (Graduate Fellowship)Alfred P. Sloan Foundation. FellowshipSimons Foundation (Simons Investigator Award)National Science Foundation (U.S.) (Award PHY-0847457

    CCN2 Enhances Resistance to Cisplatin-Mediating Cell Apoptosis in Human Osteosarcoma

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    Osteosarcoma (OS) is the most common form of malignant bone tumor and is an aggressive malignant neoplasm exhibiting osteoblastic differentiation. Cisplatin is one of the most efficacious antitumor drugs for osteosarcoma patients. However, treatment failures are common due to the development of chemoresistance. CCN2 (also known as CTGF), is a secreted protein that binds to integrins, modulates the invasive behavior of certain human cancer cells. However, the effect of CCN2 in cisplatin-mediated chemotherapy is still unknown. Here, we found that CCN2 was upregulated in human osteosarcoma cells after treatment with cisplatin. Moreover, overexpression of CCN2 increased the resistance to cisplatin-mediated cell apoptosis. In contrast, reduction of CCN2 by CCN2 shRNA promoted the chemotherapeutic effect of cisplatin. We also found that CCN2 provided resistance to cisplatin-induced apoptosis through upregulation of Bcl-xL and survivin. Knockdown of Bcl-xL or survivin removed the CCN2-mediated resistance to apoptosis induced by cisplatin. On the other hand, CCN2 also promoted FAK, MEK, and ERK survival signaling pathways to enhance tumor survival during cisplatin treatment. In a mouse xenograft model, overexpression of CCN2 promoted resistance to cisplatin. However, knockdown of CCN2 increased the therapeutic effect of cisplatin. Therefore, our data suggest that CCN2 might be a critical oncogene of human osteosarcoma for cisplatin-resistance and supported osteosarcoma cell growth in vivo and in vitro
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