Dual Identities inside the Gluon and the Graviton Scattering Amplitudes

Recently, Bern, Carrasco and Johansson conjectured dual identities inside the gluon tree scattering amplitudes. In this paper, we use the properties of the heterotic string and open string tree scattering amplitudes to refine and derive these dual identities. These identities can be carried over to loop amplitudes using the unitarity method. Furthermore, given the $M$-gluon (as well as gluon-gluino) tree amplitudes, $M$-graviton (as well as graviton-gravitino) tree scattering amplitudes can be written down immediately, avoiding the derivation of Feynman rules and the evaluation of Feynman diagrams for graviton scattering amplitudes.Comment: 43 pages, 3 figures; typos corrected, a few points clarified

Gluon fusion contribution to W+W- + jet production

We describe the computation of the $gg \to W^+W^-g$ process that contributes to the production of two $W$-bosons and a jet at the CERN Large Hadron Collider (LHC). While formally of next-to-next-to-leading order (NNLO) in QCD, this process can be evaluated separately from the bulk of NNLO QCD corrections because it is finite and gauge-invariant. It is also enhanced by the large gluon flux and by selection cuts employed in the Higgs boson searches in the decay channel $H \to W^+W^-$, as was first pointed out by Binoth {\it et al.} in the context of $gg \to W^+W^-$ production. For cuts employed by the ATLAS collaboration, we find that the gluon fusion contribution to $pp \to W^+W^-j$ enhances the background by about ten percent and can lead to moderate distortions of kinematic distributions which are instrumental for the ongoing Higgs boson searches at the LHC. We also release a public code to compute the NLO QCD corrections to this process, in the form of an add-on to the package {\tt MCFM}.Comment: 13 pages, 4 figures, 3 table

Space-like (vs. time-like) collinear limits in QCD: is factorization violated?

We consider the singular behaviour of QCD scattering amplitudes in kinematical configurations where two or more momenta of the external partons become collinear. At the tree level, this behaviour is known to be controlled by factorization formulae in which the singular collinear factor is universal (process independent). We show that this strict (process-independent) factorization is not valid at one-loop and higher-loop orders in the case of the collinear limit in space-like regions (e.g., collinear radiation from initial-state partons). We introduce a generalized version of all-order collinear factorization, in which the space-like singular factors retain some dependence on the momentum and colour charge of the non-collinear partons. We present explicit results on one-loop and two-loop amplitudes for both the two-parton and multiparton collinear limits. At the level of square amplitudes and, more generally, cross sections in hadron--hadron collisions, the violation of strict collinear factorization has implications on the non-abelian structure of logarithmically-enhanced terms in perturbative calculations (starting from the next-to-next-to-leading order) and on various factorization issues of mass singularities (starting from the next-to-next-to-next-to-leading order).Comment: 81 pages, 5 figures, typos corrected in the text, few comments added and inclusion of NOTE ADDED on recent development

Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.

Caveolin-1 (Cav1) is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori) is a major risk factor for human gastric cancer (GC) where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES) but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS), infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird") compared to AGS cells stably transfected with Cav1 (AGS/Cav1). Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1) to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87) and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1) to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs) in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells

Mammalian Neurogenesis Requires Treacle-Plk1 for Precise Control of Spindle Orientation, Mitotic Progression, and Maintenance of Neural Progenitor Cells

The cerebral cortex is a specialized region of the brain that processes cognitive, motor, somatosensory, auditory, and visual functions. Its characteristic architecture and size is dependent upon the number of neurons generated during embryogenesis and has been postulated to be governed by symmetric versus asymmetric cell divisions, which mediate the balance between progenitor cell maintenance and neuron differentiation, respectively. The mechanistic importance of spindle orientation remains controversial, hence there is considerable interest in understanding how neural progenitor cell mitosis is controlled during neurogenesis. We discovered that Treacle, which is encoded by the Tcof1 gene, is a novel centrosome- and kinetochore-associated protein that is critical for spindle fidelity and mitotic progression. Tcof1/Treacle loss-of-function disrupts spindle orientation and cell cycle progression, which perturbs the maintenance, proliferation, and localization of neural progenitors during cortical neurogenesis. Consistent with this, Tcof1+/− mice exhibit reduced brain size as a consequence of defects in neural progenitor maintenance. We determined that Treacle elicits its effect via a direct interaction with Polo-like kinase1 (Plk1), and furthermore we discovered novel in vivo roles for Plk1 in governing mitotic progression and spindle orientation in the developing mammalian cortex. Increased asymmetric cell division, however, did not promote increased neuronal differentiation. Collectively our research has therefore identified Treacle and Plk1 as novel in vivo regulators of spindle fidelity, mitotic progression, and proliferation in the maintenance and localization of neural progenitor cells. Together, Treacle and Plk1 are critically required for proper cortical neurogenesis, which has important implications in the regulation of mammalian brain size and the pathogenesis of congenital neurodevelopmental disorders such as microcephaly

R^4 counterterm and E7(7) symmetry in maximal supergravity

The coefficient of a potential R^4 counterterm in N=8 supergravity has been shown previously to vanish in an explicit three-loop calculation. The R^4 term respects N=8 supersymmetry; hence this result poses the question of whether another symmetry could be responsible for the cancellation of the three-loop divergence. In this article we investigate possible restrictions from the coset symmetry E7(7)/SU(8), exploring the limits as a single scalar becomes soft, as well as a double-soft scalar limit relation derived recently by Arkani-Hamed et al. We implement these relations for the matrix elements of the R^4 term that occurs in the low-energy expansion of closed-string tree-level amplitudes. We find that the matrix elements of R^4 that we investigated all obey the double-soft scalar limit relation, including certain non-maximally-helicity-violating six-point amplitudes. However, the single-soft limit does not vanish for this latter set of amplitudes, which suggests that the E7(7) symmetry is broken by the R^4 term.Comment: 33 pages, typos corrected, published versio

Synergistic Activation of Cardiac Genes by Myocardin and Tbx5

Myocardial differentiation is associated with the activation and expression of an array of cardiac specific genes. However, the transcriptional networks that control cardiac gene expression are not completely understood. Myocardin is a cardiac and smooth muscle-specific expressed transcriptional coactivator of Serum Response Factor (SRF) and is able to potently activate cardiac and smooth muscle gene expression during development. We hypothesize that myocardin discriminates between cardiac and smooth muscle specific genes by associating with distinct co-factors. Here, we show that myocardin directly interacts with Tbx5, a member of the T-box family of transcription factors involved in the Holt-Oram syndrome. Tbx5 synergizes with myocardin to activate expression of the cardiac specific genes atrial natriuretic factor (ANF) and alpha myosin heavy chain (α-MHC), but not that of smooth muscle specific genes SM22 or smooth muscle myosin heavy chain (SM-MHC). We found that this synergistic activation of shared target genes is dependent on the binding sites for Tbx5, T-box factor-Binding Elements (TBEs). Myocardin and Tbx5 physically interact and their interaction domains were mapped to the basic domain and the coil domain of myocardin and Tbx5, respectively. Our analysis demonstrates that the Tbx5G80R mutation, which leads to the Holt-Oram syndrome in humans, failed to synergize with myocardin to activate cardiac gene expression. These data uncover a key role for Tbx5 and myocardin in establishing the transcriptional foundation for cardiac gene activation and suggest that the interaction of myocardin and Tbx5 maybe involved in cardiac development and diseases