21 research outputs found

    Vortex counting from field theory

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    The vortex partition function in 2d N = (2,2) U(N) gauge theory is derived from the field theoretical point of view by using the moduli matrix approach. The character for the tangent space at each moduli space fixed point is written in terms of the moduli matrix, and then the vortex partition function is obtained by applying the localization formula. We find that dealing with the fermionic zero modes is crucial to obtain the vortex partition function with the anti-fundamental and adjoint matters in addition to the fundamental chiral multiplets. The orbifold vortex partition function is also investigated from the field theoretical point of view.Comment: 21 pages, no figure

    Skp2 expression is associated with high risk and elevated Ki67 expression in gastrointestinal stromal tumours

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    BACKGROUND: Gastrointestinal stromal tumors (GIST) exhibit an unpredictable clinical course and can rapidly progress to lethality. Predictions about the biological behavior of GIST are based on a number of canonical clinical and pathologic parameters whose validity in distinguishing between a benign and a malignant tumour is still imperfect. The aim of our study was to investigate the role of morphologic parameters and expression of cells cycle regulators as prognosticators in GIST. METHODS: We performed an immunohistochemical analysis for Ki67, p27Kip1, Jab1, and Skp2, on a Tissue Microarray (TMA) containing 94 GIST. Expression of the above proteins was correlated to classically used prognosticators, as well as to risk groups. Clinical significance of histologic and immunohistochemical features were evaluated in 59 patients for whom follow-up information was available. RESULTS: Overexpression of Ki67 and Skp2, and p27Kip1 loss directly correlated with the high risk group (p = 0.03 for Ki67 and Skp2, p = 0.05 for p27Kip1). Jab1 expression did not exhibit correlation with risk. In 59 cases provided with clinical follow-up, high cellularity, presence of necrosis, and Ki67 overexpression were predictive of a reduced overall survival in a univariate model. The same parameters, as well as mitotic rate, tumour size, and p27Kip1 loss were indicative of a shortened relapse free survival interval. High cellularity, and high mitotic rate retained their prognostic significance by multivariate analysis. CONCLUSION: Our data suggest that a number of histologic parameters in combination with immunohistochemical expression of cell cycle regulators can facilitate risk categorization and predict biologic behavior in GIST. Importantly this study demonstrates, for the first time, that Skp2 expression correlates with Ki67 expression and high risk in GIST

    Analysis of the masses and decay constants of the heavy-light mesons with QCD sum rules

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    In this article, we calculate the contributions of the vacuum condensates up to dimension-6 including the O(αs){\mathcal {O}}(\alpha _s) corrections to the quark condensates in the operator product expansion, then we study the masses and decay constants of the pseudoscalar, scalar, vector, and axial-vector heavy-light mesons with the QCD sum rules in a systematic way. The masses of the observed mesons (D,D)(D,D^*), (Ds,Ds)(D_s,D_s^*), (D0(2400),D1(2430))(D_0^*(2400),D_1(2430)), (Ds0(2317),Ds1(2460)),(D_{s0}^*(2317),D_{s1}(2460)), (B,B)(B,B^*), (Bs,Bs)(B_s,B_s^*) can be well reproduced, while the predictions for the masses of (B0,B1)(B^*_{0}, B_{1}) and (Bs0,Bs1)(B^*_{s0}, B_{s1}) can be confronted with the experimental data in the future. We obtain the decay constants of the pseudoscalar, scalar, vector, and axial-vector heavy-light mesons, which have many phenomenological applications in studying the semi-leptonic and leptonic decays of the heavy-light mesons

    Mechanism of Inhibition of Enveloped Virus Membrane Fusion by the Antiviral Drug Arbidol

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    The broad-spectrum antiviral arbidol (Arb) inhibits cell entry of enveloped viruses by blocking viral fusion with host cell membrane. To better understand Arb mechanism of action, we investigated its interactions with phospholipids and membrane peptides. We demonstrate that Arb associates with phospholipids in the micromolar range. NMR reveals that Arb interacts with the polar head-group of phospholipid at the membrane interface. Fluorescence studies of interactions between Arb and either tryptophan derivatives or membrane peptides reconstituted into liposomes show that Arb interacts with tryptophan in the micromolar range. Interestingly, apparent binding affinities between lipids and tryptophan residues are comparable with those of Arb IC50 of the hepatitis C virus (HCV) membrane fusion. Since tryptophan residues of membrane proteins are known to bind preferentially at the membrane interface, these data suggest that Arb could increase the strength of virus glycoprotein's interactions with the membrane, due to a dual binding mode involving aromatic residues and phospholipids. The resulting complexation would inhibit the expected viral glycoprotein conformational changes required during the fusion process. Our findings pave the way towards the design of new drugs exhibiting Arb-like interfacial membrane binding properties to inhibit early steps of virus entry, i.e., attractive targets to combat viral infection

    QCD and strongly coupled gauge theories : challenges and perspectives

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    We highlight the progress, current status, and open challenges of QCD-driven physics, in theory and in experiment. We discuss how the strong interaction is intimately connected to a broad sweep of physical problems, in settings ranging from astrophysics and cosmology to strongly coupled, complex systems in particle and condensed-matter physics, as well as to searches for physics beyond the Standard Model. We also discuss how success in describing the strong interaction impacts other fields, and, in turn, how such subjects can impact studies of the strong interaction. In the course of the work we offer a perspective on the many research streams which flow into and out of QCD, as well as a vision for future developments.Peer reviewe
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