5 research outputs found

    Integrable structure of W_3 Conformal Field Theory, Quantum Boussinesq Theory and Boundary Affine Toda Theory

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    In this paper we study the Yang-Baxter integrable structure of Conformal Field Theories with extended conformal symmetry generated by the W_3 algebra. We explicitly construct various T- and Q-operators which act in the irreducible highest weight modules of the W_3 algebra. These operators can be viewed as continuous field theory analogues of the commuting transfer matrices and Q-matrices of the integrable lattice systems associated with the quantum algebra U_q(\hat{sl}(3)). We formulate several conjectures detailing certain analytic characteristics of the Q-operators and propose exact asymptotic expansions of the T- and Q-operators at large values of the spectral parameter. We show, in particular, that the asymptotic expansion of the T-operators generates an infinite set of local integrals of motion of the W_3 CFT which in the classical limit reproduces an infinite set of conserved Hamiltonians associated with the classical Boussinesq equation. We further study the vacuum eigenvalues of the Q-operators (corresponding to the highest weight vector of the W_3 module) and show that they are simply related to the expectation values of the boundary exponential fields in the non-equilibrium boundary affine Toda field theory with zero bulk mass.Comment: LaTeX, 87 pages, 1 figure. Misprints correcte

    Treatment response in Kawasaki disease is associated with sialylation levels of endogenous but not therapeutic intravenous immunoglobulin G.

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    OBJECTIVES: Although intravenous immunoglobulin (IVIG) is highly effective in Kawasaki disease (KD), mechanisms are not understood and 10-20% of patients are treatment-resistant, manifesting a higher rate of coronary artery aneurysms. Murine models suggest that α2-6-linked sialic acid (α2-6Sia) content of IVIG is critical for suppressing inflammation. However, pro-inflammatory states also up-regulate endogenous levels of β-galactoside:α2-6 sialyltransferase-I (ST6Gal-I), the enzyme that catalyzes addition of α2-6Sias to N-glycans. We asked whether IVIG failures correlated with levels of α2-6Sia on infused IVIG or on the patient's own endogenous IgG. METHODS: We quantified levels of α2-6Sia in infused IVIG and endogenous IgG from 10 IVIG-responsive and 10 resistant KD subjects using multiple approaches. Transcript levels of ST6GAL1, in patient whole blood and B cell lines were evaluated by RT-PCR. Plasma soluble (s)ST6Gal-I levels were measured by ELISA. RESULTS: There was no consistent difference in median sialylation levels of infused IVIG between groups. However, α2-6Sia levels in endogenous IgG, ST6GAL1 transcript levels, and ST6Gal-I protein in serum from IVIG-resistant KD subjects were lower than in responsive subjects at both pre-treatment and one-year time points (p <0.001, respectively). CONCLUSIONS: Our data indicate sialylation levels of therapeutic IVIG are unrelated to treatment response in KD. Rather, lower sialylation of endogenous IgG and lower blood levels of ST6GALI mRNA and ST6Gal-I enzyme predict therapy resistance. These differences were stable over time, suggesting a genetic basis. Because IVIG-resistance increases risk of coronary artery aneurysms, our findings have important implications for the identification and treatment of such individuals
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