3,048 research outputs found

    Diffractive meson production from virtual photons with odd charge-parity exchange

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    We calculate the cross section of diffractive charge-parity C=+1 neutral meson production in virtual photon proton collision at high energies. Due to the opposite C-parities of photon and meson M (M = eta_C, pi^0, a_2) this process probes the t-channel C=-1 odderon exchange which is described here as noninteracting three-gluon exchange. Estimates for the cross section of the inelastic diffractive process gamma^* p -> eta_C X_p are presented. The total cross section of diffractive \eta_C meson photoproduction is found to be 47 pb. The cross sections for the diffractive production of light mesons (pi^0, a_2) in \gamma^* p collisions are of the same order if the photon virtuality Q^2 is m^2_C.Comment: LaTeX, 19 pages, 8 ps-figs, epsfi

    Effective Action for High-Energy Scattering in Gravity

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    The multi-Regge effective action is derived directly from the linearized gravity action. After excluding the redundant field components we separate the fields into momentum modes and integrate over modes which correspond neither to the kinematics of scattering nor to the one of exchanged particles. The effective vertices of scattering and of particle production are obtained as sums of the contributions from the triple and quartic interaction terms and the fields in the effective action are defined in terms of the two physical components of the metric fluctuation.Comment: 15 pages, LATE

    Factorization of R-matrix and Baxter's Q-operator

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    The general rational solution of the Yang-Baxter equation with the symmetry algebra sl(2) can be represented as the product of the simpler building blocks denoted as R-operators. The R-operators are constructed explicitly and have simple structure. Using the R-operators we construct the two-parametric Baxter's Q-operator for the generic inhomogeneous periodic XXX spin chain. In the case of homogeneous XXX spin chain it is possible to reduce the general Q-operator to the much simpler one-parametric operator.Comment: 17 page

    Dissociative recombination and electron-impact de-excitation in CH photon emission under ITER divertor-relevant plasma conditions

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    For understanding carbon erosion and redeposition in nuclear fusion devices, it is important to understand the transport and chemical break-up of hydrocarbon molecules in edge plasmas, often diagnosed by emission of the CH A^2\Delta - X^2\Pi Ger\"o band around 430 nm. The CH A-level can be excited either by electron-impact or by dissociative recombination (D.R.) of hydrocarbon ions. These processes were included in the 3D Monte Carlo impurity transport code ERO. A series of methane injection experiments was performed in the high-density, low-temperature linear plasma generator Pilot-PSI, and simulated emission intensity profiles were benchmarked against these experiments. It was confirmed that excitation by D.R. dominates at T_e < 1.5 eV. The results indicate that the fraction of D.R. events that lead to a CH radical in the A-level and consequent photon emission is at least 10%. Additionally, quenching of the excited CH radicals by electron impact de-excitation was included in the modeling. This quenching is shown to be significant: depending on the electron density, it reduces the effective CH emission by a factor of 1.4 at n_e=1.3*10^20 m^-3, to 2.8 at n_e=9.3*10^20 m^-3. Its inclusion significantly improved agreement between experiment and modeling

    Symmetry Properties of the Effective Action for High-Energy Scattering in QCD

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    We study the effective action describing high-energy scattering processes in the multi-Regge limit of QCD, which should provide the starting point for a new attempt to overcome the limitations of the leading logarithmic and the eikonal approximations. The action can be obtained via simple graphical rules or by integrating in the QCD functional integral over momentum modes of gluon and quark fields that do not appear explicitely as scattering or exchanged particles in the considered processes. The supersymmetry is used to obtain the terms in the action involving quarks fields from the pure gluonic ones. We observe a Weizs\"acker - Williams type relations between terms describing scattering and production of particles.Comment: 37 pages LATEX, 1 Table and 7 figures using package FEYNMA

    Behavior of tumors under nonstationary theraphy

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    We present a model for the interaction dynamics of lymphocytes-tumor cells population. This model reproduces all known states for the tumor. Futherly,we develop it taking into account periodical immunotheraphy treatment with cytokines alone. A detailed analysis for the evolution of tumor cells as a function of frecuency and theraphy burden applied for the periodical treatment is carried out. Certain threshold values for the frecuency and applied doses are derived from this analysis. So it seems possible to control and reduce the growth of the tumor. Also, constant values for cytokines doses seems to be a succesful treatment.Comment: 6 pages, 7 figure

    The BFKL Pomeron in 2+1 Dimensional QCD

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    We investigate the high-energy scattering in the spontaneously broken Yang - Mills gauge theory in 2+1 space--time dimensions and present the exact solution of the leading lns\ln s BFKL equation. The solution is constructed in terms of special functions using the earlier results of two of us (L.N.L. and L.S.). The analytic properties of the tt-channel partial wave as functions of the angular momentum and momentum transfer have been studied. We find in the angular momentum plane: (i) a Regge pole whose trajectory has an intercept larger than 1 and (ii) a fixed cut with the rightmost singularity located at j=1j=1. The massive Yang - Mills theory can be considered as a theoretical model for the (non-perturbative) Pomeron. We study the main structure and property of the solution including the Pomeron trajectory at momentum transfer different from zero. The relation to the results of M. Li and C-I. Tan for the massless case is discussed.Comment: 28 pages LATEX, 3 EPS figures include

    Self-renewal of single mouse hematopoietic stem cells is reduced by JAK2V617F without compromising progenitor cell expansion

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    Recent descriptions of significant heterogeneity in normal stem cells and cancers have altered our understanding of tumorigenesis, emphasizing the need to understand how single stem cells are subverted to cause tumors. Human myeloproliferative neoplasms (MPNs) are thought to reflect transformation of a hematopoietic stem cell (HSC) and the majority harbor an acquired V617F mutation in the JAK2 tyrosine kinase, making them a paradigm for studying the early stages of tumor establishment and progression. The consequences of activating tyrosine kinase mutations for stem and progenitor cell behavior are unclear. In this article, we identify a distinct cellular mechanism operative in stem cells. By using conditional knock-in mice, we show that the HSC defect resulting from expression of heterozygous human JAK2V617F is both quantitative (reduced HSC numbers) and qualitative (lineage biases and reduced self-renewal per HSC). The defect is intrinsic to individual HSCs and their progeny are skewed toward proliferation and differentiation as evidenced by single cell and transplantation assays. Aged JAK2V617F show a more pronounced defect as assessed by transplantation, but mice that transform reacquire competitive self-renewal ability. Quantitative analysis of HSC-derived clones was used to model the fate choices of normal and JAK2-mutant HSCs and indicates that JAK2V617F reduces self-renewal of individual HSCs but leaves progenitor expansion intact. This conclusion is supported by paired daughter cell analyses, which indicate that JAK2-mutant HSCs more often give rise to two differentiated daughter cells. Together these data suggest that acquisition of JAK2V617F alone is insufficient for clonal expansion and disease progression and causes eventual HSC exhaustion. Moreover, our results show that clonal expansion of progenitor cells provides a window in which collaborating mutations can accumulate to drive disease progression. Characterizing the mechanism(s) of JAK2V617F subclinical clonal expansions and the transition to overt MPNs will illuminate the earliest stages of tumor establishment and subclone competition, fundamentally shifting the way we treat and manage cancers
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