Electron Spectra in the Ionization of Atoms by Neutrinos

For neutrinos of O(10keV) energies, their oscillation lengths are less than a few hundred meters, thereby suggesting the fascinating idea of oscillation experiments of small geometrical size. To help evaluating this idea we calculate the ionization cross sections of H, He, Ne and Xe, using any neutrino flavor, in the few keV energy range. We find that the atomic ionization cross sections per electron are always smaller than the neutrino cross sections off free electrons, approaching it from below as the energy increases to the 100 keV region. At the 10-20 keV range though, atomic binding effects are very important, particularly for the heavier atoms, inducing a factor of two reduction of the Xe ionization cross section, compared to the free electron one.Comment: Typos corrected. Version appeared in Phys. Rev. D70:113008 (2004

Requirement for PRC1 subunit BMI1 in host gene activation by Epstein-Barr virus potein EBNA3C

Epstein–Barr virus proteins EBNA3A, EBNA3B and EBNA3C control hundreds of host genes after infection. Changes in epigenetic marks around EBNA3-regulated genes suggest that they exert transcriptional control in collaboration with epigenetic factors. The roles of polycomb repressive complex (PRC)2 subunit SUZ12 and of PRC1 subunit BMI1 were assessed for their importance in EBNA3-mediated repression and activation. ChIP-seq experiments for SUZ12 and BMI1 were performed to determine their global localization on chromatin and analysis offered further insight into polycomb protein distribution in differentiated cells. Their localization was compared to that of each EBNA3 to resolve longstanding questions about the EBNA3–polycomb relationship. SUZ12 did not co-localize with any EBNA3, whereas EBNA3C co-localized significantly and co-immunoprecipitated with BMI1. In cells expressing a conditional EBNA3C, BMI1 was sequestered to EBNA3C-binding sites after EBNA3C activation. When SUZ12 or BMI1 was knocked down in the same cells, SUZ12 did not contribute to EBNA3C-mediated regulation. Surprisingly, after BMI1 knockdown, EBNA3C repressed equally efficiently but host gene activation by EBNA3C was impaired. This overturns previous assumptions about BMI1/PRC1 functions during EBNA3C-mediated regulation, for the first time identifies directly a host factor involved in EBNA3-mediated activation and provides a new insight into how PRC1 can be involved in gene activation

Analyzing epsilon'/epsilon in the 1/N_c Expansion

We present a recent analysis of epsilon'/epsilon in the 1/N_c expansion. We show that the 1/N_c corrections to the matrix element of Q_6 are large and positive, indicating a Delta I=1/2 enhancement similar to the one of Q_1 and Q_2 which dominate the CP conserving amplitude. This enhances the CP ratio and can bring the standard model prediction close to the measured value for central values of the parameters.Comment: One reference corrected. 5 pages, talk presented by P.H. Soldan at the 3. International Conference on B Physics and CP Violation, Taipei, Taiwan, December 3 - 7, 1999. Slightly expanded version of the article submitted to the proceeding

Coherent Pion Production by Neutrinos

I concentrate in this article on the reaction--coherent pion production by neutrinos incident on nuclei. A special effort is made in order to describe the approximations entering the calculation. I conclude that the reaction is well understood and with appropriate data for hadronic reactions is can be computed for low and high energies. Because of shortage of space I omitted the resonance analysis, which is described in articles with my collaborators.Comment: 4 pages. Proceedings of Conf. to be published by APS-Proceeding

Resonance production by neutrinos: I. J=3/2 Resonances

The article contains general formulas for the production of J=3/2 resonances by neutrinos and antineutrinos. It specializes to the P_{33}(1232) resonance whose form factors are determined by theory and experiment and then are compared with experimental results at low and high energies. It is shown that the minimum in the low Q^2 region is a consequence of a combined effect from the vanishing of the vector form factors, the muon mass and Pauli blocking. Several improvements for the future investigations are suggested.Comment: 10 pages, LaTeX, misprints corrected, 1 reference adde

Transport study of charged current interactions in neutrino-nucleus reactions

Within a dynamical transport approach we investigate charged current interactions in neutrino-nucleus reactions for neutrino energies of 0.3 - 1.5 GeV with particular emphasis on resonant pion production channels via the $\Delta_{33}(1232)$ resonance. The final-state-interactions of the resonance as well as of the emitted pions are calculated explicitly for $^{12}C$ and $^{56}Fe$ nuclei and show a dominance of pion suppression at moderate momenta $p_\pi >$ 0.2 GeV/c. A comparison to integrated $\pi^+$ spectra for $\nu_\mu + ^{12}C$ reactions with the available (preliminary) data demonstrates a reasonable agreement.Comment: 13 pages incl. 6 eps-figures; computational error in final state interactions corrected; to be published in Phys. Lett.

On the probabilistic min spanning tree Problem

We study a probabilistic optimization model for min spanning tree, where any vertex vi of the input-graph G(V,E) has some presence probability pi in the final instance G′ ⊂ G that will effectively be optimized. Suppose that when this “real” instance G′ becomes known, a spanning tree T, called anticipatory or a priori spanning tree, has already been computed in G and one can run a quick algorithm (quicker than one that recomputes from scratch), called modification strategy, that modifies the anticipatory tree T in order to fit G ′. The goal is to compute an anticipatory spanning tree of G such that, its modification for any G ′ ⊆ G is optimal for G ′. This is what we call probabilistic min spanning tree problem. In this paper we study complexity and approximation of probabilistic min spanning tree in complete graphs under two distinct modification strategies leading to different complexity results for the problem. For the first of the strategies developed, we also study two natural subproblems of probabilistic min spanning tree, namely, the probabilistic metric min spanning tree and the probabilistic min spanning tree 1,2 that deal with metric complete graphs and complete graphs with edge-weights either 1, or 2, respectively

Epstein-Barr virus nuclear protein EBNA3C directly induces expression of AID and somatic mutations in B cells

Activation-induced cytidine deaminase (AID), the enzyme responsible for induction of sequence variation in immunoglobulins (Igs) during the process of somatic hypermutation (SHM) and also Ig class switching, can have a potent mutator phenotype in the development of lymphoma. Using various Epstein-Barr virus (EBV) recombinants, we provide definitive evidence that the viral nuclear protein EBNA3C is essential in EBV-infected primary B cells for the induction of AID mRNA and protein. Using lymphoblastoid cell lines (LCLs) established with EBV recombinants conditional for EBNA3C function, this was confirmed, and it was shown that transactivation of the AID gene (AICDA) is associated with EBNA3C binding to highly conserved regulatory elements located proximal to and upstream of the AICDA transcription start site. EBNA3C binding initiated epigenetic changes to chromatin at specific sites across the AICDA locus. Deep sequencing of cDNA corresponding to the IgH V-D-J region from the conditional LCL was used to formally show that SHM is activated by functional EBNA3C and induction of AID. These data, showing the direct targeting and induction of functional AID by EBNA3C, suggest a novel role for EBV in the etiology of B cell cancers, including endemic Burkitt lymphoma