34 research outputs found

    Bloom-Gilman duality of inelastic structure functions in nucleon and nuclei

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    The Bloom-Gilman local duality of the inelastic structure function of the proton, the deuteron and light complex nuclei is investigated using available experimental data in the squared four-momentum transfer range from 0.3 to 5 (GeV/c)**2. The results of our analysis suggest that the onset of the Bloom-Gilman local duality is anticipated in complex nuclei with respect to the case of the protonand the deuteron. A possible interpretation of this result in terms of a rescaling effect is discussed with particular emphasis to the possibility of reproducing the damping of the nucleon-resonance transitions observed in recent electroproduction data off nuclei.Comment: revised version, to appear in Physical Review

    Measurement of the Neutron Spin Structure Function g1ng_1^n with a Polarized ^3He Target

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    Results are reported from the HERMES experiment at HERA on a measurement of the neutron spin structure function g1n(x,Q2)g_1^n(x,Q^2) in deep inelastic scattering using 27.5 GeV longitudinally polarized positrons incident on a polarized 3^3He internal gas target. The data cover the kinematic range 0.023<x<0.60.023<x<0.6 and 1(GeV/c)2<Q2<15(GeV/c)21 (GeV/c)^2 < Q^2 <15 (GeV/c)^2. The integral 0.0230.6g1n(x)dx\int_{0.023}^{0.6} g_1^n(x) dx evaluated at a fixed Q2Q^2 of 2.5(GeV/c)22.5 (GeV/c)^2 is 0.034±0.013(stat.)±0.005(syst.)-0.034\pm 0.013(stat.)\pm 0.005(syst.). Assuming Regge behavior at low xx, the first moment Γ1n=01g1n(x)dx\Gamma_1^n=\int_0^1 g_1^n(x) dx is 0.037±0.013(stat.)±0.005(syst.)±0.006(extrapol.)-0.037\pm 0.013(stat.)\pm 0.005(syst.)\pm 0.006(extrapol.).Comment: 4 pages TEX, text available at http://www.krl.caltech.edu/preprints/OAP.htm

    Flavor Decomposition of the Polarized Quark Distributions in the Nucleon from Inclusive and Semi-inclusive Deep-inelastic Scattering

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    Spin asymmetries of semi-inclusive cross sections for the production of positively and negatively charged hadrons have been measured in deep-inelastic scattering of polarized positrons on polarized hydrogen and 3He targets, in the kinematic range 0.023<x<0.6 and 1 GeV^2<Q^2<10 GeV^2. Polarized quark distributions are extracted as a function of x for up $(u+u_bar) and down (d+d_bar) flavors. The up quark polarization is positive and the down quark polarization is negative in the measured range. The polarization of the sea is compatible with zero. The first moments of the polarized quark distributions are presented. The isospin non-singlet combination Delta_q_3 is consistent with the prediction based on the Bjorken sum rule. The moments of the polarized quark distributions are compared to predictions based on SU(3)_f flavor symmetry and to a prediction from lattice QCD.Comment: 14 pages, 6 figures (eps format), 10 tables in Latex New version contains tables of asymmetries and correlation matri

    Vesicular Stomatitis Virus Infection Promotes Immune Evasion by Preventing NKG2D-Ligand Surface Expression

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    Vesicular stomatitis virus (VSV) has recently gained attention for its oncolytic ability in cancer treatment. Initially, we hypothesized that VSV infection could increase immune recognition of cancer cells through induction of the immune stimulatory NKG2D-ligands. Here we show that VSV infection leads to a robust induction of MICA mRNA expression, however the subsequent surface expression is potently hindered. Thus, VSV lines up with human cytomegalovirus (HCMV) and adenovirus, which actively subvert the immune system by negatively affecting NKG2D-ligand surface expression. VSV infection caused an active suppression of NKG2D-ligand surface expression, affecting both endogenous and histone deacetylase (HDAC)-inhibitor induced MICA, MICB and ULBP-2 expression. The classical immune escape mechanism of VSV (i.e., the M protein blockade of nucleocytoplasmic mRNA transport) was not involved, as the VSV mutant strain, VSVΔM51, which possess a defective M protein, prevented MICA surface expression similarly to wild-type VSV. The VSV mediated down modulation of NKG2D-ligand expression did not involve apoptosis. Constitutive expression of MICA bypassed the escape mechanism, suggesting that VSV affect NKG2D-ligand expression at an early post-transcriptional level. Our results show that VSV possess an escape mechanism, which could affect the immune recognition of VSV infected cancer cells. This may also have implications for immune recognition of cancer cells after combined treatment with VSV and chemotherapeutic drugs

    Entry of Herpes Simplex Virus Type 1 (HSV-1) into the Distal Axons of Trigeminal Neurons Favors the Onset of Nonproductive, Silent Infection

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    Following productive, lytic infection in epithelia, herpes simplex virus type 1 (HSV-1) establishes a lifelong latent infection in sensory neurons that is interrupted by episodes of reactivation. In order to better understand what triggers this lytic/latent decision in neurons, we set up an organotypic model based on chicken embryonic trigeminal ganglia explants (TGEs) in a double chamber system. Adding HSV-1 to the ganglion compartment (GC) resulted in a productive infection in the explants. By contrast, selective application of the virus to distal axons led to a largely nonproductive infection that was characterized by the poor expression of lytic genes and the presence of high levels of the 2.0-kb major latency-associated transcript (LAT) RNA. Treatment of the explants with the immediate-early (IE) gene transcriptional inducer hexamethylene bisacetamide, and simultaneous co-infection of the GC with HSV-1, herpes simplex virus type 2 (HSV-2) or pseudorabies virus (PrV) helper virus significantly enhanced the ability of HSV-1 to productively infect sensory neurons upon axonal entry. Helper-virus-induced transactivation of HSV-1 IE gene expression in axonally-infected TGEs in the absence of de novo protein synthesis was dependent on the presence of functional tegument protein VP16 in HSV-1 helper virus particles. After the establishment of a LAT-positive silent infection in TGEs, HSV-1 was refractory to transactivation by superinfection of the GC with HSV-1 but not with HSV-2 and PrV helper virus. In conclusion, the site of entry appears to be a critical determinant in the lytic/latent decision in sensory neurons. HSV-1 entry into distal axons results in an insufficient transactivation of IE gene expression and favors the establishment of a nonproductive, silent infection in trigeminal neurons

    Erratum to: "Nuclear Effects on R=\sigma_L/\sigma_T in Deep-Inelastic Scattering" Phys.Lett. B475(2000)386

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    This erratum revokes the main conclusion of a Letter that reported measurements of cross sections for deep-inelastic scattering (DIS) of leptons on 3^3He and 14^{14}N targets, expressed as ratios of σA/σD\sigma_A / \sigma_D to the cross section on the deuterium target.Comment: 3 pages, 1 figur
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