The interplay of soft and hard contributions in the electromagnetic pion form factor

We consider various relativistic models for the valence Fock-state wave function of the pion. These models are obtained from simple instant-form wave functions by applying a Melosh rotation to the spin part and by imposing physical constraints on the parameters. We discuss how the soft and the hard (perturbative) parts of the electromagnetic form factor are affected by the choice of the model and by the Melosh rotation.Comment: 3 pages, 2 eps-figures, uses espcrc2.st

Space- and time-like electromagnetic pion form factors in light-cone pQCD

We present a combined analysis of the space- and time-like electromagnetic pion form factors in light-cone perturbative QCD with transverse momentum dependence and Sudakov suppression. Including the non-perturbative ``soft' QCD and power suppressed twist-3 corrections to the standard twist-2 perturbative QCD result, the experimental pion data available at moderate energies/momentum transfers can be explained reasonably well. This may help towards resolving the bulk of the existing discrepancy between the space- and time-like experimental data.Comment: 14 pages, 3 figure

The Role of Citrullinated Proteins Suggests a Novel Mechanism in the Pathogenesis of Multiple Sclerosis

The pathogenesis of MS is unknown. In our studies, we have demonstrated an important role for citrullinated myelin basic protein (MBP). The accompanying loss of positive charge compromises the ability of MBP to interact with the lipid bilayer. The conversion of arginine to citrulline in brain is carried out by an enzyme peptidyl arginine deiminase (PAD) 2. The amount of PAD 2 in brain was increased in MS normal-appearing white matter. The mechanism responsible for this increase involved hypomethylation of the promoter region in the PAD 2 gene in MS, but no change (compared to normal) was found in thymus tissue DNA from the same MS patients. In addition, no change was observed in other neurological diseases, including Alzheimer’s, Parkinson’s, and Huntington’s. We propose that citrullinated MBP, resulting from elevated levels of PAD 2 represents an important biochemical pathway in the pathogenesis of MS

Non-structural protein 1 of avian influenza A viruses differentially inhibit NF-κB promoter activation

<p>Abstract</p> <p>Background</p> <p>Influenza virus infection activates NF-κB and is a general prerequisite for a productive influenza virus infection. On the other hand, non-structural protein 1 (NS1) suppresses this viral activated NF-κB, presumably to prevent expression of NF-κB mediated anti-viral response. NS1 proteins of influenza A viruses are divided into two groups, known as allele A and allele B. The possible functional relevance of this NS1 division to viral pathogenicity is lacking.</p> <p>Findings</p> <p>The ability of NS1 protein from two avian influenza subtypes, H6N8 and H4N6, to inhibit NF-κB promoter activation was assessed. Further, efforts were made to characterize the genetic basis of this inhibition. We found that allele A NS1 proteins of H6N8 and H4N6 are significantly better in preventing dsRNA induced NF-κB promoter activation compared to allele B of corresponding subtypes, in a species independent manner. Furthermore, the ability to suppress NF-κB promoter activation was mapped to the effector domain while the RNA binding domain alone was unable to suppress this activation. Chimeric NS1 proteins containing either RNA binding domain of allele A and effector domain of allele B or vice versa, were equally potent in preventing NF-κB promoter activation compared to their wt. NS1 protein of allele A and B from both subtypes expressed efficiently as detected by Western blotting and predominantly localized in the nucleus in both A549 and MiLu cells as shown by <it>in situ </it>PLA.</p> <p>Conclusions</p> <p>Here, we present another aspect of NS1 protein in inhibiting dsRNA induced NF-κB activation in an allele dependent manner. This suggests a possible correlation with the virus's pathogenic potential.</p

Identification and characterization of a novel non-structural protein of bluetongue virus

Bluetongue virus (BTV) is the causative agent of a major disease of livestock (bluetongue). For over two decades, it has been widely accepted that the 10 segments of the dsRNA genome of BTV encode for 7 structural and 3 non-structural proteins. The non-structural proteins (NS1, NS2, NS3/NS3a) play different key roles during the viral replication cycle. In this study we show that BTV expresses a fourth non-structural protein (that we designated NS4) encoded by an open reading frame in segment 9 overlapping the open reading frame encoding VP6. NS4 is 77–79 amino acid residues in length and highly conserved among several BTV serotypes/strains. NS4 was expressed early post-infection and localized in the nucleoli of BTV infected cells. By reverse genetics, we showed that NS4 is dispensable for BTV replication in vitro, both in mammalian and insect cells, and does not affect viral virulence in murine models of bluetongue infection. Interestingly, NS4 conferred a replication advantage to BTV-8, but not to BTV-1, in cells in an interferon (IFN)-induced antiviral state. However, the BTV-1 NS4 conferred a replication advantage both to a BTV-8 reassortant containing the entire segment 9 of BTV-1 and to a BTV-8 mutant with the NS4 identical to the homologous BTV-1 protein. Collectively, this study suggests that NS4 plays an important role in virus-host interaction and is one of the mechanisms played, at least by BTV-8, to counteract the antiviral response of the host. In addition, the distinct nucleolar localization of NS4, being expressed by a virus that replicates exclusively in the cytoplasm, offers new avenues to investigate the multiple roles played by the nucleolus in the biology of the cell

Measurement of single-spin azimuthal asymmetries in semi-inclusive electroproduction of pions and kaons on a longitudinally polarised deuterium target

Single-spin asymmetries have been measured for semi-inclusive electroproduction of $\pi^+$, $\pi^-$, $\pi^0$ and $K^+$ mesons in deep-inelastic scattering off a longitudinally polarised deuterium target. The asymmetries appear in the distribution of the hadrons in the azimuthal angle $\phi$ around the virtual photon direction, relative to the lepton scattering plane. The corresponding analysing powers in the $\sin \phi$ moment of the cross section are $0.012 \pm 0.002 {(stat.)} \pm 0.002 {(syst.)}$ for $\pi^+$, $0.006 \pm 0.003 {(stat.)} \pm 0.002 {(syst.)}$ for $\pi^-$, $0.021 \pm 0.005 {(stat.)} \pm 0.003 {(syst.)}$ for $\pi^0$ and $0.013 \pm 0.006 {(stat.)} \pm 0.003 {(syst.)}$ for $K^+$. The $\sin 2\phi$ moments are compatible with zero for all particles.Comment: Revised version shortened 9 pages, 3 tables, 7 figure

Subleading-twist effects in single-spin asymmetries in semi-inclusive deep-inelastic scattering on a longitudinally polarized hydrogen target

Single-spin asymmetries in the semi-inclusive production of charged pions in deep-inelastic scattering from transversely and longitudinally polarized proton targets are combined to evaluate the subleading-twist contribution to the longitudinal case. This contribution is significantly positive for (\pi^+) mesons and dominates the asymmetries on a longitudinally polarized target previously measured by \hermes. The subleading-twist contribution for (\pi^-) mesons is found to be small

Single-spin asymmetries in semi-inclusive deep-inelastic scattering on a transversely polarized hydrogen target

Single-spin asymmetries for semi-inclusive electroproduction of charged pions in deep-inelastic scattering of positrons are measured for the first time with transverse target polarization. The asymmetry depends on the azimuthal angles of both the pion ($\phi$) and the target spin axis ($\phi_S$) about the virtual photon direction and relative to the lepton scattering plane. The extracted Fourier component \cmpi is a signal of the previously unmeasured quark transversity distribution, in conjunction with the so-called Collins fragmentation function, also unknown. The Fourier component \smpi of the asymmetry arises from a correlation between the transverse polarization of the target nucleon and the intrinsic transverse momentum of quarks, as represented by the previously unmeasured Sivers distribution function. Evidence for both signals is observed, but the Sivers asymmetry may be affected by exclusive vector meson productio

First Measurement of the Tensor Structure Function b1b_1 of the Deuteron

The \Hermes experiment has investigated the tensor spin structure of the deuteron using the 27.6 GeV/c positron beam of \Hera. The use of a tensor polarized deuteron gas target with only a negligible residual vector polarization enabled the first measurement of the tensor asymmetry \At and the tensor structure function \bd for average values of the Bj{\o}rken variable $0.01<0.45$ and of the squared four-momentum transfer $0.5 {\rm GeV^2} <5 {\rm GeV^2}$. The quantities \At and \bd are found to be non-zero. The rise of \bd for decreasing values of $x$ can be interpreted to originate from the same mechanism that leads to nuclear shadowing in unpolarized scattering