Inclusive jet cross sections and dijet correlations in D∗±D^{*\pm} photoproduction at HERA

Inclusive jet cross sections in photoproduction for events containing a $D^*$ meson have been measured with the ZEUS detector at HERA using an integrated luminosity of $78.6 {\rm pb}^{-1}$. The events were required to have a virtuality of the incoming photon, $Q^2$, of less than 1 GeV$^2$, and a photon-proton centre-of-mass energy in the range $130<W_{\gamma p}<280 {\rm GeV}$. The measurements are compared with next-to-leading-order (NLO) QCD calculations. Good agreement is found with the NLO calculations over most of the measured kinematic region. Requiring a second jet in the event allowed a more detailed comparison with QCD calculations. The measured dijet cross sections are also compared to Monte Carlo (MC) models which incorporate leading-order matrix elements followed by parton showers and hadronisation. The NLO QCD predictions are in general agreement with the data although differences have been isolated to regions where contributions from higher orders are expected to be significant. The MC models give a better description than the NLO predictions of the shape of the measured cross sections.Comment: 43 pages, 12 figures, charm jets ZEU

Dissociation of virtual photons in events with a leading proton at HERA

The ZEUS detector has been used to study dissociation of virtual photons in events with a leading proton, gamma^* p -> X p, in e^+p collisions at HERA. The data cover photon virtualities in two ranges, 0.03<Q^2<0.60 GeV^2 and 2<Q^2<100 GeV^2, with M_X>1.5 GeV, where M_X is the mass of the hadronic final state, X. Events were required to have a leading proton, detected in the ZEUS leading proton spectrometer, carrying at least 90% of the incoming proton energy. The cross section is presented as a function of t, the squared four-momentum transfer at the proton vertex, Phi, the azimuthal angle between the positron scattering plane and the proton scattering plane, and Q^2. The data are presented in terms of the diffractive structure function, F_2^D(3). A next-to-leading-order QCD fit to the higher-Q^2 data set and to previously published diffractive charm production data is presented

Study of deep inelastic inclusive and diffractive scattering with the ZEUS forward plug calorimeter

Deep inelastic scattering and its diffractive component, ep -> e'gamma*p ->e'XN, have been studied at HERA with the ZEUS detector using an integrated luminosity of 4.2 pb-1. The measurement covers a wide range in the gamma*p c.m. energy W (37 - 245 GeV), photon virtuality Q2 (2.2 - 80 GeV2) and mass Mx. The diffractive cross section for Mx > 2 GeV rises strongly with W; the rise is steeper with increasing Q2. The latter observation excludes the description of diffractive deep inelastic scattering in terms of the exchange of a single Pomeron. The ratio of diffractive to total cross section is constant as a function of W, in contradiction to the expectation of Regge phenomenology combined with a naive extension of the optical theorem to gamma*p scattering. Above Mx of 8 GeV, the ratio is flat with Q2, indicating a leading-twist behaviour of the diffractive cross section. The data are also presented in terms of the diffractive structure function, F2D(3)(beta,xpom,Q2), of the proton. For fixed beta, the Q2 dependence of xpom F2D(3) changes with xpom in violation of Regge factorisation. For fixed xpom, xpom F2D(3) rises as beta -> 0, the rise accelerating with increasing Q2. These positive scaling violations suggest substantial contributions of perturbative effects in the diffractive DIS cross section.Comment: 87 pages, 25 figure

The role of WNK in modulation of KCl cotransport activity in red cells from normal individuals and patients with sickle cell anaemia

Abstract: Abnormal activity of red cell KCl cotransport (KCC) is involved in pathogenesis of sickle cell anaemia (SCA). KCC-mediated solute loss causes shrinkage, concentrates HbS, and promotes HbS polymerisation. Red cell KCC also responds to various stimuli including pH, volume, urea, and oxygen tension, and regulation involves protein phosphorylation. The main aim of this study was to investigate the role of the WNK/SPAK/OSR1 pathway in sickle cells. The pan WNK inhibitor WNK463 stimulated KCC with an EC50 of 10.9 ± 1.1 nM and 7.9 ± 1.2 nM in sickle and normal red cells, respectively. SPAK/OSR1 inhibitors had little effect. The action of WNK463 was not additive with other kinase inhibitors (staurosporine and N-ethylmaleimide). Its effects were largely abrogated by pre-treatment with the phosphatase inhibitor calyculin A. WNK463 also reduced the effects of physiological KCC stimuli (pH, volume, urea) and abolished any response of KCC to changes in oxygen tension. Finally, although protein kinases have been implicated in regulation of phosphatidylserine exposure, WNK463 had no effect. Findings indicate a predominant role for WNKs in control of KCC in sickle cells but an apparent absence of downstream involvement of SPAK/OSR1. A more complete understanding of the mechanisms will inform pathogenesis whilst manipulation of WNK activity represents a potential therapeutic approach

Alpha-Synuclein Aggregation Induced By Brief Ischemia Negatively Impacts Neuronal Survival in Vivo: A Study in [A30P] Alpha-Synuclein Transgenic Mouse

Alpha-synuclein oligomerization and aggregation are considered to have a role in the pathogenesis of neurodegenerative diseases. However, despite numerous in vitro studies, the impact of aggregates in the intact brain is unclear. In vitro, oxidative/nitrative stress and acidity induce alpha-synuclein oligomerization. These conditions favoring alpha-synuclein fibrillization are present in the ischemic brain, which may serve as an in vivo model to study alpha-synuclein aggregation. In this study, we show that 30-minute proximal middle cerebral artery (MCA) occlusion and 72 hours reperfusion induce oligomerization of wild-type alpha-synuclein in the ischemic mouse brain. The nonamyloidogenic isoform beta-synuclein did not form oligomers. Alpha-synuclein aggregates were confined to neurons and colocalized with ubiquitin immunoreactivity. We also found that 30 minutes proximal MCA occlusion and 24 hours reperfusion induced larger infarcts in C57BL/6(Thy1)-h[A30P]alphaSYN transgenic mice, which have an increased tendency to form synuclein fibrils. Trangenics also developed more selective neuronal necrosis when subjected to 20 minutes distal MCA occlusion and 72 hours reperfusion. Enhanced 3-nitrotyrosine immunoreactivity in transgenic mice suggests that oxidative/nitrative stress may be one of the mechanisms mediating aggregate toxicity. Thus, the increased vulnerability of transgenic mice to ischemia suggests that alpha-synuclein aggregates not only form during ischemia but also negatively impact neuronal survival, supporting the idea that alpha-synuclein misfolding may be neurotoxic. Journal of Cerebral Blood Flow & Metabolism (2011) 31, 913-923; doi:10.1038/jcbfm.2010.170; published online 29 September 2010WoSScopu