258 research outputs found

    Tagged-photon events in polarized DIS process

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    Deep-inelastic events for the scattering of the longitudinally polarized electron by polarized proton with tagged collinear photon radiated from initial-state electron are considered. The corresponding cross-section is derived in the Born approximation. The model-independent radiative corrections to the Born cross-section are also calculated. Obtained result is applied to the case of elastic scattering.Comment: 14 pages, 2 figures, submitted to JET

    Neuroinflammation, autoinflammation, splenomegaly and anemia caused by bi-allelic mutations in IRAK4

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    We describe a novel, severe autoinflammatory syndrome characterized by neuroinflammation, systemic autoinflammation, splenomegaly, and anemia (NASA) caused by bi-allelic mutations in IRAK4. IRAK-4 is a serine/threonine kinase with a pivotal role in innate immune signaling from toll-like receptors and production of pro-inflammatory cytokines. In humans, bi-allelic mutations in IRAK4 result in IRAK-4 deficiency and increased susceptibility to pyogenic bacterial infections, but autoinflammation has never been described. We describe 5 affected patients from 2 unrelated families with compound heterozygous mutations in IRAK4 (c.C877T (p.Q293*)/c.G958T (p.D320Y); and c.A86C (p.Q29P)/c.161 + 1G>A) resulting in severe systemic autoinflammation, massive splenomegaly and severe transfusion dependent anemia and, in 3/5 cases, severe neuroinflammation and seizures. IRAK-4 protein expression was reduced in peripheral blood mononuclear cells (PBMC) in affected patients. Immunological analysis demonstrated elevated serum tumor necrosis factor (TNF), interleukin (IL) 1 beta (IL-1β), IL-6, IL-8, interferon α2a (IFN-α2a), and interferon β (IFN-β); and elevated cerebrospinal fluid (CSF) IL-6 without elevation of CSF IFN-α despite perturbed interferon gene signature. Mutations were located within the death domain (DD; p.Q29P and splice site mutation c.161 + 1G>A) and kinase domain (p.Q293*/p.D320Y) of IRAK-4. Structure-based modeling of the DD mutation p.Q29P showed alteration in the alignment of a loop within the DD with loss of contact distance and hydrogen bond interactions with IRAK-1/2 within the myddosome complex. The kinase domain mutation p.D320Y was predicted to stabilize interactions within the kinase active site. While precise mechanisms of autoinflammation in NASA remain uncertain, we speculate that loss of negative regulation of IRAK-4 and IRAK-1; dysregulation of myddosome assembly and disassembly; or kinase active site instability may drive dysregulated IL-6 and TNF production. Blockade of IL-6 resulted in immediate and complete amelioration of systemic autoinflammation and anemia in all 5 patients treated; however, neuroinflammation has, so far proven recalcitrant to IL-6 blockade and the janus kinase (JAK) inhibitor baricitinib, likely due to lack of central nervous system penetration of both drugs. We therefore highlight that bi-allelic mutation in IRAK4 may be associated with a severe and complex autoinflammatory and neuroinflammatory phenotype that we have called NASA (neuroinflammation, autoinflammation, splenomegaly and anemia), in addition to immunodeficiency in humans

    Measurement of Angular Distributions and R= sigma_L/sigma_T in Diffractive Electroproduction of rho^0 Mesons

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    Production and decay angular distributions were extracted from measurements of exclusive electroproduction of the rho^0(770) meson over a range in the virtual photon negative four-momentum squared 0.5< Q^2 <4 GeV^2 and the photon-nucleon invariant mass range 3.8< W <6.5 GeV. The experiment was performed with the HERMES spectrometer, using a longitudinally polarized positron beam and a ^3He gas target internal to the HERA e^{+-} storage ring. The event sample combines rho^0 mesons produced incoherently off individual nucleons and coherently off the nucleus as a whole. The distributions in one production angle and two angles describing the rho^0 -> pi+ pi- decay yielded measurements of eight elements of the spin-density matrix, including one that had not been measured before. The results are consistent with the dominance of helicity-conserving amplitudes and natural parity exchange. The improved precision achieved at 47 GeV, reveals evidence for an energy dependence in the ratio R of the longitudinal to transverse cross sections at constant Q^2.Comment: 15 pages, 15 embedded figures, LaTeX for SVJour(epj) document class Revision: Fig. 15 corrected, recent data added to Figs. 10,12,14,15; minor changes to tex

    Beam-Induced Nuclear Depolarisation in a Gaseous Polarised Hydrogen Target

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    Spin-polarised atomic hydrogen is used as a gaseous polarised proton target in high energy and nuclear physics experiments operating with internal beams in storage rings. When such beams are intense and bunched, this type of target can be depolarised by a resonant interaction with the transient magnetic field generated by the beam bunches. This effect has been studied with the HERA positron beam in the HERMES experiment at DESY. Resonances have been observed and a simple analytic model has been used to explain their shape and position. Operating conditions for the experiment have been found where there is no significant target depolarisation due to this effect.Comment: REVTEX, 6 pages, 5 figure

    Measurement of the Proton Spin Structure Function g1p with a Pure Hydrogen Target

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    A measurement of the proton spin structure function g1p(x,Q^2) in deep-inelastic scattering is presented. The data were taken with the 27.6 GeV longitudinally polarised positron beam at HERA incident on a longitudinally polarised pure hydrogen gas target internal to the storage ring. The kinematic range is 0.021<x<0.85 and 0.8 GeV^2<Q^2<20 GeV^2. The integral Int_{0.021}^{0.85} g1p(x)dx evaluated at Q0^2 of 2.5 GeV^2 is 0.122+/-0.003(stat.)+/-0.010(syst.).Comment: 7 pages, 3 figures, 1 table, RevTeX late

    The Flavor Asymmetry of the Light Quark Sea from Semi-inclusive Deep-inelastic Scattering

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    The flavor asymmetry of the light quark sea of the nucleon is determined in the kinematic range 0.02<x<0.3 and 1 GeV^2<Q^2<10 GeV^2, for the first time from semi-inclusive deep-inelastic scattering. The quantity (dbar(x)-ubar(x))/(u(x)-d(x)) is derived from a relationship between the yields of positive and negative pions from unpolarized hydrogen and deuterium targets. The flavor asymmetry dbar-ubar is found to be non-zero and x dependent, showing an excess of dbar over ubar quarks in the proton.Comment: 7 Pages, 2 figures, RevTeX format; slight revision in text, small change in extraction of dbar-ubar and comparison with a high q2 parameterizatio

    Azimuthal anisotropy and correlations in the hard scattering regime at RHIC

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    Azimuthal anisotropy (v2v_2) and two-particle angular correlations of high pTp_T charged hadrons have been measured in Au+Au collisions at sNN\sqrt{s_{NN}}=130 GeV for transverse momenta up to 6 GeV/c, where hard processes are expected to contribute significantly. The two-particle angular correlations exhibit elliptic flow and a structure suggestive of fragmentation of high pTp_T partons. The monotonic rise of v2(pT)v_2(p_T) for pT<2p_T<2 GeV/c is consistent with collective hydrodynamical flow calculations. At \pT>3 GeV/c a saturation of v2v_2 is observed which persists up to pT=6p_T=6 GeV/c.Comment: As publishe

    Activating mutations in BRAF disrupt the hypothalamo-pituitary axis leading to hypopituitarism in mice and humans

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    Germline mutations in BRAF and other components of the MAPK pathway are associated with the congenital syndromes collectively known as RASopathies. Here, we report the association of Septo-Optic Dysplasia (SOD) including hypopituitarism and Cardio-Facio-Cutaneous (CFC) syndrome in patients harbouring mutations in BRAF. Phosphoproteomic analyses demonstrate that these genetic variants are gain-of-function mutations leading to activation of the MAPK pathway. Activation of the MAPK pathway by conditional expression of the BrafV600E/+ allele, or the knock-in BrafQ241R/+ allele (corresponding to the most frequent human CFC-causing mutation, BRAF p.Q257R), leads to abnormal cell lineage determination and terminal differentiation of hormone-producing cells, causing hypopituitarism. Expression of the BrafV600E/+ allele in embryonic pituitary progenitors leads to an increased expression of cell cycle inhibitors, cell growth arrest and apoptosis, but not tumour formation. Our findings show a critical role of BRAF in hypothalamo-pituitary-axis development both in mouse and human and implicate mutations found in RASopathies as a cause of endocrine deficiencies in humans

    Azimuthal anisotropy of K0S and Lambda + Lambda -bar production at midrapidity from Au+Au collisions at sqrt[sNN]=130 GeV

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    We report STAR results on the azimuthal anisotropy parameter v2 for strange particles K0S, Lambda , and Lambda -bar at midrapidity in Au+Au collisions at sqrt[sNN]=130 GeV at the Relativistic Heavy Ion Collider. The value of v2 as a function of transverse momentum, pt, of the produced particle and collision centrality is presented for both particles up to pt~3.0 GeV/c. A strong pt dependence in v2 is observed up to 2.0 GeV/c. The v2 measurement is compared with hydrodynamic model calculations. The physics implications of the pt integrated v2 magnitude as a function of particle mass are also discussed.Alle Autoren: C. Adler, Z. Ahammed, C. Allgower, J. Amonett, B. D. Anderson, M. Anderson, G. S. Averichev, J. Balewski, O. Barannikova, L. S. Barnby, J. Baudot, S. Bekele, V. V. Belaga, R. Bellwied, J. Berger, H. Bichsel, A. Billmeier, L. C. Bland, C. O. Blyth, B. E. Bonner, A. Boucham, A. Brandin, A. Bravar, R. V. Cadman, H. Caines, M. Calderón de la Barca Sánchez, A. Cardenas, J. Carroll, J. Castillo, M. Castro, D. Cebra, P. Chaloupka, S. Chattopadhyay, Y. Chen, S. P. Chernenko, M. Cherney, A. Chikanian, B. Choi, W. Christie, J. P. Coffin, T. M. Cormier, J. G. Cramer, H. J. Crawford, W. S. Deng, A. A. Derevschikov, L. Didenko, T. Dietel, J. E. Draper, V. B. Dunin, J. C. Dunlop, V. Eckardt, L. G. Efimov, V. Emelianov, J. Engelage, G. Eppley, B. Erazmus, P. Fachini, V. Faine, K. Filimonov, E. Finch, Y. Fisyak, D. Flierl, K. J. Foley, J. Fu, C. A. Gagliardi, N. Gagunashvili, J. Gans, L. Gaudichet, M. Germain, F. Geurts, V. Ghazikhanian, O. Grachov, V. Grigoriev, M. Guedon, E. Gushin, T. J. Hallman, D. Hardtke, J. W. Harris, T. W. Henry, S. Heppelmann, T. Herston, B. Hippolyte, A. Hirsch, E. Hjort, G. W. Hoffmann, M. Horsley, H. Z. Huang, T. J. Humanic, G. Igo, A. Ishihara, Yu. I. Ivanshin, P. Jacobs, W. W. Jacobs, M. Janik, I. Johnson, P. G. Jones, E. G. Judd, M. Kaneta, M. Kaplan, D. Keane, J. Kiryluk, A. Kisiel, J. Klay, S. R. Klein, A. Klyachko, A. S. Konstantinov, M. Kopytine, L. Kotchenda, A. D. Kovalenko, M. Kramer, P. Kravtsov, K. Krueger, C. Kuhn, A. I. Kulikov, G. J. Kunde, C. L. Kunz, R. Kh. Kutuev, A. A. Kuznetsov, L. Lakehal-Ayat, M. A. C. Lamont, J. M. Landgraf, S. Lange, C. P. Lansdell, B. Lasiuk, F. Laue, A. Lebedev, R. Lednický, V. M. Leontiev, M. J. LeVine, Q. Li, S. J. Lindenbaum, M. A. Lisa, F. Liu, L. Liu, Z. Liu, Q. J. Liu, T. Ljubicic, W. J. Llope, G. LoCurto, H. Long, R. S. Longacre, M. Lopez-Noriega, W. A. Love, T. Ludlam, D. Lynn, J. Ma, R. Majka, S. Margetis, C. Markert, L. Martin, J. Marx, H. S. Matis, Yu. A. Matulenko, T. S. McShane, F. Meissner, Yu. Melnick, A. Meschanin, M. Messer, M. L. Miller, Z. Milosevich, N. G. Minaev, J. Mitchell, V. A. Moiseenko, C. F. Moore, V. Morozov, M. M. de Moura, M. G. Munhoz, J. M. Nelson, P. Nevski, V. A. Nikitin, L. V. Nogach, B. Norman, S. B. Nurushev, G. Odyniec, A. Ogawa, V. Okorokov, M. Oldenburg, D. Olson, G. Paic, S. U. Pandey, Y. Panebratsev, S. Y. Panitkin, A. I. Pavlinov, T. Pawlak, V. Perevoztchikov, W. Peryt, V. A Petrov, M. Planinic, J. Pluta, N. Porile, J. Porter, A. M. Poskanzer, E. Potrebenikova, D. Prindle, C. Pruneau, J. Putschke, G. Rai, G. Rakness, O. Ravel, R. L. Ray, S. V. Razin, D. Reichhold, J. G. Reid, F. Retiere, A. Ridiger, H. G. Ritter, J. B. Roberts, O. V. Rogachevski, J. L. Romero, A. Rose, C. Roy, V. Rykov, I. Sakrejda, S. Salur, J. Sandweiss, A. C. Saulys, I. Savin, J. Schambach, R. P. Scharenberg, N. Schmitz, L. S. Schroeder, A. Schüttauf, K. Schweda, J. Seger, D. Seliverstov, P. Seyboth, E. Shahaliev, K. E. Shestermanov, S. S. Shimanskii, V. S. Shvetcov, G. Skoro, N. Smirnov, R. Snellings, P. Sorensen, J. Sowinski, H. M. Spinka, B. Srivastava, E. J. Stephenson, R. Stock, A. Stolpovsky, M. Strikhanov, B. Stringfellow, C. Struck, A. A. P. Suaide, E. Sugarbaker, C. Suire, M. Šumbera, B. Surrow, T. J. M. Symons, A. Szanto de Toledo, P. Szarwas, A. Tai, J. Takahashi, A. H. Tang, J. H. Thomas, M. Thompson, V. Tikhomirov, M. Tokarev, M. B. Tonjes, T. A. Trainor, S. Trentalange, R. E. Tribble, V. Trofimov, O. Tsai, T. Ullrich, D. G. Underwood, G. Van Buren, A. M. VanderMolen, I. M. Vasilevski, A. N. Vasiliev, S. E. Vigdor, S. A. Voloshin, F. Wang, H. Ward, J. W. Watson, R. Wells, G. D. Westfall, C. Whitten, Jr., H. Wieman, R. Willson, S. W. Wissink, R. Witt, J. Wood, N. Xu, Z. Xu, A. E. Yakutin, E. Yamamoto, J. Yang, P. Yepes, V. I. Yurevich, Y. V. Zanevski, I. Zborovský, H. Zhang, W. M. Zhang, R. Zoulkarneev, and A. N. Zubarev (STAR Collaboration

    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
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